Congestive heart failure can be classified into two major categories based on ejection fraction: systolic heart failure with an ejection fraction < 40% and diastolic heart failure with an ejection fraction > 55%. Ejection fraction (EF) can be precisely measured using a cardiac ultrasound.
Systolic heart failure is characterized by reduced cardiac contractility leading to reduced EF, increased end-diastolic pressure, and increased EDV. Systolic heart failure can arise from conditions like coronary artery disease, which induces cardiac ischemia leading to decreased contractility, acute coronary syndrome such as acute MI with myocardial scarring, and dilated cardiomyopathy. Additional causes include valvular insufficiency (like aortic or mitral regurgitation) and left-to-right shunts (like ventricular septal defect), both of which lead to volume overload. Systolic heart failure is associated with increased preload, and causes eccentric hypertrophy (sarcomeres add in series) in response to volume-overload states.
Diastolic heart failure features reduced ventricular compliance but preserves normal diastolic volumes. This results in increased end-diastolic pressure. Common etiologies include long-standing hypertension (most common) and aortic stenosis, which induce pressure overload leading to left. Hypertrophic obstructive cardiomyopathy (HOCM) also causes diastolic heart failure due to isolated ventricular septum hypertrophy and LVOT obstruction. Restrictive cardiomyopathy & constrictive pericarditis, as well as coronary artery disease can also lead to diastolic heart failure, all of which cause a non-compliant ventricle. In response to increased afterload, such as from chronic hypertension or valvular stenosis, the heart undergoes concentric hypertrophy, where sarcomeres add in parallel. This form of heart failure with concentric hypertrophy is marked by decreased chamber size and increased wall thickness. In cases of restrictive cardiomyopathy and constrictive pericarditis, diastolic heart failure presents with a normal chamber size and wall thickness.
In both types of heart failure, decreased cardiac output activates compensatory mechanisms, including increased sympathetic activation and RAAS activation. The surge in sympathetic response increases heart rate & contractility, and prompts vasoconstriction, which increases systemic vascular resistance (SVR). The activated RAAS pathway further enhances vasoconstriction through increased angiotensin II production, and promotes salt and water retention due to elevated aldosterone levels. Decreased CO also results increases ADH activity, which increases free water retention.
When the heart experiences stress, it releases natriuretic peptides, specifically ANP from stretched atrial cardiomyocytes and BNP from ventricular cardiomyocytes. These peptides achieve several cardiac-relief functions. Firstly, they induce vasodilation, effectively reducing afterload. They also promote natriuresis, leading to diuresis, which in turn decreases preload. By inhibiting renin production, these peptides decrease aldosterone levels, amplifying the natriuretic and diuretic effects. Additionally, they instigate efferent arteriolar vasoconstriction, thus increases GFR which further supports diuresis.
Despite these protective responses, the cardiac remodeling driven by long-term neurohormonal activation (like RAAS, ADH, and sympathetic activation) combined with increased hemodynamic stress, proves detrimental. This remodeling, in turn, can further diminish cardiac output. Consequently, these compensatory mechanisms often lead to a cycle of further decreased cardiac output, exacerbating pulmonary and peripheral edema, and ultimately, deleterious cardiac remodeling.
Systolic heart failure, or heart failure with reduced ejection fraction, is characterized by the heart's inability to pump blood effectively during systole due to reduced cardiac contractility, and is typically associated with an ejection fraction < 40%. Diastolic heart failure, also referred to as heart failure with preserved ejection fraction, is characterized by the heart's inability to fill with blood adequately during diastole due to reduced ventricular compliance. It usually presents with an ejection fraction greater than 55%.
Coronary artery disease can adversely affect both systolic and diastolic of the heart. Systolic heart failure occurs when ischemia, secondary to coronary artery disease, impairs the myocardium's ability to contract effectively, leading to reduced ejection fraction. On the other hand, diastolic heart failure arises when ischemia makes the ventricular walls stiff and less compliant, thereby hindering proper filling during diastole. Both forms of heart failure result in inadequate cardiac output and the symptoms associated with heart failure.
When cardiomyocytes are stretched, BNP and ANP are released as part of a compensatory response aimed at mitigating heart failure. These peptides exert multifaceted effects: they induce vasodilation, reducing afterload; facilitate natriuresis, thereby aiding diuresis and lowering preload; inhibit renin secretion, which subsequently decreases aldosterone levels; and constrict efferent arterioles to enhance glomerular filtration rate (GFR), further contributing to natriuresis and diuresis.
Heart failure is associated with decreased cardiac output, stimulating compensatory mechanisms like sympathetic activation (leading to increased heart rate, cardiac contractility, and vasoconstriction), renin-angiotensin-aldosterone system (RAAS) activation (causing salt and water retention), and antidiuretic hormone (ADH) activation (leading to increased free water retention). While these mechanisms attempt to improve cardiac output, they can exacerbate heart failure by increasing afterload and preload, thus inducing further cardiac strain and leading to deleterious cardiac remodeling over time.
Diastolic heart failure is often associated with conditions that impair ventricular relaxation or increase ventricular stiffness, leading to inadequate filling during diastole. Hypertension is a prevalent underlying factor, as chronic elevated blood pressure imposes a greater workload on the heart, leading to left ventricular hypertrophy. Other common conditions include diabetes mellitus, ischemic heart disease, and age-related degenerative changes. Valvular diseases like aortic stenosis and certain cardiomyopathies such as restrictive or hypertrophic cardiomyopathy can also contribute to diastolic dysfunction. Overall, these conditions compromise the heart's ability to fill adequately during diastole, leading to symptoms of heart failure.