"My help comes from the LORD, the Maker of heaven and earth"

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1.Causes of Heart Failure, signs and symptoms and Medical reduced proportion of the blood that fills its ventricles during
Treatment of heart failure. (2) diastole. The increase in blood at the end of systole leads to
Definition: It is defined as failure of the heart to pump blood forward ventricular stretch, dilatation, and eccentric remodelling.
(cardiac output) at a sufficient rate to meet metabolic demands of Diastolic heart failure refers to impaired ventricular relaxation or
peripheral tissues, leading to congestion of various organ. filling. This leads to the term heart failure with preserved ejection
Classification: There are many different ways to classify heart fraction or HFpEF. Ventricular hypertrophy tends to develop and
failure, which reflect the complexity of the condition: diastolic heart failure is characterised by concentric remodelling.
Right vs left
Left-sided heart failure is the most common form of heart failure
that is associated with a reduced or preserved pumping function of
the left ventricle. It may be caused by a wide range of conditions.
Right-sided heart failure commonly occurs as a result of advanced
left-sided failure. Primary right-sided heart failure is uncommon.
The combination of left and right failure is known as congestive
cardiac failure.
Causes:
1. Vascular: These are the most common causes of heart failure.
• Ischaemic heart disease (35-40%)
• Hypertension (15-20%)
Acute vs chronic 2. Muscular: Cardiomyopathy is a common cause of heart failure.
Acute heart failure is characterised by a rapid onset of symptoms Dilated cardiomyopathies are often idiopathic.
and signs of heart failure that is usually life-threatening. The most • Dilated cardiomyopathy (30%)
common causes of acute heart failure include acute myocardial • Hypertrophic cardiomyopathy
dysfunction (ischaemic, inflammatory), acute valvular, pericardial • Congenital heart disease
tamponade. 3. Valvular: Valvular disease may lead to either acute or chronic
Chronic heart failure is due to progressive cardiac dysfunction heart failure.
from structural and/or functional cardiac abnormalities. There is a • Stenotic valves
reduction in cardiac output and/or elevated intracardiac pressure at • Regurgitant valves
rest or on stress. Chronic heart failure is usually precipitated by 4. Electrical: Arrhythmias (abnormalities of normal conduction)
conditions that affect the muscle (e.g. cardiomyopathy), vessels (e.g. may cause acute heart failure through decompensation.
ischaemic heart disease), valves (e.g. aortic stenosis), and 5. High-output: Typically heart failure is caused by a reduced
conduction (e.g. atrial fibrillation). cardiac output. In some cases, however, the cardiac output may be
Systolic vs diastolic raised but the systemic vascular resistance very low. Causes include:
Systolic heart failure refers to a reduction in the left ventricular • Anaemia • Thyrotoxicosis
ejection fraction (LVEF). In other words, the heart is pumping out a • Septicaemia • Liver failure
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Pathophysiology:
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Precipitating factors for heart failure: - Difficulty performing activities that were once
manageable.
✓ Intercurrent infections ✓ Drugs with negative 7. Sudden Weight Gain:
✓ Pulmonary embolism inotropic effect (beta - Fluid retention can lead to a sudden increase in body
✓ Anaemia blockers) weight.
✓ Pregnancy ✓ Subacute bacterial Signs:
✓ Myocardial ischaemia endocarditis 1. Elevated Jugular Venous Pressure (JVP):
or infarction ✓ Hypertension - Visible pulsation of the jugular veins in the neck due to
✓ Thyrotoxicosis ✓ Fluid retention due to increased pressure in the right side of the heart.
✓ Myocarditis high salt intake 2. Peripheral Edema:
✓ Arrhythmias - Swelling in the extremities, often noticed in the ankles,
feet, and legs.
Symptoms: 3. Hepatomegaly:
1. Shortness of Breath (Dyspnea): - Enlargement of the liver due to congestion.
- Especially during physical activity or when lying flat. 4. Ascites:
- Paroxysmal nocturnal dyspnea: Sudden onset of severe - Accumulation of fluid in the abdominal cavity.
shortness of breath during sleep, often leading to waking up 5. Cyanosis:
gasping for breath. - Bluish discoloration of the lips and skin, indicating poor
2. Fatigue and Weakness: oxygenation.
- Generalized tiredness and a reduced ability to carry out 6. Crackles in the Lungs:
daily activities. - Heard on auscultation, crackling sounds may be present
3. Swelling (Edema): due to fluid accumulation in the lungs.
- Accumulation of fluid, often noticeable in the legs, 7. S3 Gallop:
ankles, and feet (peripheral edema). - An additional heart sound (S3) may be heard on
- Abdominal swelling may also occur (ascites). auscultation, indicating impaired ventricular filling.
4. Persistent Cough: 8. Orthopnea:
- Often a dry, hacking cough or a cough with frothy or - Difficulty breathing while lying flat, often relieved by
blood-tinged sputum. sitting up or propping oneself up with pillows.
5. Increased Heart Rate: 9. Paradoxical Pulse:
- Tachycardia, or a rapid heartbeat, may be experienced. - A drop in systolic blood pressure during inspiration,
6. Reduced Exercise Tolerance: indicating cardiac tamponade or severe heart failure.
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10. Cheyne-Stokes breathing Imaging

- Cheyne-Stokes breathing is a specific pattern of Echocardiogram:
breathing characterized by a gradual increase in tidal o Evidence of previous MI
volume followed by a gradual decrease, leading to a o Left ventricular strain / hypertrophy
temporary stop in breathing known as apnea. This cycle o Conduction abnormalities / AF
then repeats. CXR:
Diagnosis: o Cardiomegaly (Cardiothoracic ratio > 50% on PA
Clinical evaluation:In patients with suspected heart film)
failure, the first step is taking a detailed history and o Alveolar shadowing oedema
performing a clinical examination. o Kerley B lines (fluid in septae of secondary lobules)
BNP:B-type natriuretic peptide (BNP) is a protein released o Pleural effusion
by cardiomyocytes in response to excessive stretching. It is o Upper lobe diversion
used to assess the likelihood of heart failure. Diagnostic Criteria based on NYHA
Echocardiography Class I No Limitation of Physical Activity
A transthoracic echocardiography (TTE) is the main No Symptoms of Physical Activity
investigation for the confirmation of heart failure. It should Class II Mild Limitation of Physical Activity
be completed in patients with an elevated BNP. This helps Comfortable At Rest
to differentiate suspected heart failure into three groups: Class III Marked Limitation of Physical Activity
• Heart failure with reduced ejection fraction (HFrEF): Comfortable Only At Rest
LVEF <40% Class IV Unable To Do Physical Activity
• Heart failure with minimally reduced ejection fraction Symptoms Even at Rest
(HFmrEF): LVEF 40-49% Treatment:
• Heart failure with preserved ejection fraction (HFpEF): General measures:
LVEF ≥50% • Rest at home or hospitalisation.
Bloods • Meals should be small; avoidance of salt food and anxiety
1. CBC - exclude anaemia, infective cause. of the patient be relieved by reassurance or by tranquillisers.
2. U&Es - exclude renal failure as a cause of oedema. • Weight reduction is advised to obese patients.
3. LFT - exclude liver failure as a cause of oedema. • Alcohol and smoking should be avoided.
4. Cholesterol and HbA1c - cardiovascular risk • Risk of deep vein thrombosis can be reduced by
stratification. anticoagulation, leg exercises and elastic stockings.
5. TFT - exclude thyroid disease.
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Medical treatment: 5.Angiotensin receptor blockers (ARBs) such as losartan

1. Angiotensin-converting enzyme (ACE) inhibitors: may be used in those individuals who have intolerable side
• Example: Enalapril 2.5 mg OD effects with ACE inhibitors.
• Started once the diagnosis is established; improve 6.Digoxin
prognosis and symptoms. Digoxin can be used to provide rate control in patients with
• Check renal function prior to initiation; repeat tests heart failure and atrial fibrillation. In patients with severe
within 1-2 weeks. heart failure. Toxic effect occurs due to large dose used for
• Double dose every 2-4 weeks until target dose is long period.
achieved (e.g. Enalapril 5 mg BD). Treatment based on NYHA Diagnostic Criteria:
2. Beta-blockers: Class I ACE Inhibitors + β Blockers
• Example: Metoprolol 1.25 mg OD Class II ACE Inhibitors + β Blockers + Diuretics (loop
• Improve prognosis and symptoms. diuretics)
• Contra-indicated in severe asthma, COPD, pulmonary Class III ACE Inhibitors + β Blockers + Diuretics (loop
oedema, or bradycardia. diuretics) + MRA
• Double dose every 4 weeks until target dose is Class IV ACE Inhibitors + β Blockers + Diuretics (loop
achieved (e.g. Bisoprolol 5 mg BD). diuretics) + MRA + Digitalis
3. Mineralocorticoid receptor antagonists (MRA): Advanced treatment
• Example: Spironolactone 25 mg OD 1. Coronary revascularization CABG or PCI may
• May be added to ACE and beta-blocker if symptoms improve function in selected patient.
persist. 2. Biventricular pacing or implantable cardioverter
• Contra-indicated in hyperkalaemia, hyponatraemia, defibrillator. Biventricular pacing is indicated in severe
acute kidney injury. heart failure due to nonreversible cause or resistant heart
• Increase dose to 50 mg as tolerated within four weeks failure.
of initiation. The implantable cardioverter defibrillator (ICD) is
4. Diuretics: useful for life-threatening ventricular arrhythmias in
▪ Example: Furosemide 20 mg OD patients with CHF.
▪ Can be started immediately if the patient has 3. Left ventricular assist device (LVAD) and artificial
symptomatic fluid overload; titrated up or down heart. These devices are used in patients with
according to the degree of oedema. transplantation or corrective surgery.
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4. Cardiac transplantation: Cardiac transplantation is the 4. Right Ventricular Hypertrophy: "Tetralogy" refers to
only hope for survival for younger patients with severe four heart problems. The fourth problem is that the right
intractable heart failure. ventricle becomes enlarged as it tries to pump blood into the
pulmonary artery.
2.Discuss the structural Anatomy, symptoms, diagnosis Embryology:
and Treatment of Tetralogy of Fallot (4) TOF occurs as the result of anterocephalad malalignment
Introduction: of the infundibular septum, resulting in a ventricular septal
Tetralogy of Fallot was first described by Louis Arthur defect, right ventricular outflow tract obstruction
Etienne Fallot in 1888, as a malformation created by a very (Pulmonary Stenosis) and overriding of the aorta.
unique combination of anatomic malformations in the heart. Hemodynamics/Pathophysiology:
It is the most common cyanotic congenital heart disease. Its Normally, oxygen-poor (blue) blood returns to the
four essential components (tetrad) are right atrium from the body, travels to the right ventricle,
1. Pulmonary stenosis (usually infundibular), then it is pumped through the pulmonary artery into the
2. Ventricular Septal Defect, lungs where it receives oxygen. Oxygen-rich (red) blood
3. Right Ventricular Hypertrophy returns to the left atrium from the lungs, passes into the left
4. Dextroposition/ overriding of the aorta. ventricle, and then is pumped through the aorta out to the
Epidemiology: body. In tetralogy of fallot, blood flow within the heart
Tetralogy of Fallot occurs in 3 of every 10,000 live births is varies, and is largely dependent on the size of the
the most common cause of cyanotic cardiac disease in ventricular septal defect and how severe the pulmonary
patients beyond the neonatal age. stenosis.
Anatomy: Acyanotic Fallot:
1.Ventricular Septal Defect (VSD): An opening in the With mild pulmonary stenosis, the pressure in the
ventricular septum or dividing wall between the two lower right ventricle can be slightly higher than the left. Some of
chambers of the heart known as the right and left ventricles. the oxygen-poor (blue) blood in the right ventricle will pass
2. Pulmonary Stenosis: A muscular obstruction in the right through the VSD to the left ventricle, mix with the oxy-
ventricle, just below the pulmonary valve, that decreases gen-rich (red) blood there and then flow into the aorta. The
the normal flow of blood. The pulmonary valve may also rest of the oxygen-poor (blue) blood will go its normal route
be small. to the lungs. These children may have slightly lower oxy-
3. Overriding aorta: The aorta is shifted towards the right gen levels than usual, but may not appear blue.
side of the heart so that it sits over the ventricular septal
defect.
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Cyanotic Fallot: 3. Clubbing of Fingers and Toes: Chronic hypoxemia can

With more serious pulmonary stenosis, it is harder for lead to clubbing, a condition characterized by enlargement
oxygen-poor (blue) blood to flow into the pulmonary artery, and rounding of the fingertips and toes.
so more of it passes through the VSD into the left ventricle, 4. Poor Weight Gain and Growth: Infants and children
mixing with oxygen-rich (red) blood and then moving on with TOF may have difficulty gaining weight and growing
out to the body. These children will have lower than normal at a normal rate due to inadequate oxygen delivery to
oxygen levels in the bloodstream and may appear blue, tissues.
especially whenever the pressure in the right ventricle is 5. Fatigue and Weakness: Inadequate oxygenation can
very high and large amounts of oxygen-poor (blue) blood lead to fatigue and weakness, particularly during exertion.
passes through the VSD to the left side of the heart. 6. Cyanosis: Cyanosis, or bluish discoloration of the skin,
Causes of Tetralogy of Fallot lips, and nail beds, is one of the hallmark signs of TOF. It
Some congenital heart defects may have a genetic occurs due to decreased oxygen levels in the blood caused
link, either occurring due to a defect in a gene, a by mixing of oxygenated and deoxygenated blood in the
chromosome abnormality or environmental exposure, heart.
causing heart problems to occur more often in certain 7. Heart Murmur: A heart murmur, caused by turbulent
families. blood flow through the defects in the heart, may be heard
Maternal abuse of alcohol during pregnancy, leading upon auscultation.
to fetal alcohol syndrome (FAS), is linked to tetralogy of 8. Syncope (Fainting): In severe cases of TOF, reduced
fallot. Mothers who take medications to control seizures oxygen supply to the brain during physical exertion may
and mothers with phenylketonuria (PKU) are also more lead to episodes of syncope.
likely to have a baby with tetralogy of fallot. 9. Difficulty Feeding: Infants with TOF may have
Clinical features difficulty feeding due to inadequate oxygenation and
1. Tet Spells (Hypercyanotic Spells): Tet spells are sudden increased work of breathing.
episodes of increased cyanosis and respiratory distress 10. Irritability: Infants and children with TOF may exhibit
triggered by factors such as crying, feeding, or physical irritability due to discomfort from cyanosis and difficulty
activity. These spells can be life-threatening if not promptly breathing.
managed. Diagnosis:
2. Dyspnea (Shortness of Breath): Individuals with TOF Blood studies show polycythemia and high hematocrit
may experience dyspnea, especially during physical (packed cell volume).
activity or feeding, due to inadequate oxygen supply to the Chest X-ray reveals oligemic lung fields (poorly
body. vascularized lungs), a small boot-shaped heart (coeur en
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sabot) with the tip of the boot turned up above the Management of the Hypercyanotic Spell
diaphragm (because of RVH) and concavity of the o Parents are taught to place their child in the knee-chest
pulmonary artery segment (small pulmonary conus). One position in an effort to increase SVR and decreases
in every 4 or 5 cases of TOF has right aortic arch. systemic venous return to the right heart (decreases
ECG shows right axis deviation, RVH with tall and beaked deoxygenated blood from entering heart)
P waves. o Oxygen is initiated to decrease peripheral pulmonary
The two-dimensional echocardiography shows the vasoconstriction, and improve oxygenation once flow of
anterior-superior displacement of the outflow ventricular blood to the lungs is reestablished.
septum, causing stenosis of the subpulmonic right o Immediate intravenous access for fluid administration.
ventricular outflow. This helps to improve right ventricular preload.
Cardiac catheterization and selective angiocardiography o Intravenous morphine is administered to decrease the
are of great value to elucidate anatomic anomalies in tract release of catecholamines. Decrease in HR will increase
and associated anterior VSD in doubtful cases. Cardiac time for right ventricular filling. Decreased HR also
catheterization shows remarkable fall in systolic pressure promotes relaxation of the infundibular spasm.
in the right ventricle as the catheter enters the pulmonary o Alternatively, IV esmolol infusion (short-acting B-
artery. blockers) can be used.
Ventriculography shows the anatomy of TOF at its best. o If the patient remains hypercyanotic after these
Aortography/coronary arteriography outlines the course measures, he/she should be paralyzed and intubated.
of the coronary arteries. o Phenylephrine/ketamine infusion aids in increasing
Complication: SVR.
▪ Heart failure Surgery:
▪ Infective endocarditis ✓ Modified blalock-Taussig shunt: It consists of
▪ Stroke anastomosing the subclavian and the pulmonary arteries.
▪ Polycythaemia This is the most popular systemic – to- pulmonary artery
▪ Death shunt today. It can be performed successfully even in a
Management: preterm neonate.
▪ Hb is maintained at or more than 14 g/dl oral iron ✓ Balloon dilation of pulmonary valve:
supplementation may be required to prevent iron i.Stenting of patent arterial duct in case it is present.
deficiency anemia. ii.Potts' operation-here, a side-to-side anastomosis of
▪ ẞ-blockers to be given in highest tolerated doses (usual pulmonary artery with aorta is created.
dose 1-4 mg/kg/day in 2-3 divided doses).
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✓ Waterson's operation: It consists of constructing a shunt • ECG: Prolongation of the PR interval. Prolonged PR
between the ascending aorta and the right pulmonary interval in itself is not a criterion for carditis.
artery. • Acute phase reactants: Laboratory evidence of acute
inflammation, such as elevated ESR or CRP, meets
3.Discuss the Etiology, pathogenesis, clinical features requirements for a minor criterion.
and treatment of Rheumatic heart disease. (4)
• Fever. The temperature is usually in the range of more
The acquired heart disease in young and middle-aged
than or equal to 38°C.
people is rheumatic heart disease which occurs in two
• Unexplained epistaxis.
forms:
• Weakness, fatigue, pallor, loss of appetite, abdominal
1.Acute rheumatic fever/acute rheumatic heart disease.
pain and weight loss.
2.Chronic rheumatic valvular heart disease.
Major Manifestation:
Acute Rheumatic Fever/Acute Rheumatic Heart
Carditis: It is common which may involve the
Disease.
endocardium (valves), myocardium and pericardium. In
Definition: Rheumatic fever is a systemic inflammatory
children there can be involvement of all the three layersen
disease caused by the antibody to Group A beta-hemolytic
the heart called rheumatic pancarditis. It is evidence by
Streptococcus. It affects mainly heart, joints and collagen
presence of
tissue, nervous system, kidney and skin.
Pathogenesis: • Muffled heart sound (ventricle gallop exists that is
It appears after a lapse of 2-3 weeks following streptococcal S3).
throat infection leading to formation of antibodies against • Friction rub (main manifestation of pericarditis).
the organism which cross-react with cardiac and other • Pericardial pain.
tissues leading to clinical manifestations of acute rheumatic • Changes in E.C.G.
fever. One attack does not confer immunity, hence, repeated Arthritis:
attacks are common. The younger the patient, more i. Affected joint is red, warm, swollen, very tender, with
frequent are the attacks. limited movements and effusion.
“RHEUMATIC FEVER LICKS THE JOINTS BUT ii. Migratory. Several joints are commonly involved, either
BITES THE HEART" together or one after another.
Clinical Manifestation: iii. Typically, the large joints are affected as knees, wrists,
Minor Manifestation: ankles and elbows. It rarely affects fingers, toes or spine.
• Arthralgia: Painful joints without swelling. iv. It disappears within 12-24 hours from start of salicylate
therapy.
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v. If untreated it doesn't persist in the same joint for more To diagnose rheumatic fever, it is necessary to have:
than 1 week. 1. Two major criteria + evidence of preceding Group A
vi. Rheumatic arthritis leaves the joint intact and doesn't Beta- Hemolytic Streptococcus pyogenes or infection.
result in chronic disease. 2. One major + 2 minor criteria + evidence of preceding
Rheumatic (Sydenham's) chorea: Chorea is characterized Group A Beta- Hemolytic Streptococcus pyogenes or
by sudden, aimless, involuntary and irregular muscular infection.
movements of the extremities. 3.Evidence for streptococcal infection by
Subcutaneous nodules: Nodules are generally identified as i. Antistreptolysin O
small (0.5 - 1 cm) and firm without any tenderness or ii. Anti – DNAse B antibody
attachment to the skin. iii. Throat culture
They can be palpated over the extensor surfaces of joints 4.Electrocardiography: Prolonged PR interval in the ECG
such as elbows, knees, ankles is a nondiagnostic criterion.
Erythema marginatum: The lesions are non-pruritic and 5.Echocardiography: Cardiac dilation and valve
appear initially as undifferentiated macules on the trunk and abnormalities.
inner aspect of the extremities (never on face). Treatment:
Diagnosis: The aims of treatment are;
JONES CRITERIA FOR DIAGNOSIS OF RHEUMATIC 1. To give rest to the body and the joints.
FEVER 2. To limit cardiac damage.
3. To eliminate streptococcal infections by appropriate
antibiotics
General Measures:
▪ During the acute febrile stage, bed rest is advised.
▪ Three months bed rest is advisable for children presenting
with severe carditis.
▪ A good nutritious light diet rich in proteins and calories is
advised to speed up the recovery.
▪ Salt restriction may be required in the presence of CCF.
Medical treatment:
1.Salicylates: Calcium aspirin is usually given in a large
dose of 1 g every 4-6 hourly in children, till the acute
symptoms are over, then the dose is reduced and tapered off.
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Toxic symptoms such as buzzing of the ears (tinnitis), in children. The disease is basically valvular heart disease
deafness, nausea and vomiting occur due to large dose but affecting the heart valves either in isolation or in
rapidly subside when the dose is reduced. combination. Mitral valve is the commonly involved
2.Corticosteroids: Prednisolone (1-2 mg/kg/day in divided followed by aortic valves.
doses) is given in severe cases of acute rheumatic carditis. Pathology
It acts as an anti-inflammatory agent, hence, relieves pain The main pathological process in chronic rheumatic heart
and inflammation. disease is chronic inflammation, irreversible destruction of
3.Antibiotics: the valves with loss of elasticity, thickening of the valve
Penicillin is started after obtaining throat cultures. cusps and fusion of the commissures between the cusps, as
Benzathine penicillin G: a result of which the valve can not function normally. Two
• 600,000 U intramuscularly once for patients 27 kg main effects of chronic inflammation are:
• 1.2 million U intramuscularly once for patients >27 kg 1. Stenosis of the valve: The cusps of the valves fuse
or together leading to narrowing of the opening of the valve
Phenoxymethylpenicillin (penicillin V): which cause obstruction to the flow of blood.
• 250 mg orally BID or TID for 10 days for patients $27 kg 2. Incompetence (regurgitation) of the valve: The loss of
• 500 mg orally BID or TID for 10 days for patients >27 kg elasticity and scarring of the cusps, distortion and dilatation
ог of the valve ring results in improper closure of the valve.
Amoxicillin 50 mg/kg orally once daily for 10 days Due to incomplete closure, the valve becomes incompetent
(maximum 1 g/dose). to prevent backflow of the blood, hence, regurgitation of
Treatment of Chorea blood occurs.
• The patient as well as the parents should be reassured and The order of frequency of valve involvement is mitral valve
told about the self-limiting course of the disease. The > aortic valve > pulmonary valve > tricuspid valve. Lastly,
patient should be provided complete physical and mental the destructive process may result in calcification and
rest. immobility of the valves.
• Phenobarbitone is prescribed 30 mg thrice daily. Clinical features seen in table 7.7
Complication Rheumatic Valvular Heart Disease:
• Chlorpromazine, diazepam, diphenhydramine or
1.Congestive Heart Failure
promethazine can be used as sedatives.
2. Subacute Bacterial Endocarditis
• Haloperidol has also been used effectively.
3. Arrhythmias
Chronic Rheumatic Valvular Heart Disease
4. Clot formation and subsequent embolization
The only chronic sequelae of rheumatic fever are rheumatic
5.Anginal pains and Myocardial ischaemia
heart disease. It is the most common acquired heart disease
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Management: 3. ACE Inhibitors: It block the conversion of angiotensin

Medical management: I to angiotensin II, a potent vasoconstrictor, thereby
1. Digoxin: Digoxin is a cardiac glycoside that works by reducing peripheral vascular resistance and decreasing
inhibiting the sodium-potassium ATPase pump in cardiac aldosterone secretion. This results in vasodilation,
cells, leading to increased intracellular calcium levels and decreased blood pressure, and reduced sodium and water
enhanced cardiac contractility. It is used in RHD to improve retention. It used to improve cardiac function, reduce
symptoms of heart failure, including dyspnea (shortness of afterload, and prevent or delay the progression of heart
breath), fatigue, and exercise intolerance, by increasing failure.
cardiac contractility and improving cardiac output. Surgical management:
2. Diuretics (e.g., Furosemide): Diuretics increase urinary 1. Balloon valvuloplasty: It is done for stenotic lesion to
excretion of sodium and water, leading to reduced blood remove obstruction to flow of the blood. Re-stenosis is a
volume and decreased preload on the heart. It help to common problem. It is used for mitral and aortic stenosis.
alleviate symptoms of heart failure and improve 2. Valve Replacement: In this process, the normal valve is
hemodynamic status in patients with RHD-associated fluid replaced by an artificial ball and socket valve or any other
retention. valve.
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4. Pathophysiology of atherosclerosis and its risk factors o The fibrous cap consists of collagen, elastin, and smooth
and prevention. (3) muscle cells and serves to stabilize the plaque.
The term atherosclerosis is derived from two Greek words. 3. Stage III - Complicated Lesions (Fibroatheroma
‘Athero’ meaning ‘Fatty Mish’ and ‘Skleros’ meaning Formation):
“Hard”. This word combination indicates that o Some fibrous plaques may undergo further changes,
atherosclerosis begins as soft deposits of fat, that hardens leading to the formation of complicated lesions known
with age. Atherosclerosis is often referred to as ‘hardening as fibroatheromas.
of the arteries’. o These lesions may exhibit features such as increased
Pathophysiology: inflammation, intraplaque hemorrhage, necrotic cores,
The American Heart Association (AHA) classification and thinning of the fibrous cap.
system describes the six stages of atherosclerosis based on o Fibroatheromas are considered unstable and prone to
histological changes observed in arterial walls. These stages rupture, leading to acute thrombotic events.
are as follows: 4. Stage IV - Plaque Rupture:
1. Stage I - Initiation (Fatty Streak Formation): o Plaque rupture occurs when the fibrous cap of
o In this initial stage, low-density lipoprotein (LDL) atherosclerotic lesions becomes thin and vulnerable to
cholesterol penetrates the endothelium and accumulates mechanical stress or inflammatory processes.
within the intima layer of the arterial wall. o Rupture exposes the thrombogenic material within the
o Monocytes adhere to the endothelium and migrate into plaque to circulating blood, resulting in platelet
the intima, where they differentiate into macrophages activation and the formation of a thrombus (blood clot)
and engulf the lipid, forming foam cells. at the site of rupture.
o The accumulation of foam cells results in the 5. Stage V - Thrombosis and Occlusion:
development of fatty streaks, which are considered the o Thrombosis refers to the formation of a blood clot within
earliest visible lesions of atherosclerosis. the artery, which can partially or completely obstruct
2. Stage II - Progression of Lesions (Fibrous Plaque blood flow.
Formation): o Thrombi can lead to acute cardiovascular events such as
o Over time, fatty streaks can progress into more myocardial infarction (heart attack) or stroke if they
advanced lesions known as fibrous plaques. occlude critical arteries supplying vital organs.
o Smooth muscle cells migrate from the media layer into 6. Stage VI - Organization and Healing:
the intima and proliferate, forming a fibrous cap over o Following thrombus formation, the body initiates a
the lipid-rich core. healing process to stabilize the thrombus and repair the
injured arterial wall.
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o Macrophages and smooth muscle cells migrate into the Risk Factors:
thrombus, leading to its organization and eventual Modifiable Risk Factors:
incorporation into the arterial wall. 1. High Blood Pressure (Hypertension): Increases the
o Over time, the thrombus may undergo fibrous tissue risk of endothelial injury and accelerates atherosclerosis
deposition and calcification, resulting in the formation of progression.
a permanent plaque. 2. High Cholesterol (Dyslipidemia): Elevated levels of
LDL cholesterol and low levels of high-density
lipoprotein (HDL) cholesterol contribute to plaque
formation.
3. Smoking: Damages the endothelium, promotes
inflammation, and accelerates plaque formation.
4. Diabetes: Hyperglycemia and insulin resistance
contribute to endothelial dysfunction and promote
atherosclerosis.
5. Obesity: Increases the risk of hypertension,
dyslipidemia, and diabetes, all of which are risk factors
for atherosclerosis.
6. Sedentary Lifestyle: Lack of physical activity is
associated with obesity, hypertension, and dyslipidemia,
all of which increase the risk of atherosclerosis.
Unmodifiable Risk Factors:
1. Age: Atherosclerosis becomes more prevalent with
advancing age.
2. Gender: Men are at higher risk of developing
atherosclerosis compared to premenopausal women;
however, the risk for women increases after menopause.
3. Family History: A family history of premature
cardiovascular disease is a risk factor for atherosclerosis.
4. Genetics: Certain genetic factors influence lipid
metabolism, inflammation, and other processes involved
in atherosclerosis development.
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Prevention: 4. Blood Pressure Control:

