title: Positive end-expiratory pressure does not compromise myocardial contractility in myocardial ischemia/reperfusion.
abstract: Therapy for severe myocardial ischemia/reperfusion sometimes necessitates intermittent positive pressure ventilation, which may impair left ventricular function by reduction of ventricular loading. It is unknown today whether positive airway pressure also affects contractile force after myocardial ischemia/reperfusion. The authors tested whether positive end-expiratory pressure (PEEP) impairs myocardial contractility in acute ischemic heart failure. In 11 anesthetized mechanically ventilated pigs (28 +/- 3 kg), cardiac output (CO, aortic flow probe), load-independent parameters of left ventricular contractility (conductance method: preload recruitable stroke work [PRSW] and end-systolic elastance [E(es)]) and preload (end-diastolic volume [EDV] conductance) were assessed before and after myocardial ischemia and reperfusion (left anterior descending artery occlusion, 60 min). Data were taken during PEEP 0, 5, and 10 cm H2O. Before myocardial ischemia, both PEEP 5 and 10 cm H2O reduced CO (P < 0.05) because of a reduction of EDV (P < 0.05, PEEP 10 cm H2O). The PRSW remained unchanged (not significant [NS]) and E(es) increased (P < 0.05, PEEP 10 cm H2O). After myocardial ischemia/reperfusion, CO and PRSW, but not E(es) (NS), deteriorated markedly. At the same time, PEEP 10 cm H2O reduced CO (P < 0.05) and, slightly, EDV (NS). Now, both PRSW (P < 0.05, PEEP 5 cm H2O) and E(es) (P < 0.05, PEEP 10 cm H2O) improved upon ventilation with PEEP. In our model, the administration of PEEP impaired global left ventricular function before and after myocardial ischemia/reperfusion. The observed impairment is not attributable to compromised contractility.
authors.affiliation: Department of Anesthesiology, Ludwig Maximilians University Munich, Klinikum Grosshadern, Munich, Germany. jkubitz@gmx.de
authors.forename: Jens Christian
authors.initials: JC
authors.lastname: Kubitz
authors.forename: Thorsten
authors.initials: T
authors.lastname: Annecke
authors.forename: Rabea
authors.initials: R
authors.lastname: Hinkel
authors.forename: Daniel Arnulf
authors.initials: DA
authors.lastname: Reuter
authors.forename: Nils
authors.initials: N
authors.lastname: Kronas
authors.forename: Steffi
authors.initials: S
authors.lastname: Forkl
authors.forename: Peter
authors.initials: P
authors.lastname: Boekstegers
authors.forename: Alwin Eduard
authors.initials: AE
authors.lastname: Goetz
authors.forename: Gregor Iwan
authors.initials: GI
authors.lastname: Kemming
mesh_terms: D000818:Animals; D001794:Blood Pressure; D002302:Cardiac Output; D006352:Heart Ventricles / Q000473:pathology; D009119:Muscle Contraction; D009200:Myocardial Contraction; D017202:Myocardial Ischemia / Q000473:pathology*; D009206:Myocardium / Q000473:pathology; D011175:Positive-Pressure Respiration; D011312:Pressure; D015427:Reperfusion Injury; D020521:Stroke; D013552:Swine; D013997:Time Factors; D014867:Water / Q000737:chemistry
chemical_list: D014867:Water