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The prognostic factors of hypotension after rapid sequence intubation
American Journal of Emergency Medicine (2008) 26, 845–851
www.elsevier.com/locate/ajem
Original Contribution
The prognostic factors of hypotension after rapid sequence intubation Chih-Chuan Lin MD a,b , Kuan Fu Chen MD a,b , Chia-Pang Shih MHA c , Chen-June Seak MD a,b , Kuang-Hung Hsu PhD c,⁎ a
Department of Emergency Medicine, Chang Gung Memorial Hospital, Linkou, Taiwan College of Medicine, Chang Gung University, Taoyuan, Taiwan c Laboratory for Epidemiology and Department of Health Care Management, Chang Gung University, Taoyuan, Taiwan b
Received 21 August 2007; revised 14 November 2007; accepted 14 November 2007
Abstract Background: Rapid sequence intubation (RSI) has achieved high success and low complication rate in the ED. However, hypotension after RSI does occur. This study aimed to identify the prognostic factors of hypotension after RSI. Methods: This study identified patients who needed emergency airway management and then divided them into 2 groups. Patients in the first group were the hypotension group, whose systolic blood pressure (SBP) was found to be greater than 90 mm Hg before RSI but less than 90 mm Hg after RSI. Patients in the second group were deemed as the control group whose pre-SBP and post-SBP were greater than 90 mm Hg. The following variables were measured in the study: age, sex, body weight, patients' underlying disease and ongoing disease, the initial vital signs, and laboratory tests. A prognostic model with multiple logistic regression was established based on significant findings from univariate analysis. Results: A total of 149 patients were recruited from the ED in this study, with 28 patients in the hypotension group and 121 patients in the control group. After univariate analysis, there were 6 factors identified as significant findings including chronic obstructive pulmonary disease, sepsis, albumin, lidocaine, low body weight (b55 kg), and preintubation blood pressure of less than 140 mm Hg. Multiple logistic regression has demonstrated that patients' underlying diseases, anthropometric parameters, and drug medications were factors related to postintubation hypotension among ED patients. Conclusions: Clinical practitioners in the ED should take a patient's predisposing factors into serious consideration before emergency intubation while a preplanned strategy is made. © 2008 Elsevier Inc. All rights reserved.
1. Introduction Rapid sequence intubation (RSI), an important technique for airway management of patients in the ED, is becoming a ⁎ Corresponding author. Tel.: +1 886 3 3281200x2505; fax: +1 886 3 3287715. E-mail address: [email protected] (K.-H. Hsu). 0735-6757/$ – see front matter © 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.ajem.2007.11.027
very important issue affecting patient prognosis in emergency medicine practice [1]. Previous reports have shown that the use of RSI in the ED could result in high success rate of patient treatment [2-9]. However, a number of immediate complications after RSI were found in some other studies, including hypoxemia, hypotension, arrhythmia, and even death [3-8,10]. To the best of our knowledge, there are scant reports on the prediction of adverse outcomes after RSI [11].
846 Nevertheless, the issue of being able to predict the immediate complications in patients after RSI is very important for emergency medicine practitioners. The level of patient safety can be improved by identifying prognostic patients in advance before performing RSI. The ultimate goal of this research was to develop a model of preventive measures for patients with hypotension undergoing RSI.
2. Material and methods 2.1. Study design, settings, and samples This study was designed with a retrospective case-control method; the samples were collected from March 2002 to September 2002. Samples of this study were collected from the patients visiting the ED of Linkou Chang Gung Memorial Hospital, a 3000-bed medical center. There were many criteria set for inclusion of study subjects: (1) nontraumatic patients admitted to the ED; (2) age older than 18 years; (3) patients needed emergency airway management and underwent RSI. Patients with the following conditions were excluded from the study: (1) apparently in shock status, cardiac arrest and ventricular arrhythmia, related to the subsequent drop of initial blood pressure to less than 90 mm Hg; (2) received fluid resuscitation and inotropic agents; (3) with esophageal intubation, tube malposition, multiple attempts (N3 times).
2.2. Airway management Airway management in the ED is typically performed by ED residents and supervised by ED faculty. Rapid sequence intubation was performed as described in a previous study according to our department policy with preoxygenation, adjunctive medications, an induction agent, and a neuromuscular blocker followed by tracheal intubation [12]. Lidocaine (1-1.5 mg/kg) was used for the following purposes: (1) to diminish the hypertension response; (2) to reduce airway reactions; (3) to prevent intracranial hypertension; (4) to decrease the incidence of dysrhythmias during intubation. Midazolam (0.05-0.1 mg/kg) or ketamine (1-2 mg/kg) was used as the sedation agent. Rocuronium (0.8-1.2 mg/kg) was used as the paralytic agent. Ketamine was used in patients with chronic obstructive pulmonary disease (COPD) as described in other references. Airway maneuver such as cricoid pressure was used to optimize airway protection and visualization. Equipment, including laryngoscopes, endotracheal tubes, bag-valve masks, and suction, was prepared before intubation. All the patients were monitored by electrocardiogram, pulse oximetry, and blood pressure noninvasively. Blood pressure and pulse rate were measured just before intubation and after the tube passed. The blood pressure was measured noninvasively by using the conventional cuff over upper arm with an electronic
C.-C. Lin et al. sphygmomanometer. Confirmatory methods were used after tracheal placement including listening for anterior breath sounds over the chest and abdomen, and chest x-ray.
2.3. Study protocol and data acquisition The study protocol was approved by the hospital ethics committee (internal review board) before implementation (Fig. 1). There were 2 groups classified from the recruited patients. Group 1, the “hypotension group,” was composed of patients whose systolic blood pressure (SBP) before RSI (preSBP) was found to be greater than 90 mm Hg but less than 90 mm Hg in SBP after RSI (post-SBP). Group 2, the “normal control group,” consisted of patients whose SBP was greater than 90 mm Hg in both pre-SBP and post-SBP. Postintubation hypotension was found in patients whose SBP was 90 mm Hg or lower within 5 minutes after intubation. The data were collected from the following 4 categories: basic anthropometrics, vital signs upon RSI, biochemistry tests of blood, and medications prescribed during RSI. The basic anthropometric variables included age, sex, body weight, and patients' underlying diseases and ongoing diseases during this admission. The body weights of the patients were obtained when they were admitted to the intensive care unit. The patients' underlying diseases were obtained by reviewing their medical records and confirmed by their accompanying family members. The ongoing diseases were abstracted from the discharge diagnoses of this admission. The selected underlying diseases in this study were as follows: chronic obstructive pulmonary disease, old stroke (old cerebrovascular accident [CVA]), diabetes mellitus, hypertension, renal disease, cancer, and heart disease. Ongoing diseases included COPD, sepsis, congestive heart failure (CHF), CVA, acute myocardial infarction, liver disease, pneumonia, renal disease, seizure disorder, upper gastrointestinal tract bleeding, intoxication, and cancer. The variables of vital signs measured within 5 minutes upon
Fig. 1
The flow chart of sample recruitment and study design.
