Cardiopulmonary resuscitation in the rat

1988 ◽  
Vol 65 (6) ◽  
pp. 2641-2647 ◽  
Author(s):  
I. von Planta ◽  
M. H. Weil ◽  
M. von Planta ◽  
J. Bisera ◽  
S. Bruno ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Cardiopulmonary Resuscitation ◽  
Aortic Pressure ◽  
Coronary Perfusion Pressure ◽  
Low Flow ◽  
Coronary Perfusion ◽  
Flow State ◽  
Successful Resuscitation ◽  
End Tidal ◽  
The Right

A standardized method of cardiopulmonary resuscitation in rodents has been developed for anesthetized, mechanically ventilated rats. Ventricular fibrillation was induced and maintained by an alternating current delivered to the right ventricular endocardium. After 4 min of ventricular fibrillation, the chest was compressed with a pneumatic piston device. Eight of 14 animals were successfully resuscitated with DC countershock after 6 min of cardiac arrest. In confirmation of earlier studies from our laboratories in dogs, pigs, and human patients, this rodent model of cardiopulmonary resuscitation demonstrated large venoarterial [H+] and PCO2 gradients associated with reduced pulmonary excretion of CO2 during the low-flow state. Mean aortic pressure, coronary perfusion pressure, and end-tidal CO2 during chest compression were predictive of successful resuscitation.

Cardiopulmonary resuscitation in the mouse

2002 ◽  
Vol 93 (4) ◽  
pp. 1222-1226 ◽  
Author(s):  
Lei Song ◽  
Max Harry Weil ◽  
Wanchun Tang ◽  
Shijie Sun ◽  
Tommaso Pellis
Keyword(s):  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Cardiopulmonary Arrest ◽  
Threshold Level ◽  
Aortic Pressure ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Successful Resuscitation ◽  
Threshold Levels ◽  
The Right

We sought to develop a model of cardiac arrest and resuscitation on mice that would be comparable to that of large mammals and would allow for more fundamental investigations on cardiopulmonary arrest and cardiac resuscitation. A model of cardiopulmonary resuscitation previously developed by our group on rats was adapted to anesthetized, mechanically ventilated adult male Institute of Cancer Research mice that weighed 46 ± 3 g. The trachea was intubated through the mouth, and end-tidal Pco 2(Pet CO2 ) was measured with a microcapnometer. Catheters were advanced into the aorta and into the right atrium, and coronary perfusion pressure (CPP) was computed. A 1.5-mA alternating current was delivered to the right ventricular endocardium, which produced ventricular fibrillation or a pulseless rhythm. Precordial compression was begun 4 min later. Ten sequential studies were performed, during which five animals were successfully resuscitated and five failed resuscitation efforts. Successful resuscitation was contingent on the restoration of threshold levels of CPP and Pet CO2 during chest compression. As in rats, swine, and human patients, threshold levels of mean aortic pressure, CPP, and Pet CO2 were critical determinates of resuscitability in this murine model of threshold level of cardiac arrest and resuscitation.

Abstract 289: Effect of Elevated Legs on Hemodynamic Performance During Cardiopulmonary Resuscitation in a Porcine Model of Cardiac Arrest

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Eric Qvigstad ◽  
Andres Neset ◽  
Theresa M Olasveengen ◽  
øystein Tømte ◽  
Morten Eriksen ◽  
...  
Keyword(s):  
Blood Flow ◽  
Supine Position ◽  
Life Support ◽  
Advanced Life Support ◽  
Aortic Pressure ◽  
Coronary Perfusion Pressure ◽  
Right Atrial ◽  
Positive Pressure ◽  
Coronary Perfusion ◽  
End Tidal

