Congestive heart failure (CHF) otherwise known as cardiac failure refers as the inability of the heart to pump sufficient blood to meet needs of tissues for oxygenation and nutrition. This disease can affect the heart’s ability to respond to circulation demands of the body. CHF is a slowly developing condition where cardiac output is lower-than-normal.


In CHF, the contractile properties of the heart are impaired. This leads to a decreased cardiac output. Cardiac output (CO) is best described by the equation CO = HR (heart rate) x SV (stroke volume). Heart rate is an autonomic nervous system function and in cases where CO falls, sympathetic nervous system increases heart rate to maintain adequate cardiac output. When the compensatory mechanism fails to maintain adequate tissue perfusion, the properties of stroke volume must adjust to maintain CO. But if the main problem in CHF is the damage of heart muscle fibers, stroke volume is impaired and CO cannot be maintained to normal output.


The amount of blood pumped in each contraction is what you call the stroke volume (SV). SV is dependent on three factors namely the preload which is the volume of blood filling the heart. Amount of blood brought to the heart is directly proportional to the pressure applied by the length of stretch of the myocardial fibers. The second factor relating to stroke volume is the changes in the force of contraction occurring at the cellular level which is termed as contractility. This factor is related to the length of myocardial fibers and the levels of calcium in the body. The third factor is referred to as afterload. This is the amount of pressure of ventricles needs to come up to be able to pump blood across the pressure gradient that is created with the arteriole resistance.

Etiology of CHF

Myocardial Weakness

Common cause of myocardium weakness is ischemia related to Atherosclerosis and its stenosis of the coronary arteries. When stenosis reaches about 50-70%, only resting myocardial oxygen can be met. When atherosclerosis progresses myocardial fibers undergo hypoxic injury leading to necrosis. These fibers are then replaced with fibrous connective tissue resulting to deteriorating pumping capacity of the heart and reduced ventricular compliance. Other myocardial ischemia cause is thrombosis in the coronary arteries. Myocardial weakness can developed with myocarditis or cardiomyopathies.

Restrictions to Pumping

Some physical factors restrict the heart’s pumping ability such as malfunction in cardiac valve. Inability of the valves to open widely causes decreased blood flow to the heart leading to a reduced cardiac output. Congenital Heart Defects also restrict the pumping of the heart by interfering the free flow of blood in myocardium. Presence of mass (may be a thrombus or tumor) within cardiac chamber can cause internal obstruction by occupying a portion of chamber’s volume, thereby reducing the chamber’s blood capacity. The most common cardiac tumor, myxoma, is of endothelial origin and is most often located at the left atrium. This type of tumor accounts for 35-50% of all primary cardiac tumors. Its presence can occlude mitral valve which can cause instant death or can serve as a site for the formation of thromboembolus. Pumping may also be restricted by cardiac dysrhythmias, pericarditis and cardiac tamponade.

Increased Afterload

Inability to maintain cardiac output may also result from overload. In cases where the myocardium is constantly exposed to high physical demand, the strain may overwhelm the heart and the result is declined contractility and stroke volume which is likely seen when cardiac afterload is increased. The right ventricle faces this type of situation in certain lung diseases such as Cor Pulmonale where vascular damage causes pulmonary hypertension. Systemic hypertension can also increase afterload as elevated BP presents an increased resistance that the left ventricle must overcome to maintain an adequate CO. Furthermore, valve disease or congenital defects in the cardiac outflow tracts, valves, pulmonary trunk or aorta can also produce excessive ventricular afterload.

Congestive Heart Failure Schematic Diagram

Schematic Diagram Credits: Pathophysiology, Concepts and Applications for Health Care Professionals by Thomas J. Nowak and A. Gordon Hanford, 3rd Edition


Two significant factors are considered when congestive heart failure pathophysiology is discussed. First, the heart is unable to clear itself with of the delivered blood. The second factor is how long it takes for the signs and symptoms to develop.

In this pathophysiology explanation, we will use mitral stenosis as the etiologic factor of CHF. Stenosis of the mitral valve produces hardened and thicker valve cusps that cannot fully open. This decreases the passageway of blood from the left atrium to left ventricle. The stenosed portion interferes with ventricular filling leading to decline in stroke volume and cardiac output. When stenosis increases, cardiac output may even fail to meet demands even at rest. As a result the affected individual experiences weakness, fatigue and fainting.

When blood cannot easily flow, it backs into the right atrium and then to the lungs. Pulmonary congestion in return produces pulmonary hypertension with pressure sometimes rising 3-5 times above normal. With high pressure, fluid accumulates in the lung interstitium, otherwise known as pulmonary edema which stiffens lungs making it less elastic and more firm. Fluids are forced from pulmonary tissues to alveolar air spaces as the condition progresses. When fluids accumulate in alveoli and bronchioles, surface for diffusion is reduced resulting to airway obstruction and manifested as difficulty of breathing or dyspnea.

In congestive heart failure, dyspnea is aggravated when lying down, a condition called orthopnea. The cause of orthopnea is the increased load placed on the failing heart. This pulmonary burden adds more pulmonary congestion, edema and aggravation of respiratory difficulty. Orthopnea is managed by assisting the individual to sitting or fowler’s position.

Patient’s diagnosed with CHF report bouts of dyspnea at nighttime. This condition is referred as paroxysmal nocturnal dyspnea. Unlike orthopnea, relied is not quickly achieved by sitting down. About 30 minutes in an upright position is needed for breathing to become easier.

Aside from breathing difficulties, pulmonary hypertension can also cause aneurysms in small pulmonary vessels which may rupture and cause hemorrhage in the lungs. Pulmonary hypertension and congestion can lead to secondary infection. A common complication of CHF is bronchopneumonia.

As CHF progresses, backup of blood in the right heart can increase the right heart’s preload. The right responds with hypertrophy that increases their strength and enables them to compensate with an increased stroke volume. This results to an enlarged heart which is called cardiomegaly. Cardiomegaly characterizes a chronically failing heart.

When the right heart congestion develops, systemic venous congestion results manifested by swelling of the major superficial veins. Often clients with CHF are noted with swelling jugular veins. With elevation of systemic venous pressure, capillary pressures also increased leading to systemic edema. Following the pull of gravity fluid accumulation in the lower parts of the body are noticed in ankles when the person is sitting or standing, a condition termed as dependent edema.

Systemic edema also has significant effects on the liver and spleen. Blood congested in the liver causes it to enlarged, a condition known as hepatomegaly. Congestion of blood in the hepatic system produces high pressures that can damage hepatocytes or cause the vessels to rupture resulting to hemorrhage.

Hepatic system hypertension may also cause back pressure leading to spleen congestion or splenomegaly, which is associated with severe and advanced CHF.

Originally posted 2015-03-15 12:00:07. Republished by Blog Post Promoter