The prognostic factors of hypotension after rapid sequence intubation RSI (pre- and post-SBP) included heart rate and blood pressure. The biochemistry test performed by clinical laboratory included white blood cell, hemoglobin, sodium, potassium, albumin, creatinine, and arterial blood gas. The medications prescribed on RSI as described above were abstracted from medical records.
2.4. Statistical methods All statistical analysis was performed using SAS statistical software version 8.1 (SAS Institute, Cary, NC). Continuous variables were expressed as mean ± SD, whereas the categorical variables were indicated as frequency (%). For univariate analysis between groups (1 vs 2), we used the Student t test for continuous variables, the χ2 test for categorical variables, and odds ratios (OR) for expression of strength of association on categorical variables. Variables found to be statistically significant in the univariate analysis were selected as candidates for the subsequent multivariable analysis. A multiple logistic regression was applied to analyze factors influencing the occurrence of hypotension after RSI. A P value less than .05 was considered statistically significant.
3. Results A total of 149 patients were enrolled in this study, including 97 males and 52 females. The average age of the study samples was 67.26 ± 17.13 years. There were 28 patients collected in the hypotension group and 121 patients in the normal control group. The statistical analysis found no
Table 1
847
difference between the hypotension and normal control group in age (66.18 ± 18.66 vs 67.51 ± 16.83, respectively, P = .71), sex (male/female: 18:10 vs 79:42, respectively, P = .92), and body weight (53.86 ± 12.15 vs 57.86 ± 12.16 kg, respectively, P = .12). Taken together, in these 2 groups, the average SBP was 144.28 ± 34.29 mm Hg and the average heart rate was 110.39 ± 25.47 beats per minute with pre-RSI hemodynamic measurements. All patients in the study groups were found to have tachypnea (with respiratory rate of 26.88 ± 8.14 per minute) and hypoxemia (with SaO2 of 88.21% ± 9.38%) (Table 1). The data have shown that patients in the hypotension group had lower pre-RSI SBP compared to those in the normal control group (127.86 ± 25.34 vs 148.08 ± 35.04 mm Hg, respectively, P = .005). The hypotension group showed a significant drop in SBP to 74.23 ± 10.78 mm Hg, a difference of 53 mm Hg, after RSI, whereas the difference in the normal control group was not significant, 8 mm Hg. Meanwhile, there were no differences found in the variables diastolic blood pressure, heart rate, and oxygen saturation between pre- and post-RSI (Table 1). The proportion of major medications prescribed was as follows: 80.53% of patients were treated with lidocaine (120/149); 93.28% with rocuronium (139/149); 53.84% with midazolam (70/130). All the patients with COPD (n = 19) were sedated by ketamine in this study. Among variables of underlying and ongoing diseases, only sepsis (OR, 6.69; P b .0001) and ongoing COPD (OR, 3.0; P = .05) have shown statistically significant difference between the hypotension group and the normal control group. Lidocaine was found to be the only drug used in RSI that was different with regard to proportion of usage and dosage between groups (Tables 2 and 3). Among
Characteristics of the patients
Variable
Group 1 (n = 28)
Group 2 (n = 121)
Total (N = 149)
Sex (male/female) Age Weight
18/10 66.18 ± 18.66 53.86 ± 12.15
79/42 67.51 ± 16.83 57.86 ± 12.16
97/52 67.26 ± 17.13 57.10 ± 12.22
.92 .71 .12
Pre-RSI vital signs SBP (mm Hg) DBP (mm Hg) HR RR SaO2
127.86 ± 25.34 68.64 ± 16.86 111.22 ± 25.59 25.89 ± 8.30 88.71 ± 10.29
148.08 ± 35.04 76.92 ± 22.35 110.21 ± 25.54 27.11 ± 8.12 88.08 ± 9.19
144.28 ± 34.29 75.36 ± 21.62 110.39 ± 25.47 26.88 ± 8.14 88.21 ± 9.38
.005 .07 .85 .48 .77
Post-RSI vital signs SBP (mm Hg) DBP (mm Hg) HR SaO2
74.23 ± 10.78 41.73 ± 7.83 102.43 ± 34.45 94.55 ± 8.00
140.59 ± 35.98 70.76 ± 22.33 111.12 ± 26.26 97.21 ± 4.11
128.85 ± 41.59 65.63 ± 23.32 109.48 ± 28.05 96.69 ± 5.17
b.0001 b.0001 .14 .10
DBP indicates diastolic blood pressure; HR, heart rate; RR, respiratory rate; SaO2, oxygen saturation.
P value
848
C.-C. Lin et al.
laboratory tests, there was statistical difference in albumin between groups (2.90 ± 0.80 vs 2.52 ± 0.83, P = .03); however, the comparisons on creatinine, hemoglobin, sodium, potassium, pH, pCO2, bicarbonate, and blood sugar (Table 3) showed no difference. The cutoff points of pre-SBP and body weight in multivariate analysis were predetermined by receiver operator calibration curve analyses and found to be optimized at 140 mm Hg and 55 kg, respectively. The logistic regression model has demonstrated that pre-SBP, sepsis, COPD, and body weight were significant prognostic factors for hypotension upon RSI. Sepsis was the most likely factor associated with the occurrence of hypotension after RSI, with an odds ratio of 9.91 (95% confidence interval [CI], 2.87-34.23). Whereas ongoing COPD was one of the prognostic factors associated with post-RSI hypotension among patients treated with intubations in the ED (OR, 4.75; 95% CI, 1.40-16.06). In consistency with our expectations, patients with SBP lower than 140 mm Hg before RSI had a 4.14fold (95% CI, 1.51-11.37) higher likelihood of developing hypotension after intubations. Patients' body weight was a
predictor for the development of post-RSI hypotension. Patients with body weight of less than 55 kg had a 3.27-fold (95% CI = 1.19-9.01) higher chance of developing hypotension than other patients (Table 4).
