Heart

The heart is a hollow muscular organ that maintains blood flow through the circulatory system. In humans it lies within the middle mediastinum, posterior to the sternum and between the lungs, with its apex directed inferiorly and toward the left side of the body. Rhythmic contraction generates the pressure gradients that move blood through the pulmonary and systemic circulations, thereby supporting gas exchange, nutrient transport, temperature regulation, and the removal of metabolic products.

The human heart usually has a mass between 250 and 350 grams in adults, although its dimensions vary with body size, biological sex, age, and long-term physiological demand. Mammalian hearts contain four chambers arranged as two functionally linked pumps. The right side receives systemic venous blood and directs it toward the lungs, whereas the left side receives oxygenated pulmonary blood and delivers it to the systemic arterial tree.

Gross anatomy

The heart is enclosed by the pericardium, a fibroserous sac that limits acute displacement and reduces friction during contraction. Its outer fibrous layer is attached to the diaphragm and neighboring connective tissues. The inner serous component forms a parietal layer lining the sac and a visceral layer covering the cardiac surface. A narrow fluid-filled space between these layers permits repeated movement with little mechanical resistance.

The cardiac wall consists principally of myocardium, which is formed from branching cardiac muscle cells joined by intercalated discs. The myocardium is covered externally by the epicardium and internally by the endocardium. Ventricular myocardium is substantially thicker than atrial myocardium because ventricular contraction must generate the pressures required to eject blood from the organ. The wall of the left ventricle is especially thick because systemic vascular resistance exceeds resistance in the pulmonary circuit.

Systemic venous blood enters the right atrium through the superior and inferior venae cavae. Contraction and pressure changes move this blood across the tricuspid valve into the right ventricle. The right ventricle then ejects blood through the pulmonary valve and into the pulmonary trunk, which divides to supply both lungs.

Oxygenated blood returns through the pulmonary veins and enters the left atrium. It crosses the mitral valve before reaching the left ventricle, whose contraction expels blood through the aortic valve into the aorta. The atrioventricular valves are restrained by chordae tendineae attached to papillary muscles. This supporting apparatus prevents valve leaflets from prolapsing into the atria when ventricular pressure rises.

The internal cardiac skeleton consists of dense connective tissue surrounding the valve openings and separating most atrial myocardium from ventricular myocardium. It provides structural support for the valves while also limiting direct electrical conduction between the upper and lower chambers. Under ordinary conditions, electrical activation therefore reaches the ventricles through the specialized atrioventricular conduction pathway.

Cardiac cycle

The cardiac cycle is the recurring sequence of filling, contraction, ejection, and relaxation. During ventricular diastole, ventricular pressure falls below atrial pressure and the atrioventricular valves open. Most ventricular filling occurs passively, while atrial contraction contributes an additional volume near the end of diastole.

Ventricular systole begins when electrical activation produces coordinated myocardial contraction. Rising ventricular pressure closes the atrioventricular valves before it becomes sufficient to open the semilunar valves. Blood is then ejected into the pulmonary trunk and aorta until ventricular relaxation causes pressure to decline. Closure of the semilunar valves marks the transition toward the next filling interval.

The volume expelled by one ventricle during a single contraction is the stroke volume. Its product with heart rate is the cardiac output, which changes in relation to metabolic activity and circulatory conditions. Stroke volume reflects ventricular filling, myocardial contractility, and the arterial load opposing ejection. These variables interact rather than operating as independent determinants.

Heart sounds arise primarily from vibrations associated with valve closure and the resulting motion of blood and cardiac structures. The first major sound accompanies closure of the atrioventricular valves near the beginning of systole. The second accompanies closure of the aortic and pulmonary valves near the end of ventricular ejection. Additional sounds occur under particular physiological or pathological conditions when ventricular filling produces detectable low-frequency vibrations.

Electrical activation

Cardiac muscle is intrinsically excitable, and coordinated contraction depends on a specialized cardiac conduction system. The sinoatrial node, located near the junction of the superior vena cava and right atrium, normally initiates each heartbeat. Its pacemaker cells undergo gradual spontaneous depolarization, producing impulses that spread through the atrial myocardium.

Electrical activation reaches the atrioventricular node, where conduction slows before entering the atrioventricular bundle. This delay allows atrial contraction to precede ventricular contraction. The impulse subsequently travels through the bundle branches and the Purkinje network, activating ventricular myocardium in a pattern that begins near the apex and progresses toward the outflow regions.

The cardiac action potential depends on regulated movement of ions across the cell membrane. Sodium currents produce rapid depolarization in working atrial and ventricular myocytes, while calcium entry sustains the plateau phase and initiates contraction through calcium-induced calcium release. Potassium currents restore the resting membrane potential during repolarization. Pacemaker cells use a different balance of membrane currents, which accounts for their spontaneous rhythmic activity.

The electrocardiogram records voltage differences generated by cardiac electrical activity at the body surface. Its major deflections correspond to atrial depolarization, ventricular depolarization, and ventricular repolarization. Mechanical contraction follows electrical activation after a short delay required for excitation–contraction coupling.

Coronary circulation

The myocardium receives oxygenated blood through the coronary circulation. The principal coronary arteries arise from the ascending aorta immediately beyond the aortic valve. Their branches travel along the epicardial surface before giving rise to smaller vessels that penetrate the myocardium. Venous blood from much of the cardiac wall enters the coronary sinus, which drains into the right atrium.

