I is the failure of the left ventricle to propel blood forwards resulting in accumulationf blood in pulmonary circulation
characterized by paroxysmal nocturnal dyspnoea, gallop rhythm, pulsus alternans and basal crepitations, Aetiology
I, Hypertension is the commonest cause,
2. Coronary thrombosis
3. Aortic valve disease, e g aortic stenosis and aortic
4. Mitral incompetence
5 Some congenital hearl disease. e g coaretation of aort
6. Curdiomyopathy
7. Ventricular tachyurrhythmia
In mitral stenosis there is ulso pulmonary oedema us nresult of left atrial failure; therefore, this disease cannot be included under causes of left ventricular failure but certainly included under left heart failure.Clinical Features
1. Dyspnoea: This is due to pulmonary venous congestion resulting in pulmonary stiffness with diminished pulmonary
compliance, which stimulates the Hering-Breuer’s reflex resulting in rapid and shallow respiralion withaccumulation of CO2. It first occurs on exertion (exertional dyspnoea) and may occur ultimately even al res (orthopnoea)
Dyspnoea on exertion or effort dyspnoea: In earlier stages patient feels out of breath only during heavy exercise but
ultimately even during normal daily activities e.g., walking on level grounds there may be breathlessness. This stage
is called compensated stage and the cardiac reserve powers are put into action. In some cases patients may restrict their
activity to hide breathlessness Dyspnoea at rest: Dysponea at rest may be paroxysma and often nocturnal. At midnight patient suddenly wakes up, sits up in bed or rushes to the window and feels suffocated. This is called paroxysmal noctural dyspnoea
(PND). This is possibly related toa) redistribution of blood with increased pulmonary congestion during recumbent posture b) Slowing of respiration rate with less absorption of alveolar moisture c) Increased heart rate during rapid eye movement (REM)
and dreams Pulmonary venous congestion leads to bronchial venous congestion and oedema of the bronchial mucosa which may give rise to reflex bronchoconstriction and bronchospasm. This is called cardiac asthma. Gradually in course of time
even during recumbent posture in bed, patient feels breathlessness. This is called orthopnoea and it is due to
persistent pulmonary congestion with decreased pulmonary compliance even in erect posture. This is called Decompensated state of Heart failure
2. Cough and Expectoration: This is also due to pulmonarycongestion with pulmonary oedema and therefore it occurs
after exertion in earlier states. During acute attack patient coughs and brings out lot of sputum. This is characteristically frothy as the bronchial secretion is mixed up with air. Sometimes, there may be haemoptysis which is either due to haemorrhagic transudate or rupture of bronchopulmonary venous circuit. increased bearl vate
sweat ofien drenching the garments may he seen which is due to eacessiveheros portalning to the undertying cause may
General Survey Age and Nes Usually elderly males above 40 years In Pheumatic cases it may develop in lower age groups and in fermales. Decuhihis is propped up as in this positlan the cadia outiu, .. less, ven.”ו” ieturn is relised and ‘here is bette,
play of respiratory museles Pacies is ansious and sweating may he present Ounasis is present and is central in type I la due to
defective oxygenation of blood in the lungs due to poor diftusion of osygen from oedematous alveoli and is also due
to mismatched pulmonary ventilation and perfusion Reynirvarinn rite is hurried (<40, there may be Cheyne
Stokes breathing present Pulse vate is always high above 100-120/min, usually gular, tension and volume may be high. Pulsus alternans may he present which is diagnosed by sphygmomanometer. Arterial wall may be thick due to sclerosis (Whip cord)
lood pressure: As hypertension is the commonest cause blood pressure is high. On an average case it is above 200
100 mm of Hg but slight rise of blood pressure may even be seen in normotensive subjeets with left ventrieular failure due
to increased catecholamine secretion. Sometimes there maybe decapitated blood pressure Examination of Heart
On inspection apex beat is more down and forceful, on palpation it may be heaving (forceful and well sustained), This
is, however, not present in myocardial infarction.On auscultation heart rate is increused, S, and S may beaudible giving rise to triple thythm or gallop thythm over the mitral area. Sometimes S and S4 may merge together in
presence of high heart rate giving rise to summation gallop Sometimes tick-tack rhythm or embryocardia may be present P2 may be accentuated: A2 may be accentuated and ringing in type in hypertensive cases, Murmur may be present over mitral
or aortic areas if valvular disease is responsible for heartfailure Examination of LungsBasal crepitations to start with and ultimately bilateral coarse moist sounds (bubbling rales) over the chest may develop due to pulmonary oedema. Expiratory wheeze and diffuse wheezing rhonchi may be present. Tracheal rattling sound mayalso be present at terminal stages Investigations
1. X-ray of the chest (P A.) will show bilateral perihilar
butterfly shadow due to pulmonary oedema. There may be tonbal This B-adrenergic agonist inhaler and IV aminophylline may be considered but better be avoided as they provoke tachycardia includingsupraventricular tachyarrhythmia

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