Prevention of atherosclerosis involves addressing - Monitor blood pressure regularly and aim for optimal
modifiable risk factors, promoting healthy lifestyle habits, levels (typically < 120/80 mmHg).
and implementing medical interventions to reduce the risk - Adopt lifestyle modifications such as weight loss,
of plaque formation, progression, and complications. Here dietary changes, physical activity, and stress reduction
are key strategies for preventing atherosclerosis: techniques to lower blood pressure.
1. Healthy Diet: - Take prescribed antihypertensive medications if lifestyle
- Adopt a heart-healthy diet rich in fruits, vegetables, modifications alone are insufficient to control blood
whole grains, lean proteins, and healthy fats (e.g., pressure.
monounsaturated and polyunsaturated fats). 5. Cholesterol Management:
- Limit intake of saturated fats, trans fats, cholesterol, - Maintain healthy cholesterol levels by following a low-
sodium, and added sugars, which can contribute to fat, low-cholesterol diet and avoiding foods high in
dyslipidemia, hypertension, and obesity. saturated and trans fats.
- Follow dietary patterns such as the Mediterranean diet - Consider medications such as statins to lower LDL
or DASH (Dietary Approaches to Stop Hypertension) diet, cholesterol levels and reduce the risk of atherosclerosis
which have been associated with reduced cardiovascular progression and cardiovascular events.
risk. - Monitor lipid levels regularly and adjust treatment
2. Regular Physical Activity: strategies as needed to achieve target cholesterol levels.
- Engage in regular aerobic exercise, such as brisk 6. Diabetes Management:
walking, jogging, swimming, or cycling, for at least 150 - Control blood glucose levels through lifestyle
minutes per week. modifications (diet, exercise, weight management) and
- Physical activity helps to maintain a healthy weight, medications as prescribed by a healthcare provider.
lower blood pressure, improve lipid profiles, and enhance - Regularly monitor blood sugar levels and undergo
overall cardiovascular health. screening for diabetes-related complications, including
3. Smoking Cessation: cardiovascular disease.
- Quit smoking and avoid exposure to secondhand smoke, 7. Weight Management:
as smoking is a major risk factor for atherosclerosis and - Maintain a healthy weight through a balanced diet and
cardiovascular disease. regular physical activity.
- Seek smoking cessation programs, counseling, or - Aim for a body mass index (BMI) within the normal
nicotine replacement therapies to quit smoking range (18.5 to 24.9 kg/m²) and waist circumference
successfully.
 I M M A N U V E L | 17

measurements that are within recommended limits to Electrocardiogram Electrocardiogram (ECG or EKG
reduce cardiovascular risk. from electrocardiogram in Dutch) is the record or graphical
9. Regular Health Check-ups: registration of electrical activities of the heart.
- Schedule regular medical check-ups with a healthcare Principle of ECG
provider to monitor cardiovascular risk factors, assess The fundamental basis of ECG is depolarisation of the heart
overall health, and receive preventive care and screenings by the electrical impulse which is propagated along the
as recommended based on individual risk profiles. length of muscle fibres and sets up electrical potentials in
10. Medications: the form of waveforms which are amplified and recorded.
- Medications such as statins to lower LDL cholesterol, Depolarisation (contraction) is followed by repolarisation
blood pressure-lowering medications (e.g., ACE inhibitors, (relaxation).
beta-blockers, calcium channel blockers), antiplatelet Types of ECG
agents (e.g., aspirin), and anticoagulants (e.g., warfarin, • Rest ECG
direct oral anticoagulants) may be prescribed to reduce • Exercise ECG or Tread Mill Test (TMT)
cardiovascular risk. • Ambulatory ECG or Holter ECG
Exercise ECG or Tread Mill Test (TMT)
5. Diagnostic tools for heart disease and prevention of An Exercise ECG, also known as a Treadmill Test or
heart disease. Exercise Stress Test, is a diagnostic procedure used to
Diagnostic tools for heart disease include a variety of tests evaluate the heart's response to physical exertion. During
and procedures that healthcare providers use to assess heart the test, the patient exercises on a treadmill while their heart
health, identify risk factors, and diagnose specific rate, blood pressure, and electrocardiogram (ECG) are
cardiovascular conditions. monitored continuously.
Electrocardiogram (ECG)
Electrocardiography Electrocardiography is the
technique by which electrical activities of the heart are
studied. The impulse is generated in the SA node, travels to
AV node, bundle of His and its branches (right and left
bundle branch) and then to the ventricles to be recorded
from the surface by electrodes.
Electrocardiograph Electrocardiograph is the instrument
(machine) by which electrical activities of the heart are
recorded.
 I M M A N U V E L | 18

The goal is to assess the heart's ability to tolerate increased Interpretation of ECG:
workload and to detect abnormalities in heart rhythm, blood
flow, or electrical activity that may indicate underlying
heart disease.
Horizontal ST segment depression>1 mm staying for > 80
msec is considered as positive test for myocardial
ischaemia.
Ambulatory ECG (Holter's monitoring)
It is continuous recording of one or more ECG leads by a
small palpable solid state taperecorder. This is useful in
detecting transient episodes of arrhythmias or ischaemia in
a patient who is up and about but is asymptomatic and
resting ECG is normal. The ECG is done during daily
normal activity for 24 hours while taperecorder remain
attached to the body. The abnormality in the rhythm or an
evidence of ischaemia can be seen.
Chest X-ray (PA view)
A posteroanterior (PA) chest X-ray renders valuable
regarding the size and shape of the heart, pulmonary
vasculature and the lung fields. The anterior posterior (AP)
chest X-ray is not preferred heart because it magnities the
cardiac shadow. Cardiac Biomarker:
The size of the heart is estimated in relation to BNP (Brain Natriuretic Peptide) is a hormone secreted
cardiothoracic ratio. Normally the heart shadow occupies primarily by the cardiac ventricles in response to increased
less than half of the transthoracic diameter on chest X-ray, myocardial stretch and pressure overload. Elevated BNP
if it occupies more than half, then heart shadow is said to be levels (>100 pg/mL) in the setting of symptoms such as
enlarged . The heart shadow is enlarged in variety of heart dyspnea, fatigue, or edema suggest heart failure.
diseases, most commonly being the valvular heart diseases Cardiac troponins (cTn) are proteins found in cardiac
and pericardial effusion. muscle cells (myocytes) that are released into the
bloodstream following myocardial injury or necrosis.
 I M M A N U V E L | 19

Troponin T (cTnT) and troponin I (cTnI) are the two main Radionuclide Scanning
isoforms used as cardiac biomarkers. Myocardial scanning using radioactive thallium or other
Cardiac troponin is the gold standard biomarker for tracers is used to distinguish ischaemic from nonischaemic
diagnosing acute myocardial infarction (heart attack) and myocardium. Radioactive pyrophosphate is used to
assessing myocardial injury. Elevated troponin levels distinguish between normal and infarcted segment.
indicate myocardial damage, even in the absence of Cardiac Catheterisation
symptoms or ECG changes. This is an invasive procedure in which a catheter is
Specialised Investigations introduced through a vein or an artery and manipulated
Echocardiogram through the heart under an X-ray monitor. It provides useful
Echocardiography is ultrasound imaging of heart and great informations regarding the pressure in the atria, ventricles
vessels. Ultrasounds reflected at interfaces between the and the great vessels. This information is vital before heart
blood and solid tissues are gathered through the transducer surgery.In addition, through these catheters, one can
on the chest and then displayed on an oscilloscope in the monitor pulmonary capillary wedge pressure (PCWP) in
form of anatomical structure which is studied for any ICCU for administration of fluid therapy in cardiac patients.
abnormality. Echocardiogram is thus useful to study the Angiocardiography
pericardium, wall of the ventricles and heart valves. Thus, It is X-ray of the heart taken after an injection of radio-
it is useful to diagnose pericardial effusion, valvular heart opaque contrast material into the individual chambers of the
disease and other heart conditions. heart, the aorta or pulmonary artery. This enables a precise
Doppler echocardiography is useful to study the flow of diagnosis to be made of many structural abnormalities
blood through the heart valves, hence, gives valuable whether congenital or acquired.
informations regarding the stenotic and regurgitant valvular Coronary Angiography
lesions and congenital heart defects (ASD, VSD). It is recording of the coronary circulation after injecting a
radio-contrast material through the catheter placed in the
Common indication echocardiography origin of the right and left coronary arteries. It gives
information to the surgeon regarding the stenoses of the
artery/arteries which can be dilated and stenting can be done
or bypass grafting may be done
Prevention of heart disease
Prevention of heart disease involves adopting a
combination of lifestyle modifications and medical
interventions aimed at reducing cardiovascular risk factors
 I M M A N U V E L | 20

and promoting overall heart health. Here are key strategies 5. Manage Stress:
for preventing heart disease: - Practice stress-reduction techniques such as mindfulness
1. Healthy Diet: meditation, deep breathing exercises, yoga, tai chi, or
- Adopt a heart-healthy diet rich in fruits, vegetables, progressive muscle relaxation.
whole grains, lean proteins (such as fish, poultry, beans, and - Seek social support, engage in enjoyable activities, and
nuts), and healthy fats (such as olive oil and avocados). prioritize self-care to cope with stress effectively and
- Limit intake of saturated fats, trans fats, cholesterol, promote overall well-being.
sodium, and added sugars, which can contribute to high 6. Regular Health Check-ups:
blood pressure, high cholesterol levels, and obesity. - Schedule regular medical check-ups with a healthcare
2. Regular Physical Activity: provider to monitor cardiovascular risk factors such as
- Engage in regular aerobic exercise such as brisk blood pressure, cholesterol levels, blood glucose levels, and
walking, jogging, swimming, cycling, or dancing for at body weight.
least 150 minutes per week. - Undergo preventive screenings for conditions such as
- Include muscle-strengthening activities on two or more diabetes, hypertension, and dyslipidemia, as recommended
days per week to improve overall fitness and maintain a based on individual risk factors and age.
healthy weight. 7. Medication Adherence:
3. Tobacco Avoidance and Smoking Cessation: - Take prescribed medications as directed by a healthcare
- Avoid tobacco use in any form, including smoking and provider to manage underlying conditions such as
exposure to secondhand smoke. hypertension, dyslipidemia, diabetes, or atrial fibrillation.
- Quit smoking if you currently smoke, and seek support - Adherence to medication regimens is crucial for
from healthcare providers, smoking cessation programs, or preventing disease progression and reducing the risk of
counseling to quit successfully. cardiovascular events.
4. Maintain a Healthy Weight: 8. Limit Alcohol Consumption:
- Achieve and maintain a healthy weight through a - If you choose to drink alcohol, do so in moderation.
combination of balanced diet, regular physical activity, and Limit alcohol intake to no more than one drink per day for
portion control. women and up to two drinks per day for men.
- Aim for a body mass index (BMI) within the normal
range (18.5 to 24.9 kg/m²) and waist circumference
measurements that are within recommended limits.
 I M M A N U V E L | 21

6. What is Cardiac Arrest and sudden Cardiac death? State its Symptoms and Signs
causes, etiology and immediate management of cardiac arrest. (3) 1. Absence of heart beat.
Cardiac Arrest: Cardiac arrest is a sudden and unexpected 2. Absence of peripheral pulses
loss of heart function, typically resulting in the cessation of 3. Cold extremities
blood circulation. During cardiac arrest, the heart's 4. Loss of consciousness or disturbed consciousness
electrical system malfunctions, causing it to stop beating 5. Stoppage of spontaneous respiration
effectively. If left untreated, cardiac arrest can quickly lead 6. Pupils are initially reactive to light; if not treated in
to irreversible brain damage and death. time, become dilated and fixed.
Sudden Cardiac Death (SCD): Sudden cardiac death 7. The ECG shows absence of waveforms, either there is
refers to a sudden, unexpected loss of heart function, straight line or undulation of the baseline.
usually resulting from a cardiac arrhythmia (abnormal heart Treatment
rhythm), such as ventricular fibrillation or ventricular It is a dire emergency and urgent resuscitative measures are
tachycardia. SCD occurs abruptly, often without warning. It needed to sustain life otherwise irreversible damage will
is a leading cause of death worldwide, particularly among occur within 3-5 minutes due to hypoxia.
individuals with underlying heart disease or risk factors for Steps
cardiovascular events. 1. Once the diagnosis is made, always call for help. A nurse
Causes of cardiac of arrest must call the doctor.
2. Give a sharp blow to the center of the chest and look for
the carotid or femoral pulse or heart sound.
3. If the heart does not start immediately, start the basic life
support.
ABC OF BASIC LIFE SUPPORT:
A. For airway
- Place the patient on firm surface (floor) or hardbed on his
back. The legs are elevated.
- Clear the mouth and airway. Extend the neck and the chin.
B. For breathing
- Direct mouth to mouth breathing after placing a gauge
piece over the mouth of the victim be started until face
mask or ambu bag becomes available.
- Breathing by ambu bag or through mask
 I M M A N U V E L | 22

C. For circulation Algorithm for cardiac arrest

Cardiac massage should be attempted simultaneously with
mouth to mouth breathing. This is a done by placing both
hands, one over the other, on the lower part of the sternum
and applying sharp, smooth forceful compressions at a rate
of 60-100/min. The success of cardiac compression is
judged by appearance of femoral pulse with each thrust.

4. Continuous ECG monitoring should be done if the

patient is not in ICCU. This will identify the underlying
rhythm and allow further treatment depending on the
findings, i.e. electromechanical dissociation, ventricular
fibrillation or asystole.
5. A life saving emergency tray with the drugs must be by
the side of patient.

LIFE SAVING DRUGS IN EMERGENCY TRAY

• Dopamine • Coramine
• Dobutamine • Frusemide
• Adrenaline • Deriphylline
• Atropine • Diazepam
• Dexamethasone • Sodium bicarbonate
• Hydrocortisone • Dilantin
• Calcium gluconate • 25% dextrose ampoule
 I M M A N U V E L | 23

7.Discuss the clinical features, etiology and management urgency, can lead to acute pulmonary edema due to
of Acute Pulmonary Edema (2) increased afterload and left ventricular strain.
Definitions: Cardiogenic pulmonary oedema is defined as 7. Toxic Inhalation: Inhalation of toxic gases, such as high
collection of fluid into lungs due to an acute increase in the concentrations of oxygen, carbon monoxide, or smoke,
left atrial pressure. can cause direct injury to the alveolar-capillary
Causes: membrane and trigger pulmonary edema.
The causes are: Some other causes:
1. Heart Failure: The most common cause of acute o Systemic hypertension
pulmonary edema is decompensated heart failure, o Aortic valvular stenosis, aortic regurgitation
typically due to left ventricular dysfunction resulting o Idiopathic hypertrophic subaortic stenosis (IHSS)
from conditions such as myocardial infarction, o Coarctation of aorta
cardiomyopathy, valvular heart disease, or hypertension. o Mitral stenosis, mitral regurgitation
2. Acute Coronary Syndrome (ACS): Acute myocardial o Left atrial myxoma (tumour of left atrial muscle)
infarction or unstable angina can precipitate acute o Endomyocardial fibrosis
pulmonary edema due to myocardial ischemia, o Ventricular septal defect, Petent ductus arteriosus
myocardial stunning, or acute mitral regurgitation. o Papillary muscle dysfunction
3. Fluid Overload: Excessive fluid retention or volume o Cardiomyopathy
overload, often secondary to renal failure, intravenous o Anterior wall myocardial infarction Endocarditis
fluid administration, or excessive salt intake, can Clinical features
overwhelm the heart's pumping capacity and lead to Dyspnea: Sudden onset of severe shortness of breath, often
pulmonary congestion. described as "air hunger" or feeling like suffocation.
4. Valvular Heart Disease: Severe mitral or aortic valve Orthopnea: Difficulty breathing while lying flat, leading to
dysfunction, particularly acute mitral regurgitation or the need to sit or stand upright to alleviate symptoms.
aortic regurgitation, can cause acute pulmonary edema Paroxysmal Nocturnal Dyspnea (PND): Episodes of
by increasing left atrial pressure and pulmonary venous sudden, severe shortness of breath that awaken the
congestion. individual from sleep.
5. Arrhythmias: Rapid atrial fibrillation, ventricular Cough: Often dry initially, but may become productive of
tachycardia, or other arrhythmias can impair cardiac frothy, pink-tinged sputum as the condition progresses.
function and precipitate acute pulmonary edema. Tachypnea: Rapid breathing, with respiratory rate often
6. Hypertensive Crisis: Severe hypertension, especially in exceeding 30 breaths per minute.
the context of hypertensive emergency or hypertensive
 I M M A N U V E L | 24

Tachycardia: Elevated heart rate, reflecting the body's Investigations

compensatory response to hypoxemia and increased 1. Electrocardiogram (ECG). It is done for left ventricular
sympathetic activity. hypertrophy or myocardial ischaemia
Hypoxemia: Low oxygen levels in the blood, leading to 2. Chest X-ray. This may show the following findings:
symptoms such as confusion, restlessness, cyanosis (blue • Cardiac shadow is enlarged and occupies more than
discoloration of the skin), and diaphoresis (profuse 50% of transthoracic diameter.
sweating). • Abnormal distension of upper lobe veins
Crackles or Rales: Adventitious lung sounds heard on • Vascularity of the lung fields is increased. Pulmonary
auscultation, indicating fluid accumulation in the alveoli. artery is dilated. In acute pulmonary oedema, there may
Hypertension or Hypotension: Acute pulmonary edema be bilateral homogenous opacities, extending from hilum
may initially present with elevated blood pressure due to to periphery
increased sympathetic tone, but hypotension can develop as • There may be an interlobular fissure effusion or pleural
cardiac output decreases and cardiogenic shock ensues. effusion.
Cyanosis: Bluish discoloration of the skin and mucous 3. Echocardiogram. This would reveal the cause of left
membranes due to inadequate oxygenation. ventricular failure such as valvulal disease, myocardial
Some other Symptoms and Signs disease etc.
• Chyne-Stokes respiration 4. Blood tests. Blood urea, electrolytes must be monitored.
• Oliguria, nocturia Full blood count, liver biochemistry, cardiac enzymes and
• Fatigue and weakness thyroid function test must be performed.
• Cerebral symptoms e.g., confusion, insomnia Management
• Extremities may be cold or pale The first aim of treatment of left heart failure is to find out
• Profuse sweating or perspiration may be present and remove any precipitating cause of decompensation,
• Low pulse volume or pulsus alternans may be present such as an arrhythmia or an intercurrent infection. The
• Central cyanosis necessary measures are:
• Third heart sound may be audible 1. Sedatives. Morphine is used intravenously in doses of 5-
• Oliguria, urine may be of high specific gravity and shows 10 mg along with an antiemetic (metoclopramide 10 mg
proteinuria IV.) and repeated frequently as desired. This drug reduces
• Hydrothorax or pleural effusion anxiety and load on the heart.
• Anxiety and depression 2. Oxygen therapy. About 60% O2 should be administered
• Cardiomegaly and signs of basic heart disease causing through a face mask and preferably under positive pressure
LVF to overcome hypxaemia.
 I M M A N U V E L | 25

3. Upright posture. The patient should be maintained in a

sitting position, with legs hanging along the side of the bed.
JNC Classification to define HYPERTENSION
This tends to reduce the venous return.
4. Loop diuretics. The high potency loop diuretics, such as
frusemide (40-100 mg) or bumetanide (1 mg) may be used
intravenously to clear the fluid overload by profuse
diuresis.
5. Reduction of afterload. Intravenous sodium nitroprusside
or i.v. glyceryl trinitrate is given to patients whose systolic
blood pressure is above 100 mg of Hg. This rapidly reduces
afterload on the heart.
6. Digitalis. If digoxin has not been used previously, can be Isolated Systolic Hypertension
administered intravenously in a small nose. This is said to be present when systolic blood pressure
7. Bronchodilatation. Sometimes aminophylline or is > 140 mm Hg and diastolic blood pressure is < 90 mmHg.
theophylline intravenously is effective in diminishing It is commonly seen in old age (above 65 years).
bronchospasm. Accelerated Hypertension
8. Noninvasive Positive Pressure Ventilation (NIPPV): A significant recent increase in blood pressure over
Continuous positive airway pressure (CPAP) or bilevel previous hypertensive levels, associated with evidence of
positive airway pressure (BiPAP) can be used to improve vascular damage on fundoscopic examination, but without
oxygenation, reduce respiratory distress, and decrease the papilloedema.
work of breathing in patients with acute pulmonary edema. Hypertensive Urgency
This is a situation in which the BP is markedly elevated, but
without any evidence of end organ damage. In this
8. Hypertension (4) condition, the control of the elevated BP can be done
Definition gradually.
Hypertension is defined as the persistent high blood Hypertensive Emergency
pressure. Clinically, when the systolic pressure remains This is a situation in which the BP is markedly elevated, but
elevated above 150 mm Hg and diastolic pressure remains with evidence of some end organ damage. In this condition,
elevated above 90 mm Hg, it is considered as hypertension. the control of the elevated BP has to be done immediately
in order to prevent further end organ damage.
 I M M A N U V E L | 26

White Coat Hypertension Symptoms and Signs (adverse effects of hypertension)

A transient increase in blood pressure in normal individuals, 1. The majority of the patients may remain asymptomatic
when BP is recorded in a physician’s consulting room, or in for many years (10-15 yrs). Headache, matiness,
a hospital. palpitations, epistaxis and ringing in the ears (tinnitis) are
Causes: the early symptoms referable to hypertension.
1. Primary or idiopathic 2. Eventually, due to persistently elevated BP, the organs
• Essential hypertension may be affected and symptoms are referable to damage to
2. Secondary to some cause the organs rather than to hypertension.
i. Renal diseases • Cardiac symptoms due to high BP occur as a result of
• Chronic pyelonephritis left ventricular failure (dyspnoea on exertion, orthopnoea,
• Acute or chronic glomerulonephritis PND, cough, expectoration) or due to coronary
• Polycystic kidney disease ischaemia/infarction. It is well known fact that acute
• Renal artery stenosis myocardial infarction is more common in hypertensive than
ii. Endocrinal causes nonhypertensives.
• Cushing's syndrome • Cerebral symptoms occur due to narrowing of the
• Primary hyperaldosteronism (Conn's syndrome) cerebral vessels (cerebral ischaemia) or rupture of the
• Phaeochromocytoma vessels. The symptoms and signs include transient
• Congenital adrenal hyperplasia ischaemic attacks (TIAS) leading to transient weakness or
• Acromegaly paralysis, completed stroke and hypertensive
• Myxoedema encephalopathy (mental changes, fits, headache and coma).
iii. Drug induced, e.g. The latter is more common in malignant than benign
• Steroids, oral contraceptives, NSAIDs, hypertension.
sympathomimetic agents • Visual symptoms occur in the form of blurring of the
iv. Collagen vascular disorders vision.
• SLE • Urinary symptoms appear in the form of haematuria
• Polyarteritis nodosa (PAN) (blood in the urine) and renal failure (features of uraemia).
v. Miscellaneous In secondary hypertension due to some identifiable
• Toxaemia of pregnancy cause, the symptoms and signs are referable to the cause
• Pregnancy associated hypertension such as polyuria and polydipsia occur in primary
• Coarctation of aorta hyperaldosteronism, moon-face, truncal obesity, abdominal
striae, weight gain in Cushing's syndrome and episodes of
 I M M A N U V E L | 27

headaches and palpitations are seen in 2. Diet. Reduction of alcohol consumption and correction
phaeochromocytomas. of obesity (BMI should be <25 kg) are both effective
Investigations antihypertensive measures. The patient is advised not to add
1. Basic (done in all patients) salt from the table (low to moderate sodium intake) and
o Urine for protein, blood and glucose. avoid foods with high sodium content. A low fat diet,
o Blood glucose/sugar (fasting and postprandial) Serum caloric restriction should be advised to patients who are
electrolytes, e.g. K¹ and Na+ overweight. Encourage fruit and vegetable consumption.
o Plasma urea/creatinine 3.Regular Exercise. Regular exercise, ie. Iso- tonic
o ECG for left ventricular hypertrophy or ischaemia exercises, fast walking (≥ 30 min/day on most of the days),
o Fundus examination for exudates and haemorrhage, jogging, swimming are better than isometric exercises
i.e. retinopathy. (weightlifting)
o Lipidogram 4. Smoking. Smoking should be strongly discouraged.
o Chest X-ray for heart size, i.e. for cardiomegaly.
2. Special investigations
o IVP (intravenous pyelography) and ultrasound for any
renal disease, e.g. polycystic kidney disease.
o Renal angiogram for renal artery stenosis, if
suspected.
o 24 hour catecholamine (vanillymandelic acid VMA)
for phaeochromocytoma.
o Urinary cortisol and dexamethasone suppression test
for cushing syndrome.
o Angiography/ MRI for coarction of aorta.
Management:
Aim of Treatment
i. To reduce the blood pressure to normal levels.
ii. To prevent development of complications. Drug Therapy: Many patients can be controlled with a
iii. To improve the life expectancy. single drug, the choice of which depends on the safety,
General measures. convenience and freedom from side effects. Another large
1.Relief of stress by avoiding unnecessary tension and group of patients may require a combination therapy
relaxation exercises. consisting of two or more drugs.
 I M M A N U V E L | 28

The antihypertensive most frequently used are: vi. Vasodilators (e.g. hydralazine, diazoxide,
i. Betablockers (e.g. metoprolol, atenolol). They are drug nitroprusside). Hydralazine is not used now-a days.
of choice in hypertension. They lower the BP by Diazoxide and nitroprusside are used for the treatment of
antagonizing the beta-adrenergic receptors. They, in hypertensive emergencies such as malignant hypertension.
addition, relieve angina.
ii. Diuretics (e.g. chlorthiazide). Their antihyper- tensive 9. Describe the cardiac cycle.
effect is through sodium diuresis (loss of Na through DEFINITION: Cardiac cycle is defined as the sequence of
kidneys) and volume depletion. They are combined with coordinated events taking place in the heart during each
betablockers to reduce moderate to severe hypertension. beat. Each heartbeat consists of two major periods called
They can be used alone in mild hypertension. systole and diastole. During systole, heart contracts and
iii. Calcium channel blockers (e.g. nifedipine, amlodi- pumps the blood through arteries. During diastole, heart
pine). They relax the smooth muscles of blood vessels and relaxes and blood is filled in the heart. All these changes are
produce vasodilatation and reduce peripheral resistance. repeated during every heartbeat, in a cyclic manner.
They are used in the treatment of hypertension as a first line EVENTS OF CARDIAC CYCLE
therapy in place of betablockers. Events of cardiac cycle are classified into two:
iv. Angiotension converting enzyme (ACE) inhibitors 1. Atrial events
(e.g. captopril, lisnopril, ramipril, etc.). These drugs block 2. Ventricular events.
the production of angiotensin II by inhibiting the ATRIAL EVENTS
angiotensin converting enzyme, thus overcome the Atrial events are divided into two divisions:
vasoconstrictive effects of angiotensin II. They are used for 1. Atrial systole = 0.11 (0.1) sec
treatment of hypertension especially when there is 2. Atrial diastole = 0.69 (0.7) sec.
associated congestive heart failure where betablockers and VENTRICULAR EVENTS
calcium antagonists can not be used. Ventricular events are divided into two divisions:
v. Angiotensin receptor blockers (e.g. losartan, irbesartan, 1. Ventricular systole = 0.27 (0.3) sec
candesartan, etc.). They are a new class of drugs used in the 2. Ventricular diastole = 0.53 (0.5) sec.
treatment of mild to moderate hypertension. They reduce Ventricular systole (0.27 sec)
BP by blocking the angiotensin receptors. They are less 1. Isometric contraction 0.05 sec
toxic than ACE inhibitors, do not produce intractable 2. Ejection period 0.22 sec
cough. These agents can be used in combination with ACE Ventricular diastole (0.53 sec)
inhibitors and other hypertensives. They are most useful in 1. Protodiastole 0.04 sec
hypertension associated with diabetes and renal disease. 2. Isometric relaxation 0.08 sec
 I M M A N U V E L | 29

3. Rapid filling 0.11 sec QRS complex. Closure of atrioventricular valves at the
4. Slow filling 0.19 sec beginning of this phase produces first heart sound.
5. Last rapid filling (atrial systole) 0.11 sec Ejection Period: Due to the opening of semilunar valves
ATRIAL EVENTS and isotonic contraction of ventricles, blood is ejected out
Atrial Systole: Atrial systole is also known as last rapid of both the ventricles. Hence, this period is called ejection
filling phase or presystole. It is usually considered as the period.
last phase of ventricular diastole. Its duration is 0.11 second. Duration of this period is 0.22 second. Ejection period
During this period, only a small amount, i.e. 10% of blood is of two stages:
is forced from atria into ventricles. In ECG it is represented 1. First Stage or Rapid Ejection Period
by P wave. Contraction of atrial musculature causes the First stage starts immediately after the opening of
production of fourth heart sound. semilunar valves. During this stage, a large amount of
Atrial Diastole: After atrial systole, the atrial diastole blood is rapidly ejected from both the ventricles. It lasts
starts. Simultaneously, ventricular systole also starts. Atrial for 0.13 second.
diastole lasts for about 0.7 sec (accurate duration is 0.69 2. Second Stage or Slow Ejection Period
sec). This long atrial diastole is necessary because, this is During this stage, the blood is ejected slowly with much
the period during which atrial filling takes place. Right less force. Duration of this period is 0.09 second.
atrium receives deoxygenated blood from all over the body In ECG it is represented by ST segment.
through superior and inferior vena cavae. Left atrium Protodiastole: Protodiastole is the first stage of ventricular
receives oxygenated blood from lungs through pulmonary diastole, hence the name protodiastole. Duration of this
veins. period is 0.04 second. Due to the ejection of blood, the
VENTRICULAR EVENTS pressure in aorta and pulmonary artery increases and
Isometric Contraction Period: Isometric contraction pressure in ventricles drops. When intraventricular pressure
period in cardiac cycle is the first phase of ventricular becomes less than the pressure in aorta and pulmonary
systole. It lasts for 0.05 second. During isometric artery, the semilunar valves close. Atrioventricular valves
contraction period, the ventricular pressure increases are already closed (see above). No other change occurs in
greatly. When this pressure increases above the pressure in the heart during this period. Thus, protodiastole indicates
the aorta and pulmonary artery, the semilunar valves open. only the end of systole and beginning of diastole. Closure
Thus, the pressure rise in ventricle, caused by isometric of semilunar valves during this phase produces second heart
contraction is responsible for the opening of semilunar sound.
valves, leading to ejection of blood from the ventricles into Isometric Relaxation Period: Isometric relaxation is the
aorta and pulmonary artery. In ECG it is represented by type of muscular relaxation, characterized by decrease in
 I M M A N U V E L | 30

tension without any change in the length of muscle fibers.

