Desflurane, sevoflurane, and isoflurane impair canine left ventricular-arterial coupling and mechanical efficiency.
BACKGROUND
The effects of desflurane, sevoflurane, and isoflurane on left ventricular-arterial coupling and mechanical efficiency were examined and compared in acutely instrumented dogs.


METHODS
Twenty-four open-chest, barbiturate-anesthetized dogs were instrumented for measurement of aortic and left ventricular (LV) pressure (micromanometer-tipped catheter), dP/dtmax, and LV volume (conductance catheter). Myocardial contractility was assessed with the end-systolic pressure-volume relation (Ees) and preload recruitable stroke work (Msw) generated from a series of LV pressure-volume diagrams. Left ventricular-arterial coupling and mechanical efficiency were determined by the ratio of Ees to effective arterial elastance (Ea; the ratio of end-systolic arterial pressure to stroke volume) and the ratio of stroke work (SW) to pressure-volume area (PVA), respectively.


RESULTS
Desflurane, sevoflurane, and isoflurane reduced heart rate, mean arterial pressure, and left ventricular systolic pressure. All three anesthetics caused similar decreases in myocardial contractility and left ventricular afterload, as indicated by reductions in Ees, Msw, and dP/dtmax and Ea, respectively. Despite causing simultaneous declines in Ees and Ea, desflurane decreased Ees/Ea (1.02 +/- 0.16 during control to 0.62 +/- 0.14 at 1.2 minimum alveolar concentration) and SW/PVA (0.51 +/- 0.04 during control to 0.43 +/- 0.05 at 1.2 minimum alveolar concentration). Similar results were observed with sevoflurane and isoflurane.


CONCLUSIONS
The present findings indicate that volatile anesthetics preserve optimum left ventricular-arterial coupling and efficiency at low anesthetic concentrations (< 0.9 minimum alveolar concentration); however, mechanical matching of energy transfer from the left ventricle to the arterial circulation degenerates at higher end-tidal concentrations. These detrimental alterations in left ventricular-arterial coupling produced by desflurane, sevoflurane, and isoflurane contribute to reductions in overall cardiac performance observed with these agents in vivo.
Hettrick
D A
DA
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226, USA.
Pagel
P S
PS
Warltier
D C
DC
D000758:Anesthesia; D018685:Anesthetics, Inhalation / Q000633:toxicity*; D000818:Animals; D001011:Aorta / Q000187:drug effects* / Q000502:physiology; D001463:Barbiturates; D001794:Blood Pressure / Q000187:drug effects; D003864:Depression, Chemical; D000077335:Desflurane; D004285:Dogs; D004987:Ethers / Q000633:toxicity; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D007530:Isoflurane / Q000031:analogs & derivatives / Q000633:toxicity; D008297:Male; D008738:Methyl Ethers; D009200:Myocardial Contraction / Q000187:drug effects; D000077149:Sevoflurane; D013318:Stroke Volume / Q000187:drug effects; D016277:Ventricular Function, Left / Q000187:drug effects* / Q000502:physiology; D017725:Ventricular Pressure / Q000187:drug effects
D018685:Anesthetics, Inhalation; D001463:Barbiturates; D004987:Ethers; D008738:Methyl Ethers; D000077149:Sevoflurane; D000077335:Desflurane; D007530:Isoflurane