Circulation
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Hypertension and atherosclerotic coronary arterial obstruction frequently coexist in patients. However, the effect of increased aortic pressure on ischemic segmental dysfunction is not well understood. We studied the effects of aortic pressure increases on segmental left ventricular function during myocardial ischemia. ⋯ Increased aortic pressure in dogs without coronary occlusion produced reversible decreases in end-diastolic wall thickness, NET and LV dP/dt. Thus, the production of systemic hypertension with diastolic pressures of 110-120 mm Hg acutely or for 6 hours during evolving canine myocardial infarction does not appear to exert an important deleterious effect on myocardial oxygen supply and demand. However, 24 hours of mildly increased aortic pressure accentuates end-diastolic wall thinning in segments with paradoxic systolic motion and results in a failure of their return to control values at this period.
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We studied the function of right internal jugular vein valves during cardiac catheterization in 32 patients and external jugular vein valves in vitro from 13 dogs. Patients with normal central venous pressure had competent valves during cough-induced transvalvular pressure gradients of 52.4 +/- 8.6 mm Hg. Ten of 15 patients with elevated central venous pressure had either incompetent or absent internal jugular valves, the latter occurring only in patients with long-standing, severe tricuspid regurgitation. ⋯ Five of six excised valves remained competent during pulsatile transvalvular pressure of 64.8 +/- 1.9 mm Hg. Thus, thoracic inlet venous valves are usually competent during sudden increases in intrathoracic pressure. These valves may play an important role in establishing the extrathoracic arteriovenous pressure gradient necessary for forward blood flow during cardiopulmonary resuscitation and other states with high intrathoracic pressure.
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The clinical entry characteristics and medical history of 142 resuscitated out-of-hospital cardiac arrest victims with coronary heart disease were studied in order to identify factors that affect their long-term survival. The cardiac arrest event was classified as being secondary to an acute myocardial infarction (AMI) in 44% (62 of 142), an ischemic event (IE) in 34% (49 of 142) and a primary arrhythmic event (PAE) in 22% (31 of 142). The majority of patients in all groups had a history of angina pectoris. ⋯ Covariate analysis for more than 40 variables indicates that a high-risk group included 22% (31 of 142) of the cardiac arrest victims had 1- and 2-year survival rates of 71% and 55%, respectively, and was characterized as having used digitalis before arrest, experiencing blood urea nitrogen elevation and pulmonary congestion during the hospitalization for the event, and classification of the cardiac arrest event as a PAE. A low-risk group comprised 78% (111 of 142) of the survivors and had 1- and 2-year survival rates of 85% and 69%, respectively. These data indicate that cardiac arrest due to coronary heart disease is secondary to several mechanisms related to subsequent survival.
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A new noninvasive method for determining arterial blood pressure is presented. Using a fast servo system, the pressure in the arm cuff is controlled so that the flow is maintained at a low value. ⋯ Mean arterial blood pressure was determined from the noninvasive recordings using the same mathematically valid procedure as was used for the invasive recordings. The deviation between the invasive and the noninvasive determinations of this measurement was -0.6 +/- 2.2 mm Hg (mean +/- SD) in 23 subjects.
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The effect of pulsatile flow during cardiopulmonary bypass on the hormonal stress response was studied in 26 patients. Thirteen had routine and 13 had pulsatile bypass with an average pulse pressure of 30 mm Hg. Plasma vasopressin levels were significantly elevated during bypass in both groups, but were lower with pulsation (66 +/- 11 vs 36.3 pg/ml, p less than 0.05). ⋯ There were no significant changes in renin activity in either group, but the increase after cardiopulmonary bypass was greater in the nonpulsatile group (2.0 +/- 0.7 vs 1.36 +/- 0.4 ng/ml/hr, NS). These data suggest that pulsatile flow significantly attenuates the vasopressin and catecholamine stress response to cardiopulmonary bypass. This may explain the increased flow requirements and better tissue perfusion and organ function and the decreased incidence of postoperative hypertension after bypass using pulsatile flow.