Invasive arterial blood pressure monitoring to detect post-intubation hypotension in patients who receive a prehospital emergency anaesthetic for suspected traumatic brain injury

Invasive arterial blood pressure monitoring to detect post-intubation hypotension in patients who receive a prehospital emergency anaesthetic for suspected traumatic brain injury | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Invasive arterial blood pressure monitoring to detect post-intubation hypotension in patients who receive a prehospital emergency anaesthetic for suspected traumatic brain injury Silas Houghton Budd, Nick Haslam, Jo Griggs, Jack Barrett, Scott Clarke, and 3 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-6229140/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Background The prehospital management of moderate/severe traumatic brain injury (TBI) centres on the prevention of secondary brain injury. In some cases, prehospital emergency anaesthesia (PHEA) may be required to provide optimal neuroprotective care. Continuous invasive arterial blood pressure (IBP) monitoring is increasingly utilised in this cohort. PHEA can result in significant blood pressure changes, particularly around induction. IBP allows for a more targeted approach to blood pressure management in these patients. The aim of this study was to analyse hypotension frequency, depth and duration in suspected TBI patients monitored with IBP before PHEA. Methods A retrospective analysis of suspected TBI patients attended by Air Ambulance Charity Kent Surrey Sussex who received IBP prior to PHEA between the 6 January 2022 and the 6 July 2024. The magnitude and duration of ‘absolute hypotension’ (systolic blood pressure (SBP) < 90mmHg) were combined to establish a ‘dose’ of absolute hypotension (mmHg*min). The primary endpoints were the incidence and dose of absolute hypotension. Results 305 patients were identified, of which 140 (45.9%) were included. Median age was 58 years (interquartile range (IQR) 42–73), predominant sex was male ( n = 108, 77%) and median Glasgow Coma Scale (GCS) was 6/15 (IQR 4.0–7.5). Thirteen patients (9.3%) were found to have an episode of absolute hypotension pre-PHEA, increasing to 53 (37.9%) post-PHEA. Twenty-five patients (47.2%) had an initial absolute hypotensive episode occur after five minutes post-PHEA, with a median duration of three minutes (IQR 1.0–4.5). The median dose of absolute hypotension was 144 mmHg*min (IQR 3.75–1675.5). Twenty-five patients (17.9%) had ‘clinically important hypotension’ (SBP < 110mmHg) pre-PHEA, increasing to 80 post-PHEA (57.1%). Pre-PHEA absolute and clinically important hypotension were found to be associated with both the incidence and dose of post-PHEA absolute hypotension. Conclusion This study highlights a higher incidence of absolute hypotension using IBP compared to previous studies utilising intermittent non-invasive blood pressure monitoring. While post-PHEA absolute hypotension was common, over half of these events were brief (less than five minutes). These findings highlight the importance of analysing depth and duration of hypotension and suggest the need for prehospital outcome-based studies utilising continuous IBP. Non-invasive blood pressure Invasive arterial blood pressure Absolute hypotension Clinically important hypotension Dose of hypotension Traumatic brain injury Prehospital emergency anaesthesia Helicopter emergency medical service Critical care Figures Figure 1 Figure 2 Figure 3 Figure 4 Background Traumatic brain injury (TBI) is a significant cause of morbidity and mortality in the United Kingdom, affecting approximately 40,000 people per year ( 1 ). While most cases are mild and recover without specialist intervention, a small subset of patients with moderate or severe TBI require enhanced medical care to reduce the chance of death or disability. Whilst the primary brain injury resulting from traumatic forces is considered irreversible ( 2 ), subsequent progressive neuronal injury, or ‘secondary brain injury’, can be mitigated through clinical intervention and, critically, avoidance of further physiological insults ( 3 , 4 ). Early, prehospital management of secondary brain injury is therefore key to reducing mortality and improving neurological outcomes for patients with TBI ( 5 , 6 ). The prehospital management of secondary brain injury centres on the maintenance of cerebral perfusion pressure and avoidance of metabolic insults to the brain ( 7 ). Two key elements of a neuroprotective bundle of care for patients with severe TBI are prehospital emergency anaesthesia (PHEA) and management of blood pressure. The aims of PHEA are to secure the airway, optimise oxygenation, and improve cerebral perfusion by regulating cerebral vasoconstriction through normocapnic ventilation ( 8 , 9 ). However, induction of anaesthesia and subsequent positive pressure ventilation can itself cause several adverse effects, including hypo- and hypertension, hypoxaemia, hypercarbia and even cardiac arrest ( 10 ). Prehospital TBI guidelines highlight the importance of proactive blood pressure management. Across multiple studies, ‘absolute hypotension’ (SBP < 90mmHg) has repeatedly been associated with worse patient outcomes and even a single episode has been associated with increased adjusted mortality ( 1 ). Whilst a significant proportion of patients with severe TBI experience spontaneous hypotension ( 11 ), many more are at risk of post-PHEA absolute hypotension and meticulous management of peri-PHEA blood pressure is therefore critical. Non-invasive blood pressure (NIBP) and invasive arterial blood pressure (IBP) monitors are the most common methods of blood pressure measurement. NIBP monitors produce discrete measurements and normally cycle every 2–5 minutes ( 12 – 15 ). In contrast, IBP monitors continuously record the pressure in the arterial vessel in which they are sited, allowing accurate, real-time identification of SBP, diastolic blood pressure (DBP) and mean arterial pressure ( 16 ). Continuous IBP monitoring is considered gold standard ( 16 ) with many studies demonstrating a poor correlation with NIBP ( 12 , 17 – 20 ). Invasive arterial blood pressure monitoring is not routinely used in the prehospital setting. However, it is becoming increasingly prevalent within enhanced care teams, driven by several reported benefits ( 7 , 10 ). Continuous IBP monitoring allows for the immediate detection of BP changes (enabling timely treatment); eliminates the risk of occult, unmeasured hypotension associated with intermittent NIBP monitoring; and reduces the effects of in-transit noise and artefact, providing more reliable and accurate measurement during patient transfer ( 20 ). These factors are presumed to ultimately reduce both the incidence and severity of post-PHEA absolute hypotension. These presumed benefits must be weighed against the risks of establishing IBP monitoring such as the potential for prolonged scene time and delay to definitive care ( 7 ). Whilst not specific to those with TBI, several in-hospital studies have found depth and duration of hypotension are associated with mortality over and above incidence of absolute hypotension ( 21 , 22 ). Prehospitally, Spaite et al. sought to test the hypothesis that extent of absolute hypotension impacts the mortality of TBI patients, combining the depth and duration of absolute hypotension to establish a ‘dose’ of hypotension (mmHg*min) ( 14 ). They demonstrated a linear relationship between this hypotensive dose and adjusted mortality. However, to date, this and other prehospital studies have been limited by discrete, infrequent and potentially inaccurate NIBP recordings. Continuous IBP monitoring on the other hand provides an opportunity to accurately analyse the depth, duration and therefore dose of hypotension in the prehospital setting. The primary aim of this study was to analyse the incidence and dose of post-PHEA absolute hypotension in suspected TBI patients monitored with IBP prior to PHEA. Methods Study setting The study was conducted at Air Ambulance Charity Kent Surrey Sussex (KSS), a Helicopter Emergency Medical Service covering a large geographical area with a resident population of 4.5 million and a transient population of 8 million. The enhanced care team comprise a doctor (with at least five years of postgraduate experience and six months of hospital anaesthesia training) and a paramedic (with specialist training, including modules on prehospital anaesthesia). Study design We performed a retrospective observational cohort study of all patients who received PHEA for suspected TBI by KSS between 6 January 2022 and 6 July 2024. IBP monitoring was introduced on 1 January 2022 and indicated for those receiving PHEA for suspected TBI. Standard Operating Procedures (SOP) outline the indications, preparation and conduct of PHEA for patients with traumatic injuries, the indications for IBP monitoring, and the management of hypotension in TBI. The indications for PHEA include actual or impending airway compromise, ventilatory failure, reduced Glasgow Coma Scale (GCS), anticipated clinical course and humanitarian reasons ( 11 ). Preparation includes patient positioning, equipment readiness and monitoring. Preoxygenation is performed for at least three minutes. For trauma patients, the standard drugs and doses are Fentanyl 3 µg/kg, Ketamine 2 mg/kg, and Rocuronium 2 mg/kg ( 3 – 2 – 2 ). Dose adjustments are made for hypovolaemic, frail, or elderly patients by reducing ( 1 – 1 – 2 ) or omitting (0-1-2) Fentanyl ( 14 ). Monitoring includes NIBP measured at three-minute intervals, and continuous IBP and other vital signs. The process for IBP monitoring is as follows: ( 1 ) an arterial catheter is placed in either the radial or femoral artery; ( 2 ) the arterial catheter is attached to a saline-filled pressure transducer system; ( 3 ) continuous monitoring is displayed on the patient monitor. In the context of brain injury, the recommended haemodynamic targets are SBP 110–150 mmHg and a mean arterial pressure > 80 mmHg with aggressive management of SBP < 90 mmHg. The options available for management of hypotension include 0.9% sodium chloride, adrenaline, noradrenaline, ephedrine and metaraminol. The objective of this study was to determine the hypotensive response to PHEA in patients with suspected TBI monitored with IBP. The primary outcome was the incidence of post-PHEA absolute hypotension. Secondary outcomes: The dose of post-intubation absolute hypotension The incidence and dose of post-intubation ‘clinically important hypotension’, defined as SBP < 110mmHg ( 23 ) The timing and occurrence of absolute and clinically important hypotensive episodes following PHEA The factors associated with the incidence and dose of post-intubation absolute hypotension Participants Adult (≥ 16 years) trauma patients who had IBP initiated at least three minutes before PHEA were included. The three-minute threshold was established by author consensus to balance the collection of sufficient pre-PHEA clinical data with the inclusion of eligible patients. Patients were excluded if they had no presumed TBI on case review, a nontraumatic brain injury (including spontaneous intracranial haemorrhage, hanging/asphyxiation associated injury), had been in cardiac arrest, IBP was not cited pre-PHEA, if there were insufficient data points for analysis, or if there was an IBP malfunction. Interfacility transfers were also excluded, as were those with IBP monitoring but no PHEA or no documented time of PHEA. Children were not included as their physiology and expected normal haemodynamic parameters differ, which would have made interpretation complex. Similarly, the pathophysiology of nontraumatic intracranial lesions is sufficiently different as not to be included ( 10 , 12 – 14 ). Data collection Invasive arterial blood pressure readings were recorded every minute from three minutes pre-PHEA until 15 minutes post-PHEA, with the time of PHEA marked as 0 minutes. We then removed spurious blood pressure readings, defined as any of: SBP > 280mmHg, SBP < 30mmHg, SBP <(DBP + 5mmHg), DBP 150 mmHg ( 24 ). As described by Spaite et al. previously, the dose of absolute hypotension was calculated by combining the depth (magnitude of BP below 90mmHg) with the duration (time with BP below threshold) and expressed as a single value (mmHg*min; Fig. 1 ) ( 14 ). Physiological data is stored on our patient monitor (Tempus Pro ALS, Philips®), and the device uploads patient information to a dedicated electronic patient clinical record system (HEMSbase V.2.0, Medic One Systems, UK), allowing for numeric and visual trend analysis. Statistical methods Categorical data are presented as frequency ( n ) and percentage (%). Continuous data are reported as mean and standard deviation (SD) for normally distributed data or median and interquartile range (IQR) for non-normally distributed data. The distribution of numerical data was assessed using visual inspection of histograms and Q-Q plots, with normality evaluated using the one-sample Kolmogorov-Smirnov test. For the primary analysis, patients were categorised based on whether they had an incident of absolute hypotension post-PHEA or not. Categorical data were compared between groups using Fisher’s exact test. For continuous variables, comparisons were performed using either the Mann-Whitney U test or t-test, depending on the normality of the data. To identify the doses, the magnitude and duration of abnormal SBP were calculated for each endpoint and expressed as a single figure (mmHg*min). This was measured from the first to the fifteenth minute post-PHEA. A binary logistic regression model was used to analyse the association between predictor variables and whether a patient would have an episode of absolute hypotension post-PHEA. A linear regression model was used to analyse the association between predictors and dose of hypotension. Predictors were identified before analysis and included the patient's age, weight (kg), time-to-PHEA (defined as the time from 999 call-to-PHEA in minutes) and pre-PHEA BP category: absolute hypotension (SBP 180mmhg). 