Chapter 18: The Cardiovascular System - The Heart

Overview of the Cardiovascular System: The Heart

• The heart functions as a transport system comprising two side-by-side pumps that serve distinct circuits:

  • Right Side: Receives oxygen-poor blood from body tissues and pumps it to the lungs to eliminate $CO_2$ and pick up $O_2$ through the pulmonary circuit. This circuit consists of arteries and veins carrying blood to and from the lungs.

  • Left Side: Receives oxygenated blood from the lungs and pumps it to body tissues to deliver $O_2$ and pick up $CO_2$ through the systemic circuit. This circuit involves blood vessels carrying blood to and from all body tissues.

• Internal Chambers:

  • Receiving Chambers: The right atrium receives blood from the systemic circuit; the left atrium receives blood from the pulmonary circuit.

  • Pumping Chambers: The right ventricle pumps blood through the pulmonary circuit; the left ventricle pumps blood through the systemic circuit.

Anatomy and Location of the Heart

• Size and Weight: The heart is roughly the size of a fist, hollow, cone-shaped, and weighs less than $1\,\text{lb}$.

• Location:

  • Situated in the mediastinum between the second rib and the fifth intercostal space.

  • Rests on the superior surface of the diaphragm, positioned between the sternum and the vertebral column.

  • Approximately $\frac{2}{3}$ of the heart's mass lies to the left of the midsternal line.

• Orientation:

  • Base: The broad, flat posterior surface directed toward the right shoulder.

  • Apex: Points toward the left hip.

  • Apical Impulse: Can be palpated between the fifth and sixth ribs, just below the left nipple.

The Pericardium and Heart Wall Layers

• Pericardium: A double-walled sac surrounding the heart.

  • Superficial Fibrous Pericardium: Functions to protect the heart, anchor it to surrounding structures, and prevent overfilling.

  • Serous Pericardium: A deep, double-layered membrane.

    • Parietal Layer: Lines the internal surface of the fibrous pericardium.

    • Visceral Layer (Epicardium): Lines the external surface of the heart.

  • Pericardial Cavity: The fluid-filled space between the parietal and visceral layers that decreases friction during heart movement.

• Homeostatic Imbalance — Pericarditis: Inflammation of the pericardium that causes membrane surfaces to roughen, leading to a "pericardial friction rub." Severe cases can lead to cardiac tamponade, where excess inflammatory fluid compresses the heart, limiting its pumping ability. Treatment involves drawing out fluid via a syringe.

• Layers of the Heart Wall:

  • Epicardium: The visceral layer of the serous pericardium.

  • Myocardium: The middle layer consisting of circular or spiral bundles of contractile cardiac muscle cells; the bulk of the heart wall.

    • Contains a non-excitable fibrous cardiac skeleton made of dense collagen and elastic fibers. It anchors muscle fibers, supports valves, and limits the spread of action potentials to specific pathways.

  • Endocardium: The innermost layer, continuous with the endothelial lining of blood vessels, lining heart chambers and covering valve skeletons.

Internal Heart Chambers and Great Vessels

• Internal Features:

  • Interatrial Septum: Separates the atria. It contains the fossa ovalis, a remnant of the fetal foramen ovale.

  • Interventricular Septum: Separates the ventricles.

• Atria (Receiving Chambers): Small, thin-walled chambers that contribute little to blood propulsion.

  • Auricles: Appendages that increase atrial volume.

  • Right Atrium: Receives blood via the superior vena cava (above diaphragm), inferior vena cava (below diaphragm), and coronary sinus (from myocardium).

  • Left Atrium: Receives blood from the lungs via four pulmonary veins. It contains pectinate muscles, primarily found in the auricles.

• Ventricles (Discharging Chambers): The actual pumps with much thicker walls than the atria.

  • Trabeculae Carneae: Irregular muscle ridges on internal walls.

  • Papillary Muscles: Project into the cavity and anchor the chordae tendineae (which in turn anchor valve cusps).

  • Right Ventricle: Pumps blood into the pulmonary trunk.

  • Left Ventricle: Pumps blood into the aorta, the largest artery in the body.

Cardiac Valves and Unidirectional Blood Flow

• Valves open and close in response to pressure changes to ensure unidirectional flow.

• Atrioventricular (AV) Valves: Prevent backflow into the atria during ventricular contraction.

  • Tricuspid Valve: Right AV valve with three cusps.

  • Mitral (Bicuspid) Valve: Left AV valve with two cusps.

