Resuscitation
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Comparative Study
The effect of cardiopulmonary bypass resuscitation on cardiac arrest induced lactic acidosis in dogs.
The adequacy of end organ blood flow following a cardiac arrest varies depending on the artificial reperfusion technique utilized and may critically affect patient outcome. Both oxygen consumption (VO2) and arterial lactate values have previously been used to assess tissue perfusion. Cardiopulmonary bypass resuscitation (CPB) is a reperfusion technique capable of providing near normal end organ blood flow. ⋯ Baseline hemodynamic and biochemical measurements were similar in both treatment groups (P greater than 0.05). Oxygen consumption (440 +/- 50 ml/min/M2) and mean arterial lactic acid values (7.44 +/- 2.25 mmol/l) were significantly higher at 1 min of resuscitation in CPB-treated dogs compared to dogs treated with CPR (60 +/- 10 ml/min/M2) (3.16 +/- 0.69 mmol/l) respectively (P less than 0.05). Mean arterial lactic acid values rose significantly at each sampling interval during CPR (P less than 0.05) but began to decrease after 5 min of resuscitation in the CPB animals and were not significantly different than baseline after 60 min of bypass (P greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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Standard external cardiopulmonary resuscitation (SECPR) produces high cerebral venous and intracranial pressure peaks, low cerebral perfusion pressure, and low cerebral blood flow (CBF). Cerebral viability seems to require 20% of normal CBF, which SECPR cannot reliably generate. We tested the hypothesis that SECPR can produce adequate CBF if started immediately, but not if started after a long period of cardiac arrest (no flow, stasis). ⋯ Decrease in mean arterial pressures (MAP) produced by SECPR during asystole paralleled CBF values. Thus, the longer the preceding period of stasis, the lower the MAP and CBF generated by SECPR without epinephrine. This effect may be the result of anoxia-induced vasoparalysis and stasis-induced increased blood viscosity.
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Transcutaneous oxygen tension (PtCO2) was observed during hemorrhagic hypoperfusion using four therapeutic modalities: pneumatic antishock garment (PASG), 20 degrees Trendelenburg positioning, combined PASG-Trendelenburg, and whole blood infusion. Anesthetized mongrel dogs were mechanically ventilated. A heated transcutaneous oxygen sensor was applied to the skin overlying the sternum. ⋯ MAP and CI fell in all groups following hemorrhage but did so less precipitously in the PASG group. The PASG and PASG-Trendelenburg groups showed the greatest increase in CI during reinfusion. These results suggest that when PtCO2 is relied upon as an indicator of adequacy of resuscitation during moderate hemorrhagic shock, that cutaneous perfusion may be improved by the PASG or Trendelenburg position, and that perfusion is most effectively restored by blood infusion.
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The efficacy of CPR has been questioned. A major criticism is that neurologic outcomes have not been adequately studied. For a 26-month period, 138 patients from six major receiving hospitals were discharged alive following prehospital cardiac arrests. ⋯ There was no significant difference at any CPC level (P not significant). Furthermore, there was no statistical difference between either group when compared for age, response time, resuscitation time, witnessing of arrest or distribution of presenting rhythms. In conclusion, no significant effect in neurologic outcome among saved cardiac arrest victims was found between bystander/first responder CPR and bystander/first responder NO CPR groups in the paramedic program studied.
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Three series of experiments were conducted to develop a model of volume-controlled severe hemorrhagic shock in the unanesthetized analgesic cynomolgus monkey. This report concerns the insult without resuscitation. In Series I, seven monkeys were sedated with 75% N2O/25% O2, bled 40% of their measured blood volume over 20 min and observed until death. ⋯ Three died due to inaccurate (preventable) MAP adjustments. At MAP 30 mmHg, all animals lost consciousness, EEG activity decreased, and brain stem reflexes disappeared. The "volume-pressure controlled" hemorrhagic shock model of Series III retains the initial natural response to bleeding, simulates the clinical picture of severe prolonged shock without anesthesia, and represents a more controllable insult than volume controlled hemorrhage alone.