95% confidence intervals (CI) for regression estimates were calculated to indicate precision. Statistical significance was set at p < 0.05 for all analyses. All statistical analyses were performed using R Statistical Software 4.4.2 ( 25 ). R packages included: tidyverse , gtsummary , diptest , and lme4 for modelling. Results Baseline characteristics Between 6 January 2022 and 6 July 2024, 305 cases were identified. 165 cases were excluded, leaving 140 (45.9%) for analysis (Fig. 2 ). Table 1 provides a summary of the included patients: the median age was 58 years (IQR 42–73), most were male sex ( n = 108, 77%) and the median GCS was 6/15 (IQR 4.0–7.5). Table 1 Baseline characteristics, mechanism and time-interval descriptors for included patients. Variable n = 140 Age (years) (Median, IQR) 58 (42, 73) Sex (n, %) Female 32 (23%) Male 108 (77%) Weight (kg) (Median, IQR) 80 (70, 80) MOI (n, %) Accidental injury 87 (62%) Assault 7 (5.0%) Exposure 1 (0.7%) Intentional self-harm 1 (0.7%) RTC 44 (31%) Code Red † (n, %) 7 (5%) Vasopressor administration 65 (46.4%) Initial GCS (Median, IQR) 6.00 (4.00, 7.50) Unreactive pupil (n, %) 55 (39%) Time-to-HEMS activation (min) (Median, IQR) 10 ( 5 , 22 ) Time-to-scene arrival (min) (Median, IQR) 33 (24, 41) Time-to-PHEA (min) (Median, IQR) 28 (23, 36) Time-to-first IBP (min) (Median, IQR) 20 ( 15 , 26 ) Legend table 1. Kg, kilograms; MOI, mechanism of injury; RTC, road traffic collision; GCS, Glasgow Coma Scale; HEMS, Helicopter Emergency Medical Services; PHEA, prehospital emergency anaesthesia; IBP, invasive arterial blood pressure; † patients suspected to have major haemorrhage. Thirteen patients (9.3%) were found to have an episode of absolute hypotension pre-PHEA, increasing to 53 (37.9%) post-PHEA. There were 25 patients (17.9%) who had clinically important hypotension pre-PHEA, increasing to 80 post-PHEA (57.1%). The dose of absolute hypotension was highest in patients classified as having pre-PHEA absolute hypotension, with a median dose of 144 mmHg*min. A wide IQR (3.75–1675.5) indicated a significant spread in absolute hypotension severity within this group. In comparison, pre-PHEA clinically important hypotensive patients experienced a median dose of 19.5 mmHg*min (IQR 0–450.75), while pre-PHEA normotensive patients experienced a median dose of 0 mmHg*min (IQR 0–23.75). As shown in Fig. 3 , 89 (63.5%) patients did not have a dose of absolute hypotension post-PHEA, these were predominantly those without pre-PHEA absolute or clinically important hypotension. Patients with a higher dose of hypotension were typically from the pre-PHEA hypotension patients. Of the 53 patients who experienced post-PHEA absolute hypotension, over half ( n = 28, 52.8%) experienced their first episode within the first five minutes post-PHEA (Fig. 4 a). The remaining 25 patients (47.2%) had their first absolute hypotensive episode occur after five minutes post-PHEA. In this latter cohort, the median duration of these episodes was three minutes (IQR 1.0–4.5). One patient experienced an absolute hypotensive episode at minute 15. This case was reviewed and the patient returned to normal blood pressure at minute 16 and remained stable. Figure 4 b presents the distribution of the duration of absolute hypotension following PHEA. Most patients experienced hypotension lasting less than six minutes ( n = 29, 54.7%) and of these, 12 (22.6%) had episodes lasting less than one minute, while 22 (41.5%) experienced episodes lasting less than three minutes. The distribution showed a steep decline after the first minute, with progressively fewer patients experiencing longer durations and only a small number having episodes lasting up to 15 minutes. We further evaluated the timing of the first clinically important hypotensive episode (Fig. 4 c); a peak was observed within the first minute post-PHEA. The distribution then tapers off, with fewer patients encountering their first absolute hypotensive episode beyond this time and a small proportion extending to minute 10. Figure 4 d illustrates the distribution of clinically important hypotensive episode durations post-PHEA. The duration of hypotensive episodes varied with the median duration of clinically important hypotension being 10 minutes (IQR 7–14). Prediction of post-PHEA absolute hypotension Variables were then explored to determine their relationship with predicting post-PHEA absolute hypotension (supplementary Table 1). In the univariate analysis pre-PHEA clinically important hypotension emerged as a significant predictor with a substantial positive association. Pre-PHEA absolute hypotension also demonstrated a strong association, although this did not reach statistical significance. Other variables did not show significant associations in the univariate analysis; however, females exhibited a trend towards a higher risk of post-PHEA absolute hypotension. In the multivariate model, pre-PHEA clinically important hypotension remained a significant independent predictor of post-PHEA absolute hypotension. None of the other variables reached statistical significance in the multivariable model. Several variables were associated with the post-PHEA dose of absolute hypotension in the univariate analysis (supplementary Table 2). Pre-PHEA clinically important hypotension emerged as a significant predictor, associated with an increase of 858 mmHg*min (95% CI: 564–1152, p < 0.001) when compared with pre-PHEA normotensive patients. Similarly, pre-PHEA absolute hypotension was associated with a higher dose, contributing an additional 464 mmHg*min (95% CI: 13.6–915, p = 0.044). Weight and initial GCS were also significant, with increases of 501 mmHg*min (95% CI: 18.4–984, p = 0.042) and 352 mmHg*min (95% CI: 120–585, p = 0.003), respectively. Meanwhile, MOI, age and time-to-PHEA did not show statistically significant associations. In the multivariable analysis, pre-PHEA clinically important hypotension remained a strong independent predictor, associated with an increase