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Cardiovascular Disorders

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0% found this document useful (0 votes)
14 views

Cardiovascular Disorders

Uploaded by

Wajeeha Ayub
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
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Cardiovascular Disorders

1. Chronic Cardiac Failure


Failure of heart to maintain Cardiac output according to body’ needs. Over a long period of time with
compensatory changes.
Forward failure – dec cardiac output.
Backward failure – damming of blood.
Left Heart Failure Right Heart Failure
Causes: Causes:
Aortic regurgitation, mitral regurgitation, Atrial septal defect, tricuspid regurgitation,
patent ductus arteriosus, aortic stenosis, pulmonary hypertension, pulmonary
hypertension + cardiomyopathy, ischemic stenosis, cardiomyopathy.
heart disease.
Clinical features: Clinical features:
(Mostly pulmonary) dyspnoea (exertional, (Mostly related to liver) Headache,
orthopnea, nocturnal), pleural effusion, restlessness, cough, dyspnoea, anorexia,
pulmonary edema (blue skin, dysnea, nausea, vomiting, pain in right
blood in sputum), fatigue, weakness, hypochondrium, tachycardia, oliguria,
nocturia, non productive chronic cough, nocturia, pedal edema, raised JVP,
cardiomegaly, 3rd heart sound (gallop hepatomegaly, putting edema, ascites,
rhythm), loud P2, apex beat displaced, pleural effusion, tricuspid regurgitation,
basal crepitations. gallop rhythm, right Ventricular
cardiomegaly.

Framingham Criteria for CCF (1 major and 2 minor)


Major Minor
Paroxysmal nocturnal dyspnoea (L), Pedal edema (R), night cough (L),
neck vein distension (R), dyspnoea on exertion (L), hepatomegaly
crepitations (L), cardiomegaly (R), pleural effusion (L), tachycardia
(R+L), acute pulmonary edema (L), (R+L), vital capacity reduced by one third
S3 gallop (R+L), inc JVP (R), (L)
positive hepatojugular reflex (R)
(to remember these easily > left failure has pulmonary symptoms predominantly and right has liver symptoms.
The letters mentioned in the table of criteria above is just to make it easy to remember)
Investigations:
ECG, xray, echo, blood CP, LFTs, cardiac enzymes, thyroid function tests, electrolytes, serum urea
creatinine, myocardial biopsy, ETT.
Management:
(Correct underlying cause. Remove precipitating factors (pneumonia, anemia etc). Control of congestive
heart failure.) Bed rest, physical and emotional rest, low salt diet, diuretics, digitalis, dobutamine,
dopamine, stop smoking.
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Cardiac failure > diuretics, ACE inhibitors, digitalis, restriction of sodium and physical activity,
vasodilator, positive Ionotropic Agents.
Complications: uremia, hypokalemia, hyponatremia, impaired liver function, thromboembolism.

2. Acute Cardiac Failure


Develops suddenly in hours or days in asymptomatic patient.
Causes: MI, VSD, mitral regurgitation, myocarditis, Cardiac tamponade, acute pulmonary embolus.
Clinical features:
• Acute cardiogenic pulmonary edema: inc fluid in tissues of lung, sudden Onset, severe acute
breathlessness, wheezing, productive cough (blood tinged, frothy sputum), rapid breathing,
crepitations, ronchi, sweating, cold skin, cyanosis, feeling of drowning, tachycardia, raised JVP,
gallop rhythm.
• Cardiogenic shock: severe clinical expression of left Ventricular failure, cold clammy skin,
cyanosis, oliguria/anuria, anxiety, confusion, fatigue, caused by infarction of large area of
ventricle.
• Acute decompensation of chronic heart failure.
Investigations:
ECG, echo, chest xray, arterial gases, inc pulmonary capillary wedge pressure.
Management:
Patient in sitting position. High concentration of O2. Morphine (metoclopromide along to prevent
vomiting). Diuretics, vasodilator. Nebulization with salbutamol, Ionotropic Agents (dobutamine etc).
Ionotropic balloon counterpulsation, thrmbolysis, angioplasty, bypass surgery, revascularization.

{Cardiogenic Shock – inability to pump due to severe left Ventricular failure. Cold clammy skin, cyanosis,
same as above. Differentiated from non cardiogenic shock by measuring pulmonary capillary wedge pressure
(inc in cardiogenic, dec in vice versa). Management same as above.

