Pathophysiology

• Reduced contractility → systolic ventricular dysfunction → decreased left ventricular ejection fraction (LVEF) → decreased cardiac output

• Causes include:

  • Damage and loss of myocytes (e.g., following myocardial infarction, coronary artery disease, dilated cardiomyopathy)

  • Cardiac arrhythmias

  • High-output conditions

• Decreased ventricular compliance → diastolic ventricular dysfunction → reduced ventricular filling and increased diastolic pressure → decreased cardiac output (while the left ventricular ejection fraction remains normal)

• Causes include:

  • Increased stiffness of the ventricle (e.g., long-standing arterial hypertension with ventricular wall hypertrophy, restrictive cardiomyopathy)

  • Impaired relaxation of the ventricle (e.g., constrictive pericarditis, pericardial tamponade)

• Increased left ventricular afterload: increased mean aortic pressure (e.g., arterial hypertension), outflow obstruction (e.g., aortic stenosis)

• Increased left ventricular preload: left ventricular volume overload (e.g., backflow into the left ventricle caused by aortic insufficiency)

• Increased right ventricular afterload: increase in pulmonary artery pressure (e.g., pulmonary hypertension)

• Increased right ventricular preload: right ventricular volume overload (e.g., tricuspid valve regurgitation, left-to-right shunt)

reduced cardiac output → poor organ perfusion → organ dysfunction (e.g., hypotension, renal dysfunction)

• Left ventricle: increased left-ventricular volumes or pressures → backup of blood into lungs → increased pulmonary capillary pressure → cardiogenic pulmonary edema (presenting with orthopnea) and increased pulmonary artery pressure

• Right ventricle: increased pulmonary artery pressure → reduced right-sided cardiac output → systemic venous congestion → peripheral edema and progressive congestion of internal organs (e.g., liver, stomach)

• Nutmeg liver: the macroscopic appearance of the liver which resembles a nutmeg seed due to ischemia and fatty degeneration from hepatic venous congestion

The compensation mechanisms are meant to maintain the cardiac output when stroke volume is reduced.

• Increased adrenergic activity : increase in heart rate, blood pressure, and ventricular contractility

• Increase of renin-angiotensin-aldosterone system activity (RAAS): activated following decrease in renal perfusion secondary to reduction of stroke volume and cardiac output

  • ↑ Angiotensin II secretion results in:

    • Peripheral vasoconstriction → ↑ systemic blood pressure → ↑ afterload

    • Vasoconstriction of the efferent arterioles → ↓ net renal blood flow and ↑ intraglomerular pressure → maintained GFR

  • ↑ Aldosterone secretion → ↑ renal Na+ and H2O resorption → ↑ preload

• Secretion of brain natriuretic peptide (BNP)

  • Definition: ventricular myocyte hormone released in response to increased ventricular filling and stretching

  • Mechanism of action: ↑ intracellular smooth muscle cGMP → vasodilation → hypotension and decreased pulmonary capillary wedge pressure