a b s t r a c t

Purpose: Postintubation hypotension (PIH) is an adverse event associated with poor outcomes in emergency de- partment (ED) endotracheal intubation. This study aimed to evaluate the association between sedative dose ad- justment and PIH during Emergency airway management. We also investigated the impact of patient and procedural factors on the incidence of PIH.

Materials and methods: This was a single-center, retrospective study that used a prospectively collected registry of airway management performed at the ED from April 2014 to February 2017. Adult patients who received emer- gency endotracheal intubation were included. Multivariable logistic regression models were used to evaluate the association of PIH with sedative dose, patient variables, and procedural variables.

Results: Overall, 689 patients were included, and 233 (33.8%) patients developed PIH. In the patients overall, mul- tivariable logistic regression demonstrated that age N 70 years, Shock Index N0.8, arterial acidosis (pH b 7.2), in- tubation indication, and use of non-depolarizing Neuromuscular blocking agent were significantly related to PIH. In patients overall, the sedative dose was not related to PIH (overdose; OR: 1.09, 95%CI: 0.57-2.06), (reduction; OR: 0.93, 95%CI: 0.61-1.42), (none used; OR: 1.28, 95%CI: 0.64-2.53). In subgroup analysis, Ketamine dose was not related to PIH (overdose; OR: 0.81, 95%CI: 0.27-2.38, reduction; OR: 1.41, 95%CI: 0.78-2.54). Reduction of etomidate dose was significantly associated with decreased PIH (reduction; OR: 0.46, 95%CI: 0.22-0.98, over- dose; OR: 1.77, 95%CI: 0.79-3.93).

Conclusions: PIH was mainly related to predisposing patient-related factors. Only adjustment of etomidate dose was associated with the incidence of PIH.

(C) 2018

Introduction

Critically ill patients who visit the emergency department (ED) often require emergency airway management due to various indications, in- cluding respiratory failures in oxygenation or ventilation, airway ob- struction, metabolic derangements, and a requirement for airway protection. Endotracheal intubation is an essential, life-saving pro- cedure for critically-ill or injured patients who require a definitive air- way in the ED. Rapid Sequence Intubation , which involves administration of a potent sedative followed by a rapidly acting neuro- muscular blocking agent to increase the success rate and reduce adverse events, is a widely used technique to facilitate ETI in the ED [1-3].

Abbreviations: ED, emergency department; PIH, Postintubation hypotension; CI, confidence interval.

* Corresponding author at: Department of Emergency Medicine, Samsung Medical

Center, Sungkyunkwan University School of Medicine, 81 Irwon-ro, Gangnam-gu, Seoul 135-710, South Korea.

E-mail address: [email protected] (T.G. Shin).

During or immediately after RSI, various complications including hy- potension, hypoxia, arrhythmia, and death can occur [4-10]. Among these, postintubation hypotension (PIH) is known to be the most com- mon undesirable hemodynamic change [11]. Previous studies in the ED and intensive care unit (ICU) have reported that hypotension after en- dotracheal intubation is associated with an increased incidence of acute myocardial infarction, renal failure, increased duration of hospi- talization, and mortality [12-17].

According to previous studies on the risk factors of PIH, hypoten- sion before endotracheal intubation, use of neuromuscular blocking agent, pre-intubation shock index, chronic renal failure, endotra- cheal intubation indications (respiratory failure), diabetes, chronic obstructive pulmonary disease, sepsis, Albumin level, body weight, and age are related to PIH [13-15,18,19]. However, most of the risk factors identified in these previous studies are difficult to modify prior to ETI, and studies for deriving strategies to reduce the inci- dence of PIH are lacking.

Considering that the dose of the drug administered for RSI can be ad- justed at the time of endotracheal intubation, this study aimed to

https://doi.org/10.1016/j.ajem.2018.09.015

0735-6757/(C) 2018

investigate whether the dose of sedative used during endotracheal intu- bation could affect PIH incidence and to identify clinical factors that af- fect PIH.

