Effects of conventional vs high-dose rocuronium on the QTc interval during anesthesia induction and intubation in patients undergoing coronary artery surgery: a randomized, double-blind, parallel trial

Myocardial ischemia, as well as the induction agents used in anesthesia, may cause corrected QT interval (QTc) prolongation. The objective of this randomized, double-blind trial was to determine the effects of high- vs conventional-dose bolus rocuronium on QTc duration and the incidence of dysrhythmias following anesthesia induction and intubation. Fifty patients about to undergo coronary artery surgery were randomly allocated to receive conventional-dose (0.6 mg/kg, group C, n=25) or high-dose (1.2 mg/kg, group H, n=25) rocuronium after induction with etomidate and fentanyl. QTc, heart rate, and mean arterial pressure were recorded before induction (T0), after induction (T1), after rocuronium (just before laryngoscopy; T2), 2 min after intubation (T3), and 5 min after intubation (T4). The occurrence of dysrhythmias was recorded. In both groups, QTc was significantly longer at T3 than at baseline [475 vs 429 ms in group C (P=0.001), and 459 vs 434 ms in group H (P=0.005)]. The incidence of dysrhythmias in group C (28%) and in group H (24%) was similar. The QTc after high-dose rocuronium was not significantly longer than after conventional-dose rocuronium in patients about to undergo coronary artery surgery who were induced with etomidate and fentanyl. In both groups, compared with baseline, QTc was most prolonged at 2 min after intubation, suggesting that QTc prolongation may be due to the nociceptive stimulus of intubation.

Effects of conventional vs high-dose rocuronium on the QTc interval during anesthesia induction and intubation in patients undergoing coronary artery surgery: a randomized, double-blind, parallel trial.

Myocardial ischemia, as well as the induction agents used in anesthesia, may cause corrected QT interval (QTc) prolongation. The objective of this randomized, double-blind trial was to determine the effects of high- vs conventional-dose bolus rocuronium on QTc duration and the incidence of dysrhythmias following anesthesia induction and intubation. Fifty patients about to undergo coronary artery surgery were randomly allocated to receive conventional-dose (0.6 mg/kg, group C, n=25) or high-dose (1.2 mg/kg, group H, n=25) rocuronium after induction with etomidate and fentanyl. QTc, heart rate, and mean arterial pressure were recorded before induction (T0), after induction (T1), after rocuronium (just before laryngoscopy; T2), 2 min after intubation (T3), and 5 min after intubation (T4). The occurrence of dysrhythmias was recorded. In both groups, QTc was significantly longer at T3 than at baseline [475 vs 429 ms in group C (P=0.001), and 459 vs 434 ms in group H (P=0.005)]. The incidence of dysrhythmias in group C (28%) and in group H (24%) was similar. The QTc after high-dose rocuronium was not significantly longer than after conventional-dose rocuronium in patients about to undergo coronary artery surgery who were induced with etomidate and fentanyl. In both groups, compared with baseline, QTc was most prolonged at 2 min after intubation, suggesting that QTc prolongation may be due to the nociceptive stimulus of intubation.

Pulmonary hypertension in patients with chronic renal failure.

BACKGROUND: Many etiologies causing pulmonary hypertension (PH) have been reported, and one of the background disease seen with patients with PH is chronic renal failure (CRF); however, the pathogenesis of PH in this group of patients is not explained satisfactorily. OBJECTIVES: The aims of this study were to evaluate the incidence of unexplained PH among patients with CRF and to suggest possible etiologic factors. METHODS: Two hundred and eleven patients with CRF were evaluated and the ones who have comorbid conditions that cause PH were excluded. Pulmonary arterial pressure (PAP) and cardiac functions were evaluated by Doppler echocardiography. Arteriovenous fistula (AVF) flow was measured by Doppler sonography. The patients were followed for at least 6 months. RESULTS: Forty-eight CRF patients (20 males, 28 females) were included: 23 were predialysis patients, and 25 patients received hemodialysis via AVF. Patients were followed for 7.5 +/- 1.01 months. Systolic PAP >35 mm Hg was found in 56% (14/25) of patients receiving hemodialysis (36.8 +/- 10.7 mm Hg) and in 39.1% (9/23) of predialysis patients (29.5 +/- 9.5 mm Hg). The parathyroid hormone level, cardiac output values and CRF duration were found to be increased in patients with elevated systolic PAP (p < 0.05). AVF flow and AVF duration were positively correlated with systolic PAP in patients receiving hemodialysis (p < 0.05). There was a negative correlation between systolic PAP and residual urine volume (p < 0.05). AVF compression in hemodialysis patients decreased systolic PAP from 36.8 +/- 10.7 to 32.8 +/- 10.5 mm Hg. Systolic PAP values were increased at the end of the study in the predialysis group, whereas they were decreased at the end of the follow-up in the hemodialysis group (36.9 +/- 10.5 and 32.04 +/- 10.5 mm Hg, respectively). CONCLUSIONS: This study demonstrates a high incidence of PH among patients with CRF. CRF duration, AVF flow, parathyroid hormone level and cardiac output may be involved in the pathogenesis of PH. The effective hemodialysis and dry weight reduction decreased systolic PAP values.