The heart operates as a dual-pump system driven by pressure gradients and electrical stimulation. Hemodynamics involves the physical principles governing blood flow through the circulatory system. Cardiac output depends directly on stroke volume and heart rate. Stroke volume relies on three distinct variables:
A failure in any of these components alters tissue perfusion and triggers compensatory neurohormonal mechanisms.
Atherosclerosis begins with endothelial injury inside the arterial wall. This injury allows low-density lipoproteins to slip beneath the endothelial lining, where they undergo oxidation. Macrophages engulf these oxidized lipids and transform into foam cells, creating the foundational fatty streak.
Over time, smooth muscle cells proliferate, forming a fibrous cap over a lipid-rich necrotic core. Vulnerable plaques feature thin fibrous caps that rupture easily. Once a plaque ruptures, platelets aggregate at the site, triggering rapid thrombus formation and obstructing coronary blood flow.
Heart failure occurs when the myocardium fails to pump blood effectively to meet the metabolic demands of body tissues. In systolic dysfunction, the left ventricle loses its contractile strength, resulting in a reduced ejection fraction. Diastolic dysfunction involves impaired ventricular relaxation and filling, even though the ejection fraction may remain normal.
To compensate for failing output, the body activates the sympathetic nervous system and the renin-angiotensin-aldosterone system. While these systems temporarily boost blood pressure and cardiac output, chronic activation causes ventricular remodeling, myocardial hypertrophy, and progressive cellular death.
Sustained high blood pressure damages arterial walls through constant mechanical stress. Elevated systemic vascular resistance forces the smooth muscle cells in arterial walls to hypertrophy and multiply, narrowing the lumen further. This vascular remodeling perpetuates the hypertensive state in a destructive feedback loop.
Endothelial dysfunction also impairs the release of local vasodilators like nitric oxide while increasing vasoconstrictors such as endothelin. Over time, target organs like the kidneys, brain, and retina suffer ischemic damage from this ongoing microvascular disease.
Normal heart rhythms rely on synchronized electrical impulse generation and propagation through specialized conduction pathways. Arrhythmias arise from disturbances in impulse formation, impulse conduction, or a combination of both.
Heart valves ensure unidirectional blood flow through the chambers. Valvular dysfunction generally manifests as stenosis or regurgitation. Stenosis involves the narrowing of the valve opening due to leaflet thickening, fusion, or calcification, which forces the upstream chamber to work harder to push blood through.
Regurgitation, or insufficiency, occurs when valve leaflets fail to close completely, allowing blood to flow backward. Common causes include rheumatic fever, infective endocarditis, and age-related degenerative calcification. Both conditions eventually lead to chamber enlargement and heart failure.
Pathological changes in the cardiovascular system translate into recognizable clinical signs. Left-sided heart failure typically presents with pulmonary congestion, dyspnea, orthopnea, and crackles in the lung bases. Right-sided heart failure causes systemic congestion, manifested by jugular venous distension, peripheral edema, and hepatomegaly.
Nurses must monitor vital signs, track fluid balance, assess peripheral pulses, and recognize early signs of low cardiac output. Patient education on medication adherence, sodium restriction, and daily weight monitoring remains vital to prevent acute decompensation and hospital readmissions.