Isometric relaxation of ventricular muscle is also called
isovolumetric relaxation. During isometric relaxation
period, once again all the valves of the heart are closed.
Now, both the ventricles relax as closed cavities without
any change in volume or length of the muscle fiber.
Intraventricular pressure decreases during this period.
Duration of isometric relaxation period is 0.08 second.
Rapid Filling Phase: When atrionventricular valves are
opened, there is a sudden rush of blood (which is
accumulated in atria during atrial diastole) from atria into
ventricles. So, this period is called the first rapid filling
period. Ventricles also relax isotonically. About 70% of
filling takes place during this phase, which lasts for 0.11
second. Rushing of blood into ventricles during this phase
causes production of third heart sound.
Slow Filling Phase: After the sudden rush of blood, the
ventricular filling becomes slow. Now, it is called the slow
filling. It is also called diastasis. About 20% of filling
occurs in this phase. Duration of slow filling phase is 0.19
second.
Last Rapid Filling Phase: Last rapid filling phase occurs
because of atrial systole. After slow filling period, the atria 10. Discuss the structural anatomy, presentation,
contract and push a small amount of blood into ventricles. diagnosis and treatment of Transposition of Great
About 10% of ventricular filling takes place during this Arteries.
period. Flow of additional amount of blood into ventricle Transposition of the great arteries is a congenital
due to atrial systole is called atrial kick. (present at birth) heart defect. Due to abnormal
development of the fetal heart during the first 8 weeks of
pregnancy, the large vessels that take blood away from the
heart to the lungs or to the body, are improperly connected.
 I M M A N U V E L | 31

Structural Anatomy: infant with transposition of the great arteries to live. An

Normally, oxygen- poor blood returns to the right opening in the atrial or ventricular septum will allow blood
atrium from the body, travels to the right ventricle, then is from one side to mix with blood from another, creating
pumped through the pulmonary artery into the lungs where "purple" blood with an oxygen level somewhere in-between
it receives oxygen. Oxygen-rich blood returns to the left that of the oxygen- poor (blue) and the oxygen-rich (red)
atrium from the lungs, passes into the left ventricle and then blood. Patent ductus arteriosus (another type of congenital
is pumped through the aorta out to the body. heart defect) will also allow mixing of oxygen-poor (blue)
In transposition of the great arteries, the aorta is and oxygen-rich (red) blood through the connection
connected to the right ventricle and the pulmonary artery is between the aorta and pulmo- nary artery. The "purple"
connected to the left ventricle - the exact opposite of a blood that results from this mixing is beneficial, providing
normal heart's anatomy: at least smaller amounts of oxygen to the body, if not a
1. Oxygen-poor blood returns to the right atrium from the normal amount of oxygen.
body, passes through the right atrium and ventricle, then Because of the low amount of oxygen provided to the body,
goes into the misconnected aorta back to the body. TGA is a heart problem that is labeled "blue-baby syn-
2. Oxygen-rich blood returns to the left atrium from the drome".
lungs, passes through the left atrium and ventricle, then Clinical Features:
goes into the pulmonary artery and back to the lungs. o Severe cyanosis (differential with legs being less cyanotic
Two separate circuits are formed-one that circulates than the arms), appearing at or shortly after birth,
oxygen-poor (blue) blood from the body back to the body constitutes the hallmark of TGV. Later, dyspnea, heart
and another that recirculates oxygen-rich (red) blood from failure and growth failure occur. Clubbing also develops
the lungs back to the lungs. in few months.
Causes: The heart is forming during the first 8 weeks of o Heart is always enlarged. Murmurs are not of a classical
fetal development. The problem occurs in the middle of pattern and are usually re=lated to the type of coexisting
these weeks, allowing the aorta and pulmonary artery to be communication. Auscultatory findings in TGA with
attached to the incorrect chamber. interatrial mixing in those who are symptomatic at birth
Some congenital heart defects may have a genetic link, with cyanosis include normal first heart sound, single
either occurring due to a defect in a gene, a chromosome second heart sound and an ejection systolic murmur
abnormality or environmental exposure, causing heart (grades 1-2) which has no significance.
problems to occur more often in certain families. o Auscultatory findings in TGA with VSD, who develop
Presentation: Other heart defects are often associated with heart failure, cyanosis, and cardiomegaly in second or
TGA and they actually may be necessary in order for an third month of life, are normal first heart sound, single or
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normally split-second heart sound and grades 2-4 ejection Surgical (Curative)
systolic murmur, apical third sound gallop or a mid- o Jatene arterial switch: The great vessels are interchanged
diastolic rumble. or switched. Ideally, it is done within 2 weeks of life. In
Diagnosis TGA with intact ventricular septum beyond 2 weeks, LV
▪ Chest X-ray shows enlarged heart with a narrow base will slowly regress and will not be able to support
(pedicle) on account of malposition of great vessels and systemic arterial pressure if arterial switch operation is
grossly plethoric lung fields (more so in the upper done very late.
portion) and often absent thymic shadow. Egg-on-side o If VSD coexists, the switch procedure is performed
appearance is characteristic. within 2 months of age.
▪ ECG reveals RVH, right axis deviation and often P
pulmonale. 11.Signs, symptoms, diagnosis and management of
▪ Echocardiography confirms the diagnosis. It shows rheumatic mitral stenosis.
equal peak systolic pressure in both ventricles, aorta and Rheumatic mitral stenosis is a condition characterized
pulmonary artery. Cardiac catheterization and selective by narrowing of the mitral valve opening due to scarring
angiocardiography help in confirming the diagnosis. and thickening of the valve leaflets and chordae tendineae,
Management: typically resulting from rheumatic fever. This narrowing
The child will most likely be admitted to the Intensive Care restricts the flow of blood from the left atrium to the left
Unit (ICU) or special care nursery once symptoms are ventricle during diastole, leading to elevated left atrial
noted. Initially, the child may be placed on oxygen and pressure, pulmonary congestion, and eventually right heart
possibly even on a ventilator, to assist his/her breathing. failure.
Intravenous (IV) medications may be given to help the heart Causes:
and lungs function more efficiently. Other important Rheumatic mitral stenosis (MS) is primarily caused by
aspects of initial treatment include the following: rheumatic fever, an inflammatory condition triggered by
Medical untreated or inadequately treated group A streptococcal
o Prostaglandin El to keep PDA open infection, particularly pharyngitis. Rheumatic fever can
o CHF is treated if identified lead to inflammation and scarring of the mitral valve,
o Cyanotic babies may be treated percutaneously with a resulting in stenosis over time.
Rashkind atrial balloon septostomy to create a more Pathophysiology:
sizable ASD (when atrial septal defect is small and - In rheumatic MS, chronic inflammation of the mitral valve
restrictive). This procedure improves oxygenation leads to fibrosis, thickening, and fusion of the valve leaflets
until definitive surgery is performed. and chordae tendineae.
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- This results in decreased mobility of the valve leaflets and to redistribution of fluid from the legs to the lungs when
narrowing of the mitral valve orifice, impeding the flow of lying down.
blood from the left atrium to the left ventricle during 8. Reduced exercise tolerance: Patients may notice a
diastole. decrease in their ability to perform physical activities due
- As a consequence, left atrial pressure increases, leading to to limited cardiac output and oxygen delivery to the tissues.
atrial dilation and eventually left atrial enlargement. 9. Signs of right heart failure: Manifestations may include
- The increased pressure within the left atrium can also lead jugular venous distension, hepatomegaly, ascites, and
to pulmonary hypertension, right ventricular hypertrophy, peripheral edema, reflecting elevated right-sided pressures
and ultimately right heart failure. and fluid retention.
Signs and symptoms: 10. Mitral facies: A dusky cyanotic hue on the cheeks and
1. Dyspnea: Shortness of breath, particularly with exertion malar eminences, resulting from chronic hypoxemia and
or when lying flat (orthopnea) due to impaired left reduced cardiac output.
ventricular filling and elevated left atrial pressure. 11. Auscultatory findings: A low-pitched rumbling
2. Fatigue: Generalized weakness and tiredness, often diastolic murmur, best heard at the apex with the patient in
exacerbated by reduced cardiac output. the left lateral decubitus position, often accompanied by an
3. Palpitations: Sensation of rapid or irregular heartbeat, opening snap, is characteristic of mitral stenosis.
commonly associated with atrial fibrillation, which often Diagnosis:
accompanies mitral stenosis. - Physical examination: Auscultation may reveal a low-
4. Cough: Dry cough or cough productive of frothy sputum, pitched rumbling diastolic murmur best heard at the apex
reflecting pulmonary congestion and possible pulmonary with the patient in the left lateral decubitus position (the
edema. "opening snap" and "rumbling" murmur of mitral stenosis).
5. Hemoptysis: Coughing up blood-tinged sputum, - Echocardiography: Transthoracic echocardiography is
resulting from rupture of small pulmonary vessels due to the primary imaging modality for diagnosing and assessing
increased pulmonary pressure. the severity of mitral stenosis. It can visualize the thickened
6. Chest discomfort: Patients may experience chest pain or mitral valve leaflets, calculate the valve area, assess the
discomfort, often described as tightness or pressure, due to degree of mitral regurgitation, and evaluate for associated
increased workload on the heart. complications such as left atrial enlargement and
7. Orthopnea and paroxysmal nocturnal dyspnea: pulmonary hypertension.
Difficulty breathing while lying flat and sudden awakening - Electrocardiogram (ECG): May show findings
from sleep with severe shortness of breath, respectively, due consistent with left atrial enlargement, such as P wave
 I M M A N U V E L | 34

abnormalities (e.g., widened P waves, prolonged PR 12.Myocardial infraction

interval) and atrial fibrillation.
- Chest X-ray: Can demonstrate left atrial enlargement,
pulmonary congestion, and signs of pulmonary
hypertension (e.g., prominent pulmonary vasculature,
Kerley B lines).
Management:
- Medical management: Symptomatic relief with diuretics
to manage volume overload and relieve symptoms of
congestion. Anticoagulation with warfarin or direct oral
anticoagulants is indicated in patients with atrial fibrillation
or a history of embolic events.
- Percutaneous balloon mitral valvuloplasty (PBMV): A
catheter-based procedure to dilate the stenotic mitral valve
using a balloon catheter, relieving the obstruction and
improving symptoms.
- Surgical mitral valve repair or replacement: Indicated
in patients with severe symptomatic mitral stenosis
refractory to medical or percutaneous interventions, or in
those with severe mitral regurgitation or other valve
abnormalities.
- Prophylactic antibiotic therapy: To prevent recurrent
episodes of rheumatic fever and mitigate the progression of
mitral valve disease in patients with a history of rheumatic
fever.
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Credits: X. JENCY B. Sc Physician Assistant

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1.Activated Clotting Time (2) - For patients undergoing PCI, the target ACT may be
Activated Clotting Time (ACT) is a laboratory test used to shorter, usually around 200 to 300 seconds.
assess the efficacy of anticoagulation during certain Clinical Significance:
medical procedures, particularly those involving - ACT monitoring is essential during procedures involving
cardiopulmonary bypass (CPB) during cardiac surgery or CPB or PCI to ensure adequate anticoagulation and
interventions such as percutaneous coronary interventions minimize the risk of thrombosis or clot formation within the
(PCI). circuit or coronary arteries.
Principle: - A prolonged ACT may indicate insufficient
The ACT measures the time taken for blood to clot after the anticoagulation, increasing the risk of clot formation and
addition of an activator (such as kaolin or celite) and a thrombotic complications.
source of calcium chloride. The activator initiates the - Conversely, a shortened ACT may indicate excessive
intrinsic pathway of the coagulation cascade, leading to the anticoagulation, increasing the risk of bleeding
formation of a fibrin clot. The time taken for clot formation complications.
is measured in seconds and represents the activated clotting Limitations:
time. - ACT is a global test of coagulation and does not
Procedure: specifically measure the activity of individual coagulation
1. A blood sample is collected from the patient via factors or platelet function.
venipuncture or an arterial line. - ACT results can be affected by various factors, including
2. The blood is immediately mixed with an activator and hematocrit level, platelet count, temperature, and the
calcium chloride in a specialized test tube or cartridge. presence of heparin or other anticoagulants.
3. The clotting time is measured using a coagulation
analyzer or dedicated point-of-care testing device. 2.Acute Rheumatic fever
4. The result is reported as the time in seconds from the Definition: It is infection caused by group A beta-
addition of the activator to the formation of a stable clot. Hemolyticus streptococci involving the skin and throat
Interpretation: (sore throat). It appears after a lapse of 2-3 weeks following
The normal range for ACT may vary depending on the streptococcal throat infection leading to formation of
laboratory and the specific activator used. However, in antibodies against the organism which cross-react with
general: cardiac and other tissues leading to clinical manifestations
- For patients undergoing CPB during cardiac surgery, the of acute rheumatic fever. One attack does not confer
target ACT is typically between 400 to 480 seconds. immunity, hence, repeated attacks are common. The
younger the patient, more frequent are the attacks.
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“RHEUMATIC FEVER LICKS THE JOINTS BUT • Pericardial pain.

BITES THE HEART" • Changes in E.C.G.
Clinical Manifestation: Arthritis: It is the most common criterion: Typical arthritis
Minor Manifestation: occurs in 70% of cases. It occurs during the first 1-2 weeks
• Arthralgia: Painful joints without swelling. the febrile period and lasts for a few days in certain affected
• ECG: Prolongation of the PR interval. Prolonged PR joints before moving to other joints.
interval in itself is not a criterion for carditis. i. Affected joint is red, warm, swollen, very tender, with
• Acute phase reactants: Laboratory evidence of acute limited movements and effusion.
inflammation, such as elevated ESR or CRP, meets ii. Migratory. Several joints are commonly involved, either
requirements for a minor criterion. together or one after another.
• Fever. The temperature is usually in the range of more iii. Typically, the large joints are affected as knees, wrists,
than or equal to 38°C. ankles and elbows. It rarely affects fingers, toes or spine.
• Unexplained epistaxis. iv. It disappears within 12-24 hours from start of salicylate
• Weakness, fatigue, pallor, loss of appetite, abdominal therapy.
pain and weight loss. v. If untreated it doesn't persist in the same joint for more
Major Manifestation: than 1 week.
Carditis: Carditis: Mitral and aortic valves are most vi. Rheumatic arthritis leaves the joint intact and doesn't
affective valves and they become scarred, fibrous areas result in chronic disease.
when healed, stenosis as the leaflets (cusps) of the valves Rheumatic (Sydenham's) chorea: Chorea is characterized
occurs because they fuse together. This process causes by sudden, aimless, involuntary and irregular muscular
obstruction to the blood flow into the left ventricle or aorta movements of the extremities.
or both. The valve edges may become so scarred that they a. Involuntary facial grimaces.
can't completely close, causing a block flower re- b. Speech disturbance.
gurgitation (valvular insufficiency) when the valves close C. Severe muscle weakness (can be profound).
so, the following manifestations will be seen: d. Muscle movements exaggerated by anxiety and at-
• Tachycardia out of proportion to degree of fever. tempts at fine motor activity are relieved by rest.
• Cardiomegaly Subcutaneous nodules: These occur rarely in the general
population, but are frequently found in individuals who
• New murmur or change in preexisting murmurs.
have severe carditis or who have had repeated attack of
• Muffled heart sound (ventricle gallop exists that is S3).
acute rheumatic fever.
• Friction rub (main manifestation of pericarditis).
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i. Nodules are generally identified as small (0.5 - 1 cm) To diagnose rheumatic fever, it is necessary to have:
and firm without any tenderness or attachment to the 1. Two major criteria + evidence of preceding Group A
skin. Beta- Hemolytic Streptococcus pyogenes or infection.
ii. They can be palpated over the extensor surfaces of joints 2. One major + 2 minor criteria + evidence of preceding
such as elbows, knees, ankles or over the scalp and Group A Beta- Hemolytic Streptococcus pyogenes or
spinous processes of the vertebrae. infection.
iii. They gradually resolve over a period of time with no 3.Evidence for streptococcal infection by
residual. i. Antistreptolysin O
Erythema marginatum: The lesions are non-pruritic and ii. Anti – DNAse B antibody
appear initially as undifferentiated macules on the trunk and iii. Throat culture
inner aspect of the extremities (never on face). 4.Electrocardiography: Prolonged PR interval in the ECG
Evanescent and if watched from hour to hour, it will is a nondiagnostic criterion.
be noted to change gradually. 5.Echocardiography: Cardiac dilation and valve
Diagnosis: abnormalities.
JONES CRITERIA FOR DIAGNOSIS OF RHEUMATIC Treatment:
FEVER The aims of treatment are;
4. To give rest to the body and the joints.
5. To limit cardiac damage.
6. To eliminate streptococcal infections by appropriate
antibiotics
General Measures:
▪ During the acute febrile stage, bed rest is advised.
▪ Three months bed rest is advisable for children presenting
with severe carditis.
▪ A good nutritious light diet rich in proteins and calories is
advised to speed up the recovery.
▪ Salt restriction may be required in the presence of CCF.
Medical treatment:
1.Salicylates: They are used to relieve the joint pain and
fever. Salicylates have no effect on the heart lesions.
Calcium aspirin is usually given in a large dose of 1 g every
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4-6 hourly in children, till the acute symptoms are over, then • Chlorpromazine, diazepam, diphenhydramine or
the dose is reduced and tapered off. Toxic symptoms such promethazine can be used as sedatives.
as buzzing of the ears (tinnitis), deafness, nausea and • Haloperidol has also been used effectively.
vomiting occur due to large dose but rapidly subside when Prophalaxis:
the dose is reduced. 1. Primary Prophylaxis: This involves the administration
2.Corticosteroids: Prednisolone (1-2 mg/kg/day in divided of antibiotics to individuals with a history of rheumatic
doses) is given in severe cases of acute rheumatic carditis. fever or a streptococcal throat infection to prevent the
It acts as an anti-inflammatory agent, hence, relieves pain development of acute rheumatic fever.
and inflammation. These steroids are, sometimes, more 2. Secondary Prophylaxis (or Secondary Prevention):
effective than salicylates in relieving pain and fever. There Also known as long-term or maintenance prophylaxis,
is no evidence till date that long term use of steroids will this involves the continuous administration of antibiotics
prevent the heart valve damage. to individuals with a history of acute rheumatic fever or
3.Antibiotics: rheumatic heart disease to prevent recurrent episodes of
Penicillin is started after obtaining throat cultures. rheumatic fever. It is typically recommended for at least
Benzathine penicillin G: 5 years after the last episode of acute rheumatic fever.
• 600,000 U intramuscularly once for patients 27 kg
• 1.2 million U intramuscularly once for patients >27 kg 3. Anatomy of long saphenous vein.
or The long saphenous vein (LSV), also known as the great
Phenoxymethylpenicillin (penicillin V): saphenous vein (GSV), is a large superficial vein located in
• 250 mg orally BID or TID for 10 days for patients $27 kg the lower extremity. It is one of the major veins of the leg
• 500 mg orally BID or TID for 10 days for patients >27 kg and plays a crucial role in venous return from the lower limb
ог to the heart. Here is an overview of the anatomy of the long
Amoxicillin 50 mg/kg orally once daily for 10 days saphenous vein:
(maximum 1 g/dose). 1. Origin and Course:
Treatment of Chorea - The long saphenous vein originates from the dorsal
• The patient as well as the parents should be reassured and venous arch of the foot, which is located on the dorsum
told about the self-limiting course of the disease. The (top) of the foot and formed by the merging of superficial
patient should be provided complete physical and mental veins.
rest. - From its origin, the long saphenous vein ascends along
• Phenobarbitone is prescribed 30 mg thrice daily. the medial aspect (inner side) of the lower limb, coursing
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anterior to the medial malleolus (ankle bone) and posterior 5. Clinical Significance:
to the medial condyle of the tibia (knee bone). - The long saphenous vein is commonly used as a conduit
- It continues its course along the medial aspect of the leg, for venous grafts in surgical procedures such as coronary
passing posterior to the medial femoral condyle (thigh artery bypass grafting (CABG) and peripheral vascular
bone) and extending into the thigh. bypass surgery.
2. Tributaries: - It is also a common site for venous access during
- The long saphenous vein receives numerous tributaries procedures such as venipuncture and venous cannulation.
along its course, including superficial veins of the foot, - Pathological conditions affecting the long saphenous
ankle, and leg, as well as perforating veins that connect with vein include chronic venous insufficiency, varicose veins,
the deep venous system. and venous thrombosis.
- Some of the major tributaries include the anterior and
posterior accessory saphenous veins, which join the long 4.Aortic aneurysm.
saphenous vein at various points along its course. An aortic aneurysm is a localized dilation or bulging of the
3. Drainage and Connections: aortic wall, which can occur anywhere along the length of
- The long saphenous vein primarily drains into the the aorta. The aorta is the main artery that carries oxygen-
femoral vein, a deep vein located in the thigh. rich blood from the heart to the rest of the body. Aneurysms
- Near its termination, the long saphenous vein may can develop in any segment of the aorta, including the
connect with the deep venous system through perforating ascending aorta, aortic arch, descending thoracic aorta, and
veins, which penetrate the deep fascia and allow abdominal aorta.
communication between the superficial and deep venous Classification:
systems. Aortic aneurysms are classified based on their location
4. Valves: include:
- The long saphenous vein contains numerous valves 1. Thoracic Aortic Aneurysm (TAA):
along its course, which help to prevent retrograde flow of - Thoracic aortic aneurysms occur in the portion of the
blood and facilitate venous return to the heart. aorta that runs through the chest cavity.
- These valves are particularly prominent in the lower leg - They can involve the ascending aorta, aortic arch, or
and thigh, where they play a crucial role in maintaining descending thoracic aorta.
venous hemodynamics and preventing venous 2. Abdominal Aortic Aneurysm (AAA):
insufficiency. - Abdominal aortic aneurysms occur in the portion of the
aorta that passes through the abdomen.
- They are the most common type of aortic aneurysm.
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Clinical Features: • Evidence of widespread vascular disease i.e. femoral and

Thoracic aortic aneurysm distal pulses in the legs or feet maynbe weak or absent.
Symptoms • Bruits may be heard over the aneurysm arising from
• Due to compression of adjacent structures: associated narrowed arteries.
• Tracheal deviation, cough, dyspnoea, haemoptysis, • Stigmata of distal embolisation.
stridor, intrapulmonary haemorrhage due to compression of • Haemorrhagic shock (hypotension, tachycardia, shock)
tracheobronchial tree and the lung. with rupture of aneurysm.
• Hoarseness-compression of recurrent laryngeal nerve. Diagnosis:
• Dysphagia-compression of oesophagus. - Aortic aneurysms are typically diagnosed using imaging
• Distended veins in the neck and over chest- superior vena studies such as ultrasound, computed tomography (CT)
cava compression. scan, magnetic resonance imaging (MRI), or angiography.
•Pain-compression and erosion of adjacent musculoskeletal - Screening for abdominal aortic aneurysms is
structures. recommended for certain high-risk populations, such as
Signs older adults with a history of smoking.
• Tracheal tug due to aneurysm of arch of aorta. Treatment:
• Suprasternal pulsations due to expansile mass. - Treatment options for aortic aneurysms depend on factors
• Aneurysm of ascending aorta may produce aortic such as the size, location, rate of growth, and presence of
regurgitation. symptoms.
• Syphilitic aneurysm involving ascending aorta may - Small aneurysms may be monitored with regular imaging
produce anginal pain. studies to assess for any changes in size.
Abdominal aortic aneurysm - Large or rapidly growing aneurysms, or those causing
Symptoms symptoms, may require surgical repair or endovascular
• Asymptomatic (especially small aneurysm, <5 cm in stent grafting to reinforce the weakened portion of the aorta
diameter). and prevent rupture.
• May present with sense of fullness in epigastrium, Complications:
backache, abdominal pain or claudication of limbs. - The main complication of aortic aneurysms is rupture,
• May present acutely with abrupt onset of severe pain and which is associated with high mortality rates.
hypotension from rupture. - Aneurysms can also compress adjacent structures, leading
Signs to symptoms such as difficulty breathing, dysphagia
• A pulsatile mass extending variably between the xiphoid (difficulty swallowing), and vocal cord paralysis.
process and the umbilicus.
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5. Atrial Fibrillation. (2) 4. Permanent AF: AF where attempts to restore normal

