Heart failure affecting the left ventricle is characterized by engorged, congested lungs. As the lungs develop chronic stasis, the lungs become more rigid and dark brown in coloration. 

Heart failure affecting the right ventricle is characterized by an enlargement of the liver which increases in consistency, the liver develops red areas in the center and yellowish areas in the periphery of the lobule as a result of the lipid dystrophy. In more advanced cases, cardiac cirrhosis of the liver occurs. 

The causes of heart failure are multiple and include:

  • Determining factors (determining here means main, these are factors which eventually lead to heart failure)
  • Immediate, accelerating factors. 

Determining factors for the left ventricle heart failure include:

  • Hypertensive disease

  • A myocardial infarction

  • Myocardial cardiosclerosis

  • Aortic defects

  • Myocarditis

Immediate, accelerating factors:

These factors include extreme physical exertions, various infections such as acute pneumopathies, influenza, re-activation of acute articular rheumatism, bacterial endocarditis, etc. Psychological trauma, obesity, pregnancy, a diet rich in salts and lacking proteins, carbohydrates and vitamin B complex, etc are all factors which may lead to the emergence of the disease, albeit more rarely. 

How does heart failure occur?

The heart resembles a pump which distributes the blood throughout all the systems and organs in the body. The amount that the heart is capable of pumping every minute is termed the cardiac output. This output is not constant, but rather fluctuates according to the physiological needs of the organism. The capacity that the heart retains in order to increase the output, depending on the needs of the organism, is called the cardiac reserve. Pathologies of the heart are characterized by a reduced potential energy of the heart. However, the heart still attempts to withstand this phenomenon via  certain mechanisms, which affect the heart muscle and cause the following cardiomyopathies (Cardiomyopathy definition: Diseases of the heart muscle, characterized by abnormality in chamber size and wall thickness, or functional contractile dysfunctions; mainly systolic or diastolic dysfunction in the absence of coronary artery disease, hypertension, valvular disease, or congenital heart disease (Elliot et al., 2018)) :

  1. Compensatory tachycardia or restrictive cardiomyopathy
    This occurs when the heart beats faster, hence increases its beat frequency (the number of beats per minute) in order to sustain the needs of organs and tissue for blood. However, this is only a temporary solution. If the heart operates in this manner, it manages to tire itself out very quickly. In addition to this, the tachycardia leads to a shorter diastole (the ventricle is not completely filled with blood) which causes a reduction in the systolic output (less blood flowing to the periphery).
  2. Enlargement (dilation) of the heart or dilated cardiomyopathy
    Enlargement/dilation of the heart causes the myocardial fibers to become elongated in the direction of the diastole more so than under normal physiological conditions. According to the law of Starling, the systolic contraction is more powerful, hence the ventricles are completely emptied, which is why the systolic output is larger. This compensation mechanism has its limits. When the muscle fibers become more elongated, their contractile power is reduced.
  3. Hypertrophy of the heart or hypertrophic cardiomyopathy
    The heart becomes hypertrophic which is the usual compensatory mechanism when the hemodynamic overload continues over a long or short period of time. The heart undergoes this transition into hypertrophy when the myocardium fibers become thicker, while their numbers do not change. It should also be noted, that the hypertrophic fibers have upregulated needs for blood flow, but the capillary network remains unchanged. This causes the development of a relative ischemia, which makes up the core cause for potential decompensation (Decompensation definition: functional deterioration of a structure or system, in this case, the cardiac system, that had been previously working with the aid of compensation. Compensation means that the system manages to function despite stressors or defects) later on in the progression of the condition. When the compensatory mechanisms are capable of maintaining the cardiac output at a level where the clinical pathological signs are not evident, the cardiovascular apparatus is compensated. In other cases, the compensatory mechanisms are so greatly diminished, that the heart muscle is not capable of fulfilling the tissues’ needs for blood flow, hence the clinical signs of heart failure appear.

Two pathogenic theories behind heart failure

1. The retrograde theory

The reduction in contractile power of the myocardium causes the cavities of the heart to become partially emptied. Due to this, the residual systolic blood and the ventricular diastolic pressure rise. Alongside the aforementioned, the atrial pressure rises, and the flow of venous blood is obstructed. When the failure affects the left ventricle, the pressure in the left atrium and pulmonary veins rises in retrograde fashion. Stasis emerges in the pulmonary circulation. 

When the failure affects the right ventricle, the pressure in the venous systemic circulation rises. This causes stasis (a stoppage or slowdown in the flow of blood or other body fluid, such as lymph) in the liver, kidneys, etc., and accumulation of liquids in the intercellular spaces, which eventually leads to edema. 

This theory is contested, because in cases such as adhesive pericarditis, tricuspid stenosis or for conditions such as ligation of the vena cava inferior, there is no edema for substantial amounts of time, regardless of the rise in venous pressure.

2. The anterograde theory

According to this theory, the heart cannot contract with as much vigor as it used to, hence the cardiac output is reduced, the renal flux is reduced and so is the glomerular filtration. In this manner, there is water and sodium retention, and as a consequence, the volume of blood increases alongside the venous pressure. The two of them in conjunction both eventually cause the edema. 

What this theory does not account for is that it cannot explain the partial decompensation that may occur, such as for example the rise in pressure in the pulmonary circulation. According to the theory, the retention of water and sodium should have global effects on the entire circulatory system.

Hence, both methods have their flaws, and in many ways complete one-another. 

Medically Reviewed by a doctor on 30 Jun 2018
Medical Author: Dr. med.