Purpose of the study: During advanced life support (ALS) end-tidal carbon dioxide (EtCO 2 ) reflects cardiac output (CO). A recent clinical study found an association between passive leg raising (PLR) and increased EtCO 2 during ALS. This may reflect a transient increase in pulmonary blood flow and CO, but might cause a detrimental decrease in coronary perfusion pressure (CPP). We evaluated the effect of PLR during experimental ALS in a randomized, factorial design. Materials and methods: In nine anesthetized domestic pigs (30±1.8 kg) ventricular fibrillation was induced electrically. After 3 minutes of no-flow, mechanical chest compressions (5cm @ 100 min -1 ) were started. During four 5-minute segments of CPR we measured CO, EtCO 2 , perfusion pressures, carotid and cerebral cortical microcirculatory blood flow (MBF) and CPP (the average of the positive pressure difference between decompression aortic pressure (AP) and right atrial pressure (RAP)) at minute 2 and 4. Interventions were provided in a randomized sequence with PLR vs supine position, with or without epinephrine (0.5mg iv). Values are given as mean±standard deviation. Results: PLR did not increase EtCO2 compared to supine position (3.1±0.7 vs 3.0±0.8 kPa), but CO was minimally increased from 1.1±0.3 to 1.2±0.3 Lmin -1 ,(p=0.003). PLR did not significantly increase AP (57±15 vs. 48±18 mmHg, p=0.3), but RAP was higher (43±10 vs. 31±7, p=0.003). However, no difference was found in CPP due to marked variation in both groups (median(range): PLR 20 (9,43) and supine 17(9,58)). The effect of epinephrine during this experimental setup was minimal. Conclusion: We did not find a positive effect of PLR during experimental ALS, but there were no obviously detrimental effects either.

Abstract 306: Similar Hemodynamic Efficacy Between 30 mm and 50 mm Compression Depth During Mechanical Chest Compression with Weil Mini Chest Compressor

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Zhengfei Yang ◽  
Ping Gong ◽  
Xiaobo Wu ◽  
Jie Qian ◽  
Shen Zhao ◽  
...  
Keyword(s):  
Chest Compression ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Compression Depth ◽  
Successful Resuscitation ◽  
Mechanical Chest Compression ◽  
Significant Difference ◽  
Manual Chest Compression ◽  
End Tidal ◽  
Mechanical Cpr

Introduction: Current guidelines require a 50 mm compression depth for manual chest compression. During mechanical chest compression, however, because of the design of each device, whether this depth yields the most optimal hemodynamic efficacy remains to be tested. In this study, we investigated the effects of compression depth on hemodynamics efficacy during mechanical CPR with the Weil Mini Chest Compressor in a porcine model. Hypothesis: There is no significant difference in hemodynamic efficacy between compression depth of 30 mm and 50 mm during mechanical CPR with the Weil Mini Chest Compressor. Methods: Ten male domestic pigs weighing 34±2 kg were utilized. Ventricular fibrillation was electrically induced and untreated for 7 min. The animals were then randomized to receive compression depth of 30 mm or 50 mm. Coincident with the start of precordial compression, the animals were mechanically ventilated at a rate of 10 breaths per minute. Defibrillation was attempted by a single 150 J shock. If resuscitation was not successful, CPR was resumed for 2 mins prior to the next defibrillation until either successful resuscitation or for a total of 15 mins. Results: All animals were successfully resuscitated. There were no differences in coronary perfusion pressure (CPP), end-tidal carbon dioxide (ETCO2) and carotid blood flow (CBF) between the two groups (Table). A significantly less rib fracture was observed in the 30 mm group [0 (0-0) vs 1.2 (0-2), p<0.05]. Conclusion: Similar hemodynamic efficacy was observed between 30 and 50 mm compression depth during mechanical CPR with the Weil Mini Chest Compressor.