Subject and methods

Study subjects

Adult (>=19 years old) ED patients who received emergency endotra- cheal intubation at a tertiary hospital ED (annual ED patients of approx- imately 70,000) from April 1, 2014 to February 28, 2017 (2 years and 11 months) were included. Patients who received endotracheal intuba- tion due to cardiac arrest or for whom incomplete data were available were excluded.

This study was approved by the relevant institutional review board, and the need to obtain informed consent was waived due to the retro- spective nature of this study.

Study method and data collection

Data collection

For this study, data were collected by retrospectively reviewing medical records. Data from the Airway Quality Improvement (QI) regis- try, which was prospectively collected from April 2014 for quality im- provement of endotracheal intubation, was analyzed. Endotracheal intubation-related information was collected, and an airway manage- ment QI team acted to improve the success rate of endotracheal intuba- tion and reduce complications. One independent emergency medical technician used a checklist to collect data for each attempted endotra- cheal intubation. After endotracheal intubation was performed, the op- erator completed the registry by filling in additional information. The registry included the patient’s age, sex, height, weight, endotracheal in- tubation indication, vital signs before and after endotracheal intubation, and the medication and doses used for endotracheal intubation. Pre- intubation vital signs were collected at the time of attempted intuba- tion. Post-intubation vital signs were collected for 30 min after intuba- tion. The shock index prior to intubation was computed based on the equation of pulse rate/systolic blood pressure (sBP).

The primary endpoint of this study was PIH; this was defined as sBP b 90 mmHg or mean blood pressure (mBP) b 65 mmHg, requiring vaso- pressor administration or an increased dose of vasopressor, or a de- crease in BP by N20%, using the lowest vital signs during 30 min after intubation. PIH was classified into five categories, as summarized in Table 1.

Endotracheal intubation process

Endotracheal intubation was performed in the ED by an emergency medicine resident or attending physicians, and other residents from the departments of internal medicine, neurology, general surgery,

Table 1

Postintubation hypotension categories.

• Before intubation^a: sBP^b >= 90 and mBP^c >= 65 without vasopressor After intubation^d: sBP b 90 or mBP b 65 or vasopressor use

• Before intubation^a: Any BP^e with vasopressor

After intubation^d: Any BP^e with increased dose of vasopressor

• Before intubation^a: sBP >= 90 and mBP >= 65 with vasopressor

After intubation^d: sBP b 90 or mBP b 65 with the same dose of vasopressor

• Before intubation^a: sBP b 90 or mBP b 65 without vasopressor After intubation^d: reduction of 20% of sBP or mBP without vasopressor

• Before intubation^a: sBP b 90 or mBP b 65 without vasopressor After intubation^d: Any BP^e with vasopressor use

^a Blood pressure before intubation was that recorded at the time of intubation.

^b sBP: systolic blood pressure.

^c mBP: mean blood pressure.

^d Blood pressure after intubation was the lowest value within 30 min of intubation, or the nearest record if no record within 30 min was available.

^e BP: blood pressure.

neurosurgery, thoracic surgery, otorhinolaryngology, intensive care medicine, Family Medicine, and anesthesiology participated. The standard RSI process was followed. The preoxygenation target was peripheral oxygen saturation (SpO₂) of N90%; patients were catego- rized on the basis of SpO₂ after at least 3 min of oxygen supply with a facial mask or bag-mask (15 L/min) at the time of decision to intubate: 1) low risk, SpO₂ N 95%; 2) high-risk, SpO₂ 91-95%;