of 802 mmHg*min (95% CI: 504–1100, p < 0.001). Similarly, pre-PHEA absolute hypotension was independently associated with an increase of 573 mmHg*min (95% CI: 55.9–1090, p = 0.030). Female sex was a significant predictor, associated with an additional 327 mmHg*min (95% CI: 120–534, p = 0.002) compared to male sex. Other factors, including age, weight, initial GCS, time-to-PHEA, and MOI were not significantly associated. Discussion To our knowledge this is the first study to utilise IBP monitoring to analyse post-PHEA absolute hypotension in suspected TBI patients. We observed a high incidence of absolute hypotension following PHEA ( n = 53, 37.9%) compared to previous studies ( 13 , 14 , 26 ). Notably, in a previous study conducted by our service ( 14 ) the incidence of absolute hypotension was less than a quarter (9%) of the rate we observed. This discrepancy likely reflects differences in frequency of BP measurement. In the previous study, two consecutive NIBP readings (at least three minutes apart) were required to meet the definition of absolute hypotension, whereas we included any single episode of absolute hypotension which was recorded every minute. Meidart et al. found that continuous BP monitoring identified nearly four times as many hypotensive episodes as intermittent NIBP ( 27 ), while Wijnberge et al. (2022) demonstrated that intermittent NIBP missed 8% of hypotensive events ( 28 ). Although these studies are hospital based and their results are therefore not directly generalisable to prehospital care, they underscore the broader issue of missed hypotension with infrequent measurements, a phenomenon likely mirrored in previous prehospital studies using NIBP only. Our study suggests that continuous IBP captures episodes of hypotension that would otherwise be missed, both clinically and in the published literature. Given a single episode of prehospital absolute hypotension has been associated with a doubling of mortality in TBI patients ( 1 , 24 ) these occult episodes of hypotension might be considered clinically relevant. However, direct comparison with prior studies that used NIBP values is difficult because the duration of a single episode of hypotension is unknown, likely variable and potentially prolonged. A deeper understanding of the impact of both the magnitude and duration of hypotension on outcomes is therefore required ( 15 , 29 , 30 ). Spaite et al. demonstrated a linear relationship between the dose of absolute hypotension and mortality, with a 19% increase in mortality risk for every doubling of hypotension dose ( 14 ). Their findings suggest that depth and duration, rather than just incidence, may be a more relevant measure. This is in-keeping with a large body of evidence from elective surgery that injury to end organs is a function of both depth and duration of hypotension ( 31 ). Interestingly, although we observed a high incidence of absolute hypotension compared to previous studies, the duration of these episodes was generally brief, with a significant proportion (54.7%) lasting less than six minutes post- PHEA. Of these episodes, 12 (22.6%) had absolute hypotension lasting less than one minute, and 22 (41.5%) experienced absolute hypotension lasting less than three minutes. This further supports our hypothesis that these episodes may have been missed in studies using intermittent NIBP and demonstrates the importance of considering duration alongside depth of hypotension. These short episodes of hypotension may also represent early recognition and intervention by the treating team because of continuous IBP monitoring ( 32 ) which would be in-keeping with previous work by Maheshwari et al. who found that continuous monitoring significantly reduced the duration of intraoperative hypotension ( 22 ). We found that in most cases the peak incidence ( n = 28, 52.8%) of absolute hypotension occurred within the first five minutes post-PHEA, coinciding with the hemodynamic effects of induction agents and positive pressure ventilation. This finding, in keeping with our clinical experience and previous studies ( 13 , 26 ), strongly supports siting arterial access prior to PHEA when possible. Not only does this allow the prompt detection and treatment of post-PHEA hypotension but also ensures the team is not task-fixated on arterial line insertion during a period of patient care associated with a heightened risk of hypotension. Furthermore, accurate and reliable pre-PHEA IBP monitoring may aid with the choice of induction drug and dose. When siting an arterial line, it therefore seems prudent to maximise clinical benefit by achieving this prior to PHEA whenever possible. Our results show that patients with both absolute and clinically important hypotension were more likely to experience a single episode of post-PHEA absolute hypotension. Conversely, we found patients without pre-PHEA absolute or clinically important hypotension were largely spared from post-PHEA absolute hypotension, a finding similar to Price et al ( 13 ). These findings raise the question of whether proactive management to achieve a SBP > 110 mmHg before PHEA and a careful induction regimen may mitigate some of the hemodynamic risks of PHEA, a question that warrants further investigation. Pre-PHEA clinically important hypotension was the only variable associated with the post-PHEA absolute hypotension in both univariate and multivariate analyses. Perhaps surprisingly, we did not observe an association of age with hypotensive episodes as others have reported ( 13 , 26 , 33 ), potentially due to the higher frequency of brief absolute hypotensive episodes in our cohort. This may also explain why pre-PHEA absolute hypotension was not significantly associated with post-PHEA absolute hypotension, however this may also be due to the team selecting a more reserved induction regimen. Analysis of hypotensive dose on the other hand identified lower initial GCS, heavier weight and female sex as significant predictors in univariate analysis, with female sex remaining significant in multivariate analysis. Heavier patient weight was not retained in multivariate analysis, which may have been due to the variability and inaccuracy associated with clinician estimation of weight ( 31 ). Lower GCS scores were similarly associated with higher doses in univariate analysis but not in multivariate models, potentially reflecting impaired compensatory mechanisms in patients with severe brain injury. Our finding that female sex predicts an increased dose of post-PHEA absolute hypotension is novel and has not previously been reported. Whilst this result should be interpreted with caution due to the retrospective nature of the study and low proportion of female