Deep hypothermia in the cat

1959 ◽  
Vol 196 (2) ◽  
pp. 354-356 ◽  
Author(s):  
Arthur F. Battista

Sixteen adult cats were cooled, using the method of hypercapnia and hypoxia. Seven cats died during the cooling or warming period due to irreversible ventricular fibrillation or cardiac arrest. Nine cats survived and the lowest body temperature obtained was 12.5°C. The rate of body cooling and the oxygen and carbon dioxide concentrations were critical parameters difficult to control in a large animal such as the cat.

Author(s):  
Awni M. Al-Subu ◽  
Timothy A. Hacker ◽  
Jens C. Eickhoff ◽  
George Ofori-Amanfo ◽  
Marlowe W. Eldridge

AbstractThe aim of this study was to examine the use of volumetric capnography monitoring to assess cardiopulmonary resuscitation (CPR) effectiveness by correlating it with cardiac output (CO), and to evaluate the effect of epinephrine boluses on both end-tidal carbon dioxide (EtCO2) and the volume of CO2 elimination (VCO2) in a swine ventricular fibrillation cardiac arrest model. Planned secondary analysis of data collected to investigate the use of noninvasive monitors in a pediatric swine ventricular fibrillation cardiac arrest model was performed. Twenty-eight ventricular fibrillatory arrests with open cardiac massage were conducted. During CPR, EtCO2 and VCO2 had strong correlation with CO, measured as a percentage of baseline pulmonary blood flow, with correlation coefficients of 0.83 (p < 0.001) and 0.53 (p = 0.018), respectively. However, both EtCO2 and VCO2 had weak and nonsignificant correlation with diastolic blood pressure during CPR 0.30 (p = 0.484) (95% confidence interval [CI], –0.51–0.83) and 0.25 (p = 0.566) (95% CI, –0.55–0.81), respectively. EtCO2 and VCO2 increased significantly after the first epinephrine bolus without significant change in CO. The correlations between EtCO2 and VCO2 and CO were weak 0.20 (p = 0.646) (95% CI, −0.59–0.79), and 0.27 (p = 0.543) (95% CI, −0.54–0.82) following epinephrine boluses. Continuous EtCO2 and VCO2 monitoring are potentially useful metrics to ensure effective CPR. However, transient epinephrine administration by boluses might confound the use of EtCO2 and VCO2 to guide chest compression.


2002 ◽  
Vol 37 (1) ◽  
pp. 60-68 ◽  
Author(s):  
J. Larry Zettler ◽  
Edwin L. Soderstrom ◽  
Richard F. Gill ◽  
Bruce E. Mackey

Fifth instars of navel orangeworm, Amyelois transitella (Walker), were exposed to controlled atmospheres to measure the effects of elevated carbon dioxide and reduced oxygen concentrations and temperature on heart contraction rate. The atmospheres contained varying concentrations of oxygen, carbon dioxide and nitrogen and were produced by blending air with carbon dioxide or nitrogen. Carbon dioxide concentrations between 50% and 99.5% caused immediate cardiac arrest in A. transitella, but the heart contractions restarted after a transient delay. The length of this delay was directly proportional to the concentration of carbon dioxide, and contraction rate following restart was inversely proportional to the concentration of carbon dioxide. Cardiac arrest was irreversible in 100% carbon dioxide. Heart contraction rate of A. transitella was directly proportional to both temperature and oxygen content of the atmosphere through a range of 15°C to 50°C.


1995 ◽  
Vol 78 (4) ◽  
pp. 1579-1584 ◽  
Author(s):  
B. A. Johnson ◽  
M. H. Weil ◽  
W. Tang ◽  
M. Noc ◽  
D. McKee ◽  
...  

During the global myocardial ischemia of cardiac arrest and during regional myocardial ischemia due to local impairment of coronary blood flow, intramyocardial carbon dioxide tensions (Pmco2) of ischemic myocardium increase to levels exceeding 400 Torr. The mechanism of such myocardial hypercarbic acidosis is as yet incompletely understood, specifically whether these increases in Pmco2 are due to increased oxidative metabolism, decreased CO2 removal, or buffering of metabolic acids. We therefore measured Pmco2 and the total CO2 content of rat hearts harvested before, during, and after resuscitation from cardiac arrest. Pmco2 significantly increased from an average of 63 to 209 Torr during a 4-min interval of untreated ventricular fibrillation. This was associated with concurrent decreases in intracellular pH from an average of 7.03 to 6.02 units. The total CO2 content of the myocardium simultaneously decreased from 17.0 to 16.5 mmol/kg. Accordingly, increases in Pmco2 and [H+] were observed in the absence of increases in the total CO2 content and therefore the calculated myocardial bicarbonate. These observations in the rat model implicate buffering of metabolic acids by bicarbonate rather than increases in CO2 production or decreases in CO2 removal as the predominant mechanism accounting for myocardial hypercarbia.


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