Pulmonary hypertension

Clinical Features Signs

Inspection Palpation Auscultation
1- Dyspnea initially on exertion & Hear sounds
later at rest . - Prominent a wave in JVP - Left parasternal heave " RV heave" 1- Accentuated S2( P2 )+ wide splitting
( due to RV pressure over load RVE) 2- If RSHF " cor pulmonales" S3
2- Dull , retrosternal chest pain - Cyanosis in late stage " due to " gallop rhythm "
( due to coronary blood flow systemic V.C resulting from markedly -Palpable PS in pulmonary area 3- Right ventricular S4.
to a marked hypertrophied RV ) reduced COP" (due to dilated pulmonary artery)
Murmurs (PS, PR, TR)
4- Ejection systolic murmur ( heard at
3- Syncope or near syncope due pulmonary area due to relative PS )
to fixed cardiac output. 5- In advanced cases :
- PR : Early diastolic murmur .
- TR : Pansystolic murmur .
Added Sounds
Systolic Ejection click in pulmonary area
Investigations
ECG X-ray Echo Cardiac catheterization
-RV & RA enlargement -Confirm the diagnosis e.g.
-RV hypertrophy -RV enlargement . -Detection of heart defects. detection the defect.
-RA hypertrophy -RA dilatation . -Thickened interventricular septum. -Measure pulmonary artery
-Enlargement of Pulmonary artery -Abnormal septal motion due to RV pressure to assess severity.
& it's main branches. pressure overload. -Measure the O2 level in
chambers and arteries.
- VSD , ASD , PDA causes pulmonary hypertension ( Left to Right shunt increasing pulmonary blood flow )
1- Signs of pulmonary hypertension
2- Symptoms : pulmonary blood flow lung plethora ( causing exertional dyspnea & recurrent chest infections ) pulmonary vasculature
resistance "pulmonary hypertension" till pulmonary artery pressure exceeds aortic artery pressure reversal shunt " Eisenmenger's
syndrome" causing cyanosis & Clubbing fingers.
- VSD , ASD causes LCOP ( signs & symptoms of LOCP ) - RV enlargement : ASD - PS
- PDA hyperdynamic circulation ( similar to peripheral signs of AR ) - LV enlargement : VSD–PDA–coarctation of aorta – AS
- Biventricular enlargement: VSD ( Later )
Accentuated S2 in VSD, ASD, PDA: accentuated P2 component Murmurs : - ASD Ejection systolic murmur(due to relative PS)
Splitting of S2 : - VSD Pansystolic murmur (left parasternal area.)
- VSD Wide splitting . - PDA Continuous murmur (Left infraclavicular area)
- ASD Wide fixed splitting.
- PDA Paradoxical splitting Thrill :
S3 : - VSD left parasternal area.
- VSD due to LV volume overload - PDA Left infraclavicular area (2nd left space )
Pulmonary area.
- ASD due to RV volume over load
S4 : Systolic ejection click :
- VSD , ASD , PDA if caused pulmonary hypertension - VSD , ASD , PDA if caused pulmonary hypertension .

VSD ASD PDA

Inspection
Gian (a) wave (a) wave equal to (v) wave ?! Gian (a) wave
If developed pulmonary hypertension cyanosis , finger clubbing , dyspnea .
Palpation
- Palpable P2 - Palpable P2 - Palpable P2
- Right ventricular heave - Right ventricular heave . - Right ventricular heave
- Thrill . - Relative stenosis causes no thrill - Thrill .
- LV volume overload apex displaced outward and - RV volume overload apex displaced outward - Pulse: is bounding ( wide pulse pressure ).
downward (with localized apex) only (with diffuse apex) - BP: Low diastolic blood pressure.
Auscultation ( shadowed = most important )
- S2 accentuated with wide splitting - S2 accentuated with wide fixed splitting - S2 accentuated with paradoxical splitting
- S3 - S3
- S4 - S4 - S4
- Pansystolic murmur with thrill ASD itself doesn't cause murmur : - Continuous machinery murmur
- Murmur of relative MS - Murmur of relative PS ( due to RV volume overload) N.B with moderate degree of pulmonary hypertension,
( due to increase blood flow through mitral valve ) the diastolic component of murmur disappears leaving
a systolic murmur only.
- Murmur of AR in high defects - Murmur of relative TS ( if the shunt is large )
" due to prolapse of a valve leaflet" - in advanced:TR (RVE dilated ventricle affect valve) - Mid-diastolic murmur : may be audible at the
- Murmur of relative PS ( due to RV volume overload) apex as a result of the increased volume of
- in advanced:TR (RVE dilated ventricle affect valve) blood flow across the mitral valve.
Systolic Ejection click in pulmonary area Systolic Ejection click in pulmonary area Systolic Ejection click in pulmonary area
Evaluation of the Infant or Child with Congenital Heart Disease
The initial evaluation for suspected congenital heart disease involves a systematic approach with three major components.
• First congenital cardiac defects can be divided into two major groups based on the presence or absence of cyanosis:
1- Acyanotic congenital heart leasions which can be determined by 1- physical examination 2- aided by pulse
2- Cyanotic congenital heart leasions oximetry.
• Second hese two groups can be further subdivided according to whether the chest radiograph shows evidence of : 1- increased 2- normal 3-
These 3 decreased pulmonary vascular markings.
markings
• Third ECG used to determine whether : right, left, or biventricular hypertrophy exists.
The character of the heart sounds AND presence & character of any murmurs further narrow the differential diagnosis.
The final diagnosis is then confirmed by : echocardiography / CT / MRI / cardiac catheterization.
ACYANOTIC CONGENITAL HEART LESIONS
• Acyanotic congenital heart lesions is classified according to the predominant physiologic load on the heart :
A. Lesions resulting in increase volume load : (the most common lesions)
right shunt lesions (commonest) Atrial septal defect (ASD) - Ventricular Septal
1- Left-to-right eptal Defect (VSD) - AV septal defects (AV canal) - Patent Ductus Arteriosus
2- Atrioventricular (AV) valve regurgitation
regurgitation.
• Although many congenital heart lesions induce more than one physiologic disturbance,
3- Cardiomyopathies.
it is helpful to focus on the primary load abnormality for purposes of classification.
B. Lesions resulting in increase pressure load : secondary to :
utflow obstruction (pulmonic or aortic valve stenosis) or
1- Outflow • Chest radiograph & Electrocardiogram are useful for differentiating between these classes.
arrowing of one of the great vessels (coarctation of the aorta).
2- Narrowing
LESIONS RESULTING IN INCREASED VOLUME LOAD LESIONS RESULTING IN INCREASED PRESSURE LOAD
1- Left-to-right
right shunt lesions
lesions: Outflow obstruction :
• circulation, which
The pathophysiologic feature is communication between the systemic & pulmonary sides of the circulation, • The most frequent are obstructions to ventricular outflow:
results in shunting of fully oxygenated blood back into the lungs. 1- Pulmonic
ulmonic stenosis,
- This shunt can be quantitated by : calculating the ratio of pulmonary to systemic blood flow (Qp : Qs) Thus, a 2:1 2- Aortic stenosis,
shunt implies twice the normal pulmonary blood flow.
3- Coarctation
oarctation of the aorta .
• The direction and magnitude of the shunt across such a communication depend on : • Less common are obstruction to ventricular inflow:
1- Size of the defect 22- Relative pulmonary & systemic pressure 3- Vascular resistance. 1- tricuspid or mitral stenosis and
• These factors are dynamic and may change dramatically with age: 2- cor triatriatum.
1- Intracardiac defects may grow smaller with time;
2- Pulmonary vascular resistance, which is high in the immediate newborn period, decreases to normal adult • Ventricular outflow obstruction can occur :
levels by several weeks of life; - At the valve,
3- Chronic exposure of the pulmonary circulation to high pressure & blood flow results in gradual increase in - below the valve
pulmonary vascular resistance pulmonary hypertension Eisenmenger syndrome (reversed shunt ). chambered right ventricle
1- double-chambered
Thus, a lesion such as a large VSD may be associated with little shunting and few symptoms during the initial weeks of life 2- subaortic membrane
When pulmonary vascular resistance declin
declines in the next several weeks, the volume of the left-to-right
left right shunt increases, and - Above the valve :
symptoms begin to appear. 1- branch pulmonary stenosis
• Increased volume of blood in the lungs , causes : 2- supravalvular aortic stenosis
1- pulmonary compliance and Obstruction is compensated by :
2- work of breathing. 1- Cardiac wall thickness (hypertrophy),
(
3- Fluid leaks into the interstitial space and alveoli and causes pulmonary edema.
edema 2- Dilatation in later stages.
The infant acquires the symptoms we refer to as heart failure, such as:
1-- Tachypnea 2- Chest retrac9ons 3- Nasal flaring 4-4 wheezing. • If obstruction is mild :
- Cardiac
ardiac output will be maintained and the clinical symptoms of HF will be either
otal left ventricular output is actually several times greater than normal, although much of this output is
- Total subtle or absent .
ineffective because it returns directly to the lungs.
evel of left ventricular output :
- To maintain this high level • If obstruction is Severe :
1- Heart rate are increased mediated by an increase in sympathetic nervous system activity. - It is usually encountered in the immediate newborn period The infant may
2- Stroke volume become critically ill within several hours of birth.
- The increase in circulating catecholamines COMBINED WITH the increased work of breathing, results in 1- Severe pulmonic stenosis (critical pulmonic stenosis) in the newborn
levation in total body oxygen consumption, beyond the oxygen transport ability of the circulation Such oxygen
elevation period results in :
consumption leads to 1-- Swea9ng 2- Irritability 3- Failure
ailure to thrive.
• Signs of right-sided
sided heart failure (hepatomegaly,
(hepatomegaly, peripheral edema),
- Remodeling of the heart occurs, with predominantly : • Cyanosis
yanosis from right-to-left
right left shunting across foramen ovale.
1- Dilatation &
esser degree of hypertrophy.
2- Lesser • In older children, severe pulmonic stenosis leads to symptoms of
right-sided
sided heart failure, but not to cyanosis unless a pathway persists
- If left untreated pulmonary vascular resistance eventually begins to rise by several years of age, the shunt for right-to-left
left shunting(e.g.,patency of the foramen ovale)
volume will decrease and eventually reverse from right to left (Eisenmenger syndrome) cyanosis.
2- Atrioventricular (AV) valve regurgitation 2- Severe aortic stenosis (critical aortic stenosis) in the newborn period is
• ugh the AV valves is most commonly encountered in patients with partial or complete AV septal
Regurgitation through characterized by:
defects (atrioseptal defects, AV canal). • Signs of left-sided
sided heart failure (pulmonary edema, poor perfusion)
- Combination of a left-to--right shunt WITH AV valve regurgitation increases the volume load on the heart and • right-sided
sided failure (hepatomegaly, peripheral edema),
leads to more severe symptoms. • may progress rapidly to total circulatory collapse.
• Isolated regurgitation through the tricuspid valve is seen in "Ebstein anomaly .
Ebstein anomaly"
• Regurgitation involving one of the semilunar valves is usually also associated
associate with some degree of stenosis. 3- Coarctation of the aorta :
• In
n older children and adolescents is usually manifested as:
as
• Aortic regurgitation may bee encountered in patients with :
- upper body hypertension and
irectly under the aortic valve (supracristal VSD) and
1- VSD directly
- diminished pulses in the lower extremities.
embranous subaortic stenosis.
2- Membranous
• In the immediate newborn period :
3- Cardiomyopathies. - Occurrence
ccurrence of coarctation may be delayed because of the
• The major causes of cardiomyopathy in infants and children include : presence of a patent ductus arteriosus.
1-- Viral myocardi9s 2- Metabolic disorders 3-
3 Genetic defects - In these patients, the open aortic end of the ductus may
• Heart muscle function is decreased in the cardiomyopathies (In contrast to left-to-right
left right shunts, in which intrinsic cardiac serve as a conduit for blood flow to partially
artially bypass the
muscle function is generally either normal or increased) obstruction These infants then become symptomatic,
• Cardiomyopathies may affect 1- systolic contractility or 2- diastolic relaxation
re or both. often dramatically, when the ductus finally closes.