sex ( n = 32, 23%), it is not an isolated observation in prehospital trauma management ( 33 ) and merits further investigation. Limitations There are several limitations to this study which we should acknowledge. Firstly, the absence of patient outcome data such as mortality or neurological recovery limited our ability to correlate hypotensive dose with clinical endpoints. We have described that most patients who experience absolute hypotension post-PHEA have a relatively low dose, however without patient outcome data we are unable to describe the clinical significance of this. Previous work would suggest that these low doses are not associated with poor patient outcomes ( 15 ), but these data were based on infrequent NIBP measurements. Large, in-hospital, peri-operative datasets suggest a linear relationship between the duration of hypotension and end-organ damage with evidence of renal and/or cardiac harm even with very brief exposure (1–5 minutes). As the injured brain is arguably more sensitive to hypotensive episodes ( 34 ) even very short episodes of hypotension (i.e. those with low doses) may be clinically relevant. A prospective prehospital study utilising continuous IBP measurements and clinical outcomes is required to better understand this relationship. Several factors influence the accuracy of SBP as measured by IBP monitoring. Changes in the position of the transducer relative to the patient in the vertical axis can lead to significant under or overestimates of the true BP, a significant risk in the dynamic environment of prehospital care. To mitigate this all clinicians at KSS secure the transducer with tape to the regimental badge area of the lower deltoid for radial arterial lines and upper thigh for common femoral arterial lines. Nevertheless, unrecognised movement of the transducer may have led to erroneous readings. Similarly, underdamping and overdamping can lead to overestimation and underestimation of the true SBP respectively. KSS utilise the same transducer set up for every patient, minimising but not eliminating the risk of these artifacts. Seventeen (5.57%) cases were excluded from this study due to arterial line malfunction identified by clinicians on scene. This may be due to discontinuity at any point from the artery to the transducer or failure of the mechanical and/or electrical components within the system. It’s possible that in this cohort of patients, arterial line placement was technically more challenging leading to subsequent displacement or a markedly damped trace. We cannot elucidate the aetiology of malfunction for each case from documentation but recognise this may be an important group of patients who were excluded from this study. Regarding diagnosis of TBI, this was a retrospective study in which patients were included based on the teams’ suspicion of TBI, as opposed to a confirmed diagnosis following diagnostic imaging. It is therefore possible that some patients included in this study did not have intracranial pathology, however this reflects the limitations of current prehospital diagnostics and allows extrapolation of results to clinical practice. The times of induction and intubation were recorded by the enhanced care team manually using recorded electronic patient record time stamps. Although cases were reviewed to address any apparent timing issues, this may mean the recorded time of PHEA and the actual time were not identical. Therefore, a pre-PHEA hypotensive event occurring one minute before the documented induction time could be related to the PHEA rather than the underlying pathology. Several patients had their arterial line placed post-PHEA which may represent those who were clinically deteriorating, whose need for clinical intervention outweighed the benefit of real-time monitoring or those in whom arterial line placement was technically more challenging and abandoned pre-PHEA. This exclusion may bias our results towards underestimating the overall risk of post-PHEA hypotension. We recognise our assumption that the increased incidence of absolute hypotension in this study compared to prior published literature reflects increased frequency of measurement as opposed to a true increased incidence. Whilst it is possible that there was a lower true incidence of absolute hypotension in previous studies this is not in-keeping with prior work comparing IBP and NIBP ( 27 , 28 ) nor have there been any substantial changes in our service that would explain such a finding. Constraints of our data collection software meant we were unable to evaluate continuous IBP recordings and instead relied on single entries at one-minute intervals. While this is more frequent and reliable than NIBP, there still exists the risk of missed hypotensive episodes, albeit very brief. The reliance on estimated weights introduced variability into our data. While weight was a borderline predictor of hypotensive dose in univariate analysis, this was based on clinician estimation of weight, which is known to be inaccurate ( 35 ) undermining the validity of this finding. Finally, it was not possible to review the impact of vasopressor drugs such as adrenaline, noradrenaline, ephedrine or metaraminol on hypotensive episodes, as these are most often documented as the total amount given and not time-stamped at the exact time of administration. As such, clinical teams may have seen a hypotensive episode occur and treated it immediately with a vasopressor in less than a minute, hiding an incidence of hypotension. Conclusion To our knowledge this is the first study to utilise IBP monitoring to analyse post-PHEA absolute hypotension in patients with suspected TBI. We report a high incidence of absolute hypotension compared to previous studies utilising NIBP, likely reflective of the increased frequency of measurements. We demonstrate the potential value of considering dose when analysing IBP measurements, as despite an increased incidence of absolute hypotension, most of these episodes were of short duration and low dose. These findings also suggest benefit in pre-PHEA IBP monitoring. Further studies utilising continuous IBP monitoring to analyse dose of hypotension and its association with clinical outcome measures such as mortality and long-term neurological function are required. Abbreviations BP Blood pressure CI Confidence interval DBP Diastolic blood pressure GCS Glasgow Coma Scale IBP Invasive arterial blood pressure IQR Interquartile range Kg Kilogram KSS Air Ambulance Charity Kent Surrey Sussex NIBP Non-invasive blood pressure PHEA Prehospital emergency anaesthesia SBP Systolic blood pressure SD Standard deviation SOP Standard operating procedure TBI Traumatic brain injury Declarations Ethical