2010
DOI: 10.1016/j.resuscitation.2010.09.241
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Difference in end-tidal carbon dioxide between asphyxial cardiac arrest and ventricular fibrillation/pulseless ventricular tachycardia cardiac arrest in cardiopulmonary resuscitation—Comparison of 2000 and 2005 CPR guidelines

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“…Longer-lasting tissue hypoperfusion due to disease causes lactic acidosis [4,6] which leads to compensatory tachypnea and respiratory alkalosis [7][8][9]. If homeostasis is not achieved, the deepening of metabolic acidosis leads to respiratory failure, which results in secondary CA presented as an initial non-shockable rhythm, and higher levels of end-tidal carbon dioxide (EtCO 2 ) and lactate are expected [4,8,[10][11][12].…”
Section: Introductionmentioning
confidence: 99%
“…Longer-lasting tissue hypoperfusion due to disease causes lactic acidosis [4,6] which leads to compensatory tachypnea and respiratory alkalosis [7][8][9]. If homeostasis is not achieved, the deepening of metabolic acidosis leads to respiratory failure, which results in secondary CA presented as an initial non-shockable rhythm, and higher levels of end-tidal carbon dioxide (EtCO 2 ) and lactate are expected [4,8,[10][11][12].…”
Section: Introductionmentioning
confidence: 99%
“…[7][8][9] If homeostasis is not achieved deepening of metabolic acidosis leads to respiratory failure which results in secondary CA presented initial non-shockable rhythm, higher levels of EtCO2 (end tidal carbon dioxide) and lactate are expected. [4,8,[10][11][12] Some studies showed poor neurological outcome of patients after return of spontaneous circulation (ROSC) with high levels of lactate at hospital admission. [13][14][15] A clear association between lactate levels and prognosis of OHCA still remains to be proven.…”
Section: Introductionmentioning
confidence: 99%