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Heart Anatomy and Physiology
Sources: Guyton and Hall Textbook of Medical Physiology; Goldman-Cecil Medicine; Costanzo Physiology 7th Ed; Gray's Anatomy for Students; Barash Clinical Anesthesia 9th Ed
1. Gross Anatomy
The heart is a four-chambered muscular pump enclosed within the pericardium, which has two layers - a fibrous outer layer and a serous inner layer (parietal and visceral/epicardium) with a pericardial space in between. The heart wall itself consists of three layers:
- Endocardium - inner smooth lining
- Myocardium - the contractile muscle bulk
- Epicardium - outer visceral pericardial layer
Chambers
| Chamber | Wall | Function |
|---|
| Right atrium | Thin | Receives deoxygenated blood from SVC, IVC, coronary sinus |
| Right ventricle | Thin | Pumps blood to lungs via pulmonary artery |
| Left atrium | Thin | Receives oxygenated blood from 4 pulmonary veins |
| Left ventricle | Thick | Pumps blood into systemic circulation via aorta |
The interventricular septum divides the two ventricles. The left ventricle is the primary pumping chamber, composed of billions of cardiomyocytes connected end-to-end through gap junctions. - Goldman-Cecil Medicine
The LV has a unique double-helix muscle fiber architecture: subepicardial fibers spiral leftward, subendocardial fibers spiral rightward. This creates a wringing/twisting (torsion) motion during systole, pulling the base toward the apex. At end-systole the ventricle is like a loaded spring and recoils during diastole to rapidly fill. - Guyton & Hall, p.122
Valves
| Valve | Location | Opens During |
|---|
| Tricuspid (3 leaflets) | Right AV junction | Ventricular diastole |
| Mitral/Bicuspid (2 leaflets) | Left AV junction | Ventricular diastole |
| Pulmonary (semilunar) | RV-pulmonary artery | Ventricular systole |
| Aortic (semilunar) | LV-aorta junction | Ventricular systole |
AV valves are tethered to papillary muscles via chordae tendineae, which prevent leaflet prolapse (regurgitation) during ventricular contraction. The pressure gradient between ventricles and atria opens and closes the AV valves.
2. Conduction System
The conduction system initiates and coordinates contraction in a precise unidirectional sequence. - Gray's Anatomy for Students
SA Node → Atrial muscle → AV Node → Bundle of His
→ Right & Left Bundle Branches → Purkinje Fibers → Ventricular myocardium
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Sinoatrial (SA) node - the primary pacemaker, located at the junction of the superior vena cava and right atrium (crista terminalis). Discharges spontaneously at 60-100 bpm.
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Atrioventricular (AV) node - near the opening of the coronary sinus, close to the septal cusp of the tricuspid valve. Introduces a delay (~0.12 s) allowing atrial contraction to complete before ventricular activation.
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Bundle of His - direct continuation of the AV node, travels along the lower border of the membranous interventricular septum before splitting into right and left bundle branches.
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Right and left bundle branches - travel down respective sides of the interventricular septum toward the apex.
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Purkinje fibers - subendocardial plexus with the most functional contacts to working myocardium. Ensure rapid, near-simultaneous activation of ventricular muscle from apex to base.
The conduction pathway is insulated from surrounding myocardium by connective tissue to prevent premature activation. Coronary artery disease can disrupt the blood supply to these cells and cause dysrhythmias. - Gray's Anatomy for Students
3. Cardiac Action Potentials
Ventricular/Atrial action potential (phases 0-4):
- Phase 0 - rapid upstroke; fast Na+ channels open
- Phase 1 - early rapid repolarization; transient K+ outflow
- Phase 2 - plateau; slow L-type Ca2+ channels open (balanced by K+ outflow) - unique to cardiac muscle, prevents tetanic contraction
- Phase 3 - rapid repolarization; K+ channels open
- Phase 4 - resting potential (-85 to -90 mV)
SA node action potential - no fast Na+ channels; slow spontaneous diastolic depolarization (Phase 4 "funny current" via If channels + T-type Ca2+), followed by upstroke via L-type Ca2+ channels. Resting potential only around -55 to -65 mV.