Calcium-entry blockers during porcine cardiopulmonary resuscitation

1990 ◽  
Vol 78 (2) ◽  
pp. 207-213 ◽  
Author(s):  
Martin von Planta ◽  
Max Harry Weil ◽  
Raul J. Gazmuri ◽  
Marc A. Ritz ◽  
Eric C. Rackow
Keyword(s):  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Co2 Concentration ◽  
Coronary Perfusion Pressure ◽  
Calcium Entry ◽  
Coronary Perfusion ◽  
Calcium Entry Blockers ◽  
Coronary Vein ◽  
End Tidal ◽  
Canine Myocardium

1. Calcium-entry blockers increase the intramyo-cardial pH and decrease the intramyocardial Pco2 of ischaemic canine myocardium. However, the evidence documenting improvements in myocardial acidosis and in myocardial resuscitability after administration of calcium-entry blockers during cardiac arrest is incomplete. We therefore compared the effects of verapamil (0.05 mg/kg) and diltiazem (0.075 mg/kg) with those of saline placebo in an established porcine model of cardiac arrest and cardiopulmonary resuscitation. 2. After verapamil, six of 11 animals were successfully resuscitated; after diltiazem, five of 10; and after saline placebo, six of 10. Coronary perfusion and mean aortic pressures together with end-tidal CO2 concentration during precordial compression were predictive of resuscitation, independently of the drug or placebo. 3. Coronary vein pH decreased to 6.91 ± 0.06 units (mean ± sem) with concurrent increases in Pco2 to levels exceeding 100 mmHg. Coronary vein lactate increased to a maximum of 7.5 ± 0.6 mmol/l. Coronary vein acidaemia was accompanied by decreases in intramyocardial pH to 6.64 ± 0.06 units. However, each of these differences between success and failure of resuscitation was unrelated to treatment with calcium-entry blockers. 4. Accordingly, neither verapamil nor diltiazem selectively altered coronary perfusion pressure, attenuated intramyocardial acidosis or improved resuscitability after porcine cardiac arrest and cardiopulmonary resuscitation.

Endobronchial Vasopressin Improves Survival during Cardiopulmonary Resuscitation in Pigs 

1997 ◽  
Vol 86 (6) ◽  
pp. 1375-1381 ◽  
Author(s):  
Volker Wenzel ◽  
Karl H. Lindner ◽  
Andreas W. Prengel ◽  
Keith G. Lurie ◽  
Hans U. Strohmenger
Keyword(s):  
Placebo Group ◽  
Cardiopulmonary Resuscitation ◽  
Drug Administration ◽  
Porcine Model ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Spontaneous Circulation ◽  
Coronary Perfusion ◽  
Successful Resuscitation ◽  
Short Period

Background Intravenous administration of vasopressin during cardiopulmonary resuscitation (CPR) has been shown to be more effective than optimal doses of epinephrine. This study evaluated the effect of endobronchial vasopressin during CPR. Methods After 4 min of untreated ventricular fibrillation and 3 min of CPR, 21 pigs were randomized to be treated with 0.8 U/kg intravenous vasopressin (n = 7), 0.8 U/kg endobronchial vasopressin (n = 9), or an endobronchial placebo of normal saline (n = 5). Defibrillation was performed 5 min after drug administration to attempt return of spontaneous circulation. Results All animals in the intravenous and endobronchial vasopressin group were resuscitated successfully, but only two of five animals in the placebo group were. At 2 and 5 min after drug administration, coronary perfusion pressure in the intravenous and endobronchial vasopressin group was significantly higher than in the placebo group (50 +/- 10, 34 +/- 5 vs. 16 +/- 6 mmHg, respectively; and 35 +/- 10, 39 +/- 10 vs. 19 +/- 5 mmHg, respectively; P &lt; 0.05). Conclusions Endobronchial vasopressin is absorbed during CPR, coronary perfusion pressure is increased significantly within a short period, and the chance of successful resuscitation is increased in this porcine model of CPR. Endobronchial vasopressin may be an alternative for vasopressor administration during CPR, when intravenous access is delayed or not available.

scholarly journals Cardiac arrest complicating cardiogenic shock: from pathophysiological insights to Impella-assisted cardiopulmonary resuscitation in a pheochromocytoma-induced Takotsubo cardiomyopathy—a case report