3) hypoxemic, SpO₂ b 91%. noninvasive positive pressure ventilation and Apneic oxygenation were considered in high-risk or hypoxemic patients. Depending on the patient, pre-treatment drugs, sedative, and Neuromuscular blocking agents were administered prior to en- dotracheal intubation. The sedative dose was determined by the at- tending doctor, based on the recommended dose for the patient’s hemodynamic status and age. The recommended dose for sedatives were as follows: etomidate 0.3 mg/kg, ketamine 1.5 mg/kg, and mid- azolam 0.1 mg/kg. The sedative dose was categorized as a dose re- duction when b75%, as overdose when N125%, and as standard dose when N75% but b125%, relative to the recommended dose. For neuro- muscular blocking agents, succinylcholine (1-1.5 mg/kg), rocuronium (1 mg/kg), and vecuronium (0.1 mg/kg) were used. For sedation after intubation, remifentanil, midazolam, and fentanyl were continuously administered.

Statistical analysis

For statistical analysis, STATA version 14.0 (Stata Corp LP, College Station, TX, USA) was used. Continuous variables are presented as means and standard deviation, and Student’s t-test was used for com- parisons. Categorical variables are presented as numbers and percent- ages, and the chi-square test was used for comparison. In order to investigate the association with PIH, univariate regression was per- formed for age, weight, body mass index (BMI), intubation indication, shock index, arterial acidosis, type of neuromuscular blocking agent, pre-treatment drug use, pre-intubation hypoxia, and type and dose of sedative, and results are presented as odds ratio (ORs) and 95% confi- dence intervals (CIs). For multivariable logistic regression models, sed- ative dose and variables with p values b0.1 in the univariate analysis were included. In order to analyze subgroups based on the drug type, the incidence of PIH according to drug dose was compared between the ketamine and etomidate group, and multivariate regression analysis was performed using adjustment for variables identified as statistically significant in univariate regression analysis. p values b0.05 were consid- ered statistically significant.

Results

Patient characteristics

During the study period, from April 1, 2014 to February 28, 2017, a total of 1087 endotracheal intubations were performed in the ED. Among them, 398 cases, including 373 intubations performed due to cardiac arrest and 25 cases with incomplete data, were excluded; thus, a total of 689 intubations were analyzed. Of these 689 cases, 233 cases (33.8%) developed PIH, and according to the predefined PIH criteria (Table 1), 144 cases (20.9%) were classified as category (1), 43 cases

(6.2%) as category (2), 8 cases (1.2%) as category (3), 6 cases (0.9%) as

category (4), and 32 cases (4.6%) as category (5).

The baseline characteristics of the patients are shown in Table 2. The mean age was 64.1 +- 15.9 years, and most patients (61.4%) were male. The intubation indications were primarily for decreased level of con- sciousness (32.4%) and respiratory failure (52.0%). Most commonly used sedatives during endotracheal intubation were etomidate (49.6%) and ketamine (35.1%). There was a significant difference be- tween the PIH and non-PIH groups in terms of age, weight, BMI, shock index prior to intubation, arterial blood pH, intubation indication, types of sedative and neuromuscular blocking agent used, fentanyl

