Understanding Coronary Blood Flow

Abstract

Fick's principle states that oxygen consumption of an organ or organism is equal to the product of blood flow and oxygen extraction from the blood. Among all organs, the heart is unique in that oxygen extraction is constantly close to maximal. Thus, the only way that this metabolically demanding organ can increase oxygen consumption is by increasing coronary blood flow. In this aspect of oxygen delivery, the heart also is unique because most flow occurs in diastole instead of in systole. In other organs, blood flows down a pressure gradient from its arterial source through the resistance of the arterioles into the capillary bed and thence venous return. In the heart, the compression of the vasculature by its surrounding muscle during systole impedes flow so that while the pressure head for flow is maximum in systole, flow is maximum in diastole. Thus, a simple "vascular waterfall" model in which flow moves from highest to lowest pressure does not fully explain observed myocardial flow phenomena. Article p 1768In this week's Circulation, Davies et al 1 used computer analysis of recordings of blood flow and pressure to detect and quantify intracoronary waves and to study coronary flow events in normal subjects and those with left ventricular hypertrophy (LVH). Waves were generated from both ends of the coronary tree. Proximal waves moved forward; distal waves moved backward. In this schema, proximal "pushing" waves and distal suction waves accelerate forward blood flow, while proximal suction waves and distal pushing waves do the opposite. Although the authors consistently detected 6 waves, 2 were dominant: a forward-moving pushing wave and a backward-moving suction wave (although this wave moves proximally, it propels blood forward). The forwardmoving pushing wave is generated by systolic pressure. It probably drives blood primarily into the epicardial coronaries where it might be stored until it is released for forward flow when the myocardium relaxes. The second important wave, typically the largest, is a suction wave generated by relaxation of the left ventricle and is probably the main driver in diastolic coronary blood flow. Coronary Blood Flow in Normal Subjects and Those With LVHIn normal subjects, endocardial blood flow exceeds epicardial flow, so the ratio of endocardial to epicardial blood flow is Ϸ1.2:1. 2,3 It is generally held that this distribution matches the nutrient requirements of the endocardium where wall stress higher than that of the epicardium increases endocardial oxygen demand. It has been known for decades that this distribution is reversed in the presence of concentric LVH, predisposing toward endocardial ischemia. 2-5 Indeed, such ischemically mediated endocardial contractile dysfunction has been demonstrated. 6,7 Furthermore, it is known that coronary flow reserve is reduced in LVH. 8 Although normal myocardium can increase its flow 5-to 8-fold under stress, it can be reduced by Ն50% in concentric LVH. This mechanism must play a role in the angina observed in some patients with LVH wh...

The compression and expansion waves of the forward and backward flows: An in-vitro arterial model

“…Pulling (expansion) waves were observed in the pulmonary venous [27] and left side of the circulatory system [4,28]. Carabello [29] indicated that the second peak of coronary flow waveform is a pulling wave, which is generated by the relaxation of the left ventricle. Further, it is thought that pulling waves generated owing to left ventricular relaxation play a major role in shaping the pulsatile nature of pulmonary venous flow, whose characteristics are being used clinically in several areas such as, first, estimation of the left ventricular filling pressure, second, evaluation of the left ventricular and left atria diastolic function, and, thirdly, grading the severity of mitral valve regurgitation [30].…”

A mathematical model of coronary blood flow control: simulation of patient-specific three-dimensional hemodynamics during exercise

“…We emphasize that is not the total blood oxygen content but rather that oxygen content that will be extracted as the blood passes through the myocardial vasculature. Opting to hold this constant is a simplification, but a reasonable one, as coronary blood oxygen extraction is constantly close to maximum ( 6 , 70 ). P̄ cor was discussed in Mathematical Model of Coronary Flow Control ; k fb and g remain to be discussed.…”

“…the mass of oxygen delivered to the left-ventricular myocardium (O 2 D) is defined to be the product of coronary blood flow and arterial blood oxygen content ( 34 ). It is physiologically maintained at a value very close to that of the left-ventricular myocardial oxygen demand (MV̇ o 2 ) ( 6 , 65 ). Such close matching requires a delicate balancing of coronary intrinsic and extrinsic control systems, which operate together to achieve rapid and accurate adjustment of O 2 D in response to changes in MV̇ o 2 ( 42 ).…”

Rationale and Pitfalls of Noninvasive Coronary Flow Reserve Estimation in Assessment of Microvascular Disease

“…CFR could be diminished in the presence of left ventricular hypertrophy 15 . The decrease in CFR in left ventricular hypertrophy is probably due to a combination of reduced capillary density per unit of myocardium, increased resistance to flow, microvessel disease, and diastolic dysfunction 16 . Hence, it can be a challenge to tease out the effect of microvessel disease and its contribution to decreased CFR in patients with left ventricular hypertrophy.…”

“…15 The decrease in CFR in left ventricular hypertrophy is probably due to a combination of reduced capillary density per unit of myocardium, increased resistance to flow, microvessel disease, and diastolic dysfunction. 16 Hence, it can be a challenge to tease out the effect of microvessel disease and its contribution to decreased CFR in patients with left ventricular hypertrophy. As mentioned above, the presence of left ventricular diastolic dysfunction can also affect the measured CFR by Doppler echocardiography, 17 and this can be a challenge in high-risk population such as diabetics, obese, and hypertensives, in whom there is high prevalence of diastolic dysfunction.…”