EISENMENGER’S SYNDROME

CAUSATION:

TYPES

Pulmonary hypertension with reversal of arteriovenous shunt is called EISENMENGER’S SYNDROME.  It is seen in cases of ventricular septal defect (EISENMENGER’S SYNDROME  complex), patent ductus arteriosus and sometimes in atrial septal defect (rare under the age of twentyone or in secundum type). It may also be seen in more complex defects like AVSD, Aorto-pulmonary window, common truncus and single ventricular heart. Eisenmenger’s syndrome reaction comprises shunt reversal in ASD or PDA, after puberty due to pulmonary hypertension. The causes of pulmonary hypertension is not clear and possibly due to development of pulmonary vascular disease or increased resistance. This will give rise to decreased pulmonary compliance with increased pressure in infancy or childhood due to reactive pulmonary vasoconstriction.

CLINICAL FEATURES:

Easy fatiguability, syncope, palpitation (flutter fibrillation), ventricular trachycardia, tiredness and angina may develop. Angina is due to reduced myocardial oxygenation and increased right ventricular wall stress. There may be features of CCF, haemoptysis (due to bleeding from bronchial vessels or pulmonary infarction), features of endocarditis.

CAUSATION:

Pulmonary hypertension with reversal of arteriovenous shunt is called EISENMENGER’S SYNDROME.  It is seen in cases of ventricular septal defect (EISENMENGER’S SYNDROME  complex), patent ductus arteriosus and sometimes in atrial septal defect (rare under the age of twentyone or in secundum type). It may also be seen in more complex defects like AVSD, Aorto-pulmonary window, common truncus and single ventricular heart. Eisenmenger’s syndrome reaction comprises shunt reversal in ASD or PDA, after puberty due to pulmonary hypertension. The causes of pulmonary hypertension is not clear and possibly due to development of pulmonary vascular disease or increased resistance. This will give rise to decreased pulmonary compliance with increased pressure in infancy or childhood due to reactive pulmonary vasoconstriction.

CLINICAL FEATURES:

Easy fatiguability, syncope, palpitation (flutter fibrillation), ventricular trachycardia, tiredness and angina may develop. Angina is due to reduced myocardial oxygenation and increased right ventricular wall stress. There may be features of CCF, haemoptysis (due to bleeding from bronchial vessels or pulmonary infarction), features of endocarditis.

Central cyanosis, polycythaemia, clubbing of fingers and toes, prominent ‘a’ wave in the neck, left due to right ventricular hypertrophy, palpable P2, very loud sound heart sound (p2) associated with closed splitting and ejection click are present. There may be roght-sided s4. Decrescendo diastolic murmur (graham steelle’s murmur) over pulmonary ares may be audible. In cases of PDA with Eisenmenger’s syndrome lower limbs will show cyanosis and clubbing, which is called differential cyanosis. Exertional dyspnoea with pedal oedema may be present due to right heart failure.

ECG shows right ventricular hypertrophy,x-ray shows dilate pulmonary artery with peripheral pruning, right ventricular enlargement and increased vascularity  of the lung Echo Doppler may show a jet of tricuspid insufficiency. Cardiac catheterization shows increased pulmonary artery pressure with reactivity of pulmonary vasculature. Open lung biopsy may be helpful.

TREATMENT

This is mainly conservative to prevent bacterial endocarditis and heart failure or thromboembolic complications. Surgical repair of the defect is strongly contraindicated as the mortality is high. Nifedepine, ACE inhibitors and prostacyclin are said to be useful.

Central cyanosis, polycythaemia, clubbing of fingers and toes, prominent ‘a’ wave in the neck, left due to right ventricular hypertrophy, palpable P2, very loud sound heart sound (p2) associated with closed splitting and ejection click are present. There may be roght-sided s4. Decrescendo diastolic murmur (graham steelle’s murmur) over pulmonary ares may be audible. In cases of PDA with Eisenmenger’s syndrome lower limbs will show cyanosis and clubbing, which is called differential cyanosis. Exertional dyspnoea with pedal oedema may be present due to right heart failure.

CAUSATION:

TYPES

Pulmonary hypertension with reversal of arteriovenous shunt is called EISENMENGER’S SYNDROME.  It is seen in cases of ventricular septal defect (EISENMENGER’S SYNDROME  complex), patent ductus arteriosus and sometimes in atrial septal defect (rare under the age of twentyone or in secundum type). It may also be seen in more complex defects like AVSD, Aorto-pulmonary window, common truncus and single ventricular heart. Eisenmenger’s syndrome reaction comprises shunt reversal in ASD or PDA, after puberty due to pulmonary hypertension. The causes of pulmonary hypertension is not clear and possibly due to development of pulmonary vascular disease or increased resistance. This will give rise to decreased pulmonary compliance with increased pressure in infancy or childhood due to reactive pulmonary vasoconstriction.

CLINICAL FEATURES:

Easy fatiguability, syncope, palpitation (flutter fibrillation), ventricular trachycardia, tiredness and angina may develop. Angina is due to reduced myocardial oxygenation and increased right ventricular wall stress. There may be features of CCF, haemoptysis (due to bleeding from bronchial vessels or pulmonary infarction), features of endocarditis.

Central cyanosis, polycythaemia, clubbing of fingers and toes, prominent ‘a’ wave in the neck, left due to right ventricular hypertrophy, palpable P2, very loud sound heart sound (p2) associated with closed splitting and ejection click are present. There may be roght-sided s4. Decrescendo diastolic murmur (graham steelle’s murmur) over pulmonary ares may be audible. In cases of PDA with Eisenmenger’s syndrome lower limbs will show cyanosis and clubbing, which is called differential cyanosis. Exertional dyspnoea with pedal oedema may be present due to right heart failure.

ECG shows right ventricular hypertrophy,x-ray shows dilate pulmonary artery with peripheral pruning, right ventricular enlargement and increased vascularity  of the lung Echo Doppler may show a jet of tricuspid insufficiency. Cardiac catheterization shows increased pulmonary artery pressure with reactivity of pulmonary vasculature. Open lung biopsy may be helpful.

TREATMENT

This is mainly conservative to prevent bacterial endocarditis and heart failure or thromboembolic complications. Surgical repair of the defect is strongly contraindicated as the mortality is high. Nifedepine, ACE inhibitors and prostacyclin are said to be useful.

ECG shows right ventricular hypertrophy,x-ray shows dilate pulmonary artery with peripheral pruning, right ventricular enlargement and increased vascularity  of the lung Echo Doppler may show a jet of tricuspid insufficiency. Cardiac catheterization shows increased pulmonary artery pressure with reactivity of pulmonary vasculature. Open lung biopsy may be helpful.

TREATMENT

This is mainly conservative to prevent bacterial endocarditis and heart failure or thromboembolic complications. Surgical repair of the defect is strongly contraindicated as the mortality is high. Nifedepine, ACE inhibitors and prostacyclin are said to be useful.

EISENMENGER’S SYNDROME

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