  • Chordae Tendineae: Anchor valve flaps to papillary muscles to prevent eversion into the atria during systole.

• Semilunar (SL) Valves: Prevent backflow from major arteries into the ventricles during relaxation. Each has three crescent-shaped cusps.

  • Pulmonary Valve: Between the right ventricle and pulmonary trunk.

  • Aortic Valve: Between the left ventricle and aorta.

• Venous Junctions: No valves exist between major veins and the atria because the inertia of incoming blood and the compression of venous openings during contraction prevent significant backflow.

• Clinical Conditions:

  • Incompetent (Insufficient) Valve: Blood backflows, forcing the heart to repump the same blood.

  • Valvular Stenosis: Stiff flaps constrict the opening, forcing the heart to generate more force.

Hemodynamics of the Systemic and Pulmonary Circuits

• Both circuits pump equal volumes of blood, but the ventricles possess unequal workloads.

• Right Ventricle: Pumps into the shorter, low-resistance, low-pressure pulmonary circuit. It is crescent-shaped.

• Left Ventricle: Pumps into the longer, high-resistance, high-pressure systemic circuit. It is cylindrical and its walls are much thicker to generate greater pressure.

Coronary Circulation

• The functional blood supply of the heart, representing the body's shortest circulation. Blood is delivered primarily when the heart is relaxed.

• Arterial Supply:

  • Left Coronary Artery: Branches into the anterior interventricular artery (supplies the septum/anterior walls) and the circumflex artery (supplies the left atrium/posterior wall).

  • Right Coronary Artery: Branches into the right marginal artery (supplies the right side) and the posterior interventricular artery (supplies the posterior walls).

• Anastomoses: Junctions between arterial branches provide collateral routes but cannot compensate for sudden major occlusions.

• Venous Drainage: Cardiac veins collect blood; the coronary sinus empties it into the right atrium.

• Homeostatic Imbalances:

  • Angina Pectoris: Thoracic pain from temporary oxygen deficiency.

  • Myocardial Infarction (Heart Attack): Prolonged blockage leads to cell death and replacement with noncontractile scar tissue. Left ventricular damage is most critical.

Microscopic Anatomy of Cardiac Muscle

• Cardiac Myocytes: Short, fat, branched, interconnected cells with one or two central nuclei.

• Endomysium: Loose connective tissue connecting cells to the fibrous skeleton.

• Intercalated Discs: Contain desmosomes (structural integrity) and gap junctions (electrical coupling). This allows the heart to function as a functional syncytium.

• Metabolism: Numerous large mitochondria ($25\%$ to $35\%$ of cell volume) provide high fatigue resistance. Cardiac muscle is almost exclusively aerobic.

• Structure: Myofibrils contain sarcomeres (with Z discs, A bands, and I bands). The sarcoplasmic reticulum (SR) is simpler than in skeletal muscle, lacking triads, and T tubules are wider and enter at Z discs.

Comparison of Skeletal and Cardiac Muscle Physiology

• Similarities: Both use action potentials (AP), excitation-contraction coupling, and calcium binding to troponin for the sliding filament mechanism.

• Differences:

  • Automaticity: Approximately $1\%$ of cardiac cells are special pacemaker cells that spontaneously depolarize; no neural input is required for initiation.

  • Unit Contraction: Myocytes contract as a single unit or not at all (syncytium); skeletal units act independently.

  • Refractory Period: The absolute refractory period in cardiac muscle is nearly as long as the contraction itself, preventing tetanic contractions.

  • Calcium Source: Cardiac muscle uses both the SR and external influx from the extracellular fluid (ECF). ECF $Ca^{2+}$ triggers the release of $80\%$ to $90\%$ of the $Ca^{2+}$ stored in the SR.

  • Respiration: Cardiac muscle relies strictly on aerobic metabolism; skeletal muscle can sustain anaerobic activity.

The Intrinsic Conduction System and Pacemaker Physiology

• Pacemaker Potentials: Unstable resting potentials that continuously drift toward a threshold of $-40\,\text{mV}$.

• Action Potential Steps in Pacemaker Cells:

  1. Pacemaker Potential: $K^+$ channels close, slow $Na^+$ channels open, moving the potential toward threshold.

  2. Depolarization: At threshold, $Ca^{2+}$ channels open, causing a large influx of $Ca^{2+}$.

  3. Repolarization: $Ca^{2+}$ channels close, $K^+$ channels open, causing $K^+$ efflux.

• Sequence of Excitation:

  1. Sinoatrial (SA) Node: The primary pacemaker, depolarizing at approximately $75\,\text{beats\,min}^{-1}$ (sinus rhythm).

