The Cardiovascular System: The Heart – Structure, Function, and Physiology

The Cardiovascular System: The Heart

Heart Anatomy and Location

The heart is a muscular organ responsible for pumping blood throughout the body. It is located in the mediastinum, resting on the superior surface of the diaphragm, with two-thirds of its mass to the left of the midsternal line. The heart lies anterior to the vertebral column and posterior to the sternum.

• Size: Approximately the size of a fist.

• Enclosure: The heart is enclosed in the pericardium, a double-walled sac that protects, anchors, and prevents overfilling.

Pericardium and Heart Wall Layers

The pericardium consists of two main layers: the superficial fibrous pericardium and the deep serous pericardium. The serous pericardium is further divided into the parietal and visceral (epicardium) layers, separated by the fluid-filled pericardial cavity, which reduces friction during heartbeats.

• Epicardium: Visceral layer of the serous pericardium.

• Myocardium: Composed of spiral bundles of cardiac muscle cells and the fibrous skeleton of the heart, which anchors muscle fibers, supports valves, and limits the spread of action potentials.

• Endocardium: Continuous with the endothelial lining of blood vessels.

Chambers of the Heart

The heart contains four chambers: two atria (receiving chambers) and two ventricles (discharging chambers). The atria are separated by the interatrial septum, and the ventricles by the interventricular septum. Externally, the coronary sulcus separates the atria from the ventricles, and auricles increase atrial volume.

• Atria: Right atrium receives blood from the superior and inferior vena cava and the coronary sinus; left atrium receives blood from the right and left pulmonary veins.

• Ventricles: Right ventricle pumps blood into the pulmonary trunk; left ventricle pumps blood into the aorta.

Internal Features of the Heart

The walls of the atria are ridged by pectinate muscles (mainly in the right atrium), while the walls of the ventricles are ridged by trabeculae carneae. Papillary muscles project into the ventricular cavities and are attached to the atrioventricular (AV) valves via chordae tendineae.

Pathway of Blood Through the Heart

The heart functions as two side-by-side pumps: the right side pumps blood through the pulmonary circuit (to and from the lungs), and the left side pumps blood through the systemic circuit (to and from body tissues).

• Right atrium → tricuspid valve → right ventricle → pulmonary semilunar valve → pulmonary trunk → pulmonary arteries → lungs → pulmonary veins → left atrium → bicuspid (mitral) valve → left ventricle → aortic semilunar valve → aorta → systemic circulation

Coronary Circulation

Coronary circulation provides the functional blood supply to the heart muscle itself. The arterial supply varies and contains many anastomoses (junctions) among branches, providing collateral routes for blood delivery. Major arteries include the right and left coronary arteries, which branch into the marginal, circumflex, and anterior/posterior interventricular arteries. Venous blood is collected by the great, middle, and small cardiac veins, which join to form the coronary sinus.

Heart Valves

Heart valves ensure unidirectional blood flow through the heart. The atrioventricular (AV) valves (tricuspid and mitral) prevent backflow into the atria when the ventricles contract. The semilunar (SL) valves (aortic and pulmonary) prevent backflow into the ventricles when the ventricles relax. Chordae tendineae anchor AV valve cusps to papillary muscles.

Microscopic Anatomy of Cardiac Muscle

Cardiac muscle cells are striated, short, branched, and interconnected. They contain numerous large mitochondria and are connected by intercalated discs, which contain desmosomes (prevent cell separation during contraction) and gap junctions (allow ions to pass, electrically coupling cells). This structure allows the heart to function as a functional syncytium (all cells contract together).

Cardiac Muscle Contraction

Cardiac muscle contraction is initiated by depolarization, which is rhythmic and spontaneous. About 1% of cardiac cells are self-excitable (automaticity). Depolarization opens voltage-gated fast Na+ channels, causing a reversal of membrane potential. The depolarization wave in T tubules causes the sarcoplasmic reticulum (SR) to release Ca2+, and slow Ca2+ channels in the sarcolemma prolong the depolarization phase (plateau).

• Depolarization: Na+ influx through fast voltage-gated channels.

• Plateau phase: Ca2+ influx through slow channels keeps the cell depolarized.