Table 2 Baseline characteristics.
	Total	PIHa	Non-PIHa	p value
	(n = 689)	(n = 233)	(n = 456)
Age (years)	64.1 +- 15.9	67.5 +- 14.6	62.3 +- 16.3	b0.001
Age N 70	292 (42.4%)	121 (51.9%)	171 (37.4%)	b0.001
Sex (male)	423 (61.4%)	144 (61.8%)	279 (61.2%)	0.875
Weight (kg)	62.8 +- 13.7	60.2 +- 12.5	64.2 +- 14.1	b0.001
Weight b 60 kg	249 (36.1%)	99 (42.5%)	150 (32.9%)	0.013
BMIb (kg/m2) Underweight (b18.5 kg/m2)	83 (12.1%)	39 (16.7%)	44 (9.7%)	0.019
Normal weight (18.5-25 kg/m2)	459 (66.6%)	151 (64.8%)	308 (67.5%)
Overweight (N25 kg/m2)	147 (21.3%)	43 (18.5%)	104 (22.8%)
Intubation indication				b0.001
Altered mental status	223 (32.4%)	53 (22.8%)	170 (37.3%)
Respiratory failure	350 (50.1%)	126 (54.1%)	222 (49.1%)
Shock	49 (7.1%)	28 (12.0%)	21 (4.6%)
drug intoxication	13 (1.9%)	6 (2.6%)	7 (1.5%)
Airway obstruction	8 (1.2%)	5 (2.2%)	3 (0.7%)
Trauma	34 (4.9%)	9 (3.9%)	25 (5.5%)
Others	12 (1.8%)	6 (2.6%)	6 (1.3%)
Shock index	0.87 +- 0.39	1.04 +- 0.44	0.78 +- 0.33	b0.001
Shock index N 0.8	356 (52.9%)	155 (69.8%)	201 (44.6%)	b0.001
Arterial acidosis (pH b 7.2)	148 (21.5%)	64 (27.5%)	84 (18.4%)	0.006
Sedative				0.003
Ketamine	242 (35.1%)	99 (42.5%)	143 (31.4%)
Etomidate	342 (49.6%)	95 (40.8%)	247 (54.2%)
Others	45 (6.5%)	13 (5.6%)	32 (7.0%)
None NMBc	60 (8.7%)	26 (11.2%)	34 (7.5%)	b0.001
Succinylcholine	435 (63.1%)	154 (35.4%)	281 (64.6%)
Non-depolarizing NMBc	184 (26.7%)	43 (23.4%)	141 (76.6%)
None	70 (10.2%)	36 (51.4%)	34 (48.6%)
Pretreatment (fentanyl)	75 (10.9%)	17 (7.30%)	58 (12.7%)	0.031
Post-intubation continuous sedative	241 (35.0%)	87 (37.3%)	154 (33.8%)	0.353
Low SpO2 before intubationd	198 (28.7%)	83 (35.6%)	115 (25.2%)	0.004
Sedative dose				0.281
Overdose (N125%)	61 (8.9%)	23 (9.9%)	38 (8.3%)
Standard (75%-125%)	342 (49.6%)	107 (45.9%)	235 (51.5%)
Reduction (b75%)	226 (32.8%)	77 (33.1%)	149 (32.7%)
No use	60 (8.7%)	26 (11.2%)	34 (7.5%)
Multiple attempts of intubation, >=3 times	53 (7.7%)	18 (7.7%)	35 (7.7%)	0.981
In-hospital mortality (%)	233 (33.8%)	93 (49.2)	140 (28.0)	b0.001
a PIH: postintubation hypotension.

^b BMI: body mass index.

^c NMB: neuromuscular blocking agent.

^d SpO₂ was b90% at the time of intubation, although the preoxygenation method was applied.

administration status, and SpO₂ below 90% prior to intubation. There was no statistically significant difference between the PIH and non- PIH groups in terms of the distribution of the sedative dose used during intubation (p = 0.281). In-hospital mortality was significantly higher in the PIH group (49.2%), compared with the non-PIH group (28.0%) (p b 0.001).

Multivariable logistic regression analysis for variables associated with PIH

In multivariate logistic regression analysis, after adjusting for confounding variables, dose reduction (adjusted OR: 0.93, 95% CI: 0.61-1.42, p = 0.735) or overdose (adjusted OR: 1.09, 95% CI: 0.57-2.06, p = 0.794) of sedative, as compared to the standard dose, and no use of sedative (adjusted OR: 1.28, 95% CI: 0.64-2.53, p = 0.483) demonstrated no significant association with PIH (Table 3). However, the following clinical factors were associated with PIH after endotracheal intubation: age over 70 (adjusted OR: 2.16, 95% CI: 1.50-3.10, p b 0.001), shock index over 0.8 (adjusted

OR: 2.43, 95% CI: 2.05-4.05, p b 0.001), arterial blood pH below 7.2

(adjusted OR: 1.58, 95% CI: 1.04-2.41, p = 0.033), use of a non- depolarizing neuromuscular blocking agent (adjusted OR: 0.53, 95% CI: 0.34-0.81, p = 0.003).