Table 2 Comparisons between group 1 and group 2 in underlying, ongoing disease, and RSI medications
In this study, we identified sepsis and COPD as 2 important prognostic factors in predicting hypotension after RSI. It was found that there is a high chance of developing hypotension among patients with these diseases, owing to their disease nature. There were approximately 50% of patients with sepsis being identified to have some form of impairment in left ventricular systolic function [13]. Even in patients with normotensive sepsis, an impairment in intrinsic myocardial performance was also found [14]. Myocardial depression with peripheral vasodilatation and a reduced systemic vascular resistance was also a major hemodynamic feature acknowledged in patients with sepsis. The effective intravascular volume was found reduced in patients with sepsis and was granted as a major factor leading to circulatory instability and collapse [15-17]. The sympathetic tone in patients with sepsis who required emergency intubation was found to be higher compared to others. Abrupt abatement of sympathetic tone after replacement of an airway may lead to profound hemodynamic changes regardless of the technique of induction, which results in postintubation hypotension [18]. A similar mechanism may also be applied to the postintubation hypotension of patients with COPD. Securing the airway and initiating mechanical ventilation will alleviate the stress of hypoxia and hypercarbia of patients with COPD. The decrease in sympathetic vascular tone may involve hemodynamic compromise by decreasing the cardiac parameters of preload and afterload. Besides, hypovolemia will further complicate the clinical situations, rendering patients far more sensitive to the effects of controlled ventilation. Positive ventilation pressure and positive endexpiratory pressure were also found to increase intrathoracic
Variables Ongoing disease Cancer Congestive heart failure COPD CVA Heart disease Liver disease Pneumonia Renal disease Seizure disorder Sepsis Intoxication Upper gastrointestinal tract bleeding
Group 1 Group 2 Odds P value (n = 28) (n = 121) ratio 3 4 7 0 6 3 14 5 0 9 0 5
13 17 12 9 25 12 66 14 3 8 5 23
1.00 1.02 3.00 0.22 1.05 1.09 0.83 1.66 0.70 6.69 0.41 0.93
.99 1.00 .05 .21 .93 1.00 .66 .36 1.00 b.0001 .58 .88
Underlying disease COPD CVA Diabetes mellitus Hypertension Cancer Renal disease Heart disease
7 2 6 10 2 5 6
18 15 33 51 14 18 17
1.91 0.54 0.73 0.76 0.59 1.24 1.67
.26 .53 .53 .53 .74 .77 .38
RSI medication Lidocaine Rocurorium Ketamine Midazolam
27 28 4 11
93 111 15 59
8.13 5.05 1.18 0.68
.02 .21 .76 .37
4. Discussion This study addresses the issue of prognostic factors associated with the development of hypotension after RSI, which is deemed as a novelty in the field. Previous studies focused primarily on the effectiveness and safety of RSI practiced by emergency physicians. Consequently, complications of RSI, such as hypoxemia, hypotension, and arrhythmia, were the main focus of such literatures. Few, if any, focused on the risk factors of developing hypotension after RSI in the ED. The results of this study have shown that the development of hypotension after RSI was a multifactorial model among these patients.
4.1. Influence of sepsis and COPD on the hemodynamic status of patients who received RSI
The prognostic factors of hypotension after rapid sequence intubation Table 3
849
Comparisons between group 1 and group 2 in laboratory studies
Variable
Group 1 (n = 28)
Group 2 (n = 121)
Total (N = 149)
P value
Laboratory tests White blood cell Hemoglobin Creatinine Albumin Potassium Sodium Blood sugar Arterial blood gas, pH pCO2 HCO3
12.06 ± 4.73 11.52 ± 2.69 2.45 ± 2.10 2.52 ± 0.83 4.00 ± 0.69 135.29 ± 6.88 164.36 ± 106.62 7.32 ± 0.16 44.85 ± 22.94 22.71 ± 10.04
11.85 ± 6.43 11.65 ± 2.92 2.09 ± 2.19 2.90 ± 0.80 4.62 ± 3.91 135.49 ± 13.41 187.72 ± 118.68 7.33 ± 0.15 44.69 ± 20.29 22.63 ± 8.47
11.89 ± 6.13 11.63 ± 2.87 2.16 ± 2.17 2.83 ± 0.81 4.50 ± 3.54 135.45 ± 12.42 183.30 ± 116.51 7.33 ± 0.15 44.72 ± 20.73 22.65 ± 8.75
.87 .83 .44 .03 .11 .91 .34 .68 .97 .96
78.75 ± 22.84 6.79 ± 17.01 43.93 ± 7.25 1.82 ± 2.36
65.58 ± 40.97 6.82 ± 19.92 43.76 ± 15.16 3.13 ± 6.60
68.05 ± 38.51 6.81 ± 19.35 43.79 ± 13.99 2.88 ± 6.05
.02 .99 .93 .08
Drug dosage(mg) Lidocaine Ketamine Rocurorium Midazolam
pressure, which impedes venous return to the right ventricle and increases right ventricular afterload. This problem may be further exacerbated in patients who have significant obstructive lung disease [18]. Consequently, the combined effects from the loss of sympathetic tone after RSI and the decrease in preload from positive pressure ventilation can result in profound hypotension, often with reflex tachycardia as demonstrated by our cases.
intravascular colloid osmotic pressure. This relative hypovolemia may have contributed to the postintubation hypotension of the patients in this study [19]. As indicated by previous documents, patients with low body weight were associated with increased mortality as opposed to the those with normal weight [20,21]. It is not surprising that patients with low body weight were more likely to develop hypotension after RSI owing to the deficiency of hemodynamic status.
4.2. Influence of albumin and lower body weight on the hemodynamic status of patients who received RSI
4.3. Influence of RSI medications on the hemodynamic status of patients who received RSI
In this study, we have noticed that albumin was a significant prognostic factor in univariate analysis. Particularly, the significant reduction of plasma albumin in patients with sepsis was granted as the main association. An explanation of increased capillary membrane permeability was proposed, which was associated with marked fluid shifts into the tissues and resulted in the subsequent loss of
Ketamine was used as a sedative agent in all patients with COPD. Chronic obstructive pulmonary disease was one of the significant prognostic factors of developing hypotension after RSI whereas ketamine use was not. This finding suggested that hypotension after RSI was not related to the use of ketamine but COPD was. Lidocaine was used as an intravenous agent to blunt the sympathetic stimulation
Table 4
Logistic model for predicting hypotension after RSI
Variables
Pre-SBP (mm Hg) COPD Sepsis Body weight (kg)
≦140 N140 Yes No Yes No ≦55 N55
Group 1 (n = 28)
Group 2 (n = 121)
Estimate
P value
20 8 7 21 9 19 20 8
50 71 12 108 8 113 55 66
1.42
.01
1.56
.01
2.29
.00
1.19
.02
odds ratio
95% CI Lower
Upper
4.14 1.00 4.75 1.00 9.91 1.00 3.27 1.00
1.51
11.37
1.40
16.06
2.87
34.23
1.19
9.01
850 during RSI. The beneficial effects of intravenous lidocaine were inconsistent and therefore its use in these settings was controversial [22-24]. In our study, the frequency and dosage of lidocaine were higher in the hypotension group than in the normal control group. The evidence of this study points to the association of lidocaine use with the development of hypotension after RSI. Lidocaine was normally applied to the patients who required RSI while blunting the sympathetic stimulation. It is possible that the sympathetic stimulation leads to the occurrence of hypotension after the use of lidocaine, particularly in the patients with sepsis and COPD. Thus, the use of lidocaine in RSI requires some precaution in some cases. Midazolam was reported in previous studies [25-27] as one of the agents that probably caused hypotension after RSI. However, controversies still existed among these studies owing to different patient profiles and conditions. One study has demonstrated that midazolam was dose related to hypotension in prehospital RSI with subjects including patients with traumatic brain injury, which was different from our study subjects. Choi et al [27] stated that midazolam is more likely to cause hypotension than etomidate in the ED during RSI. Whereas Swanson et al [25] found that there was low incidence of hypotension with both midazolam and etomidate in prehospital RSI. The present study suggests a large scale randomized control study is required for the clarifications of the association. Different RSI protocols were found to yield different adverse outcomes in one literature [11]. The present study has demonstrated here the multifactorial nature of postintubation hypotension among patients in the ED, which gives valuable information on both etiological analysis and risk estimation for future practice in emergency medicine. There are different kinds of patients who need emergent airway intervention. The hemodynamic statuses of these patients may be varied among patients. We should keep in mind that not only the medications but also disease factors will cause hypotension in RSI. The interactions between medications and disease should not be overlooked in patients who need to be intubated in the future.
