Left Coronary Artery
Left coronary splits into the LAD (represented by V3-5 on the EKG, supplies the interventricular groove via diagonal and septal perforator branches) and the circumflex (follows the AV groove, giving off the obtuse marginal and supplying the posterior LV as well as some of the RV, represented by lead I and aVL).
Right Coronary Artery
Right coronary artery supplies the sinus node artery (also supplies the RA) and AV nodal artery, and usually terminates in the posterior descending artery. In 10% of patients, the AV node is supplied by the septal perforating branches of the LAD [James TN. Am Heart J 62: 756, 1961]. Occlusion of the RCA leads to EKG changes in II, III, and aVF. 50% of humans are “right dominant” in that the RCA supplies the posterior descending. 30% of humans are co-dominant (mixed perfusion) and 20% are left-dominant.
In 50% of humans, the RCA supplies the posterior descending artery. In 30% of humans, both the RCA and LCA supply the posterior descending, and in 20% of humans the LCA (left-dominant) supplies the posterior descending exclusively.
Coronary Blood Flow
4% of total cardiac output (250 mL/min). The right ventricle, which rarely develops pressures in excess of systemic diastolic blood pressure, receives a constant supply of blood flow (except in the setting of severe pulmonary hypertension). The left ventricle, by contrast, only receives blood flow during diastole. The healthy heart is capable of matching oxygen supply to demand, although the exact mechanism is not known – most likely an intrinsic capability, possibly related to oxygen depletion, CO2 production, or other factors such as adenosine, ATP, or [H+].
Coronary Vascular Resistance
Unlike most of the systemic circulation, in which arterioles < 50 um in diameter are the predominant source of resistance, in the coronary circulation most of the resistance originates from larger (> 100 um in diameter) vessels, although 10% comes from coronary veins [Marcus ML et al. Circulation82: 1, 1990]. Beta agonists dilate coronary blood vessels, and alpha agonists lead to vasoconstriction, but whether or not these changes are significant enough to overcome local metabolite-mediated supply:demand matching and actually change coronary blood flow is controversial [Kaplan JA, ed. Essentials of Cardiac Anesthesia. Saunders, 2008 p 71].
Nitric oxide (NO), which functions by increasing cGMP production and whose release is caused by a variety of stimuli, causes vascular relaxation as well as inhibition of platelet adhesion/aggregation [Kaplan JA, ed. Essentials of Cardiac Anesthesia. Saunders, 2008 p 69]. Prostacyclin (PGI2) also causes vascular relaxation as well as inhibition of platelet adhesion/aggregation but works by increasing cAMP.
Endothelin, thromboxane A1, and prostaglandin H2 [Kaplan JA, ed. Essentials of Cardiac Anesthesia. Saunders, 2008 p 69] are all released by the endothelium and all cause vasoconstriction.
In addition to NO and PGI2, both of which cause vascular relaxation as well as inhibition of platelet adhesion/aggregation, endothelial cells also release protein C, thrombomodulin, and TPA.