Temperature-dependent skeletal muscle dysfunction in rats with congestive heart failure.

Abnormalities in the excitation-contraction coupling of slow-twitch muscle seem to explain the slowing and increased fatigue observed in congestive heart failure (CHF). However, it is not known which elements of the excitation-contraction coupling might be affected. We hypothesize that the temperature sensitivity of contractile properties of the soleus muscle might be altered in CHF possibly because of alterations of the temperature sensitivity of intracellular Ca(2+) handling. We electrically stimulated the in situ soleus muscle of anesthetised rats that had 6-wk postinfarction CHF using 1 and 50 Hz and using a fatigue protocol (5-Hz stimulation for 30 min) at 35, 37, and 40 degrees C. Ca(2+) uptake and release were measured in sarcoplasmic reticulum vesicles at various temperatures. Contraction and relaxation rates of the soleus muscle were slower in CHF than in sham at 35 degrees C, but the difference was almost absent at 40 degrees C. The fatigue protocol revealed that force development was more temperature sensitive in CHF, whereas contraction and relaxation rates were less temperature sensitive in CHF than in sham. The Ca(2+) uptake and release rates did not correlate to the difference between CHF and sham regarding contractile properties or temperature sensitivity. In conclusion, the discrepant results regarding altered temperature sensitivity of contraction and relaxation rates in the soleus muscle of CHF rats compared with Ca(2+) release and uptake rates in vesicles indicate that the molecular cause of slow-twitch muscle dysfunction in CHF is not linked to the intracellular Ca(2+) cycling.

Oxygen delivery and return of spontaneous circulation with ventilation:compression ratio 2:30 versus chest compressions only CPR in pigs.

The need for rescue breathing during the initial management of sudden cardiac arrest is currently being debated and reevaluated. The present study was designed to compare cerebral oxygen delivery during basic life support (BLS) by chest compressions only with chest compressions plus ventilation in pigs with an obstructed airway mimicked by a valve hindering passive inhalation. Resuscitability was then studied during the subsequent advanced life support (ALS) period. After 3 min of untreated ventricular fibrillation (VF) BLS was started. The animals were randomised into two groups. One group received chest compressions only. The other group received ventilations and chest compressions with a ratio of 2:30. A gas mixture of 17% oxygen and 4% carbon dioxide was used for ventilation during BLS. After 10 min of BLS, ALS was provided. All six pigs ventilated during BLS attained a return of spontaneous circulation (ROSC) within the first 2 min of advanced cardiopulmonary resuscitation (CPR) compared with only one of six compressions-only pigs. While all except one compressions-only animal achieved ROSC before the experiment was terminated, the median time to ROSC was shorter in the ventilated group. With a ventilation:compression ratio of 2:30 the arterial oxygen content stayed at 2/3 of normal, but with compressions-only, the arterial blood was virtually desaturated with no arterio-venous oxygen difference within 1.5-2 min. Haemodynamic data did not differ between the groups. In this model of very ideal BLS, ventilation improved arterial oxygenation and the median time to ROSC was shorter. We believe that in cardiac arrest with an obstructed airway, pulmonary ventilation should still be strongly recommended.

Quality of CPR with three different ventilation:compression ratios.

Current adult basic cardiopulmonary resuscitation (CPR) guidelines recommend a 2:15 ventilation:compression ratio, while the optimal ratio is unknown. This study was designed to compare arterial and mixed venous blood gas changes and cerebral circulation and oxygen delivery with ventilation:compression ratios of 2:15, 2:50 and 5:50 in a model of basic CPR. Ventricular fibrillation (VF) was induced in 12 anaesthetised pigs, and satisfactory recordings were obtained from 9 of them. A non-intervention interval of 3 min was followed by CPR with pauses in compressions for ventilation with 17% oxygen and 4% carbon dioxide in a randomised, cross-over design with each method being used for 5 min. Pulmonary gas exchange was clearly superior with a ventilation:compression ratio of 2:15. While the arterial oxygen saturation stayed above 80% throughout CPR for 2:15, it dropped below 40% during part of the ventilation:compression cycle for both the other two ratios. On the other hand, the ratio 2:50 produced 30% more chest compressions per minute than either of the two other methods. This resulted in a mean carotid flow that was significantly higher with the ratio of 2:50 than with 5:50 while 2:15 was not significantly different from either. The mean cerebrocortical microcirculation was approximately 37% of pre-VF levels during compression cycles alone with no significant differences between the methods. The oxygen delivery to the brain was higher for the ratio of 2:15 than for either 5:50 or 2:50. In parallel the central venous oxygenation, which gives some indication of tissue oxygenation, was higher for the ratio of 2:15 than for both 5:50 and 2:50. As the compressions were done with a mechanical device with only 2-3 s pauses per ventilation, the data cannot be extrapolated to laypersons who have great variations in quality of CPR. However, it might seem reasonable to suggest that basic CPR by professionals should continue with ratio of 2:15 at present if it can be shown that similar brief pauses for ventilation can be achieved in clinical practice.