Congestive Heart Failure - Clinical Manifestations

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Congestive heart failure presents with distinct symptoms that can be traced to either left-sided or right-sided heart failure. Left-sided heart failure (LHF) predominantly affects the lungs, leading to symptoms like dyspnea with exertion due to reduced lung compliance and orthopnea. The sensation of dyspnea arises when pulmonary C fibers detect pulmonary edema. Paroxysmal nocturnal dyspnea (PND) is also associated with LHF. Auscultation reveals bibasilar inspiratory crackles and sometimes wheezing due to peribronchial edema.

Left-sided heart failure presents with pulmonary edema, evidenced by frothy pink transudate on the intra-alveolar surface and the presence of hemosiderin-laden alveolar macrophages, colloquially termed as ‘heart failure cells.’ Imaging via a chest x-ray (CXR) is an essential diagnostic tool that often reveals findings such as cephalization of the pulmonary vessels, fluffy ‘batwing’ shaped bilateral opacities, Kerley B lines (indicative of fluid accumulation between lobes), air bronchogram (dark airway set against an opacified interstitium), and cardiomegaly. Acoustic findings include the S3 heart sound, more prevalent in systolic heart failure, and the S4 heart sound, frequently seen in diastolic heart failure.

Left-sided heart failure can also cause dilation of the mitral annulus, resulting in mitral regurgitation. Complications such as atrial fibrillation can also arise from atrial dilation. The pathology of left-sided heart failure also involves damage to the pulmonary vascular endothelium, leading to decreased NO production & increased endothelins, resulting in vasoconstriction. Over time, this leads to pulmonary vascular remodeling, characterized by collagen deposition (intimal hypertrophy) and smooth muscle cell proliferation (medial hypertrophy). A consequential effect of left-sided heart failure is pulmonary artery hypertension—the most common cause of right-sided heart failure.

Right-sided heart failure (RHF) primarily affects the systemic circulation, manifesting as jugular vein distension (JVD), hepato-jugular reflux, and peripheral edema. Hepatic involvement leads to zone 3 (centrilobular) necrosis, or ‘nutmeg liver,’ and painful hepatomegaly. Portal hypertension can also occur in RHF due to congestion of blood in the hepatic vein, which can cause ascites. LHF is the most common cause of RHF through a sequence of pulmonary artery hypertension and subsequent cor pulmonale. S3 heart sound (common in systolic HF) and S4 heart sound (common in diastolic HF) can be heard on auscultation. Systolic murmurs due to mitral regurgitation in left-sided HF and tricuspid regurgitation in right-sided HF are also common. Both forms involve vascular remodeling and can result in atrial fibrillation due to atrial dilation.

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What clinical manifestations are associated with left-sided heart failure and how do they arise?

Left-sided heart failure often leads to clinical signs such as pulmonary edema, orthopnea, and paroxysmal nocturnal dyspnea. These symptoms manifest when the failing left ventricle elevates pressure in the pulmonary circulation, causing fluid to leak into the alveoli. This alveolar fluid accumulation, sensed by pulmonary C fibers, results in the sensation of dyspnea. Additional findings may include bibasilar inspiratory crackles and wheezing due to peribronchial edema. At the microscopic level, the alveoli may contain frothy pink transudate and hemosiderin-laden alveolar macrophages, commonly known as "heart failure cells.

What findings are commonly seen on a chest X-ray (CXR) in left-sided heart failure?

A chest X-ray (CXR) for suspected left-sided heart failure typically reveals several characteristic features. These include cephalization of the pulmonary vessels, indicative of increased pulmonary venous pressure. Pulmonary edema is often visible as bilateral fluffy opacities, sometimes referred to as "batwing" opacities. Additional features like Kerley B lines suggest interlobular fluid accumulation, and air bronchograms may also be present. Cardiomegaly, or enlargement of the heart, is another common finding. In some cases, the X-ray may also suggest dilation of the mitral annulus, which can be an indirect sign of mitral regurgitation—a condition frequently associated with left-sided heart failure.

What alterations in heart sounds are commonly observed in heart failure?

Heart failure can result in significant changes to cardiovascular sounds: an S3 heart sound is more common with systolic heart failure, often reflective of increased filling pressures; an S4 heart sound is more common in diastolic heart failure and it represents a stiff or noncompliant ventricle, which needs greater filling pressure. Left-sided heart failure can present with a systolic murmur due to mitral regurgitation.

What is the most common cause of right-sided heart failure and how does it develop?

The most common cause of right-sided heart failure is left-sided heart failure. When the left ventricle fails, it leads to an increase in pressure within the pulmonary circulation, causing pulmonary hypertension. This heightened pressure burdens the right ventricle, ultimately leading to right-sided heart failure, known as cor pulmonale. Other contributing factors can include chronic pulmonary emboli or a saddle pulmonary embolism, which place additional strain on the right side of the heart and can lead to right-sided heart failure.

What are the typical signs and symptoms associated with right-sided heart failure?

Right-sided heart failure manifests with various clinical signs such as jugular vein distension (JVD), hepato-jugular reflux, and Kussmaul sign, which is a rise in JVD during inspiration. Peripheral edema, pleural and pericardial effusions, and painful hepatomegaly from hepatic congestion are also common. Additionally, a dilated tricuspid annulus may result in a systolic murmur indicative of tricuspid regurgitation. Portal hypertension can lead to ascites, and hepatic venous congestion may result in centrilobular necrosis, manifesting as "nutmeg liver" upon gross pathological examination.