Left ventricular dysfunction during extracorporeal membrane oxygenation in a hypoxemic swine model.

BACKGROUND: Perfusion of the coronary circulation with hypoxemic blood from the left ventricle has been postulated to cause myocardial dysfunction during venoarterial extracorporeal membrane oxygenation for respiratory support. METHODS: We investigated this hypothesis in 10 anesthetized open-chest piglets (7 to 9 kg) undergoing venoarterial extracorporeal membrane oxygenation after placement of minor-axis sonomicrometry crystals and left ventricular micromanometer. The left atrial partial pressure of oxygen was made hypoxemic (25 to 40 mm Hg) after initiation of extracorporeal membrane oxygenation by ventilation with a hypoxic gas mixture. Left ventricular contractile function, including peak LV pressure, shortening fraction, maximum rate of increase of left ventricular pressure, velocity of circumferential fiber shortening, end-systolic pressure-minor axis dimension relationship, and preload recruitable dimensional stroke work, was measured or calculated on extracorporeal membrane oxygenation before (baseline) and at 4 and 6 hours after rendering the left atrial blood hypoxemic. RESULTS: Left ventricular shortening fraction and velocity of circumferential fiber shortening were significantly lower (p < 0.05) at 4 and 6 hours when compared with baseline. The slope of the end-systolic pressure-minor axis dimension relationship decreased but was not significantly different at 4 and 6 hours when compared with baseline owing to poor linear correlation (r = 0.30 to 0.93). The preload recruitable dimensional stroke work was more linear (r = 0.87 to 0.99), and the slope was significantly lower (p < 0.01) at 4 and 6 hours when compared with baseline. CONCLUSIONS: Hypoxemic cardiac output from the left ventricle during venoarterial extracorporeal membrane oxygenation is associated with depression of left ventricular systolic function in this animal model. Current use of venoarterial extracorporeal membrane oxygenation for respiratory support may not provide adequate oxygen supply to the myocardium.

Blood conservation with membrane oxygenators and dipyridamole.

Cardiopulmonary bypass induces platelet activation and dysfunction, which result in platelet deposition and depletion. Reduced platelet numbers and abnormal platelet function may contribute to postoperative bleeding. A membrane oxygenator may preserve platelets and reduce bleeding more than a bubble oxygenator, and the antiplatelet agent dipyridamole may protect platelets intraoperatively and reduce bleeding postoperatively. A prospective randomized trial was performed in 44 patients undergoing elective coronary artery bypass grafting to assess the effects of the membrane oxygenator and dipyridamole on platelet counts, platelet activation products, and postoperative bleeding. Patients who were randomized to receive a bubble oxygenator and no dipyridamole had the lowest postoperative platelet counts, the greatest blood loss, and the most blood products transfused. Platelet counts were highest and blood loss was least in patients randomized to receive a membrane oxygenator and dipyridamole (p less than .05). A bubble oxygenator with dipyridamole and a membrane oxygenator without dipyridamole resulted in intermediate postoperative platelet counts and blood loss. Arterial thromboxane B2 and platelet factor 4 concentrations were elevated on cardiopulmonary bypass in all groups. Both the membrane oxygenator and dipyridamole were independently effective (by multivariate analysis) in preserving platelets. Optimal blood conservation was achieved with a membrane oxygenator and dipyridamole.

Diltiazem cardioplegia. A balance of risk and benefit.

Calcium channel blockers may prevent myocardial injury during cardioplegia and reperfusion. A prospective, randomized trial was instituted to evaluate the hemodynamic and myocardial metabolic recovery in 40 patients undergoing elective aorta-coronary bypass with either diltiazem in crystalloid potassium cardioplegia (n = 20) or crystalloid potassium cardioplegia (n = 20). In a preliminary trial, doses between 150 and 250 micrograms/kg reduced the period of heart block after cross-clamp removal (90 +/- 110 minutes) from that found with higher doses and improved myocardial metabolism. In the randomized trial, diltiazem cardioplegia (150 micrograms/kg) produced coronary vasodilatation during cardioplegia and produced less reactive hyperemia during reperfusion. Myocardial oxygen extraction was lower and myocardial lactate production was less after diltiazem cardioplegia during reperfusion. Tissue adenosine triphosphate and creatine phosphate concentrations were preserved better after diltiazem cardioplegia. The postoperative creatine kinase MB levels were less (p less than 0.05) after diltiazem cardioplegia, which indicated less myocardial injury. Postoperative volume loading demonstrated that systolic function (the relation between systolic blood pressure and end-systolic volume index) was depressed after diltiazem cardioplegia compared to crystalloid cardioplegia, but cardiac index was higher because afterload (mean arterial pressure) was lower and preload (end-diastolic volume index) was higher. Diltiazem cardioplegia preserved high-energy phosphates, improved postoperative myocardial metabolism, and reduced ischemic injury after elective coronary bypass. However, diltiazem was a potent negative inotrope and produced prolonged periods of electromechanical arrest. Diltiazem cardioplegia may be of value in patients with severe ischemia but should be used with caution in patients with ventricular dysfunction, and a dose-response relation must be established at each institution before clinical use.