Risk factors for mortality after failed coronary angioplasty: an anesthesia perspective.

Monitored anesthesia care (MAC) for percutaneous transluminal coronary angioplasty (PTCA), and anesthesia for emergent coronary artery bypass graft (CABG) surgery due to failed PTCA, have added relatively new challenges to the cardiac anesthesiologist in community practice. This study attempted to define easily identifiable preangioplasty and periangioplasty risk factors for mortality after failed PTCA. A total of 1,380 angioplasties performed in a single community hospital were retrospectively reviewed; 120 (8.7%) were attempted PTCAs requiring subsequent CABG during the same hospital stay. The 120 failures included 10 surgical mortalities (8.3%); multivariate analysis revealed several significant differences between the mortality and survivor groups. Mortality tended to be higher in insulin-dependent diabetics (P = 0.003), females (P = 0.005), and patients 70 years or over (P = 0.043). Previous CABG, decreased left ventricular ejection fraction, and number of vessels with significant disease did not differ between the groups. Patients who died required more vasopressor agents (P = 0.011) during PTCA and experienced cardiac arrests (P = 0.011) at significantly higher rates than survivors. Left system (left anterior descending or circumflex coronary artery) angioplasty, inability to pass the angioplasty guidewire, and antiarrhythmic drug use did not differ between groups. Data concerning endotracheal intubation in the catheterization laboratory and time from laboratory exit to initiation of cardiopulmonary bypass, while bivariately significant, were too sparse for multivariate analysis. The authors believe that several risk factors for postangioplasty surgical mortality are easily determined without access to diagnostic angiographic studies.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of sufentanil on the hemodynamic and respiratory response to exercise.

The effects of the potent opioid, sufentanil, were studied in 11 athletes. Sufentanil was administered intravenously (up to 0.5 microgram.kg-1 over 10 min) to the subjects while they ran at 14 km.hr-1 on a level treadmill. Prior to, and after, the drug infusion, the treadmill was inclined by 6% for 4 min and CO2 was inhaled for 4 min. Two groups were studied: group 1 (six subjects) breathed room air and group 2 (five subjects) breathed O2 enriched air. During level running the ventilation (liters.min-1) of the group 1 subjects was reduced (65.3 +/- 8.6 to 55.9 +/- 4.9, P = 0.09, mean +/- standard error) and PaCO2 (mm Hg) increased from 37.6 +/- 0.7 to 44.0 +/- 0.5 (P less than 0.05). PaO2 (mm Hg) was substantially reduced from 92.0 +/- 2.0 to 70.0 +/- 2.0 (P less than 0.05). In group 2, where hypoxia did not occur, ventilation was reduced from 62.5 +/- 1.5 to 47.6 +/- 1.0 (P less than 0.05). The ventilatory response to the CO2 was shifted to the right but the slope was unchanged by sufentanil. The 6% grade did not cause any significant change in the PaCO2 in either group 1 (0.1 +/- 0.4 prior and 0.8 +/- 0.5 mm Hg increase after sufentanil) or group 2 (1.0 +/- 1.5 prior and 0.4 +/- 0.9 mm Hg increase after sufentanil). The heart rate response was unaffected by sufentanil but the blood pressure increase in response to the 6% grade was blocked with the drug.(ABSTRACT TRUNCATED AT 250 WORDS)

An analysis of serum enzyme changes and clinical biochemical abnormalities of the anemia in Olympic runners.

In order to assess the changes in the clinical biochemistry of runner's anemia and its evolution during a prolonged period of high-intensity training, 11 male international class distance runners (mean time for 1 mile 4 min, 2.5 sec) were followed over a 10-month period prior to the 1984 U.S. Olympic Trials. Mean values of hemoglobin, hematocrit, and mean corpuscular hemoglobin (MCH) decreased modestly over the period of study. Means of haptoglobin, iron, and total iron binding capacity (TIBC) remained roughly constant. Percentage of saturation of TIBC by iron (% sat) averaged 30% or less in 5 of 11 runners, suggesting mild iron deficiency. Most measured haptoglobin levels were below normal range throughout the study period. The cause of runner's anemia has been demonstrated to be multifactorial, including disordered iron metabolism, iron deficiency, and hemolysis. Other studies have shown absent bone marrow iron in male athletes, secondary to hematuria, ischemia of the intestinal mucosa with bleeding, and iron losses due to heavy perspiring. Cardiorespiratory fitness, evaluated through repetitive treadmill testing, was not adversely affected in our athletes. Total creatine kinase (CK) increased significantly after a training session, while the MB fraction of CK never exceeded 3%. Total lactate dehydrogenase (LD) also rose after exercise, but the fractions represented by isozymes 1-5 were unaltered; specifically, there was no change in the LD-1/LD-2 ratio. Enzyme elevations were thus derived from skeletal muscle and not from heart.

Changes in serum enzymes, lactate, and haptoglobin following acute physical stress in international-class athletes.

Skeletal muscle is rich in creatine kinase (CK), lactate dehydrogenase (LD), and other enzymes. Many reports describe changes in serum CK and LD following exercise. In our study, 11 male international-class medium-distance runners were followed over a 10-month period prior to the 1984 US Olympic Trials. Cardiorespiratory fitness, evaluated through repetitive treadmill testing, was unchanged in our athletes. Total CK increased significantly during the course of training, and the CK-MB activity was higher than that of sedentary individuals; CK-MB never rose to more than 3% of the total CK. Total LD also rose following acute exercise; however, the proportions of the five isoenzymes were unaltered. There was no change in the LD-1/LD-2 ratio from normal. The origin of the increased serum enzymes was believed to be primarily skeletal muscle. A decrease of serum haptoglobin following acute stress was attributed to intravascular hemolysis and binding of hemoglobin. As expected, serum lactate was dramatically increased immediately postexercise.