• Decreased cardiac function results in increased atrial & ventricular filling pressure pulmonary edema occurs
secondary to increased capillary pressure.
CYANOTIC CONGENITAL HEART LESIONS
CYANOTIC LESIONS WITH DECREASED PULMONARY BLOOD FLOW CYANOTIC LESIONS WITH INCREASED PULMONARY BLOOD FLOW.
• These lesions must include both : • These lesions is not associated with obstr
obstruction
uction to pulmonary blood flow, Cyanosis is caused by either:
either
bstruction to pulmonary blood flow , at :
1- Obstruction 1- Abnormal
bnormal ventricular
ventricular-arterial
arterial connections :
- Tricuspid valve a- Transposition of the great vesselss (most common):
ight ventricular level
- Right - Aorta arises from the RV AND Pulmonary
P artery arises from the LV
ulmonary valve level
- Pulmonary
athway by which systemic venous blood can shunt from right to left & enter systemic circulation, via
2- Pathway
- Systemic venous blood returning to the right atrium is pumped directly back to the body,
and oxygenated blood returning from the lungs to left atrium is pumped back into lungs.
1- patent foramen ovale,
2- ASD , VSD - The persistence of fetal pathways (foramen ovale and ductus arteriosus) allows for a
small degree of mixing in the immediate newborn period; when the ductus begins to
• Common lesions in this group include
include: close, these infants become extremely cyanotic.
1- Tetralogy of Fallot
ricuspid atresia,
2- Tricuspid 2- Total
otal mixing of systemic venous and pulmonary venous blood within the heart , include:
arious forms of single ventricle with pulmo
3- Various pulmonary
nary stenosis . a- Cardiac
ardiac defects with a common atrium or ventricle,
In these lesions, the degree of cyanosis depends on the degree of obstruction to pulmonary blood b- Total anomalous
malous pulmonary venous return
flow. If the obstruction is mild, cyanosis may be absent at rest. c- Truncus arteriosus
- Deoxygenated
eoxygenated systemic venous blood and oxygenated pulmonary venous blood mix
These patients may have hypercyanotic (“tet”) spells during conditions of stress.
completely in the heart so,, oxygen saturation is equal in the pulmonary artery and aorta.
tion is se
In contrast, if the obstruction severe, pulmonary blood flow may be dependent
depe on patency of the - If pulmonary blood flow is nott obstruc
obstructed, these infants have a combination
ation of ccyanosis & HF.
ductus arteriosus When n the du
ductus closes in the 1st few days of life, the neonate experiences - In contrast, if pulmonary stenosis
osis is pr
present, these infants have cyanosiss alone, similar
s to
profound hypoxemia and shock . patients with the tetralogy of Fallot
DISORDERS OF HEART RATE, RHYTHM AND CONDUCTION ( Source: Davidson )
Introduction 3 main mechanisms of tachycardia:
- The heart beat is normally initiated by an electrical discharge from the sinoatrial (sinus) node. 1- Increased automaticity.
- The atria and ventricles then depolarise sequentially as electrical depolarisation passes through specialised conducting tissues. The tachycardia is produced by repeated spontaneous depolarisation of an ectopic
- The sinus node acts as a pacemaker and its intrinsic rate is regulated by the autonomic nervous system; focus, often in response to catecholamines
a- vagal activity slows the heart rate,
b- sympathetic activity accelerates it via cardiac sympathetic nerves and circulating catecholamines.
2- Re-entry.
- The tachycardia is initiated by an ectopic beat and sustained by a re-entry circuit.
- If the sinus rate becomes unduly slow, a lower centre may assume the role of pacemaker. This is known as an escape rhythm and may arise in: - Most tachyarrhythmias are due to re-entry.
a- the AV node or His bundle (junctional rhythm) or
b- the ventricles (idioventricular rhythm). 3- Triggered activity.
- This can cause ventricular arrhythmias in patients with coronary heart disease.
A cardiac arrhythmia is a disturbance of the electrical rhythm of the heart. Arrhythmias are :
- It is a form of secondary depolarisation arising from an incompletely repolarised cell
1- often a manifestation of structural heart disease
membrane.
2- or because of abnormal conduction or
3- because of abnormal depolarisation in an otherwise healthy heart. Bradycardia :
1- Reduced automaticity, e.g. sinus bradycardia.
A heart rate > 100/min is called a tachycardia and a heart rate < 60/min is called a bradycardia. 2- Blocked or abnormally slow conduction, e.g. AV block.
Sinus rhythms
Sinus arrhythmia Sinus bradycardia Sinus tachycardia
Phasic alteration of the heart rate during respiration, sinus rate : This is defined a sinus rate < 60/min may occur in healthy people at This is defined as a sinus rate > 100/min,
- increases during inspiration rest
- slows during expiration  Physiological : common finding in athletes.  Physiological :
 pathological causes: increase sympathetic activity associated with exercise,emotion, pregnancy
Normally : - MI - Sinus node disease (sick sinus syndrome) – Hypothermia
It is a consequence of normal parasympathetic nervous system N.B. Young adults can produce a rapid sinus rate, up to 200/min, during
- Hypothyroidism - Cholestatic jaundice - Raised intracranial intense exercise.
activity & can be pronounced in children. pressure - Drugs, e.g. β-blockers, digoxin, verapamil
Abnormally :  Treatment :  pathological causes:
Absence of this normal variation in heart rate with breathing or with 1- No treatment : Asymptomatic sinus bradycardia requires no treatment. -- Anxiety – fever – anemia – heart failure – Thyrotoxicosis
changes in posture may be a feature of autonomic neuropathy. 2- Drugs : Symptomatic acute sinus bradycardia usually responds to - Phaeochromocytoma - Drugs, e.g. β-agonists (bronchodilators).
intravenous atropine 0.6-1.2 mg.
3- Surgery : Patients with recurrent or persistent symptomatic sinus
bradycardia should be considered for pacemaker implantation.
Atrial tachyarrhythmias
Atrial fibrillation Atrial flutter
Incidence :  Paroxysmal atrial fibrillation  - Atrial flutter is characterised by a large (macro) re-entry circuit, usually within
- Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, - Occasional attacks that are well tolerated do not necessarily require treatment. the RA encircling the tricuspid annulus.
- Overall prevalence of 0.5% in the adult population of the UK. - Beta-blockers: - The atrial rate is approximately 300/min :
- Prevalence rises with age, affecting 2-5% and 8% of those aged over 70 and 80 years respectively. 1- Used as first-line therapy if symptoms are troublesome, 1- Usually associated with 2:1, 3:1 or 4:1 2nd degree AV block (with
Atrial fibrillation is a complex arrhythmia characterised by both : 2- Useful for treating patients with AF associated with ischaemic heart disease, corresponding heart rates of 150, 100 or 75/min).
hypertension and cardiac failure.
3- Abnormal automatic firing: 2- Rarely, in young patients, every beat is conducted, producing:
Beta-blockers reduce the ectopic firing that normally initiates AF.
Episodes of atrial fibrillation are usually initiated by rapid bursts of ectopic a- a heart rate of 300/min
beats arising from : - Class Ic drugs (see Box later), such as propafenone or flecainide, are : b- and potentially haemodynamic compromise.
o Effective at preventing episodes but
- conducting tissue in the pulmonary veins o Should not be given to patients with coronary disease or left ventricular dysfunction. - Atrial flutter should always be suspected when there is a narrow complex
- or diseased atrial tissue. tachycardia of 150/min.
Flecainide is usually prescribed along with a rate limiting β-blocker because it occasionally
4- Presence of multiple interacting re-entry circuits looping around atria : precipitates atrial flutter.
- AF becomes sustained because of : - Amiodarone :
 is the most effective agent for preventing AF
1- initiation of re-entrant conduction within the atria
 but its side-effects restrict its use to patients in whom other measures fail.
2- or sometimes because of continuous ectopic firing .
- Digoxin & Verapamil :
- Re-entry is more likely to occur in :  Not effective drugs for preventing paroxysms of AF,
 although they serve to limit the heart rate when AF occurs by blocking the AV node.
1- atria that are enlarged (prolonged pathway),
2- many forms of heart disease(in which conduction - Catheter ablation :
 Used If β-blockers or class Ic drugs are ineffective or cause side-effects
is slow). (1) Ectopic beats, often arising from
 Used to isolate electrically the pulmonary veins from the LA, preventing ectopic
the pulmonary veins, trigger atrial
 During episodes of AF, the atria beat rapidly but in (1) Ectopic beats, often arising from
fibrillation. triggering of AF.
the pulmonary
(2) veins,the
Re-entry within trigger atrial
atria maintains  Sometimes Used to create lines of conduction block within atria to prevent re-entry.
an uncoordinated and ineffective manner. fibrillation.
atrial fibrillation, with multiple  Ablation prevents AF in approximately 70% of patients with prior drug-resistant
(2) Re-entry
interacting within circuits
re-entry the atriaoperating
maintains
 The ventricles are activated irregularly at a rate atrial fibrillation, with multiple episodes, although drugs may subsequently be needed to maintain sinus rhythm.
simultaneously.
determined by conduction through the AV node interacting re-entry circuits operating  Ablation for AF is an evolving treatment which is associated with a small risk of (atrial flutter with 3:1 AV block; flutter waves are only visible in leads II and III.)
simultaneously. embolic stroke or cardiac tamponade.
 This produces the characteristic 'irregularly irregular' pulse.  Specialised 'AF suppression' pacemakers have been developed which pace the - The ECG shows saw-toothed flutter waves.
atria to prevent paroxysms (but this has not proved to be as effective as was initially hoped) - When there is regular 2:1 AV block, it may be difficult to identify flutter waves
 Persistent and permanent atrial fibrillation which are buried in the QRS complexes and T waves.
-There are two options for treating persistent AF: - Carotid sinus pressure or intravenous adenosine :
A) Rhythm control: attempting to restore & maintain sinus rhythm may help to establish the diagnosis by temporarily increasing the degree of AV
B) Rate control: using treatments to : control the ventricular rate & prevention of embolism. block and revealing the flutter waves.
A) Rhythm control
- Attempt to restore and maintain sinus rhythm is particularly appropriate if:
- Two examples of atrial fibrillation. The QRS complexes are irregular and there are no P waves. a- the arrhythmia has precipitated troublesome symptoms
A) There is usually a fast ventricular rate, e.g. between 120 and 160/min, at the onset of atrial fibrillation. b- and there is a modifiable or treatable underlying cause.
B) In chronic AF, the ventricular rate may be much slower due to the effects of medication and AV nodal fatigue. - Attempts to restore and maintain sinus rhythm are most successful if :
a- AF has been present for < 3 months, b- the patient is young
- The ECG (Fig.) shows : c- there is no important structural heart disease.
1- normal but irregular QRS complexes; Electrical cardioversion : Management
2- there are no P waves but the baseline may show irregular fibrillation waves. - It is successful in three-quarters of patients but relapse is frequent (25-50% at 1 month A) Control the ventricular rate :
AF can be classified as: & 70-90% at 1 year). Digoxin, β-blockers or verapamil can be used
1- Paroxysmal (intermittent, self-terminating episodes), - Immediate DC cardioversion after the administration of intravenous heparin is B) Preferable to Restore sinus rhythm by :
appropriate if AF has been present for < 48 hours.
2- Persistent (prolonged episodes that can be terminated by electrical or 1- direct current (DC) cardioversion .
chemical cardioversion) - In other situations, DC cardioversion should be deferred until the patient has been
established on warfarin, with an international normalised ratio (INR) > 2.0 for a minimum 2- or using intravenous amiodarone.
3- Permanent. of 4 weeks, and any underlying problems, such as hypertension, have been eliminated. C) Prevent recurrent episodes of atrial flutter :
- Patients seen for the first time, it can be difficult to identify which of these is present. Alternative to electrical cardioversion ( Flecainide ) : Beta-blockers or amiodarone can also be used
- Unfortunately for many patients, paroxysmal AF will become permanent as the underlying disease - Infusing intravenous flecainide (2 mg/kg over 30 minutes, maximum dose 150 mg) is a D) Patients with persistent, troublesome symptoms.
process that predisposes to AF progresses. safe alternative if  there is no underlying structural heart disease. Catheter ablation offers a 90% chance of complete cure
Electrical remodeling : Anticoagulants : ( the treatment of choice for those patients )
Electrophysiological changes occur in the atria within a few hours of the onset of AF that tend
- Anticoagulation should be maintained for at least 3 months following successful
to maintain fibrillation
cardioversion; if relapse occurs, a second (or third) cardioversion may be appropriate.  Flecainide :
Structural remodelling - Although flecainide can also be used for acute treatment or prophylaxis, it
When AF persists for a period of months, structural remodelling occurs with atrial fibrosis and Concomitant therapy :
should be avoided because there is a risk of slowing the flutter circuit and
dilatation that further predispose to AF. - Concomitant therapy with amiodarone or β-blockers may reduce the risk of recurrence.
facilitating 1:1 AV nodal conduction  This can cause a paradoxical
Thus early treatment of AF will prevent this and reinitiation of the arrhythmia. Catheter ablation :
tachycardia and haemodynamic compromise.
Common causes of atrial fibrillation : AF may be the first manifestation of many - Catheter ablation is sometimes used to help restore and maintain sinus rhythm in resistant
- If used, it should always be prescribed along with an AV node-blocking drug,
- Coronary artery disease (including acute MI) forms of heart disease (), cases, but it is a less effective treatment for persistent AF than for paroxysmal AF.
such as a β-blocker.
- Valvular heart disease, especially particularly those that are associated with B) Rate control
rheusssmatic mitral valve disease enlargement or dilatation of the atria. - If sinus rhythm cannot be restored (accepting that AF will be permanent) , treatment should Premature atrial contraction
- Hypertension be directed at maintaining an appropriate heart rate.
Common causes : ( Atrial ectopic beats, extrasystoles, premature beats )
- Sinoatrial disease - Alcohol excess, hyperthyroidism and A) control the ventricular rate :
- Hyperthyroidism chronic lung disease, - Digoxin, - will reduce the ventricular rate by:
increasing the degree of AV block.
- Alcohol - multiple aetiological factors often coexist - β-blockers -
- Combination therapy (e.g. digoxin + atenolol) is advisable.
- Cardiomyopathy such as the combination of alcohol, - rate-limiting calcium antagonist
- Congenital heart disease hypertension and coronary disease. N.B. This alone may produce a striking improvement in overall cardiac function, particularly in patients with MS .