Atrial fibrillation is the most common cardiac condition sinus rhythm have been abandoned, and the
characterized by irregularly irregular heartbeat for about arrhythmia is accepted as a permanent condition.
more than 350 beats per minute, that occurs when the Symptoms and Signs
electrical signals in the atria fire rapidly at the same time. 1. Patients may complain of "missed beats" and
Pathogenesis: palpitations due to complete irregularity of the heart
(1) Ectopic beats, often arising from the pulmonary veins, rhythm. The heart rate is irregular, often varies between
trigger atrial fibrillation. 100-150/min.
(2) Re-entry within the atria maintains atrial fibrillation, 2. There may be pulse deficit of > 10 beats/min. The pulse
with multiple interacting re-entry circuits operating deficit is the difference between the pulse rate on
simultaneously. palpation and heart rate on auscultation of heart. The
difference is due to the presence of missed beats, i.e. the
weak beats produced in the heart are not transmitted to
the pulse, hence, the deficit.
3. The symptoms and signs of the underlying heart disease,
e.g. rheumatic heart disease or thyrotoxicosis may be
present.
4. Other Symptoms and Signs
o Chest pain
o Palpitation
o Dyspnea/Faintness
Diagnosis:
Types of Atrial Fibrillation: • Electrocardiogram (ECG): ECG shows irregular R-
1. Paroxysmal AF: Episodes of AF that spontaneously R intervals and baseline is wavy and undulating
terminate within 7 days. Instead of P waves, small fibrillation (f) waves are
2. Persistent AF: AF that lasts for more than 7 days and seen. No effect of carotid massage.
requires intervention (e.g., pharmacological or • Holter monitoring, event recording, or telemetry
electrical cardioversion) to restore normal sinus may be used to document paroxysmal AF.
rhythm.
3. Long-standing Persistent AF: Continuous AF
lasting for more than 1 year.
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Treatment: 4. Thromboembolism: Apart from stroke, AF can also

Rate control: Medications (e.g., beta-blockers, calcium lead to systemic embolization to other organs, such as
channel blockers, digoxin) are used to slow the ventricular the kidneys, spleen, or extremities.
response in AF.
Rhythm control: Strategies to restore and maintain sinus 6.Atrial septal defect (3)
rhythm include antiarrhythmic drugs and cardioversion An atrial septal defect is an opening in the atrial
(electrical or pharmacological). septum, or dividing wall between the two upper chambers
Anticoagulation: Oral anticoagulants (e.g., warfarin, direct of the heart known as the right and left atria. ASD is a
oral anticoagulants) are prescribed to reduce the risk of congenital heart defect. As the fetus is growing, something
thromboembolic events, particularly stroke. occurs to affect heart development during the first eight
Cardioversion: Electrical cardioversion may be performed weeks of pregnancy, resulting in an ASD.
to restore normal sinus rhythm in selected patients. Structural Anatomy:
Ablation therapy: Catheter ablation may be considered for Normally, oxygen-poor blood returns to the right atrium
patients with symptomatic AF refractory to medical from the body, travels to the right ventricle, then is pumped
therapy, particularly in those with paroxysmal AF. into the lungs where it receives oxygen. Oxygen- rich (red)
Treatment of underlying cause: When the atrial blood returns to the left atrium from the lungs, passes into
fibrillation is due to thyrotoxicosis such as in old persons, the left ventricle and then is pumped out to the body through
treatment of thyroid disorder leads to restoration of sinus the aorta.
rhythm. In atrial septal defect it allows oxygen-rich (red) blood to
Complications: pass from the left atrium, through the opening in the septum
1. Stroke: AF increases the risk of stroke due to the and then mixes with oxygen-poor blood in the right atrium.
formation of atrial thrombi, which can embolize to the Causes:
cerebral circulation. The heart forms during the first eight weeks of fetal
2. Heart failure: AF can exacerbate or precipitate heart development. It begins as a hollow tube, then partitions
failure by reducing cardiac output and promoting within the tube develop that eventually become the septa (or
atrial remodeling. walls) dividing the right side of the heart from the left.
3. Tachycardia-induced cardiomyopathy: Prolonged Atrial septal defects occur when the partitioning process
periods of rapid ventricular response in AF can lead to does not occur completely, leaving an opening in the atrial
ventricular dysfunction and heart failure. septum.
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Some congenital heart defects may have a genetic link, Chest X-ray shows right atrial and ventricular
either occurring due to a defect in a gene, a chromosome enlargement, increased pulmonary vascularity, enlarged
abnormality or environmental exposure. pulmonary artery and rather small left ventricle and aorta.
Types: ECG
1. Secundum ASD: The most common type, involving an a. Ostium secundum: RAD with RV dominance and
opening in the central part of the atrial septum. incomplete RBBB
2. Primum ASD: Involves an opening in the lower part of b. Ostium primum: LAD with incomplete RBBB
the atrial septum, near the atrioventricular valves. c. Sinus venosus: Inverted P-wave in inferior leads.
3. Sinus venosus ASD: Involves an opening near the Junctional rhythm may be present. Rarely ostium primum
entrance of the superior or inferior vena cava into the defects may be associated with complete heart block.
right atrium. Cardiac catheterization shows oxygen content of blood
4. Coronary sinus ASD: Rare type involving an opening from right atrium to be far more than that from SVC.
near the coronary sinus, which drains blood from the Echocardiography: The primary imaging modality used to
heart muscle. diagnose ASDs and assess their size, location, and
Signs and Symptoms: associated complications. Transthoracic echocardiography
• Many individuals with small ASDs may be (TTE) and transesophageal echocardiography (TEE) are
asymptomatic and the condition may only be detected commonly performed.
incidentally during routine medical examinations. Complications
• Symptoms, when present, may include fatigue, shortness These are infrequent, especially in infants:
of breath (especially with exertion), recurrent • Heart failure seldom occurs in infancy
respiratory infections, palpitations, and difficulty • Infective endocarditis is infrequent
feeding or poor growth in infants. • Pulmonary hypertension
• With significant shunting and long-standing ASDs, • Eisenmenger complex
individuals may develop symptoms of right-sided heart Treatment
failure, such as hepatomegaly, ascites, and peripheral o Heart failure and arrhythmias should be managed
edema. medically
Diagnosis: o Antibiotic prophylaxis during dental procedures is
Physical examination: May reveal a widely split-second necessary.
heart sound (S2) and a systolic ejection murmur along the o In view of risk of complications, closure of defects, if
left sternal border. needed, should be done before school entry
 I M M A N U V E L | 50

o Small defects (<8mm) are likely to undergo • Skin changes: Skin discoloration, pallor, or cyanosis
spontaneous closure and are best observed and followed (bluish discoloration) of the affected areas, particularly
up during episodes of ischemia.
o Fossa ovalis defects usually respond to occlusive • Ulcers and gangrene: Development of non-healing
devices placed percutaneously through catheter. A ulcers, open sores, or gangrenous tissue, particularly in
proportion of them need surgical closure the fingers and toes.
o The closure of defect by open-heart surgery gives • Raynaud's phenomenon: Recurrent episodes of digital
gratifying results. It is best done in childhood. vasospasm, leading to changes in skin color (pallor,
cyanosis, redness) and sensation in response to cold or
7. Burger’s disease (Thrombo Angitis Obliterans). stress.
Definition: It is an inflammatory occlusive vascular Diagnosis:
disorder involving the small and medium-sized arteries and Diagnosis of Buerger's disease is based on clinical
veins in the distal upper and lower extremities. evaluation, medical history, and imaging studies.
Causes: The exact cause of Buerger's disease is unknown, • Angiography: Contrast-enhanced imaging studies, such
but it is strongly associated with tobacco use. Smoking and as angiography or magnetic resonance angiography
other forms of tobacco exposure are considered significant (MRA), may reveal characteristic findings of arterial
risk factors for the development and progression of the occlusion, segmental narrowing, and collateral vessel
disease. It is believed that tobacco toxins trigger an formation in the affected extremities.
inflammatory response in the blood vessels, leading to • Blood tests: Laboratory tests may be performed to rule
endothelial injury and subsequent thrombosis and out other conditions and assess for markers of
vasculitis. inflammation and thrombosis.
Signs and Symptoms: Management:
• Claudication: Intermittent claudication (pain or • Smoking cessation: The most important aspect of
cramping) in the affected extremities, typically during managing Buerger's disease is complete cessation of
physical activity and relieved with rest. tobacco use in all forms, including smoking and chewing
• Pain: Persistent pain in the fingers, toes, hands, feet, or tobacco.
other affected areas, often described as sharp, burning, or • Medications: Vasodilators, antiplatelet agents, and
throbbing. anticoagulants may be prescribed to improve blood flow
• Cold sensitivity: Sensitivity to cold temperatures in the and prevent thrombosis.
affected extremities. • Regular leg exercises (Buerger's exercises) should be
undertaken to improve the collateral circulation in the
 I M M A N U V E L | 51

legs. The patient lies flat on the couch. The legs are 3. Iatrogenic: Complications of cardiac procedures (e.g.,
supported 45° above the horizontal until the feet blanch, cardiac catheterization, pacemaker insertion) or
usually after a few minutes. The legs are then lowered complications of anticoagulation therapy can lead to
over the side until the feet flush pink. After a rest in the bleeding into the pericardial sac.
horizontal position the cycle is then repeated. 4. Malignancy: Cancerous tumors involving the
• Symptomatic treatment: Pain management, wound pericardium or adjacent structures can lead to pericardial
care, and supportive measures to alleviate symptoms and effusion and tamponade.
prevent complications such as infection and tissue loss. 5. Idiopathic: In some cases, the cause of pericardial
• Revascularization procedures: In some cases, surgical effusion leading to tamponade may be unknown
or endovascular interventions may be considered to (idiopathic).
restore blood flow to the affected areas, particularly in Pathophysiology: In cardiac tamponade, the accumulation
individuals with severe ischemia or tissue necrosis. of fluid in the pericardial sac leads to increased pressure
surrounding the heart. This pressure compresses the cardiac
8. Cardiac tamponade (3) chambers, impairing their ability to fill during diastole. As
Cardiac tamponade is a life-threatening medical a result, cardiac output decreases, leading to decreased
emergency characterized by the accumulation of fluid or perfusion of vital organs. Additionally, the decreased filling
blood in the pericardial sac, leading to compression of the of the heart chambers causes a reduction in stroke volume,
heart and impaired cardiac function. The pericardial sac is leading to further reductions in cardiac output.
a double-layered membrane that surrounds the heart and Signs and Symptoms:
provides protection and lubrication. When fluid 1. Beck's Triad:
accumulates rapidly within this space, it can exert pressure • Hypotension: Due to decreased cardiac output.
on the heart chambers, impairing their ability to fill and • Jugular venous distention (JVD): Due to impaired
pump effectively. venous return to the heart.
Causes: • Muffled heart sounds: Due to the dampening effect of
1. Trauma: Blunt or penetrating chest trauma can cause the fluid-filled pericardial sac on heart sounds.
blood to accumulate in the pericardial sac, leading to 2. Pulsus paradoxus: Exaggerated decrease in systolic
tamponade. blood pressure (>10 mmHg) during inspiration, due to
2. Pericarditis: Inflammation of the pericardium can lead increased right ventricular filling and leftward shift of
to the accumulation of fluid (pericardial effusion), the interventricular septum during inspiration, leading to
which, if excessive, can cause tamponade. further impairment of left ventricular filling.
 I M M A N U V E L | 52

3. Tachycardia: Compensatory response to decreased 2. Supportive measures: Intravenous fluids and

cardiac output. vasopressors may be administered to maintain blood
4. Dyspnea: Due to decreased cardiac output and pressure and organ perfusion.
pulmonary congestion. 3. Treatment of underlying cause: Once stabilized, the
5. Tachypnea: Secondary to dyspnea and compensatory underlying cause of cardiac tamponade (e.g.,
respiratory effort. pericarditis, trauma, malignancy) should be identified
6. Chest discomfort: Typically retrosternal or pleuritic in and managed appropriately.
nature, but may be absent in some cases. 4. Surgical intervention: In cases of recurrent tamponade
7. Weakness, fatigue, altered mental status: Secondary or underlying structural heart disease, surgical
to decreased organ perfusion. interventions such as pericardial window or
Diagnosis: pericardiectomy may be necessary to prevent recurrence.
1. Clinical evaluation: Based on history, physical
examination findings, and clinical suspicion. 9. Causes of chest pain and how will you identify
2. Echocardiography: The diagnostic modality of choice, ischemic cardiac pain? (2)
allowing visualization of pericardial effusion and Chest pain can have numerous causes, ranging from
assessment of its hemodynamic significance. benign conditions to life-threatening emergencies. Here are
3. Electrocardiography (ECG): May show electrical some common causes of chest pain:
alternans (alternating QRS amplitude) due to the 1. Gastrointestinal causes:
swinging of the heart within the fluid-filled pericardial • Gastroesophageal reflux disease (GERD):
sac. Retrosternal burning or discomfort that may be
4. Chest X-ray: May show an enlarged cardiac silhouette exacerbated by lying down, eating spicy or acidic
and/or signs of pulmonary congestion. foods, or bending over.
5. CT scan or MRI: May be used to assess pericardial • Peptic ulcer disease: Epigastric or retrosternal
effusion and identify the underlying cause. burning pain that may be relieved by antacids or food.
Management: • Esophageal spasm: Intermittent episodes of
1. Emergent pericardiocentesis: The definitive treatment squeezing or sharp chest pain that may mimic cardiac
for cardiac tamponade involves the insertion of a needle pain.
or catheter into the pericardial sac to drain the • Identifying features: Symptoms such as dysphagia,
accumulated fluid or blood and relieve the pressure on regurgitation, acidic taste in the mouth, and response
the heart. to antacids can suggest gastrointestinal causes.
 I M M A N U V E L | 53

2. Musculoskeletal causes: • Angina: Typically described as pressure, tightness,

• Costochondritis: Inflammation of the cartilage that or squeezing in the chest, often provoked by exertion
connects the ribs to the sternum, causing localized or stress and relieved with rest or nitroglycerin.
chest pain that may worsen with palpation or • Acute Coronary Syndrome (ACS): Includes
movement. unstable angina, non-ST segment elevation
• Rib fractures: Sharp, localized chest pain that myocardial infarction (NSTEMI), and ST-segment
worsens with breathing or movement. elevation myocardial infarction (STEMI). Chest pain
• Muscle strain: Chest pain related to overuse or in ACS is often more severe and prolonged than
trauma to the chest wall muscles. stable angina and may not be relieved with rest or
• Identifying features: Chest pain reproducible with nitroglycerin.
palpation or movement, absence of radiation to other Identifying Ischemic Cardiac Pain:
areas, and absence of associated symptoms such as 1. Characteristics of pain: Ischemic cardiac pain is
dyspnea or diaphoresis. often described as pressure, tightness, or squeezing in
3. Pulmonary causes: the chest, typically located substernally and may
• Pneumonia: Chest pain that may be pleuritic radiate to the left arm, jaw, or back.
(worsened by deep breathing or coughing) and 2. Associated symptoms: Symptoms such as dyspnea,
associated with fever, cough, and sputum production. diaphoresis, nausea, and vomiting may accompany
• Pulmonary embolism: Acute onset pleuritic chest ischemic cardiac pain.
pain associated with dyspnea, tachypnea, and 3. Exacerbating factors: Ischemic cardiac pain may be
occasionally hemoptysis. triggered or exacerbated by exertion or emotional
• Pneumothorax: Sudden-onset sharp chest pain stress and relieved with rest or nitroglycerin.
associated with dyspnea and decreased breath sounds 4. Medical history: Risk factors for coronary artery
on the affected side. disease (e.g., hypertension, hyperlipidemia, diabetes,
• Identifying features: Symptoms such as cough, smoking) and history of previous cardiac events can
dyspnea, hemoptysis, and signs of respiratory increase the likelihood of ischemic cardiac pain.
distress can suggest pulmonary causes. 5. Response to treatment: Ischemic cardiac pain may
4. Cardiac causes: respond to nitroglycerin or other antianginal
• Ischemic cardiac pain occurs when the blood flow to medications.
the heart muscle is inadequate, usually due to 6. Diagnostic testing: Electrocardiogram (ECG),
coronary artery disease (CAD). cardiac enzymes (troponin), and imaging studies (e.g.,
stress testing, coronary angiography) can help
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confirm the presence of ischemic cardiac pain and during or after the procedure. This can occur due to
identify underlying coronary artery disease. inadequate blood flow to the heart muscle during surgery
or complications such as graft occlusion or thrombosis.
10.Complications after CABG surgery 5. Stroke: Stroke is a rare but serious complication of
Coronary artery bypass grafting (CABG) surgery is a CABG surgery. It can occur due to embolization of
common and effective treatment for coronary artery disease plaque or blood clots from the heart or blood vessels
(CAD) in which blocked or narrowed coronary arteries are during surgery or as a result of manipulation of the aorta
bypassed with grafts to improve blood flow to the heart during surgery.
muscle. While CABG surgery is generally safe, like any 6. Pulmonary complications: Postoperative pulmonary
surgical procedure, it carries potential risks and complications, such as atelectasis (lung collapse),
complications. Here are some of the common complications pneumonia, or respiratory failure, can occur due to
that can occur after CABG surgery: factors such as anesthesia, immobility, and impaired lung
1. Bleeding: Bleeding is a common complication after function.
CABG surgery, particularly at the site where the grafts 7. Renal dysfunction: Some patients may experience
are harvested (e.g., the leg vein or radial artery). temporary or permanent kidney dysfunction after CABG
Excessive bleeding may require blood transfusions or surgery, particularly those with pre-existing kidney
surgical re-exploration to control bleeding. disease or risk factors such as diabetes and hypertension.
2. Infection: Surgical site infections, pneumonia, urinary 8. Neurological complications: In addition to stroke, other
tract infections, and bloodstream infections can occur neurological complications such as cognitive
after CABG surgery. Prophylactic antibiotics are dysfunction, delirium, or peripheral neuropathy can
typically administered before and after surgery to reduce occur after CABG surgery, particularly in older adults or
the risk of infection. those with pre-existing neurological conditions.
3. Arrhythmias: Heart rhythm disturbances, such as atrial 9. Deep vein thrombosis (DVT) and pulmonary
fibrillation, atrial flutter, or ventricular arrhythmias, can embolism (PE): Blood clots can form in the legs (DVT)
occur after CABG surgery. Most arrhythmias are and travel to the lungs (PE) after CABG surgery,
temporary and resolve on their own, but some may particularly in patients who are immobile or have other
require medical intervention or antiarrhythmic risk factors for thromboembolism.
medications. 10. Wound complications: Surgical site complications,
4. Myocardial infarction (heart attack): Although such as wound infection, dehiscence (wound opening),
CABG surgery is performed to improve blood flow to or sternotomy (chest incision) complications, can occur
the heart, there is a small risk of myocardial infarction
 I M M A N U V E L | 55

after CABG surgery and may require additional • Structural anatomy: Aorta arises from the right
treatment or surgical intervention. ventricle, and the pulmonary artery arises from the
11. Graft failure: Over time, grafts used in CABG left ventricle.
surgery may become blocked or narrowed (graft failure), • Clinical features: Cyanosis shortly after birth,
leading to recurrent symptoms of angina or the need for respiratory distress, poor feeding, failure to thrive.
additional interventions such as percutaneous coronary • Treatment: Arterial switch operation (also known as
intervention (PCI) or repeat CABG surgery. the Jatene procedure) is the primary surgical
treatment for TGA. This involves switching the
11.Congenital cyanotic heart disease. position of the great arteries to restore the normal
1. Tetralogy of Fallot (TOF): circulation pattern. Additionally, a septostomy
• Structural anatomy: TOF consists of four primary (balloon atrial septostomy) may be performed as a
abnormalities: temporary measure to increase mixing of oxygenated
• Ventricular septal defect (VSD): Opening between and deoxygenated blood until surgery can be
the right and left ventricles. performed.
• Pulmonary stenosis: Narrowing of the pulmonary 3. Tricuspid atresia:
valve or pulmonary artery. • Structural anatomy: Absence or severe
• Overriding aorta: The aorta is positioned over both underdevelopment of the tricuspid valve, leading
the left and right ventricles. to an obstruction between the right atrium and right
• Right ventricular hypertrophy: Thickening of the ventricle.
muscle of the right ventricle. • Clinical features: Cyanosis, respiratory distress,
• Clinical features: Cyanosis, episodes of hypoxia (tet poor feeding, failure to thrive, hepatomegaly,
spells), dyspnea, failure to thrive, clubbing of fingers, clubbing of fingers.
squatting behavior. • Treatment: Surgical options for tricuspid atresia
• Treatment: Surgical repair is typically performed in may include a staged approach. Initial procedures
infancy and may involve a procedure called a may involve creating a connection between the
"complete repair" or "intracardiac repair" to close the right atrium and ventricle (e.g., Blalock-Taussig
VSD, relieve pulmonary stenosis, and reposition the shunt) to increase pulmonary blood flow.
overriding aorta. This often includes patching the Subsequent surgeries may include Fontan
VSD, widening the pulmonary outflow tract, and procedure to redirect blood flow from the right
correcting the position of the aorta. atrium directly to the pulmonary arteries,
2. Transposition of the Great Arteries (TGA): bypassing the right ventricle altogether.
 I M M A N U V E L | 56

4. Ebstein's anomaly: 12.Constrictive pericarditis

• Structural anatomy: Malformation of the Constrictive pericarditis is a condition characterized
tricuspid valve, displacement of the valve leaflets by the thickening, fibrosis, and calcification of the
into the right ventricle. pericardium, the sac-like membrane surrounding the heart.
• Clinical features: Cyanosis, respiratory distress, This leads to the loss of pericardial elasticity and restricts
heart murmur, palpitations, fatigue, exercise the normal expansion and filling of the heart during the
intolerance. cardiac cycle, impairing cardiac function. As a result,
• Treatment: Surgical repair of Ebstein's anomaly patients with constrictive pericarditis may experience
may involve various techniques to reconstruct or symptoms of heart failure and hemodynamic compromise.
replace the malformed tricuspid valve. Procedures Causes: Constrictive pericarditis can have various causes,
may include tricuspid valve repair, cone including:
reconstruction, or tricuspid valve replacement. 1. Idiopathic or unknown cause.
Additional procedures may be needed to address 2. Prior episodes of pericarditis, including viral or bacterial
associated defects such as closure of atrial septal pericarditis.
defects or repair of anomalous pulmonary venous 3. Radiation therapy to the chest for conditions such as
connections. cancer.
5. Total anomalous pulmonary venous connection 4. Cardiac surgery or interventions involving the
(TAPVC): pericardium.
• Structural anatomy: Pulmonary veins do not connect 5. Connective tissue disorders.
normally to the left atrium but instead drain into other 6. Tuberculosis.
veins or the right atrium. 7. Chronic renal failure.
• Clinical features: Cyanosis, respiratory distress, poor 8. Inflammatory conditions such as rheumatoid arthritis.
feeding, failure to thrive, heart murmur. Pathophysiology: In constrictive pericarditis, the
• Treatment: Surgical repair involves redirecting the thickened and rigid pericardium restricts the normal
pulmonary veins to drain into the left atrium. This diastolic filling of the heart chambers, leading to elevated
typically involves an intracardiac repair to reroute the pressures within the heart. This impairs cardiac output and
pulmonary veins and close any associated atrial septal causes systemic venous congestion. The filling of the
defects. The specific technique used may vary ventricles becomes more rapid and less compliant, resulting
depending on the anatomy of the anomalous in the characteristic hemodynamic findings of "square root"
connections. or "dip-and-plateau" pressure tracings on cardiac
catheterization.
 I M M A N U V E L | 57

Clinical Features: Treatment:

1. Dyspnea: Particularly on exertion due to impaired 1. Medical management: Symptomatic relief with
cardiac output. diuretics to reduce volume overload and optimize fluid
2. Fatigue and weakness: Resulting from reduced balance.
systemic perfusion. 2. Pericardiectomy: Surgical removal of the thickened
3. Peripheral edema and ascites: Due to elevated right- pericardium is the definitive treatment for constrictive
sided pressures and venous congestion. pericarditis, aiming to restore normal cardiac function.
4. Orthopnea and paroxysmal nocturnal dyspnea: This procedure may be performed via a median
Symptoms of heart failure exacerbated by lying flat. sternotomy or minimally invasive approaches depending
5. Kussmaul's sign: Paradoxical increase in jugular on the individual patient's condition and surgical
venous pressure during inspiration, indicating impaired expertise.
right ventricular filling. 3. Treat underlying cause: if found – In case of TB
6. Pericardial knock: A high-pitched early diastolic sound antitubercular drugs may be given.
heard on cardiac auscultation.
7. Hepatomegaly: Due to hepatic congestion. 13.Coronary Artery Bypass Grafting/ Surgical
8. Pulsus paradoxus: Exaggerated decrease in systolic management of coronary artery disease
blood pressure during inspiration, due to decreased left Coronary Artery Bypass Grafting (CABG) is a
ventricular filling. surgical procedure used to treat coronary artery disease
Diagnosis: (CAD), a condition characterized by narrowing or
1. Echocardiography: May demonstrate thickened blockages in the coronary arteries that supply blood to the
pericardium, abnormal septal motion, and signs of heart muscle. CABG is commonly performed to improve
ventricular interdependence. blood flow to the heart and relieve symptoms such as angina
2. Cardiac catheterization: May reveal equalization of (chest pain) and reduce the risk of heart attack.
diastolic pressures in all cardiac chambers and a dip-and- Procedure: During CABG surgery, a cardiothoracic
plateau pressure waveform. surgeon creates new routes for blood flow to bypass
3. CT/MRI: Can provide detailed imaging of the blocked or narrowed coronary arteries. The procedure
pericardium and surrounding structures. typically involves the following steps:
4. Pericardial biopsy: May be performed in cases of 1. Preparation: The patient is placed under general
uncertain etiology, such as suspected tuberculosis or anesthesia, and monitoring devices are attached to
neoplastic disease. monitor vital signs throughout the procedure. The
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surgical site is prepared, and the chest may be shaved and technique may be suitable for some patients who are at
cleaned. higher risk for complications associated with CPB.
2. Harvesting of grafts: The surgeon harvests healthy Indications: CABG may be recommended for patients
blood vessels, typically from the patient's own body with:
(autologous grafts), such as the internal mammary artery • Severe coronary artery disease (CAD) involving
(IMA) from the chest wall or saphenous vein from the multiple vessels.
leg. Occasionally, arteries from the arm (radial artery) or • Left main coronary artery disease.
other blood vessels may also be used. • Failed percutaneous coronary intervention (PCI) or
3. Cardiopulmonary bypass (CPB): In traditional CABG stenting.
surgery, the patient is connected to a heart-lung bypass • Persistent angina or symptoms despite optimal medical
machine, which temporarily takes over the function of the therapy.
heart and lungs. This allows the surgeon to perform the • High-risk features such as reduced left ventricular
procedure on a motionless and bloodless field. function or diabetes.
4. Graft insertion: The harvested blood vessels are then Recovery:
attached (grafted) to the coronary arteries, creating new • After CABG surgery, patients are closely monitored in
routes for blood flow to bypass the blockages. The grafts the intensive care unit (ICU) or cardiac care unit (CCU)
are usually sewn distal to the blockage, allowing blood to to ensure stability and manage any complications.
flow around the obstruction and reach the heart muscle. • Patients typically stay in the hospital for several days to
5. Closure: After the grafts are in place, the heart-lung a week, depending on their recovery progress.
bypass machine is gradually weaned off, and the heart is • Cardiac rehabilitation programs may be recommended to
allowed to resume pumping on its own. The chest help patients regain strength, improve cardiovascular
incision(s) are closed with sutures or staples, and a sterile fitness, and reduce the risk of future cardiac events.
dressing is applied.
Types of CABG: 14. Coronary perfusion. (2)
1. Traditional CABG (On-pump CABG): The surgery is Coronary perfusion refers to the process by which blood is
performed using a heart-lung bypass machine to delivered to the myocardium (heart muscle) through the
maintain circulation during the procedure. coronary arteries to supply oxygen and nutrients and
2. Off-pump CABG (Beating heart surgery): The remove waste products. Adequate coronary perfusion is
surgery is performed while the heart is still beating, essential for the normal functioning of the heart and
without the use of a heart-lung bypass machine. This maintenance of cardiac output.
 I M M A N U V E L | 59

