Makindo Medical Notes

Related Subjects: | Cardiac Anatomy and Physiology | Coronary Artery Anatomy and Physiology | Cardiac Electrophysiology | Cardiac Embryology

Cardiac Anatomy and Physiology

The heart is a muscular, cone-shaped organ located in the middle mediastinum of the thoracic cavity. Enclosed by the fibrous pericardium, it sits between the lungs and rests on the diaphragm. The heart is oriented obliquely, with the apex pointing downward and to the left, typically found at the 5th intercostal space along the mid-clavicular line. The base faces posteriorly toward the vertebral column.

Structural Overview

• Chambers: The heart consists of four chambers:
  • Right Atrium: Receives deoxygenated blood from the systemic circulation via the superior and inferior vena cava and the coronary sinus.
  • Right Ventricle: Pumps deoxygenated blood into the pulmonary arteries through the pulmonary valve, leading to the lungs for gas exchange.
  • Left Atrium: Receives oxygenated blood from the lungs via four pulmonary veins.
  • Left Ventricle: Pumps oxygenated blood into the systemic circulation through the aortic valve and aorta. It has the thickest muscular wall to generate high pressure for systemic circulation.
• Valves: Ensure unidirectional blood flow:
  • Atrioventricular (AV) Valves:
    • Tricuspid Valve: Between the right atrium and right ventricle.
    • Mitral (Bicuspid) Valve: Between the left atrium and left ventricle.
  • Semilunar Valves:
    • Pulmonary Valve: Between the right ventricle and pulmonary artery.
    • Aortic Valve: Between the left ventricle and aorta.

Heart Borders and Surfaces

• Right Border: Formed mainly by the right atrium.
• Left Border: Formed primarily by the left ventricle and partially by the left atrial appendage superiorly.
• Inferior (Diaphragmatic) Surface: Composed of both right and left ventricles; rests on the diaphragm.
• Base (Posterior Surface): Formed mainly by the left atrium, positioned anterior to the esophagus—important for transesophageal echocardiography.

Cardiac Physiology

The heart functions as a dual pump system, coordinating the pulmonary and systemic circulations. Its primary role is to maintain adequate blood flow to meet the metabolic demands of the body.

The Cardiac Cycle

The cardiac cycle consists of a series of events that occur during one heartbeat, divided into systole and diastole.

• Systole: Ventricular contraction phase where blood is ejected into the aorta and pulmonary artery. Includes:
  • Isovolumetric Contraction: Ventricles contract with no volume change; all valves are closed.
  • Ventricular Ejection: Semilunar valves open; blood is expelled into the arterial system.
• Diastole: Ventricular relaxation phase allowing ventricular filling. Includes:
  • Isovolumetric Relaxation: Ventricles relax; all valves are closed.
  • Ventricular Filling: AV valves open; blood flows from atria to ventricles.
  • Atrial Systole: Atria contract to complete ventricular filling.

Electrical Conduction System

The heart's rhythmic contractions are regulated by its intrinsic electrical conduction system.

• Sinoatrial (SA) Node: Primary pacemaker located in the right atrium; initiates impulses at ~60-100 beats per minute (bpm).
• Atrioventricular (AV) Node: Located at the atrioventricular junction; delays impulses to allow ventricular filling.
• Bundle of His: Pathway from AV node into the interventricular septum.
• Bundle Branches: Left and right branches transmit impulses to respective ventricles.
• Purkinje Fibers: Network of fibers that distribute impulses throughout ventricles, causing coordinated contraction.

Action Potentials in Cardiac Cells

Cardiac cells generate action potentials that differ between pacemaker cells and contractile myocytes.

Pacemaker Cells (SA and AV Nodes)

• Phase 4 (Spontaneous Depolarization): Slow influx of Na⁺ through "funny" channels (I_f) and Ca²⁺ through T-type calcium channels.
• Phase 0 (Depolarization): Influx of Ca²⁺ through L-type calcium channels triggers action potential.
• Phase 3 (Repolarization): Efflux of K⁺ returns the cell to resting potential.

Ventricular Myocytes

• Phase 0 (Rapid Depolarization): Sudden influx of Na⁺ through fast sodium channels.
• Phase 1 (Initial Repolarization): Transient outward K⁺ current.
• Phase 2 (Plateau Phase): Influx of Ca²⁺ balances K⁺ efflux, prolonging depolarization.
• Phase 3 (Repolarization): Increased K⁺ efflux repolarizes the cell.
• Phase 4 (Resting Potential): Resting membrane potential maintained by Na⁺/K⁺ ATPase pump.

Excitation-Contraction Coupling

• Depolarization opens voltage-gated L-type calcium channels during the plateau phase.
• Calcium influx triggers calcium release from the sarcoplasmic reticulum (calcium-induced calcium release).
• Calcium binds to troponin C, initiating cross-bridge cycling between actin and myosin filaments.
• Contraction occurs as sarcomeres shorten.
• Relaxation follows as calcium is re-sequestered into the sarcoplasmic reticulum by SERCA pumps and removed from the cell via the Na⁺/Ca²⁺ exchanger.