- Chest infection - About 50% of all patients with paroxysmal  During exercise  Beta-blockers and rate-limiting calcium antagonists are often - Premature, normal QRS complex
- Pulmonary embolism 20% of patients with persistent or more effective than digoxin at controlling the heart rate during exercise - The P wave of this beat occurred too soon in the heart cycle;
- Pericardial disease permanent AF have structurally normal  And may have additional benefits in patients with hypertension or structural heart disease. - The P-R interval is shortened, indicating that the ectopic origin of the beat is
hearts; this is known as 'lone atrial in the atria near the A-V node.
- Idiopathic (lone AF) - Pace and ablate strategy : In poorly controlled and symptomatic AF (exceptional cases)
fibrillation'. - The interval between the premature contraction and the next succeeding
They can be treated by deliberately inducing complete AV nodal block with catheter contraction is slightly prolonged, which is called a compensatory pause.
Clinical Features ablation; a permanent pacemaker must be implanted beforehand.
AF is often completely asymptomatic, in which case it is usually discovered as a result
- Usually cause no symptoms
of a routine examination or ECG. B) Prevention of thromboembolism ( Anti-Coagulation ) :
- but can give the sensation of a missed beat or an abnormally strong beat.
- AF can cause palpitation, breathlessness and fatigue. - Loss of atrial contraction & left atrial dilatation cause  stasis of blood in the LA and
- In patients with poor ventricular function or valve disease it may precipitate or may lead to thrombus formation in the left atrial appendage. - In most cases these are of no consequence,
aggravate cardiac failure because of loss of atrial function and heart rate - This predisposes patients to stroke & other forms of systemic embolism. - very frequent atrial ectopic beats may predisposes to atrial fibrillation.
control. - The annual risk of these events in patients with persistent AF is approximately 5% but it is
influenced by many factors (Box 1) and may range from less than 1% to 12% (Box 2) - Treatment is rarely necessary.
- A fall in BP may cause lightheadedness, - β-blockers can be used if symptoms are intrusive.
- chest pain may occur with underlying coronary disease. - Treatment with warfarin (target INR 2.0-3.0) reduces the risk of stroke by about two-
thirds, at the cost of an annual risk of bleeding of approximately 1-1.5%, Atrial tachycardia
Prognosis: AF is associated with significant morbidity and a twofold increase in Indications of warfarin :
Atrial tachycardia may be a manifestation of :
mortality that are largely attributable to the effects of the underlying heart disease and  Warfarin is indicated in patients at high or very high risk of stroke
1- increased atrial automaticity,
the risk of cerebral embolism  For patients with intermittent AF, the risk of stroke is proportionate to the frequency & duration
of AF episodes Those with frequent, prolonged (> 24 hours) episodes of AF should be 2- sinoatrial disease
Management considered for warfarin anticoagulation. 3- digoxin toxicity.
1) Assessment of patients: Relative contraindications :
- With newly diagnosed AF, assessment includes: a full history, physical  Warfarin is indicated in patients at high or very high risk of stroke, unless anticoagulation poses
- It produces a narrow complex tachycardia with abnormal P
examination, 12-lead ECG, echocardiogram & thyroid function tests . unacceptable risks. wave morphology .
Biochemical evidence of hyperthyroidism is found in a small minority of patients with  Comorbid conditions that may be complicated by bleeding, such as peptic ulcer, uncontrolled - Sometimes associated with AV block if the atrial rate is rapid.
hypertension, alcohol misuse, frequent falls, poor drug compliance and potential drug interactions.
otherwise unexplained AF - Reduce automaticity :
- Treatment with aspirin reduces the risk of stroke by only one-fifth.
- Additional investigations such as exercise testing may be needed to determine  Respond to β-blockers which reduce automaticity,
Indications: Young patients (under 65 years) with no evidence of structural heart disease have a very
the nature and extent of any underlying heart disease. low risk of stroke; they do not require warfarin but may benefit from aspirin  or class I or III anti-arrhythmic drugs .
- Warfarin reduces the risk of ischaemic stroke in non-rheumatic atrial fibrillation by about 62% (absolute risk reduction 2.7% for - Rapid atrial tachycardias :
2) Treatment : primary prevention and 8.4% for secondary prevention), The ventricular response in rapid atrial tachycardias may be controlled by
- When AF complicates an acute illness (e.g. chest infection, pulmonary embolism), - Aspirin reduces the risk by only 22% (absolute risk reduction 1.5% for primary prevention and 2.5% for secondary prevention). AV node-blocking drugs.
effective treatment of the primary disorder will often restore sinus rhythm. - NNTB for 1 year (warfarin vs placebo) = 18.' - Recurrent atrial tachycardia :
- Otherwise, the main objectives are : to restore sinus rhythm as soon as possible,  Patients at moderate risk of stroke may be treated with warfarin or aspirin after  Catheter ablation, can be used to target the ectopic site
prevent recurrent episodes of AF, optimise the heart rate during periods of AF, discussing the balance of risk and benefit with the individual.  Should be offered as an alternative to anti-arrhythmic drugs in patients with
minimise the risk of thromboembolism and treat any underlying disease. - Assessment of the risk of embolism: helps to define possible benefits of antithrombotic therapy (see Box 3). recurrent atrial tachycardia.
- Echocardiography is valuable in risk stratification.
 Paroxysmal Supraventricular tachycardias
- The term 'supraventricular tachycardia' (SVT) is commonly used to describe a range of regular tachycardias that have a similar appearance on an ECG.
- These are usually associated with a narrow QRS complex and are characterised by a re-entry circuit or automatic focus involving the atria.
- The term SVT is misleading, as in many cases the ventricles also form part of the re-entry circuit, such as in patients with AV re-entrant tachycardia .
Atrioventricular nodal re-entrant tachycardia (AVNRT) Wolff-Parkinson-White syndrome & atrioventricular re-entrant tachycardia
This is due to re-entry in a circuit involving the AV node and its two right atrial input In these conditions, an abnormal band of conducting tissue connects the atria and ventricles.
pathways: a superior 'fast' pathway and an inferior 'slow' pathway (see Fig. ). A It resembles Purkinje tissue in that it conducts very rapidly, and is known as an accessory pathway.
The mechanism of AVNRT occurs via two right atrial AV nodal input pathways: - In 50% of cases, this pathway only conducts in the retrograde direction (from ventricles to atria) and thus does
the slow (S) and fast (F) pathways. Antegrade conduction occurs via the slow not alter the appearance of the ECG in sinus rhythm. This is known as a concealed accessory pathway.
pathway; the wavefront enters the AV node and passes into the ventricles, at B) Manifest accessory pathway
the same time re-entering the atria via the fast pathway. - Conduction occurs partly through the AV node and partly through the accessory pathway. Premature activation of
ventricular tissue via the pathway produces (B) :
- This produces a regular tachycardia with a rate of 120-240/min.
1- a short PR interval &
- It tends to occur in hearts that are otherwise normal and episodes may last from a
2- a 'slurring' of the QRS complex, called a delta wave. This is known as a manifest accessory pathway.
few seconds to many hours.
C) Wolff-Parkinson-White syndrome.
Clinical Features: - As the AV node & accessory pathway have different conduction speeds & refractory periods, a re-entry circuit
- Usually: fast heart beat & may feel: faint or breathless. can develop, causing tachycardia. when this is associated with symptoms, this is know as  Wolff-Parkinson-
- Release of atrial natriuretic peptide  polyuria, White syndrome
- If there is coexisting structural heart disease  cardiac pain or heart failure - The ECG appearance of this tachycardia may be indistinguishable from that of AVNRT (A), Carotid sinus pressure
may occur. or intravenous adenosine can terminate the tachycardia.
ECG : D) pre-excited atrial fibrillation .
The ECG (Fig. 18.44) usually shows a: - If atrial fibrillation occurs, it may produce a dangerously rapid ventricular rate because the accessory pathway lacks
- tachycardia with normal narrow QRS complexes the rate-limiting properties of the AV node This is known as pre-excited atrial fibrillation .
- but there may be rate-dependent bundle branch block. - It should be treated as an emergency, usually with DC cardioversion.
- Catheter ablation is first-line treatment in symptomatic patients and is nearly always curative.
Management : - Prophylactic anti-arrhythmic drugs, such as flecainide, propafenone or amiodarone, can also be used.
- Treatment is not always necessary. - These slow the conduction rate and prolong the refractory period of the accessory pathway.
- Episode may be terminated by: a- carotid sinus pressure or - Digoxin and verapamil shorten the refractory period of the accessory pathway and should be avoided.
b- other measures that increase vagal tone (e.g. Valsalva man[oelig ]uvre).
- Restore sinus rhythm: by - Adenosine, β-blockers , (Ca) Verapamil , flecainide.
- DC cardioversion, severe haemodynamic compromise

