Since it was first described by Trendelenburg in the 1860s, the head-down tilt position has been used in various clinical situations for a long time.1 Although this position has been frequently used to augment venous return in hypovolaemic hypotensive patients, previous studies have failed to demonstrate that it has a meaningful haemodynamic effect,2–6 and consequently, it has been recommended that this position should not to be used during the resuscitation of hypotensive patients.7
However, in patients undergoing spinal anaesthesia, the head-down tilt position is effective in increasing blood pressure8 and cardiac output (CO).9 These results suggest that the effect of the head-down tilt position may be different during anaesthesia. Although the head-down tilt position is commonly used to treat hypotension on induction of general anaesthesia, there are few studies exploring the effectiveness of this practice in patients under general anaesthesia. In a study performed on paediatric patients, Kardos et al.10 demonstrated that the head-down tilt position did not improve either CO or blood pressure. These results suggest that the effect of head-down tilt position may be dependent on the type of anaesthesia or even the type of patient population.
We hypothesised that the head-down tilt position might increase blood pressure and CO in hypotensive patients following the induction of general anaesthesia. To evaluate our hypothesis, we undertook this randomised clinical study, in which we measured and compared haemodynamic parameters and the use of vasopressors in a head-down tilt group and a supine group during hypotension after general anaesthesia in patients undergoing cardiac surgery.
Ethical approval for this study (H-0811-065-263) was provided by the Seoul National University Hospital Institutional Review Board, Seoul, Korea (President Sang Goo Shim) on 14 January 2010.
After obtaining institutional review board approval, written informed consents were obtained from all enrolled patients. Ninety eight patients scheduled for cardiac surgery at Seoul National University Hospital were enrolled and 40 were included in this study. The exclusion criteria applied were as follows: emergency surgery, age less than 19 or more than 85 years, an ejection fraction less than 40%, acute myocardial infarction less than a month before surgery, raised intracranial pressure, severe pulmonary disease [as indicated by a forced expiratory volume in 1 s (FEV1) of <1.0 l], arrhythmia and the pre-operative use of vasopressor. Pre-operative medication of the patient was continued except angiotensin-converting enzyme inhibitor (ACEI), which was stopped at least 3 days before the surgery. If hypotension did not occur during the induction of anaesthesia, the patients were also excluded.
Anaesthesia and monitoring
Before anaesthesia induction, an arterial line was placed in the radial artery and connected to a FloTrac-Vigileo system (Edward Lifesciences, Irvine, California, USA). An arterial line transducer was placed and zeroed to the fourth intercostal space in the midaxillary line. In addition, a 5-lead electrocardiography (ECG), a pulse oximeter, a capnometer, a pulmonary artery catheter, a transesophageal echocardiography and a nasopharyngeal temperature monitoring device were used. Anaesthesia was induced with midazolam 0.15 mg kg−1 IBW (ideal body weight), vecuronium 10 mg and sufentanil 1 μg kg−1 IBW. Anaesthesia was maintained with continuous infusions of midazolam (0.05 mg kg−1 h−1 IBW), sufentanil (2.5 μg kg−1 h−1 IBW) and vecuronium (0.1 mg kg−1 h−1 IBW). IBW was calculated using Devine's formula. Minimal crystalloid fluid was infused during the study to maintain the intravenous line.
When hypotension occurred between anaesthesia induction and skin incision, the patient was placed in the supine position or in the 15° head-down tilt position according to randomisation until skin incision. Hypotension was defined as a mean arterial pressure (MAP) of less than 70% of pre-operative baseline MAP or a SBP of less than 90 mmHg. Pre-operative baseline MAP was determined by averaging three pre-operative MAP values obtained at least 8 h apart. If hypotension did not occur during this period, the patient was excluded.
Group allocations were performed by an anaesthesia nurse unrelated to the study using a randomisation programme available on the internet (http://www.randomizer.org). Anaesthesiologists were not given any information regarding group allocations until the occurrence of hypotension.
