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

Standard

Positive end-expiratory pressure does not compromise myocardial contractility in myocardial ischemia/reperfusion. / Kubitz, Jens; Annecke, Thorsten; Hinkel, Rabea; Reuter, Daniel; Kronas, Nils; Forkl, Steffi; Boekstegers, Peter; Goetz, Alwin Eduard; Kemming, Gregor Iwan.

In: SHOCK, Vol. 27, No. 6, 6, 2007, p. 638-643.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

Harvard

Kubitz, J, Annecke, T, Hinkel, R, Reuter, D, Kronas, N, Forkl, S, Boekstegers, P, Goetz, AE & Kemming, GI 2007, 'Positive end-expiratory pressure does not compromise myocardial contractility in myocardial ischemia/reperfusion.', SHOCK, vol. 27, no. 6, 6, pp. 638-643. <http://www.ncbi.nlm.nih.gov/pubmed/17505303?dopt=Citation>

APA

Kubitz, J., Annecke, T., Hinkel, R., Reuter, D., 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, 27(6), 638-643. [6]. http://www.ncbi.nlm.nih.gov/pubmed/17505303?dopt=Citation

Vancouver

Kubitz J, Annecke T, Hinkel R, Reuter D, Kronas N, Forkl S et al. Positive end-expiratory pressure does not compromise myocardial contractility in myocardial ischemia/reperfusion. SHOCK. 2007;27(6):638-643. 6.

Bibtex

@article{15ad35009b3b4ec59ec3a8d1193f5ca6,
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.",
author = "Jens Kubitz and Thorsten Annecke and Rabea Hinkel and Daniel Reuter and Nils Kronas and Steffi Forkl and Peter Boekstegers and Goetz, {Alwin Eduard} and Kemming, {Gregor Iwan}",
year = "2007",
language = "Deutsch",
volume = "27",
pages = "638--643",
journal = "SHOCK",
issn = "1073-2322",
publisher = "Lippincott Williams and Wilkins",
number = "6",

}

RIS

TY - JOUR

T1 - Positive end-expiratory pressure does not compromise myocardial contractility in myocardial ischemia/reperfusion.

AU - Kubitz, Jens

AU - Annecke, Thorsten

AU - Hinkel, Rabea

AU - Reuter, Daniel

AU - Kronas, Nils

AU - Forkl, Steffi

AU - Boekstegers, Peter

AU - Goetz, Alwin Eduard

AU - Kemming, Gregor Iwan

PY - 2007

Y1 - 2007

N2 - 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.

AB - 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.

M3 - SCORING: Zeitschriftenaufsatz

VL - 27

SP - 638

EP - 643

JO - SHOCK

JF - SHOCK

SN - 1073-2322

IS - 6

M1 - 6

ER -