- Prevention recurrence (prophylaxis) β-blocker , Amiodarone .

- Catheter ablation offers a high chance of complete cure.

B) C) D)
Sinus rhythm. Orthodromic tachycardia. Atrial fibrillation.

The main uses, dosages and side-effects of the most widely used anti-arrhythmic drugs
Drug Main uses Route Dose (adult) Important side-effects
Class I
Disopyramide Prevention and treatment of atrial and I.v. 2 mg/kg at 30 mg/min, then 0.4 mg/kg/hr (max 800 mg/day) Myocardial depression, hypotension, dry
ventricular tachyarrhythmias mouth, urinary retention
Oral 300-800 mg daily in divided dosage
Lidocaine Treatment and short-term prevention of I.v. Bolus 50-100 mg, 4 mg/min for 30 mins, then 2 mg/min for 2 Myocardial depression, confusion, convulsions
VT and VF hrs, then 1 mg/min for 24 hrs
Prevention and treatment of ventricular I.v. Loading dose: 100-250 mg at 25 mg/min, then 250 mg in 1 hr, Myocardial depression, GI irritation, confusion,
Mexiletine tachyarrhythmias then 250 mg in 2 hrs dizziness, tremor, nystagmus, ataxia
Maintenance therapy: 0.5 mg/min
Oral 200-250 mg 8-hourly
Flecainide Prevention and treatment of atrial and I.v. 2 mg/kg over 10 mins, then 1.5 mg/kg/hr for 1 hr, then 0.1 Myocardial depression, dizziness
ventricular tachyarrhythmias mg/kg/hr
Oral 50-100 mg 12-hourly
Propafenone Prevention and treatment of atrial and Oral 150 mg 8-hourly for 1 wk, then 300 mg 12-hourly Myocardial depression, dizziness
ventricular tachyarrhythmias

Class II
Atenolol Treatment and prevention of SVT and I.v. 2.5 mg at 1 mg/min repeated at 5-min intervals (max 10 mg)
AF Oral 25-100 mg daily Myocardial depression, bradycardia,
Bisoprolol Prevention of VEs and exercise- Oral 2.5-10 mg daily bronchospasm, fatigue, depression,
Metoprolol induced VT I.v. 5 mg over 2 mins to a maximum of 15 mg nightmares, cold peripheries

Sotalol Oral 50-100 mg 8- or 12-hourly

I.v. 10-20 mg slowly Sotalol can cause torsades de pointes
Oral 40-160 mg 12-hourly
Class III
I.v. 5 mg/kg over 20-120 mins, then up to 15 mg/kg/24 hrs Photosensitivity, skin discoloration, corneal
deposits, thyroid dysfunction, alveolitis, nausea
Amiodarone Serious or resistant atrial and and vomiting, hepatotoxicity, peripheral
ventricular tachyarrhythmias neuropathy, torsades de pointes; potentiates
digoxin and warfarin
Oral Initially 600-1200 mg/day, then 100-400 mg daily
Class IV
Verapamil Treatment of SVT, control of AF I.v. 5-10 mg over 30 secs Myocardial depression, hypotension,
Oral 40-120 mg 8-hourly or 240 mg SR daily bradycardia, constipation

