• Myocardial O₂ uptake = (A-V) O₂ x Coronary Blood Flow
• since the heart extracts almost all of the O₂ from the blood, coronary blood flow must increase to meet increase demand
• if one is anemic (ß hemoglobin), then one needs Ý CBF to make up the difference in oxygen supply
• at rest the LV gets 60-90 mL/100g/min, the RV 40-60 mL/100g/min. CBF can Ý 4-6 x’s during increased demand.
• coronary reserve Þ difference between resting flow and maximal flow
• Demand
• Most important: Wall Stress, Contractility, Heart rate
• Moderate importance: external work (cardiac work Þ fiber shortening or SV; actual ejection of blood)
• Less important: basal O₂ requirement, activation energy of the contractile mechanism
• Wall Stress – a dilated heart requires more O₂. Compensatory hypertrophy lowers O₂ requirement per gram of tissue.
• Wall stress = (P x r) / 2h [where P = intraventricular pressure, r = radius of ventricle, and h = wall thickness]
• if a patient’s HR or BP goes up, then the metabolic rate of the heart also increases
• Supply
• Anatomy:
• RCA – gives rise to; 1) Sinus node branch, 2) Marginal branch, 3) PDA, 4) AV nodal branch.
• LCA – gives rise to 1) LAD, 2) Circumflex
• In 85% of hearts the RCA supplies the posterior aspect of the heart. The other 15% use the LCA
• penetrating branches of the coronary arteries reach down into the subepicardial and subendocardial regions.
• most of the resistance comes from the microvasculature of the heart
• Autoregulation – blood flow is regulated via resistance in the coronary circulation to supply the heart with the amount of oxygenated blood it requires. As BP drops the vessels dilate to allow more flow until they reach the Autoregulatory threshold when ß BP translates linearly with ß CBF.
• Flow is at a maximum during diastole because the blood vessels get squeezed during systole
• R1 = viscosity of flow during diastole(affected by plaques in epicardial vessels)
• R2 = autoregulation by the microvasculature - major component
• R3 = compressive forces during systole (higher in the subendocardium than the subepicardium; this is why the subendocardium is most vulnerable to ischemia (ST depression))
• R_total = R₁ + R₂ + R₃

• Metabolic – metabolic products can cause vasodilation (Adenosine, PG’s, CO₂, H⁺)
• Myogenic – as BP rises the vessels constrict (autoregulation), maintains a steady flow
• Endothelial – EDRF-NO and PGI₂ cause vasodilation, 5-HT, TA₂, and endothelin cause vasoconstriction.
• injured endothelium loses its capacity to produce vasodilating substances so the vasoconstrictors remain unopposed
• causes of endothelial injury include: HTN, DM, smoking, and hyperlipidemia
• Neurohumoral – a-agonists vasoconstrict, b and parasympathetic vasodilate. (metabolic effects are more important; e.g. Epi speeds up the heart, vagal stimulation slows it down.)

Coronary Collateral Vessels – small channels connecting large coronary vessels (small in size and # in normal hearts)