After the patients were placed in the supine or head-down tilt position according to group assignment, the same hypotension treatment protocol was used in the two groups. Briefly, ephedrine 0.1 mg kg−1 IBW was administered when the heart rate was less than 70 beats per minute or phenylephrine 0.5 μg kg−1 IBW when the heart rate was at least 70 beats per minute. If blood pressure was not restored within 30 s after vasopressor administration, the treatment regimen was repeated until the total amount of administered drug reached its maximum dose. The maximum doses of ephedrine and phenylephrine were 0.5 mg kg−1 IBW and 4 μg kg−1 IBW, respectively. If the total amount of administered drug exceeded the maximum dose and the patient did not recover from hypotension, the patient was defined as having refractory hypotension and vasopressin or epinephrine was administered according to attending anaesthesiologist's decision. Total amounts and the numbers of drug administrations were recorded. Haemodynamic data were collected at 1-min intervals for 10 min from the occurrence of hypotension and included SBP and DBP, MAP, heart rate, cardiac index (CI) and stroke volume index. SBP, DBP, MAP and heart rate were measured by invasive arterial pressure monitoring. CI and stroke volume index were measured using a FloTrac-Vigileo system.
Data are presented as mean ± SD. To compare demographic data between the two groups, we used the Mann–Whitney rank-sum test and Fisher's exact test to compare continuous and categorical variables, respectively. To compare haemodynamic data between the two groups, the Mann–Whitney rank-sum test was used at each time point. Longitudinal intragroup haemodynamic data were compared using repeated-measures analysis of variance (ANOVA) on ranks with the Tukey's test for multiple comparisons. The Mann–Whitney rank-sum test was used to compare the percentage of patients in whom vasopressors were used and Fisher's exact test was used to compare the number of vasopressor administrations. Fisher's exact test was used to compare occurrences of refractory hypotension. Statistical significance was accepted for P values of less than 0.05. Statistical analysis was performed using SPSS version 12.0 (SPSS Inc., Chicago, Illinois, USA). Using the results of our pilot study, we expected that a standard deviation of MAP would be 5.2 mmHg. We expected that MAP would increase by 5 mmHg. Assuming an alpha of 0.05 and power 0.8, we calculated the required sample size to be 19 in each group using SigmaStat version 3.5 (Systat Software Inc., San Jose, California, USA).
Of the 98 enrolled patients, 40 patients [40/98, (40.1%)] developed hypotension and were included. These 40 patients were then randomly allocated to the supine (n = 19) or head-down tilt groups (n = 21), and completed the study (Fig. 1). No significant differences were found between patient characteristics, pre-operative baseline MAP (Table 1) and the initial haemodynamic parameters upon the group allocations (Table 2) in the two groups. None of the patients developed abnormal ECG changes during the study.
Three patients (15.8%) in the supine group and no patient in the head-down tilt group went into a refractory hypotensive state, respectively (3/19 vs. 0/21, P = 0.098 with Fisher's exact test). None of these refractory patients were pre-operatively on ACEI. Minimal haemodynamic differences were observed between the two groups. SBP changes from baseline at 1 min (−3.98 ± 6.31 vs. 1.84 ± 8.25%, P = 0.004 with Mann–Whitney rank-sum test) and 2 min (1.51 ± 14.34 vs. 9.37 ± 10.57%, P = 0.032 with Mann–Whitney rank-sum test) were greater in the head-down tilt group (Fig. 2a), but no other intergroup haemodynamic difference was found (Figs 2 and 3). However, the number of vasopressor administrations (1.79 ± 1.13 vs. 0.67 ± 0.80, P = 0.002 with Fisher's exact test), the total dosage of ephedrine used (10.17 ± 5.82 vs. 4.26 ± 5.16 mg, P = 0.004 with Mann–Whitney rank-sum test) and the percentage of the patients requiring vasopressor [19/19 (100%) vs. 10/21 (47.62%), P < 0.001 with Mann–Whitney rank-sum test] were greater in the supine group (Fig. 4). Phenylephrine was used in only one patient in the supine group at a dose of 30.5 μg.
