Left-Sided Heart Failure, Its Morphology And Clinical Features

Left-Sided Heart Failure, Its Morphology And Clinical Features In Full Detail

Heart failure can affect the left or right side of the heart, or it can affect both sides. The most common causes of left ventricular heart failure are ischemic heart disease (CHD), systemic hypertension, mitral valve or aortic disease, and primary myocardial disease.

The morphological and clinical effects of left ventricular heart failure (eg, amyloidosis) are due to a decrease in systemic perfusion and an increase in posterior pressure in the pulmonary circulation.



Cardiac microscopic symptoms depend on the underlying disease process, for example, there may be a brain infection or valve dysfunction. In addition to regurgitation due to mitral valve stenosis or obstruction cardiomyopathy (described below), the left ventricle is usually hypertrophic and can sometimes spread widely.

Left ventricular proliferation can cause mitral regurgitation and left atrial dilation, which are associated with increased incidence of atrial fibrillation. Microscopic changes in heart failure are non-specific and mostly consist of myocyte hypertrophy with interstitial fibrosis of varying severity. Other lesions that contribute to the development of heart failure (such as recent or previous myocardial infarction) may be treated against this background.


In severe left ventricular failure of the lungs, the increased pressure in the pulmonary veins eventually transmits to the capillaries and pulmonary arteries, resulting in congestion and inflammation.

Simultaneously, pleural effusion due to an increase in hydrostatic pressure in the visceral pleural venula. The lungs are heavy and swollen, prevascular and medial, which can be detected microscopically.

Transudate, swelling of the alveolar septum and accumulation of edematous fluid in the alveolar space. In chronic heart failure, a variable number of red blood cells emerge from the capillaries with increased permeability in the alveolar space, where they are defagocytosis by macrophages.

Subsequent breakdown of erythrocytes and hemoglobin reveals hemosiderin-loaded alveolar macrophages, called heart failure cells, which reflect the later episodes of pulmonary edema.

Clinical Features

Dyspnea with difficulty (breathing difficulties) is usually the earliest and most prominent symptom of left ventricular heart failure. Coughing is also common due to fluid leakage into the air. If failure occurs, the patient develops shortness of breath in the supine position (orthopnea). This is because the supine position increases the return of veins from the lower leg and also raises the diaphragm.

Orthopedics are usually relaxed by sitting or standing, so patients often sleep in a semi-sitting position. Paroxysmal nocturnal dyspnea is a dramatic form of dyspnea that wakes the patient from sleep with a feeling of difficulty breathing.

Other manifestations of left ventricular failure include a large heart (cardiomegaly), tachycardia, third heart sound (S3), and mild spots at the base of the lungs due to the opening of edematous pulmonary alveoli. As the ventricles expand, the papillary muscles move from behind, causing mitral regurgitation and systolic murmur. Later chronic left atrial enlargement can lead to atrial fibrillation, as indicated by a “random” heartbeat.

Irregular and chaotic atrial contraction reduces the participation of the atria in the ventricular filling, thus reducing the number of ventricular heartbeats. Atrial fibrillation also causes blood stasis (especially in the atria), which often leads to blood clots, which can lead to rejection of embolism and lead to heart attacks and strokes in other organs.

Decreased cardiac output leads to a decrease in renal perfusion, which in turn stimulates the renin-angiotensin-aldosterone axis, which increases intravascular volume and pressure. Unfortunately, in heart failure, this compensatory effect is exacerbated by pulmonary edema. With further development of CHF, prenatal isotemia may occur with residual nitrogen excretion and metabolic disturbances.

In severe CHF, a decrease in cerebral perfusion may manifest as hypoxic encephalopathy, characterized by irritability, cognitive impairment, and restlessness that can lead to convulsions and coma.

Heart failure is usually treated, at least initially, with a underlying cause, such as valve failure or low heart perfusion. As an alternative to such options, the medical approach involves limiting the amount of salts or pharmacological agents that reduce the volume overload (e.g., diuretics), increasing myocardial compression (so-called “Positive inotropes”), or reducing cardiac output.

Angiotensin converting enzyme inhibitors benefit patients not only by resisting aldosterone-mediated salt and water retention but also by limiting cardiomyocyte hypertrophy and reconstituting it by unknown mechanisms.

Although cardiac synchronization therapy (external stimulation of the right and left ventricles) and modulation of cardiac contraction (external stimulation of the heart muscle) have recently been added to the arsenal of cardiologists, CHF is one of the leading causes of disease and death in humans.

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