3. The “dominance” of the coronary circulation is determined on the basis of which major coronary artery feeds the posterior descending coronary artery (PDA). A “right-dominant” circulation occurs when the RCA supplies blood to the PDA and is observed in approximately 80% of patients. A “left-dominant” circulation in which the PDA is supplied by the LCCA is observed in the remaining 20% of patients.

4. RA, LA, and RV coronary perfusion occurs during both systole and diastole because aortic blood pressure always exceeds the pressure within each of these chambers (Fig. 10-2).

5. The extent of development of the coronary collateral circulation may determine whether myocardial ischemia or infarction is likely in patients with coronary artery disease.

6. The coronary veins converge and terminate in the coronary sinus, which empties into the posterior aspect of the RA above the tricuspid valve (accounts for about 85% of the total coronary blood flow to the LV. The remaining blood flow empties directly into the atrial and ventricular cavities via the thebesian veins. The RV veins drain into the anterior cardiac veins; these empty individually into the RA.

D. Impulse Conduction

1. How the heart is electrically activated is essential to its mechanical performance. The primary cardiac pacemaker is the sinoatrial node, although declines in firing rate and delays or blockade of normal conduction may result in the appearance of secondary pacemakers.

2. The atria are electrically isolated from the ventricles by the heart’s cartilaginous skeleton. As a result, atrial depolarization is directed solely to the RV and the LV through the AV node. Because AV node conduction is relatively slow compared with the pathways proximal and distal to it, the AV node is responsible for the sequential contraction pattern of the atria and the ventricles.

3. Accessory pathways that bypass the AV node and establish abnormal conduction between the atria and ventricles may produce supraventricular tachyarrhythmias.

II. CORONARY PHYSIOLOGY

A. Coronary Blood Supply

1. Blood supply to the LV is directly dependent on the difference between the aortic pressure and LV end-diastolic pressure (coronary perfusion pressure) and inversely related to the vascular resistance to flow, which varies to the fourth power of the radius of the vessel (Poiseuille’s law).

2. Resting coronary blood flow in an adult is approximately 250 mL/min (1 mL/min/g) or 5% of total cardiac output.

3. The LV subendocardium is exposed to a higher pressure than the subepicardial layer during systole (systolic intraventricular pressure may be higher than the peak LV systolic pressure). Because of these differences in tissue pressure, the subendocardial layer is more susceptible to ischemia in the presence of coronary artery stenoses, pressure-overload hypertrophy, or pronounced tachycardia.

4. The heart normally extracts between 75% and 80% of arterial O₂ content, by far the greatest O₂ extraction of all the body’s organs.

5. Myocardial O₂ consumption is a major determinant of coronary blood flow.

III. CARDIAC MYOCYTE ANATOMY AND FUNCTION

A. Ultrastructure

1. The heart contracts and relaxes nearly 3 billion times during an average lifetime based on a heart rate of 70 beats per minute and a life expectancy of 75 years.

2. The sarcolemma is the external membrane of the cardiac muscle cell (contains ion channels and receptors) and deep invaginations of the sarcolemma (transverse [“T”] tubules) penetrate the internal structure of the myocyte, ensuring rapid, uniform transmission of the depolarizing impulses that initiate contraction to be simultaneously distributed throughout the cell.

B. Contractile Apparatus

1. Myosin, actin, tropomyosin, and the three-protein troponin complex comprise the six major components of the contractile apparatus.

2. The maximum velocity of sarcomere shortening has been shown to be dependent on the activity of this actin-activated myosin ATPase.

C. Calcium–Myofilament Interaction. Binding of Ca²⁺ to troponin C precipitates a series of conformational changes in the troponin–tropomyosin complex that lead to the exposure of the myosin binding site on the actin molecule.

D. Myosin–Actin Interaction. Binding of adenosine triphosphate with high affinity to the catalytic domain of myosin initiates the series of chemical and mechanical events that cause contraction of the sarcomere to occur.

IV. THE CARDIAC CYCLE (Fig. 10-3)

A. The QRS complex of the electrocardiogram indicates that RV and LV depolarization has occurred. This electrical event initiates contraction (systole) and is associated with rapid increases in pressure in both chambers. When RV and LV pressures are greater than RA and LA pressures, the tricuspid and mitral valves close, thereby producing the first heart sound (S₁).

B. The maximum rate of rise of LV pressure (+dP/dt), a commonly used index of myocardial contractility, also occurs during LV isovolumic contraction.

C. Aortic and PA pressures briefly exceed LV and RV pressures as this slower ejection phase comes to an end, and the aortic and pulmonic valves close in response to these pressure gradient reversals.

1. Closure of the aortic and pulmonic valves causes the second heart sound (S₂); this event denotes end-systole.

2. S₂ is normally split because the aortic valve closes slightly before the pulmonic valve.

3. The mitral valve opens when LA pressure exceeds LV pressure, and the pressure gradient between the chambers drives blood stored in the LA into the LV.

D. Age and cardiac disease (myocardial ischemia, pressure-overload hypertrophy) often delay LV relaxation, which blunts early LV filling by reducing the LA-to-LV pressure gradient.

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