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The effects of intentional hyperthermia on the Thrombelastograph and the Sonoclot analyser.

The effect of whole-body hyperthermia (WBH) on viscoelastic properties of whole blood, as measured by the thrombelastogram (TEG) and Sonoclot analyser, was investigated in 10 patients undergoing WBH-carboplastin therapy for metastatic disease. Blood was taken from an existing central line at baseline (37 degrees C), during warming (39 and 41 degrees C) and cooling (39 and 37 degrees C). Sonoclot and TEG samples were analysed simultaneously at 37 degrees C and at the patient's temperature with a temperature-compensated unit, except at 41 degrees C for the Sonoclot (maximum temperature adjustment of 40 degrees C). TEG measurements included R time (time to initial fibrin formation [mm]), K time (mm) and alpha angle (degrees) (both reflecting fibrinogen-platelet interaction), maximum amplitude (representing qualitative platelet function [mm]) and per cent fibrinolysis at 30 and 60 min. The Sonoclot ACT (SonACT-secs), initial rate of clot formation (%), time to peak amplitude (min) and peak amplitude of the Sonoclot signature (mm) were recorded. Decreased R time of the TEG compared to a marginally elevated baseline was found at all times during warming and cooling (p < 0.05). The K time was decreased at 41 degrees C compared to a normal baseline (p < 0.05). The SonACT was decreased (from an elevated baseline) at all other times, without differences in measures at patient temperature versus 37 degrees C (p < 0.05). The data suggest acceleration of fibrin formation during WBH to 41 degrees C in patients with malignancy. Implications for defining thromboembolic risk require further investigation.

Adult↗

PubMedDate not supplied

The use of esmolol in whole-body hyperthermia: cardiovascular effects.

Whole-body hyperthermia (WBH) is a well-described investigational adjunct to systemic chemotherapy for the treatment of advanced malignancies. The hemodynamic consequences of this physiologic state may include tachycardia, which can produce acute myocardial ischemia in patients with coronary artery disease. Ischemic heart disease is currently considered a contraindication to WBH. We chose to investigate the consequences of using a new beta 1-adrenergic antagonist, esmolol, to attempt to control the tachycardia associated with WBH. After institutional approval and patient consent, nine consecutive patients with normal cardiac function presenting for WBH with carboplatin infusion were studied. Along with standard monitors, radial arterial and oximetric thermodilution pulmonary artery catheters were placed. Patients were sedated and heated in a radiant warmer (Enthermics). Spontaneous ventilation was maintained and hemodynamic data were gathered at 37 degrees C, and at 41.8 degrees C (before, during and after esmolol infusion). Heart rate and cardiac output increased (by 46% (p = 0.001) and 35% (p = 0.04) respectively) while mean arterial pressure and systemic vascular resistance fell (by 18% (p = 0.02) and 44% (p = 0.006) respectively) during hyperthermia. Heart rate was significantly reduced during esmolol administration (mean dose 180 micrograms/kg/min) in the absence of changes in cardiac index and calculated oxygen delivery. Ventricular filling pressures and stroke work were unchanged. No heart failure, pulmonary edema, or other adverse event was observed. Hemodynamic changes seen during esmolol administration were completely reversed 15 min after the infusion was stopped. We conclude that the administration of moderate doses of esmolol is safe for this population of patients undergoing WBH, and that this technique raises the question of whether patients with ischemic heart disease could safely undergo WBH.

Adrenergic beta-Antagonists↗