Chapter 19 – Cardiovascular System: Heart

19.1 Introduction to the Cardiovascular System

  • Cardiovascular system = heart + blood vessels
  • Overall mission: transport blood throughout the body
    • Delivers \mathrm{O_2} & nutrients
    • Removes \mathrm{CO_2} & metabolic wastes
  • Key requirement = adequate perfusion
    • Perfusion = “mL of blood / minute / gram of tissue”
    • Must be high enough to maintain cellular health
    • Maintained by continuous heart pumping & patent (open, healthy) vessels

19.1a General Function

  • Heart creates pressure gradients that keep blood moving
  • Failure anywhere (pump or pipes) ↓ perfusion → cell injury/death

19.1b Overview of Major Components

  • Blood vessels = “soft pipes”
    • Arteries, veins, capillaries
  • The heart
    • Hollow, four-chambered pump at system center
    • Two functional sides (right & left)
    • Chambers = 2 atria (receiving) + 2 ventricles (pumping)

19.1c Pulmonary vs. Systemic Circulation (concept only – diagrams on slides)

  • Pulmonary circuit: right heart → lungs (gas exchange) → left heart
  • Systemic circuit: left heart → systemic tissues (delivery) → right heart
  • Closed loop; outputs must balance

19.3 Heart Anatomy

External Features (Figures 19.4–19.6)

  • Anterior & posterior surfaces show major grooves (sulci) that house coronary vessels
  • Apex points left & inferior; base faces posterior-superior

19.3b Heart Wall

  • Wall thickness varies
    • Ventricles thicker than atria
    • Left ventricle thickest (must generate systemic pressure)
  • Three distinct layers (superficial → deep)
    1. Epicardium (visceral pericardium) – serous membrane
    2. Myocardium – spiral bundles of cardiac muscle; largest layer
    3. Endocardium – endothelium + areolar CT lining chambers & valves

Internal Anatomy (Fig 19.7)

  • Interatrial & interventricular septa separate right vs. left chambers
  • Trabeculae carneae = ridges in ventricular walls
  • Pectinate muscles = ridges in atrial walls (auricles)

Heart Valves (19.3d–19.3c)

Atrioventricular (AV) Valves

  • Right AV = tricuspid
  • Left AV = bicuspid / mitral
  • Prevent backflow into atria during ventricular systole
  • Supported by:
    • Papillary muscles (cone-shaped; 3 in right ventricle typically)
    • Chordae tendineae (collagen cords) – prevent valve inversion

Semilunar (SL) Valves

  • Pulmonary SL (right ventricle → pulmonary trunk)
  • Aortic SL (left ventricle → aorta)
  • Open when ventricular P > arterial P; close when ventricles relax
  • Closure catches “back-sliding” blood, producing S₂ (“dupp”)

Valve Pathology (Clinical View: Heart Murmurs)

  • Valvular insufficiency = cusps don’t seal → regurgitation & chamber enlargement
  • Valvular stenosis = scarred, narrowed cusps → high resistance, ↓ output
  • Murmur = auscultated turbulence; may reflect either defect

Fibrous Skeleton (19.3e)

  • Dense irregular CT; forms fibrous rings around valves
  • Provides:
    • Structural support
    • Anchor point for myocardium
    • Electrical insulation between atria & ventricles (ensures sequential contraction)
  • Spiral muscle arrangement → atrial squeeze “inward”; ventricular contraction “wrings” apex → base

Coronary Circulation (19.3f)

  • Purpose: supply myocardium, which is too thick for diffusion
  • Arteries (Fig 19.11a) branch off ascending aorta:
    • Right coronary → marginal & posterior interventricular branches
    • Left coronary → circumflex & anterior interventricular (LAD) branches
  • Veins (Fig 19.11b) drain into coronary sinus → right atrium
  • Flow is intermittent: vessels patent in diastole; compressed in systole
  • Functional end-arteries: anastomoses exist but too small to fully compensate occlusion

Clinical: CHD, Angina, MI

  • Atherosclerosis or spasm ↓ flow
  • Angina pectoris: transient ischemic pain; treat with vasodilators
  • Myocardial infarction: complete occlusion → cell death
    • Severe chest pain ± left arm/jaw, dyspnea, diaphoresis, nausea

19.4 Microscopic Structure & Metabolism of Cardiac Muscle

Cell Structure

  • Short, branched cells; 1–2 central nuclei; abundant mitochondria
  • Intercalated discs:
    • Desmosomes = mechanical coupling
    • Gap junctions = ionic/electrical coupling → functional syncytium

Metabolism

  • High ATP demand; rich blood supply, myoglobin, creatine kinase
  • Utilizes multiple fuels (fatty acids, glucose, lactate, ketones, AAs)
  • Relies almost exclusively on aerobic respiration → sensitive to ischemia

19.5 Conduction System & ANS Control

Conduction Pathway

  1. SA node (posterior wall RA) – pacemaker
  2. Internodal pathways & AV node (interatrial septum)
  3. AV bundle (Bundle of His) → right & left bundle branches
  4. Purkinje fibers (apex → ventricular walls)

