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Coronary blood flow (basics)
This document discusses coronary blood flow and its control. It begins by introducing the unique nature of the coronary circulation and the importance of balancing oxygen supply and demand. It then covers several topics in depth: the control of coronary blood flow during different parts of the cardiac cycle; the determinants of myocardial oxygen consumption; coronary autoregulation and how it can become impaired; transmural variations in coronary blood flow; endothelium-dependent modulation of coronary tone through factors like nitric oxide, prostacyclin, and endothelin; and the components of coronary vascular resistance. The overall goal is to provide an in-depth overview of coronary circulation and the factors that influence blood flow to the heart.
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Coronary blood flow (basics)
- 1. Coronary Blood Flow By Dr. SafwatIbrahim AlNahrawi Cardiology Resident at National Heart Institute.
- 2. Introduction: The coronary circulationis unique in that the heart is responsible for generating the arterial pressure that is required to perfuse the systemic circulation and yet, at the same time, has its own perfusion impeded during the systolic portion of the cardiac cycle . The balance between oxygen supply and demand is a critical determinant of the normal beat-to- beat function of the heart. Introduction
- 3. The importance ofthe coronary circulation is that myocardial contraction is closely related, so when this relation is acutely disrupted by diseases affecting coronary blood flow the resulting imbalance can immediately precipitate a vicious cycle, whereby ischemia-induced contractile dysfunction precipitates hypotension and further myocardial ischemia. Introduction
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- 5. Control of coronaryblood flow : Introduction Control of Coronary Blood flow During Diastole.During Systole. Coronary arterial inflow increases with a tran-smural gradient that favors perfusion to the subendocardial vessels. Increases tissue pressure, redistributes perfusion from the subendocardial to the subepicardial layers of the heart, and impedes coronary arterial inflow, which reaches it’s lowest level. coronary venous outflow falls.Compression reduces the diameter of intramyocardial microcirculatory vessels (arterioles, capillaries, and venules) and increases coronary venous outflow, which peaks during systole
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- 10. Myocardial Oxygen Consumption myocardialoxygen extraction is maximal at rest (60% to 80% of arterial oxygen content). increase oxygen extraction to increase oxygen delivery is limited to sympathetic activation and acute subendocardial ischemia. So, the increases in myocardial oxygen consumption are met by proportional increases in coronary flow. Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption
- 11. Myocardial Oxygen Consumption Themajor determinants of myocardial oxygen consumption are heart rate systolic pressure (or myocardial wall stress) left ventricular (LV) contractility. Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption
- 12. Coronary Autoregulation: Regional coronaryblood flow remains constant as coronary artery pressure is reduced below aortic pressure over a wide range when the determinants of myocardial oxygen consumption are kept constant. Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation
- 13. Coronary Autoregulation: Resting coronaryblood flow under normal hemodynamic conditions averages 0.7 to 1.0 mL/min/g and can increase between four to five fold during vasodilation. coronary flow reserve Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation
- 14. Coronary Autoregulation: coronary flowreserve reduced when • the diastolic time available for subendocardial perfusion is decreased (tachycardia) • the compressive determinants of diastolic perfusion (preload) are increased. Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation
- 15. Coronary Autoregulation: coronary flowreserve anything that increases resting flow, including: • increases in the hemodynamic determinants of oxygen consumption (systolic pressure, heart rate, and contractility) • reductions in arterial oxygen supply (anemia and hypoxia) Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation
- 16. Coronary Autoregulation: coronary flowreserve subendocardial ischemia in the presence of normal coronary arteries. Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation
- 17. Coronary Autoregulation: Trans-mural variationsIn coronary Blood flow: Subendocardial flow occurs primarily in diastole and begins to decrease below a mean coronary pressure of 40 mm Hg. By contrast, subepicardial flow occurs throughout the cardiac cycle and is maintained until coronary pressure falls below 25 mm Hg. So, vulnerability of the sub- endocardium to ischemia increased Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation
- 18. Coronary Autoregulation: Trans-mural variationsIn coronary Blood flow: Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation
- 19. Coronary Autoregulation: Endothelium-Dependent Modulation ofCoronary Tone. Epicardial conduit arteries do not contribute significantly to coronary vascular resistance. arterial diameter is regulated by • platelets paracrine factors • circulating neurohormonal agonists • neural tone • local control (vascular shear stress). Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation
- 20. Coronary Autoregulation: Endothelium-Dependent Modulation ofCoronary Tone. The net effect of many of these agonists is dependent on whether a functional endothelium is present. Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation Acetyl choline Endothelial dependent relaxing factor (Nitric oxide) cGMP Smooth muscle relaxation