Process of Coronary Perfusion: coronary perfusion pressure decreases, coronary

1. Coronary Arteries: The coronary arteries are the blood resistance vessels dilate to increase blood flow, and vice
vessels that supply oxygenated blood to the heart muscle. versa.
The right coronary artery (RCA) and the left coronary 5. Factors Affecting Coronary Perfusion: Several factors
artery (LCA) are the two main coronary arteries. The influence coronary perfusion, including systemic blood
LCA further divides into the left anterior descending pressure, heart rate, myocardial oxygen demand,
artery (LAD) and the left circumflex artery (LCx). coronary artery diameter, and vascular resistance.
2. Diastole: Coronary perfusion primarily occurs during Conditions such as coronary artery disease, vasospasm,
diastole, the resting phase of the cardiac cycle when the and thrombosis can impair coronary perfusion and lead
heart relaxes and fills with blood. During diastole, the to myocardial ischemia and angina.
coronary arteries are perfused with blood as they are 6. Clinical Implications: Adequate coronary perfusion is
compressed by the contracting myocardium. The crucial for maintaining myocardial oxygenation and
compression of the coronary arteries during systole helps preventing ischemia and myocardial infarction.
to expel blood from the coronary vessels, while Conditions that compromise coronary perfusion, such as
relaxation during diastole allows for the filling of the coronary artery disease, hypertension, and heart failure,
coronary arteries with oxygenated blood. can increase the risk of adverse cardiac events.
3. Coronary Perfusion Pressure: Coronary perfusion
pressure (CPP) is the difference between the pressure in 15. Cyanotic Spell. (2)
the aorta (aortic pressure) and the pressure in the A cyanotic spell, also known as a tet spell or
coronary arteries (coronary sinus pressure) during hypercyanotic spell, is a characteristic event seen in infants
diastole. CPP represents the driving force for coronary and young children with certain congenital heart defects,
blood flow and is calculated by subtracting the coronary particularly Tetralogy of Fallot (TOF). It is a sudden
sinus pressure from the aortic pressure. A higher CPP is episode of profound cyanosis (bluish discoloration of the
associated with increased coronary blood flow and better skin and mucous membranes) accompanied by respiratory
myocardial perfusion. distress and potentially life-threatening hemodynamic
4. Autoregulation: The coronary circulation is regulated instability.
by various mechanisms to ensure adequate blood flow to Features of a Cyanotic Spell:
meet the metabolic demands of the myocardium. 1. Cyanosis: The hallmark feature of a cyanotic spell is the
Autoregulation helps to maintain coronary perfusion sudden onset of cyanosis, where the skin, lips, and
within a narrow range despite changes in systemic blood mucous membranes appear bluish due to decreased
pressure, cardiac output, and metabolic demands. When
 I M M A N U V E L | 60

oxygenation of the blood. This cyanosis can be severe 3. Sedation: Sedation or calming measures may be
and may progress rapidly. employed to reduce agitation and minimize triggering
2. Respiratory Distress: Children experiencing a cyanotic factors for cyanotic spells.
spell often exhibit respiratory distress, including rapid or 4. IV Fluids: Intravenous fluids may be administered to
labored breathing, grunting, and nasal flaring. They may optimize hydration and improve cardiac output.
also appear agitated or restless. 5. Pharmacotherapy: Medications such as morphine,
3. Decreased Oxygen Saturation: Measurement of which reduces systemic vascular resistance and
oxygen saturation using pulse oximetry typically reveals decreases the severity of cyanotic spells, may be used in
a significant decrease in arterial oxygen saturation some cases. Propranolol or other beta-blockers may also
during a cyanotic spell, often below normal levels. be beneficial in certain situations.
4. Hemodynamic Instability: Cyanotic spells can lead to 6. Emergency Treatment: In severe cases with
hemodynamic instability, characterized by decreased hemodynamic instability, immediate medical attention is
cardiac output, hypotension, and decreased systemic required. Measures such as providing supplemental
perfusion. This can result in lethargy, altered mental oxygen, initiating positive pressure ventilation,
status, or even loss of consciousness. administering intravenous fluids, and preparing for
5. Triggering Factors: Cyanotic spells are often emergent intubation and mechanical ventilation may be
precipitated by events that increase right ventricular necessary.
outflow obstruction or decrease pulmonary blood flow, Prevention: The prevention of cyanotic spells in children
such as crying, feeding, defecation, or agitation. These with congenital heart defects involves careful monitoring,
activities can exacerbate the imbalance between avoidance of triggers, optimization of cardiac function, and
pulmonary and systemic blood flow in children with timely surgical intervention to correct underlying cardiac
congenital heart defects like TOF. abnormalities when appropriate.
Management of Cyanotic Spells:
1. Positioning: Place the child in a knee-to-chest or 16.Dilated Cardiomyopathy
squatting position, which helps increase systemic Dilated cardiomyopathy (DCM) is a condition
vascular resistance and decrease right-to-left shunting of characterized by enlargement (dilation) of the heart
blood, improving systemic oxygenation. chambers, particularly the left ventricle, along with
2. Oxygen Therapy: Administer supplemental oxygen to impaired systolic function, leading to reduced cardiac
improve oxygenation and alleviate hypoxemia. High- output and heart failure. DCM can affect both children and
flow oxygen via a face mask or nasal cannula is often adults and is one of the most common forms of
used initially. cardiomyopathy.
 I M M A N U V E L | 61

Causes: The exact cause of dilated cardiomyopathy may 5. S3 gallop: Presence of an extra heart sound (S3) on
not always be clear, but it can be attributed to a variety of auscultation, indicating impaired ventricular function.
factors, including: 6. Arrhythmias: DCM increases the risk of various
1. Genetic factors: DCM can be inherited in an cardiac arrhythmias, including atrial fibrillation,
autosomal dominant, autosomal recessive, or X- ventricular tachycardia, or ventricular fibrillation.
linked pattern, with mutations in multiple genes Diagnosis:
implicated in its development. 1. Echocardiography: The primary diagnostic modality
2. Alcohol excess (alcoholic cardiomyopathy), certain for DCM, echocardiography can assess cardiac chamber
toxins (cocaine, cobalt). size, wall thickness, and ventricular function.
3. Peripartum cardiomyopathy (developing in last 2. Electrocardiography (ECG): ECG may reveal
trimester or within 6 months after delivery in nonspecific changes, such as ST-segment and T-wave
multiparous woman). abnormalities, atrial or ventricular arrhythmias, or
4. Metabolic diseases, e.g. haemochromatosis, conduction defects.
sarcoidosis, amyloidosis, diabetes. 3. Cardiac MRI: Provides detailed imaging of the heart
5. Neuromuscular diseases e.g. Friedreich's ataxia, structure, function, and tissue characterization, helpful
muscular dystrophy. for diagnosis and assessing myocardial viability.
6. Drugs e.g. doxorubicin, cyclophosphamide. 4. Laboratory tests: Blood tests may be performed to
7. Nutritional, e.g. thiamine, deficiency (Beriberi). evaluate for markers of heart failure, electrolyte
Clinical Features: The clinical presentation of dilated imbalances, or evidence of myocardial injury.
cardiomyopathy can vary widely and may include: Treatment:
1. Heart failure symptoms: Dyspnea (shortness of 1. Medications: Pharmacotherapy for DCM aims to reduce
breath), fatigue, orthopnea (difficulty breathing while symptoms, improve cardiac function, and slow disease
lying flat), paroxysmal nocturnal dyspnea, and exercise progression. This may include angiotensin-converting
intolerance. enzyme (ACE) inhibitors, beta-blockers, diuretics,
2. Peripheral edema: Swelling of the legs, ankles, or feet aldosterone antagonists, and inotropic agents.
due to fluid retention. 2. Device therapy: In some cases, implantable
3. Ascites: Accumulation of fluid in the abdominal cavity, cardioverter-defibrillators (ICDs) or cardiac
leading to abdominal distension. resynchronization therapy (CRT) devices may be
4. Jugular venous distention: Visible bulging of the indicated to prevent sudden cardiac death or improve
jugular veins in the neck, indicating increased central cardiac function.
venous pressure.
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3. Lifestyle modifications: Patients with DCM are advised 3. Assessment of Jugular Venous Pressure (JVP): The
to follow a heart-healthy diet, limit alcohol intake, quit JVP is estimated by measuring the vertical distance
smoking, and engage in regular exercise as tolerated. between the highest point of venous pulsation and the
4. Surgical intervention: In select cases, heart sternal angle (also known as the angle of Louis), which
transplantation or ventricular assist device (VAD) correlates with the right atrial pressure. The JVP is
implantation may be considered for patients with typically measured in centimeters of water (cmH2O) or
advanced heart failure refractory to medical therapy. millimeters of mercury (mmHg).
Importance of Jugular Venous Pulse Examination:
17.Examination of jugular venous pulse and its 1. Assessment of Volume Status: Changes in the JVP
importance. (4) can provide valuable information about intravascular
The examination of the jugular venous pulse (JVP) is volume status. A high or elevated JVP may indicate
a valuable clinical tool to assess the hemodynamic status of volume overload or fluid retention, while a low JVP may
patients, particularly those with suspected or known suggest hypovolemia or dehydration.
cardiovascular conditions. The jugular venous pulse 2. Evaluation of Right-Sided Cardiac Function: The
provides important information about right-sided cardiac JVP reflects right atrial pressure, which is influenced by
function, fluid status, and intravascular volume. right-sided cardiac function, venous return, and preload.
Technique: The examination of the jugular venous pulse Abnormalities in the JVP waveform or contour can
involves observing the pulsations of the internal jugular indicate right heart dysfunction, such as right heart
vein (IJV) in the neck while the patient is in a semi- failure or tricuspid valve abnormalities.
recumbent position (usually at a 45-degree angle). The 3. Diagnosis of Cardiac Conditions: Examination of
following steps are typically followed: the JVP is particularly useful in the diagnosis and
1. Patient Positioning: The patient is placed in a semi- monitoring of conditions such as heart failure,
recumbent position with the head of the bed elevated to constrictive pericarditis, cardiac tamponade, and
approximately 45 degrees. This position allows for pulmonary hypertension. Changes in the JVP waveform,
better visualization and assessment of the jugular such as loss of normal pulsatility or exaggerated a or v
venous pulsations. waves, can provide diagnostic clues.
2. Identification of the Internal Jugular Vein: The 4. Assessment of Fluid Responsiveness: In critically ill
internal jugular vein is located medial to the patients, assessment of the JVP can help guide fluid
sternocleidomastoid muscle in the neck. It is typically management strategies by evaluating the response to
visible as a pulsating column of blood when the patient volume expansion. An increase in the JVP with volume
is positioned appropriately. infusion may indicate fluid responsiveness, whereas no
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change or a decrease in the JVP may suggest non- Evaluation and Selection Process: Patients undergoing
responsiveness. heart transplantation undergo a comprehensive evaluation
5. Prognostic Indicator: The JVP can serve as a process to assess their candidacy for transplantation. This
prognostic indicator in patients with cardiovascular evaluation includes:
diseases. Persistent elevation of the JVP despite 1. Medical history and physical examination.
treatment may be associated with worse outcomes and 2. Cardiac imaging studies (echocardiography, cardiac
increased mortality risk. MRI) to assess cardiac function and anatomy.
3. Laboratory tests to evaluate organ function and screen
18.Heart transplantation for infectious diseases.
Heart transplantation is a surgical procedure 4. Psychosocial assessment to evaluate social support,
performed to replace a diseased or failing heart with a coping mechanisms, and adherence to medical therapy.
healthy donor heart from a deceased individual. It is 5. Assessment by a multidisciplinary team, including
considered the gold standard treatment for patients with cardiologists, cardiac surgeons, transplant coordinators,
end-stage heart failure who have exhausted medical therapy psychologists, and social workers.
and other treatment options. Heart transplantation offers the Surgical Procedure: The heart transplantation procedure
potential for improved quality of life and long-term survival involves several key steps:
in carefully selected patients. 1. Donor heart procurement: A suitable donor heart is
Indications for Heart Transplantation: Heart identified based on compatibility criteria such as blood
transplantation may be considered for patients with end- type, size, and tissue matching. The donor heart is
stage heart failure who meet specific criteria, including: harvested from a deceased donor and preserved for
1. Severe symptoms of heart failure despite optimal transplantation.
medical therapy. 2. Recipient preparation: The recipient patient is prepared
2. Impaired left ventricular function with reduced ejection for surgery, including anesthesia induction and
fraction. placement of monitoring devices.
3. Presence of debilitating symptoms such as dyspnea, 3. Cardiopulmonary bypass (CPB): The recipient's heart
fatigue, and exercise intolerance. is stopped, and cardiopulmonary bypass is initiated to
4. Inability to perform activities of daily living due to heart maintain circulation during the procedure.
failure symptoms. 4. Donor heart implantation: The recipient's diseased
5. Absence of significant comorbidities or heart is removed, and the donor heart is sewn into place,
contraindications to transplantation. connecting the major blood vessels and cardiac
chambers.
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5. Weaning from CPB: The recipient's heart is gradually exceeds 85%, and the five-year survival rate is
allowed to resume beating, and CPB is discontinued. approximately 70-75%. However, long-term survival is
6. Closure: The surgical incisions are closed, and the influenced by factors such as age, comorbidities, graft
patient is transferred to the intensive care unit (ICU) for rejection, and complications related to immunosuppression.
postoperative monitoring and care.
Postoperative Care and Immunosuppression: After heart 19.Holter test.
transplantation, patients require intensive postoperative A Holter monitor, also known as ambulatory
care and monitoring to prevent complications and optimize electrocardiography, is a portable device used to
graft function. Key aspects of postoperative care include: continuously record the electrical activity of the heart over
1. Immunosuppressive therapy: Patients receive lifelong an extended period, typically 24 to 48 hours or longer. It is
immunosuppressive medications to prevent rejection of a non-invasive diagnostic tool used to evaluate cardiac
the donor heart. This typically includes a combination of rhythm disturbances and assess for symptoms such as
drugs such as calcineurin inhibitors (e.g., tacrolimus, palpitations, dizziness, syncope (fainting), or suspected
cyclosporine), antimetabolites (e.g., mycophenolate arrhythmias.
mofetil), and corticosteroids. Purpose: The primary purposes of a Holter monitor test
2. Infection prophylaxis: Patients are at increased risk of include:
infection due to immunosuppression and receive 1. Detection of Arrhythmias: Holter monitoring allows
prophylactic antibiotics, antiviral agents, and antifungal for the detection and documentation of various cardiac
medications to prevent opportunistic infections. arrhythmias, including bradyarrhythmias (slow heart
3. Cardiac monitoring: Patients undergo frequent cardiac rhythms), tachyarrhythmias (fast heart rhythms), atrial
monitoring, echocardiography, and endomyocardial fibrillation, atrial flutter, ventricular ectopy, and pauses.
biopsies to assess graft function and detect signs of 2. Symptom Correlation: Holter monitoring can help
rejection or complications. correlate symptoms such as palpitations, dizziness, or
4. Rehabilitation: Cardiac rehabilitation and exercise syncope with specific arrhythmias or changes in heart
programs are initiated to promote physical recovery, rhythm patterns.
optimize cardiovascular fitness, and improve quality of 3. Evaluation of Cardiac Function: Continuous
life. monitoring of the heart's electrical activity provides
Outcomes and Prognosis: Heart transplantation can valuable information about cardiac function, conduction
significantly improve quality of life and long-term survival abnormalities, and the occurrence of silent or
in carefully selected patients with end-stage heart failure. asymptomatic arrhythmias.
The one-year survival rate after heart transplantation
 I M M A N U V E L | 65

4. Assessment of Treatment Efficacy: Holter monitoring • Palpitations or other symptoms suggestive of

may be used to evaluate the effectiveness of arrhythmias.
antiarrhythmic medications, pacemakers, or other • Syncope (fainting) or unexplained loss of consciousness.
interventions in managing cardiac rhythm disturbances. • Evaluation of known or suspected arrhythmias,
Procedure: The Holter monitor test typically involves the including atrial fibrillation, ventricular ectopy, or pauses.
following steps: • Assessment of antiarrhythmic drug therapy efficacy or
1. Placement of Electrodes: Small adhesive electrodes are pacemaker function.
attached to the patient's chest, which are connected to a • Risk stratification in patients with underlying heart
portable recording device worn on a belt or shoulder disease or cardiovascular risk factors.
strap. Limitations: While Holter monitoring is a valuable
2. Recording Period: The patient is instructed to resume diagnostic tool, it has some limitations, including:
their usual activities while wearing the Holter monitor • Limited duration of monitoring compared to implantable
for the specified recording period, usually 24 to 48 hours loop recorders or event monitors.
or longer. They are provided with a diary to record • Inability to capture symptoms that occur infrequently or
symptoms, activities, and events during the monitoring intermittently.
period. • Patient discomfort or inconvenience associated with
3. Recording Analysis: After the monitoring period is wearing the monitor and electrodes.
complete, the recorded data is downloaded from the • Potential for artifact or noise interference that may affect
Holter monitor to a computer for analysis. The the accuracy of recordings.
electrocardiographic tracings are reviewed to identify
arrhythmias, abnormalities, and correlations with 20.Hypertensive Emergencies.
symptoms. Hypertensive emergencies involve systolic blood
4. Interpretation and Reporting: The findings of the pressure (SBP) greater than 180 mmHg and/or diastolic
Holter monitor test are interpreted, and a report is blood pressure (DBP) greater than 120 mmHg along with
generated summarizing the recorded cardiac rhythm, evidence of acute target organ damage. The term
arrhythmias detected, symptomatic events, and any "hypertensive crisis" encompasses both hypertensive
relevant clinical findings. Recommendations for further emergencies and urgencies, with emergencies being the
evaluation or management may be provided based on the more severe category.
results. Causes: Hypertensive emergencies can occur due to
Indications: Holter monitoring may be indicated for various underlying conditions, including:
patients with: 1. Uncontrolled essential hypertension.
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2. Acute kidney injury or chronic kidney disease. 2. Laboratory tests: Complete blood count, serum
3. Acute myocardial infarction or unstable angina. electrolytes, renal function tests, cardiac enzymes,
4. Aortic dissection or other aortic pathologies. coagulation studies, and urinalysis to assess for end-
5. Intracerebral hemorrhage or ischemic stroke. organ damage and identify underlying causes.
6. Hypertensive encephalopathy. 3. Electrocardiogram (ECG): To evaluate for evidence of
7. Pre-eclampsia or eclampsia during pregnancy. cardiac ischemia, arrhythmias, or left ventricular
8. Adrenal gland disorders such as pheochromocytoma or hypertrophy.
adrenal crisis. 4. Imaging studies: Chest X-ray, echocardiography,
9. Drug-induced hypertension, such as from stimulant computed tomography (CT) scan, or magnetic resonance
overdose or abrupt cessation of antihypertensive imaging (MRI) may be indicated based on clinical
medications. suspicion to assess for acute complications such as
Clinical Features: Patients with hypertensive emergencies pulmonary edema, aortic dissection, or stroke.
may present with symptoms related to acute target organ Treatment: The primary goal of treatment in hypertensive
damage, including: emergencies is to rapidly lower blood pressure to prevent or
1. Severe headache. minimize acute end-organ damage while avoiding
2. Visual disturbances or changes in vision. precipitous decreases that could lead to hypoperfusion.
3. Altered mental status, confusion, or seizures. Treatment modalities may include:
4. Chest pain or shortness of breath. 1. Intravenous antihypertensive medications: Agents
5. Focal neurologic deficits, such as hemiparesis or such as nitroglycerin, sodium nitroprusside, nicardipine,
aphasia. labetalol, or fenoldopam are commonly used for
6. Nausea, vomiting, or abdominal pain. controlled reduction of blood pressure.
7. Signs of end-organ damage, such as acute kidney injury 2. Management of underlying conditions: Treatment of
(oliguria, elevated creatinine), pulmonary edema, or the underlying cause, such as reperfusion therapy for
hypertensive retinopathy. acute myocardial infarction or aortic repair for aortic
Diagnosis: Diagnosis of a hypertensive emergency is dissection.
primarily clinical, based on the presence of severely 3. Monitoring and supportive care: Continuous
elevated blood pressure and evidence of acute target organ monitoring of vital signs, cardiac rhythm, urine output,
damage. Diagnostic workup may include: and neurologic status. Supportive measures may include
1. Measurement of blood pressure: Repeated supplemental oxygen, intravenous fluids, and correction
measurements to confirm elevated blood pressure. of electrolyte imbalances.
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4. Admission to intensive care unit (ICU): Patients with cardiomyopathies, valvular heart disease, pericardial
hypertensive emergencies often require close monitoring diseases, and intracardiac masses.
and intensive care management to optimize outcomes • Doppler echocardiography enables assessment of
and prevent complications. blood flow patterns, velocities, and pressures, aiding
Prognosis: The prognosis of hypertensive emergencies in the diagnosis of valvular regurgitation or stenosis,
depends on various factors, including the underlying cause, intracardiac shunts, and assessing hemodynamic
severity of end-organ damage, promptness of treatment, and severity.
comorbidities. Early recognition and prompt initiation of 2. Assessment of Cardiac Function:
appropriate treatment are essential to improve outcomes • Echocardiography allows for the evaluation of cardiac
and minimize morbidity and mortality associated with function, including left ventricular (LV) and right
hypertensive emergencies. Long-term management focuses ventricular (RV) systolic and diastolic function,
on blood pressure control and addressing modifiable risk ejection fraction, and wall motion abnormalities.
factors to prevent future hypertensive crises. • It provides quantitative measurements such as LV
dimensions, wall thickness, volumes, and myocardial
21.Importance of Echocardiography (3) strain, which are crucial for assessing cardiac
Echocardiography, also known as cardiac ultrasound, is performance and detecting dysfunction or
a non-invasive imaging modality that utilizes high- remodeling.
frequency sound waves (ultrasound) to visualize the 3. Monitoring Disease Progression:
structures and function of the heart in real-time. It plays a • Echocardiography plays a key role in monitoring
crucial role in the diagnosis, assessment, and management disease progression and treatment response in patients
of various cardiovascular conditions. Some key aspects with cardiovascular diseases, such as heart failure,
highlighting the importance of echocardiography include: ischemic heart disease, or cardiomyopathies.
1. Diagnostic Utility: • Serial echocardiographic assessments enable
• Echocardiography allows for the visualization of clinicians to track changes in cardiac structure,
cardiac structures, including the chambers, valves, function, and hemodynamics over time, guiding
myocardium, and great vessels, enabling the detection therapeutic decisions and optimizing patient
of abnormalities such as structural defects, tumors, management.
thrombi, or congenital heart diseases. 4. Guidance for Interventional Procedures:
• It provides valuable diagnostic information in the • Echocardiography provides real-time imaging
evaluation of conditions such as heart failure, guidance for various interventional procedures,
including transesophageal echocardiography (TEE)
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for intracardiac device placement, valve supply to the myocardium during exertion, suggestive of
interventions, or percutaneous structural heart underlying CAD.
interventions. Assessment of Exercise Capacity:
• It facilitates procedural planning, device sizing, and o TMT provides valuable information about exercise
intra-procedural monitoring, enhancing the safety and capacity, functional status, and cardiovascular fitness by
efficacy of interventional procedures. measuring parameters such as exercise duration,
5. Risk Stratification and Prognostication: workload achieved, and metabolic equivalents (METs)
• Echocardiography aids in risk stratification and achieved.
prognostication by identifying high-risk features, o Poor exercise tolerance or premature termination of the
such as severe valvular disease, ventricular test may indicate underlying cardiac or pulmonary
dysfunction, or pulmonary hypertension, which may limitations, deconditioning, or reduced functional
influence treatment decisions and predict outcomes. capacity.
• It provides valuable information for assessing Risk Stratification and Prognostication:
perioperative risk in patients undergoing non-cardiac o TMT serves as a risk stratification tool for patients with
surgery and guiding management in critically ill suspected or known CAD, helping to identify individuals
patients in the intensive care unit. at increased risk of adverse cardiovascular events, such
as myocardial infarction, unstable angina, or cardiac
22.Importance of TMT. death.
Treadmill Exercise Testing (TMT), commonly known as a o Abnormal exercise test results, including significant ST-
stress test or exercise ECG, is a non-invasive diagnostic segment changes, exercise-induced symptoms (e.g.,
procedure used to evaluate cardiac function and detect chest pain, dyspnea), or hemodynamic instability, are
coronary artery disease (CAD) by assessing the heart's associated with a higher risk of future cardiac events and
response to physical exertion. Here are some key points may guide further management and treatment decisions.
highlighting the importance of TMT: Evaluation of Symptomatic Patients:
Detection of Coronary Artery Disease (CAD): o TMT is particularly useful in evaluating patients with
o TMT is widely used for the detection of CAD, which is exertional symptoms suggestive of CAD, such as chest
characterized by reduced blood flow to the heart muscles pain (angina pectoris), dyspnea, or unexplained fatigue.
due to narrowing or blockage of coronary arteries. o The reproduction of symptoms during exercise, along
o Exercise-induced ischemia, manifested by ST-segment with ECG changes indicative of ischemia, provides
depression on the electrocardiogram (ECG), is a hallmark diagnostic clues and helps confirm the presence of CAD
finding during TMT and indicates inadequate oxygen or other cardiovascular conditions.
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Assessment of Treatment Response: 4. Sick Sinus Syndrome: Pacemakers are indicated for
o TMT may be employed to assess the efficacy of medical patients with sick sinus syndrome, a condition
therapy, lifestyle modifications, or revascularization characterized by dysfunction of the sinus node, leading
procedures (e.g., coronary angioplasty, coronary artery to bradycardia or pauses in heart rhythm.
bypass grafting) in patients with CAD. 5. Heart Failure: In select cases, pacemakers with cardiac
o Improvement in exercise tolerance or resolution of resynchronization therapy (CRT) capabilities
exercise-induced ischemia following treatment suggests (biventricular pacing) may be indicated for patients with
a favorable response and may guide ongoing heart failure and ventricular dyssynchrony to improve
management and follow-up care. cardiac function and symptoms.
Components of a Pacemaker:
23.Pacemaker (2) 1. Pulse Generator: The pulse generator contains the
A pacemaker is a small electronic device implanted in the battery and electronic circuitry that generate electrical
chest to regulate the heart's rhythm by delivering electrical impulses. It is typically implanted beneath the skin in the
impulses to the heart muscle. Pacemakers are commonly chest or abdomen.
used to treat various cardiac arrhythmias, including 2. Leads: Leads are thin, insulated wires that deliver
bradycardia (slow heart rate), heart block, and certain types electrical impulses from the pulse generator to the heart
of tachyarrhythmias (fast heart rate). chambers. Endocardial leads are inserted through a vein
Indications for Pacemaker Implantation: into the heart chambers and are attached to the
1. Symptomatic Bradycardia: Pacemakers are indicated myocardium.
for patients with symptomatic bradycardia (e.g., 3. Sensing and Pacing Electrodes: The leads contain
dizziness, syncope, fatigue) due to sinus node sensing electrodes that detect the heart's electrical
dysfunction or atrioventricular (AV) block. activity (e.g., intrinsic rhythm) and pacing electrodes that
2. Heart Block: Pacemakers are indicated for patients with deliver electrical impulses to the myocardium to initiate
advanced AV block (second-degree or third-degree heart or maintain a desired heart rhythm.
block) or bundle branch block associated with 4. Programming Device: Pacemakers are programmable
symptomatic bradycardia. devices that can be adjusted or reprogrammed using an
3. Tachybrady Syndrome: Pacemakers with dual- external programming device. Clinicians can customize
chamber pacing capabilities may be indicated for parameters such as pacing mode, rate, sensitivity, and
patients with tachybrady syndrome, characterized by timing to optimize device function and patient outcomes.
alternating episodes of bradycardia and tachycardia. Implantation Procedure: Pacemaker implantation is
typically performed under local anesthesia with sedation in
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an electrophysiology laboratory or operating room. The 2. Angiotensin II Receptor Blockers (ARBs):

procedure involves making a small incision in the chest or • Examples: Losartan, Valsartan, Irbesartan.
abdomen, inserting the leads into a vein, advancing them to • Mechanism of Action: ARBs selectively block the
the desired heart chamber under fluoroscopic guidance, and binding of angiotensin II to its receptors, preventing
securing them to the myocardium. The pulse generator is vasoconstriction and aldosterone release, resulting in
then implanted subcutaneously and connected to the leads. vasodilation and blood pressure reduction.
After implantation, the device is tested to ensure proper • Clinical Benefits: ARBs are similar to ACE inhibitors
sensing, pacing, and function. in their blood pressure-lowering effects and are often
used as an alternative in patients intolerant to ACE
24.Oral anti hypertension drugs inhibitors.
Oral antihypertensive drugs are medications used to • Side Effects: Hyperkalemia, hypotension, renal
lower blood pressure and manage hypertension; a common dysfunction.
cardiovascular condition characterized by elevated blood • Contraindications: Pregnancy, history of angioedema
pressure levels. Here are some commonly prescribed with ARBs, bilateral renal artery stenosis.
classes of oral antihypertensive drugs: 3. Calcium Channel Blockers (CCBs):
1. Angiotensin-Converting Enzyme (ACE) Inhibitors: • Examples: Amlodipine, Nifedipine, Diltiazem,
• Examples: Enalapril, Lisinopril, Ramipril. Verapamil.
• Mechanism of Action: ACE inhibitors block the • Mechanism of Action: CCBs inhibit the influx of
conversion of angiotensin I to angiotensin II, a potent calcium ions into vascular smooth muscle cells,
vasoconstrictor, thereby reducing systemic vascular leading to vasodilation and relaxation of arterial
resistance and lowering blood pressure. walls, which reduces peripheral vascular resistance
• Clinical Benefits: ACE inhibitors are effective in and blood pressure.
reducing blood pressure, slowing the progression of • Clinical Benefits: CCBs are effective in lowering
kidney disease in patients with diabetes or proteinuria, blood pressure, particularly in patients with
and improving outcomes in heart failure and post- hypertension and concomitant angina, atrial
myocardial infarction patients. fibrillation, or migraine headaches.
• Side Effects: Cough, hyperkalemia, hypotension, • Side Effects: Peripheral edema, flushing, dizziness,
renal dysfunction, angioedema (rare but serious). constipation (verapamil, diltiazem), reflex
• Contraindications: Pregnancy (especially in the tachycardia (nifedipine).
second and third trimesters), history of angioedema • Contraindications: Severe aortic stenosis, heart
with ACE inhibitors, bilateral renal artery stenosis. failure (in some cases), hypotension.
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4. Diuretics: angina, heart failure, or previous myocardial