Intrinsic Cardiac Conduction System

The intrinsic conduction system consists of noncontractile autorhythmic cells that initiate and distribute impulses to coordinate the depolarization and contraction of the heart. The sequence of excitation is as follows:

1. Sinoatrial (SA) node: Pacemaker; generates impulses about 75 times per minute.

2. Atrioventricular (AV) node: Delays impulses by ~0.1 second; depolarizes 50 times per minute without SA node input.

3. AV bundle (bundle of His): Only electrical connection between atria and ventricles.

4. Right and left bundle branches: Carry impulses toward the apex of the heart.

5. Purkinje fibers: Complete the pathway into the apex and ventricular walls.

Electrocardiography (ECG/EKG)

An electrocardiogram (ECG or EKG) is a composite recording of all the action potentials generated by nodal and contractile cells at a given time. It consists of three main waves:

• P wave: Depolarization of the SA node.

• QRS complex: Ventricular depolarization.

• T wave: Ventricular repolarization.

Heart Sounds and the Cardiac Cycle

Two main heart sounds ("lub-dup") are associated with the closing of heart valves. The first sound occurs as AV valves close (beginning of systole), and the second as SL valves close (beginning of ventricular diastole). The cardiac cycle includes all events associated with blood flow during one heartbeat, including systole (contraction) and diastole (relaxation).

Phases of the Cardiac Cycle

1. Ventricular filling: AV valves open; 80% of blood flows passively into ventricles, atrial systole delivers remaining 20% (end diastolic volume, EDV).

2. Ventricular systole: Atria relax, ventricles contract, AV valves close, SL valves open when ventricular pressure exceeds arterial pressure (end systolic volume, ESV).

3. Isovolumetric relaxation: Ventricles relax, SL valves close, causing a brief rise in aortic pressure (dicrotic notch).

Cardiac Output (CO)

Cardiac output is the volume of blood pumped by each ventricle in one minute.

• Formula: $CO = HR \times SV$

• Stroke Volume (SV): $SV = EDV - ESV$

• At rest: $CO = 75 \text{ beats/min} \times 70 \text{ ml/beat} = 5,250 \text{ ml/min} = 5.25 \text{ L/min}$

• Cardiac reserve: Difference between resting and maximal CO.

Regulation of Stroke Volume

Three main factors affect stroke volume:

Factor	Description
Preload	Degree of stretch of cardiac muscle cells before contraction (Frank-Starling law)
Contractility	Contractile strength at a given muscle length, independent of muscle stretch and EDV
Afterload	Pressure that must be overcome for ventricles to eject blood (force SL valves open)

• Preload: Increased by slow heartbeat and exercise (increases venous return and EDV).

• Contractility: Increased by positive inotropic agents (e.g., hormones, sympathetic stimulation); decreased by negative inotropic agents (e.g., acidosis, high K+, calcium channel blockers).

• Afterload: Increased by hypertension, resulting in increased ESV and reduced SV.

Regulation of Heart Rate

• Positive chronotropic factors: Increase heart rate (e.g., sympathetic stimulation, hormones).

• Negative chronotropic factors: Decrease heart rate (e.g., parasympathetic stimulation, medications).

• Autonomic nervous system: Sympathetic stimulation increases rate and force; parasympathetic stimulation (vagal tone) decreases rate.

• Atrial (Bainbridge) reflex: Increased venous return stretches atrial walls, stimulating the SA node and sympathetic reflexes.

• Other factors: Age, gender, exercise, and body temperature also influence heart rate.

Homeostatic Imbalances

• Angina pectoris: Thoracic pain due to fleeting deficiency in blood delivery to the myocardium; cells are weakened.

• Myocardial infarction (heart attack): Prolonged coronary blockage; areas of cell death are repaired with noncontractile scar tissue.

• Tachycardia: Abnormally fast heart rate (>100 bpm); may lead to fibrillation if persistent.

• Bradycardia: Heart rate slower than 60 bpm; may result in inadequate blood circulation but can be normal in athletes.

• Congestive heart failure (CHF): Progressive condition where CO is too low to meet tissue needs; caused by coronary atherosclerosis, high blood pressure, multiple myocardial infarcts, or dilated cardiomyopathy.

Developmental and Age-Related Changes

• Congenital heart defects: May lead to mixing of systemic and pulmonary blood or narrowed valves/vessels, increasing cardiac workload.

• Age-related changes: Sclerosis and thickening of valve flaps, decline in cardiac reserve, fibrosis of cardiac muscle, and atherosclerosis.