Date Published: July 29, 2013
Publisher: Hindawi Publishing Corporation
Author(s): Tanyong Pipanmekaporn, Yodying Punjasawadwong, Somrat Charuluxananan, Worawut Lapisatepun, Pavena Bunburaphong.
The purpose of this study was to determine the effect of dexmedetomidine on hemodynamic responses to DLT intubation compared to placebo and to assess the adverse effects related to dexmedetomidine. Sixty patients were randomly allocated to receive 0.7 μg/kg dexmedetomidine (n = 30) or normal saline (n = 30) 10 minutes before general anesthesia. Systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), heart rate (HR), and rate pressure product (RPP) between groups were recorded. During intubation and 10 minutes afterward (T1-T10), the mean SBP, DBP, MAP, HR, and RPP in the control group were significantly higher than those in the dexmedetomidine group throughout the study period except at T1. The mean differences of SBP, DBP, MAP, HR, and RPP were significantly higher in the control group, with the value of 15.2 mmHg, 10.5 mmHg, 14 mmHg, 10.5 beats per minute, and 2,462.8 mmHg min−1. Four patients in the dexmedetomidine group and 1 patient in the control group developed hypotension, while 2 patients in the dexmedetomidine group had bradycardia. Prophylactic dexmedetomidine can attenuate the hemodynamic responses to laryngoscopy and DLT intubation with minimal adverse effects. This trial is registered with ClinicalTrials.gov NCT01289769.
A double-lumen endotracheal tube (DLT) is a device frequently used in thoracic surgery. It effectively provides lung separation and facilitates changing from two- to one-lung ventilation . A previous study found that both laryngoscopy and DLT intubation could stimulate significant hemodynamic responses and increase the plasma concentration of catecholamines . Although these hemodynamic responses including tachycardia and hypertension are transient, they can be harmful to patients with hypertension, myocardial ischemia, or cerebrovascular disease [3, 4]. The supplement of an inhaled anesthetic agent during anesthetic induction and intubation using a nondepolarizing muscle relaxant is a normal practice at our hospital. However, we observe that this practice is found ineffective to attenuate the hemodynamic responses to intubation and rescue treatment is frequently required. Therefore, some measures should be added in order to optimize this condition.
After approval from the institutional review board and written informed consent were obtained, 60 patients with the American Society of Anesthesiologists (ASA) physical status I-III, aged 18–65 years, undergoing scheduled thoracic surgery between March and December 2011 were enrolled in the study. Exclusion criteria were preoperative arrhythmias, bradycardia (heart rate < 50 beats per minute), second- or third-degree atrioventricular block, tachycardia (heart rate > 100 beats per minute), coronary artery disease, previous cerebrovascular accident, poorly controlled hypertension, renal or liver impairment and suspected difficult intubation. All patients had 0.2 mg/kg of diazepam orally two hours before surgery. In the operating theater the following monitoring was established: noninvasive blood pressure monitoring, electrocardiography (ECG) using the three-lead electrode system, peripheral oxygen saturation, and radial artery catheterization with a 20 G catheter. Patients were randomly allocated into two groups: the dexmedetomidine group and the control group, using a block of four randomizations with each randomized number concealed in a sealed, opaque envelope which would be opened after radial artery catheterization. The dexmedetomidine group received dexmedetomidine, 0.7 μg/kg in 0.9% NaCl 20 mL, while the control group received 0.9% NaCl 20 mL. Both the dexmedetomidine solution and 0.9% NaCl were prepared by a nurse who was not involved in the study so that the investigators would be unaware of the group identity. The designated solution was infused over 10 minutes before the induction of anesthesia. Propofol 2.5 mg/kg and fentanyl 1 μg/kg were given followed by rocuronium 0.6 mg/kg to facilitate endotracheal intubation. Anesthesia was maintained with 1% vaporizer setting of concentration of sevoflurane until tracheal intubation. Four minutes later, the laryngoscopy and endotracheal intubation were performed using a 39 Fr, 37 Fr, or 35 Fr endobronchial tube as recommended by Slinger and Campos . All intubation attempts were performed by the same anesthesiologist (TP). Hemodynamic parameters (systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), heart rate (HR), and rate pressure product (RPP, SBP × HR)) were recorded at baseline, just before intubation, during intubation, and every minute after intubation for 10 minutes. Recording of parameters including intubation time (time from applying a laryngoscopy to tracheal cuff inflation) was done by another nurse who was not involved in the study. The incidences of hypotension (a decrease in SBP > 25% of baseline or SBP < 90 mmHg) and bradycardia (a decrease in HR > 25% of baseline or HR < 50 beats per minute) were