The goals of this study were to quantify the effects of epinephrine on myocardial and cerebral blood flow during conventional cardiopulmonary resuscitation (CPR) and CPR with simultaneous chest compression-ventilation and to test the hypothesis that epinephrine would improve myocardial and cerebral blood flow by preventing collapse of intrathoracic arteries and by vasoconstricting other vascular beds, thereby increasing perfusion pressures. Cerebral and myocardial blood flow were measured by the radiolabeled microsphere technique, which we have previously validated during CPR. We studied the effect of epinephrine on established arterial collapse during CPR with simultaneous chest compression-ventilation with the abdomen bound or unbound. Epinephrine reversed arterial collapse, thereby eliminating the systolic gradient between aortic and carotid pressures and increasing cerebral perfusion pressure and cerebral blood flow while decreasing blood flow to other cephalic tissues. Epinephrine produced higher cerebral and myocardial perfusion pressures during CPR with simultaneous chest compression-ventilation when the abdomen was unbound rather than bound because abdominal binding increased intracranial and venous pressures. In other experiments we compared the effect of epinephrine on blood flow during 1 hr of either conventional CPR or with simultaneous chest compression-ventilation with the abdomen unbound. Epinephrine infusion during conventional CPR produced an average cerebral blood flow of 15 ml/min-100 g (41 + 15% of control) and an average myocardial blood flow of 18 mI/min 100 g (15 ± 8% of control). In our previous studies, cerebral and myocardial blood flow were less than 3 ±+ 1 % of control during conventional CPR without epinephrine. Although flows during CPR with simultaneous chest compression-ventilation without epinephrine were initially higher than those during conventional CPR, arterial collapse developed after 20 min, limiting cerebral and myocardial blood flow. The use of epinephrine throughout 50 min of CPR with simultaneous chest compression-ventilation maintained cerebral blood flow at 22 + 2 ml/min 100 g (73 ± 25% control) and left ventricular blood flow at 38 ± 9 ml/min 100 g (28 ± 8% control). The improved blood flows with epinephrine correlated with improved electroencephalographic activity and restoration of spontaneous circulation. The mechanisms responsible for the increased brain and myocardial blood flow with epinephrine include the prevention of arterial collapse and the intense vasoconstriction of other vascular beds, which prevents the run off of blood into these tissues and preferentially increases cerebral and myocardial perfusion pressures. We conclude that epinephrine substantially improves cerebral and myocardial blood flow during both conventional CPR and CPR with simultaneous chest compression-ventilation and that the combined use of epinephrine and CPR with simultaneous chest compression-ventilation with the abdomen unbound maintains high levels of blood flow to the ...

These data, while limited to a small number of patients, suggest that CM can reverse remodeling of the dilated failing heart. While systolic squeezing assist effects of CM may play a role in some patients, our study found that this was not required to achieve substantial benefits from the procedure. We speculate that CM may act more passively, like an elastic girdle around the heart, to help reverse chamber remodeling.

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In this preliminary study, vest CPR, despite its late application, successfully increased aortic pressure and coronary perfusion pressure, and there was an insignificant trend toward a greater likelihood of the return of spontaneous circulation with vest CPR than with continued manual CPR. The effect of vest CPR on survival, however, is currently unknown and will require further study.

ALTHOUGH bicuspid venous valves in the internal jugular and subclavian veins at the thoracic inlet in man were identified by sixteenth century anatomists' and are included in modern textbooks of anatomy,2 many physicians are unaware of their existence. The function and competence of these thoracic inlet venous valves have been controversial for several hundred years. In 1628, Harvey wrote, "the edges of the valves in the jugular veins hang downwards, and are so contrived that they prevent blood from rising upwards."3 Nearly 3 centuries later, Mackenzie4 reviewed the evidence and could not reach any firm conclusion about the competence of the internal jugular vein valve. In patients with tricuspid regurgitation, Muller and Shillingford found sudden decreases in systolic pressure (v) waves as the catheter was withdrawn from the superior vena cava past the subclavian vein valves.5 Wood claimed that in tricuspid regurgitation, the venous valves take on the function of the tricuspid valve.6 Keith,7 however, concluded that in man, the internal jugular vein valves were the weakest set of venous valves separating the thorax and abdomen from the extremities because they were the only set of From the Peter