Automaticity

  • SA nodal cells spontaneously depolarize (pacemaker potential)
    • RMP ≈ -60\,\text{mV} but unstable
    • Fires every 0.8\,\text{s} → \approx 75\,\text{bpm}
    • Intrinsic rate \approx 100\,\text{bpm}; parasympathetic vagal tone slows resting HR

ANS Innervation (Fig 19.13)

  • Cardiac centers in medulla:
    • Cardioacceleratory (sympathetic) ↑ HR & force
    • Cardioinhibitory (parasympathetic via vagus) ↓ HR
  • Inputs from baro- & chemoreceptors modulate output

Ectopic Pacemakers

  • Non-SA foci can pace when SA damaged
    • AV node rhythm: 40–50 bpm (life-sustaining)
    • Ventricular focus: 20–40 bpm (usually insufficient)

19.6–19.7 Electrical & Mechanical Events in the Heart

SA Node Action Potential

  1. Slow Na⁺ influx (funny channels) → threshold
  2. Rapid Ca²⁺ influx → depolarization
  3. K⁺ efflux → repolarization; cycle repeats

Conduction to Ventricles (Fig 19.17)

  • Rapid spread via Purkinje fibers ensures synchronous ventricular systole
  • Papillary muscle stimulation slightly precedes pressure rise → stabilizes AV cusps

Cardiac Muscle Cell Action Potential

  1. Depolarization: Na⁺ influx
  2. Plateau: Ca²⁺ influx balanced by K⁺ efflux (maintains depolarization, prolongs refractory period ≈ 250\,\text{ms})
  3. Repolarization: Ca²⁺ channels close; K⁺ continues outward
  • Long refractory period prevents tetany

ECG (19.7d)

  • P wave = atrial depolarization
  • QRS complex = ventricular depolarization (& atrial repolarization)
  • T wave = ventricular repolarization
  • PR, QT, ST segments/intervals give conduction & repolarization timing

Arrhythmias (Clinical View)

  • Heart blocks (1°, 2°, 3°) = slowed/failed AV conduction
  • PVCs – premature ventricular contractions; benign if isolated
  • Atrial fibrillation – chaotic atrial activity
  • Ventricular fibrillation – fatal pump failure; treat with defibrillation

19.8 Cardiac Cycle

  • One heartbeat = coordinated systole & diastole of all chambers
  • Pressure changes drive valve operation & blood flow (high → low)

Sequence of Events

  1. Atrial systole: completes ventricular filling; EDV reached
  2. Isovolumic ventricular contraction: AV valves close (S₁ “lubb”); pressure rises, SL valves still shut
  3. Ventricular ejection: pressure > arterial; SL open; blood leaves; SV ejected, ESV = EDV - SV
  4. Isovolumic relaxation: ventricles relax; SL close (S₂ “dupp”); all valves closed
  5. Ventricular filling (passive): atria & ventricles in diastole; AV valves open; cycle repeats

Heart Sounds & Murmurs

  • S₁ = AV closure, S₂ = SL closure; S₃, S₄ useful in pathology
  • Murmurs reflect turbulence (insufficiency vs. stenosis)

Ventricular Balance

  • Both ventricles pump equal volumes; mismatch → systemic or pulmonary edema

19.9 Cardiac Output (CO)

  • CO = HR \times SV (L min^{-1}) – measure of CV performance
  • Cardiac reserve = max CO – resting CO (↑ 4× in non-athlete, 7× in athlete)

Heart Rate Modulation (Chronotropic Agents)

  • Positive agents: sympathetic NE/EPI, TH, caffeine, nicotine ↑ HR
  • Negative agents: parasymp ACh, beta-blockers ↓ HR
  • Reflexes:
    • Baroreceptor input adjusts HR to BP
    • Bainbridge (atrial) reflex: ↑ venous return stretches atria → ↑ HR

Stroke Volume Determinants

  1. Venous return / preload
    • Frank-Starling Law: ↑ EDV → optimal filament overlap → ↑ force → ↑ SV
    • ↑ with exercise (muscle pump) or slower HR; ↓ with hemorrhage, tachycardia
  2. Inotropic state (contractility)
    • Positive agents (sympathetic NE/EPI, digitalis) ↑ Ca²⁺ → ↑ cross-bridges → ↑ SV
    • Negative agents (acidosis, hyperkalemia, Ca²⁺ channel blockers) ↓ SV
  3. Afterload
    • Arterial pressure that ventricles must overcome
    • ↑ afterload (e.g., hypertension, aortic stenosis) ↓ SV

Overall CO Control

  • HR influenced primarily by nodal activity & ANS/hormonal status
  • SV influenced by preload, contractility, afterload
  • Clinical extremes:
    • Bradycardia < 60 bpm (athletes, hypothyroid, electrolyte imbalance, CHF)
    • Tachycardia > 100 bpm (fever, anxiety, heart disease)

19.10 Heart Development

  • Begins wk 3: two endothelial heart tubes (mesoderm) form & fuse
  • Beats by day 22; folds & bends during wk 4 to form primitive chambers
  • Key fetal shunt: foramen ovale (RA → LA); closes post-birth → fossa ovalis