3. Hypertension
Sustained high BP (140/90) – atleast 2 readings on different occasions.
BP = cardiac output × peripheral resistance
Classification:
Optimal – systolic <120 diastolic <80
Normal - <130, <85
Pre hypertension – 130-139, 85-89

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Hypertension stage 1 (mild) – 140-159, 90-99
Stage 2 (moderate) – 160-179, 100-109
Stage 3 (severe) - >180, >110
Etiology: P°hypertension – 95% of cases are idiopathic precipitated by smoking, alcohol, caffeine, excess salt –
25-55 y/o. S°hypertension- 5%. Has a cause. Renal disease, endocrine disease, drugs.
Clinical features:
Mostly asymptomatic. Suboccipital pulsating headache (usually in morning), somnolence, confusion,
visual disturbances (these last 3 are in hypertensive encephalopathy), nausea, vomiting. Patients with
pheochromocytoma present with palpitations, perspiration, anxiety etc.
Complications: left Ventricular hypertrophy, stroke, IHD, hypertensive encephalopathy, subarachnoid
Hemorrhage, retinal changes, progressive renal failure.
{Take BP with patient lying down and standing. Increase in diastolic on standing occurs usually when it is
primary whereas decrease occurs when it is secondary.}
Investigations:
Urine analysis, hematocrit, serum urea creatinine, serum K, FBS, lipid profile, serum uric acid, ECG,
echo, xray (all these to detect causes of HT).
Management:
Weight reduction, reduce alcohol, stop smoking, salt restriction, avoid stress, thiazide diuretics, beta
blockers, ACE inhibitors, Ca channel blockers, alpha blockers. Combination Therapy:
>diuretic+BB+vasodilator/CCB. >diuretic+ACEI+CCB/BB. >CCB+ACEI+BB.
{Hypertensive crises: persistent diastolic >130. Hypertensive urgency: diastolic >125, can be controlled in few
hours, no organ damage. Hypertensive emergency: rapid decrease in BP in one hour required to prevent organ
failure.}

4. Ischemic Heart Disease


Decreased supply of O2 to cardiac muscles.
Causes: atherosclerosis (atheroma)
Risk factors: fixed>age, males, family history. Modifiable>hyperlipidemia, HT, smoking, diabetes, obesity, no
excercise, alcohol etc.

5. Coronary Artery Disease


Caused by atheroma/thrombosis. Presented by stable/unstable angina, MI, heart failure, arrhythmia, death.
Angina Pectoris
Paroxysmal chest pain due to MI.

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Causes: atherosclerosis, aortic stenosis, cardiomyopathy.
Types:
• Stable: coronary perfusion is impaired by fixed or stable atheroma. Patient has fixed capacity by
exertion.
• Unstable: rapidly worsening pain at rest or even during sleep (pain on minimal exertion-angina at rest,
partial obstruction)
• MI: mechanism is same as unstable (thrombus formation) but there is complete obstruction +necrosis of
cardiac cells.
Other types are:
• Exertional Angina: inc myocardial O2 demand during exertion. Relieved by nitroglycerine and rest.
• Prinzmetals/variant Angina: occurs at rest, awaking people from sleep. ST elevation.
• Unstable Angina: recent onset that inc in frequency, episodes and duration – Angina at rest not Relieved
by medication.
• Decubitus Angina: when Patient lies down.
• Nocturnal Angina: awakes people at night.
• Cardiac syndrome X: angina+positive excercise test+angiographically normal arteries.
Clinical features:
Chest pain, dysnea, nausea, fainting, radiating pain (dermatome from C8 to T4), relieved by sublingual
nitroglycerine, tightness in chest (sense of pressure, choking, heaviness in chest), may be sharp and
piercing, less than 30 minutes (usually 1-4 min), pale face, cold sweats.
Grading:
Grade 1 – ordinary physical activity does not cause angina.
Grade 2 – walking uphill, climbing more than one flight of stairs causes angina.
Grade 3 – walking on level/climbing one flight of stairs causes angina.
Grade 4 – inability to carry out any physical activity.
Investigations:
ECG (ST depression, T inversion except for Prinzmetals angina where there is elevation), excercise
tolerance test, isotope scanning, echo, coronary Angiography.
Management:
No smoking, ideal body weight, regular excercise, avoid exertion, sublingual nitrate before physical
exertion that may induce angina.
Sublingual nitroglycerine (Angised) acts in 1-2 mins. Repeated after 3-5 minute intervals. 3 tablets
maximum otherwise it’s just evolving MI so seek medical help. Nitrates, b blockers, Ca channel blockers,
aspirin, statins, coronary angioplasty, coronary artery bypass grafting.