  2. Atrioventricular (AV) Node: Located in the inferior interatrial septum; delays the impulse by $0.1\,\text{s}$ to allow atria to finish contracting. Inherent rate is $50\,\text{beats\,min}^{-1}$.

  3. Atrioventricular (AV) Bundle (Bundle of His): The only electrical link between atria and ventricles.

  4. Right and Left Bundle Branches: Carry impulses down the interventricular septum.

  5. Subendocardial Conducting Network (Purkinje Fibers): Complete the pathway to the apex and ventricular walls. Contraction proceeds from the apex toward the atria. Inherent rate is $30\,\text{beats\,min}^{-1}$.

• Total time from SA node to complete ventricular depolarization is approximately $0.22\,\text{s}$.

Extrinsic Regulation and Clinical Rhythm Disorders

• Autonomic Control: The medulla oblongata contains heart centers.

  • Cardioacceleratory Center: Sends sympathetic signals to increase HR and force.

  • Cardioinhibitory Center: Sends parasympathetic signals via the vagus nerve to decrease HR.

• Homeostatic Imbalances:

  • Arrhythmias: Irregular heart rhythms.

  • Fibrillation: Rapid, uncoordinated contractions; circulation stops. Treated by defibrillation.

  • Ectopic Focus: An abnormal pacemaker (e.g., AV node setting a junctional rhythm of $40$ to $60\,\text{beats\,min}^{-1}$).

  • Extrasystole: Premature contraction often caused by caffeine or nicotine.

  • Heart Block: Failure of impulses to reach the ventricles due to AV node damage. Requires an artificial pacemaker.

Action Potentials in Contractile Cardiac Cells

• These cells make up the bulk of the heart wall.

• Action Potential Phases:

  1. Depolarization: Fast voltage-gated $Na^+$ channels open ($Na^+$ influx).

  2. Plateau Phase: Depolarization opens slow $Ca^{2+}$ channels. The influx of $Ca^{2+}$ prolongs the depolarization, ensuring efficient blood ejection and a long refractory period.

  3. Repolarization: $Ca^{2+}$ channels close, voltage-gated $K^+$ channels open ($K^+$ efflux).

Electrocardiography (ECG/EKG)

• A graphic recording of total electrical activity (not a single AP).

• Waves and Intervals:

  • P wave: Atrial depolarization.

  • QRS complex: Ventricular depolarization and atrial repolarization.

  • T wave: Ventricular repolarization.

  • P-R Interval: Time from the start of atrial depolarization to the start of ventricular depolarization.

  • S-T Segment: Entire ventricular myocardium is depolarized (plateau phase).

  • Q-T Interval: Duration of ventricular depolarization through repolarization.

• Diagnostic Value: Enlarged R waves suggest enlarged ventricles; S-T changes suggest ischemia; prolonged Q-T suggests repolarization abnormalities.

The Cardiac Cycle: Mechanical Phases

• Systole: Contraction period. Diastole: Relaxation period.

• 1. Ventricular Filling (Mid-to-late Diastole): Pressure is low. > 80\% of blood flows passively. Atrial contraction (P wave) adds the remaining $20\%$.

  • End Diastolic Volume (EDV): The volume of blood in the ventricle at the end of diastole ($\approx 120\,cm^3$).

• 2. Ventricular Systole:

  • Isovolumic Contraction: Pressure rises, AV valves close. All valves are closed; volume is constant.

  • Ventricular Ejection: Ventricular pressure exceeds arterial pressure. SL valves open. Aortic pressure reaches $120\,\text{mmHg}$; pulmonary trunk pressure reaches $24\,\text{mmHg}$.

• 3. Isovolumic Relaxation (Early Diastole): Ventricles relax (T wave). Pressure drops, and arterial backflow closes SL valves.

  • End Systolic Volume (ESV): Blood remaining after systole ($\approx 50\,cm^3$).

  • Dicrotic Notch: Brief rise in aortic pressure caused by backflow hitting closed SL valves.

• Timing: At $75\,\text{beats\,min}^{-1}$, one cycle is $0.8\,\text{s}$. (Atrial systole: $0.1\,\text{s}$; Ventricular systole: $0.3\,\text{s}$; Quiescent period: $0.4\,\text{s}$).