Other
Atropine Treatment of bradycardia and/or I.v. 0.6-3 mg Dry mouth, thirst, blurred vision, atrial and
hypotension due to vagal overactivity ventricular extrasystoles
Adenosine Treatment of SVT, aid to diagnosis in I.v. 3 mg over 2 secs, followed if necessary by 6 mg, then 12 mg Flushing, dyspnoea, chest pain Avoid in
unidentified tachycardia at intervals of 1-2 mins asthma
Treatment and prevention of SVT, rate I.v. Loading dose: 0.5-1 mg (total), 0.5 mg over 30 mins, then GI disturbance, xanthopsia, arrhythmias (see
Digoxin control of AF 0.25-0.5 mg 4- to 8-hourly to maximum total of 1 mg, Box 18.43)
assessing response before each additional dose
Oral 0.5 mg 6-hourly for 2 doses, then 0.125-0.25 mg daily
Treatment of Heart Failure
Management of chronic heart failure
New York Heart Association (NYHA)
Classification of heart failure
No limitation. Normal physical
Class I
exercise does not cause fatigue,
dyspnoea or palpitations
Mild limitation. Comfortable at rest
Class II but normal physical activity produces
fatigue, dyspnoea or palpitations
Marked limitation. Comfortable at rest
Class III but gentle physical activity produces
marked symptoms of heart failure
Symptoms of HF occur at rest AND
Class IV exacerbated by any physical activity

Diagnosis of heart failure (European

Society of Cardiology guidelines)
Essen al features (criteria 1 and 2)
1. Symptoms and signs of heart failure (e.g.
breathlessness, fatigue, ankle swelling)
2. Objective evidence of cardiac dysfunction (at
rest, e.g. echocardiogram)
Non-essential features Neurohumoral activation & sites of action of drugs used in TTT of HF
3. Response to treatment directed towards heart
failure(in cases where the diagnosis is in doubt)
Stages of heart failure and treatment options for systolic heart failure
General measures
Education Diet Obesity control Smoking Exercise Vaccination
 Explanation of :  Large meals is avoided .  For those with exacerbations of CHF  bed rest , reduces  Consider :
 Maintain desired BMI  Cessation
- Nature of disease  Weight reduction. the demands on the heart - influenza vaccination
- Treatment  Salt restriction.  Regular moderate aerobic exercise within limits of symptoms. - pneumococcal vaccination
- Self-help strategies  Severe HF fluid restriction.
Drug therapy
Diuretics Mechanism:
 Diuretics produce an increase in urinary sodium & water excretion, leading to reduction in blood & plasma volume.
Monitoring : - It reduces preload  improves pulmonary & systemic venous congestion.
1- Serum electrolytes * Although a fall in preload (ventricular filling pressure) tends to reduce cardiac output, the ‘Starling curve’ in heart failure is flat, so there may be a beneficial fall in filling pressure with little change in cardiac output!!
2- Renal function tests - It may also reduce afterload & ventricular volume  leading to a fall in ventricular wall tension & increased cardiac efficiency.
must be monitored regularly , for risk Regimens :
of : - Hypokalaemia 1- Loop diuretics (e.g. furosemide ) or Thiazide diuretics (e.g. bendroflumethiazide , hydrochlorothiazide) should be given in patients with fluid overload.
- Hypomagnesaemia  In some patients with severe chronic heart failure particularly if there is associated renal impairment,  oedema may persist, despite oral loop diuretic therapy :
a- Intravenous infusion of furosemide (5–10 mg/hr) may ini ate a diuresis.
They may cause hyperkalaemia, b- Combining a loop diure c with a thiazide diure c (e.g. bendroflumethiazide 5 mg daily)
particularly when used with an ACEIs. 2- Aldosterone antagonists (spironolactone and eplerenone) :
- Potassium-sparing diuretics  particular benefit in patients with : 1- Heart failure with severe left ventricular systolic dysfunction. 2- Improve outcome in heart failure following acute MI.
Angiotensin-converting Mechanism:
 Angiotensin-converting enzyme (ACE) inhibition therapy interrupts the vicious circle of neurohumoral activation  by preventing the conversion of angiotensin I to angiotensin II,  thereby
enzyme inhibitors (ACEI) 1- Preventing peripheral vasoconstriction 2- Activation of the sympathetic nervous system 3- Salt and water retention due to aldosterone release.
S.E.- Hypotension :  These drugs also prevent the undesirable activation of the renin–angiotensin system caused by diuretic therapy.
introduced gradually with low initial dose
with regular blood pressure monitoring Indications : (Davidson's note 18.16 page: 551: ACE inhibitors in chronic heart failure due to ventricular dysfunction reduce mortality & re-admission rates)
-Hyperkalaemia : 1- In moderate & severe heart failure : can produce a substantial improvement in effort tolerance & in mortality.
*Aldosterone should be discontinued . 2- Asymptomatic heart failure following myocardial infarction : improve outcome & prevent the onset of overt heart failure.
*offset loop diuretic hypokalaemia Contraindications : Monitoring therapy : Renal function & serum potassium
- Renal dysfunction : creatin. measured. 1- Renal artery stenosis 2- Pregnancy 3- Previous angioedema
Angiotensin II receptor Mechanism :
Act by blocking the action of angiotensin II on : Heart  inhibit the sympathetic activity , resulting in bradycardia.
antagonists (ARA) Peripheral vasculature  inhibit vasoconstriction , resulting in vasodilation.
 Same all side effects of ACE inhibitors. Kidney  prevent aldosterone release , resulting in decrease salt & water retention.
 Unlike ACEI : Indications :
- Don't affect bradykinin metabolism 1- Alternative to ACEI as a second-line therapy in patients intolerant of ACEI. ( Compared with ACE inhibitors, ARBs are better tolerated and have similar efficacy in reducing cardiovascular events ).
- Don't produce cough. 2- Both ACEI & ARA two can be combined in patients with resistant or recurrent heart failure.

Vasodilators Indications : When ACE inhibitor or ARB drugs are contraindicated (e.g. in severe renal failure) or intolerant.
Regimen : The combination of Nitrates  reduce preload AND Hydralazine  arterial dilators reduce afterload.
Mechanism :
 Counteract the deleterious effects of enhanced sympathetic stimulation AND reduces the risk of arrhythmias & sudden death.
Beta-blockers Regimen : (When initiated in standard doses, they may precipitate acute-on-chronic heart failure)
Bisoprolol  Given in small incremental doses (e.g. bisoprolol started at a dose of 1.25 mg daily, and increased gradually over a 12-week period to a target maintenance dose of 10 mg daily).
Effects :
1- Increase ejec on frac on 2- Improve symptoms 3- Reduce the frequency of hospitalisation 4- Reduce mortality in patients with chronic heart failure .
Indications :
Cardiac glycosides  Provide rate control in patients with heart failure & atrial fibrillation.
 Used as add-on therapy in symptomatic heart failure patients already receiving ACEI & beta-blockers
Digoxin  In patients with severe heart failure (NYHA class III–IV), digoxin reduces the likelihood of hospitalisation for heart failure, although it has no effect on long-term survival.
Inotropic & vasopressors Indications :
 IV inotropes & vasopressor agents  are used in patients with chronic heart failure who are not responding to oral medication. ( they have not been shown to improve long-term mortality).
Amiodarone Indications :
1- It has little negative inotropic effect  may valuable in patients with poor left ventricular function.
2- It is only effective in the treatment of symptomatic arrhythmias ( and should not be used as a preventative agent in asymptomatic patients).
Other medications Ivabradine Mechanism : inhibits the IF channels in the SA node resulting in reduction if heart rate.
Indications : best suited to patients who cannot take β-blockers or in whom the heart rate remains high despite β-blockade.
It reduces hospital admission & mortality rates in patients with heart failure due to moderate or severe left ventricular systolic impairment.
N.B. In patients with known ischaemic Indications :
heart disease antiplatelet therapy 1- In hospital: all patients require prophylactic anticoagulation (BECAUSE Heart failure is associated with a four-fold increase in the risk of a stroke).
(aspirin, clopidogrel) and statin Anticoagulants 2-Patients with atrial fibrillation
therapy should be continued 3-Patients with sinus rhythm with a history of thromboembolism, left ventricular thrombus or aneurysm.
Implantable Cardiac Defibrillators / and Cardiac Resynchronisation Therapy
1- Implantable cardiac defibrillator :
 Patients with symptomatic ventricular arrhythmias AND heart failure  Irrespective of their response to anti-arrhythmic drug therapy, all should be considered for implantation of a cardiac defibrillator because it improves survival.
2- Cardiac resynchronization therapy :
 In patients with marked intraventricular conduction delay,  prolonged depolarisation may lead to: uncoordinated L.V contraction. When this is associated with severe symptomatic heart failure, cardiac resynchronization
therapy should be considered : Here, both the LV and RV are paced simultaneously to generate a more coordinated left ventricular contraction and improve cardiac output. This is associated with improved symptoms & survival.
Coronary revascularisation
‘Hibernating’ myocardium can be defined as reversible left ventricular dysfunction due to chronic coronary artery disease that responds positively to inotropic stress and indicates the presence of viable heart muscle that may recover after
revascularization. It is due to reduced myocardial perfusion, which is just sufficient to maintain viability of the heart muscle. (‘hibernating’ myocardium can be identified by : stress echocardiography & specialized nuclear or MR imaging).
1- Coronary artery bypass surgery or May improve function in areas of the myocardium that are ‘hibernating’ because of inadequate blood supply, used to treat selected patients with HF & CHD.
2- Percutaneous coronary intervention
Heart transplantation 1-year survival over 90% / 5-year is 75%
Indications : treatment of choice for younger patients with : Intractable heart failure whose life expectancy is <6 months 1- Coronary artery disease & 2- Dilated cardiomyopathy are the most common indications
Ventricular assist devices
Because of the limited supply of donor organs, ventricular assist devices (VADs) have been employed as:
• a bridge to cardiac transplantation • potential long-term therapy • short-term restoration therapy following a potentially reversible insult, e.g. viral myocarditis.
- VADs assist cardiac output by using a roller, centrifugal or pulsatile pump that, in some cases, is implantable and portable.
- They withdraw blood through cannulae inserted in the atria or ventricular apex and pump it into the pulmonary artery or aorta.
- They are designed not only to unload the ventricles but also to provide support to the pulmonary and systemic circulations.
- Their more widespread application is limited by high complication rates (haemorrhage, systemic embolism, infection), although some improvements in survival .
Source: Davidson & Kumar.
 Management of acute heart failure ( acute pulmonary edema )
The goals of treatment in a patient with AHF include:
1- Immediate relief of symptoms and stabilization of haemodynamics (short-term benefits).
2- Reduction in length of hospital stay & hospital readmissions.
3- Reduction in mortality from heart failure.
A) Patients with haemodynamic compromise , may require :
 Arterial lines (invasive blood pressure monitoring and arterial gases),
 Central venous cannulation (intravenous medication, inotropic support, monitoring of central venous pressure)
 Pulmonary artery cannulation (calculation of cardiac output/index, peripheral vasoconstriction and pulmonary wedge pressure).
B) Initial therapy :
1- Sit the patient up to reduce pulmonary congestion.
2- Give  a- Oxygen / Non-invasive positive pressure ventilation (con nuous posi ve airways pressure (CPAP) of 5–10 mmHg).
b- Loop diuretic: furosemide (50–100 mg IV).
c- Vasodilator "Nitrates" : IV glyceryl trinitrate (10–200 μg/min )  until : 1- Clinical improvement occurs or 2- systolic BP falls to < 110 mmHg.
e- All pa ents require prophylac c an coagula on with low molecular weight heparin, e.g. enoxaparin 1 mg/kg s.c. ×2 daily.
C) In patients who don't respond to the initial therapy :  Inotropic support : Dobutamine / Phosphodiesterase inhibitors / levosimendan can be added.
If blood pressure is low, use : noradrenaline (norepinephrine).
D) With acute cardiogenic pulmonary oedema & shock  Intra-aortic balloon pump may be beneficial.
E) Monitoring: regular measurements of temperature, heart rate, blood pressure and cardiac monitoring.
 Mitral valve disease
Mitral stenosis Mitral regurgitation
Etiology & Pathophysiology Etiology & Pathophysiology
- The mitral valve orifice is normally about 5 cm 2 in diastole Mitral regurgitation may also follow mitral valvotomy or valvuloplasty.
- Patients usually remain asymptomatic until the stenosis is < 2 cm 2 ( 1 cm2 in severe stenosis)

