Successful treatment of peripartum massive pulmonary embolism with extracorporeal membrane oxygenation and catheter-directed pulmonary thrombolytic therapy.

Chronic thromboembolic pulmonary hypertension during pregnancy is uncommon but is associated with maternal mortality in excess of 35%. We report a case of decompensated thromboembolic pulmonary hypertension requiring emergency caesarean section and postpartum treatment with extracorporeal membrane oxygenation and thrombolytic therapy with urokinase. The use of extracorporeal membrane oxygenation, catheter-directed pulmonary thrombolytic therapy and other pulmonary vasodilators for management of this life-threatening disease is discussed.

Effect of pump prime on acidosis, strong-ion-difference and unmeasured ions during cardiopulmonary bypass.

We tested the hypothesis that a cardiopulmonary bypass prime with lactate would be associated with less acidosis than a prime with only chloride anions because of differences in the measured strong-ion-difference. We randomised 20 patients to a 1500 ml bypass prime with either a chloride-only solution (Ringer's Injection; anions: chloride 152 mmol/l) or a lactated solution (Hartmann's solution; anions: chloride 109 mmol/l, lactate 29 mmol/l). Arterial blood was sampled before bypass and then two, five, 15 and 30 minutes after initiating bypass. We used repeated measures analysis of variance to compare groups. In both groups, the base-excess and measured strong-ion-difference decreased markedly from baseline after two minutes of bypass. The chloride-only group had greater acidosis with lower base-excess and pH (P < 0.05), greatest after five minutes of bypass (C5). Contrary to our hypothesis, however, the difference between the groups was not due to a difference in the measured strong-ion-difference, P = 0.88. At C5 when the difference in standard base-excess between the groups was greatest, 1.9 mmol/l (95% confidence interval: 0.1 to 3.6 mmol/l, P < 0.05), the difference in the measured strong-ion-difference was only 0.2 mmol/l (95% confidence interval: -2.4 to 2.7 mmol/l, P > 0.05). There was, however a difference in the net-unmeasured-ions (strong-ion-gap). We conclude that acid-base changes with cardiopulmonary bypass may differ with the prime but that the early differences between chloride-only and lactated primes appear not to be due to differences in the measured strong-ion-difference. We suggest future studies examine other possible mechanisms including unmeasured ions.

Pulmonary arteriovenous malformation causing massive haemoptysis and complicated by coronary air embolism.

We report the case of a 20-year-old man with possible Osler-Rendu-Weber syndrome (hereditary haemorrhagic telangiectasia) who developed an episode of massive haemoptysis from a bleeding pulmonary arteriovenous malformation in the left lower lobe of his lung. During the acute haemorrhage, he also appeared to suffer a coronary air embolism, possibly due to introduction of air into the bleeding arteriovenous malformation during intermittent positive pressure ventilation through the endotracheal tube. His electrocardiogram showed extensive ST elevation (>2 mm) in the inferolateral leads associated with raised troponin I and creatine kinase levels. These changes resolved within thirty minutes. The pulmonary arteriovenous malformation was successfully treated with a combination of alcohol injection and coil embolization.

Role of pump prime in the etiology and pathogenesis of cardiopulmonary bypass-associated acidosis.

BACKGROUND: The development of metabolic acidosis during cardiopulmonary bypass (CPB) is well recognized but poorly understood. The authors hypothesized that the delivery of pump prime fluids is primarily responsible for its development. Accordingly, acid-base changes induced by the establishment of CPB were studied using two types of priming fluid (Haemaccel, a polygeline solution, and Ringer's Injection vs. Plasmalyte 148) using quantitative biophysical methods. METHODS: A prospective, double-blind, randomized trial was conducted at a tertiary institution with 22 patients undergoing CPB for coronary artery bypass surgery. Sampling of arterial blood was performed at three time intervals: before CPB (t1), 2 min after initiation of CPB at full flows (t2), and at the end of the case (t3). Measurements of Na+, K+, Mg2+, Cl-, HCO3-, phosphate, Ca2+, albumin, lactate, and arterial blood gases at each collection point were performed. Results were analyzed in a quantitative manner. RESULTS: Immediately on delivery of pump prime fluids, all patients developed a metabolic acidosis (base excess: 0. 95 mEq/l (t1) to -3.65 mEq/l (t2) (P < 0.001) for Haemaccel-Ringer's and 1.17 mEq/l (t1) to -3.20 mEq/l (t2). The decrease in base excess was the same for both primes (-4.60 vs. -4.37; not significant). However, the mechanism of metabolic acidosis was different. With the Haemaccel-Ringer's prime, the metabolic acidosis was hyperchloremic (Delta Cl-, +9.50 mEq/l; confidence interval, 7.00-11.50). With Plasmalyte 148, the acidosis was induced by an increase in unmeasured anions, most probably acetate and gluconate. The resolution of these two processes was different because the excretion of chloride was slower than that of the unmeasured anions (Delta base excess from t1 to t3 = -1.60 for Haemaccel-Ringer's vs. +1.15 for Plasmalyte 148; P = 0.0062). CONCLUSIONS: Cardiopulmonary bypass-induced metabolic acidosis appears to be iatrogenic in nature and derived from the effect of pump prime fluid on acid-base balance. The extent of such acidosis and its duration varies according to the type of pump prime.

Hormonal effects of norepinephrine on acute glucose disposal in humans: a minimal model analysis.

It is not known whether circulating norepinephrine (NE) has a direct hormonal influence on glucose disposal. This study examines whether moderate elevation of NE alters the disposal of an acute intravenous (IV) glucose load, as analysed by the minimal model of Bergman. Eight healthy normal subjects were infused with either 25 ng/kg/min NE (plasma NE 1,284 +/- 259 pg/mL) or normal saline (plasma NE 314 +/- 86 pg/mL), 30 minutes prior to and during an IV glucose tolerance test (GTT). There was a small but significant rise (P less than .05) in basal blood glucose levels during the initial 30-minute NE infusion which was accompanied by a 40% increase (0.39 +/- .02 to 0.59 +/- .07 nmol/L, P less than .01) in nonesterified fatty acid levels (NEFA). Insulin, C-peptide, and glucagon levels did not change. NE impaired the rate of acute glucose disposal (Kg 1.74 +/- 0.24 v 2.10 +/- 0.23 (min-1, P less than .05). Minimal model analysis revealed a corresponding 35% decrease in insulin sensitivity (SI 4.85 +/- 1.51 v 7.28 +/- 1.16 min-1 microU-1 mL-1 x 10(4), P less than .05) but no significant differences between glucose-mediated glucose disposal or pancreatic B-cell responsiveness. The glucose disposition index (si* phi2), a direct measure of an individual's overall insulin- mediated glucose disposal, was reduced by 70% in the NE-infussed subjects (si* phi2 69 +/-22 v 223 +/- 76 mg-1 ml-1 min-3 x 10(2), p< .05).(ABSTRACT TRUNCATED AT 250 WORDS)