6. Acute Coronary Syndrome


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Unstable angina and non-ST elevation MI. ST segment depression or T wave flattening or inversion. If cardiac
enzymes are not elevated – this is Unstable angina. If enzymes elevated – its non-ST elevation MI.
Investigations:
ECG, cardiac enzymes troponin T/I.
Management:
Hospitalization, bed rest, O2, sedation, BP maintained, heparin, antiplatelets (clopidogrel, aspirin), nitrates, b
blockers, revascularization, statins, ACEI, cessation of smoking, excercise, weight reduction, low fat diet.

7. Myocardial Infarction
Acute ischemic necrosis of area of myocardium. Usually in left ventricle. Usually btw 6 am and 12 noon
(circulatory periodicity).
Causes: atheroma, embolism, chest wall injury, vasculitis, polycythemia, DIC, congenital coronary abnormality,
thyrotoxicosis, valvular disease, arrhythmia.
Clinical features:
Sternal pain (radiating, severe than angina, lasts more than 30 minutes), similar to angina but occurs at
rest/less activity, not relieved by nitroglycerin. Dyspnoea, chest tightness, marked weakness or syncope,
nausea, vomiting, palpitations, cold sweating, ischemia, pallor, tachycardia, cold peripheries, 3 rd heart
sound.
{Painless/silent infarction – pain absent. Detected in routine ECG. Sudden death sometimes due to
arrythmia/Ventricular fibrillation.}
Investigations:
Patient appears anxious, restless, describes pain with clenched fist held against sternum, cold
perspiration, pallor. Pulse: tachycardia (Bradycardia if inf wall infarction), high BP, may develop fever in 24-
48 hours, raised RR (basal crepitations, raised JVP, wheezing (ronchi).
ECG (ST-elevation, T inversion), cardiac enzymes raised, serum myoglobin raised, serum AST and LDH
raised, blood cp/ESR high, echo, Radionuclide scan.
Management:
General>bed rest, CCU, nothing/clear liquids by mouth, bed side commode, O2, sedation. Specific>pain
relief- nitrates, morphine, oral aspirin. Nitroglycerin sublingually, O2, IV blockers if tachycardia,
thrombolytic streptokinase, acute angioplasty. Isosorbide dinitrate for 24-48 hours. Watch for
Ventricular fibrillation. Alprazolam, diet control, smoking cessation.
{Extra: UQ:
>Non-ST elevation MI, also called subendocardial infarction/non Q wave/ non occlusive thrombi.
>prognosis of non ST elevation MI better than MI with ST elevation.
Types: >Q wave: ECG has pathologic Q waves, T waves peaked then ST elevated, poor prognosis.

Asma Usman General Medicine


>Non Q Wave: No Q waves, T wave inversion, ST segment depression, better prognosis.
Cardiac enzymes: Troponin T and I are specific as they remain elevated (T – 10-14 days) (I – 7-10 days). LDH
also elevated but is non specific. Creatine kinase rises within 4-8 hours, peaks at 24 then normal by 2-3 days
(CK-MB more specific).
Higher the ST elevation, extensive is MI, Higher mortality. Higher the quantity of CK-MB, larger the infarct
and higher the mortality.}