- Etiology: - Causes of mitral regurgitation (Etiology) :

1- Mitral stenosis is almost always rheumatic in origin, 1- Rheumatic disease
2- Caused by heavy calcification of the mitral valve apparatus.(in older people) 2- Mitral valve prolapse (common cause)
3- Congenital mitral stenosis (rare) 3- Dilatation of the LV and mitral valve ring (e.g. coronary artery disease, cardiomyopathy):

- In rheumatic mitral stenosis : - Mitral valve function depends on the chordae tendineae and their papillary muscles;
dilatation of the LV distorts the geometry of these and may cause mitral regurgitation.
the mitral valve orifice is slowly diminished by:
- progressive fibrosis, - Dilated cardiomyopathy and heart failure from coronary artery disease are common causes
- calcification of the valve leaflets, of so-called 'functional' mitral regurgitation
- fusion of the cusps and subvalvular apparatus.
4- Damage to valve cusps and chordae (e.g. rheumatic heart disease, endocarditis),
The flow of blood from LA to LV is restricted and left atrial pressure rises, leading to: 5- Ischaemia or infarction of the papillary muscle.
- - pulmonary venous congestion & breathlessness & low cardiac output which 6- MI
- may cause fatigue. 7- Mitral regurgitation may also follow mitral valvotomy or valvuloplasty.
- - There is dilatation and hypertrophy of the LA,
- - and left ventricular filling becomes more dependent on left atrial contraction.
 Chronic mitral regurgitation causes  a- gradual dilatation of the LA with b- little increase in pressure  therefore relatively few symptoms.
 Progressive dilatation of the LA  causes atrial fibrillation which precipitates pulmonary oedema because: The LV dilates slowly and the a-left ventricular diastolic & b- left atrial pressures gradually increase as a result of chronic volume overload of LV.
1- the accompanying tachycardia lead to marked haemodynamic deterioration with a rapid rise in left atrial pressure.
2- loss of atrial contraction
 In contrast, Acute mitral regurgitation causes  a rapid rise in left atrial pressure (because left atrial compliance is normal) and marked symptoms .
Mitral valve prolapse ( known as 'floppy' mitral valve )
 A more gradual rise in left atrial pressure tends to cause an increase in pulmonary vascular resistance, which leads to  pulmonary hypertension - It is caused by:
that may protect the patient from pulmonary oedema,,, Pulmonary hypertension leads to: 1- congenital anomalies 2- degenerative myxomatous changes, 3- a feature of connective tissue disorders such as Marfan's syndrome.
1- Right ventricular hypertrophy & dilatation,
2- Tricuspid regurgitation - In its mildest forms, the valve remains competent but bulges back into the atrium during systole, causing a midsystolic click but no murmur.
3- Right heart failure.
- In the presence of a regurgitant valve, the click is followed by a late systolic murmur which lengthens as the regurgitation becomes more severe.
 Fewer than 20% of patients remain in sinus rhythm; many of these have a small fibrotic LA and severe pulmonary hypertension. A click is not always audible and the physical signs may vary with both posture and respiration.
N.B. - Progressive elongation of the chordae tendineae leads to  increasing mitral regurgitation, and if chordal rupture occurs, regurgitation suddenly
- Any increase in heart rate shortens diastole when the mitral valve is open  produces a further rise in left atrial pressure. becomes severe. ( This is rare before the fifth or sixth decade of life )
- Situations that demand an increase in cardiac output (exercise and pregnancy ) increases left atrial pressure  so, poorly tolerated.
Mitral valve prolapse is associated with : 1- a variety of typically benign arrhythmias, 2- atypical chest pain and 3- a very small risk of embolic stroke or TIA.
Symptoms Explanation of symptoms & signs
The overall long-term prognosis is good.
- Breathlessness (pulmonary congestion) - Effort-related dyspnea is common, exercise tolerance typically diminishes very slowly over many years  AND
Cough (pulmonary congestion) eventually symptoms occur at rest.
- Symptoms Explanation of symptoms & signs
- Chest pain (pulmonary hypertension) - Acute pulmonary oedema or pulmonary hypertension can lead to  haemoptysis.
- All patients, Particularly those with atrial fibrillation, are at risk from left atrial thrombosis and systemic - Dyspnoea (pulmonary venous congestion) Symptoms depend on how suddenly the regurgitation develops.
- Haemoptysis (pulmonary congestion, pulmonary embolism) thromboembolism. ( emboli caused one-quarter of all deaths.) - Fatigue (low cardiac output) - Chronic mitral regurgitation produces a symptom complex that is similar to that of mitral
- Fatigue (low cardiac output) - Palpitation (atrial fibrillation, increased stroke volume) stenosis but sudden-onset mitral regurgitation usually presents with acute pulmonary oedema.
- Oedema, ascites (right heart failure)  The physical signs of mitral stenosis are often found before symptoms develop : - Oedema, ascites (right heart failure)
- Palpitation (atrial fibrillation) The forces that open and close the mitral valve increase as left atrial pressure rises : - The regurgitant jet causes an apical systolic murmur (see Fig. 18.88) which radiates into the
- Thromboembolic complications (e.g. stroke, ischaemic limb) 1- The first heart sound (S1) is therefore loud and can be palpable (tapping apex beat). Signs axilla and may be accompanied by a thrill.
Signs 2- An opening snap may be audible and moves closer to the second sound (S2) as the stenosis becomes
Atrial fibrillation more severe & left atrial pressure rises.
 - Atrial fibrillation/flutter - Increased forward flow through the mitral valve causes:
3- However, the first heart sound and opening snap may be inaudible if the valve is heavily calcified.
 Mitral facies - Cardiomegaly: displaced hyperdynamic apex beat 1- a loud third heart sound
 Auscultation Turbulent flow produces: - Apical pansystolic murmur ± thrill 2-and even a short mid-diastolic murmur.
o Loud first heart sound, opening snap - the characteristic low-pitched mid-diastolic murmur & sometimes a thrill. - Soft S1, apical S3
- The apex beat feels active and rocking due to left ventricular volume overload and is usually
o Mid-diastolic murmur - The murmur is accentuated by: a- exercise & b-during atrial systole (pre-systolic accentuation). - Signs of pulmonary venous congestion (crepitations,
Crepitations, pulmonary oedema, effusions (raised - Early in the disease, a pre-systolic murmur may be the only auscultatory abnormality, but in patients displaced to the left as a result of left ventricular dilatation.
 pulmonary oedema, effusions)
pulmonary capillary pressure) with symptoms the murmur extends from the opening snap to the first heart sound.
- Coexisting mitral regurgitation causes a pansystolic murmur that radiates towards the axilla.
- Signs of pulmonary hypertension and right heart failure N.B. in ivestigations :
 RV heave, loud P2 (pulmonary hypertension) - Atrial fibrillation is common, as a consequence of atrial dilatation.
Pulmonary hypertension may ultimately lead to right ventricular hypertrophy & dilatation with secondary - At cardiac catheterisation, the severity of mitral regurgitation can be assessed by left ventriculography and
tricuspid regurgitation, which causes  a systolic murmur & giant 'v waves' in the venous pulse. by the size of the v (systolic) waves in the left atrial or pulmonary artery wedge pressure trace.
Investigations Investigations
ECG Chest X-ray Echo Doppler Cardiac catheterisation ECG Chest X-ray Echo Doppler Cardiac catheterisation
 P mitrale or atrial  Enlarged LA and  Thickened immobile  Pressure gradient  Coronary artery  Left atrial hypertrophy  Enlarged LA  Dilated LA, LV  Detects & quantifies  Dilated LA, dilated LV,
fibrillation appendage cusps across mitral valve disease (if not in AF)  Enlarged LV  Dynamic LV (unless regurgitation mitral regurgitation
 Right ventricular  Signs of pulmonary  Reduced valve area  Pulmonary artery  Mitral stenosis and  Left ventricular  Pulmonary venous myocardial dysfunction  Pulmonary
hypertrophy: tall R venous congestion  Reduced rate of pressure regurgitation hypertrophy congestion predominates) hypertension
waves in V1-V3 diastolic filling of LV  Left ventricular  Pulmonary artery  Pulmonary oedema  Structural abnormalities  Coexisting coronary
 Enlarged LA function pressure (if acute) of mitral valve (e.g. artery disease
prolapse)

