Related Subjects:
| Cardiac Anatomy and Physiology
| Coronary Artery Anatomy and Physiology
| Cardiac Electrophysiology
| Cardiac Embryology
Cardiac Anatomy
- The heart is a cone-shaped structure with an apex and a base, located in the middle mediastinum, enveloped by the fibrous pericardium. It is positioned between the lungs.
- The apex points downward and laterally, with its anatomical surface marking at the 5th intercostal space, mid-clavicular line. The base faces posteriorly.
- The heart consists of four chambers:
- Two atria that act as reservoirs for blood returning to the heart.
- Two ventricles that function as pumps, propelling blood to the body and lungs.
Basic Heart Structure
- The left ventricle receives oxygenated blood from the left atrium via the mitral valve and pumps it into the systemic circulation. It has a thick muscular wall due to the high pressure it must generate.
- The right ventricle receives deoxygenated blood from the vena cava through the right atrium and pumps it into the pulmonary artery through the pulmonary valve.
- The borders of the heart:
- The right border consists almost entirely of the right atrium.
- The left border is mostly formed by the left ventricle, with the left atrial appendage superiorly.
- The base (posterior surface) is primarily formed by the left atrium, lying in close proximity to the esophagus (important for transesophageal echocardiography).
- The inferior (diaphragmatic) surface is made up of both the right and left ventricles.
Pressure Comparison: Right vs. Left
Cardiac Physiology
- Systole: The phase when the ventricles contract, ejecting blood into the systemic and pulmonary circulations.
- Diastole: The phase when the ventricles relax, allowing the atria to fill with blood. Diastole shortens as heart rate increases.
Cardiac Output
- Total blood volume is approximately 5 liters.
- Left ventricular volume at the end of diastole = 100 ml; at the end of systole = 30 ml.
- Stroke volume (SV) = 70 ml, and the average heart rate is 70 beats per minute (bpm).
- Cardiac output (CO) = SV (70 ml) x HR (70 bpm) ≈ 5 liters per minute.
Cardiac Cycle
Measuring Cardiac Output
- Thermodilution Technique: A cold solution is injected into the left atrium, and temperature changes in the pulmonary artery help estimate cardiac output.
- Esophageal Doppler: Uses Doppler ultrasound to measure blood flow in the descending aorta, combined with patient-specific factors to estimate cardiac output.
- Resistance and Flow: Arterioles and small arteries are the primary regulators of blood flow resistance, with small changes in arterial diameter causing significant changes in flow.
Systemic and Pulmonary Circulations
- The systemic and pulmonary circulations work in parallel and in series, maintaining the same flow.
- Resistance in the pulmonary circulation is only 10% of that in the systemic circulation.
- Systemic pressures: 120/80 mmHg, Pulmonary pressures: 25/10 mmHg.
Coronary Anatomy
- The first organ supplied by the heart is itself.
- Left Coronary Artery: Arises from the left posterior aortic sinus, branching into the left anterior descending artery (LAD) and the circumflex artery (Cx).
- The LAD supplies the anterior wall and septum of the heart, with diagonal and septal branches.
- The Cx runs in the left atrioventricular groove, supplying the lateral wall of the left ventricle. In 10% of people, it also supplies the posterior descending artery (PDA).
- Right Coronary Artery: Arises from the anterior aortic sinus, supplying the right ventricle and, in 65% of individuals, the inferior wall of the left ventricle via the posterior descending artery.
Cardiac Cycle
- The SA node (SAN) is the primary pacemaker, generating an intrinsic rate of 100 bpm, reduced to 70 bpm by vagal tone.
- Depolarization spreads through atrial tissue, creating the P wave on an ECG, followed by atrial contraction (atrial systole).
- The AV node delays the impulse, allowing ventricular filling, before passing the signal through the His-Purkinje system, causing ventricular contraction (QRS complex).
- As the ventricles contract, mitral and tricuspid valves close (first heart sound), followed by the ejection of blood.
- Ventricular relaxation and repolarization result in the closing of the aortic and pulmonary valves (second heart sound), followed by passive ventricular filling.
Cellular Mechanism of Cardiac Contraction
- Pacemaker cells in the SAN, AVN, and Purkinje fibers depolarize spontaneously. Calcium entry triggers contraction.
- Myocardial cells depolarize via Na+ and Ca2+ influx, initiating the sliding of actin and myosin filaments, leading to contraction.
- Excitation-contraction coupling relies on calcium released from the sarcoplasmic reticulum, mediated by calcium-induced calcium release (CICR).
- Calcium levels rise during depolarization, triggering ATP hydrolysis and sarcomere shortening (contraction), followed by relaxation as calcium is reabsorbed.
- Digoxin increases intracellular calcium, enhancing contractility, a mechanism exploited in treating heart failure.
Starling’s Law
- Increased preload (ventricular filling) stretches the cardiac muscle, enhancing contraction strength and stroke volume.
- In heart failure, this relationship may break down, leading to reduced contractile efficiency.
Exercise Physiology
- Physiological Response:
- Adrenaline (epinephrine) and noradrenaline (norepinephrine) increase heart rate, stroke volume, and vasoconstriction in non-essential organs.
- Heart rate rises from 50 bpm to 150 bpm, stroke volume increases from 80 ml to 160 ml, and cardiac output can increase up to 6 times (up to 24 l/min).
Pacemaker Action Potential at the SA Node
Pacemaker cells depolarize differently from other cardiac cells. These specialized cells in the SAN, AVN, and Purkinje fibers control the heart's rhythm, with the SA node having the fastest rate of depolarization.
Ventricular Myocyte Action Potential (5 Phases)
- Phase 0: Rapid depolarization due to Na+ influx.
- Phase 1: Brief repolarization as K+ moves out.
- Phase 2: Plateau phase with balanced K+ outflow and Ca2+ inflow.
- Phase 3: Repolarization with decreased Ca2+ conductance and increased K+ outflow.
- Phase 4: Return to resting potential, near the K+ equilibrium potential.
SA Node Pacemaker Action Potential (3 Phases)
- Phase 0: Depolarization driven by Ca2+ influx through transient and long-acting calcium channels.
- Phase 3: Repolarization with increased K+ conductance and reduced Ca2+ influx.
- Phase 4: Resting potential returns, with Na+ influx through "funny" channels (If), leading to slow spontaneous depolarization.