Elsevier

Resuscitation

Volume 84, Issue 5, May 2013, Pages 696-701
Resuscitation

Experimental paper
Hemodynamic directed CPR improves short-term survival from asphyxia-associated cardiac arrest

https://doi.org/10.1016/j.resuscitation.2012.10.023Get rights and content

Abstract

Aim

Adequate coronary perfusion pressure (CPP) during cardiopulmonary resuscitation (CPR) is essential for establishing return of spontaneous circulation. The objective of this study was to compare short-term survival using a hemodynamic directed resuscitation strategy versus an absolute depth-guided approach in a porcine model of asphyxia-associated cardiac arrest. We hypothesized that a hemodynamic directed approach would improve short-term survival compared to depth-guided care.

Methods

After 7 min of asphyxia, followed by induction of ventricular fibrillation, 19 female 3-month old swine (31 ± 0.4 kg) were randomized to receive one of three resuscitation strategies: (1) hemodynamic directed care (CPP-20): chest compressions (CCs) with depth titrated to a target systolic blood pressure of 100 mmHg and titration of vasopressors to maintain CPP > 20 mmHg; (2) depth 33 mm (D33): target CC depth of 33 mm with standard American Heart Association (AHA) epinephrine dosing; or (3) depth 51 mm (D51): target CC depth of 51 mm with standard AHA epinephrine dosing. All animals received manual CPR guided by audiovisual feedback for 10 min before first shock.

Results

45-Min survival was higher in the CPP-20 group (6/6) compared to D33 (1/7) or D51 (1/6) groups; p = 0.002. Coronary perfusion pressures were higher in the CPP-20 group compared to D33 (p = 0.011) and D51 (p = 0.04), and in survivors compared to non-survivors (p < 0.01). Total number of vasopressor doses administered and defibrillation attempts were not different.

Conclusions

Hemodynamic directed care targeting CPPs > 20 mmHg improves short-term survival in an intensive care unit porcine model of asphyxia-associated cardiac arrest.

Introduction

The success of cardiopulmonary resuscitation (CPR) depends on adequate myocardial blood flow.1, 2, 3, 4 Nevertheless, current guidelines for the treatment of cardiac arrest assume that all patients can be treated with a uniform chest compression (CC) depth despite a paucity of data indicating that a specific depth consistently provides adequate myocardial blood flow.5, 6 A treatment strategy to titrate compression depth and vasopressor dosing to physiological parameters that are more closely related to myocardial blood flow would presumably be a more successful approach, and would be a major paradigm shift in the field of resuscitation.

During CPR, coronary perfusion pressure (CPP), the aortic pressure minus the right atrial pressure during the relaxation (“diastolic”) phase of CPR, is the primary determinant of myocardial blood flow.2, 7, 8 Therefore, it is not surprising that in both human and animal studies, CPP is also associated with resuscitation outcome.3, 4, 9, 10, 11 Failure to generate a CPP of at least 15–20 mmHg during CPR is rarely associated with a successful resuscitation.2, 3, 11 Importantly, many patients with in-hospital cardiac arrests are in intensive care units and have invasive hemodynamic monitoring,12, 13 so a hemodynamic directed CPR strategy targeted to attain an adequate CPP could be implemented.

This randomized investigation compared short-term survival with a hemodynamic directed resuscitation strategy intended to attain CPPs > 20 mmHg (CPP-20) versus absolute depth-guided CPR in a porcine model of asphyxia-associated cardiac arrest. We further subdivided the depth-guided CPR into two groups: one with CC depth targeted to previously documented “usual care” of 33 mm (D33) and one with CCs targeted to the American Heart Association (AHA) 2010 guideline recommended depth of 51 mm (D51). We hypothesized that the CPP-20 resuscitation strategy would improve short-term survival compared to either D33 or D51.

Section snippets

Animal preparation

The experimental protocol was approved by The University of Pennsylvania Institutional Animal Care and Use Committee. Nineteen healthy 3-month old female domestic swine were anesthetized and mechanically ventilated using a Datex Ohmeda anesthesia machine (Modulus SE) on a mixture of room air and titrated isoflurane (∼1.0–2.5%) with a tidal volume of 12 mL/kg, PEEP 6 cm H2O, rate of 12 breaths/min, and titration of rate to maintain end-tidal carbon dioxide (ETCO2) at 38–42 mmHg (NICO, Novametrix

Results

The primary outcome variable of 45-min ICU survival and the secondary outcome variable of any ROSC were both significantly different across treatments (Table 1) with superior survival rates in the CPP-20 group. In a model using generalized estimating equations (GEE), coronary perfusion pressure (Fig. 2) was significantly higher in the CPP-20 group compared to both D33 (p = 0.011) and D51 (p = 0.04), and higher in survivors compared to non-survivors irrespective of treatment group (p < 0.01).

Discussion

This study establishes that short-term survival from asphyxia-associated cardiac arrest can be superior after hemodynamic directed CPR to maintain coronary perfusion pressure >20 mmHg (CPP-20) compared to resuscitation with depth of compressions guided to either 33 mm or 51 mm and standard AHA vasopressor dosing. Congruent with previous investigations,2, 3, 11 coronary perfusion pressures were higher in survivors compared to non-survivors irrespective of treatment group, providing mechanistic

Conclusions

In this novel intensive care unit model of asphyxia-associated cardiac arrest, short-term survival was improved when resuscitation therapy was titrated to CPR-generated physiology with specific hemodynamic goals as compared to currently recommended uniform guidelines even with excellent 51 mm compression depth. This treatment protocol individualizes therapy to the patient's hemodynamic status in contrast to the usual “one-size-fits-all” strategy. As more in-hospital cardiac arrests are occurring

Conflict of interest statement

This study was funded by the Laerdal Foundation for Acute Care Medicine, the National Institute of Child Health and Human Development (RMS K23), the National Institute of Neurological Disorders and Stroke (SHF K08), and CHOP CCM Endowed Chair Funds.

Acknowledgments

We would also like to thank Lori Boyle, Jessica Leffelman, and Stephanie Tuttle who have supported resuscitation science at the University of Pennsylvania and Children's Hospital of Philadelphia.

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    A Spanish translated version of the summary of this article appears as Appendix in the final online version at http://dx.doi.org/10.1016/j.resuscitation.2012.10.023.

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