Management Management
Patients with minor symptoms should be treated medically.  Mitral regurgitation of moderate severity can be treated medically : 1- Diuretics 2- Vasodilators, e.g. ACE inhibitors 3- Digoxin if atrial fibrillation is prese
Intervention by balloon valvuloplasty, mitral valvotomy or mitral valve replacement should be considered if the patient remains symptomatic despite medical treatment or if pulmonary hypertension develops. 4- Anticoagulants if atrial fibrillation is present
Medical management Mitral balloon valvuloplasty and valve replacement
 In all patients with mitral regurgitation, high afterload may worsen the degree of regurgitation and hypertension should be treated with vasodilators such as ACE inhibitors.
- -Valvuloplasty is the treatment of choice if specific criteria are fulfilled :
1- Significant symptoms, 2- Isolated mitral stenosis, 3- No (or trivial) mitral regurgitation
1- Anticoagulation to reduce the risk of systemic embolism, 4- Mobile, non-calcified valve/subvalve apparatus on echo, 5- LA free of thrombus  Indications for mitral valve replacement or repair : Patients should be reviewed at regular intervals because
1- worsening symptoms, 2- progressive cardiomegaly 3- echocardiographic evidence of deteriorating left ventricular function
2- Ventricular rate control (digoxin, β-blockers or rate-limiting calcium -
antagonists) in atrial fibrillation, - Surgical closed or open mitral valvotomy are acceptable alternatives. N.B. Mitral valve repair is used to treat mitral valve prolapse and offers many advantages when compared to mitral valve replacement, :
- 1- it is now advocated for severe regurgitation, even in asymptomatic patients.
3- Diuretic therapy to control pulmonary congestion.
- Valve replacement is indicated if there is substantial mitral reflux or if the valve is 2- results are excellent .
4- Antibiotic prophylaxis against infective endocarditis is no longer routinely 3-early repair prevents irreversible left ventricular damage.
rigid and calcified
recommended. -  Mitral regurgitation of coronary heart disease :
- Patients who have undergone mitral valvuloplasty or valvotomy should be followed up - Mitral regurgitation often accompanies the ventricular dilatation and dysfunction that are concomitants of coronary artery disease.
at 1-2-yearly intervals because restenosis may occur. - If such patients are to undergo coronary bypass graft surgery, it is common practice to repair the valve and restore mitral valve function by inserting an annuloplasty ring to
- overcome annular dilatation and to bring the valve leaflets closer together.
- Clinical symptoms & signs are a guide to the severity of mitral restenosis but Doppler
It can be difficult, however, to determine whether it is the ventricular dilatation or the mitral regurgitation that is the predominant problem.
echocardiography provides a more accurate assessment. If ventricular dilatation is the underlying cause of mitral regurgitation, mitral valve repair or replacement may actually worsen ventricular function, as the ventricle can no longer empty into the low-pressure LA.
 Aortic valve disease
Aortic stenosis Aortic regurgitation
Etiology & Pathophysiology Etiology & Pathophysiology
- Etiology depends on the age of the patient : -Etiology :
This condition is due to  A) disease of the aortic valve cusps or b) dilatation of the aortic root
Infants, children, adolescents Young adults to middle-aged Middle-aged to elderly
- Congenital aortic stenosis - Calcification and fibrosis of - Senile degenerative aortic stenosis. - Congenital :
- Congenital subvalvular aortic stenosis congenitally bicuspid aortic valve. - Calcification of bicuspid aortic valve. Bicuspid valve or disproportionate cusps
- Congenital supravalvular aortic stenosis - Rheumatic aortic stenosis. - Rheumatic aortic stenosis.
- Acquired :
- In congenital aortic stenosis, obstruction is present from birth or becomes apparent in infancy. 1- Rheumatic disease
- In congenitally bicuspid aortic valves, obstruction may take years to develop as the valve becomes 2- Infective endocarditis
fibrotic and calcified. 3- Trauma
- In normal tricuspid aortic valve (In older people), may be affected by fibrosis and calcification, in a 4- Aortic dilatation (Marfan's syndrome, aneurysm, dissection, syphilis,
process that is histologically similar to that of atherosclerosis affecting the arterial wall. ankylosing spondylitis).
- Haemodynamically significant stenosis develops slowly, typically occurring at:
* 30-60 years in those with rheumatic disease, - The LV dilates and hypertrophies to compensate for the regurgitation.
* 50-60 in those with bicuspid aortic valves - The stroke volume of the LV may eventually be doubled or trebled, and the major arteries are
* 70-90 in those with degenerative calcific disease. then conspicuously pulsatile.
- As the disease progresses, left ventricular diastolic pressure rises and breathlessness develops.
 The LV becomes increasingly hypertrophied (compensation)  resulting in :
1- increasing pressure gradient across the aortic valve so, cardiac output is initially maintained .
The fixed outflow obstruction limits the increase in cardiac output required on exercise. Symptoms Explanation of symptoms & signs
2- Coronary blood flow may then be inadequate resulting in developing angina, even in the Mild to moderate AR Severe AR - Until the onset of breathlessness, the only symptom may be an awareness of the heart beat, particularly when
absence of coronary disease. lying on the left side, which results from the increased stroke volume.
- Often asymptomatic - Breathlessness.
- Awareness of heart - Angina. - First symptom is sometimes Paroxysmal nocturnal dyspnoea, then peripheral oedema or angina may occur.
 Eventually, the LV can no longer overcome the outflow tract obstruction and pulmonary beat, 'palpitations'
oedema occurs. - Murmurs:
-The characteristic murmur is best heard to the left of the sternum during held expiration; a thrill is rare.
Signs - A systolic murmur due to the increased stroke volume is common and does not necessarily indicate stenosis.
N.B. In contrast to mitral stenosis, which tends to progress very slowly, patients with aortic stenosis : - Signs Pulses - The regurgitant jet causes fluttering of the mitral valve and, if severe, causes partial closure of the anterior mitral
1- Remain asymptomatic for many years. - Large-volume or 'collapsing' pulse leaflet leading to functional mitral stenosis and a soft mid-diastolic (Austin Flint) murmur.
2- Deteriorate rapidly when symptoms develop. - Low diastolic and increased pulse pressure
3- Death usually ensues within 3-5 years of these. - Bounding peripheral pulses Heart failure
Symptoms Explanation of symptoms & signs - Capillary pulsation in nail beds: Quincke's sign - In acute severe regurgitation (e.g. perforation of aortic cusp in endocarditis) there may be no time for
- Aortic stenosis is commonly picked up in asymptomatic patients at routine clinical examination. - Femoral bruit ('pistol shot'): Duroziez's sign compensatory left ventricular hypertrophy and dilatation to develop and the features of heart failure may
- Mild or moderate stenosis: usually asymptomatic - Head nodding with pulse: de Musset's sign
- The three cardinal symptoms are: angina, breathlessness and syncope. predominate.
- Exertional dyspnoea (breathlessness) - Murmurs: - In this situation, the classical signs of aortic regurgitation may be masked by :
- Angina Angina Exertional Breathlessness Exertional Syncope - Early diastolic murmur a- tachycardia &
- Exertional syncope Angina arises because of: Exertional breathlessness Syncope usually occurs on - Systolic murmur (increased stroke volume) b- brupt rise in left ventricular end-diastolic pressure; thus :
- Sudden death 1- the increased demands of the hypertrophied LV working suggests: - Austin Flint murmur (soft mid-diastolic) 1- the pulse pressure may be near normal
exertion when cardiac
against the high-pressure outflow tract obstruction, - Other signs:
- Episodes of acute pulmonary oedema. cardiac decompensation as output fails to rise to meet 2- the diastolic murmur may be short or even absent .
leading to a mismatch between oxygen demand & supply. - Displaced, heaving apex beat (volume overload)
a consequence of the demand, leading to a fall in
2- may also due to coexisting coronary artery disease, - Presystolic impulse
Signs excessive pressure overload BP.
especially in old age when it affects over 50% of patients. - Fourth heart sound
placed on the LV.
- Crepitations (pulmonary venous congestion).
- Ejection systolic murmur.
- Slow-rising carotid pulse. The characteristic clinical signs :
- Narrow pulse pressure. 1- Ejection systolic murmur radiates to the neck, Investigations
Thrusting apex beat (LV pressure overload). 2- Soft second heart sound, particularly in those with calcific valves.
- - Doppler  Regurgitation is detected by Doppler echocardiography.
3- The murmur is often likened to a saw cutting wood and may (especially in older patients) have a musical quality
- Signs of pulmonary venous congestion (e.g. In severe acute aortic regurgitation, the rapid rise in left ventricular diastolic pressure may cause premature mitral valve closure.
like the 'mew' of a seagull.
crepitations). - Cardiac catheterisation & aortography  can help in 1-assessing the severity of regurgitation 2-dilatation of the aorta 3-the presence of coexisting coronary artery disease.
N.B.
1- The severity of aortic stenosis may be difficult to gauge clinically, as older patients with a non-compliant 'stiff' arterial - MRI  is useful in assessing the degree and extent of aortic dilatation.
system may have an apparently normal carotid upstroke in the presence of severe aortic stenosis.
2- Milder degrees of stenosis may be difficult to distinguish from aortic sclerosis in which the valve is thickened
ECG Chest X-ray Echo Doppler Cardiac catheterization
(may not be required)
or calcified but not obstructed.
Initially normal, later left - Cardiac dilatation, - Dilated LV Regurgitation is detected by - Dilated LV
Investigations ventricular hypertrophy and T- - maybe aortic dilatation - Hyperdynamic LV Doppler - Aortic regurgitation
- ECG features of hypertrophy in advanced cases (check ECG in CVS books). Nevertheless, especially in old age, the ECG can be normal despite severe stenosis. wave inversion - Features of left heart failure. - Fluttering anterior mitral leaflet - Dilated aortic root
- Echocardigraphy demonstrates restricted valve opening - Doppler detects reflux
- Doppler assessment 1- permits calculation of the systolic gradient across the aortic valve, from which the severity of stenosis can be assessed.
2- Detection of associated aortic regurgitation Management
- In patients with an impaired left ventricle  velocities across the aortic valve may be diminished because of a reduced stroke volume, - Treatment may be required for underlying conditions such as endocarditis or syphilis.
- In patients with aortic regurgitation  velocities are increased because of an increased stroke volume. - Systolic BP should be controlled with vasodilating drugs such as nifedipine or ACE inhibitors.
- CT and MRI are useful in assessing the degree of valve calcification and stenosis respectively but are rarely necessary.
ECG Chest X-ray Echo Doppler Cardiac catheterisation Aymptomatic patients Symptomatic patients
- Left ventricular hypertrophy - May be normal; - Measurement of severity of - Mainly to identify associated
- Calcified valve with restricted
(usually) stenosis coronary artery disease A) Reporting : - Aortic valve replacement is indicated if :
- sometimes enlarged LV & opening,
- Left bundle branch block dilated ascending aorta on - Detection of associated - May be used to measure Those with chronic aortic regurgitation can remain asymptomatic for many 1- If evidence of increasing ventricular size or if the end-systolic dimension
- Hypertrophied LV
PA view, calcified valve on aortic regurgitation gradient between LV and years because compensatory ventricular dilatation and hypertrophy occur, increases to ≥ 55 mm,
lateral view aorta BUT should be advised to report the development of any symptoms of 2- aortic regurgitation causes symptoms, and this may need to be
breathlessness or angina. combined with :
Management a- aortic root replacement &
Patients with asymptomatic (Irrespective of the severity) aortic stenosis Patients with symptomatic severe aortic stenosis b- coronary bypass surgery.
conservative management surgery - Those patients should have prompt aortic valve replacement.
B) Following Up :
Those patients have a good Such patients should be kept under review, - Old age is not a contraindication to valve replacement and results are very good in They should also be followed up annually with echocardiography for evidence
immediate prognosis & conservative as the development of : experienced centres, even for those in their eighties (Box 18.110). of increasing ventricular size. - Aortic root replacement is indicated if :
management is appropriate. 1- angina, - Incidence: the most common form of valve disease affecting the very old.
- Symptoms: a common cause of syncope, angina and heart failure in the very old. Aortic root dilatation is the cause of aortic regurgitation (e.g. Marfan's
2- syncope, Aortic
3- symptoms of low cardiac output stenosis
- Signs: because of increasing stiffening in the central arteries, low pulse pressure and a slow rising pulse may not be present. C) Aortic valve replacement : syndrome)
- Surgery: can be successful in those aged 80 or more in the absence of comorbidity, but with a higher operative mortality. The prognosis
4- heart failure in old age without surgery is poor once symptoms have developed.
There is conflicting evidence regarding the need for aortic valve replacement
- Valve replacement type: a biological valve is often preferable to a mechanical, because this obviates the need for anticoagulation, and the in asymptomatic patients with severe aortic regurgitation.
has a poor prognosis and is an indication for durability of biological valves usually exceeds the patient's anticipated life expectancy.
prompt surgery. - Delay exposes the patient to the risk of sudden death or irreversible deterioration in ventricular function.
- Patients with moderate or severe stenosis are evaluated every 1-2 years with - Some patients with severe aortic stenosis deny symptoms, and if this could be due to a sedentary lifestyle, a
careful exercise test may reveal symptoms on modest exertion.
Doppler echocardiography to detect progression in severity;
- this is more rapid in older patients with heavily calcified valves. - Aortic balloon valvuloplasty  is useful in congenital aortic stenosis but is of no value in
older patients with calcific aortic stenosis.
- Anticoagulants  are only required in a- patients who have atrial fibrillation or
b- those who have had a valve replacement with a mechanical
prosthesis.
 Tricuspid valve disease
Tricuspid stenosis Tricuspid regurgitation
Etiology Etiology
Tricuspid regurgitation is common, &is most frequently 'functional' as a result of right ventricular dilatation
- Usually rheumatic in origin
Primary Secondry
- Occurs in fewer than 5% of patients with rheumatic heart disease. - Rheumatic heart disease. - Right ventricular dilatation due
Nearly always in association with mitral & aortic valve disease. to chronic left heart failure
- - Endocarditis, particularly in ('functional tricuspid regurgitation')
- seldom seen in developed countries. injection drug-users - Right ventricular infarction
- Ebstein's congenital anomaly - Pulmonary hypertension (e.g.
cor pulmonale)
Tricuspid stenosis and regurgitation are also features of the carcinoid syndrome
Clinical Features Clinical Features
Symptoms : Symptoms :
- Although the symptoms of mitral & aortic valve disease predominate, Symptoms are usually non-specific, with:
-Tricuspid stenosis may cause symptoms of right heart failure, 1- tiredness related to reduced forward flow,
including : 2- oedema
Hepatic discomfort, Peripheral oedema, presystolic pulsation 3- hepatic enlargement due to venous congestion.
(large a wave), ascites. Signs :
Signs : 1- 'giant' v wave in the jugular venous pulse (a cv wave replaces the
1- Raised JVP with a prominent a wave (main feature), normal x descent).
2- Slow y descent due to the loss of normal rapid right 2- Pansystolic murmur at the left sternal edge
ventricular filling. 3- Pulsatile Liver.
3- Mid-diastolic murmur: Investigations
- best heard at the lower left or right sternal edge. Echocardiography :
- generally higher-pitched than murmur of mitral stenosis - may reveal dilatation of the RV.

