Pericardial effusion complicating acute myocardial infarction.

The acute fibrinous pericarditis that complicates acute myocardial infarction is usually of no functional significance. Uncommonly, hemorrhagic effusion may compound this process. In the case reported here, the pericardial aspect of acute lateral myocardial infarction dominated the clinical picture, thus posing a diagnostic problem. This phase of the disease stimulates us to place it on record.

Influence of the salt moiety on the effectiveness of corticosteroid therapy in cardiogenic shock.

Using closed chest coronary artery microsphere embolization, myocardial infarction and subsequent shock were produced in healthy adult mongrel dogs. Following infarction animals were distributed among the following groups: (1) control; (2) methylprednisolone sodium succinate (MPSS); (3) methylprednisolone sodium phosphate (MPSP); (4) sodium phosphate (SP); and (5) sodium succinate (SS). Drug doses of equivalent anti-inflammatory activity were administered i.v. 15 min after infarction. Compared to control animals, only dogs treated with MPSS exhibited significant improvements in hemodynamic parameters and permanent survival. Survival in MPSS dogs was significantly (P = 0.02) better than that of either group treated with SP or SS and substantially (P = 0.02) better than that of either group treated with SP or SS and substantially (P = 0.065) better than the survival rate of dogs receiving MPSP. It appears that succinate is permissive, while phosphate is restrictive, with respect to efficacy of methylprednisolone in experimental cardiogenic shock. Possible explanations for these observations are discussed.

Protective effects of epinephrine tolerance in experimental cardiogenic shock.

To evaluate the mechanism of protection of epinephrine tolerance in shock, we studied the hemodynamic and regional blood flow response to cardiogenic shock in dogs rendered tolerant to lethal doses of epinephrine. Shock was induced by coronary embolization. Regional organ perfusion was evaluated with radioactive microspheres. The survival of tolerant dogs following embolization was 8/12 (62%) compared to 5/31 (16%) in control dogs (P = 0.008). Heart and adrenal organ weights were significantly greater in the tolerant animals. Ventricular hypertrophy in the tolerant dogs was accompanied by greater myocardial blood flow and greater myocardial contractility both before and during cardiogenic shock. There was significantly greater regional flow to spleen, gastrointestinal tract, and pancreas during shock in the epinephrine-tolerant group.

Comparative effects of intravenous and intra-arterial methylprednisolone in cardiogenic shock.

This study was undertaken to determine if a portion of intravenously administered methylprednisolone sodium succinate (MPSS) might be metabolized by the lung during cardiogenic shock. With plastic microsphere coronary artery embolization, myocardial infarction and shock were produced in mongrel dogs. Animals were assigned to control, intra-arterial MPSS, and intravenous MPSS groups, with the treated dogs receiving 30 mg/kg of MPSS 15 minutes after infarction. Compared to control animals, the group receiving intra-arterial MPSS had significantly higher mean blood pressure, cardiac index, and blood glucose levels and a lower peripheral resistance during shock. Compared with the intravenous MPSS group, dogs treated with intra-arterial MPSS had significantly lower peripheral resistance and a nearly significantly higher cardiac index. Permanent survival rates were 26% in the control group, 60% in the intravenous MPSS group, and 50% in the intra-arterial MPSS group. Although treatment with intra-arterial MPSS was associated with a better hemodynamic profile than that following intravenous MPSS (suggesting the possibility of corticosteroid metabolism by the lung), survival was not enhanced. It was concluded that functionally insignificant amounts of corticosteroids given intravenously might be inactivated by the lung. Hence, intravenous MPSS injection is a practical and adequate means of administering this valuable agent in cardiogenic shock.

Effects of intra-arterial ethanol in cardiogenic shock.

Unanaesthetized mongrel dogs in cardiogenic shock received a 30-min intra-arterial infusion of 1 X 9 g/kg of 40% ethanol. Alcohol produced significant vasodilatation and improvements in the mean blood pressure and cardiac output. Arterial pH and the arteriovenous oxygen difference were markedly reduced, and the blood glucose concentration was significantly increased. Despite a considerable reduction in serum CPK levels, survival was not improved by ethanol.

The use of methylprednisolone during cardiopulmonary bypass. A review of 427 cases.

A study was designed to evaluate the hemodynamic effects of massive doses of methylprednisolone (30 mg. per kilogram) during cardiopulmonary bypass at normothermia and hypothermia. In 427 patients studied, significantly less vasoconstriction (p less than 0.01) and improved perfusion flows (p less than 0.0005) were obtained at comparable pressure levels in the steroid-treated group (272 patients) compared with the control group (155 patients). Because of these measured parameters, methylprednisolone should be considered a valuable adjunct to improving tissue perfusion during cardiopulmonary bypass.

Therapeutic effects of corticosteroids in septic shock.

PIP: After a brief summary of the pathophysiology of gram-negative septic shock, a laboratory animal experiment testing the therapeutic efficacy of corticosteroids in such shock cases is presented. Healthy adult mongrel dogs were injected intravenously with 2 mg/kg of E. coli endotoxin to produce endotoxin shock. Overall, the survival of untreated animals was 17% and this was not significantly altered by volume replacement with either Ringers or dextran solution. With treatment (dexamethasone phosphate or methylprednisolone succinate) administered intravenously, in addition to volume replacement, survival increased to 70% of endotoxin-shocked dogs. However, hydrocortisone succinate did not improve survival. The precise mechanism by which the efficacious agents worked is unclear, though both clearly did significantly lower total peripheral vascular resistance. The type of fluid replacement used did not affect the enhanced survival found with dexamethasone phosphate or methylprednisolone succinate.^ieng