The ventricular refractory period lasts 0.25-0.30 s (matching the plateau duration), preventing re-excitation and tetanus - physiologically essential so the heart can relax and fill between beats. - Guyton & Hall
4. Excitation-Contraction Coupling
The key process linking electrical excitation to mechanical contraction:
- Action potential spreads into T tubules (5x wider in cardiac vs. skeletal muscle - hold large calcium stores)
- L-type Ca2+ channels (LTCC/dihydropyridine receptors) in T tubule membrane open - small Ca2+ influx
- This triggers ryanodine receptors (RyR2) in the sarcoplasmic reticulum (SR) to release a far larger Ca2+ store - "calcium-induced calcium release"
- Cytosolic Ca2+ rises, binds troponin C on thin filaments
- Troponin C-Ca2+ binding causes tropomyosin to shift, exposing myosin-binding sites on actin
- Cross-bridge cycling: myosin heads bind actin, ATPase activity causes power stroke (sliding filaments) → contraction
- Relaxation: Ca2+ pumped back into SR by SERCA2 (ATP-dependent), and out of cell via Na+/Ca2+ exchanger (NCX) and Ca2+-ATPase
Cardiac muscle depends on Ca2+ influx from T tubules as well as SR stores - unlike skeletal muscle which relies almost entirely on SR. This makes cardiac contractility responsive to extracellular Ca2+ and drugs like digoxin. - Guyton & Hall, p.125
5. The Cardiac Cycle
The cardiac cycle consists of 7 phases (as defined in Costanzo Physiology):
| Phase | Event | Valves | Heart Sound |
|---|
| A - Atrial systole | Atria contract; final ventricular filling; P wave | Mitral/tricuspid open | S4 (if present) |
| B - Isovolumetric ventricular contraction | Ventricles contract; pressure rises; all valves closed; volume constant | Mitral closes | S1 |
| C - Rapid ventricular ejection | Peak pressure; blood ejected; ventricular volume falls | Aortic opens | - |
| D - Reduced ventricular ejection | Slower ejection; min. ventricular volume; aortic pressure starts to fall | - | - |
| E - Isovolumetric ventricular relaxation | Ventricles relax; pressure falls; all valves closed; volume constant | Aortic closes | S2 |
| F - Rapid ventricular filling | Passive filling from atria; ventricular volume rises | Mitral opens | S3 (if present) |
| G - Reduced ventricular filling (diastasis) | Slow filling phase; near-equalization of atrial/ventricular pressures | - | - |
Key pressures (left heart, normal):
- LV systolic pressure: ~120 mmHg
- LV diastolic pressure: ~0-12 mmHg
- Aortic pressure: ~120/80 mmHg
Heart sounds: S1 = mitral valve closure (start of systole); S2 = aortic valve closure (start of diastole). S3 is heard in rapid filling (normal in children; pathological in adults = heart failure). S4 is heard with atrial contraction against a stiff ventricle (hypertension, hypertrophy).
6. Determinants of Cardiac Performance
Cardiac output (CO) = Heart rate (HR) × Stroke volume (SV). Normal CO at rest = ~5 L/min.
Stroke volume is determined by three factors:
Preload (end-diastolic volume / venous return)
The Frank-Starling Law: as end-diastolic volume (EDV) increases, stretch of myocardial fibers increases, leading to greater force of contraction and a larger stroke volume. This ensures the heart ejects whatever volume is returned to it. - Costanzo Physiology, p.155
Afterload (aortic pressure / peripheral vascular resistance)
The resistance against which the ventricle must pump. Increased afterload (e.g., hypertension, aortic stenosis) reduces stroke volume for a given preload.
Contractility (inotropy)
The intrinsic force-generating capacity of the myocardium independent of preload and afterload:
- Positive inotropes (digoxin, catecholamines, Ca2+): shift the Frank-Starling curve upward - greater SV at any given EDV; increased ejection fraction
- Negative inotropes (beta-blockers, Ca2+ channel blockers, heart failure): shift curve downward
7. Coronary Blood Flow
The coronary arteries arise from the aorta just above the aortic valve. Key points:
- Left coronary artery (LCA): divides into left anterior descending (LAD - supplies anterior LV, septum) and left circumflex (supplies lateral LV)
- Right coronary artery (RCA): supplies right ventricle, inferior LV, SA node, AV node in most individuals
Blood flow pattern:
- Subepicardial flow: during both systole and diastole
- Subendocardial flow: predominantly during diastole (compressed by intramyocardial pressure during systole)
The LV extracts ~70-80% of O2 from coronary blood under basal conditions (near maximal extraction). Therefore, increases in O2 demand (exercise, increased HR, hypertrophy) can only be met by increasing coronary blood flow - not by increased extraction. Key vasodilators that increase flow (up to 6-fold): nitric oxide, adenosine, bradykinin, prostaglandins, CO2. - Goldman-Cecil Medicine; Barash Clinical Anesthesia
Summary Table: Key Numbers
| Parameter | Normal Value |
|---|
| Heart rate | 60-100 bpm |
| Stroke volume | ~70 mL |
| Cardiac output | ~5 L/min |
| Ejection fraction | 55-70% |
| LV systolic pressure | ~120 mmHg |
| LV diastolic pressure | 0-12 mmHg |
| Ventricular refractory period | 0.25-0.30 s |
| Atrial refractory period | ~0.15 s |
| Coronary flow reserve (max increase) | ~6-fold |