• Examples: Hydrochlorothiazide, Chlorthalidone, infarction.
Furosemide. • Side Effects: Bradycardia, fatigue, cold extremities,
• Mechanism of Action: Diuretics increase urine bronchospasm (in patients with asthma or chronic
production by promoting sodium and water excretion obstructive pulmonary disease), worsening of heart
from the kidneys, resulting in decreased blood failure symptoms (in some cases).
volume and reduced cardiac preload, which lowers • Contraindications: Severe bradycardia, heart block,
blood pressure. asthma (non-selective beta-blockers), decompensated
• Clinical Benefits: Diuretics are widely used as first- heart failure.
line agents in the management of hypertension, 6. Renin Inhibitors:
particularly in patients with volume overload, heart • Example: Aliskiren.
failure, or renal dysfunction. Side Effects: Common • Mechanism of Action: Renin inhibitors block the
side effects include hypokalemia (with thiazide and conversion of angiotensinogen to angiotensin I,
loop diuretics), hyperkalemia (with potassium- thereby reducing the formation of angiotensin II and
sparing diuretics), electrolyte imbalances, aldosterone, resulting in vasodilation and blood
dehydration, hypotension, and metabolic pressure reduction.
disturbances. • Clinical Benefits: Renin inhibitors are used as
• Contraindications: Contraindications include severe adjunctive therapy in patients with hypertension, often
renal impairment, electrolyte imbalances, anuria, and in combination with other antihypertensive agents.
hypersensitivity to specific diuretic agents. • Side Effects: Common side effects include
5. Beta-Blockers: hyperkalemia, cough, hypotension, dizziness, and
• Examples: Atenolol, Metoprolol, Carvedilol, renal dysfunction.
Propranolol. • Contraindications: Contraindications include a
• Mechanism of Action: Beta-blockers block the effects history of angioedema related to direct renin
of catecholamines (e.g., epinephrine, norepinephrine) inhibitors, pregnancy, and bilateral renal artery
on beta-adrenergic receptors, leading to decreased stenosis.
heart rate, reduced cardiac output, and vasodilation, 7. Alpha-Blockers:
resulting in blood pressure reduction. • Examples: Prazosin, Doxazosin, Terazosin.
• Clinical Benefits: Beta-blockers are effective in • Mechanism of Action: Alpha-blockers inhibit the
lowering blood pressure and reducing heart rate, alpha-adrenergic receptors in peripheral blood vessels,
making them useful in patients with hypertension, leading to vasodilation and decreased peripheral
 I M M A N U V E L | 72

vascular resistance, resulting in blood pressure • This left-to-right shunt causes pulmonary
reduction. overcirculation and can result in pulmonary
• Clinical Benefits: Alpha-blockers are effective in hypertension, increased work on the left side of the heart,
lowering blood pressure and are often used in patients and eventual volume overload of the left atrium and left
with hypertension and concomitant benign prostatic ventricle.
hyperplasia. • Over time, PDA can lead to complications such as
• Side Effects: Common side effects include dizziness, congestive heart failure, pulmonary edema, and
orthostatic hypotension, fatigue, headache, and nasal increased risk of infective endocarditis.
congestion. First-dose phenomenon, characterized by Clinical Presentation:
severe orthostatic hypotension, may occur with some • Many infants with PDA may be asymptomatic in the
alpha-blockers. neonatal period, with symptoms becoming apparent
• Contraindications: Contraindications include later in infancy or childhood.
hypotension, syncope, and a history of orthostatic • Symptoms in infants may include poor feeding, failure
hypotension. to thrive, tachypnea, increased work of breathing, and
frequent respiratory infections.
25.Patent ductus arteriosus (4) • Older children and adults may present with symptoms
Patent ductus arteriosus (PDA) is a congenital heart defect such as exertional dyspnea, palpitations, fatigue, or
characterized by the persistence of a fetal blood vessel, the symptoms related to complications such as infective
ductus arteriosus, after birth. Normally, the ductus endocarditis.
arteriosus connects the pulmonary artery to the descending • Physical examination may reveal a continuous
aorta in the fetus, allowing oxygenated blood to bypass the "machinery-like" murmur heard best at the left upper
lungs. However, it usually closes within hours to days after sternal border, bounding pulses, and signs of pulmonary
birth in response to changes in oxygen levels and pressure overcirculation (e.g., tachycardia, widened pulse
in the newborn circulation. In cases of PDA, the ductus pressure).
arteriosus fails to close, resulting in the abnormal shunting Diagnosis:
of blood between the systemic and pulmonary circulations. • Echocardiography: The primary diagnostic modality
Pathophysiology: for assessing the presence and hemodynamic
• In PDA, oxygenated blood from the aorta is shunted back significance of PDA. It can visualize the patent ductus
into the pulmonary artery, leading to increased blood arteriosus and assess the degree of left-to-right shunting,
flow to the lungs. pulmonary overcirculation, and associated cardiac
abnormalities.
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• Chest X-ray: May show evidence of pulmonary Procedure:

overcirculation, such as cardiomegaly, increased 1. Preparation: The patient is typically instructed to avoid
pulmonary vascularity, and signs of heart failure. eating or drinking caffeine-containing beverages for
• Electrocardiogram (ECG): Typically normal in several hours before the test. They are outfitted with
uncomplicated PDA but may show signs of left ECG electrodes attached to their chest, which
ventricular hypertrophy or left atrial enlargement in continuously monitor the heart's electrical activity
cases of significant left-to-right shunting. throughout the test. Blood pressure cuffs may also be
Treatment: placed on the patient's arm to monitor blood pressure
• Pharmacologic Closure: In preterm infants or neonates during exercise.
with small PDAs and no significant symptoms, 2. Baseline Measurements: Before beginning exercise,
pharmacologic agents such as indomethacin or ibuprofen baseline measurements of the patient's resting heart rate,
may be used to promote closure of the ductus arteriosus. blood pressure, and ECG are recorded.
• Surgical Ligation: For larger or symptomatic PDAs, 3. Exercise Protocol: The patient walks or runs on a
surgical ligation of the ductus arteriosus may be motorized treadmill at gradually increasing speed and
performed. This involves a thoracotomy or minimally incline levels, according to a standardized exercise
invasive procedure to ligate or clip the ductus arteriosus, protocol tailored to the patient's age, physical fitness,
thereby interrupting the abnormal blood flow. and clinical condition. The goal is to achieve an
• Transcatheter Closure: A less invasive alternative to appropriate level of exercise intensity, usually based on
surgical ligation, transcatheter closure involves the the patient's age-predicted maximum heart rate.
insertion of a device (e.g., coil, plug) via a catheter into 4. Monitoring: Throughout the exercise session, the
the PDA to occlude the abnormal vessel. patient's heart rate, blood pressure, symptoms (such as
chest pain or shortness of breath), and ECG changes are
26.Tread mill test. (2) closely monitored by healthcare providers. The ECG
The treadmill test, also known as exercise stress tracing displays the electrical activity of the heart and
testing or treadmill exercise ECG, is a diagnostic procedure can detect abnormalities such as arrhythmias, ischemic
used to evaluate the heart's response to physical exertion changes (ST-segment depression or elevation), or
and assess for signs of coronary artery disease (CAD) or conduction disturbances.
other cardiovascular abnormalities. It involves walking or 5. Termination Criteria: The test is typically terminated
running on a treadmill while continuously monitoring the when the patient reaches a target heart rate, achieves
patient's heart rate, blood pressure, and electrocardiogram maximal exertion, develops significant symptoms, or
(ECG) changes during exercise.
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exhibits ECG changes suggestive of myocardial 27.Trans-esophageal Echocardiogram.

ischemia or other cardiovascular abnormalities. Transesophageal echocardiogram (TEE) is a specialized
6. Recovery: After exercise, the patient is monitored imaging technique used to obtain high-resolution
during a brief recovery period to assess for any lingering ultrasound images of the heart structures by inserting a
symptoms, ECG changes, or abnormal blood pressure probe into the esophagus, located directly behind the heart.
responses. TEE provides detailed images of the heart's anatomy,
Indications: valves, chambers, and great vessels, offering valuable
• Evaluation of suspected coronary artery disease (CAD) diagnostic information that may not be as well visualized
• Assessment of exercise capacity and functional status with standard transthoracic echocardiography (TTE).
• Risk stratification in patients with known or suspected Procedure:
CAD 1. Patient Preparation: The patient is usually sedated
• Evaluation of symptoms such as chest pain, dyspnea, or to minimize discomfort and facilitate probe insertion.
palpitations during exertion They are asked to refrain from eating or drinking for
Interpretation: a specified period before the procedure.
• Normal Test: No significant ECG changes or symptoms 2. Probe Insertion: A flexible probe with an ultrasound
during exercise; appropriate increase in heart rate and transducer at its tip is inserted through the mouth and
blood pressure with exercise; no evidence of ischemia or guided into the esophagus, which lies adjacent to the
other abnormalities. heart structures.
• Abnormal Test: Presence of significant ECG changes 3. Imaging: The transducer emits ultrasound waves,
(ST-segment depression, elevation, arrhythmias) which are directed towards the heart structures. By
suggestive of myocardial ischemia, exercise-induced adjusting the position and angle of the probe, detailed
symptoms (such as chest pain or dyspnea), abnormal images of the heart valves, chambers, and great
blood pressure response, or failure to achieve target heart vessels from various perspectives.
rate or workload. 4. Real-time Monitoring: Throughout the procedure,
Limitations: the echocardiographer monitors the images in real-
• False-positive results due to non-ischemic ST-segment time on a monitor, assessing cardiac structure and
changes, arrhythmias, or other factors. function, blood flow patterns, and detecting any
• False-negative results in patients with early or mild CAD, abnormalities.
inadequate exercise effort, or inability to reach target 5. Probe Removal: Once the imaging is complete, the
heart rate. probe is carefully removed from the esophagus, and
the patient is allowed to recover from sedation.
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Indications: Limitations:
• Evaluation of cardiac structures not well visualized by • Invasive Procedure: TEE requires insertion of a probe
TTE, such as the posterior heart structures (e.g., left into the esophagus, which may cause discomfort,
atrium, mitral valve, aorta) and prosthetic heart valves. gagging, or sore throat in some patients.
• Assessment of cardiac function, including left • Sedation: Patients typically require sedation or
ventricular function, valve morphology and function, anesthesia for comfort during TEE, which carries its own
intracardiac masses or thrombi, and atrial septal defects. risks and may limit the procedure's feasibility in certain
• Diagnosis and management of complex cardiovascular patient populations.
conditions, such as infective endocarditis, aortic • Risk of Complications: Although rare, complications of
dissection, intracardiac shunts, or evaluation of embolic TEE may include esophageal injury, bleeding,
sources. aspiration, arrhythmias, or adverse reactions to sedation.
Advantages:
1. High Spatial Resolution: TEE provides superior image 28.Right heart failure
quality and resolution compared to TTE, allowing for Right heart failure, also known as cor pulmonale
detailed visualization of cardiac structures and when it's caused by pulmonary disease, is a condition
abnormalities. characterized by the inability of the right ventricle of the
2. Close Proximity to Heart Structures: The esophagus heart to effectively pump blood to the lungs and then to the
lies directly behind the heart, enabling the probe to be rest of the body. Unlike left heart failure, which primarily
positioned closer to the cardiac structures, resulting in affects the systemic circulation, right heart failure
clearer images with less interference from overlying predominantly impacts the pulmonary circulation.
tissues. Causes and Risk Factors:
3. Less Artifact: TEE is less affected by lung or chest wall 1. Chronic Lung Diseases: Conditions such as chronic
interference, making it particularly useful in patients obstructive pulmonary disease (COPD), pulmonary
with obesity, lung disease, or suboptimal TTE images. hypertension, interstitial lung disease, and cystic fibrosis
4. Real-time Monitoring: Echocardiographers can adjust can lead to increased pulmonary vascular resistance,
the probe position in real-time to obtain optimal imaging causing the right ventricle to work harder to pump blood
views and assess dynamic changes in cardiac function or through the lungs.
blood flow patterns. 2. Left Heart Failure: When left heart failure progresses,
it can cause fluid buildup in the lungs (pulmonary
edema), leading to increased pressure in the pulmonary
circulation and subsequent right heart strain.
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3. Coronary Artery Disease: Severe coronary artery 7. Cyanosis: Bluish discoloration of the lips, nail beds, or
disease can lead to right heart failure, especially when it skin, indicating poor oxygenation.
affects the right coronary artery and leads to myocardial Diagnosis:
infarction involving the right ventricle. 1. Physical Examination: Assessment of vital signs,
4. Pulmonary Embolism: Acute pulmonary embolism, a jugular venous pressure, heart sounds, and signs of fluid
blockage in the pulmonary arteries, can lead to acute overload.
right heart strain or failure due to increased pressure in 2. Imaging Studies: Chest X-ray, echocardiography, and
the pulmonary circulation. sometimes cardiac MRI or CT scan to evaluate heart
5. Chronic Kidney Disease: Renal dysfunction can lead to size, function, and presence of fluid accumulation.
fluid retention and volume overload, which can 3. Blood Tests: B-type natriuretic peptide (BNP) or N-
exacerbate right heart failure. terminal pro-BNP (NT-proBNP) levels may be elevated
6. Congenital Heart Defects: Certain congenital heart in heart failure.
defects, such as atrial septal defect or ventricular septal Treatment:
defect, can cause right heart failure, especially if they 1. Underlying Cause Management: Addressing the
lead to pulmonary hypertension or shunting of blood underlying cause of right heart failure, such as treating
from the left to the right side of the heart. lung disease, managing pulmonary hypertension, or
Signs and Symptoms: optimizing fluid balance in renal disease.
1. Dyspnea: Shortness of breath, especially with exertion 2. Medications: Diuretics to reduce fluid overload,
or lying flat (orthopnea). vasodilators (e.g., ACE inhibitors, angiotensin receptor
2. Fatigue: Generalized weakness and fatigue, often due to blockers, phosphodiesterase inhibitors) to reduce
reduced cardiac output and decreased tissue perfusion. pulmonary vascular resistance, and inotropic agents to
3. Peripheral Edema: Swelling of the legs, ankles, or improve right ventricular function in severe cases.
abdomen due to fluid retention. 3. Oxygen Therapy: Supplemental oxygen may be
4. Jugular Venous Distention (JVD): Visible distention of provided to improve oxygenation and alleviate
the jugular veins in the neck, indicating increased central symptoms.
venous pressure. 4. Lifestyle Modifications: Sodium restriction, fluid
5. Ascites: Accumulation of fluid in the abdominal cavity, restriction, and avoidance of alcohol and tobacco to
often seen in more advanced cases of right heart failure. reduce exacerbations.
6. Hepatomegaly: Enlargement of the liver due to 5. Mechanical Support: In advanced cases, devices such
congestion of blood flow. as ventricular assist devices (VADs) or extracorporeal
membrane oxygenation (ECMO) may be considered as
 I M M A N U V E L | 77

bridge therapy or as destination therapy in select lasting about 1 second each. Ensure adequate chest rise
patients. with each breath.
6. Heart Transplantation: For end-stage heart failure • Continue cycles of compressions and breaths in a ratio
refractory to medical and device therapy, heart of 30:2.
transplantation may be considered. 3. Early Defibrillation:
• If an automated external defibrillator (AED) is
29.Management of cardiac arrest. available, apply it to the victim's chest as soon as
Management of cardiac arrest involves immediate possible.
recognition of the condition and prompt initiation of • Follow the prompts provided by the AED for rhythm
cardiopulmonary resuscitation (CPR) followed by analysis and shock delivery.
advanced life support measures. The goal is to restore • Deliver a shock if advised and resume CPR
spontaneous circulation and preserve brain function. Here immediately afterward.
are the key steps in the management of cardiac arrest: 4. Advanced Life Support:
1. Recognition and Activation of Emergency Response: • Advanced airway management: Endotracheal
• Immediately recognize signs of cardiac arrest, such as intubation or supraglottic airway insertion may be
unresponsiveness, absence of breathing, and absence of performed to secure the airway and facilitate
pulse. ventilation.
• Activate the emergency medical services (EMS) system • Medications: Administer medications as indicated,
or call for help, and ensure that a defibrillator is brought such as epinephrine to support circulation and
to the scene if available. vasopressin or amiodarone for cardiac rhythm
2. Initiation of CPR: management.
• Begin chest compressions: Place the heel of one hand 5. Post-Resuscitation Care:
on the center of the victim's chest (lower half of the • Once spontaneous circulation is restored, focus on
sternum), place the other hand on top, and interlock post-cardiac arrest care to optimize hemodynamics,
fingers. Compress the chest to a depth of at least 2 oxygenation, and neurological outcomes.
inches (5 centimeters) at a rate of 100 to 120 • Consider therapeutic hypothermia or targeted
compressions per minute. temperature management to reduce neurological injury
• Provide rescue breaths: After 30 compressions, open and improve outcomes in select patients with return of
the airway using the head tilt-chin lift maneuver, pinch spontaneous circulation after cardiac arrest.
the victim's nose shut, and provide 2 rescue breaths
 I M M A N U V E L | 78

6. Monitoring and Rehabilitation: 2. Hypertension: Chronic high blood pressure increases the
• Continuously monitor the patient's vital signs, cardiac workload on the left ventricle, causing hypertrophy and
rhythm, oxygen saturation, and neurological status. eventual dysfunction.
• Initiate early rehabilitation and multidisciplinary care to 3. Valvular Heart Disease: Conditions such as aortic
optimize recovery and minimize complications in stenosis or mitral regurgitation can impair left ventricular
survivors of cardiac arrest. function by affecting valvular integrity and
7. Prevention: hemodynamics.
• Emphasize the importance of bystander CPR training 4. Cardiomyopathies: Diseases of the heart muscle,
and public access to AEDs to improve outcomes in cases including dilated cardiomyopathy, hypertrophic
of cardiac arrest. cardiomyopathy, or restrictive cardiomyopathy, can lead
• Encourage lifestyle modifications and management of to left heart failure.
underlying risk factors (e.g., smoking cessation, blood 5. Myocardial Infarction: Acute damage to the heart
pressure control, diabetes management) to prevent muscle from a heart attack can weaken the left ventricle
cardiac arrest. and impair its contractile function.
6. Arrhythmias: Abnormal heart rhythms, such as atrial
30.Left heart failure fibrillation or ventricular tachycardia, can contribute to
Left heart failure, also known as congestive heart failure heart failure by disrupting cardiac function and impairing
(CHF), is a chronic condition characterized by the inability hemodynamics.
of the left ventricle of the heart to pump blood efficiently to 7. Chronic Kidney Disease: Renal dysfunction can lead to
meet the body's metabolic demands. This leads to a cascade fluid retention and volume overload, exacerbating left
of physiological changes and clinical symptoms due to heart failure.
inadequate tissue perfusion and congestion. Left heart Pathophysiology:
failure is a common cardiovascular disorder associated with 1. Impaired Pump Function: Decreased contractility of
significant morbidity and mortality. the left ventricle reduces its ability to eject blood
Causes and Risk Factors: effectively, leading to decreased stroke volume and
1. Coronary Artery Disease (CAD): Narrowing or cardiac output.
blockage of the coronary arteries reduces blood flow to 2. Fluid Retention: Reduced forward flow of blood
the heart muscle, leading to myocardial ischemia and triggers compensatory mechanisms, including activation
impaired left ventricular function. of the renin-angiotensin-aldosterone system and release
of antidiuretic hormone (ADH), resulting in sodium and
water retention and volume overload.
 I M M A N U V E L | 79

3. Neurohormonal Activation: Activation of sympathetic abnormalities; chest X-ray to evaluate for cardiomegaly
nervous system and renin-angiotensin-aldosterone and pulmonary congestion.
system leads to vasoconstriction, sodium retention, and 3. Laboratory Tests: B-type natriuretic peptide (BNP) or
increased preload and afterload, further exacerbating N-terminal pro-BNP (NT-proBNP) levels may be
heart failure. elevated in heart failure and can aid in diagnosis and
4. Ventricular Remodeling: Structural changes in the left prognosis.
ventricle, including hypertrophy, dilation, and fibrosis, 4. Electrocardiogram (ECG): May show signs of left
occur as adaptive responses to chronic pressure or ventricular hypertrophy, conduction abnormalities, or
volume overload but can ultimately lead to progressive arrhythmias.
deterioration of cardiac function. 5. Cardiac Catheterization: Invasive procedure to assess
Signs and Symptoms: coronary artery anatomy and hemodynamics in select
1. Dyspnea: Shortness of breath, especially with exertion cases.
or lying flat (orthopnea) or awakening at night Treatment:
(paroxysmal nocturnal dyspnea). 1. Lifestyle Modifications: Sodium restriction, fluid
2. Fatigue: Generalized weakness and fatigue, often due to restriction, smoking cessation, and regular exercise to
reduced cardiac output and decreased tissue perfusion. improve symptoms and outcomes.
3. Fluid Retention: Peripheral edema (swelling of the legs, 2. Medications:
ankles, or abdomen) and pulmonary congestion (cough, • Diuretics: To reduce fluid overload and relieve
wheezing, or frothy sputum). symptoms of congestion.
4. Exercise Intolerance: Decreased exercise tolerance and • Angiotensin-Converting Enzyme (ACE) Inhibitors
easy fatigability due to reduced cardiac reserve and or Angiotensin Receptor Blockers (ARBs): To
skeletal muscle dysfunction. inhibit the renin-angiotensin-aldosterone system,
5. Tachycardia: Increased heart rate may occur as a reduce afterload, and improve cardiac function.
compensatory mechanism to maintain cardiac output. • Beta-Blockers: To reduce heart rate, improve
Diagnosis: myocardial oxygen supply-demand balance, and slow
1. History and Physical Examination: Evaluation of disease progression.
symptoms, medical history, risk factors, and signs of • Aldosterone Antagonists: To reduce sodium and
fluid overload (e.g., jugular venous distention, water retention and improve outcomes in select
pulmonary crackles, peripheral edema). patients.
2. Imaging Studies: Echocardiography to assess left
ventricular function, size, and wall motion
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• Hydralazine and Isosorbide Dinitrate: Vasodilator 31.Infective endocarditis

therapy for patients unable to tolerate ACE inhibitors Infective endocarditis (IE) is a serious infection of the
or ARBs. endocardium, which is the inner lining of the heart
• Sacubitril/Valsartan (ARNI): Combined neprilysin chambers and heart valves. It is typically caused by the
inhibitor and ARB therapy for select patients with colonization of microorganisms, primarily bacteria, on the
reduced ejection fraction. damaged or abnormal endothelial surfaces of the heart. IE
3. Device Therapy: can lead to the formation of vegetations (collections of
• Implantable Cardioverter-Defibrillator (ICD): For infected material) on the heart valves or endocardium,
primary or secondary prevention of sudden cardiac which can cause valvular dysfunction, embolic events, and
death in patients at high risk. systemic complications.
• Cardiac Resynchronization Therapy (CRT): Causes and Risk Factors:
Biventricular pacing for patients with heart failure and 1. Bacterial Infections: Most cases of IE are caused by
electrical dyssynchrony. bacteria, with the most common pathogens being
4. Surgical Interventions: Staphylococcus aureus, Streptococcus viridans, and
• Coronary artery bypass grafting (CABG) for Enterococcus species. Less commonly, fungi, such as
revascularization in patients with significant CAD. Candida species, may also cause IE.
• Valve repair or replacement for severe valvular heart 2. Predisposing Factors:
disease contributing to heart failure. • Pre-existing valvular heart disease, such as rheumatic
• Left ventricular assist device (LVAD) as destination heart disease, degenerative valve disease, or prosthetic
therapy or bridge to transplantation in select patients heart valves.
with end-stage heart failure. • Congenital heart defects, such as ventricular septal
5. Heart Transplantation: Considered in eligible patients defects, atrial septal defects, or bicuspid aortic valves.
with refractory heart failure who meet criteria for • Previous episodes of endocarditis.
transplantation. • Intravenous drug use (IVDU).
6. Lifestyle Modifications: • Invasive procedures, such as dental procedures,
• Sodium restriction to reduce fluid retention. surgery, or instrumentation, which can introduce
• Fluid restriction in advanced cases of heart failure. bacteria into the bloodstream.
• Smoking cessation, weight management, regular • Indwelling intravascular devices, such as central
exercise within tolerance, and alcohol moderation. venous catheters or pacemaker leads.
• Influenza and pneumococcal vaccinations to reduce
the risk of respiratory infections.
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Pathophysiology: 3. Systemic Symptoms: Malaise, fatigue, weight loss,

1. Endothelial Damage: Endothelial injury or disruption anorexia, and night sweats may be present.
of the endocardial surface provides a substrate for 4. Cutaneous Manifestations: Petechiae, splinter
bacterial adherence and colonization. hemorrhages, Osler's nodes (painful subcutaneous
2. Bacterial Colonization: Bacteria circulating in the nodules on the pads of the fingers or toes), and Janeway
bloodstream (bacteremia) adhere to the damaged lesions (non-tender macules or papules on the palms or
endothelium and form microcolonies. soles) may be observed.
3. Vegetation Formation: Proliferation of bacteria within 5. Ophthalmologic Findings: Retinal hemorrhages, Roth
the microcolonies leads to the formation of vegetations spots (retinal hemorrhages with white centers), or
composed of bacteria, fibrin, platelets, and embolic occlusions of retinal arteries may be detected on
inflammatory cells. fundoscopic examination.
4. Valvular Dysfunction: Vegetations may interfere with Diagnosis:
valvular function, leading to valvular regurgitation or 1. Blood Cultures: Blood cultures are essential for
stenosis. identifying the causative organism and guiding antibiotic
5. Embolic Events: Fragments of vegetations or thrombi therapy. Multiple sets of blood cultures should be
may break off and embolize to distant organs, causing obtained before initiating antibiotic therapy.
infarctions or abscesses. 2. Echocardiography:
6. Systemic Complications: Bacteremia and systemic • Transthoracic echocardiography (TTE) is often the
inflammation can lead to septic emboli, septic shock, initial imaging modality and may demonstrate
multiorgan dysfunction, or immunologic phenomena vegetations, valvular abnormalities, or evidence of
(e.g., glomerulonephritis, Osler's nodes, Janeway regurgitation.
lesions). • Transesophageal echocardiography (TEE) provides
Clinical Presentation: higher sensitivity and specificity for detecting
1. Fever: Fever is a common presenting symptom, vegetations, particularly in patients with prosthetic
although it may be absent in some cases, particularly in valves, complex native valve disease, or intracardiac
patients receiving antibiotics or those with subacute IE. devices.
2. Cardiac Symptoms: Symptoms may include new or 3. Other Investigations: Laboratory studies, such as
changing murmurs, heart failure symptoms (e.g., complete blood count (CBC), inflammatory markers
dyspnea, orthopnea, paroxysmal nocturnal dyspnea), or (e.g., erythrocyte sedimentation rate [ESR], C-reactive
symptoms related to embolic events (e.g., stroke, protein [CRP]), and serologic testing for specific
peripheral embolism). pathogens, may be useful in the diagnostic evaluation.
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Treatment: 1. Sinoatrial (SA) Node:

1. Antimicrobial Therapy: Empiric antibiotic therapy • Located in the wall of the right atrium near the entrance
should be initiated promptly after blood cultures are of the superior vena cava.
obtained, with subsequent adjustment based on culture • Often referred to as the "pacemaker" of the heart.
results and susceptibility testing. Antibiotic regimens are • Initiates the electrical impulses that stimulate atrial
tailored to the causative organism, underlying valvular contraction.
disease, and clinical severity. • Under normal conditions, it generates rhythmic
2. Surgical Intervention: impulses at a rate of approximately 60-100 beats per
• Surgical management may be indicated in certain minute, setting the heart's baseline rhythm.
cases, such as severe valvular dysfunction, large or 2. Atrioventricular (AV) Node:
mobile vegetations, recurrent embolic events, or heart • Located at the junction between the atria and ventricles,
failure refractory to medical therapy. near the lower portion of the interatrial septum.
• Surgical options include valve repair, valve • Functions as a relay station that delays the transmission
replacement, or debridement of infected tissue. of electrical impulses from the atria to the ventricles,
3. Supportive Care: Supportive measures may include allowing for sequential atrial contraction followed by
hemodynamic support, management of heart failure ventricular contraction.
symptoms, anticoagulation for prevention of embolic • Delays the impulse for a brief period to ensure that the
events, and treatment of systemic complications. atria have ejected blood into the ventricles before
ventricular contraction begins.
32.Conducting system of the heart. (2) 3. Bundle of His:
Conductive system of the heart is formed by the modified • A bundle of specialized cardiac muscle fibers that
cardiac muscle fibers. These fibers are the specialized cells, originates from the AV node and travels through the
which conduct the impulses rapidly from SA node to the interventricular septum.
ventricles. Conductive tissues of the heart are also called • Divides into the left bundle branch and the right bundle
the junctional tissues. branch, which conduct electrical impulses to the
Components of Conductive System in Human Heart respective left and right ventricles.
o SA node 4. Purkinje Fibers:
o AV node • Specialized cardiac muscle fibers that arise from the
o Bundle of His bundle branches and spread throughout the ventricular
o Purkinje fibers. myocardium.
 I M M A N U V E L | 83

• Rapidly transmit electrical impulses from the bundle • Troponin I (cTnI) and troponin T (cTnT) are specific to
branches to the ventricular myocardium, stimulating cardiac muscle and are released into the bloodstream
ventricular contraction. following myocardial cell death or injury.
• Responsible for the rapid and coordinated • Elevated troponin levels indicate myocardial damage
depolarization of the ventricles, ensuring efficient and are used to diagnose acute myocardial infarction
contraction and ejection of blood into the pulmonary (AMI) and assess its severity.
and systemic circulations. • Troponin levels rise within 3-4 hours of symptom
The coordinated depolarization and repolarization of onset, peak within 12-48 hours, and may remain
cardiac muscle cells orchestrated by the conducting system elevated for several days.
result in the sequential contraction and relaxation of the 2. Creatine Kinase (CK) and CK-MB:
atria and ventricles, producing the rhythmic heartbeat. • CK is an enzyme found in various tissues, including
Dysfunctions or abnormalities in the cardiac conduction skeletal muscle, brain, and heart.
system can lead to arrhythmias, conduction blocks, or other • CK-MB is a cardiac-specific isoform of creatine
electrical disturbances that may impair cardiac function and kinase that is predominantly found in the heart.
hemodynamics. • Elevated levels of total CK and CK-MB may indicate
Understanding the anatomy and function of the cardiac myocardial injury, particularly in the context of acute
conducting system is essential for diagnosing and managing coronary syndromes.
various cardiac rhythm disorders. • CK-MB levels rise within 3-6 hours of symptom
onset, peak within 12-24 hours, and return to normal
33.Cardiac markers within 48-72 hours.
Cardiac markers are substances released into the 3. Myoglobin:
bloodstream in response to cardiac injury or stress. These • Myoglobin is an oxygen-binding protein found in
markers play a crucial role in the diagnosis, risk cardiac and skeletal muscle.
stratification, and management of various cardiovascular • Elevated myoglobin levels are not specific to cardiac
conditions, particularly acute coronary syndromes (ACS) injury but may rise rapidly following myocardial
such as myocardial infarction (heart attack). Cardiac damage.
markers are classified into several categories, including: • Myoglobin levels rise within 1-3 hours of symptom
1. Troponins: onset, peak within 6-9 hours, and return to normal
• Troponins are considered the gold standard cardiac within 24-36 hours.
markers for diagnosing myocardial injury.
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• Myoglobin is often used as an early marker of cardiac troponin I (cTnI) and cardiac troponin T (cTnT) are
myocardial injury, particularly in conjunction with the most widely used and clinically relevant markers of
troponins. myocardial injury.
4. Brain Natriuretic Peptide (BNP) and N-terminal Clinical Implications of Cardiac Troponin
pro-BNP (NT-proBNP): Measurement:
• BNP and NT-proBNP are peptides released by the 1. Diagnosis of Acute Myocardial Infarction (AMI):
heart in response to increased ventricular wall stress, • Elevated cardiac troponin levels are the cornerstone for
particularly in the setting of heart failure. diagnosing acute myocardial infarction (heart attack).
• Elevated BNP and NT-proBNP levels are indicative of • Myocardial injury results in the release of cardiac
myocardial stretch and are used for diagnosing and troponins into the bloodstream, with cTnI and cTnT
assessing the severity of heart failure. being highly specific to cardiac muscle.
• BNP and NT-proBNP levels are elevated in patients • The 4th Universal Definition of Myocardial Infarction
with acute decompensated heart failure and can help defines myocardial infarction as a rise and/or fall of
guide treatment and prognostication. cardiac troponin levels with at least one value above the
5. High-Sensitivity C-Reactive Protein (hs-CRP): 99th percentile upper reference limit, in the setting of
• hs-CRP is a marker of systemic inflammation and is evidence of acute myocardial ischemia (symptoms,
associated with an increased risk of cardiovascular ECG changes, imaging evidence).
events. 2. Risk Stratification and Prognostication:
• Elevated hs-CRP levels are observed in various • Cardiac troponin levels correlate with the extent of
cardiovascular conditions, including atherosclerosis, myocardial damage and are prognostic indicators of
unstable angina, and myocardial infarction. adverse outcomes in patients with acute coronary
• hs-CRP levels may be used for risk stratification and syndromes (ACS).
monitoring response to treatment in patients with • Higher levels of cardiac troponins are associated with
cardiovascular disease. increased mortality, recurrent myocardial infarction,
heart failure, and other cardiovascular events.
34.Cardiac Troponin and clinical implications. (3) • Serial measurement of cardiac troponins, particularly
Cardiac troponins are regulatory proteins found high-sensitivity assays, allows for risk stratification and
exclusively in cardiac muscle cells (cardiomyocytes) and prognostication in patients with ACS and other cardiac
are integral to the regulation of cardiac muscle contraction. conditions.
They consist of three subunits: troponin C (TnC), troponin
I (TnI), and troponin T (TnT). Among these subunits,
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3. Detection of Myocardial Injury:

• Cardiac troponins are highly sensitive markers of
myocardial injury and can detect minor degrees of
myocardial damage, even in the absence of clinically
apparent symptoms.
• Elevated troponin levels may occur in various cardiac
conditions, including myocarditis, pericarditis, cardiac
contusion, arrhythmias, pulmonary embolism, and
heart failure, reflecting ongoing myocardial damage or
strain.
4. Monitoring Response to Treatment:
• Serial measurement of cardiac troponins is used to
monitor response to treatment and guide therapeutic
interventions in patients with acute myocardial
infarction and other cardiac conditions.
• A decrease in troponin levels over time may indicate
successful reperfusion, resolution of myocardial injury,
or efficacy of medical therapy.
5. Risk Assessment in Non-Cardiac Settings:
• Elevated cardiac troponin levels have been associated
with adverse outcomes in non-cardiac settings, such as
sepsis, acute respiratory distress syndrome (ARDS), and
chronic kidney disease, serving as markers of multiorgan
dysfunction and poor prognosis.
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1. Acute limb ischemia 5. Paresthesia: Numbness, tingling, or loss of sensation in

Acute limb ischemia (ALI) is a sudden decrease in blood the affected limb.
flow to a limb, typically caused by arterial occlusion, 6. Poikilothermia: Coolness of the affected limb due to
embolism, or thrombosis. The condition can affect both reduced blood flow.
upper and lower extremities. 7. Pallor: Loss of normal capillary refill, delayed capillary
Causes of Acute Limb Ischemia: refill time.
1. Arterial Embolism: Embolization of thrombi or plaque Diagnosis:
debris from the heart or proximal arteries can occlude 1. Clinical Assessment: History and physical examination
peripheral arteries, leading to ALI. to evaluate for characteristic signs and symptoms of ALI,
2. Arterial Thrombosis: Formation of a blood clot within including pain, pallor, pulselessness, paralysis, and
an artery, often in the setting of underlying paresthesia.
atherosclerosis or arterial injury, can cause acute 2. Vascular Imaging: Doppler ultrasonography, computed
occlusion and ischemia. tomography angiography (CTA), magnetic resonance
3. Arterial Trauma: Penetrating or blunt trauma to an angiography (MRA), or conventional angiography to
artery can disrupt blood flow and lead to acute ischemia. identify the location and extent of arterial occlusion.
4. Arterial Dissection: Spontaneous or traumatic 3. Laboratory Tests: Complete blood count, coagulation
dissection of an artery can impair blood flow and cause studies, serum lactate, and arterial blood gas analysis to
ischemia. assess for metabolic derangements and thrombotic
5. Arterial Compression: External compression of an disorders.
artery by a mass, hematoma, or vascular anomaly can Treatment:
obstruct blood flow and lead to ischemia. 1. Revascularization: Emergent revascularization to
Clinical Presentation: restore blood flow to the ischemic limb and salvage
1. Pain: Severe, sudden onset of pain in the affected limb, viable tissue.
often out of proportion to physical findings. • Thrombolysis: Administration of thrombolytic
2. Pallor: Pale or mottled skin color in the affected limb agents to dissolve arterial thrombi.
due to reduced perfusion. • Percutaneous Transluminal Angioplasty (PTA):
3. Pulselessness: Absent or diminished pulses distal to the Mechanical dilation of arterial stenosis or occlusion
site of arterial occlusion. using a balloon catheter.
4. Paralysis: Weakness or paralysis of the affected limb, • Surgical Thrombectomy: Open surgical removal of
particularly in severe cases. thrombus or embolus from the affected artery.
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• Bypass Grafting: Surgical placement of a graft to 3. Metabolic Effects:

bypass the occluded segment of the artery. • stimulates glycogenolysis (breakdown of glycogen
2. Supportive Measures: Pain management, fluid into glucose) in the liver and skeletal muscles.
resuscitation, and systemic anticoagulation to prevent • increased blood glucose levels (hyperglycemia).
further thrombosis. 4. Central Nervous System Effects:
3. Monitoring: Serial clinical assessment, vascular • modulating arousal, attention, and alertness.
examination, and imaging to monitor response to • enhances cognitive function
treatment and assess for complications. 5. Pupillary Dilation: Adrenaline causes dilation of the
4. Complications Management: Management of pupils (mydriasis), which improves visual acuity and
complications such as compartment syndrome, peripheral vision, enhancing the ability to detect
infection, or tissue necrosis, which may necessitate potential dangers in the environment.
further interventions or surgical debridement. Clinical Uses:
1. Anaphylaxis: Adrenaline is the first-line treatment for
2.Adrenaline. anaphylaxis, a severe allergic reaction characterized by
Adrenaline, also known as epinephrine, is a hormone and rapid onset and potentially life-threatening symptoms
neurotransmitter produced by the adrenal glands, which are such as respiratory distress, hypotension, and
located on top of the kidneys. It plays a crucial role in the cardiovascular collapse. Intramuscular or intravenous
body's response to stress and emergency situations, often administration of adrenaline helps reverse airway
referred to as the "fight or flight" response. constriction, improve blood pressure, and alleviate
Physiological Effects: symptoms.
1. Cardiovascular Effects: 2. Cardiac Arrest: Adrenaline is used during
• Increase heart rate (positive chronotropic effect) cardiopulmonary resuscitation (CPR) to stimulate the
• Enhance myocardial contractility (positive inotropic heart and increase systemic vascular resistance, thereby
effect) improving blood flow to vital organs. It is administered
• Dilate blood vessels in skeletal muscles intravenously or via endotracheal tube during advanced
• increase cardiac output and blood flow to vital cardiac life support (ACLS) protocols.
organs. 3. Severe Asthma: Adrenaline may be administered as a
2. Respiratory Effects: bronchodilator in severe asthma exacerbations that do
• bronchodilation not respond adequately to conventional treatments such
• increased airflow into the lungs as inhaled beta-agonists and systemic corticosteroids. It
• improves oxygenation
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helps relieve bronchospasm and improve airflow in the 2. Sinuses of Valsalva: The space between the cusps of the
lungs. aortic valve forms three dilated pockets called the
Side Effects and Adverse Reactions: sinuses of Valsalva. These sinuses provide support to the
1. Tachycardia: Adrenaline can cause rapid heart rate and valve leaflets and help maintain proper valve function.
palpitations, which may be undesirable in patients with 3. Annulus: The base of the aortic valve leaflets attaches
certain cardiac conditions. to the annulus, a fibrous ring that surrounds the orifice of
2. Hypertension: Adrenaline-induced vasoconstriction the aorta. The annulus provides structural support and
can lead to elevated blood pressure, particularly in anchors the valve leaflets in place.
susceptible individuals. 4. Commissures: The points of contact between adjacent
3. Arrhythmias: Adrenaline may trigger cardiac valve leaflets are called commissures. These regions
arrhythmias, especially in patients with pre-existing allow for smooth closure and opening of the valve during
heart rhythm disorders. the cardiac cycle.
4. Anxiety and Restlessness: Adrenaline's stimulatory Function: During systole (contraction phase) of the cardiac
effects on the central nervous system can manifest as cycle:
anxiety, restlessness, or agitation. • The left ventricle contracts, generating high pressure
5. Hyperglycemia: Adrenaline-induced glycogenolysis that forces blood through the open aortic valve into the
can result in elevated blood glucose levels, which may aorta.
be problematic for individuals with diabetes mellitus. • As blood is ejected into the aorta, the pressure within the
aorta rises, causing the cusps of the aortic valve to fill
3.Anatomy of Aortic Valve. the sinuses of Valsalva and close tightly.
The aortic valve is one of the four valves in the human heart, • The closed valve prevents blood from flowing back into
located between the left ventricle and the aorta. It plays a the left ventricle (preventing regurgitation) and directs
crucial role in ensuring one-way blood flow from the left it into the systemic circulation.
ventricle to the aorta, which then distributes oxygen-rich During diastole (relaxation phase) of the cardiac cycle:
blood to the rest of the body. • The left ventricle relaxes, and the pressure within it
Structure: drops below that of the aorta.
1. Leaflets/Cusps: The aortic valve consists of three • The pressure gradient causes the cusps of the aortic
semilunar cusps or leaflets, each resembling a half-moon valve to open, allowing blood to flow from the left
shape. These leaflets are composed of dense connective ventricle into the aorta and onward to the systemic
tissue covered by endocardium. circulation.
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Clinical Significance: considered a medical emergency due to the increased

• Aortic Stenosis: Narrowing of the aortic valve orifice risk of myocardial infarction (heart attack).
due to thickening or calcification of the valve leaflets, 3. Variant (Prinzmetal's) Angina: Caused by coronary
leading to obstruction of blood flow from the left artery spasm, often occurring at rest and during sleep.
ventricle to the aorta. It may be associated with transient ST-segment
• Aortic Regurgitation: Incompetence of the aortic valve elevation on electrocardiogram (ECG).
resulting in backflow of blood from the aorta into the left Risk Factors:
ventricle during diastole. 1. Coronary Artery Disease (CAD)
• Bicuspid Aortic Valve: A congenital heart defect 2. Hypertension
characterized by the presence of two instead of three 3. Hyperlipidemia
cusps in the aortic valve, which may predispose 4. Diabetes Mellitus
individuals to valve dysfunction and aortic pathology. 5. Smoking
• Valve Replacement: Surgical or transcatheter 6. Family History
replacement of the aortic valve is indicated in patients Diagnostic Evaluation:
with severe aortic stenosis or regurgitation who are 1. History and Physical Examination: Detailed history
symptomatic or at risk of adverse outcomes. of symptoms, risk factors, and medical history, along
with a physical examination to assess for signs of
4.Angina pectoris. cardiovascular disease.
Angina pectoris, commonly referred to as angina, is a 2. Electrocardiogram (ECG): Detects changes in the
symptom of coronary artery disease (CAD) characterized heart's electrical activity during episodes of angina,
by chest discomfort or pain caused by reduced blood flow such as ST-segment depression or T-wave inversion.
to the heart muscle. 3. Exercise Stress Test: Evaluates heart function and
Types of Angina: symptoms during physical exertion, often combined
1. Stable Angina: Typically triggered by physical with ECG monitoring.
exertion or emotional stress and relieved by rest or 4. Coronary Angiography: Invasive procedure to
medication. The pattern of symptoms is usually visualize the coronary arteries and identify areas of
predictable and consistent over time. narrowing or blockage.
2. Unstable Angina: Occurs unpredictably and may Management:
worsen in severity, frequency, or duration over time. 1. Lifestyle Modifications: Smoking cessation, healthy
It may occur at rest or with minimal exertion and is diet, regular exercise, weight management, and stress
reduction techniques.
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2. Medications: Nitroglycerin for acute relief of angina partial thromboplastin time (aPTT) and activated
symptoms, beta-blockers, calcium channel blockers, clotting time (ACT).
nitrates, and antiplatelet agents to reduce the 3. Heparin Reversal: At the end of CPB, heparin is
frequency and severity of angina episodes. reversed using protamine sulfate. Protamine binds to
3. Revascularization: Percutaneous coronary heparin, neutralizing its anticoagulant effects and
intervention (PCI) with stent placement or coronary restoring normal coagulation function. The dose of
artery bypass grafting (CABG) may be indicated in protamine is titrated based on the patient's ACT and
patients with severe or refractory angina. heparin dose to achieve adequate reversal without
Complications: excessive bleeding.
1. Myocardial Infarction (Heart Attack) 4. Other Anticoagulants: In some cases, alternative
2. Heart Failure anticoagulants such as bivalirudin or argatroban may be
3. Arrhythmias used, especially in patients with heparin allergies or
heparin-induced thrombocytopenia (HIT). These
5.Anticoagulation during Cardiopulmonary Bypass. medications work through different mechanisms
During cardiopulmonary bypass (CPB), anticoagulation is compared to heparin and may require different
crucial to prevent clotting within the CPB circuit and to monitoring strategies.
maintain adequate blood flow through the bypass machine.
Here's an overview of the anticoagulation protocol 6.Antiplatelet
commonly used during CPB: Antiplatelet medications are a class of drugs used to prevent
1. Heparinization: Heparin is the most commonly used blood clot formation by inhibiting platelet aggregation,
anticoagulant during CPB. It is typically administered as which plays a key role in the formation of arterial thrombi.
a bolus dose to achieve a target activated clotting time Here are some commonly used antiplatelet medications:
(ACT) of around 400-480 seconds. This high level of 1. Aspirin (Acetylsalicylic Acid):
anticoagulation is necessary to prevent clotting within • Mechanism of Action: Aspirin irreversibly inhibits
the CPB circuit, which consists of non-endothelial cyclooxygenase (COX) enzyme, thereby blocking the
surfaces that can activate the coagulation cascade. synthesis of thromboxane A2, a potent platelet
2. Monitoring: ACT is the primary method used to monitor aggregator.
the level of anticoagulation during CPB. It measures the • Indications: Aspirin is indicated for the prevention of
time it takes for blood to clot in response to a specific myocardial infarction, stroke, and cardiovascular
activator. Additional monitoring may include activated events in patients with atherosclerotic disease or risk
factors.
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• Dosage: Typically administered as low-dose aspirin • Indications: Ticagrelor and prasugrel are indicated
(81-100 mg daily) for long-term prevention. for the prevention of thrombotic events in patients
• Side Effects: Common side effects include with acute coronary syndromes undergoing PCI.
gastrointestinal irritation, peptic ulcers, and bleeding. • Dosage: Ticagrelor is typically administered as a
Rare but serious adverse effects include loading dose followed by a maintenance dose (90 mg
gastrointestinal bleeding, intracranial hemorrhage, and twice daily), while prasugrel is administered as a
hypersensitivity reactions. loading dose followed by a maintenance dose (10 mg
2. Clopidogrel (Plavix): once daily).
• Mechanism of Action: Clopidogrel irreversibly • Side Effects: Common side effects include bleeding,
inhibits the P2Y12 adenosine diphosphate (ADP) dyspnea (with ticagrelor), and gastrointestinal
receptor on platelets, preventing ADP-induced symptoms. Ticagrelor may also cause bradycardia
platelet activation and aggregation. and ventricular pauses in some patients.
• Indications: Clopidogrel is used in combination with
aspirin for the prevention of myocardial infarction, 7.Aortic root
stroke, and cardiovascular events in patients with The aortic root is the portion of the aorta that arises from
acute coronary syndromes, recent myocardial the left ventricle of the heart and serves as the attachment
infarction, or prior percutaneous coronary site for the aortic valve. It is a crucial anatomical structure
intervention (PCI). involved in the regulation of blood flow from the heart to
• Dosage: Typically administered as a loading dose the systemic circulation.
followed by a maintenance dose (75 mg once daily). Location: The aortic root is located at the base of the heart,
• Side Effects: Common side effects include directly above the left ventricle and adjacent to the
gastrointestinal upset, diarrhea, and bleeding. atrioventricular (mitral) valve. It is the starting point of the
Clopidogrel may also cause neutropenia and ascending aorta, which carries oxygenated blood from the
thrombotic thrombocytopenic purpura (TTP) in rare heart to the rest of the body.
cases. Components:
3. Ticagrelor (Brilinta) and Prasugrel (Effient): Aortic Valve: The aortic root contains the aortic valve, a
• Mechanism of Action: Ticagrelor and prasugrel are tricuspid semilunar valve that separates the left ventricle
potent P2Y12 receptor antagonists that inhibit from the ascending aorta. The aortic valve consists of three
platelet activation and aggregation, similar to cusps (leaflet-like structures) – the left coronary cusp, right
clopidogrel. coronary cusp, and non-coronary cusp – which open and
close to regulate blood flow.
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Sinuses of Valsalva: The aortic root is surrounded by three bradyarrhythmias. It acts by blocking the
dilated pockets called the sinuses of Valsalva, named after parasympathetic (vagal) tone to the heart, leading to
the Italian anatomist Antonio Maria Valsalva. These sinuses increased heart rate and improved cardiac output.
provide support to the aortic valve leaflets and help 2. Antispasmodic: Atropine can be used to reduce
maintain proper valve function. smooth muscle spasms in various organs, such as the
Aortic Annulus: The base of the aortic valve leaflets gastrointestinal tract and urinary bladder. It inhibits
attaches to the aortic annulus, a fibrous ring that surrounds gastrointestinal motility and secretions, making it
the orifice of the aorta. The annulus provides structural useful in the treatment of conditions such as irritable
support and anchors the valve leaflets in place. bowel syndrome and overactive bladder.
Clinical Significance: 3. Preanesthetic Medication: Atropine is sometimes
• Aortic Root Dilation administered before anesthesia to reduce salivary and
• Aortic Valve Disorders respiratory tract secretions and prevent bradycardia
associated with vagal stimulation during surgery.
8.Atropine 4. Ophthalmic Use: Atropine eye drops are used to
Atropine is a medication classified as an anticholinergic induce mydriasis (pupillary dilation) and cycloplegia
agent, specifically an antimuscarinic drug. It acts by (paralysis of accommodation) for ophthalmic
blocking the action of acetylcholine at muscarinic receptors examinations and procedures.
in various tissues throughout the body. Side Effects:
Mechanism of Action: • Common side effects of atropine include dry mouth,
• Atropine competitively inhibits the binding of blurred vision, urinary retention, constipation,
acetylcholine to muscarinic receptors, thereby blocking tachycardia, and flushing.
the effects of parasympathetic stimulation mediated by • Central nervous system effects such as restlessness,
acetylcholine. confusion, hallucinations, and delirium may occur
• By inhibiting muscarinic receptors, atropine produces a with higher doses or in susceptible individuals.
variety of pharmacological effects, including increased • Overdose of atropine can lead to anticholinergic
heart rate (positive chronotropic effect), bronchodilation, toxicity, characterized by symptoms such as
decreased gastrointestinal motility, and pupillary dilation hyperthermia, agitation, seizures, and cardiac
(mydriasis). arrhythmias.
Clinical Uses:
1. Bradycardia: Atropine is commonly used to increase
heart rate in patients with symptomatic bradycardia or
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9.Beta blockers. reduce myocardial oxygen demand by slowing heart