also noted. Rescue medication was comprised of ephedrine 3 mg increments for hypotension (SBP < 90 mmHg for 60 seconds), nicardipine 0.5 mg increments for hypertension (SBP > 200 mmHg or DBP > 120 mmHg for 60 seconds) [2, 14, 15], and atropine 0.3 mg increments for bradycardia (HR < 50 beats per minute). The flow diagram of the study, recommended by the Consolidated Standards of Reporting Trials, is presented in Figure 1. Sixty patients were randomized and completed the study. Patient characteristics, baseline hemodynamic variables, and intubation time were comparable between both groups (Table 1). Before intubation, mean SBP, DBP, MAP, and RPP in both groups were not significantly different; however, mean HR in the dexmedetomidine group was significantly lower than that of the control group (P < 0.05). During DLT intubation (T0) and 10 minutes afterward (T1–T10), the mean SBP, DBP, MAP, HR, and RPP in the control group were significantly higher than those of the dexmedetomidine group throughout the study period except T1, in which the blood pressures (BP) were not statistically different (Figures 2, 3, 4, and 5). A maximal increase of mean HR was observed at T0 in the control group, while a maximal increase of the mean HR in the dexmedetomidine group occurred at T1. Meanwhile, the mean differences of SBP, DBP, MAP, HR, and RPP were significantly higher in the control group between baseline, before intubation, during intubation, and T1–T10 after being adjusted for age, gender, ASA, concurrent disease, intubation time, baseline hemodynamic variables, and intubation attempts (P < 0.001) as shown in Table 2. In the dexmedetomidine group, the mean SBP, DBP, and MAP decreased significantly from the baseline before intubation, during intubation, and all through 10 minutes afterward except at T1 (P < 0.05). The mean SBP before intubation was 106.5 ± 20.7 mmHg, while the lowest mean SBP was observed at T7 (97.2 ± 13.2 mmHg). Significant decreases of mean HR from the baseline were before intubation and from T6 to T10, with the lowest mean value of 67.3 ± 13.1 beats per minute before intubation (P < 0.05). The mean values of SBP, DBP, MAP, HR, and RPP at different time points in both groups were presented in Table 3. Table 4 shows the incidences of adverse effects during and after intubation, which were not significantly different between groups. Four patients in the dexmedetomidine group and 1 patient in the control group developed hypotension, all of whom but 1 in the dexmedetomidine group required rescue medications. No patient in the control group had bradycardia. In the dexmedetomidine group, 2 patients had bradycardia and only 1 patient required treatment. All patients who received rescue medications responded very well to treatment. There was no episode of respiratory obstruction observed during administration of the study drug. NNT to prevent an increase of MAP more than 25% of baseline for dexmedetomidine was 10 (95% CI: 3.4–10.6). All patients were able to be extubated after the operation. An inhaled anesthetic agent is commonly used in combination with an intravenous anesthetic agent before a nondepolarizing muscle relaxant reaches its onset. In our practice, 1% concentration of sevoflurane may be sufficient to prevent awareness during induction of anesthesia ; however, this concentration does not effectively attenuate the hemodynamic responses to intubation. This study found that the mean SBP, DBP, MAP, HR, and RPP in the control group were significantly higher than those of the dexmedetomidine group all through 10 minutes after DLT intubation, except mean SBP, DBP, and MAP between groups at T1. Corresponding to a previous study, this study showed that maximal increases of blood pressure and heart rate occurred 1 to 2 minutes after DLT intubation in the control group and returned to baseline within 5 minutes . Thompson et al. showed that an increase of hemodynamic responses after DLT intubation in patients with an adequate depth of anesthesia was associated with an increase of the plasma level of norepinephrine . In addition, previous studies reported that RPP was one of the major determinants of myocardial oxygen consumption and RPP > 20,000 mmHg min−1 could precipitate angina pectoris . Four patients (13%) in the control group and 1 patient (3%) in the dexmedetomidine group had an RPP of more than 20,000 mmHg min−1, which could increase the risk of myocardial ischemia [17, 18]. The effect of dexmedetomidine on lowering SBP, HR, and RPP could decrease the myocardial oxygen requirement and may be advantageous for patients at risk of coronary artery disease . Moreover, the effect of dexmedetomidine in the controlling of blood pressure and heart rate during intubation may be beneficial in patients with preexisting hypertension or risk of stroke .
Prophylactic dexmedetomidine can attenuate the hemodynamic responses to laryngoscopy and DLT intubation with minimal adverse effects. This application may be useful to patients who are at risk of cardiovascular complications related to severe hypertension and tachycardia after DLT intubation.