Newly Published
Review Article  |   October 2017
Right Ventricular Perfusion: Physiology and Clinical Implications
Author Notes
  • From the Department of Anesthesiology, University of Illinois College of Medicine, Chicago, Illinois (G.J.C.); and Anesthesia Service, Clement J. Zablocki Veterans Affairs Medical Center, Milwaukee, Wisconsin (P.S.P.).
  • Submitted for publication December 19, 2016. Accepted for publication August 1, 2017.
    Submitted for publication December 19, 2016. Accepted for publication August 1, 2017.×
  • Research Support: Support was provided solely from institutional and/or departmental sources.
    Research Support: Support was provided solely from institutional and/or departmental sources.×
  • Competing Interests: The authors declare no competing interests.
    Competing Interests: The authors declare no competing interests.×
  • Correspondence: Address correspondence to Dr. Crystal: 1340 N. Astor Street, Unit 605, Chicago, Illinois 60610. gcrystal@uic.edu. Information on purchasing reprints may be found at www.anesthesiology.org or on the masthead page at the beginning of this issue. Anesthesiology’s articles are made freely accessible to all readers, for personal use only, 6 months from the cover date of the issue.
Article Information
Review Article / Cardiovascular Anesthesia
Review Article   |   October 2017
Right Ventricular Perfusion: Physiology and Clinical Implications
Anesthesiology Newly Published on October 5, 2017. doi:10.1097/ALN.0000000000001891
Anesthesiology Newly Published on October 5, 2017. doi:10.1097/ALN.0000000000001891
Abstract

Regulation of blood flow to the right ventricle differs significantly from that to the left ventricle. The right ventricle develops a lower systolic pressure than the left ventricle, resulting in reduced extravascular compressive forces and myocardial oxygen demand. Right ventricular perfusion has eight major characteristics that distinguish it from left ventricular perfusion: (1) appreciable perfusion throughout the entire cardiac cycle; (2) reduced myocardial oxygen uptake, blood flow, and oxygen extraction; (3) an oxygen extraction reserve that can be recruited to at least partially offset a reduction in coronary blood flow; (4) less effective pressure–flow autoregulation; (5) the ability to downregulate its metabolic demand during coronary hypoperfusion and thereby maintain contractile function and energy stores; (6) a transmurally uniform reduction in myocardial perfusion in the presence of a hemodynamically significant epicardial coronary stenosis; (7) extensive collateral connections from the left coronary circulation; and (8) possible retrograde perfusion from the right ventricular cavity through the Thebesian veins. These differences promote the maintenance of right ventricular oxygen supply–demand balance and provide relative resistance to ischemia-induced contractile dysfunction and infarction, but they may be compromised during acute or chronic increases in right ventricle afterload resulting from pulmonary arterial hypertension. Contractile function of the thin-walled right ventricle is exquisitely sensitive to afterload. Acute increases in pulmonary arterial pressure reduce right ventricular stroke volume and, if sufficiently large and prolonged, result in right ventricular failure. Right ventricular ischemia plays a prominent role in these effects. The risk of right ventricular ischemia is also heightened during chronic elevations in right ventricular afterload because microvascular growth fails to match myocyte hypertrophy and because microvascular dysfunction is present. The right coronary circulation is more sensitive than the left to α-adrenergic–mediated constriction, which may contribute to its greater propensity for coronary vasospasm. This characteristic of the right coronary circulation may increase its vulnerability to coronary vasoconstriction and impaired right ventricular perfusion during administration of α-adrenergic receptor agonists.