Beta blockers, also known as beta-adrenergic blocking rate and decreasing myocardial contractility.
agents, are a class of medications that primarily block the 3. Heart Failure: In patients with heart failure, beta
effects of catecholamines (such as adrenaline and blockers can improve symptoms, reduce
noradrenaline) on beta-adrenergic receptors in the body. hospitalizations, and prolong survival by blocking the
Mechanism of Action: detrimental effects of excessive sympathetic
• Beta blockers competitively block beta-adrenergic stimulation on the heart.
receptors, specifically beta-1 (β1) receptors in the 4. Arrhythmias: Beta blockers are used to manage
heart and beta-2 (β2) receptors in the lungs and blood various cardiac arrhythmias, including atrial
vessels. fibrillation, supraventricular tachycardia, and
• By blocking beta-1 receptors in the heart, beta ventricular arrhythmias, by slowing conduction
blockers reduce the effects of sympathetic stimulation through the atrioventricular node and reducing
on the heart, resulting in decreased heart rate, reduced automaticity of cardiac cells.
myocardial contractility (negative inotropic effect), 5. Myocardial Infarction: Beta blockers are often
and decreased cardiac output. prescribed after myocardial infarction (heart attack) to
• Beta blockers also inhibit the release of renin from the reduce the risk of recurrent events and improve
kidneys, leading to decreased production of outcomes. They help to stabilize the heart, reduce
angiotensin II and aldosterone, which helps to lower myocardial oxygen demand, and prevent arrhythmias.
blood pressure. Common Beta Blockers:
Clinical Uses: • Non-selective beta blockers: Propranolol, nadolol,
1. Hypertension: Beta blockers are commonly used as timolol.
first-line or adjunctive therapy for the management of • Beta-1 selective blockers: Atenolol, metoprolol,
hypertension (high blood pressure). They help to bisoprolol, nebivolol.
reduce blood pressure by decreasing heart rate and • Beta blockers with additional vasodilatory properties:
cardiac output, as well as by reducing renin release Carvedilol, labetalol.
from the kidneys. Side Effects:
2. Angina Pectoris: Beta blockers are effective in the • Common side effects of beta blockers include
treatment of stable angina (angina pectoris), a bradycardia (slow heart rate), hypotension (low blood
condition characterized by chest pain or discomfort pressure), fatigue, dizziness, and cold extremities.
due to reduced blood flow to the heart muscle. They • Other potential side effects include
bronchoconstriction (especially in patients with
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asthma or chronic obstructive pulmonary disease), 11.Cardiac catheterization

worsening of peripheral vascular disease, and Cardiac catheterization, also known as coronary
masking of hypoglycemia symptoms in diabetic angiography or coronary catheterization, is a minimally
patients. invasive procedure used to diagnose and treat various heart
conditions. It involves inserting a thin, flexible tube called
10.Blalock–Taussig shunt a catheter into a blood vessel and advancing it to the heart
The Blalock–Taussig shunt (often abbreviated as BT shunt) or coronary arteries under X-ray guidance. Here's an
is a surgical procedure used to palliate cyanotic congenital overview of cardiac catheterization:
heart defects, particularly those involving inadequate blood Indications:
flow to the lungs (pulmonary circulation). It was first 1. Diagnostic Purposes: Cardiac catheterization is
introduced by Alfred Blalock and Helen Taussig in 1944 as primarily used to diagnose coronary artery disease
a treatment for cyanotic heart disease, specifically (CAD) by assessing the anatomy and function of the
Tetralogy of Fallot, where there is reduced blood flow to the coronary arteries, heart chambers, and valves. It helps
lungs due to obstruction of the pulmonary outflow tract. identify blockages, narrowing, or abnormalities in blood
Procedure: During a Blalock–Taussig shunt procedure, a flow within the heart and coronary arteries.
small tube (shunt) is surgically created to connect a 2. Interventional Procedures: In addition to diagnosis,
systemic artery (typically the subclavian artery) to the cardiac catheterization can also be used for therapeutic
pulmonary artery. This shunt allows oxygen-rich blood interventions such as:
from the systemic circulation to flow directly into the • Percutaneous coronary intervention (PCI): Including
pulmonary circulation, bypassing the obstructed or angioplasty and stent placement to open narrowed or
underdeveloped pulmonary arteries. The increased blocked coronary arteries and restore blood flow to
pulmonary blood flow helps alleviate cyanosis and the heart muscle.
improves oxygenation of the blood. • Valvuloplasty: Balloon valvuloplasty to treat stenotic
Indications: The Blalock–Taussig shunt is primarily heart valves by dilating the valve opening.
indicated for congenital heart defects associated with • Closure of congenital heart defects: Such as atrial
reduced pulmonary blood flow and cyanosis, such as: septal defects (ASDs), ventricular septal defects
• Tetralogy of Fallot (VSDs), and patent ductus arteriosus (PDA) using
• Pulmonary atresia with ventricular septal defect catheter-based devices.
• Tricuspid atresia
• Transposition of the great arteries with ventricular
septal defect and pulmonary stenosis
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12.Cardiac myxoma/ Left Atrial Myxoma. excision of the tumor while preserving normal cardiac
Cardiac myxomas are the most common primary cardiac function and preventing embolic events.
tumors, typically benign in nature, and are characterized by • Minimally invasive techniques, such as video-assisted
their location within the heart, usually arising from the atria, thoracoscopic surgery (VATS) or robotic-assisted
particularly the left atrium. surgery, may be considered for select cases.
Clinical Presentation: • Long-term follow-up is necessary to monitor for
• Cardiac myxomas can present with a wide range of recurrence, particularly in patients with familial
symptoms, including: syndromes associated with multiple or recurrent
• Systemic symptoms such as fever, weight loss, and myxomas.
fatigue.
• Cardiovascular symptoms such as dyspnea, 13.Cardiac output
palpitations, chest pain, syncope, or signs of heart Cardiac output (CO) is a fundamental physiological
failure. parameter that represents the volume of blood ejected by
• Embolic events resulting in stroke or peripheral the heart per unit of time, usually expressed in liters per
embolization. minute (L/min).
• Symptoms may vary depending on the size, location, and Calculation: Cardiac output is calculated by multiplying
mobility of the tumor within the heart. the stroke volume (SV) by the heart rate (HR).
Diagnosis: Mathematically, it can be expressed as: CO=SV×HR
• Echocardiography, particularly transesophageal Components:
echocardiography (TEE), is the primary imaging 1. Stroke Volume (SV): Stroke volume refers to the
modality for diagnosing cardiac myxomas. It allows volume of blood ejected by the heart with each
for visualization of the tumor's size, location, contraction (systole). It is determined by several
mobility, and attachment site within the heart. factors, including preload (volume of blood in the
• Other imaging modalities such as cardiac magnetic ventricles at the end of diastole), contractility
resonance imaging (MRI) or computed tomography (strength of ventricular contraction), and afterload
(CT) may be used to further characterize the tumor (resistance against which the heart must pump blood).
and assess its relationship with surrounding 2. Heart Rate (HR): Heart rate represents the number
structures. of times the heart contracts (beats) per minute. It is
Treatment: influenced by factors such as autonomic nervous
• Surgical resection is the mainstay of treatment for system activity, hormonal regulation, and metabolic
cardiac myxomas. The goal of surgery is complete demands.
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Clinical Significance: absence of other identifiable causes of hypertrophy (such

• Cardiac output is a key parameter in the assessment of as hypertension or aortic stenosis).
cardiovascular function and is often monitored in 3. Restrictive Cardiomyopathy (RCM): RCM is
critically ill patients, patients undergoing surgery, and characterized by stiffness and impaired relaxation of the
those with cardiovascular diseases. heart muscle, leading to reduced ventricular compliance
• Abnormalities in cardiac output can indicate various and diastolic dysfunction.
pathological conditions, including heart failure, 4. Arrhythmogenic Right Ventricular Cardiomyopathy
myocardial infarction, arrhythmias, shock, and fluid (ARVC): ARVC is characterized by fibrofatty
overload or depletion. replacement of the right ventricular myocardium,
• Measurement of cardiac output can be performed using leading to arrhythmias, right ventricular dysfunction,
various techniques, including echocardiography, and progressive dilation of the right ventricle.
thermodilution (pulmonary artery catheter), impedance Clinical Presentation:
cardiography, and cardiac magnetic resonance imaging • The clinical presentation of cardiomyopathy varies
(MRI). depending on the type, severity, and underlying cause.
Common symptoms may include dyspnea (shortness of
14.Cardiomyopathy breath), fatigue, palpitations, chest pain, edema
Cardiomyopathy is a group of diseases characterized by (swelling), and syncope (fainting).
abnormalities in the size, shape, and function of the heart • Complications of cardiomyopathy may include heart
muscle, which can impair the heart's ability to pump blood failure, arrhythmias, thromboembolism (blood clots),
effectively. and sudden cardiac death.
Classification: Diagnosis:
1. Dilated Cardiomyopathy (DCM): DCM is the most • Diagnosis of cardiomyopathy typically involves a
common type of cardiomyopathy and is characterized by combination of clinical evaluation, imaging studies
enlargement (dilation) of the heart chambers, (such as echocardiography and cardiac MRI),
particularly the left ventricle. This leads to impaired electrocardiography (ECG), and laboratory tests (such as
contraction and systolic dysfunction, resulting in biomarkers of heart damage).
reduced cardiac output and heart failure. • Endomyocardial biopsy may be performed in certain
2. Hypertrophic Cardiomyopathy (HCM): HCM is cases to evaluate for myocardial inflammation, fibrosis,
characterized by abnormal thickening (hypertrophy) of or infiltrative diseases.
the heart muscle, particularly the left ventricle, in the
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Treatment: 16.Draw and mark a normal ECG.

• Treatment of cardiomyopathy aims to alleviate
symptoms, improve cardiac function, and reduce the
risk of complications. This may include lifestyle
modifications (such as salt restriction and exercise),
pharmacotherapy (such as beta-blockers, ACE
inhibitors, diuretics, and antiarrhythmic drugs),
device therapy (such as implantable cardioverter-
defibrillators or cardiac resynchronization therapy),
and in some cases, heart transplantation.

15.Classification of congenital heart diseases.

17.Heart block.
Definition: Heart blocks are defined as blockage in the
transmission of sinus beats to the ventricles through
conduction pathway. The block occurs at the level of AV
node, hence, they are called AV blocks.
Heart block can be classified into first-degree, second-
degree, or third-degree (complete) blocks, depending on the
severity of the conduction disturbance.
Causes of heart blooks
1. Congenital
2. Acquired
• Myocardial infarction, e.g. inferior wall.
• Myocarditis, cardiomyopathy, Chagas disease.
• Calcific valvular disease, e.g. aortic stenosis
• Drugs, e.g. digoxin, beta blockers.
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• Cardiac surgery 19.Ventricular ectopic beats.

• Hypothyroidism Definition: The premature beats/contractions arising from
• Degenerative one of the ventricles are called VPCs or ventricular
Symptoms may vary depending on the degree of heart ectopics. They occur prematurely than the next expected
block and can include dizziness, fatigue, syncope (fainting), ventricular beat.
and palpitations. Characteristics
Treatment: 1. The VPC has a wide QRS complex (> 0.14 sec)
o With first-degree heart block, you might not need 2. There is a pause following the VPC.
treatment. 3. They may have same shape (monomorphic) or different
o With second-degree heart block, you may need a shapes (polymorphic)
pacemaker. Causes:
o With third-degree heart block, you will most likely need 1.Physiological: Occasionally occur following exertion,
a pacemaker. coffee or anxiety.
2. Pathological (due to disease)
18.Prolonged QT. • Coronary artery disease/ischaemic heart disease
Prolonged QT interval refers to an abnormal delay in • Hypertension
the repolarization of the ventricles during the cardiac cycle, • Myocarditis, cardiomyopathy
as seen on an electrocardiogram (ECG). The QT interval • Thyrotoxicosis
represents the time from the start of ventricular • Valvular heart disease, e.g. rheumatic
depolarization (Q wave) to the end of ventricular • Digitalis-induced
repolarization (T wave). A prolonged QT interval is defined Symptoms may include palpitations, chest discomfort, and
as QT interval exceeding 450 milliseconds in men and 470 in some cases, dizziness or syncope.
milliseconds in women. Treatment
Causes: Prolonged QT interval can be congenital (due to 1. An isolated VPC in the absence of heart Stew does not
genetic mutations) or acquired (due to medications, require treatment.
electrolyte imbalances, or certain medical conditions). 2. If they are digitalis-induced, stop the drug
Treatment for prolonged QT may include lifestyle 3. Medication – Anxiolytics, antiarrhythmic such as
changes, medications, and surgery or other procedures. betablockers, quinidine, amiodarone are helpful in VPC
Medication: Beta blockers, Mexiletine 4. Catheter ablation may be considered.
Surgery: Left cardiac sympathetic denervation (LCSD)
surgery, Implantable cardioverter-defibrillator.
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20.Torsade’s de pointes (ventricular tachycardia). (3) 21.Raynaud’s disease.

Definition: Three or more than three VPCs occurring in a Raynaud's disease, also known as Raynaud's phenomenon
quick succession or a continuous run of VPCs on ECG at a or Raynaud's syndrome, is a condition characterized by
rate of ≥100/min is called ventricular tachycardia. episodic vasospasm of the small arteries, most commonly
ECG Characteristics affecting the fingers and toes. This vasospasm leads to
1. The ECG shows a continuous run of wide, bizarre QRS temporary interruption of blood flow to the affected areas,
complexes. resulting in color changes (pallor, cyanosis, and erythema)
2. Heart rate is > 100/min. and sensations of coldness, numbness, or tingling induced
Management by exposure to cold or emotional stimulus.
1. Make the Patient to lie comfortably. Give O₂ and Treatment
maintain I.V. 1. Reassurance: Patient should be reassured about the
2. Check the pulse: If there is no pulse (pulseless VT), treat benign nature of this disorder.
it as ventricular fibrillation or cardiac arrest. 2. Patient should avoid smoking and precipitating factors,
3. If there is a pulse, evaluate the vital signs and clinical e.g. cold, drugs.
symptoms; 3. Patient need to be instructed to dress warmly by using
i. If the patient is conscious, acceptable vital parameters wollen gloves and stockings. Electrically charged gloves
are present and there is no complaint of angina, proceed are now available to keep the hands warm.
with the drug therapy. 4. Vasodilators and calcium channel blockers, e.g.
• Give I.V. xylocaine (50-100 mg bolus followed by 1-4 nifedipine reduces the frequency and severity of attacks.
mg/min as an infusion till it reverts) followed by an oral 5. In severe case, sympathectomy may be useful.
antiarrhythmic, e.g. amiodarone, disopyramide, mexiletine,
etc. The acidosis and electrocyte disturbance must be 22.Types of pulse
corrected. Pulse can be classified by
• If unresponsive to drug therapy, perform cardioversion Based on their location
(DC shock starting at 200 joules increased if required). 1. Radial Pulse: Located on the radial artery in the wrist,
ii. If the patient is unconscious and has an adverse effect just below the base of the thumb on the thumb side of the
of arrhythmia, e.g. hypotension or angina pain, give a forearm.
precordial thump, if not reverted them proceed 2. Carotid Pulse: Located on the carotid artery in the neck,
immediately with defibrillation (20 joules initially, along the medial border of the sternocleidomastoid
increase it if required). Begin the drug therapy after muscle.
reversion.
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3. Brachial Pulse: Located on the brachial artery in the Causes: Pulsus paradoxus can occur in various conditions
upper arm, between the biceps and triceps muscles. that affect cardiac or respiratory function. Common causes
4. Femoral Pulse: Located on the femoral artery in the include cardiac tamponade, severe asthma or chronic
groin, midway between the pubic symphysis and anterior obstructive pulmonary disease (COPD) exacerbations,
superior iliac spine. tension pneumothorax, and severe hypovolemia.
5. Popliteal Pulse: Located on the popliteal artery behind
the knee joint, deep within the popliteal fossa. 24.Types of Cyanosis.
Based on their character Definition: It is defined as bluish discolouration of skin and
1.Anacrotic is low volume rising pulse seen in aortic mucous membrane. It may be peripheral, central or mixed.
stenosis. Peripheral cyanosis is due to excessive extraction of O₂
2. Pulsus alternans means alternation of a large volume from the blood when circulation is slow, i.e. congestive
and low volume pulse regularly. It is seen in left heart heart failure and shock. It can occur due to vasoconstriction
failure. in severe cold weather. It is seen on lips, nails, tip of nose
3. Pulsus paradoxus: Normal pulse volume increases and ear lobule.
during inspiration but it decreases instead of normal Central cyanosis results from poor oxygenation of the
increase in pulsus-paradoxus. It is seen in constrictive blood in the lungs, hence, commonly seen in a wide variety
pericarditis, pericardial effusion, asthma, etc. of respiratory and cardiovascular diseases leading to
4. Pulsus bisferiens: It is a double peaked (two peaks at a pulmonary oedema. It can occur in congenital heart
stroke) pulse seen in combined aortic stenosis and aortic diseases with right to left shunt. It is seen on the under
regurgitation or idiopathic hypertrophic subaortic stenosis surface of tongue, lips, oral cavity and palate.
(IHSS). Mixed cyanosis is a combination of the above two types.

23.Pulsus paradoxus. 25.Clinical features of Acute Coronary Syndrome

Pulsus paradoxus is a clinical phenomenon characterized by (ACS):
an exaggerated decrease in systolic blood pressure during • Chest pain or discomfort: This is the hallmark
inspiration. Normally, during inspiration, there is a slight symptom of ACS and is often described as pressure,
decrease in systolic blood pressure due to increased tightness, squeezing, or heaviness in the chest. The pain
intrathoracic pressure and decreased venous return to the may radiate to the arms (usually the left arm), neck, jaw,
heart. However, in pulsus paradoxus, this decrease in back, or stomach.
systolic blood pressure is more pronounced and exceeds 10
mmHg.
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• Shortness of breath (dyspnea): Patients with ACS may • Head bobbing (Corrigan's sign): A visible pulsation
experience difficulty breathing, especially with exertion or bobbing of the head with each heartbeat, often
or at rest. observed in severe cases of aortic regurgitation.
• Nausea, vomiting, or indigestion: Some individuals • Water-hammer pulse (Corrigan pulse): A rapid and
with ACS may report gastrointestinal symptoms, which forceful arterial pulse that collapses suddenly,
can be mistaken for heartburn or indigestion. resembling the movement of a water hammer.
• Sweating (diaphoresis): Profuse sweating, particularly • Signs of left ventricular failure: These may include
cold and clammy sweat, may occur with ACS. dyspnea on exertion, orthopnea, paroxysmal nocturnal
• Fatigue: Patients may feel unusually tired or fatigued, dyspnea, fatigue, and pedal edema.
even with minimal physical activity.
• Anxiety or sense of impending doom: Some 27.Clinical features of Shock:
individuals may experience feelings of anxiety, • Hypotension: Low blood pressure is a hallmark
restlessness, or a sense of impending doom. feature of shock. Systolic blood pressure is typically
• Dizziness or lightheadedness: Patients may feel dizzy <90 mmHg or a decrease of >40 mmHg from baseline.
or lightheaded, especially when standing up or exerting • Tachycardia: The heart rate increases to compensate
themselves. for decreased cardiac output and maintain tissue
perfusion.
26.Clinical features of Aortic Regurgitation: • Altered mental status: Patients may appear confused,
• Bounding pulse: A strong and forceful pulse may be disoriented, lethargic, or unconscious.
palpated due to the increased stroke volume resulting • Cool, clammy skin: Peripheral vasoconstriction and
from regurgitation of blood back into the left ventricle reduced tissue perfusion lead to cool and clammy skin.
during diastole. • Weak or absent peripheral pulses: Peripheral pulses
• Widened pulse pressure: The difference between may be weak or difficult to palpate due to decreased
systolic and diastolic blood pressure may be widened cardiac output.
due to increased systolic pressure and decreased • Pallor or cyanosis: Pallor (pale skin color) or cyanosis
diastolic pressure. (bluish discoloration) may be present, especially in
• Diastolic murmur: A high-pitched blowing murmur severe cases of shock.
heard best at the left sternal border in the 2nd • Oliguria: Decreased urine output may occur due to
intercostal space during diastole. reduced renal perfusion.
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• Respiratory distress: Tachypnea, shallow breathing, 4. Technique: Place the stethoscope firmly against the
or respiratory distress may be present in patients with skin at each auscultation site. Listen systematically to
shock, especially in cardiogenic or distributive shock. each area for the presence of heart sounds (S1 and S2)
and any additional sounds, such as murmurs. Move
28.What is murmur? How to assess heart murmur. the stethoscope in a methodical pattern, listening
A heart murmur is an abnormal sound heard during carefully for any abnormalities.
auscultation of the heart with a stethoscope. Murmurs are 5. Characteristics of Murmurs: Assess the
caused by turbulent blood flow within the heart or blood characteristics of any murmurs detected:
vessels, resulting from structural abnormalities or • Timing: Determine if the murmur occurs during
physiological conditions. systole (between S1 and S2) or diastole (after S2).
Assessment of Heart Murmur: • Location: Note the specific auscultation site where
1. Preparation: Ensure a quiet environment and the murmur is loudest.
adequate lighting. Position the patient appropriately, • Radiation: Determine if the murmur radiates to
typically in a supine or seated position. Provide other areas of the chest or neck.
draping for patient comfort and exposure of the chest • Intensity: Grade the intensity of the murmur on a
area. scale of 1 to 6, with 1 being the softest and 6 being
2. Equipment: Use a high-quality stethoscope with a the loudest.
bell and diaphragm. The bell is used to detect low- • Pitch: Describe the pitch of the murmur as low,
frequency sounds, while the diaphragm is used to medium, or high.
detect high-frequency sounds. • Quality: Describe the quality of the murmur (e.g.,
3. Auscultation Sites: Begin by auscultating the heart at blowing, harsh, musical).
specific anatomical landmarks where heart sounds
and murmurs are best heard: 29.Heart Sounds
• Aortic area: Second right intercostal space at the Heart sounds are the sounds produced by mechanical
right sternal border. activities of heart during each cardiac cycle.
• Pulmonary area: Second left intercostal space at the Heart sounds are produced by:
left sternal border. 1. Flow of blood through cardiac chambers
• Tricuspid area: Lower left sternal border or fourth 2. Contraction of cardiac muscle
intercostal space. 3. Closure of valves of the heart.
• Mitral area: Fifth intercostal space at the Four heart sounds are produced during each cardiac cycle:
midclavicular line. 1. First heart sound
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2. Second heart sound • The left coronary artery arises from the left
3. Third heart sound coronary sinus of the aortic root, just above the
4. Fourth heart sound. aortic valve.
1. First heart sound is produced due to closure of the • It typically divides into two main branches:
mitral and tricuspid valves. It is best heard at apex. It is loud • Left Anterior Descending (LAD) Artery: Also
in mitral and tricuspid stenosis and weak or muffled in known as the anterior interventricular artery, the
mitral and tricuspid regurgitation. LAD artery travels down the anterior
2. Second heart sound is produced by closure of the aortic interventricular groove (also called the anterior
and pulmonary valves. It is weak in aortic and pulmonary interventricular sulcus) between the right and
stenosis but loud in systemic hypertension and pulmonary left ventricles, supplying the anterior wall of the
arterial hypertension. left ventricle and a portion of the
3. Third heart sound is produced by rapid flow of the interventricular septum.
blood from the atria to the ventricles during rapid filling • Left Circumflex (LCx) Artery: The left
phase. It may be audible normally in young persons. It is circumflex artery travels along the left
present in certain athletes and abnormally it is a sign of left atrioventricular groove (also called the coronary
heart failure due to mitral regurgitation. sulcus) between the left atrium and left
4. Normally, the fourth heart sound is an inaudible sound. ventricle, supplying the lateral wall of the left
It becomes audible only in pathological conditions. Fourth ventricle and sometimes giving off branches to
heart sound is produced by contraction of atrial the left atrium and posterior left ventricle.
musculature. It is seen in conditions like ventricular 2. Right Coronary Artery (RCA):
hypertrophy, long standing hypertension and aortic • The right coronary artery arises from the right
stenosis. coronary sinus of the aortic root, adjacent to the left
coronary artery.
30.Coronary artery anatomy. • It travels along the right atrioventricular groove
The coronary arteries are a network of blood vessels that (also called the atrioventricular sulcus) between the
supply oxygenated blood to the heart muscle right atrium and right ventricle.
(myocardium). Here's an overview of coronary artery • The RCA typically gives off branches including:
anatomy: • Right Marginal Artery: Supplies the lateral
1. Left Coronary Artery (LCA): aspect of the right ventricle.
• Posterior Descending Artery (PDA) or
Posterior Interventricular Artery: Travels in
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the posterior interventricular groove, supplying through the bloodstream and becomes lodged in a
the posterior walls of both ventricles and the blood vessel, obstructing blood flow to downstream
posterior portion of the interventricular septum. tissues.
• Emboli can originate from various sources, including
31.Protamine Reaction: blood clots, air bubbles, fat globules, foreign bodies,
• Protamine is a medication commonly used to reverse the or pieces of tissue. When an embolus becomes lodged
anticoagulant effects of heparin following surgery or in a blood vessel, it can cause tissue ischemia or
other medical procedures. It works by binding to heparin, infarction, depending on the size and location of the
forming a stable complex that is then removed from vessel affected.
circulation. • Clinical manifestations of embolization vary
• A protamine reaction refers to an adverse reaction that depending on the affected organ or tissue. For
occurs in response to the administration of protamine example, pulmonary embolism (when an embolus
sulfate. These reactions can range from mild to severe and lodges in the pulmonary arteries) can present with
may manifest as: symptoms such as chest pain, shortness of breath,
• Hypotension (low blood pressure) cough, and hemoptysis (coughing up blood).
• Bradycardia (slow heart rate) • Treatment of embolization depends on the
• Flushing or erythema (redness of the skin) underlying cause and the location and size of the
• Dyspnea (difficulty breathing) or bronchospasm embolus. Strategies may include anticoagulant
• Anaphylaxis, in rare cases, which is a severe allergic therapy, thrombolytic therapy, surgical embolectomy,
reaction characterized by swelling, hives, respiratory or catheter-based interventions such as thrombectomy
distress, and potentially life-threatening symptoms. or embolization coil placement.
• Protamine reactions are more common in individuals
with a history of fish allergy, as protamine is derived 33.Deep Vein Thrombosis (DVT):
from fish sperm. Patients with known allergies or • Deep vein thrombosis (DVT) is a condition characterized
sensitivities to protamine should be closely monitored by the formation of blood clots (thrombi) within the deep
and may require alternative management strategies for veins of the body, most commonly in the lower
heparin reversal. extremities.
• Risk factors for DVT include immobility (such as
32.Embolisation prolonged bed rest or long-distance travel), surgery,
• Embolization refers to the process by which an trauma, cancer, obesity, pregnancy, hormonal
embolus (a detached fragment of material) travels
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contraception or hormone replacement therapy, and Mechanism of Action: LMWH primarily acts by
inherited or acquired blood clotting disorders. enhancing the activity of antithrombin III, a natural
• Clinical features of DVT may include unilateral leg anticoagulant protein in the body. By binding to
swelling, pain or tenderness in the affected limb antithrombin III, LMWH accelerates its inhibition of
(particularly upon palpation or with dorsiflexion of the coagulation factors, particularly factor Xa, which plays a
foot), warmth, redness, and dilated superficial veins key role in the coagulation cascade.
(collateral vessels) in the affected limb. Indications: LMWH is commonly used for the prevention
• Complications of DVT can include pulmonary embolism and treatment of venous thromboembolism (VTE),
(when a clot dislodges from the leg veins and travels to including deep vein thrombosis (DVT) and pulmonary
the lungs), post-thrombotic syndrome (chronic leg pain, embolism (PE). It is also used in various other clinical
swelling, and skin changes), and recurrent venous settings, such as during surgery to prevent blood clots, in
thromboembolism. patients with acute coronary syndromes, and in the
• Diagnosis of DVT typically involves imaging studies management of certain medical conditions associated with
such as ultrasound (compression ultrasonography) of the increased thrombotic risk.
lower extremities to visualize the presence of thrombi Side Effects and Monitoring: Common side effects of
within the deep veins. LMWH include bleeding, bruising at the injection site, and
• Treatment of DVT aims to prevent clot propagation, thrombocytopenia. LMWH should be used with caution in
reduce the risk of embolization, and alleviate symptoms. patients with renal impairment, as dose adjustments may be
It often involves anticoagulant therapy (such as heparin necessary based on kidney function. Routine monitoring of
and warfarin or direct oral anticoagulants) and may platelet counts and renal function may be recommended in
include measures to promote venous return and prevent certain patient populations.
complications (e.g., compression stockings, ambulation).
In some cases, catheter-directed thrombolysis or surgical
35.Mitral valve
thrombectomy may be considered for severe or extensive The mitral valve, also known as the bicuspid valve, is one
DVT. of the four valves in the human heart. It is located between
the left atrium and the left ventricle and plays a crucial role
34.Low molecular weight heparin. in ensuring the unidirectional flow of blood through the
Low molecular weight heparin (LMWH) is a type of heart. Here are some key aspects of the mitral valve:
anticoagulant medication that works by inhibiting blood 1. Anatomy: The mitral valve consists of two leaflets or
clot formation. It is derived from unfractionated heparin cusps, hence the term "bicuspid." These leaflets are
named the anterior (or aortic) leaflet and the posterior (or
 I M M A N U V E L | 106

mural) leaflet. The leaflets are attached to the fibrous

annulus, which surrounds the valve orifice and provides
structural support.
2. Function: The primary function of the mitral valve is to
prevent the backflow of blood from the left ventricle into
the left atrium during ventricular contraction (systole).
When the left ventricle contracts, the mitral valve leaflets
close, forming a tight seal and preventing blood from
regurgitating back into the atrium.
3. Clinical Correlations: Mitral Valve Prolapse, Mitral
Regurgitation, Mitral Stenosis.

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Reference Books:
1. Davidson`S - Principles and Practices of Medicine
2. R Alagappan - Manual of Practical Medicine
3. Suraj Gupte – The Short Text Book of Pediatrics
4. Santhanam – Illustrated Text Book of Pediatrics
5. Sethi,Aswathi – Essential Of Pediatric Nursing
6. SN Chugh – Medicine For Nurses
7. K Sembulingam – Essential of Medical Physiology
8. RS Sharma – Cardiology
9. Jayant C Bhalerao - Essentials of Clinical Cardiology

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EDITED ON: 28.05.2024