Vascular ultrasound screening for asymptomatic abdominal aortic aneurysm.

This health technology assessment examines vascular ultrasound screening for abdominal aortic aneurysm (AAA) in asymptomatic populations. Screening reduces the incidence of AAA ruptures, rates of emergency surgical repair and AAA-attributable mortality in males ages 65 to 74. The benefit of screening women has not been established. Ontario data suggest that AAA is underdiagnosed in women, and that women are systematically undertreated. Targeting smokers for screening was found to maximize cost-effectiveness. Economic analysis found that screening may generate savings from the avoidance of emergency surgeries. Based on these findings, the Ontario Health Technology Advisory Committee has recommended screening for AAA in both male and female ever-smokers ages 65 to 74.

Failure to wean from cardiopulmonary bypass after myocardial revascularization: successful treatment with verapamil via the aortic root.

Severe ventricular dysfunction in a patient prevented weaning from cardiopulmonary bypass after myocardial revascularization. Calcium chloride and increasing doses of dopamine had no effect. Coronary vasospasm was diagnosed based on ST elevation and myocardial failure. Verapamil 0.5 mg, injected into the aortic root, was followed by a dramatic improvement in cardiac contractility and successful weaning from cardiopulmonary bypass without inotropic support.

Prolonged hemorrhagic shock does not impair regeneration of plasma coagulant masses in the rabbit.

BACKGROUND AND METHODS: Twelve adult male albino rabbits were assigned alternately to normotensive and hypotensive groups to assess the effect of hypovolemic shock on spontaneous correction of dilutional coagulopathy. All animals underwent dilutional exchange transfusion with 200 mL of rabbit RBCs and 5% human albumin. Half the animals were then acutely hemorrhaged and subsequent aliquots of blood removed as needed to maintain the mean arterial pressure at 40 mm Hg. RESULTS: By 6 hr after production of dilutional coagulopathy, masses and plasma concentrations of fibrinogen and Factor II had increased modestly but significantly, and Factor VII mass and concentration and in vitro coagulation had returned almost to normal; plasma volume was unchanged in the normotensive animals. In the hypovolemic shock animals, where coagulant mass regeneration was as rapid as in the normotensive animals, a doubling of total plasma volume (p less than .01) prevented the concentrations of fibrinogen and Factor II, and hence the coagulation times, from improving. CONCLUSIONS: Dilutional coagulopathy corrects spontaneously within hours. Normovolemic shock prolongs dilutional coagulopathy not by impairment of factor regeneration but because of further (internal) dilution due to plasma expansion. Rapid correction of dilutional coagulopathy is likely to necessitate cryoprecipitate administration.

Randomized placebo-controlled trial of propafenone for treatment of atrial tachyarrhythmias after cardiac surgery.

Fourteen patients with atrial fibrillation or flutter and a ventricular rate of greater than or equal to 120 beats/min occurring after cardiac surgery entered a double-blind placebo-controlled conditional crossover trial of intravenous propafenone. Patients randomly received either propafenone (2 mg/kg body weight) or placebo during a 10 minute intravenous infusion. If 20 minutes after the initiation of this infusion there was no conversion to sinus rhythm, the patient received a second intravenous infusion over 10 minutes (either propafenone or placebo, whichever was not given first). The electrocardiogram was recorded continuously throughout the study. Fourteen patients received propafenone and 10 received placebo. No patient's rhythm converted to sinus rhythm after placebo. In six patients (43%) (p less than 0.001), the arrhythmia converted to sinus rhythm between 5 and 10 minutes after the end of the propafenone infusion. After propafenone, the ventricular response to atrial fibrillation or flutter decreased significantly from 141.6 +/- 15.2 to 116.0 +/- 15.5 beats/min. Ventricular rate did not change after placebo. The mean propafenone plasma concentration was 3.46 +/- 2.17 mg/liter. The only side effect of propafenone noted was a decrease in systolic blood pressure of 9 +/- 9 mm Hg. Propafenone was useful for management of atrial fibrillation after cardiac surgery both for control of rapid ventricular response and for conversion to sinus rhythm.

Coagulopathy related to dilution and hypotension during massive transfusion.

A retrospective review of 64 patients receiving more than 10 units of red cell concentrate plus crystalloid within 12 h revealed two consecutive patterns of elevation of the partial thromboplastin time (PTT). The PTT at 3 to 4 h (PTT3-4) correlated with the number of liters of crystalloid (LC) infused over the first 3 h (PTT3-4 = 37 + 7 LC, r = .7643, p less than .001); the PTT thereafter (PTT4+) correlated with the number of hours of closely antecedent hypotension (AH) (PTT4+ = 37 + 21AH, r = .8680, p less than .001). These data indicate a transient dilutional coagulopathy, followed by coagulopathy related to the duration of closely AH. Whether this latter is due to impaired production, disseminated intravascular coagulation, or dilution due to internal shifts of fluids and/or proteins, remains to be clarified. Therapeutic implications of these data are discussed.

Complete recovery of the heart following exposure to profound hypothermia.

Cold injury has been suggested as a potential limitation to the use of temperatures below 10 degrees to 15 degrees C in clinical myocardial preservation. The isolated effects of profound hypothermia on myocardial function and energy metabolism were studied in the working rat heart preparation. Each heart was isolated and stabilized; then initial aortic flow, coronary flow, and heart rate were measured. The heart then was perfused in the Langendorf mode with oxygenated Krebs-Henseleit buffer for 20 minutes at 0.5 degree, 4 degrees, 10 degrees, 15 degrees, or 20 degrees C. After being rewarmed to 37 degrees C, the heart was returned to the working mode for final functional measurements. In a control group, the perfusion was kept at 37 degrees C. Recovery of function in hearts exposed to hypothermic perfusion was not significantly different from that observed in the hearts kept at 37 degrees C. When cold exposure time to 0.5 degree C perfusion was extended to 2 hours, heart function still returned to the same level as that of control hearts maintained at 37 degrees C, and adenosine triphosphate (ATP) and glycogen levels were higher than those in the control group. Thus, under these conditions, cold exposure per se, even for 2 hours at temperatures near 0 degree C, has no deleterious effect upon myocardial function and energy metabolism.