Acute Left Ventricular Failure
Acute left ventricular failure is defined as sudden onset of dyspnea at rest
or worsening dyspnoea of pre-existing chronic congestive cardiac failure
occurring in patients with a cardiac condition. It is not a disease but a syndrome
and complication of heart disease.
Acute pulmonary edema is another term used synonymously with the
same meaning. This can also mean that the left ventricle has not failed but the
left atrium alone has failed as in the case of mitral stenosis.
Acute pulmonary edema can also be due to non-cardiac causes. Non-
cardiac pulmonary edema can occur in adult respiratory distress syndrome and
organo phosphate insecticide poisoning. Neurogenic pulmonary edema follows
Acute left ventricular failure can occur in any condition, which increases
the left ventricular pressure to significantly high levels like aortic valve stenosis,
systemic hypertension, or any condition, which produces an acute volume over
load of the left ventricle as in acute mitral or aortic valve regurgitation.
Coronary artery heart disease is another important cause of acute left
ventricular failure by causing diastolic dysfunction of the left ventricle.
Acute left ventricular failure may be precipitated by a major event like
acute myocardial infarction or a minor event like the onset of atrial fibrillation in
chronic valvular heart disease. The increase in left ventricular diastolic pressure
causes a passive increase in pressure in the left atrium and the pulmonary veins.
This is transmitted to the pulmonary capillaries.
When the hydrostatic pressure in the pulmonary capillaries exceeds the
oncotic pressure of plasma, which is approximately 25 to 27 mmHg, the fluid
exudes from the pulmonary capillaries into the alveoli, causing pulmonary
edema. This stimulates the respiration through a series of autonomic reflexes
resulting in increase in respiratory rate.
In the case of mitral stenosis since the development of pulmonary venous
hypertension is very slow, occurring over a period of several years, this is
followed by the development of pulmonary arterial hypertension. This actually
protects the patient from developing acute pulmonary edema.
Acute left ventricular failure presents with sudden onset of dyspnoea at
rest. It then rapidly progresses to orthopnoea and severe respiratory distress, the
patient sitting up and gasping for breath.
Acute pulmonary edema is the classical description of a terrifying
experience. The patient will describe it as a sensation of fighting for breath. This
might occur after mid night after a few hours of sleep. Patient sits up with acute
onset of breathlessness. Sitting or standing will only give little or no relief. There
will be cough and wheezing and plenty frothy expectoration of pink or blood
Confusion and memory impairment can occur in later stages. Severe
prostration, acute anxiety and feeling of impending death can also occur. Death
is likely in all untreated patients, who have not received immediate treatment.
The patient appears to be pale and agitated. The extremities are cold and
sweating. He is acutely dyspnoeic and orthopnoeic. The pulse rate is increased
out of proportion to the general condition of the patient. There may be pulsus
alternans in severe left ventricular failure. This means the alternating pulse beats
have lower volume. Extreme tachycardia and bradycardia are ominous in the
setting of acute left ventricular failure.
The systemic blood pressure maybe altered in acute left ventricular failure
due to the underlying cause itself. In aortic stenosis, the systolic pressure will be
low, the diastolic pressure normal and the pulse pressure narrow. In systemic
hypertension, which is another cause for acute left ventricular failure, the systolic
as well as the diastolic blood pressure will be elevated.
But in case of acute left ventricular failure due to other causes, the blood
pressure is not significantly changed. Only in severe acute left ventricular failure,
the cardiac output is reduced and the systolic pressure is lowered.
The jugular venous pressure also does not show an increase unless there
is right ventricular failure or fluid over load in association. The jugular pulse
waves also remain unaltered in isolated acute left ventricular failure.
The apex beat is usually shifted downwards and outwards in most cases
of acute left ventricular failure and the character of the apex is usually heaving in
nature. On percussion of the heart cardiomegaly is detected and in presence of
pericardial effusion the percussed out left heart border is outside the palpated
The First and second heart sounds are normally heard or altered
depending upon the underlying cardiac lesion. Tachycardia invariably evident
and sometimes associated with irregularity as in the case of atrial fibrillation,
which is another important cause or precipitating factor in acute left ventricular
The diagnostic hallmark of acute left ventricular failure is the presence of a
third heart sound or a ventricular gallop. This is best heard over the apex in the
left lateral position with the breath held in expiration. The presence of a third
heart sound indicates the presence of severe left ventricular dysfunction.
There may be a murmur heard depending upon the presence of
underlying heart lesion. For example a mid-diastolic murmur of mitral stenosis or
ejection systolic murmur of aortic stenosis may be heard.
Another clinical finding that is diagnostic of acute left ventricular failure is
the presence of bilateral fine crepitations over the lung base. This is sometimes
more extensive and heard all over the lung fields as in acute pulmonary edema.
If there is significant bronchospasm there will be bilateral rhonchi also. This might
create confusion in the diagnosis as acute bronchial asthma which also presents
in a similar fashion.
The patient with acute left ventricular failure is always a very anxious and
dyspnoeic. Hence he should be comfortably positioned and supported with a
backrest in the propped up position. Patient may be given a mild sedative like
alprazolam if needed
Oxygen inhalation should be started immediately using a face mask or nasal
probes containing high concentration of oxygen flowing a at a rate of 4-6 liters
Morphine sulphate is administered as slow IV injection after diluting with
dextrose. Morphine of one ampoule containing 15 mg of the drug, is diluted in 9
ml of dextrose. One ml will then contain 3 mg. It is given as slow IV injection and
repeated at 15 minutes intervals till the patient is either relieved from dyspnoea
Diuretics such as frusemide 40 mg are given intravenously as a first line of
treatment. They can be repeated at short interval till desired action is obtained.
Precaution should be taken against the induction of hypokalemia. Diuretics
increase the urinary excretion of sodium and reduce the blood and plasma
Digoxin is indicated in all cases of acute left ventricular failure except in the
setting of acute myocardial infarction, where it is contraindicated. It is the drug of
choice when heart failure is associated with atrial fibrillation, Digoxin tablet
containing 0.25mg is administered either as a slow digitalization if the patient is
already on a daily maintenance dose of the drug or as a rapid digitalizing dose.
0.5 to 0.75mg is given initially fooled by 0.25mg after eight hours and 8hrly for 4
doses and then reduced to a maintenance dose of one tablet a day
Nitrates are indicated in acute left ventricular failure due causes other than aortic
stenosis. Tablets of isosorbide dinitrate are given as thrice daily doses of 10mg.
Care should be taken to avoid hypotension or syncope. Vasodilators like nitrates
are more useful in chronic heart failure than acute heart failure.
After all other measures fail the technique of reducing the venous return by
rotating tourniquet should be applied. It can reduce the venous return up to 20%.
Rubber tourniquet or blood pressure cuffs are tied to the three limbs and rotated
at intervals of fifteen minute.
Surgical venesection is the last resort in trying to relieve the acute left
ventricular failure in bedside settings. 100 to 150 ml of blood is let out by
venepuncture and there by reducing the pre load.