approval and consent to participate The project met the National Institute for Healthcare Research (NIHR, UK) criteria for service evaluation and formal ethical approval was waived. Consent for publication Not applicable. Availability of data and materials The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request. Competing interests The authors declare that they have no competing interests. Funding Not applicable. Authors contributions All authors fulfilled the ICMJE criteria for authorship. SHB conceived the study. LB provided supervisor oversight. SC retrieved the data. SHB/SC/JB/JG analysed the data and performed the statistical analysis. SHB/NH/JB/JG drafted the manuscript. All authors read and approved the final manuscript. Acknowledgements We are grateful for the support of our clinical and operational support colleagues at Air Ambulance Charity Kent Surrey Sussex for providing both clinical governance and operational experience to support the implementation of invasive arterial blood pressure monitoring at our service. References Lee JW, Wang W, Rezk A, Mohammed A, Macabudbud K, Englesakis M, et al. 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Prehospital invasive arterial blood pressure monitoring in critically ill patients attended by a UK helicopter emergency medical service- a retrospective observational review of practice. Scand J Trauma Resusc Emerg Med. 2024;32(1):20. Ter Avest E, Ragavan D, Griggs J, Dias M, Mitchinson SA, Lyon R. Haemodynamic effects of a prehospital emergency anaesthesia protocol consisting of fentanyl, ketamine and rocuronium in patients with trauma: a retrospective analysis of data from a Helicopter Emergency Medical Service. BMJ Open. 2021;11(12):e056487. King C, Lewinsohn A, Keeliher C, McLachlan S, Sherrin J, Khan-Cheema H, et al. Cardiovascular complications of prehospital emergency anaesthesia in patients with return of spontaneous circulation following medical cardiac arrest: a retrospective comparison of ketamine-based and midazolam-based induction protocols. Emerg Med J. 2022;39(9):672–8. Price J, Moncur L, Lachowycz K, Major R, Sagi L, McLachlan S, et al. Predictors of post-intubation hypotension in trauma patients following prehospital emergency anaesthesia: a multi-centre observational study. Scand J Trauma Resusc Emerg Med. 2023;31(1):26. ter Avest E, Griggs J, Wijesuriya J, Russell MQ, Lyon RM. Determinants of prehospital lactate in trauma patients: a retrospective cohort study. BMC Emerg Med. 2020;20(1):18. Spaite DW, Hu C, Bobrow BJ, Chikani V, Sherrill D, Barnhart B, et al. Mortality and Prehospital Blood Pressure in Patients With Major Traumatic Brain Injury: Implications for the Hypotension Threshold. JAMA Surg. 2017;152(4):360–8. Lam S, Liu H, Jian Z, Settels J, Bohringer C. Intraoperative Invasive Blood Pressure Monitoring and the Potential Pitfalls of Invasively Measured Systolic Blood Pressure. Cureus 13(8):e17610. Kaufmann T, Cox EGM, Wiersema R, Hiemstra B, Eck RJ, Koster G, et al. Non-invasive oscillometric versus invasive arterial blood pressure measurements in critically ill patients: A post hoc analysis of a prospective observational study. J Crit Care. 2020;57:118–23. Ribezzo S, Spina E, Di Bartolomeo S, Sanson G. Noninvasive Techniques for Blood Pressure Measurement Are Not a Reliable Alternative to Direct Measurement: A Randomized Crossover Trial in ICU. ScientificWorldJournal [Internet]. 2014 Jan 30 [cited 2017 Nov 30];2014. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3926274/ Riley LE, Chen GJ, Latham HE. Comparison of noninvasive blood pressure monitoring with invasive arterial pressure monitoring in medical ICU patients with septic shock. Blood Press Monit. 2017;22(4):202. Perera Y, Raitt J, Poole K, Metcalfe D, Lewinsohn A. Non-invasive versus arterial pressure monitoring in the pre-hospital critical care environment: a paired comparison of concurrently recorded measurements. Scand J Trauma Resusc Emerg Med. 2024;32(1):77. Maleczek M, Laxar D, Geroldinger A, Gleiss A, Lichtenegger P, Kimberger O. Definition of clinically relevant intraoperative hypotension: A data-driven approach. PLoS ONE. 2024;19(11):e0312966. Maheshwari K, Turan A, Mao G, Yang D, Niazi AK, Agarwal D, et al. The association of hypotension during non-cardiac surgery, before and after skin incision, with postoperative acute kidney injury: a retrospective cohort analysis. Anaesthesia. 2018;73(10):1223–8. Carney N, Totten AM, O’Reilly C, Ullman JS, Hawryluk GWJ, Bell MJ, et al. Guidelines for the Management of Severe Traumatic Brain Injury. Fourth Ed Neurosurg. 2017;80(1):6. Manley G, Knudson MM, Morabito D, Damron S, Erickson V, Pitts L. Hypotension, Hypoxia, and Head Injury: Frequency, Duration, and Consequences. Arch Surg. 2001;136(10):1118–23. R: The R Project for Statistical Computing [Internet]. [cited 2025 Feb 28]. Available from: https://www.r-project.org/ Bayliss RA, Bird R, Turner J, Chatterjee D, Lockey DJ. Haemodynamic response to pre-hospital emergency anaesthesia in trauma patients within an urban helicopter emergency medical service. Eur J Trauma Emerg Surg. 2024;50(3):987–94. Meidert AS, Dolch ME, Mühlbauer K, Zwissler B, Klein M, Briegel J, et al. Oscillometric versus invasive blood pressure measurement in patients with shock: a prospective observational study in the emergency department. J Clin Monit Comput. 2021;35(2):387–93. Wijnberge M, Schenk J, Terwindt LE, Mulder MP, Hollmann MW, Vlaar AP, et al. The use of a machine-learning algorithm that predicts hypotension during surgery in combination with personalized treatment guidance: study protocol for a randomized clinical trial. Trials. 2019;20(1):582. Badjatia N, Carney N, Crocco TJ, Fallat ME, Hennes HMA, Jagoda AS, et al. Guidelines for prehospital management of traumatic brain injury 2nd edition. Prehosp Emerg Care. 2008;12(Suppl 1):S1–52. Brenner LA. Beck Anxiety Inventory. In: Kreutzer JS, DeLuca J, Caplan B, editors. Encyclopedia of Clinical Neuropsychology [Internet]. New York, NY: Springer; 2011 [cited 2024 Jan 23]. pp. 359–61. Available from: https://doi.org/10.1007/978-0-387-79948-3_1972 Sessler DI, Bloomstone JA, Aronson S, Berry C, Gan TJ, Kellum JA, et al. Perioperative Quality Initiative consensus statement on intraoperative blood pressure, risk and outcomes for elective surgery. Br J Anaesth. 2019;122(5):563–74. Kouz K, Bergholz A, Timmermann LM, Brockmann L, Flick M, Hoppe P, et al. The Relation Between Mean Arterial Pressure and Cardiac Index in Major Abdominal Surgery Patients: A Prospective Observational Cohort Study. Anesth Analg. 