5. Limitations The major findings of this study were derived from patients with diseases in internal medicine; the interpretation should be cautious when including traumatic or pediatric patients. Different patient groups were suggested to be customized with RSI protocols with which could yield different complication rates [11]. The risk estimation provided by this study was subjected to the patient profiles and conditions for intervention. Is there any measure that we can use to prevent postintubation hypotension? We have found some clues in this study but needed further studies. Postintubation hypotension was found in this study to be associated with sepsis or COPD, which was attributed to hypovolemia.
C.-C. Lin et al. Therefore, fluid challenge with normal saline may have its role in preventing postintubation hypotension in the future [28]. Unfortunately, we did not measure the status of fluid volume among our patients as the main focus was in searching for risk factors for postintubation hypotension. Suggestions can be made in future studies, which include the group undergoing fluid resuscitation or patients undergoing inotropic agent for clarifications. There was no previous report regarding the consequences of the post-RSI hypotension based on our best knowledge. Although it was not the primary aim of this study, the importance should not be ignored because any of the consequences of hypotension would be a critical condition for ER patients such as respiratory distress and severe sepsis.
6. Conclusions Data from this study suggested that it is not a single factor that induces postintubation hypotension. Sepsis, COPD, lower body weight, and lower initial SBP were the key risk factors for developing hypotension after RSI. Based on this study, the elements of a safe plan for securing the airway should include a review of the patient's clinical diagnosis, consideration of the factors affecting the patient's hemodynamics, assessment of the patient's present and anticipated postintubation volume status, formulation of a plan for induction of anesthesia (including muscle relaxant and sedative use), and confirmation of the availability of emergency drugs based on anticipated liability of the patient's hemodynamics [29]. However, future studies are warranted for validating the risk model and intervention plans to reduce the chance of hypotension induced by RSI.
References [1] American College of Emergency Physicians. Rapid-sequence intubation. Ann Emerg Med 1997;29:573. [2] Kovacs G, Law JA, Ross J, et al. Acute airway management in the emergency department by non-anesthesiologists. Can J Anaesth 2004; 51:174-80. [3] Reid C, Chan L, Tweeddale M. The who, where, and what of rapid sequence intubation: prospective observational study of emergency RSI outside the operating theatre. Emerg Med J 2004;21:296-301. [4] Butler JM, Clancy M, Robinson N, et al. An observational survey of emergency department rapid sequence intubation. Emerg Med J 2001; 18:343-8. [5] Li J, Murphy-Lavoie H, Bugas C, et al. Complications of emergency intubation with and without paralysis. Am J Emerg Med 1999;17: 141-3. [6] Tayal VS, Riggs RW, Marx JA, et al. Rapid-sequence intubation at an emergency medicine residency: success rate and adverse events during a two-year period. Acad Emerg Med 1999;6:31-7. [7] Sakles JC, Laurin EG, Rantapaa AA, et al. Airway management in the emergency department: a one-year study of 610 tracheal intubations. Ann Emerg Med 1998;31:325-32.
The prognostic factors of hypotension after rapid sequence intubation [8] Dufour DG, Larose DL, Clement SC. Rapid sequence intubation in the emergency department. J Emerg Med 1995;13:705-10. [9] Kenny JF, Molloy K, Pollock M, et al. Rapid-sequence induction technique for orotracheal intubation of adult nontrauma patients in a community hospital setting. Ann Emerg Med 1995;25:432-3. [10] Sivilotti ML, Ducharme J. Randomized, double-blind study on sedatives and hemodynamics during rapid-sequence intubation in the emergency department: The SHRED Study. Ann Emerg Med 1998;31: 313-24. [11] Marvez E, Weiss SJ, Houry DE, et al. Predicting adverse outcomes in a diagnosis-based protocol system for rapid sequence intubation. Am J Emerg Med 2003;21:23-9. [12] Reynolds SF, Heffner J. Airway management of the critically ill patient: rapid-sequence intubation. Chest 2005;127:1397-412. [13] Charpentier J, Luyt CE, Fulla Y, et al. Brain natriuretic peptide: A marker of myocardial dysfunction and prognosis during severe sepsis. Critical Care Medicine 2004;32(3):660-5. [14] Ognibene FP, Parker MM, Natanson C, et al. Depressed left ventricular performance. Response to volume infusion in patients with sepsis and septic shock. Chest 1988;93:903-10. [15] Carroll GC, Snyder JV. Hyperdynamic severe intravascular sepsis depends on fluid administration in cynomolgus monkey. Am J Physiol 1982;243:R131-41. [16] Rackow EC, Kaufman BS, Falk J, et al. Hemodynamic response to fluid repletion in patients with septic shock: evidence for early depression of cardiac performance. Circ Shock 1987;22:11-22. [17] Weil MH, Nishjima H. Cardiac output in bacterial shock. Am J Med 1978;64:920-2. [18] Klinger JR. Hemodynamics and positive end-expiratory pressure in critically ill patients. Crit Care Clin 1996;12:841-64. [19] Goldwasser P, Feldman J. Association of serum albumin and mortality risk. J Clin Epidemiol 1997;50:693-703.
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[20] Flegal KM, Graubard BI, Williamson DF, et al. Excess deaths associated with underweight, overweight, and obesity. JAMA 2005; 293:1861-7. [21] Kuriyama S, Ohmori K, Miura C, et al. Body mass index and mortality in Japan: the Miyagi Cohort Study. J Epidemiol 2004;14(Suppl 1): S33-8. [22] Kindler CH, Schumacher PG, Schneider MC, et al. Effects of intravenous lidocaine and/or esmolol on hemodynamic responses to laryngoscopy and intubation: a double-blind, controlled clinical trial. J Clin Anesth 1996;8:491-6. [23] Singh H, Vichitvejpaisal P, Gaines GY, et al. Comparative effects of lidocaine, esmolol, and nitroglycerin in modifying the hemodynamic response to laryngoscopy and intubation. J Clin Anesth 1995;7:5-8. [24] Tam S, Chung F, Campbell M. Intravenous lidocaine: optimal time of injection before tracheal intubation. Anesth Analg 1987;66:1036-8. [25] Swanson ER, Fosnocht DE, Jensen SC. Comparison of etomidate and midazolam for prehospital rapid-sequence intubation. Prehosp Emerg Care 2004;8:273-9. [26] Davis DP, Kimbro TA, Vilke GM. The use of midazolam for prehospital rapid-sequence intubation may be associated with a dose-related increase in hypotension. Prehosp Emerg Care 2001;5: 163-8. [27] Choi YF, Wong TW, Lau CC. Midazolam is more likely to cause hypotension than etomidate in emergency department rapid sequence intubation. Emerg Med J 2004;21:700-2. [28] el-Beheiry H, Kim J, Milne B, et al. Prophylaxis against the systemic hypotension induced by propofol during rapid-sequence intubation. Can J Anaesth 1995;42:875-8. [29] Horak J, Weiss S. Emergent management of the airway. New pharmacology and the control of comorbidities in cardiac disease, ischemia, and valvular heart disease. Crit Care Clin 2000;16:411-27.
