Mechanisms of Oxygen Demand/Supply Balance in the Right Ventricle

Abstract

Few studies have investigated factors responsible for the O2 demand/supply balance in the right ventricle. Resting right coronary blood flow is lower than left coronary blood flow, which is consistent with the lesser work of the right ventricle. Because right and left coronary artery perfusion pressures are identical, right coronary conductance is less than left coronary conductance, but the signal relating this conductance to the lower right ventricular O2 demand has not been defined. At rest, the left ventricle extracts approximately 75% of the O2 delivered by coronary blood flow, whereas right ventricular O2 extraction is only ~50%. As a result, resting right coronary venous PO2 is approximately 30 mm Hg, whereas left coronary venous PO2 is approximately 20 mm Hg. Right coronary conductance does not sufficiently restrict flow to force the right ventricle to extract the same percentage of O2 as the left ventricle. Endogenous nitric oxide impacts the right ventricular O2 demand/supply balance by increasing the right coronary blood flow at rest and during acute pulmonary hypertension, systemic hypoxia, norepinephrine infusion, and coronary hypoperfusion. The substantial right ventricular O2 extraction reserve is used preferentially during exercise-induced increases in right ventricular myocardial O2 consumption. An augmented, sympathetic-mediated vasoconstrictor tone blunts metabolically mediated dilator mechanisms during exercise and forces the right ventricle to mobilize its O2 extraction reserve, but this tone does not limit resting right coronary flow. During exercise, right coronary vasodilation does not occur until right coronary venous PO2 decreases to approximately 20 mm Hg. The mechanism responsible for right coronary vasodilation at low PO2 has not been delineated. In the poorly autoregulating right coronary circulation, reduced coronary pressure unloads the coronary hydraulic skeleton and reduces right ventricular systolic stiffness. Thus, normal right ventricular external work and O2 demand/supply balance can be maintained during moderate coronary hypoperfusion.

Endothelin receptor blockade combined with phosphodiesterase-5 inhibition increases right ventricular mitochondrial capacity in pulmonary arterial hypertension

“…However, the increased demand of power output of the RV in PAH requires a rise in O 2 delivery to RV cardiomyocytes to maintain sufficient ATP synthesis. The increased O 2 consumption and diffusion distances for O 2 in hypertrophied cardiomyocytes, in combination with the reduced capillary density, can lead to a mismatch between O 2 supply and demand (15,54). In turn, this can cause hypoxia in individual cardiomyocytes and may lead to cellular damage, contributing to RV failure (45, 51).…”

A jobb kamrai anatómia és funkció korszerű echokardiográfiás vizsgálata: patológiás és fiziológiás eltérések

“…Az esetek egy részében a bal koszorúér körbefutó ága (CX) és az elülső leszálló ág (LAD) is jelentékeny mértékben hozzájárul a jobb szívfél perfúzió-jához [5], a populáció nagyjából 30%-ában pedig az infundibulumot közvetlenül az aortából eredő ér látja el [6], így izomzata változatos kollaterális ellátással bír. A bal kamrával ellentétben a jobb kamra falában szignifikáns véráramlás mutatható ki nem csupán diasztoléban, hanem a teljes szívciklus alatt [6], továbbá jóval magasabb oxigénextrakciós rezervvel is bír (nyugalomban mindössze 50%-át vonja ki az artériás vér oxigéntartal-mának, szemben a bal kamra 75%-ával) [7]. Mindezek a tényezők lényeges elemei a jobb kamra ischaemiával szembeni magasabb toleranciájának.…”

Right Ventricular Metabolism and Its Efficiency

“…Oxygen demand in the RV may also increase with elevated PAP [10]. In LV, heart failure is considered to be an energy-depleted state.…”

“…RV MVO 2 was originally measured through right coronary venous blood sampling [10]. As noninvasive approaches, 11 C-acetate and 15 O-labeled tracers PET have also been applied for RV oxidative measurements in HF and PH [15,17,22,26,39,40].…”

“…Before myocardial fibrosis and RV heart failure develop, moderate to severe PH often leads to initial RV adaptation [9]. Given the increased arterial pressure in pulmonary circulation, the RV may require a significant power output in response to increased afterload, and this may increase the demand for oxygen in the RV [10]. In this circumstance, the RV may require improved mechanical efficiency in order to increase the power output.…”