Hyperoxia may reduce coronary artery blood flow, increase systemic vascular resistance, and decrease cardiac output. This paper argues that if the baseline arterial oxygen saturations are >90%, high concentration oxygen does not increase oxygen transport, as the reductions in cardiac output are in excess of the increase in oxygen content. The balance of the limited evidence that exists suggests that the routine use of oxygen in uncomplicated MI (no failure or shock) may increase infarct size and possibly increase the risk of mortality, owing to its haemodynamic effects, including a reduction in coronary blood flow.
Routine use of oxygen in the treatment of myocardial infarction: systematic review
Heart. 2009 Mar;95(3):198-202
OBJECTIVE: During mechanical ventilation, inspiration cyclically decreases the left cardiac preload. Thus, an end-expiratory occlusion may prevent the cyclic impediment in left cardiac preload and may act like a fluid challenge. We tested whether this could serve as a functional test for fluid responsiveness in patients with circulatory failure.
DESIGN: Prospective study.
SETTING: Medical intensive care unit.
PATIENTS: Thirty-four mechanically ventilated patients with shock in whom volume expansion was planned.
INTERVENTION: A 15-second end-expiratory occlusion followed by a 500 mL saline infusion.
MEASUREMENTS: Arterial pressure and pulse contour-derived cardiac index (PiCCOplus) at baseline, during passive leg raising (PLR), during the 5-last seconds of the end-expiratory occlusion, and after volume expansion.
MAIN RESULTS: Volume expansion increased cardiac index by >15% (2.4 +/- 1.0 to 3.3 +/- 1.2 L/min/m, p < 0.05) in 23 patients ("responders"). Before volume expansion, the end-expiratory occlusion significantly increased arterial pulse pressure by 15% +/- 15% and cardiac index by 12% +/- 11% in responders whereas arterial pulse pressure and cardiac index did not change significantly in nonresponders. Fluid responsiveness was predicted by an increase in pulse pressure >or=5% during the end-expiratory occlusion with a sensitivity and a specificity of 87% and 100%, respectively, and by an increase in cardiac index >or=5% during the end-expiratory occlusion with a sensitivity and a specificity of 91% and 100%, respectively. The response of pulse pressure and cardiac index to the end-expiratory occlusion predicted fluid responsiveness with an accuracy that was similar to the response of cardiac index to PLR and that was significantly better than the response of pulse pressure to PLR (receiver operating characteristic curves area 0.957 [95% confidence interval [CI:] 0.825-0.994], 0.972 [95% CI: 0.849-0.995], 0.937 [95% CI: 0.797-0.990], and 0.675 [95% CI: 0.497-0.829], respectively).
CONCLUSIONS:The hemodynamic response to an end-expiratory occlusion can predict volume responsiveness in mechanically ventilated patients.
Predicting volume responsiveness by using the end-expiratory occlusion in mechanically ventilated intensive care unit patients.
Crit Care Med. 2009 Mar;37(3):951-6
The risk of apnoea in neonates requiring prostaglandin E1 infusions for duct-dependent congenital heart disease is well described and often results in the recommendation to intubate prior to transfer. An American study of 202 transported infants on PGE1 shows a higher rate of transport-related complications in those that had been intubated. None of the 73 (36%) unintubated patients required intubation for apneoa during transport. These data are in keeping with a previous Australian study of 300 infants receiving PGE1 in which only 2 of 78 unintubated patients experienced apnoea.
To intubate or not to intubate? Transporting infants on prostaglandin E1
Pediatrics. 2009 Jan;123(1):e25-30
A review of 1954 out-of-hospital tracheal intubation (ETI) attempts by EMS crews revealed 444 (22.7%) patients experienced one or more ETI errors, including tube misplacement or dislodgement in 61 (3%), multiple ETI attempts in 62 (3%) and failed ETI in 359 (15%). Pneumonitis was associated with failed ETI (n=20, 19%; univariable OR 2.54; 95% CI 1.24-5.25). The authors conclude that out-of-hospital ETI errors are not associated with mortality, but failed out-of-hospital ETI increases the odds of pneumonitis.