Analysis according to the type of sedative used

For the most commonly used drugs, ketamine and etomidate, an ad- ditional analysis was performed to assess association between the drug dose and PIH (Tables 4, 5). In the group that used ketamine, the mean dose was 1.20 +- 0.54 mg/kg. Reduced dose (adjusted OR: 1.41, 95%

CI: 0.78-2.54, p = 0.261) or overdose (adjusted OR: 0.81, 95% CI: 0.27-2.38, p = 0.697) of ketamine was not significantly associated with PIH. In the group that used etomidate, the mean dose was 0.29 +-

0.23 mg/kg. Reduced dose (adjusted OR: 0.46, 95% CI: 0.22-0.98, p = 0.044) of etomidate was statistically significantly associated with a de- creased incidence of PIH.

Discussion

Endotracheal intubation is a core, life-saving technique in the treat- ment of critically ill patients. In a considerable number of patients, hy- potension that can affect the patient’s prognosis may occur after endotracheal intubation. In this study, the incidence of PIH was 33.8%, which is similar to that of previous studies [11-17,19,20]. Reduction or increase of the sedative dose prior to intubation did not show a signifi- cant association with PIH in the patients overall, but in the etomidate group, dose reduction was significantly associated with decreased PIH

Table 3

Logistic repression analysis for postintubation hypotension.

Variables	Univariable analysis				Multivariable analysis
	ORa	95% CIb	p value		ORa	95% CIb	p value
Age N 70	1.80	1.31-2.48	b0.001		2.16	1.50-3.10	b0.001
Weight b 60 kg BMIc Normal weight (18.5-25 kg/m2)	1.51 Reference	1.09-2.09	0.013		1.11	0.71-1.73	0.652
Underweight (b18.5 kg/m2)	1.81	1.13-2.90	0.014		1.24	0.68-2.23	0.482
Overweight (N25 kg/m2)	0.84	0.56-1.26	0.410		0.94	0.59-1.52	0.814
Intubation indication
AMSd	Reference
Respiratory failure	1.85	1.27-2.70	0.001	1.20		0.78-1.86	0.409
Others	2.66	1.63-4.34	b0.001	2.43		1.39-4.24	0.002
Shock index N0.8	2.88	2.05-4.05	b0.001	2.67		1.84-3.87	b0.001
Arterial acidosis (pH b 7.2)	1.68	1.16-2.43	0.007	1.58		1.04-2.41	0.033
Sedative
Etomidate	Reference			Reference
Ketamine	1.80	1.27-2.55	0.001	1.48		0.98-2.24	0.065
Others	1.06	0.53-2.10	0.876	1.10		0.49-2.49	0.810
None	0.39	1.13-3.49	0.017
NMBe
Succynylcholine Non-depolarizing NMBe	Reference 0.56	0.38-0.83	0.004	0.53		0.34-0.81	0.003
None	1.93	1.16-3.21	0.011	1.48		0.81-2.70	0.199
Pretreatment (fentanyl)	0.54	0.31-0.95	0.033	0.67		0.34-1.29	0.227
Post-intubation sedative	1.17	0.84-1.62	0.353
Low SpO2 before intubation Sedative dose	1.64	1.17-2.31	0.004	1.35		0.92-1.98	0.128
Standard (75%-125%)	Reference
Overdose (N125%)	1.33	0.75-2.34	0.324	1.09		0.57-2.06	0.794
Reduction (b75%)	1.13	0.79-1.62	0.488	0.93		0.61-1.42	0.735
No use	1.68	0.96-2.94	0.069	1.28		0.64-2.53	0.483

^a OR: odds ratio.

^b CI: confidence intervals.

^c BMI: body mass index.

^d AMS; Altered mental status.