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Original Contribution
The prognostic factors of hypotension after rapid sequence intubation Chih-Chuan Lin MD a,b , Kuan Fu Chen MD a,b , Chia-Pang Shih MHA c , Chen-June Seak MD a,b , Kuang-Hung Hsu PhD c,⁎ a
Department of Emergency Medicine, Chang Gung Memorial Hospital, Linkou, Taiwan College of Medicine, Chang Gung University, Taoyuan, Taiwan c Laboratory for Epidemiology and Department of Health Care Management, Chang Gung University, Taoyuan, Taiwan b
Received 21 August 2007; revised 14 November 2007; accepted 14 November 2007
Abstract Background: Rapid sequence intubation (RSI) has achieved high success and low complication rate in the ED. However, hypotension after RSI does occur. This study aimed to identify the prognostic factors of hypotension after RSI. Methods: This study identified patients who needed emergency airway management and then divided them into 2 groups. Patients in the first group were the hypotension group, whose systolic blood pressure (SBP) was found to be greater than 90 mm Hg before RSI but less than 90 mm Hg after RSI. Patients in the second group were deemed as the control group whose pre-SBP and post-SBP were greater than 90 mm Hg. The following variables were measured in the study: age, sex, body weight, patients' underlying disease and ongoing disease, the initial vital signs, and laboratory tests. A prognostic model with multiple logistic regression was established based on significant findings from univariate analysis. Results: A total of 149 patients were recruited from the ED in this study, with 28 patients in the hypotension group and 121 patients in the control group. After univariate analysis, there were 6 factors identified as significant findings including chronic obstructive pulmonary disease, sepsis, albumin, lidocaine, low body weight (b55 kg), and preintubation blood pressure of less than 140 mm Hg. Multiple logistic regression has demonstrated that patients' underlying diseases, anthropometric parameters, and drug medications were factors related to postintubation hypotension among ED patients. Conclusions: Clinical practitioners in the ED should take a patient's predisposing factors into serious consideration before emergency intubation while a preplanned strategy is made. © 2008 Elsevier Inc. All rights reserved.
1. Introduction Rapid sequence intubation (RSI), an important technique for airway management of patients in the ED, is becoming a ⁎ Corresponding author. Tel.: +1 886 3 3281200x2505; fax: +1 886 3 3287715. E-mail address: [email protected] (K.-H. Hsu). 0735-6757/$ – see front matter © 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.ajem.2007.11.027
very important issue affecting patient prognosis in emergency medicine practice [1]. Previous reports have shown that the use of RSI in the ED could result in high success rate of patient treatment [2-9]. However, a number of immediate complications after RSI were found in some other studies, including hypoxemia, hypotension, arrhythmia, and even death [3-8,10]. To the best of our knowledge, there are scant reports on the prediction of adverse outcomes after RSI [11].
846 Nevertheless, the issue of being able to predict the immediate complications in patients after RSI is very important for emergency medicine practitioners. The level of patient safety can be improved by identifying prognostic patients in advance before performing RSI. The ultimate goal of this research was to develop a model of preventive measures for patients with hypotension undergoing RSI.
2. Material and methods 2.1. Study design, settings, and samples This study was designed with a retrospective case-control method; the samples were collected from March 2002 to September 2002. Samples of this study were collected from the patients visiting the ED of Linkou Chang Gung Memorial Hospital, a 3000-bed medical center. There were many criteria set for inclusion of study subjects: (1) nontraumatic patients admitted to the ED; (2) age older than 18 years; (3) patients needed emergency airway management and underwent RSI. Patients with the following conditions were excluded from the study: (1) apparently in shock status, cardiac arrest and ventricular arrhythmia, related to the subsequent drop of initial blood pressure to less than 90 mm Hg; (2) received fluid resuscitation and inotropic agents; (3) with esophageal intubation, tube malposition, multiple attempts (N3 times).
2.2. Airway management Airway management in the ED is typically performed by ED residents and supervised by ED faculty. Rapid sequence intubation was performed as described in a previous study according to our department policy with preoxygenation, adjunctive medications, an induction agent, and a neuromuscular blocker followed by tracheal intubation [12]. Lidocaine (1-1.5 mg/kg) was used for the following purposes: (1) to diminish the hypertension response; (2) to reduce airway reactions; (3) to prevent intracranial hypertension; (4) to decrease the incidence of dysrhythmias during intubation. Midazolam (0.05-0.1 mg/kg) or ketamine (1-2 mg/kg) was used as the sedation agent. Rocuronium (0.8-1.2 mg/kg) was used as the paralytic agent. Ketamine was used in patients with chronic obstructive pulmonary disease (COPD) as described in other references. Airway maneuver such as cricoid pressure was used to optimize airway protection and visualization. Equipment, including laryngoscopes, endotracheal tubes, bag-valve masks, and suction, was prepared before intubation. All the patients were monitored by electrocardiogram, pulse oximetry, and blood pressure noninvasively. Blood pressure and pulse rate were measured just before intubation and after the tube passed. The blood pressure was measured noninvasively by using the conventional cuff over upper arm with an electronic
C.-C. Lin et al. sphygmomanometer. Confirmatory methods were used after tracheal placement including listening for anterior breath sounds over the chest and abdomen, and chest x-ray.
2.3. Study protocol and data acquisition The study protocol was approved by the hospital ethics committee (internal review board) before implementation (Fig. 1). There were 2 groups classified from the recruited patients. Group 1, the “hypotension group,” was composed of patients whose systolic blood pressure (SBP) before RSI (preSBP) was found to be greater than 90 mm Hg but less than 90 mm Hg in SBP after RSI (post-SBP). Group 2, the “normal control group,” consisted of patients whose SBP was greater than 90 mm Hg in both pre-SBP and post-SBP. Postintubation hypotension was found in patients whose SBP was 90 mm Hg or lower within 5 minutes after intubation. The data were collected from the following 4 categories: basic anthropometrics, vital signs upon RSI, biochemistry tests of blood, and medications prescribed during RSI. The basic anthropometric variables included age, sex, body weight, and patients' underlying diseases and ongoing diseases during this admission. The body weights of the patients were obtained when they were admitted to the intensive care unit. The patients' underlying diseases were obtained by reviewing their medical records and confirmed by their accompanying family members. The ongoing diseases were abstracted from the discharge diagnoses of this admission. The selected underlying diseases in this study were as follows: chronic obstructive pulmonary disease, old stroke (old cerebrovascular accident [CVA]), diabetes mellitus, hypertension, renal disease, cancer, and heart disease. Ongoing diseases included COPD, sepsis, congestive heart failure (CHF), CVA, acute myocardial infarction, liver disease, pneumonia, renal disease, seizure disorder, upper gastrointestinal tract bleeding, intoxication, and cancer. The variables of vital signs measured within 5 minutes upon
Fig. 1
The flow chart of sample recruitment and study design.
The prognostic factors of hypotension after rapid sequence intubation RSI (pre- and post-SBP) included heart rate and blood pressure. The biochemistry test performed by clinical laboratory included white blood cell, hemoglobin, sodium, potassium, albumin, creatinine, and arterial blood gas. The medications prescribed on RSI as described above were abstracted from medical records.
