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. Encased in the fibrous pericardium, it rests between the lungs on the diaphragm. Oriented obliquely, the heart’s apex points downward and to the left—typically at the 5th intercostal space along the mid-clavicular line—while its base faces posteriorly toward the vertebral column.

Structural Overview

• Chambers: The heart consists of four chambers:
  • Right Atrium: Receives deoxygenated blood from systemic circulation via the superior and inferior vena cava and the coronary sinus.
  • Right Ventricle: Pumps deoxygenated blood through the pulmonary valve into the pulmonary arteries for gas exchange in the lungs.
  • Left Atrium: Receives oxygenated blood from the lungs through four pulmonary veins.
  • Left Ventricle: Pumps oxygenated blood into systemic circulation via the aortic valve and aorta. Its thick muscular wall generates the high pressure required for systemic perfusion.
• 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: Mainly formed by the right atrium.
• Left Border: Primarily formed by the left ventricle, with a minor contribution from the left atrial appendage superiorly.
• Inferior (Diaphragmatic) Surface: Composed of both the right and left ventricles, resting on the diaphragm.
• Base (Posterior Surface): Mainly formed by the left atrium and positioned anterior to the esophagus—a key landmark in transesophageal echocardiography.

Cardiac Physiology

The heart acts as a dual pump, coordinating both pulmonary and systemic circulations to meet the body’s metabolic demands.

The Cardiac Cycle

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

• Systole: The ventricular contraction phase during which blood is ejected into the aorta and pulmonary artery. This phase includes:
  • Isovolumetric Contraction: Ventricular contraction occurs with no change in volume, as all valves are closed.
  • Ventricular Ejection: The semilunar valves open, allowing blood to flow into the arterial system.
• Diastole: The ventricular relaxation phase, allowing filling of the ventricles. This phase includes:
  • Isovolumetric Relaxation: Ventricles relax with all valves closed.
  • Ventricular Filling: The AV valves open, permitting blood flow from the atria into the ventricles.
  • Atrial Systole: Atrial contraction completes ventricular filling.

Electrical Conduction System

The heart’s rhythmic contractions are regulated by an intrinsic electrical conduction system:

• Sinoatrial (SA) Node: The primary pacemaker located in the right atrium, initiating impulses at 60–100 beats per minute.
• Atrioventricular (AV) Node: Located at the AV junction, it delays impulses to allow for complete ventricular filling.
• Bundle of His: Transmits impulses from the AV node into the interventricular septum.
• Bundle Branches: Right and left branches that convey impulses to their respective ventricles.
• Purkinje Fibers: A network that distributes impulses throughout the ventricles, ensuring coordinated contraction.

Action Potentials in Cardiac Cells

Cardiac cells generate action potentials with distinct profiles in pacemaker cells versus contractile myocytes.

Pacemaker Cells (SA and AV Nodes)

• Phase 4 (Spontaneous Depolarization): A gradual influx of Na⁺ via "funny" channels (I_f) and Ca²⁺ through T-type channels slowly depolarizes the cell.
• Phase 0 (Depolarization): A rapid influx of Ca²⁺ through L-type channels initiates the action potential.
• Phase 3 (Repolarization): Efflux of K⁺ returns the cell to its resting potential.

Ventricular Myocytes

• Phase 0 (Rapid Depolarization): Fast sodium channels open, allowing a rapid influx of Na⁺.
• Phase 1 (Initial Repolarization): A transient outward K⁺ current initiates repolarization.
• Phase 2 (Plateau Phase): A balance between Ca²⁺ influx and K⁺ efflux maintains depolarization.
• Phase 3 (Repolarization): Increased K⁺ efflux restores the resting membrane potential.
• Phase 4 (Resting Potential): The Na⁺/K⁺ ATPase pump maintains the resting potential.

Excitation-Contraction Coupling

• Depolarization opens L-type calcium channels during the plateau phase.
• Calcium influx triggers further calcium release from the sarcoplasmic reticulum (calcium-induced calcium release).
• Calcium binds to troponin C, initiating actin-myosin cross-bridge cycling and contraction.
• Relaxation occurs as calcium is re-sequestered by SERCA pumps and extruded via the Na⁺/Ca²⁺ exchanger.

