Effects of Left Ventricular Versus Traditional Chest Compressions in a Traumatic Pulseless Electrical Activity Model.

BACKGROUND: Prehospital cardiopulmonary resuscitation has commonly been considered ineffective in traumatic cardiopulmonary arrest because traditional chest compressions do not produce substantial cardiac output. However, recent evidence suggests that chest compressions located over the left ventricle (LV) produce greater hemodynamics when compared to traditional compressions. We hypothesized that chest compressions located directly over the LV would result in an increase in return of spontaneous circulation (ROSC) and hemodynamic variables, when compared to traditional chest compressions, in a swine model of traumatic pulseless electrical activity (PEA). METHODS: Transthoracic echocardiography was used to mark the location of the aortic root (traditional compressions) and the center of the LV on animals (n = 34) that were randomized to receive chest compressions in one of the two locations. Animals were hemorrhaged to mean arterial pressure <20 to simulate traumatic PEA. After 5 minutes of PEA, basic life support (BLS) with mechanical cardiopulmonary resuscitation was initiated and performed for 10 minutes followed by advanced life support for an additional 10 minutes. Hemodynamic variables were averaged over the final 2 minutes of BLS and advanced life support periods. RESULTS: Six of the LV group (35%) achieved ROSC compared to eight of the traditional group (47%) (P = .73). There was an increase in aortic systolic blood pressure (P < .01), right atrial systolic blood pressure (P < .01), and right atrial diastolic blood pressure (P = .02) at the end of BLS in the LV group compared to the traditional group. CONCLUSIONS: In our swine model of traumatic PEA, chest compressions performed directly over the LV improved blood pressures during BLS but not ROSC.

The Effect of Chest Compression Location and Occlusion of the Aorta in a Traumatic Arrest Model.

BACKGROUND: Recent evidence demonstrates that closed chest compressions directly over the left ventricle (LV) in a traumatic cardiac arrest (TCA) model improve hemodynamics and return of spontaneous circulation (ROSC) when compared with traditional compressions. Resuscitative endovascular balloon occlusion of the aorta (REBOA) also improves hemodynamics and controls hemorrhage in TCA. We hypothesized that chest compressions located over the LV would result in improved hemodynamics and ROSC in a swine model of TCA using REBOA. MATERIALS AND METHODS: Transthoracic echo was used to mark the location of the aortic root (traditional location) and the center of the LV on animals (n = 26), which were randomized to receive chest compressions in one of the two locations. After hemorrhage, ventricular fibrillation was induced to simulate TCA. After a period of 10 min of ventricular fibrillation, basic life support (BLS) with mechanical cardiopulmonary resuscitation was initiated and performed for 10 min followed by advanced life support for an additional 10 min. REBOA balloons were inflated at 6 min into BLS. Hemodynamic variables were averaged during the final 2 min of the BLS and advanced life support periods. Survival was compared between this REBOA cohort and a control group without REBOA (no-REBOA cohort) (n = 26). RESULTS: There was no significant difference in ROSC between the two REBOA groups (P = 0.24). Survival was higher with REBOA group versus no-REBOA group (P = 0.02). CONCLUSIONS: There was no difference in ROSC between LV and traditional compressions when REBOA was used in this swine model of TCA. REBOA conferred a survival benefit regardless of compression location.

A Traumatic Pulseless Electrical Activity Model: Mortality Increases With Hypovolemia Time.

BACKGROUND: There currently are no well-defined animal models for traumatic pulseless electrical activity (PEA). Our objective was to develop a swine model of traumatic PEA that would be useful for laboratory research where mortality is an outcome of interest. In this pilot study, we hypothesized that animals that remained in PEA without intervention for a longer period would have increased mortality. MATERIALS AND METHODS: Sixteen Yorkshire swine were alternately allocated to either 5 or 10 min of traumatic PEA without intervention. After the nonintervention period, basic life support (BLS) with mechanical cardiopulmonary resuscitation was initiated and performed for 10 min followed by advanced life support (ALS) for an additional 10 min. Hemodynamic and laboratory values are reported for baseline, posthemorrhage, end of BLS, and end of ALS periods. RESULTS: Mortality in the 10-min PEA group (100%) was higher than the 5-min group (38%) (P = 0.03). Animals in the 5-min group had improved aortic diastolic blood pressure, coronary perfusion pressure, and end-tidal CO2 at the end of both the BLS (P = 0.02, 0.002, and 0.02, respectively) and ALS (P = 0.009, 0.005, and 0.008, respectively). The 10-min animals had increased hyperkalemia at the end of the BLS (P = 0.004) and ALS (P = 0.005) periods. All animals in the 10-min group developed ventricular fibrillation (VF) and 38% of the 5-min animals developed VF (P = 0.03). CONCLUSIONS: In our pilot study of traumatic PEA in a swine model, a shorter period of nonintervention resulted in increased survival, improved hemodynamics during resuscitation, decreased hyperkalemia, and less incidence of conversion to VF arrest.

Left ventricular compressions improve return of spontaneous circulation and hemodynamics in a swine model of traumatic cardiopulmonary arrest.