2022;134(2):322–9. Nutbeam T, Roberts I, Weekes L, Shakur-Still H, Brenner A, Ageron FX. Use of tranexamic acid in major trauma: a sex-disaggregated analysis of the Clinical Randomisation of an Antifibrinolytic in Significant Haemorrhage (CRASH-2 and CRASH-3) trials and UK trauma registry (Trauma and Audit Research Network) data. Br J Anaesth. 2022;129(2):191–9. White H, Venkatesh B. Cerebral perfusion pressure in neurotrauma: a review. Anesth Analg. 2008;107(3):979–88. Darnis S, Fareau N, Corallo CE, Poole S, Dooley MJ, Cheng AC. Estimation of body weight in hospitalized patients. QJM. 2012;105(8):769–74. Additional Declarations No competing interests reported. Supplementary Files Supplementarymaterial.docx Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-6229140","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":432710654,"identity":"7aaa7c04-9202-409d-91ee-e66e1a07afcc","order_by":0,"name":"Silas Houghton Budd","email":"data:image/png;base64,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","orcid":"","institution":"Air Ambulance Charity Kent Surrey Sussex","correspondingAuthor":true,"prefix":"","firstName":"Silas","middleName":"Houghton","lastName":"Budd","suffix":""},{"id":432710656,"identity":"0fad9a1b-f6bc-4e92-b1ef-03a69c188946","order_by":1,"name":"Nick Haslam","email":"","orcid":"","institution":"Air Ambulance Charity Kent Surrey Sussex","correspondingAuthor":false,"prefix":"","firstName":"Nick","middleName":"","lastName":"Haslam","suffix":""},{"id":432710657,"identity":"1f5403b3-289a-44cb-9175-cb88a34552b6","order_by":2,"name":"Jo Griggs","email":"","orcid":"","institution":"Air Ambulance Charity Kent Surrey Sussex","correspondingAuthor":false,"prefix":"","firstName":"Jo","middleName":"","lastName":"Griggs","suffix":""},{"id":432710659,"identity":"142fc379-1c3b-4ea1-8efc-9b1f145aeee3","order_by":3,"name":"Jack Barrett","email":"","orcid":"","institution":"Air Ambulance Charity Kent Surrey Sussex","correspondingAuthor":false,"prefix":"","firstName":"Jack","middleName":"","lastName":"Barrett","suffix":""},{"id":432710660,"identity":"3293b850-d870-46c9-af28-409655c990e3","order_by":4,"name":"Scott Clarke","email":"","orcid":"","institution":"Air Ambulance Charity Kent Surrey Sussex","correspondingAuthor":false,"prefix":"","firstName":"Scott","middleName":"","lastName":"Clarke","suffix":""},{"id":432710662,"identity":"5a47265b-4c33-48f8-b0ea-74178b5579b5","order_by":5,"name":"Lisa Burrell","email":"","orcid":"","institution":"Essex and Hertfordshire Air Ambulance Trust","correspondingAuthor":false,"prefix":"","firstName":"Lisa","middleName":"","lastName":"Burrell","suffix":""},{"id":432710664,"identity":"b01bf24f-df20-4fea-a70f-e666813e0432","order_by":6,"name":"Duncan Bootland","email":"","orcid":"","institution":"Air Ambulance Charity Kent Surrey Sussex","correspondingAuthor":false,"prefix":"","firstName":"Duncan","middleName":"","lastName":"Bootland","suffix":""},{"id":432710665,"identity":"07c50e73-bbda-4d3d-857f-e029ec220f29","order_by":7,"name":"Richard Lyon","email":"","orcid":"","institution":"Air Ambulance Charity Kent Surrey Sussex","correspondingAuthor":false,"prefix":"","firstName":"Richard","middleName":"","lastName":"Lyon","suffix":""}],"badges":[],"createdAt":"2025-03-14 20:53:13","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-6229140/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-6229140/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":79327043,"identity":"6730f77c-e9bf-4d26-b570-c0df17148eb3","added_by":"auto","created_at":"2025-03-27 05:41:55","extension":"jpg","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":128625,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eGraphical example of the calculation for hypotensive dose.\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eLegend Figure 1.\u003c/strong\u003e SBP; systolic blood pressure, Nb. Graphical example highlights a hypotensive dose of 66.2 mmHg*min.\u003c/p\u003e","description":"","filename":"Picture1.jpg","url":"https://assets-eu.researchsquare.com/files/rs-6229140/v1/80164c8243a41803f0572acc.jpg"},{"id":79326271,"identity":"5b5fa758-c846-4f8a-a930-22c37c13b4df","added_by":"auto","created_at":"2025-03-27 05:33:55","extension":"jpg","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":148136,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eStudy population flow diagram for included patients.\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eLegend Figure 2. \u003c/strong\u003eTBI, traumatic brain injury; ICH, intracerebral haemorrhage; PHEA, prehospital emergency anaesthesia; IBP, intra-arterial blood pressure.\u003c/p\u003e\n\u003cp\u003eI would have this as a stand alone page for clarity\u003c/p\u003e","description":"","filename":"Picture2.jpg","url":"https://assets-eu.researchsquare.com/files/rs-6229140/v1/4127927d416e29f6828a7f19.jpg"},{"id":79326265,"identity":"318fc5c4-5d9d-4078-8b51-f098d67d97ec","added_by":"auto","created_at":"2025-03-27 05:33:55","extension":"jpg","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":63966,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eDistribution of dose of absolute hypotension\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eLegend Figure 3. \u003c/strong\u003ePHEA, prehospital emergency anaesthesia.\u003c/p\u003e\n\u003cp\u003eIt’s a lot more expensive to publish in colour – I would convert to black/white if possible\u003c/p\u003e","description":"","filename":"Picture3.jpg","url":"https://assets-eu.researchsquare.com/files/rs-6229140/v1/7152e9482264115f2fe4626b.jpg"},{"id":79327046,"identity":"cc7b8c40-a6db-47fb-b4bb-3310bb6b4dc0","added_by":"auto","created_at":"2025-03-27 05:41:55","extension":"jpg","order_by":4,"title":"Figure 4","display":"","copyAsset":false,"role":"figure","size":159924,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eDistribution of hypotensive episodes and doses.\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eLegend Figure 4. \u003c/strong\u003ePHEA, prehospital emergency anaesthesia.