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. 2018 Apr 1;197(7):905-912.
doi: 10.1164/rccm.201709-1818OC.

Pulmonary Vasodilator Therapy in Shock-associated Cardiac Arrest

Ryan W Morgan  1 , Robert M Sutton  1 , Michael Karlsson  1 , Andrew J Lautz  1   2 , Constantine D Mavroudis  1 , William P Landis  1 , Yuxi Lin  1 , Sejin Jeong  1 , Nancy Craig  1 , Vinay M Nadkarni  1 , Todd J Kilbaugh  1 , Robert A Berg  1
Affiliations

Pulmonary Vasodilator Therapy in Shock-associated Cardiac Arrest

Ryan W Morgan et al. Am J Respir Crit Care Med. .

Abstract

Rationale: Many in-hospital cardiac arrests are precipitated by hypotension, often associated with systemic inflammation. These patients are less likely to be successfully resuscitated, and novel approaches to their treatment are needed.

Objectives: To determine if the addition of inhaled nitric oxide (iNO) to hemodynamic-directed cardiopulmonary resuscitation (HD-CPR) would improve short-term survival from cardiac arrest associated with shock and systemic inflammation.

Methods: In 3-month-old swine (n = 21), LPS was intravenously infused, inducing systemic hypotension. Ventricular fibrillation was induced, and animals were randomized to blinded treatment with either: 1) HD-CPR with iNO, or 2) HD-CPR without iNO. During HD-CPR, chest compression depth was titrated to peak aortic compression pressure of 100 mm Hg, and vasopressor administration was titrated to coronary perfusion pressure greater than or equal to 20 mm Hg. Defibrillation attempts began after 10 minutes of resuscitation. The primary outcome was 45-minute survival.

Measurements and main results: The iNO group had higher rates of 45-minute survival (10 of 10 vs. 3 of 11; P = 0.001). During cardiopulmonary resuscitation, the iNO group had lower pulmonary artery relaxation pressure (mean ± SEM, 10.9 ± 2.4 vs. 18.4 ± 2.4 mm Hg; P = 0.03), higher coronary perfusion pressure (21.1 ± 1.5 vs. 16.9 ± 1.0 mm Hg; P = 0.005), and higher aortic relaxation pressure (36.6 ± 1.6 vs. 30.4 ± 1.1 mm Hg; P < 0.001) despite shallower chest compressions (5.88 ± 0.25 vs. 6.46 ± 0.40 cm; P = 0.02) and fewer vasopressor doses in the first 10 minutes (median, 4 [interquartile range, 3-4] vs. 5 [interquartile range, 5-6], P = 0.03).

Conclusions: The addition of iNO to HD-CPR in LPS-induced shock-associated cardiac arrest improved short-term survival and intraarrest hemodynamics.

Keywords: cardiopulmonary resuscitation; heart arrest; inhaled nitric oxide; shock.

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Figures

Figure 1.
Figure 1.
Experimental protocol. CoPP = coronary perfusion pressure; CPR = cardiopulmonary resuscitation; HD-CPR = hemodynamic-directed cardiopulmonary resuscitation; iNO = inhaled nitric oxide; ppm = parts per million; ROSC = return of spontaneous circulation; VF = ventricular fibrillation.
Figure 2.
Figure 2.
Study flowchart. HD-CPR = hemodynamic-directed cardiopulmonary resuscitation; iNO = inhaled nitric oxide.
Figure 3.
Figure 3.
Coronary perfusion pressure during cardiopulmonary resuscitation. Coronary perfusion pressure during 10 minutes of cardiopulmonary resuscitation (CPR) in hemodynamic-directed (HD)-CPR with inhaled nitric oxide (iNO) versus HD-CPR without iNO. Error bars represent SEM. Comparison between groups using generalized estimating equation regression model.
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