BACKGROUND: Prehospital cardiopulmonary resuscitation, including closed chest compressions, has commonly been considered ineffective in traumatic cardiopulmonary arrest (TCPA) because traditional chest compressions do not produce substantial cardiac output. However, recent evidence suggests that chest compressions located over the left ventricle (LV) produce greater hemodynamics when compared to traditional compressions. We hypothesized that chest compressions located directly over the LV would improve return of spontaneous circulation (ROSC) and hemodynamics when compared with traditional chest compressions, in a swine model of TCPA. METHODS: Transthoracic echocardiography was used to mark the location of the aortic root (traditional compressions), and the center of the LV on animals (n = 26) which were randomized to receive chest compressions in one of the two locations. After hemorrhage, ventricular fibrillation was induced. After 10 minutes of ventricular fibrillation, basic life support (BLS) with mechanical cardiopulmonary resuscitation was initiated and performed for 10 minutes followed by advanced life support (ALS) for an additional 10 minutes. During BLS, the area of maximal compression was verified using transesophageal echocardiography. Hemodynamic variables were averaged over the final 2 minutes of the BLS and ALS periods. RESULTS: Five (38%) of the LV group achieved ROSC compared with zero of the aortic root group (p = 0.04). Additionally, there was an increase in aortic systolic blood pressure (SBP), aortic diastolic blood pressure (DBP) and coronary perfusion pressure (CPP) at the end of both the BLS (95% confidence interval, SBP, -49 to -21; DBP, -14 to -5.6; and CPP, -15 to -7.4) and ALS (95% confidence interval: SBP, -66 to -21; DBP, -49 to -6.8; and CPP, -51 to -7.5) resuscitation periods among the LV group. CONCLUSION: In our swine model of TCPA, chest compressions performed directly over the LV improved ROSC and hemodynamics when compared with traditional chest compressions.

Left Ventricular Compressions Improve Hemodynamics in a Swine Model of Out-of-Hospital Cardiac Arrest.

INTRODUCTION: We hypothesized that chest compressions located directly over the left ventricle (LV) would improve hemodynamics, including coronary perfusion pressure (CPP), and return of spontaneous circulation (ROSC) in a swine model of cardiac arrest. METHODS: Transthoracic echocardiography (echo) was used to mark the location of the aortic root and the center of the left ventricle on animals (n = 26) which were randomized to receive chest compressions in one of the two locations. After a period of ten minutes of ventricular fibrillation, basic life support (BLS) with mechanical cardiopulmonary resuscitation (CPR) was initiated and performed for ten minutes followed by advanced cardiac life support (ACLS) for an additional ten minutes. During BLS the area of maximal compression was verified using transesophageal echo. CPP and other hemodynamic variables were averaged every two minutes. RESULTS: Mean CPP was not significantly higher in the LV group during all time intervals of resuscitation; mean CPP was significantly higher in the LV group during the 12-14 minute interval of BLS and during minutes 22-30 of ACLS (p < 0.05). Aortic systolic and diastolic pressures, right atrial systolic pressures, and end-tidal CO2 (ETCO2) were higher in the LV group during all time intervals of resuscitation (p < 0.05). Nine of the left ventricle group (69%) achieved ROSC and survived to 60 minutes compared to zero of the aortic root group (p < 0.001). CONCLUSIONS: In our swine model of cardiac arrest, chest compressions over the left ventricle improved hemodynamics and resulted in a greater proportion of animals with ROSC and survival to 60 minutes.

Intravenous Lipid Emulsion Therapy for Severe Diphenhydramine Toxicity: A Randomized, Controlled Pilot Study in a Swine Model.

STUDY OBJECTIVE: Diphenhydramine is a moderately lipophilic antihistamine with sodium channel blockade properties. It is consumed recreationally for mild hallucinogenic and hypnotic effects and causes dysrhythmias, seizures, and death with overdose. Intravenous lipid emulsion is a novel agent used to treat lipophilic drug overdose. Two case reports describe clinical improvement with intravenous lipid emulsion after diphenhydramine toxicity, but no prospective studies have been reported. Our objective is to determine whether intravenous lipid emulsion improved hypotension compared with sodium bicarbonate for severe diphenhydramine toxicity in a model of critically ill swine. METHODS: Twenty-four swine weighing 45 to 55 kg were infused with diphenhydramine at 1 mg/kg per minute until the mean arterial pressure reached 60% of baseline. Subjects were randomized to receive intravenous lipid emulsion (bolus of 7 mL/kg and then 0.25 mL/kg per minute) or sodium bicarbonate (2 mEq/kg plus an equal volume of normal saline solution). We measured pulse rate, systolic blood pressure, mean arterial pressure, cardiac output, QRS interval, and serum diphenhydramine level. Twelve animals per group provided a power of 0.8 and α of .05 to detect a 50% difference in mean arterial pressure. We assessed differences between groups with a repeated-measures linear model (MIXED) and Kaplan-Meier estimation methods. We compared systolic blood pressure, mean arterial pressure, and cardiac output with repeated measures ANOVA. RESULTS: Baseline weight, hemodynamic parameters, QRS interval, time to hypotension, and diphenhydramine dose required to achieve hypotension were similar between groups. After hypotension was reached, there was no overall difference between intravenous lipid emulsion and sodium bicarbonate groups for cardiac output or QRS intervals; however, there were transient differences in mean arterial pressure and systolic blood pressure, favoring intravenous lipid emulsion (difference: mean arterial pressure, sodium bicarbonate versus intravenous lipid emulsion -20.7 [95% confidence interval -31.6 to -9.8]; systolic blood pressure, sodium bicarbonate versus intravenous lipid emulsion -24.8 [95% confidence interval -37.6 to -12.1]). Time to death was similar. One intravenous lipid emulsion and 2 sodium bicarbonate pigs survived. End-of-study mean total serum diphenhydramine levels were similar. The mean lipid layer diphenhydramine level was 6.8 µg/mL (SD 3.1 µg/mL) and mean aqueous layer level 8.6 µg/mL (SD 5.5 µg/mL). CONCLUSION: In our study of diphenhydramine-induced hypotensive swine, we found no difference in hypotension, QRS widening, or diphenhydramine levels in aqueous layers between intravenous lipid emulsion and sodium bicarbonate.