Resuscitation
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In a swine model of out-of-hospital ventricular fibrillation (VF) cardiac arrest, we established that automated external defibrillator (AED) defibrillation could worsen outcome from prolonged VF compared with manual defibrillation. Worse outcomes were due to substantial interruptions and delays in chest compressions for AED rhythm analyses and shock advice. In particular, the mean interval from first AED shock to first post-shock compressions was 46+/-6s. We hypothesized that the delay from shock to provision of chest compressions is similar in the out-of-hospital setting. ⋯ Substantial delays in the provision of post-shock chest compressions are typical in this EMS system with AED-equipped first responders.
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To determine the error of measurement in pulse oximetry with a decreased arterial perfusion and to identify a systolic pressure threshold for (1) initial detection and (2) a reliable reading of oxygen saturation. ⋯ Pulse oximetry is reliable with a systolic blood pressure > 80 mmHg. The lower the BP, the lower the pulse oximetry readings leading to a bias of up to -45%.
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During CPR, an inspiratory time of 2 s is recommended when the airway is unprotected; indicating that approximately 30% of the resuscitation attempt is spent on ventilation, but not on chest compressions. Since survival rates may not decrease when ventilation levels are relatively low, and uninterrupted chest compressions with a constant rate of approximately 100/min have been shown to be lifesaving, it may be beneficial to cut down the time spent on ventilation, and instead, increase the time for chest compressions. In an established bench model of a simulated unprotected airway, we evaluated if inspiratory time can be decreased from 2 to 1 s at different lower oesophageal sphincter pressure (LOSP) levels during ventilation with a bag-valve-mask device. ⋯ Total cumulative stomach inflation volume over constantly decreasing LOSP levels with an inspiratory time of 2 s versus 1 s was higher (6820 ml versus 5920 ml). In conclusion, in this model of a simulated unprotected airway, a reduction of inspiratory time from 2 to 1 s resulted in a significant increase of peak airway pressure and peak inspiratory flow rate, while lung tidal volumes remained clinically comparable (up to approximately 15% difference), but statistically different due to the precise measurements. Theoretically, this may increase the time available for, and consequently the actual number of, chest compressions during CPR by approximately 25% without risking an excessive increase in stomach inflation.
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Recent data suggest that generation of negative intrathoracic pressure during the decompression phase of CPR improves hemodynamics, organ perfusion and survival. ⋯ Incomplete chest wall recoil during the decompression phase of CPR increases endotracheal pressure, impedes venous return and decreases mean arterial pressure, and coronary and cerebral perfusion pressures.