The addition of interposed abdominal compression (IAC) to otherwise standard CPR provides external pressure over the abdomen in counterpoint to the rhythm of chest compression. Interposed abdominal compression is a simple manual technique that can supplement the use of adrenergic drugs to increase both coronary perfusion pressure and total blood flow during CPR. Mechanistically, manual abdominal compressions induce both central aortic and central venous pressure pulses. However, owing to differences in venous versus arterial capacitance, the former are usually greater than the latter, so that systemic perfusion pressure is enhanced. Moreover, practical experience and theoretical analysis have suggested subtle refinements in the hand position and technique for abdominal compression that may further improve the ratio of arterial to venous pressure augmentation. Clinical studies confirm that IAC-CPR can improve perfusion pressures and carbon dioxide excretion during CPR in humans. The incidence of abdominal trauma, regurgitation, or other complications is not increased by IAC. Randomized trials have shown that short-term and long-term survival of patients resuscitated in the hospital by IAC-CPR are about twice that of control patients resuscitated by standard CPR. The technique of IAC has thus evolved to become a highly promising adjunct to normal CPR, which is likely to be implemented in an increasing number of clinical protocols.
The iron chelating agent deferoxamine was studied in an animal model as post-resuscitation therapy to prevent late deaths and brain damage following total circulatory arrest and resuscitation. Cardio-respiratory arrest was induced by injection of cold, 1% KC1 into the left ventricles of ketamine anesthetized rats pretreated with succinylcholine chloride, and by discontinuation of positive pressure ventilation. CPR was begun after six minutes, and animals with return of spontaneous circulation were entered into the study. Within five minutes after return of spontaneous circulation, treated animals received deferoxamine (50 mg/kg, IV). At ten days, 16 of 25 (64%) of treated animals had survived without neurologic deficit, compared to nine of 25 (36%) of controls (chi square = 3.92, P < .05). Chelation of intracellular iron by deferoxamine may have prevented free-radical-mediated reactions that led to late deaths in control animals.
Power output and blood flow were determined in dogs for four muscles (gastrocnemius, latissimus dorsi, rectus abdominis, and triceps) to determine effects of choice of muscle, tetany or twitch rates, force loading of the muscle, and blood flow on muscle power output. Total power for a 20‐Kg dog was greatest for triceps at 0.77 watts (W) and least for rectus at 0.22 W; power per gram was greatest for gastrocnemius at 5.77 mW/g. Muscle perfusion of latissimus and rectus is greatly decreased by overstretching of the muscle. Overstretching also produces severe, persistent, power loss in latissimus and rectus muscles. Gastrocnemius and triceps tolerate stretching much better. We conclude that power can be improved without causing muscle fatigue by choice of muscle, choice of electrical stimulation parameters, linear geometry for contraction of the muscle, and matching the force load to each individual muscle.
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