2.4. Statistical methods All statistical analysis was performed using SAS statistical software version 8.1 (SAS Institute, Cary, NC). Continuous variables were expressed as mean ± SD, whereas the categorical variables were indicated as frequency (%). For univariate analysis between groups (1 vs 2), we used the Student t test for continuous variables, the χ2 test for categorical variables, and odds ratios (OR) for expression of strength of association on categorical variables. Variables found to be statistically significant in the univariate analysis were selected as candidates for the subsequent multivariable analysis. A multiple logistic regression was applied to analyze factors influencing the occurrence of hypotension after RSI. A P value less than .05 was considered statistically significant.
3. Results A total of 149 patients were enrolled in this study, including 97 males and 52 females. The average age of the study samples was 67.26 ± 17.13 years. There were 28 patients collected in the hypotension group and 121 patients in the normal control group. The statistical analysis found no
Table 1
847
difference between the hypotension and normal control group in age (66.18 ± 18.66 vs 67.51 ± 16.83, respectively, P = .71), sex (male/female: 18:10 vs 79:42, respectively, P = .92), and body weight (53.86 ± 12.15 vs 57.86 ± 12.16 kg, respectively, P = .12). Taken together, in these 2 groups, the average SBP was 144.28 ± 34.29 mm Hg and the average heart rate was 110.39 ± 25.47 beats per minute with pre-RSI hemodynamic measurements. All patients in the study groups were found to have tachypnea (with respiratory rate of 26.88 ± 8.14 per minute) and hypoxemia (with SaO2 of 88.21% ± 9.38%) (Table 1). The data have shown that patients in the hypotension group had lower pre-RSI SBP compared to those in the normal control group (127.86 ± 25.34 vs 148.08 ± 35.04 mm Hg, respectively, P = .005). The hypotension group showed a significant drop in SBP to 74.23 ± 10.78 mm Hg, a difference of 53 mm Hg, after RSI, whereas the difference in the normal control group was not significant, 8 mm Hg. Meanwhile, there were no differences found in the variables diastolic blood pressure, heart rate, and oxygen saturation between pre- and post-RSI (Table 1). The proportion of major medications prescribed was as follows: 80.53% of patients were treated with lidocaine (120/149); 93.28% with rocuronium (139/149); 53.84% with midazolam (70/130). All the patients with COPD (n = 19) were sedated by ketamine in this study. Among variables of underlying and ongoing diseases, only sepsis (OR, 6.69; P b .0001) and ongoing COPD (OR, 3.0; P = .05) have shown statistically significant difference between the hypotension group and the normal control group. Lidocaine was found to be the only drug used in RSI that was different with regard to proportion of usage and dosage between groups (Tables 2 and 3). Among
Characteristics of the patients
Variable
Group 1 (n = 28)
Group 2 (n = 121)
Total (N = 149)
Sex (male/female) Age Weight
18/10 66.18 ± 18.66 53.86 ± 12.15
79/42 67.51 ± 16.83 57.86 ± 12.16
97/52 67.26 ± 17.13 57.10 ± 12.22
.92 .71 .12
Pre-RSI vital signs SBP (mm Hg) DBP (mm Hg) HR RR SaO2
127.86 ± 25.34 68.64 ± 16.86 111.22 ± 25.59 25.89 ± 8.30 88.71 ± 10.29
148.08 ± 35.04 76.92 ± 22.35 110.21 ± 25.54 27.11 ± 8.12 88.08 ± 9.19
144.28 ± 34.29 75.36 ± 21.62 110.39 ± 25.47 26.88 ± 8.14 88.21 ± 9.38
.005 .07 .85 .48 .77
Post-RSI vital signs SBP (mm Hg) DBP (mm Hg) HR SaO2
74.23 ± 10.78 41.73 ± 7.83 102.43 ± 34.45 94.55 ± 8.00
140.59 ± 35.98 70.76 ± 22.33 111.12 ± 26.26 97.21 ± 4.11
128.85 ± 41.59 65.63 ± 23.32 109.48 ± 28.05 96.69 ± 5.17
b.0001 b.0001 .14 .10
DBP indicates diastolic blood pressure; HR, heart rate; RR, respiratory rate; SaO2, oxygen saturation.
P value
848
C.-C. Lin et al.
laboratory tests, there was statistical difference in albumin between groups (2.90 ± 0.80 vs 2.52 ± 0.83, P = .03); however, the comparisons on creatinine, hemoglobin, sodium, potassium, pH, pCO2, bicarbonate, and blood sugar (Table 3) showed no difference. The cutoff points of pre-SBP and body weight in multivariate analysis were predetermined by receiver operator calibration curve analyses and found to be optimized at 140 mm Hg and 55 kg, respectively. The logistic regression model has demonstrated that pre-SBP, sepsis, COPD, and body weight were significant prognostic factors for hypotension upon RSI. Sepsis was the most likely factor associated with the occurrence of hypotension after RSI, with an odds ratio of 9.91 (95% confidence interval [CI], 2.87-34.23). Whereas ongoing COPD was one of the prognostic factors associated with post-RSI hypotension among patients treated with intubations in the ED (OR, 4.75; 95% CI, 1.40-16.06). In consistency with our expectations, patients with SBP lower than 140 mm Hg before RSI had a 4.14fold (95% CI, 1.51-11.37) higher likelihood of developing hypotension after intubations. Patients' body weight was a
predictor for the development of post-RSI hypotension. Patients with body weight of less than 55 kg had a 3.27-fold (95% CI = 1.19-9.01) higher chance of developing hypotension than other patients (Table 4).