^e NMB: neuromuscular blocking agent.

incidence. Patient baseline characteristics, such as hemodynamic status prior to intubation were more strongly associated with PIH.

Hypotension in endotracheal intubation can be explained by the ef- fect of the administered drug and positive pressure ventilation. Notably, positive pressure ventilation can directly or indirectly cause PIH. Medi- cations used during intubation could decrease or block sympathetic out- flow. Moreover, they directly affect the cardiovascular system [11,21]. Previously, such phenomena were considered to be a temporary and be- nign process, but recently, its association with poor prognosis has been confirmed through a number of studies [12-17]. The present study showed an association between a reduced etomidate dose (as com- pared to the recommended dose, based on the patient’s weight), and a decreased incidence of PIH. This seems reasonable considering the mechanism of PIH. Furthermore, it suggests that an appropriate reduc- tion of etomidate dose according to the patient’s condition may be a strategy for preventing PIH.

Unlike etomidate, the ketamine dose used was not significantly as- sociated with PIH, and a tendency for a relatively higher PIH incidence in the ketamine group was observed. This may be due to the following factors. First, ketamine is a sedative with relatively stable hemodynam- ics, as compared to other drugs, due to its sympathetic nerve system stimulation. Based on our additional analysis, the ketamine group showed a significantly higher shock index than the etomidate group, and its use was more frequent in hemodynamically unstable patients. Second, for airway management QI, it has been recommended to reduce the sedative dose in hemodynamically unstable patients; thus, the dose reduction group tended to have unstable hemodynamics prior to intu- bation. In fact, the PIH group had received a lower dose of ketamine. Considering that previous studies reported ketamine administration to cause considerable PIH, the results of this study cannot be interpreted as indicating no association between ketamine dose adjustment and PIH.

Table 4

Comparisons of ketamine and etomidate doses according to the occurrence of postintubation hypotension.

Ketamine	Total (n = 242)	PIHa (n = 99)	Non-PIHa (n = 143)	p value
Dose (mg/kg)	1.20 +- 0.54	1.13 +- 0.49	1.25 +- 0.57	0.035
Overdose (N125%)	22	7 (31.8%)	15 (68.2%)	0.461
Standard (75%-125%)	91	35 (38.5%)	56 (61.5%)
Reduction (b75%)	129	57 (44.2%)	72 (55.8%)
Etomidate	Total (n = 342)	PIHa (n = 95)	Non-PIHa (n = 247)	p value
Dose (mg/kg)	0.30 +- 0.20	0.31 +- 0.10	0.29 +- 0.23	0.787
Overdose (N125%)	35	16 (45.7%)	19 (54.3%)	0.008
Standard (75%-125%)	237	67 (28.3%)	170 (71.7%)
Reduction (b75%)	70	12 (17.1%)	58 (82.9%)

Values with % show the proportion of PIH or non-PIH cases.

^a PIH: postintubation hypotension.

Table 5 Results of logistic repression analysis for postintubation hypotension in subgroups accord- ing to ketamine and etomidate use.

Univariable analysis Multivariable analysis

	ORa	95% CIb	p value		ORa	95% CIb	p value
Ketamine
Standard (75%-125%)	Reference
Overdose (N125%)	0.75	0.28-2.01	0.564	0.81		0.27-2.38	0.697
Reduction (b75%)	1.27	0.73-2.19	0.397	1.41		0.78-2.54	0.261
Etomidate
Standard (75%-125%)	Reference
Overdose (N125%)	2.14	1.04-4.40	0.039	1.77		0.79-3.93	0.163
Reduction (b75%)	0.52	0.27-1.04	0.064	0.46		0.22-0.98	0.044
a OR: odds ratio.
b CI: confidence intervals.