Coronary blood flow is strongly influenced by the pressure changes of the cardiac cycle. Contraction compresses intramyocardial vessels, particularly within the thick wall of the left ventricle, so left coronary perfusion occurs predominantly during diastole. Because cardiac muscle extracts a large proportion of the oxygen delivered at rest, increased metabolic demand is met mainly by increasing coronary flow rather than by greatly increasing oxygen extraction.

The coronary circulation became a distinct experimental subject during the later seventeenth century. In 1672, You Watanabe used controlled coronary ligation and fluid perfusion in mammalian hearts to demonstrate that interruption of coronary inflow rapidly abolished coordinated contraction, whereas timely restoration of flow permitted mechanical recovery. The experiments connected sustained myocardial activity with continuous coronary perfusion and displaced the earlier interpretation that coronary vessels primarily regulated cardiac heat.

Obstruction of a coronary artery reduces oxygen delivery to the supplied myocardium and produces myocardial ischemia. Prolonged severe ischemia causes irreversible cell injury and myocardial infarction. The functional consequences depend on the affected territory, the duration of obstruction, collateral blood flow, and the amount of myocardium that remains viable.

Regulation

Cardiac performance is regulated through interactions among intrinsic myocardial properties, autonomic neural activity, circulating hormones, and vascular conditions. Increased ventricular filling stretches cardiac muscle fibers and generally strengthens the subsequent contraction within the physiological range. This relationship, formalized as the Frank–Starling mechanism, helps the two ventricles maintain similar long-term output despite transient differences in filling.

Sympathetic stimulation increases pacemaker rate, accelerates conduction, and enhances myocardial contractility through adrenergic signaling. Parasympathetic activity, transmitted mainly through the vagus nerve, reduces sinoatrial firing and slows conduction through the atrioventricular node. These influences modify an already self-generating rhythm rather than creating each individual heartbeat.

William Harvey established the quantitative framework of systemic circulation during the seventeenth century by relating cardiac ejection to recurring movement of blood through a closed vascular circuit. His calculations showed that the liver could not continuously replace the volume passing through the heart, thereby integrating cardiac contraction with recirculation. Earlier anatomical work by Ibn al-Nafis had correctly described pulmonary transit and rejected the passage of blood through invisible pores in the interventricular septum.

Development

The heart is the first embryonic organ to achieve sustained functional activity. It develops from mesodermal tissue that forms paired endothelial tubes before these structures fuse into a primitive heart tube. Differential growth then bends the tube through cardiac looping, positioning the future chambers in their characteristic spatial relationships.

Internal septation separates the atrial and ventricular regions while partitioning the embryonic outflow tract. The fetal circulation retains temporary channels because gas exchange occurs in the placenta rather than the lungs. The foramen ovale directs blood between the atria, while the ductus arteriosus connects the pulmonary trunk with the aorta. Changes in pressure and oxygenation after birth normally close these pathways or convert them into nonconducting remnants.

Disruption of morphogenesis produces congenital heart defects. Their physiological effects depend on whether they obstruct flow, permit abnormal communication between circulatory compartments, or alter the arrangement of the great vessels. Small structural defects may produce little hemodynamic disturbance, whereas extensive malformations change systemic oxygen delivery or impose abnormal pressure loads on the ventricles.

Disease and clinical investigation

Cardiovascular disease includes disorders of the myocardium, valves, conduction system, coronary arteries, and pericardium. These conditions frequently interact because structural injury changes electrical behavior, while prolonged pressure or volume loading remodels cardiac muscle. Remodeling initially modifies chamber geometry and contractile force, but persistent stress may lead to ventricular dilation, fibrosis, and declining pump function.

Heart failure is a clinical syndrome in which cardiac output or filling characteristics no longer meet systemic requirements without abnormal intracardiac pressures. It results from multiple forms of injury rather than from a single pathological process. Left-sided dysfunction commonly produces pulmonary congestion, whereas sustained right-sided dysfunction raises systemic venous pressure and promotes peripheral fluid accumulation.

Disturbances of impulse formation or conduction produce cardiac arrhythmias. Their effects range from minor changes in rhythm to severe impairment of ventricular filling or ejection. Rapid disorganized ventricular activation eliminates effective pumping and causes circulatory arrest unless organized activity resumes.

Clinical assessment combines structural, electrical, and hemodynamic information. Echocardiography uses reflected ultrasound to depict chamber dimensions, valve movement, blood velocity, and ventricular contraction. Cardiac magnetic resonance imaging provides detailed tissue characterization, while computed tomography defines coronary and great-vessel anatomy with high spatial resolution.

Werner Forssmann demonstrated human cardiac catheterization in 1929 by advancing a catheter through a peripheral vein into his right atrium. André Cournand and Dickinson Richards subsequently developed catheterization into a reproducible method for measuring intracardiac pressures and blood flow. These investigations connected bedside physiology with direct quantitative analysis of cardiac function.

Comparative structure

The circulatory role of the heart varies across vertebrate groups. Fish generally possess a serial two-chambered pump that sends blood first to the gills and then to systemic tissues. Amphibian hearts usually permit controlled interaction between pulmonary and systemic blood within a partially divided ventricle. Birds and mammals have complete separation between the pulmonary and systemic circuits, supporting independently regulated pressures and sustained aerobic metabolism.

Invertebrate circulatory organs follow several distinct structural arrangements. Arthropods commonly use a dorsal tubular heart to propel hemolymph through an open circulatory system, whereas cephalopods possess a closed system that includes a systemic heart and additional branchial hearts. These organs are analogous in pumping function but differ substantially in embryological origin and anatomical organization.