2021 ◽  
Vol 5 (3) ◽  
Author(s):  
Filippo Zilio ◽  
Simone Muraglia ◽  
Roberto Bonmassari
Keyword(s):  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Left Ventricle ◽  
Cardiogenic Shock ◽  
Takotsubo Cardiomyopathy ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Coronary Perfusion ◽  
Refractory Cardiac Arrest

Abstract Background A ‘catecholamine storm’ in a case of pheochromocytoma can lead to a transient left ventricular dysfunction similar to Takotsubo cardiomyopathy. A cardiogenic shock can thus develop, with high left ventricular end-diastolic pressure and a reduction in coronary perfusion pressure. This scenario can ultimately lead to a cardiac arrest, in which unloading the left ventricle with a peripheral left ventricular assist device (Impella®) could help in achieving the return of spontaneous circulation (ROSC). Case summary A patient affected by Takotsubo cardiomyopathy caused by a pheochromocytoma presented with cardiogenic shock that finally evolved into refractory cardiac arrest. Cardiopulmonary resuscitation was performed but ROSC was achieved only after Impella® placement. Discussion In the clinical scenario of Takotsubo cardiomyopathy due to pheochromocytoma, when cardiogenic shock develops treatment is difficult because exogenous catecholamines, required to maintain organ perfusion, could exacerbate hypertension and deteriorate the cardiomyopathy. Moreover, as the coronary perfusion pressure is critically reduced, refractory cardiac arrest could develop. Although veno-arterial extra-corporeal membrane oxygenation (va-ECMO) has been advocated as the treatment of choice for in-hospital refractory cardiac arrest, in the presence of left ventricular overload a device like Impella®, which carries fewer complications as compared to ECMO, could be effective in obtaining the ROSC by unloading the left ventricle.

scholarly journals Esmolol during cardiopulmonary resuscitation reduces neurological injury in a porcine model of cardiac arrest

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Laura Ruggeri ◽  
Francesca Nespoli ◽  
Giuseppe Ristagno ◽  
Francesca Fumagalli ◽  
Antonio Boccardo ◽  
...  
Keyword(s):  
Cardiopulmonary Resuscitation ◽  
Porcine Model ◽  
Neuronal Degeneration ◽  
Neuron Specific Enolase ◽  
Coronary Perfusion Pressure ◽  
Neurological Injury ◽  
Saline Control ◽  
Preclinical Model ◽  
Coronary Perfusion ◽  
To Receive

AbstractPrimary vasopressor efficacy of epinephrine during cardiopulmonary resuscitation (CPR) is due to its α-adrenergic effects. However, epinephrine plays β1-adrenergic actions, which increasing myocardial oxygen consumption may lead to refractory ventricular fibrillation (VF) and poor outcome. Effects of a single dose of esmolol in addition to epinephrine during CPR were investigated in a porcine model of VF with an underlying acute myocardial infarction. VF was ischemically induced in 16 pigs and left untreated for 12 min. During CPR, animals were randomized to receive epinephrine (30 µg/kg) with either esmolol (0.5 mg/kg) or saline (control). Pigs were then observed up to 96 h. Coronary perfusion pressure increased during CPR in the esmolol group compared to control (47 ± 21 vs. 24 ± 10 mmHg at min 5, p < 0.05). In both groups, 7 animals were successfully resuscitated and 4 survived up to 96 h. No significant differences were observed between groups in the total number of defibrillations delivered prior to final resuscitation. Brain histology demonstrated reductions in cortical neuronal degeneration/necrosis (score 0.3 ± 0.5 vs. 1.3 ± 0.5, p < 0.05) and hippocampal microglial activation (6 ± 3 vs. 22 ± 4%, p < 0.01) in the esmolol group compared to control. Lower circulating levels of neuron specific enolase were measured in esmolol animals compared to controls (2[1–3] vs. 21[16–52] ng/mL, p < 0.01). In this preclinical model, β1-blockade during CPR did not facilitate VF termination but provided neuroprotection.

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