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