Table 2 Comparisons between group 1 and group 2 in underlying, ongoing disease, and RSI medications
In this study, we identified sepsis and COPD as 2 important prognostic factors in predicting hypotension after RSI. It was found that there is a high chance of developing hypotension among patients with these diseases, owing to their disease nature. There were approximately 50% of patients with sepsis being identified to have some form of impairment in left ventricular systolic function [13]. Even in patients with normotensive sepsis, an impairment in intrinsic myocardial performance was also found [14]. Myocardial depression with peripheral vasodilatation and a reduced systemic vascular resistance was also a major hemodynamic feature acknowledged in patients with sepsis. The effective intravascular volume was found reduced in patients with sepsis and was granted as a major factor leading to circulatory instability and collapse [15-17]. The sympathetic tone in patients with sepsis who required emergency intubation was found to be higher compared to others. Abrupt abatement of sympathetic tone after replacement of an airway may lead to profound hemodynamic changes regardless of the technique of induction, which results in postintubation hypotension [18]. A similar mechanism may also be applied to the postintubation hypotension of patients with COPD. Securing the airway and initiating mechanical ventilation will alleviate the stress of hypoxia and hypercarbia of patients with COPD. The decrease in sympathetic vascular tone may involve hemodynamic compromise by decreasing the cardiac parameters of preload and afterload. Besides, hypovolemia will further complicate the clinical situations, rendering patients far more sensitive to the effects of controlled ventilation. Positive ventilation pressure and positive endexpiratory pressure were also found to increase intrathoracic
Variables Ongoing disease Cancer Congestive heart failure COPD CVA Heart disease Liver disease Pneumonia Renal disease Seizure disorder Sepsis Intoxication Upper gastrointestinal tract bleeding
Group 1 Group 2 Odds P value (n = 28) (n = 121) ratio 3 4 7 0 6 3 14 5 0 9 0 5
13 17 12 9 25 12 66 14 3 8 5 23
1.00 1.02 3.00 0.22 1.05 1.09 0.83 1.66 0.70 6.69 0.41 0.93
.99 1.00 .05 .21 .93 1.00 .66 .36 1.00 b.0001 .58 .88
Underlying disease COPD CVA Diabetes mellitus Hypertension Cancer Renal disease Heart disease
7 2 6 10 2 5 6
18 15 33 51 14 18 17
1.91 0.54 0.73 0.76 0.59 1.24 1.67
.26 .53 .53 .53 .74 .77 .38
RSI medication Lidocaine Rocurorium Ketamine Midazolam
27 28 4 11
93 111 15 59
8.13 5.05 1.18 0.68
.02 .21 .76 .37
4. Discussion This study addresses the issue of prognostic factors associated with the development of hypotension after RSI, which is deemed as a novelty in the field. Previous studies focused primarily on the effectiveness and safety of RSI practiced by emergency physicians. Consequently, complications of RSI, such as hypoxemia, hypotension, and arrhythmia, were the main focus of such literatures. Few, if any, focused on the risk factors of developing hypotension after RSI in the ED. The results of this study have shown that the development of hypotension after RSI was a multifactorial model among these patients.
4.1. Influence of sepsis and COPD on the hemodynamic status of patients who received RSI
The prognostic factors of hypotension after rapid sequence intubation Table 3
849
Comparisons between group 1 and group 2 in laboratory studies
Variable
Group 1 (n = 28)
Group 2 (n = 121)
Total (N = 149)
P value
Laboratory tests White blood cell Hemoglobin Creatinine Albumin Potassium Sodium Blood sugar Arterial blood gas, pH pCO2 HCO3
12.06 ± 4.73 11.52 ± 2.69 2.45 ± 2.10 2.52 ± 0.83 4.00 ± 0.69 135.29 ± 6.88 164.36 ± 106.62 7.32 ± 0.16 44.85 ± 22.94 22.71 ± 10.04
11.85 ± 6.43 11.65 ± 2.92 2.09 ± 2.19 2.90 ± 0.80 4.62 ± 3.91 135.49 ± 13.41 187.72 ± 118.68 7.33 ± 0.15 44.69 ± 20.29 22.63 ± 8.47
11.89 ± 6.13 11.63 ± 2.87 2.16 ± 2.17 2.83 ± 0.81 4.50 ± 3.54 135.45 ± 12.42 183.30 ± 116.51 7.33 ± 0.15 44.72 ± 20.73 22.65 ± 8.75
.87 .83 .44 .03 .11 .91 .34 .68 .97 .96
78.75 ± 22.84 6.79 ± 17.01 43.93 ± 7.25 1.82 ± 2.36
65.58 ± 40.97 6.82 ± 19.92 43.76 ± 15.16 3.13 ± 6.60
68.05 ± 38.51 6.81 ± 19.35 43.79 ± 13.99 2.88 ± 6.05
.02 .99 .93 .08
Drug dosage(mg) Lidocaine Ketamine Rocurorium Midazolam
pressure, which impedes venous return to the right ventricle and increases right ventricular afterload. This problem may be further exacerbated in patients who have significant obstructive lung disease [18]. Consequently, the combined effects from the loss of sympathetic tone after RSI and the decrease in preload from positive pressure ventilation can result in profound hypotension, often with reflex tachycardia as demonstrated by our cases.
intravascular colloid osmotic pressure. This relative hypovolemia may have contributed to the postintubation hypotension of the patients in this study [19]. As indicated by previous documents, patients with low body weight were associated with increased mortality as opposed to the those with normal weight [20,21]. It is not surprising that patients with low body weight were more likely to develop hypotension after RSI owing to the deficiency of hemodynamic status.
4.2. Influence of albumin and lower body weight on the hemodynamic status of patients who received RSI
4.3. Influence of RSI medications on the hemodynamic status of patients who received RSI
In this study, we have noticed that albumin was a significant prognostic factor in univariate analysis. Particularly, the significant reduction of plasma albumin in patients with sepsis was granted as the main association. An explanation of increased capillary membrane permeability was proposed, which was associated with marked fluid shifts into the tissues and resulted in the subsequent loss of
Ketamine was used as a sedative agent in all patients with COPD. Chronic obstructive pulmonary disease was one of the significant prognostic factors of developing hypotension after RSI whereas ketamine use was not. This finding suggested that hypotension after RSI was not related to the use of ketamine but COPD was. Lidocaine was used as an intravenous agent to blunt the sympathetic stimulation
Table 4
Logistic model for predicting hypotension after RSI
Variables
Pre-SBP (mm Hg) COPD Sepsis Body weight (kg)
≦140 N140 Yes No Yes No ≦55 N55
Group 1 (n = 28)
Group 2 (n = 121)
Estimate
P value
20 8 7 21 9 19 20 8
50 71 12 108 8 113 55 66
1.42
.01
1.56
.01
2.29
.00
1.19
.02
odds ratio
95% CI Lower
Upper
4.14 1.00 4.75 1.00 9.91 1.00 3.27 1.00
1.51
11.37
1.40
16.06
2.87
34.23
1.19
9.01
850 during RSI. The beneficial effects of intravenous lidocaine were inconsistent and therefore its use in these settings was controversial [22-24]. In our study, the frequency and dosage of lidocaine were higher in the hypotension group than in the normal control group. The evidence of this study points to the association of lidocaine use with the development of hypotension after RSI. Lidocaine was normally applied to the patients who required RSI while blunting the sympathetic stimulation. It is possible that the sympathetic stimulation leads to the occurrence of hypotension after the use of lidocaine, particularly in the patients with sepsis and COPD. Thus, the use of lidocaine in RSI requires some precaution in some cases. Midazolam was reported in previous studies [25-27] as one of the agents that probably caused hypotension after RSI. However, controversies still existed among these studies owing to different patient profiles and conditions. One study has demonstrated that midazolam was dose related to hypotension in prehospital RSI with subjects including patients with traumatic brain injury, which was different from our study subjects. Choi et al [27] stated that midazolam is more likely to cause hypotension than etomidate in the ED during RSI. Whereas Swanson et al [25] found that there was low incidence of hypotension with both midazolam and etomidate in prehospital RSI. The present study suggests a large scale randomized control study is required for the clarifications of the association. Different RSI protocols were found to yield different adverse outcomes in one literature [11]. The present study has demonstrated here the multifactorial nature of postintubation hypotension among patients in the ED, which gives valuable information on both etiological analysis and risk estimation for future practice in emergency medicine. There are different kinds of patients who need emergent airway intervention. The hemodynamic statuses of these patients may be varied among patients. We should keep in mind that not only the medications but also disease factors will cause hypotension in RSI. The interactions between medications and disease should not be overlooked in patients who need to be intubated in the future.