8. Rheumatic Fever
Acute inflammatory disease following pharyngeal infection. Usually age 5-17. Cross reaction btw body
immune response to streptococcal antigens and tissue antigens principally in heart. Heart, joints, skin, lungs,
vessels, specially aortic/mitral valves affected.
Clinical features:
Sudden Onset of fever, joint pain, malaise, loss of appetite, palpable spleen, epitaxis, abdominal pain.
Duckett Jones Criteria - (For initial episodes of RF, not recurrent)
Diagnosis confirmed if: 2 major OR 1 major 2 minor OR 4 minor present.
Major: >carditis >polyarthritis >chorea >erythema marginatum >subcutaneous nodules.
Minor: >fever, arthralgia, previous RF, raised ESR/c reactive protein, leukocytosis, prolonged PR
interval.
Supporting evidence: preceding streptococcal infection such as raised ASO titer or positive throat
culture.
Complications:
Congestive HF, rheumatic heart disease, arrhythmia, pericarditis, pericardial effusion, rheumatic pneumonitis.
Investigations:
Throat swab culture, antistreptolysin O titer, raised ESR, C reactive protein, blood CP, chest xray, ECG,
echocardiography.
Management:
Bed rest (until fever, ESR, ECG, pulse return to normal), aspirin (2 weeks then tapered over 6 weeks),
corticosteroids (2 weeks then tapered over 3 weeks).
(Primary prevention – penicillin IM, erythromycin, azithromycin, cephalexin)
Chronic Rheumatic Heart Disease – rigidity of valves cusps, fusion of commissures, stenosis, regurgitation.

9. Infective Endocarditis
Microbial infection of heart valves or lining of cardiac chamber.

Asma Usman General Medicine


Causes: rheumatic heart disease, congenital heart disease, valvular disease, prosthetic valves, old age,
malignancy, DIC, uremia, burns, SLE. Organisms: strep viridans, bovis, staph aureus, enterococcus, gram
negative bacilli, fungi.
Types: >subacute endocarditis: most common organism is strep viridans. Low virulence. Congenital heart
disease or already defective valves are cause.
>acute endocarditis: staph aureus. Large vegetation, greater valve destruction, IV drug users.
>prosthetic endocarditis: s epidermidis and aureus. After cardiac surgery.
Clinical features:
Fever, Petechial Hemorrhage, Roth spots, spleenomegaly. Immune complexes: janeway lesions(small/flat
macules), splinter Hemorrhage(develop under finger/toe nails), oslers nodes (hard painful subcutaneous
swellings). Valvular dysfunction: murmurs, regurgitation. There is history of dental treatment or drug
abuse, fever, malaise, night sweats, myalgia, clubbing, weight loss.
Investigations:
Blood culture. Blood CP (raised ESR and CRP, WBCS elevated and anemia). Echo (to detect vegetation,
valve damage). ECG. Xray. Urine analysis. Serological tests.
Duke’s Criteria
Diagnosis confirmed by: 2 major OR 1 major 3 minor OR 5 minor. Possible if 1 major 1 minor OR 3
minor.
Major: >positive blood culture. >echo consistent/new murmurs of regurgitation.
Minor: >fever >predisposing factors >vascular phenomena >immunological phenomena >microbiological
evidence of infections microorganisms >positive echo.
Complications: congestive HF, valvular damage, pulmonary abscess.
Management:
Strep viridans: benzyl penicillin + gentamicin
Strep fecalis: amoxycillin + gentamicin
Staph aureus: first one if sensitive. If not, then vancomycin + gentamicin.
Prophylaxis Procedure Antibiotic
LA Dental procedure Amoxycilin oral 3g 1 hour
before.
If penicillin allergy, then
clindamycin oral 600mg
before.
GA Dental procedure Amoxycillin 1g then 0.5g 6
hourly.
If allergic, vancomycin +
gentamicin
GIT procedure Amoxicillin + gentamicin

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If allergic, vancomycin +
gentamicin.
{Scenario: systemic features + spleenomegaly + murmurs + established valve disease = infective Endocarditis.}

10. Mitral Stenosis


Causes: rheumatic heart disease, congenital, fibrosis/calcification of valves in elderly.
Clinical features:
Localized or normal apex beat at 5th intercostal space, opening snap, mid diastolic murmur,
breathlessness, fatigue, edema, ascites, palpitation, hemoptysis, cough, chest pain, thromboembolic
complications, loud first heart sound, crepitations, pulmonary edema, effusion, hoarseness, RV heave.
Investigations:
Left parasternal pulsation (bec of right ventricular hypertrophy), apex beat not displaced, loud 1st heart
sound, loud P2, opening snap, mid diastolic rumbling murmur, malar flesh. Echo, xray, ECG (tall R
waves and right Ventricular hypertrophy), doppler.
Management:
Anticoagulants (for systemic embolism), digoxin, b blockers, Ca channel blockers, diuretics, antibiotics.
Surgical: open/closed valvotomy, mitral valve repair, mitral valve replacement.