In this randomised clinical study, the head-down tilt position decreased the use of vasopressors during the treatment of general anaesthesia-induced hypotension in patients undergoing cardiac surgery. However, although minimal haemodynamic benefits were observed for the head-down tilt position, these might have been caused by the appropriate and precise use of vasopressors during the treatment of hypotension. Additionally, the haemodynamic effects by the head-down tilt position might have been attenuated by larger amount of vasopressor use in the control group.
In several previous studies,4–5,10 the head-down tilt position was concluded to be ineffective. However, the haemodynamic effect induced by the head-down tilt position is affected by many factors and has not been studied during induction of general anaesthesia in adult patients. Most importantly, patients in the present study were anaesthetised, and anaesthesia could attenuate the baroreceptor reflex, which may offset the beneficial haemodynamic effect of the head-down tilt position by vasodilation and bradycardia.5,10 Kardos et al.10 conducted a similar study on paediatric patients after inducing general anaesthesia. The adult and paediatric patients are different in their body ratios and reflexes, which may affect the effect of the head-down tilt position. Moreover, in the study by Kardos et al.,10 all patients were randomly allocated to the supine or head-down tilt position after induction of general anaesthesia, so normotensive patients were not excluded as in our study. We expected that preload increase might be ineffective in normotensive patients and the inclusion of normotensive patients might attenuate the beneficial effect on hypotensive patients in statistical analyses.
In a study by Terai et al.,11CO increased by 16% after 1 min in a 10° head-down tilt position. However, 10 min after this position change, all parameters had returned to baseline levels. It was concluded that the beneficial effects of the head-down tilt position in hypovolaemic patients were transient, and that they disappeared within 10 min. Furthermore, in a study by Reuter et al.,6 when patients were returned to a supine position after 15 min in a head-down tilt position, MAP, CI, central venous pressure and pulmonary artery occlusion pressure significantly decreased. These two features, a temporary effect and a blood pressure decrease after return to the supine position, may be the reason that head-down tilt position is usually not recommended in hypotensive patients.7 However, in our study, the head-down tilt position reduced the use of vasopressors in hypotensive patients from anaesthesia induction to surgical incision. Although this period is the most vulnerable period to hypotension during general anaesthesia, hypotension usually disappears and blood pressure increases, sometimes too high, when surgical incision commences. Consequently, these features of head-down tilt position could be advantageous for the hypotension after general anaesthesia induction.
There are several limitations in this study. First, we used the FloTrac-Vigileo system to measure CO, and this device analyses arterial waveforms without calibration to measure CO. Although the FloTrac-Vigileo system is easy to use and non-invasive, its accuracy has been disputed. However, a recent software upgrade enhanced its accuracy,12 and after that, it has been reported to show acceptable agreement with the thermodilution technique.13,14 Furthermore, our main finding is that the head-down tilt position decreased vasopressor administration, which was guided by SBP and MAP, but not by CO. Second, we could not adopt a double-blind technique in our study because patient positioning was difficult to conceal. Third, we included cardiac surgery patients with various cardiac diseases and different pathophysiologies. However, we could not conduct the statistical analysis based on subgroup classification due to the small number of patients recruited. Finally, we enrolled cardiac surgery patients. Many of these patients were on medications such as β-blockers and calcium channel blockers, which may affect the results of the study. Additionally, larger doses of anaesthetics, including opioids were used during anaesthesia induction compared to those used in non-cardiac patients. Moreover, the patients enrolled in this study may be different from the patients without cardiac disease in terms of comorbidity and vascular function. So, the result of this study could not be generalised to other patients and we may need further studies on patients without cardiac diseases.
In conclusion, the head-down tilt position decreases vasopressor administration for the treatment of hypotension following the induction of general anaesthesia in cardiac patients undergoing elective coronary artery bypass graft or valvular heart surgeries. This position is effective in the management of hypotension after the induction of general anaesthesia in patients undergoing these procedures.
We would like to thank the members of Medical Research Collaborating Center, Seoul National University Hospital, Seoul National College of Medicine for statistical analysis. This work was only supported by the Department of Anesthesiology and Pain Medicine, Seoul National University Hospital, Seoul National College of Medicine, Seoul, Korea. None of the authors has any conflict of interest.
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