5. Limitations The major findings of this study were derived from patients with diseases in internal medicine; the interpretation should be cautious when including traumatic or pediatric patients. Different patient groups were suggested to be customized with RSI protocols with which could yield different complication rates [11]. The risk estimation provided by this study was subjected to the patient profiles and conditions for intervention. Is there any measure that we can use to prevent postintubation hypotension? We have found some clues in this study but needed further studies. Postintubation hypotension was found in this study to be associated with sepsis or COPD, which was attributed to hypovolemia.
C.-C. Lin et al. Therefore, fluid challenge with normal saline may have its role in preventing postintubation hypotension in the future [28]. Unfortunately, we did not measure the status of fluid volume among our patients as the main focus was in searching for risk factors for postintubation hypotension. Suggestions can be made in future studies, which include the group undergoing fluid resuscitation or patients undergoing inotropic agent for clarifications. There was no previous report regarding the consequences of the post-RSI hypotension based on our best knowledge. Although it was not the primary aim of this study, the importance should not be ignored because any of the consequences of hypotension would be a critical condition for ER patients such as respiratory distress and severe sepsis.
6. Conclusions Data from this study suggested that it is not a single factor that induces postintubation hypotension. Sepsis, COPD, lower body weight, and lower initial SBP were the key risk factors for developing hypotension after RSI. Based on this study, the elements of a safe plan for securing the airway should include a review of the patient's clinical diagnosis, consideration of the factors affecting the patient's hemodynamics, assessment of the patient's present and anticipated postintubation volume status, formulation of a plan for induction of anesthesia (including muscle relaxant and sedative use), and confirmation of the availability of emergency drugs based on anticipated liability of the patient's hemodynamics [29]. However, future studies are warranted for validating the risk model and intervention plans to reduce the chance of hypotension induced by RSI.
References [1] American College of Emergency Physicians. Rapid-sequence intubation. Ann Emerg Med 1997;29:573. [2] Kovacs G, Law JA, Ross J, et al. Acute airway management in the emergency department by non-anesthesiologists. Can J Anaesth 2004; 51:174-80. [3] Reid C, Chan L, Tweeddale M. The who, where, and what of rapid sequence intubation: prospective observational study of emergency RSI outside the operating theatre. Emerg Med J 2004;21:296-301. [4] Butler JM, Clancy M, Robinson N, et al. An observational survey of emergency department rapid sequence intubation. Emerg Med J 2001; 18:343-8. [5] Li J, Murphy-Lavoie H, Bugas C, et al. Complications of emergency intubation with and without paralysis. Am J Emerg Med 1999;17: 141-3. [6] Tayal VS, Riggs RW, Marx JA, et al. Rapid-sequence intubation at an emergency medicine residency: success rate and adverse events during a two-year period. Acad Emerg Med 1999;6:31-7. [7] Sakles JC, Laurin EG, Rantapaa AA, et al. Airway management in the emergency department: a one-year study of 610 tracheal intubations. Ann Emerg Med 1998;31:325-32.
The prognostic factors of hypotension after rapid sequence intubation [8] Dufour DG, Larose DL, Clement SC. Rapid sequence intubation in the emergency department. J Emerg Med 1995;13:705-10. [9] Kenny JF, Molloy K, Pollock M, et al. Rapid-sequence induction technique for orotracheal intubation of adult nontrauma patients in a community hospital setting. Ann Emerg Med 1995;25:432-3. [10] Sivilotti ML, Ducharme J. Randomized, double-blind study on sedatives and hemodynamics during rapid-sequence intubation in the emergency department: The SHRED Study. Ann Emerg Med 1998;31: 313-24. [11] Marvez E, Weiss SJ, Houry DE, et al. Predicting adverse outcomes in a diagnosis-based protocol system for rapid sequence intubation. Am J Emerg Med 2003;21:23-9. [12] Reynolds SF, Heffner J. Airway management of the critically ill patient: rapid-sequence intubation. Chest 2005;127:1397-412. [13] Charpentier J, Luyt CE, Fulla Y, et al. Brain natriuretic peptide: A marker of myocardial dysfunction and prognosis during severe sepsis. Critical Care Medicine 2004;32(3):660-5. [14] Ognibene FP, Parker MM, Natanson C, et al. Depressed left ventricular performance. Response to volume infusion in patients with sepsis and septic shock. Chest 1988;93:903-10. [15] Carroll GC, Snyder JV. Hyperdynamic severe intravascular sepsis depends on fluid administration in cynomolgus monkey. Am J Physiol 1982;243:R131-41. [16] Rackow EC, Kaufman BS, Falk J, et al. Hemodynamic response to fluid repletion in patients with septic shock: evidence for early depression of cardiac performance. Circ Shock 1987;22:11-22. [17] Weil MH, Nishjima H. Cardiac output in bacterial shock. Am J Med 1978;64:920-2. [18] Klinger JR. Hemodynamics and positive end-expiratory pressure in critically ill patients. Crit Care Clin 1996;12:841-64. [19] Goldwasser P, Feldman J. Association of serum albumin and mortality risk. J Clin Epidemiol 1997;50:693-703.
851
[20] Flegal KM, Graubard BI, Williamson DF, et al. Excess deaths associated with underweight, overweight, and obesity. JAMA 2005; 293:1861-7. [21] Kuriyama S, Ohmori K, Miura C, et al. Body mass index and mortality in Japan: the Miyagi Cohort Study. J Epidemiol 2004;14(Suppl 1): S33-8. [22] Kindler CH, Schumacher PG, Schneider MC, et al. Effects of intravenous lidocaine and/or esmolol on hemodynamic responses to laryngoscopy and intubation: a double-blind, controlled clinical trial. J Clin Anesth 1996;8:491-6. [23] Singh H, Vichitvejpaisal P, Gaines GY, et al. Comparative effects of lidocaine, esmolol, and nitroglycerin in modifying the hemodynamic response to laryngoscopy and intubation. J Clin Anesth 1995;7:5-8. [24] Tam S, Chung F, Campbell M. Intravenous lidocaine: optimal time of injection before tracheal intubation. Anesth Analg 1987;66:1036-8. [25] Swanson ER, Fosnocht DE, Jensen SC. Comparison of etomidate and midazolam for prehospital rapid-sequence intubation. Prehosp Emerg Care 2004;8:273-9. [26] Davis DP, Kimbro TA, Vilke GM. The use of midazolam for prehospital rapid-sequence intubation may be associated with a dose-related increase in hypotension. Prehosp Emerg Care 2001;5: 163-8. [27] Choi YF, Wong TW, Lau CC. Midazolam is more likely to cause hypotension than etomidate in emergency department rapid sequence intubation. Emerg Med J 2004;21:700-2. [28] el-Beheiry H, Kim J, Milne B, et al. Prophylaxis against the systemic hypotension induced by propofol during rapid-sequence intubation. Can J Anaesth 1995;42:875-8. [29] Horak J, Weiss S. Emergent management of the airway. New pharmacology and the control of comorbidities in cardiac disease, ischemia, and valvular heart disease. Crit Care Clin 2000;16:411-27.