11. Mitral Regurgitation


Causes: rheumatic heart disease, mitral valve prolapse, aortic valve disease, myocarditis, RF, cardiomyopathy,
IHD, MI, CT disorders, IE, coronary artery disease.
Clinical features:
Displaced apex beat, pansystolic murmur + thrill, soft S1 and S3 is loud, dysnea, fatigue, palpitation,
edema, ascites, cardiomegaly, pulmonary venous congestion, pulmonary hypertension.
Investigations:
ECG (left Atrial hypertrophy, bifid P wave, left Ventricular hypertrophy), chest xray, echo (dilated LA,
LV), doppler, cardiac catheterization.
Management:
Vasodilators (ACE inhibitors, hydralazine) in symptomatic patients not asymptomatic chronic MR.
Diuretics, digoxin, oral anticoagulants, antibiotic Prophylaxis, mitral valve replacement/repair.

12. Mitral Valve Prolapse


Floppy/myxomatous MV. Bulging back of MV into left atrium during systolic. There is mid diastolic click first
– leads to mitral regurgitation.

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Causes: RF, CT disorders, myxomatous degeneration of valves.
Clinical features:
Usually asymptomatic. Symptomatic – chest pain(angina like but lasts for hours/days), dyspnea, fatigue,
palpitation, syncope, MR.
Examination: mid systolic click (mild cases), BP (normal or low), pan systolic murmur (in MR).
Investigations:
ECG, echo, doppler.
Complications: IE, MR, arythmias, sudden death.
Management:
Asymptomatic patients are reassured and follow up checkups. Symptomatic patients – b blockers, aspirin, IE
Prophylaxis, surgically valve repair/replacement.

13. Aortic Stenosis


Causes: congenital, rheumatic aortic stenosis, calcification of bicuspid valve.
Clinical features:
Apex beat normal/localized, ejection click (systolic murmur), slow rising pulse, signs of pulmonary
congestion (crepitations), exertional dysnea, exertional syncope, angina, sudden death, HF, GI bleeding.
Examination: (first 3 points above) + systolic thrill. S1 normal or soft. Prominent 4th sound. Systolic ejection
click. Mid systolic murmur.
Investigations:
ECG (left Ventricular hypertrophy, left bundle branch block), chest xray (enlarged LV and dilated
ascending aorta, may be normal), echo, doppler, cardiac catheterization.
Management:
Choice is surgery (people who develop angina, syncope, HF). Valve replacement. Aortic balloon
valvoplasty. Medical treatment for people who are inoperable (avoid strenuous activity, b blockers,
nitrates avoided).

14. Aortic Regurgitation


Causes: RF, IE, dissection of aorta, trauma, failure of prosthetic heart valve, congenital.
Clinical features:
Palpation, breathlessness, angina, collapsing pulse, low diastolic pressure, inc pulse pressure, bouncing
peripheral pulses, femoral bruit pistol shot, displaced apex beat, crepitations, quinkes sign, deMussets sign.
Investigations:

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ECG (left Ventricular hypertrophy, T inversion), chest xray (cardiac dilation, features of left HF) echo,
MRI.
Management:
Hydralazine, ACEI, diuretics, digoxin, IE Prophylaxis, RF Prophylaxis, aortic valve replacement.

15. Tricuspid Stenosis


RHD – common cause. Abdominal pain (due to hepatomegaly), swelling, peripheral edema, giant a wave in
JVP, pulsating liver, mid diastolic murmur at tricuspid area. Diuretic therapy, salt restriction, surgical
replacement of tricuspid valve.

16. Tricuspid Regurgitation


Causes: IE, RHD, cor pulmonale, pulmonary HT. Features of right HF. JVP (large v waves). Pansystolic
murmur. Murmur increases during inspiration. Pulsatile liver. Chest xray (dilated RA and RV), echo.
Treatment: diuretics. Replacing mitral valve (p° cause). Valvoplasty, tricuspid valve replacement.