Heart Sounds and Clinical Valve Imbalances

• "Lub": Closure of AV valves at the start of ventricular systole.

• "Dup": Closure of SL valves at the start of ventricular diastole.

• Heart Murmurs: Result from turbulent blood flow.

  • Incompetent Valve: Swishing sound due to regurgitation.

  • Stenotic Valve: High-pitched or clicking sound due to restricted flow through a narrow opening.

Cardiac Output (CO)

• Definition: Volume of blood pumped by each ventricle in $1\,\text{min}$.

• Formula: $CO = HR \times SV$.

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

• Average Resting Values: $75\,\text{beats\,min}^{-1} \times 70\,cm^3\,\text{beat}^{-1} = 5250\,cm^3\,\text{min}^{-1} = 5.25\,dm^3\,\text{min}^{-1}$.

• Cardiac Reserve: Difference between resting and maximal CO. Max CO is $20$ to $25\,dm^3\,\text{min}^{-1}$ in nonathletes and up to $35\,dm^3\,\text{min}^{-1}$ in athletes.

Regulation of Stroke Volume (SV)

• Ejection Fraction: $\frac{SV}{EDV} \times 100\%$. Normal is $\approx 60\%$.

• Preload: Degree of muscle stretch before contraction. Venous return is the main factor. Increases in preload increase SV (Frank-Starling law).

• Contractility: Contractile strength independent of muscle length. Increased by positive inotropic agents (epinephrine, high extracellular $Ca^{2+}$, glucagon, digitalis). Decreased by negative inotropic agents (acidosis, high extracellular $K^+$, calcium channel blockers).

• Afterload: Back pressure exerted by arterial blood ($80\,\text{mmHg}$ in aorta, $10\,\text{mmHg}$ in pulmonary trunk). Hypertension (> 90\,\text{mmHg}) increases afterload, which increases ESV and decreases SV.

Regulation of Heart Rate (HR)

• Autonomic Regulation:

  • Sympathetic: Stress triggers norepinephrine release, binding to $\beta\text{-adrenergic}$ receptors, increasing HR and contractility.

  • Parasympathetic: Acetylcholine hyperpolarizes pacemaker cells, slowing HR. The heart at rest exhibits vagal tone (dominant PSNS influence), which reduces HR by approximately $25\,\text{beats\,min}^{-1}$.

  • Atrial (Bainbridge) Reflex: Sympathetic reflex initiated by increased venous return and atrial stretching.

• Chemical Regulation:

  • Hormones: Epinephrine and thyroxine increase HR.

  • Ions:

    • Hypocalcemia: Depresses the heart.

    • Hypercalcemia: Increases HR and contractility.

    • Hyperkalemia: Can lead to heart block and cardiac arrest.

    • Hypokalemia: Causes feeble heartbeat and arrhythmias.

• Other Factors: HR is higher in fetuses ($140$ to $160\,\text{beats\,min}^{-1}$), females, and with increased body temperature.

• Pathological Rates: Tachycardia (> 100\,\text{beats\,min}^{-1}); Bradycardia (< 60\,\text{beats\,min}^{-1}).

Congestive Heart Failure and Pathologies

• CHF: Progressive condition where CO is inadequate for tissue needs. Causes include coronary atherosclerosis, persistent high BP, multiple infarcts, and dilated cardiomyopathy (DCM).

• Failure Modes:

  • Left-side failure: Pulmonary congestion and edema.

  • Right-side failure: Peripheral congestion and edema.

• Treatment: Diuretics (remove fluid), antihypertensives (reduce afterload), and digitalis (increase contractility).

Developmental Anatomy of the Heart

• Derived from mesoderm.

• Day 22: Heart begins as two fused endothelial chambers and starts pumping.

• Day 35: Heart contorts into a four-chambered structure.

• Fetal Bypasses:

  • Foramen Ovale: Connects atria (becomes fossa ovalis).

  • Ductus Arteriosus: Connects pulmonary trunk to aorta (becomes ligamentum arteriosum).

• Congenital Defects: Most common birth defects. Types include mixing of oxygen-rich/poor blood (septal defects) or narrowed vessels (coarctation of the aorta). Tetralogy of Fallot involves multiple disorders.

Lifespan Transitions and Age-Related Changes

• Exercise increases pumping efficiency and limits atherosclerosis.

• Aging effects: Thicker/sclerotic valve flaps, declining cardiac reserve, fibrosed cardiac muscle (scars), and increased atherosclerosis risk.