Cardiac Output and Hemodynamics

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

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

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

Factors Influencing Cardiac Output

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

Frank-Starling Law

This principle states that, within physiological limits, the force of ventricular contraction increases as the end-diastolic volume rises, optimizing cardiac output relative to venous return.

Coronary Circulation and Blood Flow Regulation

• Left Coronary Artery (LCA): Divides into:
  • Left Anterior Descending (LAD) Artery: Supplies the anterior interventricular septum and the anterior walls of both ventricles.
  • Circumflex Artery: Supplies the lateral and posterior walls of the left ventricle.
• Right Coronary Artery (RCA): Supplies the right atrium, right ventricle, and—via the posterior descending artery (PDA)—typically the inferior portion of the left ventricle.
• Coronary Dominance: Determined by which artery gives rise to the PDA, with right dominance being most common (approximately 70%).
• Blood Flow Regulation: Coronary blood flow is autoregulated by local metabolic factors (e.g., adenosine), endothelial-derived substances (such as nitric oxide), and neural influences to ensure adequate myocardial oxygenation.

Autonomic Regulation

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

Neurohormonal Regulation

Beyond the autonomic nervous system, several hormonal systems play crucial roles in regulating cardiovascular function:

• Renin-Angiotensin-Aldosterone System (RAAS): Activation of RAAS increases blood pressure and blood volume through vasoconstriction and sodium/water retention. Chronic RAAS activation is implicated in heart failure and hypertension.
• Natriuretic Peptides: Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) are released in response to increased cardiac wall stress; they promote vasodilation and diuresis, counteracting RAAS.
• Vasopressin (ADH): Contributes to water retention and vasoconstriction, further influencing blood pressure and volume.

Exercise Physiology

• Heart Rate: Rises due to increased sympathetic activity and reduced parasympathetic tone, potentially exceeding 150 bpm.
• Stroke Volume: Increases with enhanced venous return and myocardial contractility, potentially doubling from 70 mL to 140 mL.
• Cardiac Output: May increase up to 5–6 times the resting level, reaching 20–25 L/min in healthy adults.
• Blood Flow Redistribution: Enhanced perfusion to skeletal muscles and skin occurs, while blood flow to nonessential organs is reduced.

Cardiac Imaging and Diagnostics

• Electrocardiography (ECG): Records the electrical activity of the heart and helps detect arrhythmias, ischemia, and conduction abnormalities.
• Echocardiography: Uses ultrasound to visualize heart chambers, valves, and wall motion; Doppler techniques assess blood flow.
• Cardiac Magnetic Resonance Imaging (MRI): Provides high-resolution images for detailed evaluation of cardiac structure, function, and tissue characterization.
• Computed Tomography (CT) Angiography: Visualizes coronary anatomy and detects calcifications or stenoses.
• Nuclear Imaging: Techniques such as myocardial perfusion scintigraphy evaluate blood flow and viability of cardiac tissue.

Measuring Cardiac Output

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

Cellular Mechanisms of Cardiac Contraction

• Excitation-Contraction Coupling: Depends on calcium influx and subsequent 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: Binding to troponin C initiates actin-myosin cross-bridge formation and contraction.
• Relaxation: Occurs as calcium is reabsorbed into the sarcoplasmic reticulum and extruded from the cell.

Pharmacological Influence

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

Clinical Correlations

• Heart Failure: A condition in which the heart cannot pump blood effectively, involving systolic or diastolic dysfunction. Neurohormonal activation and remodeling further complicate this pathology.
• Arrhythmias: Abnormal heart rhythms due to conduction disturbances that may compromise cardiac output.
• Ischemic Heart Disease: Reduced myocardial blood flow from coronary artery disease, potentially causing angina or myocardial infarction.
• Valvular Heart Diseases: Dysfunction of heart valves that disrupts normal blood flow.
• Cardiac Murmurs and Heart Sounds: Abnormal heart sounds (such as S3 and S4 gallops or split S2) may indicate underlying pathology, including valvular disorders and ventricular dysfunction.

Summary

The heart’s intricate anatomy and physiology ensure the efficient circulation of blood throughout the body. A comprehensive understanding—from cellular contraction mechanisms to systemic hemodynamic and neurohormonal regulation—is essential for appreciating how various factors and diseases impact cardiovascular health.