- increased by inspiration. - If the valve has been affected by rheumatic disease, the leaflets
will appear thickened, and in endocarditis vegetations may be
Investigations seen.
On Doppler echocardiography: - Ebstein's anomaly, is a congenital abnormality in which the tricuspid valve is
the valve has similar appearances to those of rheumatic mitral stenosis displaced towards the right ventricular apex, with consequent enlargement of the
RA. It is commonly associated with tricuspid regurgitation.
Management Management
A) Medical :
A) In patients who require surgery to other valves, Tricuspid regurgitation due to right ventricular dilatation often improves when
either 1- the tricuspid valve is replaced or the cause of right ventricular overload is corrected, with diuretic and
2- valvotomy is performed at the time of surgery. vasodilator treatment of congestive cardiac failure.
B) Surgery :
B) isolated tricuspid stenosis (rare): - Patients with a normal pulmonary artery pressure tolerate isolated
Balloon valvuloplasty can be used tricuspid reflux well, and valves damaged by endocarditis do not usually
need to be replaced.
- Patients undergoing mitral valve replacement who have tricuspid
regurgitation due to marked dilatation of the tricuspid annulus benefit from
repair of the valve with an annuloplasty ring to bring the leaflets closer
together.
- Patients with rheumatic damage may require tricuspid valve replacement.
Pulmonary valve disease
Pulmonary stenosis Pulmonary regurgitation
- Etiology : - Etiology :
- Congenital (usually), in which case it may be isolated or associated - Rare in isolation
with other abnormalities such as Fallot's tetralogy. - usually associated with pulmonary artery dilatation due to pulmonary
- Carcinoid syndrome hypertension.

- Signs The pulmonary hypertension may be secondary to :

1- Ejection systolic murmur (principal finding), loudest at the left upper 1- other disease of the left side of the heart,
sternum & radiating towards the left shoulder. 2- primary pulmonary vascular disease
2- Thrill, best felt when the patient leans forward and breathes out. 3- Eisenmenger's syndrome.
3- Click  The murmur is often preceded by an Ejection sound (click).
4- S.S. Delay in right ventricular ejection may cause wide Splitting of the
Second heart sound. - It may complicate mitral stenosis, producing :
5- Severe pulmonary stenosis is characterised by :
a- loud harsh murmur, b- inaudible pulmonary closure sound (P2), an early diastolic decrescendo murmur at the left sternal edge
c- increased right ventricular heave, d- prominent a waves in the jugular pulse, that is difficult to distinguish from aortic regurgitation
- ECG : (Graham Steell murmur).
evidence of right ventricular hypertrophy,
- chest X-ray - Trivial pulmonary regurgitation is a frequent finding in normal individuals and
and post-stenotic dilatation in the pulmonary artery has no clinical significance.
- Doppler echocardiography :
is the definitive investigation.
Mild to moderate isolated pulmonary stenosis is relatively common &
does not usually progress or require treatment.
Severe pulmonary stenosis (resting gradient > 50 mmHg with a normal
cardiac output) is treated by : a- percutaneous pulmonary balloon valvuloplasty
b- or, by surgical valvotomy.
- Long-term results are very good.
- Post-operative pulmonary regurgitation is common but benign.