This study identified clinically important PIH risk factors. First, the association between older age and PIH is consistent with the findings of previous studies, and may be due to the higher possibility of comor- bidities and lower hemodynamic reservoir with increasing age [13,14]. Shock index, which considers blood pressure and pulse prior to en- dotracheal intubation, is known to be an important predictor of PIH, and it was also identified as a significant factor in this study [13]. Arterial acidosis was also significantly correlated with PIH, and is likely to be re- lated to decreased cardiac contractility, arterial vasodilation, and de- creased catecholamine response. Additional studies regarding PIH Prevention strategies, such as appropriately adjusting the sedative dose or rapidly correcting the aforementioned PIH risk factors prior to attempted intubation, including vasopressor administration, fluid chal-

lenge, and acidosis correction, are necessary.

The results of this study showed that the incidence of PIH was lower in the non-depolarizing neuromuscular blocking agent group than in the succinylcholine group. This is in contrast to the theory that the vasodilatory effect of non-depolarizing neuromuscular blocking agents may cause blushing, with lowering of blood pressure and increasing of the pulse rate [22]. Additional research comparing depolarizing and non-depolarizing neuromuscular blocking agents in terms of PIH inci- dence is necessary. Furthermore, there is still controversy regarding the use of neuromuscular blocking agents and PIH. Studies by Heffner et al. and Greene et al. have reported that the use of neuromuscular blocking agents decreased hemodynamic instability [13,14], but a study by Smischney et al. reported an association between the use of neuromuscular blocking agents and PIH [15].

The limitations of this study are as follows. First, this study was a single-center, observational study, and thus, the results cannot be gen- eralized and should be cautiously interpreted. In particular, the drugs administered for endotracheal intubation can vary, depending on the preference of the operator and medical institution. Second, most data were prospectively collected, but the incidence of PIH was investigated by retrospectively reviewing the medical records. We collected vital signs immediately after intubation, but they were not recorded with a predefined interval. Third, the criteria used to define PIH in this study were broader than those used in previous studies. The definition of PIH has not yet been firmly established and has been reported to vary from 19% to 52% [12-17,19,20]. Heffner et al. conducted a study in which patients with confirmed hypotension prior to endotracheal intu- bation were excluded [13,17], while Green et al. investigated the inci- dence of PIH in a broader sense by including patients whose blood pressure was decreased by N20% and patients who required vasopressor or required increased dose of vasopressor [12,14,16]. The results of this study may have been different if PIH had been defined differently. Fourth, this study investigated the sedative type and dose based on the administered dose clinically determined by the endotracheal intu- bation operator. Thus, although multivariable regression models were used to correct the confounding variables as much as possible, bias

may have affected the results. Intubation-related factors, including the time to successful intubation or preoxygenation, were not included. Fifth, the sedative dose adjustment range was not segmented and ana- lyzed in subgroups due to the small number of samples. Sixth, we did not evaluate the association between mortality and PIH. Seventh, we used patient-related variables as adjusting factors rather than the expe- rience of the physician performing the intubation; however, there might have been a strong selection bias in that senior physicians were more often responsible for additional analysis of patients with unstable vital signs, and in that attending EM physicians supervised every intuba- tion procedure to ensure adherence to standardized protocols during the airway QI program.

Conclusion

Among sedatives used during endotracheal intubation, dose reduc- tion of etomidate had a significant association with decreased PIH. In addition, the clinical condition of the patient prior to intubation, includ- ing age, shock index, and arterial acidosis were risk factors of PIH. Based on these findings, additional research on Preventive strategies for re- ducing PIH prevention is necessary.

Sources of support

None.

Previous presentations

None.

Conflicts of interest

The authors have no potential conflicts of interest or funding sources to declare.