- 21. Coronary Autoregulation: Endothelium-Dependent Modulation ofCoronary Tone. Nitric Oxide (Endothelium-Derived Relaxing Factor). • produced in endothelial cells by conversion of l-arginine to citrulline by type III NO synthase (NOS). • NO diffuse into Smooth muscle and increase cGMP which increase relaxation via decrease in intracellular calcium Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation
- 22. • NO-mediated vasodilationis enhanced by cyclic or pulsatile changes in coronary shear stress. • Chronic up regulation of NOS occurs in response to episodic increases in coronary flow (such as during exercise training). • NO-mediated vasodilation is impaired in many disease states and in patients risky for coronary artery disease (CAD), (in CAD oxidative stress generate superoxide anion which inactivate NO). This is the hallmark of impaired NO- mediated vasodilation in atherosclerosis, hypertension, and diabetes Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation
- 23. Coronary Autoregulation: Endothelium-Dependent Modulationof Coronary Tone. Endothelium-Dependent Hyperpolarizing Factor (EDHF) • endothelium-dependent mechanism for selected agonists (bradykinin), as well as shear stress–induced vasodilation. • produced by the endothelium, hyperpolarizes vascular smooth muscle and dilates arteries by opening calcium-activated potassium channels Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation
- 24. Coronary Autoregulation: Endothelium-Dependent Modulationof Coronary Tone. Prostacyclin (vasodilator prostaglandins) • Metabolism of arachidonic acid via cyclooxygenase. • Produce tonic coronary vasodilation • inhibitors of cyclooxygenase do not alter flow during ischemia distal to an acute stenosis or limit oxygen consumption in response to increases in metabolism. • This suggests that it is overcome by other compensatory vasodilator pathways. Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation
- 25. Coronary Autoregulation: Endothelium-Dependent Modulationof Coronary Tone. Endothelin (ET-1, ET-2, and ET-3) • are peptide endothelium-dependent constricting factors. • Their constricting function is mediated by binding to both ETA and ETB receptors. • ETA-mediated constriction is caused by the activation of protein kinase C in vascular smooth muscle. • ETB-mediated constriction is less pronounced and counterbalanced by ETB- mediated endothelium-dependent NO production and vasodilation. Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation
- 26. Coronary Autoregulation: Endothelium-Dependent Modulationof Coronary Tone. Endothelin (ET-1, ET-2, and ET-3) • Unlike the rapid vascular smooth muscle relaxation and recovery characteristic of endothelium-derived vasodilators (NO, EDHF, and prostacyclin), the constriction to endothelin is prolonged. • marginally involved in regulating coronary blood flow in the normal heart but concentrations increase in diseases such as heart failure Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation
- 27. Coronary Autoregulation: Endothelium-Dependent Modulation ofCoronary Tone. Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation
- 28. Coronary Vascular Resistance. Theresistance to coronary blood flow can be divided into three major components: 1-(R1) negligible conduit resistance . • hemodynamically significant epicardial artery narrowing (more than 50% diameter reduction), the fixed conduit artery resistance begins to contribute an increasing component to total coronary resistance • when severely narrowed (more than 90%), may reduce resting flow. Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation Coronary Vascular Resistance.
- 29. Coronary Vascular Resistance. Theresistance to coronary blood flow can be divided into three major components: 2- (R2) is dynamic : arises primarily from microcirculatory resistance arteries and arterioles. . Differ according to the microcirculatory resistance vessel sizes (20 to 400 µm in diameter) and changes in response to physical forces (intraluminal pressure and shear stress), as well as the metabolic needs of the tissue. Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation Coronary Vascular Resistance.
- 30. Coronary Vascular Resistance. Theresistance to coronary blood flow can be divided into three major components: 3- (R3) extravascular compressive resistance: • varies with time during the cardiac cycle and is related to cardiac contraction and systolic pressure of LV • In heart failure, the elevated ventricular diastolic pressure raise R3 impede perfusion of microcirculatory vessels from elevated extravascular tissue pressure during diastole. Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation Coronary Vascular Resistance.
- 31. Coronary Vascular Resistance. Introduction Controlof Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation Coronary Vascular Resistance. R1 is epicardial conduit artery resistance, which normally is insignificant R2 is resistance secondary to metabolic and autoregulatory adjustments in flow and occurs in arterioles and small arteries R3 is the time-varying compressive resistance that is higher in subendocardial than subepicardial layers. In the normal heart
- 32. Coronary Vascular Resistance. Microcirculationorganization Resistance vessel needs to dilate in an orchestrated fashion: • Epicardial arteries (<400 µm in diameter) serve a conduit artery function, with diameter primarily regulated by shear stress, and contribute little pressure drop (>5%) over a wide range of coronary flow. • resistance vessels can be divided into small arteries (100 to 400 µm), which regulate their tone in response to local shear stress and luminal pressure changes (myogenic response), and arterioles (<100 µm), which are sensitive to changes in local tissue metabolism and directly control perfusion of the low-resistance coronary capillary bed. Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation Coronary Vascular Resistance.
