title: Equivalent pressure-volume area accounts for oxygen consumption of fibrillating heart.
abstract: We attempted to find cardiac mechanical parameters to account for myocardial O2 consumption (VO2) during ventricular fibrillation (VF). We fully utilized the concept of pressure-volume (P-V) area (PVA), which is equivalent to the total mechanical energy generated by a ventricular contraction. We also utilized a multicompartment model consisting of multiple asynchronously contracting compartments, which we previously proposed to simulate the mechanics of a fibrillating ventricle. The model analysis had already validated the application of PVA to VF in terms of "equivalent PVA" (ePVA). ePVA is the area surrounded by the end-systolic and end-diastolic P-V relations in beating state and the isobaric P-V line at the VF pressure. ePVA is supposed to represent the total mechanical energy generated by single contractions of each compartment (or myocyte) in a fibrillating ventricle. We determined ePVA and correlated it with measured VO2 per minute (mVO2) at various ventricular volumes in electrically induced fibrillating left ventricles of the excised cross-circulated canine heart preparation. Correlation coefficient (r) of the mVO2-ePVA relation during VF was high (r = 0.95, P less than 0.01). Comparing mVO2 during VF with that in beating state at an unloaded ventricular volume, we calculated equivalent heart rate (eHR) as an estimate of the frequency of contractions of individual compartments (myocytes). With the use of both ePVA and eHR, mVO2 during VF at various ventricular volumes was estimated. The relation between estimated mVO2 and directly measured mVO2 was highly linear (r = 0.88, P less than 0.01), and the regression line almost agreed with the identity line (regression coefficient = 1.05). We conclude that the new ePVA and eHR concepts can reasonably account for VO2 during VF.
authors.affiliation: Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Osaka, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Yaku
authors.forename: Y
authors.initials: Y
authors.lastname: Goto
authors.forename: S
authors.initials: S
authors.lastname: Futaki
authors.forename: Y
authors.initials: Y
authors.lastname: Ohgoshi
authors.forename: O
authors.initials: O
authors.lastname: Kawaguchi
authors.forename: H
authors.initials: H
authors.lastname: Suga
mesh_terms: D000818:Animals; D003326:Coronary Circulation; D004285:Dogs; D004837:Epinephrine / Q000494:pharmacology; D006321:Heart / Q000187:drug effects / Q000502:physiology / Q000503:physiopathology*; D006323:Heart Arrest / Q000378:metabolism / Q000503:physiopathology; D006339:Heart Rate; D008433:Mathematics; D008955:Models, Cardiovascular; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption / Q000187:drug effects; D011433:Propranolol / Q000494:pharmacology; D014693:Ventricular Fibrillation / Q000378:metabolism / Q000503:physiopathology*
chemical_list: D011433:Propranolol; D004837:Epinephrine