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Volume infusion cooling increases end-tidal carbon dioxide and results in faster and deeper cooling during intra-cardiopulmonary resuscitation hypothermia induction.
Intensive Care Medicine Experimental 2015 December
BACKGROUND: Intra-arrest hypothermia induction may provide more benefit than inducing hypothermia after return of spontaneous circulation. However, little is understood about the interaction between patient physiology and hypothermia induction technology choice during ongoing chest compressions.
METHODS: After 10 min of untreated ventricular fibrillation, mechanical chest compressions were provided for 60 min (100 CPM, 1.25" deep) in 26 domestic swine (30.5 ± 1.7 kg) with concurrent hypothermia induction using one of eight cooling methods. Four cooling methods included volume infusion with cold saline or an ice particulate slurry through the femoral vein or carotid artery (volume infusion cooling group, VC); three included cooling via an intra-vascular heat exchange catheter, nasal cooling, or surface ice bags (no volume cooling group, NVC); and the other was a control group with no cooling (no cooling group, NC). Physiological monitoring included end-tidal carbon dioxide, aortic pressure, right atrial pressure, brain temperature, esophageal temperature, and rectal temperature.
RESULTS: During cardiopulmonary resuscitation (CPR), the volume infusion cooling group cooled faster and to lower temperatures than the other groups (VC vs. NVC or NC; ∆T = -5.6 vs. -2.1 °C or -0.6 °C; p < 0.01). The aortic pressure and right atrial pressure were higher in the volume cooling group than the other groups (VC vs. NVC or NC; AOP = 23.6 vs. 16.7 mmHg or 14.7 mmHg; p < 0.02). End-tidal carbon dioxide measurements during CPR were also higher in the volume cooling group (VC vs. NVC; EtCO2 = 23.4 vs. 13.1 mmHg; p < 0.05). Intra-corporeal temperature gradients larger than 3 °C were created by volume cooling during ongoing chest compressions.
CONCLUSIONS: Volume infusion cooling significantly altered physiology relative to other cooling methods during ongoing chest compressions. Volume cooling led to faster cooling rates, lower temperatures, higher end-tidal carbon dioxide levels, and higher central vascular pressures. IACUC protocol numbers: UPenn (803178), CHOP (997).
METHODS: After 10 min of untreated ventricular fibrillation, mechanical chest compressions were provided for 60 min (100 CPM, 1.25" deep) in 26 domestic swine (30.5 ± 1.7 kg) with concurrent hypothermia induction using one of eight cooling methods. Four cooling methods included volume infusion with cold saline or an ice particulate slurry through the femoral vein or carotid artery (volume infusion cooling group, VC); three included cooling via an intra-vascular heat exchange catheter, nasal cooling, or surface ice bags (no volume cooling group, NVC); and the other was a control group with no cooling (no cooling group, NC). Physiological monitoring included end-tidal carbon dioxide, aortic pressure, right atrial pressure, brain temperature, esophageal temperature, and rectal temperature.
RESULTS: During cardiopulmonary resuscitation (CPR), the volume infusion cooling group cooled faster and to lower temperatures than the other groups (VC vs. NVC or NC; ∆T = -5.6 vs. -2.1 °C or -0.6 °C; p < 0.01). The aortic pressure and right atrial pressure were higher in the volume cooling group than the other groups (VC vs. NVC or NC; AOP = 23.6 vs. 16.7 mmHg or 14.7 mmHg; p < 0.02). End-tidal carbon dioxide measurements during CPR were also higher in the volume cooling group (VC vs. NVC; EtCO2 = 23.4 vs. 13.1 mmHg; p < 0.05). Intra-corporeal temperature gradients larger than 3 °C were created by volume cooling during ongoing chest compressions.
CONCLUSIONS: Volume infusion cooling significantly altered physiology relative to other cooling methods during ongoing chest compressions. Volume cooling led to faster cooling rates, lower temperatures, higher end-tidal carbon dioxide levels, and higher central vascular pressures. IACUC protocol numbers: UPenn (803178), CHOP (997).
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