17. Pulmonary Stenosis


Causes: congenital, RF (rare). Features: exertional fatigue, dysnea, light headedness, chest discomfort, cyanosis.
Right Ventricular hypertrophy. S1 normal. Single S2. Diminished P2. Ejection systolic murmur. JVP prominent
a wave. ECG (hypertrophied RA and RV), chest xray (RA and RV enlargement), echo. Treatment: balloon
valvoplasty.

18. Pulmonary regurgitation


Features: right HF, early diastolic murmur, loud P2. ECG (right Ventricula hypertrophy), chest xray, echo
(dilated RV, hypertrophic RA). Treatment: digoxin (for HF), treating underlying cause, valve replacement.

19. Congenital Heart Disease


Features: central cyanosis, pulmonary hypertension, clubbing of fingers, paradoxical embolism, reduced
growth, syncope.

20. Cor Pulmonale


Right Heart Ventricula hypertrophy and dilatation secondary to pulmonary hypertension caused by diseases of
lungs.

21. Acute Pericarditis

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May be because of infection or systemic disease. Pericardial inflammation.
Causes: Acute MI, viral (common), tuberculosis, bacterial malignancy.
Clinical features:
Fever, retrosternal chest pain that radiates to neck and shoulders, pain aggravated by
breathing/swallowing/change in posture, pericardial friction rub (usually audible in systole, to and fro
quality), scratchy sound over pericardium.
Investigations:
ECG (ST elevation – concave shape. PR depression. T wave inversion – myocarditis). Chest xray. Echo.
Viral titer.
Management:
Aspirin, indomethacin, colchicine, corticosteroids. For purulent pericarditis: antibiotics,
pericardiocentesis, surgical drainage.

22. Atrial Fibrillation


Continuous rapid 400 or more beats per minute. Activation of atria. They beat but ineffectively. Ventricles
respond at irregular intervals giving characteristic irregularly regular pulse.
Causes: coronary artery disease (MI), valvular heart disease, idiopathic, HT, thyrotoxicosis, cardiomyopathy,
alcohol, pneumonia, pericardial diseases.
ECG: P wave absent, QRS rhythm rapid and irregular.
Clinical features: palpitations, systemic embolism (abdominal/leg pain, stroke), decreased cardiac output.
Management:
Electrical DC cardioversion. Rate control strategy (digoxin, b blockers, verapamil). If unsuccessful then
transesophageal echo (to look for thrombus). Elective cardioversion (first anticoagulate patient then
amiodarone). Refractory Atrial fibrillation. Anticoagulants (warfarin).

Pericardial effusion: retrosternal oppression, heart sounds become quieter, QRS voltages reduced, inc size of
cardiac silhouette (xray), globular appearance of cardiac silhouette. Echo is investigation of choice.
Cardiac tamponade: Acute HF due to compression of heart by rapidly developing effusion. Raised JVP.
Hypotension. Pulsus paradoxicus. Oliguria.
Pericardial aspiration: pericardiocentesis: aspiration of cardiac effusion.
Complications: arrhythmia, damage to coronary artery, bleeding with exacerbation of tamponade.
Contraindicated in cardiac rupture or aortic dissection.

Important points:

Asma Usman General Medicine


IE and RF are causes of mitral regurgitation so in scenario with systemic features (fever etc) + spleenomegaly +
valve disease + murmurs = IE with mitral regurgitation. If it’s a child and fever and murmurs then RF with
mitral regurgitation.
Mitral regurgitation alone is with fatigue, dyspnea, edema, not systemic upsets like fever, weight loss,
spleenomegaly.
IE occurs in an established MV disease so murmurs plus its own features.
RF: joint pain/vague pain, age 5-17 (must). IE: no pain as such given, clubbing, hematuria. (Spleen is palpable
in both).
UQ: NYHA Grading system:
Class 1: no limitation during ordinary activity.
Class 2: slight limitation during ordinary activity.
Class 3: marked limitation of normal activities without symptoms at rest.
Class 4: unable to undertake physical activity without symptoms, symptoms may be present at rest.
(Identifying points):
Mitral regurgitation – pansystolic murmur.
Aortic regurgitation – ejection systolic murmur, early diastolic, Mussets sign, Quineks sign, drousseus sign,
low diastolic pressure, collapsing pulse.
Aortic stenosis: same as above but without collapsing pulse.

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