References

1. Mace SE. Challenges and advances in intubation: rapid sequence intubation. Emerg Med Clin North Am 2008;26:1043-68 [x].
2. Walls RM, Brown 3rd CA, Bair AE, Pallin DJ. Emergency airway management: a multi-center report of 8937 emergency department intubations. J Emerg Med 2011;41:347-54.
3. Brown 3rd CA, Bair AE, Pallin DJ, Walls RM. Techniques, success, and adverse events of emergency department adult intubations. Ann Emerg Med 2015;65 [363-7370. e1].
4. Sivilotti M, Ducharme J. Randomized, double-blind study on sedatives and hemody- namics during Rapid-sequence intubation in the emergency department: the SHRED study. Ann Emerg Med 1998;31:313-24.
5. Dufour DG, Larose DL, Clement SC. Rapid sequence intubation in the emergency de- partment. J Emerg Med 1995;13:705-10.
6. Sakles JC, Laurin EG, Rantapaa AA, Panacek EA. Airway management in the emer- gency department: a one-year study of 610 tracheal intubations. Ann Emerg Med 1998;31:325-32.
7. Tayal VS, Riggs RW, Marx JA, Tomaszewski CA, Schneider RE. Rapid-sequence intu- bation at an emergency medicine residency: success rate and adverse events during a two-year period. Acad Emerg Med 1999;6:31-7.
8. Li J, Murphy-Lavoie H, Bugas C, Martinez J, Preston C. Complications of emergency intubation with and without paralysis. Am J Emerg Med 1999;17:141-3.
9. Butler JM, Clancy M, Robinson N, Driscoll P. An observational survey of emergency department rapid sequence intubation. Emerg Med J 2001;18:343-8.
10. Reid C, Chan L, Tweeddale M. The who, where, and what of rapid sequence intuba- tion: prospective observational study of emergency RSI outside the operating the- atre. Emerg Med J 2004;21:296-301.
11. Mort TC. Complications of emergency tracheal intubation: hemodynamic alterations-part I. J Intensive Care Med 2007;22:157-65.
12. Green RS, Butler MB. Postintubation hypotension in general anesthesia: a retrospec- tive analysis. J Intensive Care Med Dec. 2016;31(10):667-75.
13. Heffner AC, Swords DS, Nussbaum ML, Kline JA, Jones AE. Predictors of the compli- cation of postintubation hypotension during emergency airway management. J Crit Care 2012;27:587-93.
14. Green RS, Edwards J, Sabri E, Fergusson D. Evaluation of the incidence, risk factors, and impact on patient outcomes of postintubation hemodynamic instability. CJEM 2012;14:74-82.
15. Smischney NJ, Demirci O, Diedrich DA, Barbara DW, Sandefur BJ, Trivedi S, et al. In- cidence of and risk factors for post-intubation hypotension in the critically ill. Med Sci Monit 2016;22:346-55.
16. Green RS, Turgeon AF, McIntyre LA, Fox-Robichaud AE, Fergusson DA, Doucette S, et al. Postintubation hypotension in intensive care unit patients: a multicenter co- hort study. J Crit Care 2015;30:1055-60.
17. Heffner AC, Swords D, Kline JA, Jones AE. The frequency and significance of postintubation hypotension during emergency airway management. J Crit Care 2012;27:417.e9-417.e13.
18. Trivedi S, Demirci O, Arteaga G, Kashyap R, Smischney NJ. Evaluation of preintubation shock index and modified shock index as predictors of postintubation hypotension and other Short-term outcomes. J Crit Care 2015;30:861.e1-7.
19. Lin CC, Chen KF, Shih CP, Seak CJ, Hsu KH. The prognostic factors of hypotension after rapid sequence intubation. Am J Emerg Med 2008;26:845-51.
20. Smischney NJ, Seisa MO, Cambest J, Wiegand RA, Busack KD, Loftsgard TO, et al. The incidence of and risk factors for postintubation hypotension in the immunocompro- mised critically ill adult. J Intensive Care Med 2017;885066617704844.
21. Manthous CA. Avoiding circulatory complications during endotracheal intubation and initiation of positive pressure ventilation. J Emerg Med 2010;38:622-31.
22. M RD. Miller’s Anesthesia8th ed. ; 2015.