DEFINITION OF LEFT VENTRICULAR FAILURE

It is the failure of the left ventricle to propel blood forwards resulting in accumulation of blood in pulmonary circulation characterized by paroxysmal nocturnal dyspnoea, gallop rhythm, pulsus alternans and basal crepitations.

AETIOLOGY OF LEFT VENTRICULAR FAILURE

1. Hypertension is the commonest cause.
2. Coronary thrombosis.
3. Aortic valve disease, e.g. aortic stenosis and aortic incompetence.
4. Mitral incompetence.
5. Some congenital heart disease, e.g. coarctation of aorta, PDA etc.
6. Cardiomyopathy.
7. Ventricular tachyarrhythmia.

In mitral stenosis there is also pulmonary oedema as a result 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 respiration with accumulation of CO2. It first occurs on exertion (exertional dyspnoea) and may occur ultimately even at rest (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 paroxysmal 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 to:

1. a) redistribution of blood with increased pulmonary congestion during recumbent posture.
2. b) Slowing of respiration rate with less absorption of alveolar moisture.
3. 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 pulmonary congestion 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.
3. Palpitation: It is not an important symptom and is due to increased heart rate or cardiac dysrhythmia.
4. Perspiration: Cold clammy sweat often drenching the garments may be seen which is due to excessive catecholamine secretion.
5. Other symptoms pertaining to the underlying cause may also be present.

GENERAL SURVEY

Age and Sex: Usually elderly males above 40 years. In rheumatic cases it may develop in lower age groups and in females. Decubitus is propped up as in this position the cardiac output is less, venous return is reduced and there is better play of respiratory muscles.

Facies is anxious and sweating may be present.

Cyanosis is present and is central in type. It is due to defective oxygenation of blood in the lungs due to poor diffusion of oxygen from oedematous alveoli and is also due to mismatched pulmonary ventilation and perfusion.

Respiration rate is hurried (<40), there may be Cheyne- Stokes breathing present.

Pulse rate is always high above 100-120/min, usually regular, tension and volume may be high. Pulsus alternans may be present which is diagnosed by sphygmomanometer. Arterial wall may be thick due to sclerosis (Whip cord).

Blood 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 subjects with left ventricular failure due to increased catecholamine secretion. Sometimes there may be 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 increased, Sa and S4 may be audible giving rise to triple rhythm or gallop rhythm over the mitral area. Sometimes Są 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; A, 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 heart failure.LEFT VENTRICULAR FAILURE

Examination of Lungs

Basal 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 may also be present at terminal stages.

INVESTIGATIONS OF LEFT VENTRICULAR FAILURE

1. X-ray of the chest (P.A.) will show bilateral perihilar butterfly shadow due to pulmonary oedema. There may be signs of pulmonary vascular redistribution, blurring of vascular outlines and increased interstitial markings. Karley’s A and B lines may also be present in long standing cases. Left ventricular enlargement may also be seen.
2. ECG will show left ventricular enlargement, strain pattern, ischaemic changes or infarction
3. Echocardiogram will show abnormalities of segmental global wall motion, size of the cardiac chambers or even the aetiology of heart failure. This is the most useful test as considerable number of patients may have normal ejection faction with elevated atrial pressure due to diastolic dysfunction.
4. Radionuclide ventriculography will also show abnormalities of regional wall motion, chamber size and ejection fraction. This is very helpful when Echo is equivocal.

4. Cardiac catheterization: This is not usually done except to detect valvular disease or intracardiac shunt or cardiac aneurysm. In cardiogenic pulmonary oedema the pulmonary capillary wedge pressure is usually high (>25mm of Hg).
5. Miscellaneous Test: This includes various tests to find out the aetiological causes.