Cardiac Output and Hemodynamics

Cardiac Output (CO) is the volume of blood the heart pumps per minute and is calculated as:

CO = Stroke Volume (SV) × Heart Rate (HR)

• Stroke Volume: The amount of blood ejected with each ventricular contraction (approximately 70 mL at rest).
• Heart Rate: Beats per minute (average resting HR is about 70 bpm).
• Normal CO: Approximately 5 liters per minute at rest.

Factors Influencing Cardiac Output

• Preload: The degree of ventricular stretch due to end-diastolic volume; increased preload enhances SV via the Frank-Starling mechanism.
• Afterload: The resistance the ventricles must overcome to eject blood; increased afterload (e.g., hypertension) can decrease SV.
• Contractility: The intrinsic strength of myocardial contraction; influenced by sympathetic stimulation and circulating catecholamines.
• Heart Rate: Affects CO directly; however, excessively high HR can reduce ventricular filling time, decreasing SV.

Frank-Starling Law

States that the force of ventricular contraction increases with an increase in end-diastolic volume (within physiological limits), optimizing cardiac output based on venous return.

Coronary Circulation

• Left Coronary Artery (LCA): Divides into:
  • Left Anterior Descending (LAD) Artery: Supplies anterior interventricular septum and anterior walls of both ventricles.
  • Circumflex Artery: Supplies lateral and posterior walls of the left ventricle.
• Right Coronary Artery (RCA): Supplies right atrium, right ventricle, and, in most individuals, the inferior portion of the left ventricle via the posterior descending artery (PDA).
• Coronary Dominance: Determined by which artery gives rise to the PDA; right dominance is most common (~70%).

Systemic and Pulmonary Circulations

• The heart pumps equal volumes of blood into both circuits per beat.
• Systemic Circulation: High-pressure system (approximately 120/80 mmHg); supplies oxygenated blood to the body.
• Pulmonary Circulation: Low-pressure system (approximately 25/10 mmHg); facilitates gas exchange in the lungs.
• Pulmonary vascular resistance is about one-tenth that of systemic resistance.

Autonomic Regulation

• Sympathetic Nervous System: Increases HR, contractility, and conduction velocity via norepinephrine acting on β₁-adrenergic receptors.
• Parasympathetic Nervous System: Decreases HR and conduction velocity via acetylcholine acting on muscarinic receptors, primarily through the vagus nerve.

Exercise Physiology

During exercise, the cardiovascular system adapts to meet increased metabolic demands.

• Heart Rate: Increases due to sympathetic activation and reduced parasympathetic tone; can rise from 70 bpm to over 150 bpm.
• Stroke Volume: Increases due to enhanced venous return and myocardial contractility; may double from 70 mL to 140 mL.
• Cardiac Output: Can increase up to 5-6 times resting levels, reaching 20-25 L/min in healthy adults.
• Blood Flow Redistribution: Increased flow to skeletal muscles and skin; reduced flow to non-essential organs.

Measuring Cardiac Output

• Thermodilution Technique: Involves injecting a cold saline bolus via a pulmonary artery catheter and measuring temperature changes to calculate CO.
• Esophageal Doppler: Uses ultrasound to measure blood flow velocity in the descending aorta; estimates CO based on flow and cross-sectional area.
• Fick Principle: Calculates CO based on oxygen consumption and arteriovenous oxygen content difference.

Cellular Mechanisms of Cardiac Contraction

• Excitation-Contraction Coupling: Dependent on calcium influx and release from the sarcoplasmic reticulum.
• Calcium-Induced Calcium Release (CICR): Calcium entry through L-type channels triggers further calcium release from the sarcoplasmic reticulum.
• Role of Calcium: Binds to troponin C, causing conformational changes that allow actin-myosin cross-bridge formation and contraction.
• Relaxation: Calcium is reabsorbed into the sarcoplasmic reticulum and extruded from the cell, leading to muscle relaxation.

Pharmacological Influence

• Positive Inotropes: Increase contractility (e.g., digoxin enhances intracellular calcium).
• Negative Inotropes: Decrease contractility (e.g., β-blockers reduce sympathetic stimulation).
• Chronotropes: Affect heart rate; positive chronotropes increase HR, negative chronotropes decrease HR.
• Dromotropes: Affect conduction velocity through the AV node.

Clinical Correlations

• Heart Failure: Impaired ability of the heart to pump blood effectively; may involve systolic or diastolic dysfunction.
• Arrhythmias: Abnormal heart rhythms due to conduction system disturbances; can lead to inadequate cardiac output.
• Ischemic Heart Disease: Reduced blood flow to the myocardium due to coronary artery disease; can cause angina or myocardial infarction.
• Valvular Heart Diseases: Dysfunction of heart valves affecting blood flow direction and efficiency.

Summary

The heart's anatomy and physiology are intricately designed to ensure efficient circulation of blood throughout the body. Understanding cardiac function—from the cellular mechanisms of contraction to the systemic regulation of heart rate and blood pressure—is essential for recognizing how various factors and diseases can impact cardiovascular health.