Resuscitation
-
The 2005 revised guidelines for cardiopulmonary resuscitation (CPR) suggest a universal compression-to-ventilation (C:V) ratio of 30:2. The effects of this ratio in a realistic CPR scenario have not been investigated completely. ⋯ Increasing the chest compression ratio from 15:2 to 30:2 resulted in changes in arterial, but not mixed-venous, blood gases; therefore, the advantages of more chest compressions may outweigh a decrease in gas exchange.
-
Randomized Controlled Trial
Instructions to "push as hard as you can" improve average chest compression depth in dispatcher-assisted cardiopulmonary resuscitation.
Cardiopulmonary resuscitation (CPR) with adequate chest compression depth appears to improve first shock success in cardiac arrest. We evaluate the effect of simplification of chest compression instructions on compression depth in dispatcher-assisted CPR protocol. ⋯ Modifying dispatcher-assisted CPR instructions by changing "push down firmly 2in. (5cm)" to "push as hard as you can" achieved improvement in chest compression depth at no cost to total release or average chest compression rate.
-
Increased serum concentrations of brain-derived proteins neuron-specific enolase (NSE) and protein S-100beta (S-100b) are used as early predictors of long-term outcome in unconscious survivors after cardiopulmonary resuscitation (CPR). We investigated whether use of short-term Left Ventricular Assist Devices (LVAD) in patients undergoing percutaneous coronary intervention (PCI) effect serum concentrations of NSE and S-100b, because use of such devices in resuscitated cardiogenic shock patients increased during the last years. ⋯ LVAD support after PCI is associated with a significant increase in NSE serum concentration as well as in S-100b. We therefore postulate an overestimation of the extent of hypoxic brain damage in unconscious survivors after CPR if treatment include LVAD support or PCI or both procedures. The increase in NSE can be partly explained by alteration of thrombocytes and other blood cells. However, the increase in S-100b remains unexplained since S-100b does not occur in peripheral blood cells. An additional release of both biomarkers from ischemic myocardium or cerebral microembolism should be drawn into consideration.
-
Whether the ventilator-induced lung injury (VILI) superimposed on ischemia/reperfusion injury (I/R) causes synergistic damage has not been well explored. Whether nuclear factor-kappa B (NF-kappaB) antibody has protective effects for both injuries is also unknown. ⋯ VILI and I/R cause synergistic damage on the lung. I/R or VILI alone or combined can be attenuated by NF-kappaB antibody. NF-kappaB plays an important role in both forms of lung injury. We propose anti-NF-kappaB antibody pretreatment to be beneficial for VILI, I/R and lung transplantation.