- 33. Coronary Vascular Resistance. Microcirculationorganization Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation Coronary Vascular Resistance.
- 34. Coronary Vascular Resistance. Microcirculationorganization Capillary density of the myocardium averages 3500/mm2 (resulting in an average intercapillary distance of 17 µm), which is greater in the subendocardium than in the subepicardium. Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation Coronary Vascular Resistance.
- 35. Coronary Vascular Resistance. Microcirculationorganization Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation Coronary Vascular Resistance.
- 36. Coronary Vascular Resistance. Microcirculationorganization Flow-Mediated Resistance Artery Control. Coronary small arteries and arterioles regulate their diameter in response to changes in local shear stress (Flow- induced dilation ) which is endothelium-dependent and mediated by NO. Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation Coronary Vascular Resistance.
- 37. Coronary Vascular Resistance. Microcirculationorganization Myogenic Regulation (Pressure-Mediated Resistance Artery Control. The myogenic response refers to the ability of vascular smooth muscle to oppose changes in coronary arterial diameter, Thus vessels relax when distending pressure is decreased and constrict when distending pressure is elevated. Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation Coronary Vascular Resistance.
- 38. Coronary Vascular Resistance. Microcirculationorganization Metabolic Mediators of Coronary Resistance Vessel Control. Adenosine: • It is released from cardiac myocytes when the rate of ATP hydrolysis exceeds its synthesis during ischemia. • Its production and release also increase with myocardial metabolism. Adenosine has an extremely short half-life (less than 10 seconds) • Bind to A2 receptors on vascular smooth muscle, increases (cAMP), and opens KATP and intermediate calcium- activated potassium channels dilating vessels smaller than 100 µm. Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation Coronary Vascular Resistance.
- 39. Coronary Vascular Resistance. Microcirculationorganization Metabolic Mediators of Coronary Resistance Vessel Control. Oxygen Sensing. • Coronary flow increases in proportion to reductions in arterial oxygen content (reduced Po2 or anemia) • there is a twofold increase in perfused capillary density in response to hypoxia. Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation Coronary Vascular Resistance.
- 40. Coronary Vascular Resistance. Microcirculationorganization Metabolic Mediators of Coronary Resistance Vessel Control. Acidosis. • Arterial hypercapnia and acidosis (Pco2) are potent stimuli that produce coronary vasodilation independent of hypoxia. Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation Coronary Vascular Resistance.
- 41. Coronary Vascular Resistance. Microcirculationorganization Neural Control of Coronary Conduit and Resistance Arteries. Cholinergic Innervation • Resistance arteries dilate to acetylcholine, resulting in increases in coronary flow. • In conduit arteries, acetylcholine normally causes mild coronary vasodilation, the net action of a direct muscarinic constriction of vascular smooth muscle counterbalanced by an endothelium dependent vasodilation (NO) Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation Coronary Vascular Resistance.
- 42. Coronary Vascular Resistance. Microcirculationorganization Neural Control of Coronary Conduit and Resistance Arteries. Sympathetic Innervation • At basal conditions, there is no resting sympathetic tone in the heart and thus there is no effect of denervation on resting perfusion. • During sympathetic activation, coronary tone is modulated by norepinephrine released from myocardial sympathetic nerves, as well as by circulating norepinephrine and epinephrine. Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation Coronary Vascular Resistance.
- 43. Coronary Vascular Resistance. Microcirculationorganization Neural Control of Coronary Conduit and Resistance Arteries. Sympathetic Innervation • In conduit arteries, sympathetic stimulation leads to alpha1 constriction & B-mediated vasodilation. net effect is to dilate epicardial coronary arteries. (concomitant flow-mediated vasodilation ) • coronary resistance vessel tone are complex and dependent on the net actions of beta1- mediated increases in myocardial oxygen consumption, direct beta2-mediated coronary vasodilation, and alpha1-mediated coronary constriction. Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation Coronary Vascular Resistance.
- 44. Coronary Vascular Resistance. Microcirculationorganization Neural Control of Coronary Conduit and Resistance Arteries. The neural control mechanism produces transient vasodilation before the build up of local metabolites during exercise and prevents the development of subendocardial ischemia during abrupt changes in demand. Introduction Control of Coronary Blood flow Myocardial Oxygen Consumption Coronary Autoregulation Coronary Vascular Resistance.
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