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Kubitz JC, Annecke T, Hinkel R, et al. Positive end-expiratory pressure does not compromise myocardial contractility in myocardial ischemia/reperfusion. Shock. 2007;27(6):638-43doi: 10.1097/01.shk.0000246906.32519.8e.
Kubitz, J. C., Annecke, T., Hinkel, R., Reuter, D. A., Kronas, N., Forkl, S., Boekstegers, P., Goetz, A. E., & Kemming, G. I. (2007). Positive end-expiratory pressure does not compromise myocardial contractility in myocardial ischemia/reperfusion. Shock (Augusta, Ga.), 27(6), 638-43. https://doi.org/10.1097/01.shk.0000246906.32519.8e
Kubitz, Jens Christian, et al. "Positive end-expiratory pressure does not compromise myocardial contractility in myocardial ischemia/reperfusion." Shock (Augusta, Ga.) vol. 27,6 (2007): 638-43. doi: https://doi.org/10.1097/01.shk.0000246906.32519.8e
Kubitz JC, Annecke T, Hinkel R, Reuter DA, Kronas N, Forkl S, Boekstegers P, Goetz AE, Kemming GI. Positive end-expiratory pressure does not compromise myocardial contractility in myocardial ischemia/reperfusion. Shock. 2007 Jun;27(6):638-43. doi: 10.1097/01.shk.0000246906.32519.8e. PMID: 17505303.
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Shock. 2007 Jun;27(6):638-43. doi: 10.1097/01.shk.0000246906.32519.8e.

Positive end-expiratory pressure does not compromise myocardial contractility in myocardial ischemia/reperfusion.

Shock (Augusta, Ga.)

Jens Christian Kubitz, Thorsten Annecke, Rabea Hinkel, Daniel Arnulf Reuter, Nils Kronas, Steffi Forkl, Peter Boekstegers, Alwin Eduard Goetz, Gregor Iwan Kemming

Affiliations

  1. Department of Anesthesiology, Ludwig Maximilians University Munich, Klinikum Grosshadern, Munich, Germany. [email protected]

PMID: 17505303 DOI: 10.1097/01.shk.0000246906.32519.8e

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.

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