\u003c/p\u003e\n\u003cp\u003eThe x axis numerator scale isn't visible on 4D - presumably it's the same as the graph above but as it's visible on both 4A and 4C, it should be visible on 4D\u003c/p\u003e\n\u003cp\u003e\u003ca href=\"mailto:[email protected]\"\u003e@Jack Barrett\u003c/a\u003e\u003c/p\u003e","description":"","filename":"Picture4.jpg","url":"https://assets-eu.researchsquare.com/files/rs-6229140/v1/4a1c8968af19e8e23279a043.jpg"},{"id":80466277,"identity":"3187e7b1-9b29-4b29-98d3-548a09f351c1","added_by":"auto","created_at":"2025-04-13 04:01:33","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1279903,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-6229140/v1/eb9caf9e-e013-411e-9d0e-635e6b8dc1e8.pdf"},{"id":79326264,"identity":"48924ffc-58ac-4774-bec9-3631bdce9e8a","added_by":"auto","created_at":"2025-03-27 05:33:55","extension":"docx","order_by":1,"title":"","display":"","copyAsset":false,"role":"supplement","size":22074,"visible":true,"origin":"","legend":"","description":"","filename":"Supplementarymaterial.docx","url":"https://assets-eu.researchsquare.com/files/rs-6229140/v1/afb2614e8d115739a6ea4ea5.docx"}],"financialInterests":"No competing interests reported.","formattedTitle":"Invasive arterial blood pressure monitoring to detect post-intubation hypotension in patients who receive a prehospital emergency anaesthetic for suspected traumatic brain injury","fulltext":[{"header":"Background","content":"\u003cp\u003eTraumatic brain injury (TBI) is a significant cause of morbidity and mortality in the United Kingdom, affecting approximately 40,000 people per year (\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e). While most cases are mild and recover without specialist intervention, a small subset of patients with moderate or severe TBI require enhanced medical care to reduce the chance of death or disability. Whilst the primary brain injury resulting from traumatic forces is considered irreversible (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e), subsequent progressive neuronal injury, or \u0026lsquo;secondary brain injury\u0026rsquo;, can be mitigated through clinical intervention and, critically, avoidance of further physiological insults (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e). Early, prehospital management of secondary brain injury is therefore key to reducing mortality and improving neurological outcomes for patients with TBI (\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e, \u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eThe prehospital management of secondary brain injury centres on the maintenance of cerebral perfusion pressure and avoidance of metabolic insults to the brain (\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e). Two key elements of a neuroprotective bundle of care for patients with severe TBI are prehospital emergency anaesthesia (PHEA) and management of blood pressure. The aims of PHEA are to secure the airway, optimise oxygenation, and improve cerebral perfusion by regulating cerebral vasoconstriction through normocapnic ventilation (\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e, \u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e). However, induction of anaesthesia and subsequent positive pressure ventilation can itself cause several adverse effects, including hypo- and hypertension, hypoxaemia, hypercarbia and even cardiac arrest (\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e).\u003c/p\u003e \u003cp\u003e Prehospital TBI guidelines highlight the importance of proactive blood pressure management. Across multiple studies, \u0026lsquo;absolute hypotension\u0026rsquo; (SBP\u0026thinsp;\u0026lt;\u0026thinsp;90mmHg) has repeatedly been associated with worse patient outcomes and even a single episode has been associated with increased adjusted mortality (\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e). Whilst a significant proportion of patients with severe TBI experience spontaneous hypotension (\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e), many more are at risk of post-PHEA absolute hypotension and meticulous management of peri-PHEA blood pressure is therefore critical.\u003c/p\u003e \u003cp\u003eNon-invasive blood pressure (NIBP) and invasive arterial blood pressure (IBP) monitors are the most common methods of blood pressure measurement. NIBP monitors produce discrete measurements and normally cycle every 2\u0026ndash;5 minutes (\u003cspan additionalcitationids=\"CR13 CR14\" citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e). In contrast, IBP monitors continuously record the pressure in the arterial vessel in which they are sited, allowing accurate, real-time identification of SBP, diastolic blood pressure (DBP) and mean arterial pressure (\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e). Continuous IBP monitoring is considered gold standard (\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e) with many studies demonstrating a poor correlation with NIBP (\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e, \u003cspan additionalcitationids=\"CR18 CR19\" citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eInvasive arterial blood pressure monitoring is not routinely used in the prehospital setting. However, it is becoming increasingly prevalent within enhanced care teams, driven by several reported benefits (\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e, \u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e). Continuous IBP monitoring allows for the immediate detection of BP changes (enabling timely treatment); eliminates the risk of occult, unmeasured hypotension associated with intermittent NIBP monitoring; and reduces the effects of in-transit noise and artefact, providing more reliable and accurate measurement during patient transfer (\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e). These factors are presumed to ultimately reduce both the incidence and severity of post-PHEA absolute hypotension. These presumed benefits must be weighed against the risks of establishing IBP monitoring such as the potential for prolonged scene time and delay to definitive care (\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eWhilst not specific to those with TBI, several in-hospital studies have found depth and duration of hypotension are associated with mortality over and above incidence of absolute hypotension (\u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e, \u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e). Prehospitally, Spaite et al. sought to test the hypothesis that extent of absolute hypotension impacts the mortality of TBI patients, combining the depth and duration of absolute hypotension to establish a \u0026lsquo;dose\u0026rsquo; of hypotension (mmHg*min) (\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e). They demonstrated a linear relationship between this hypotensive dose and adjusted mortality. However, to date, this and other prehospital studies have been limited by discrete, infrequent and potentially inaccurate NIBP recordings. Continuous IBP monitoring on the other hand provides an opportunity to accurately analyse the depth, duration and therefore dose of hypotension in the prehospital setting. The primary aim of this study was to analyse the incidence and dose of post-PHEA absolute hypotension in suspected TBI patients monitored with IBP prior to PHEA.\u003c/p\u003e"},{"header":"Methods","content":"\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003ch2\u003eStudy setting\u003c/h2\u003e \u003cp\u003eThe study was conducted at Air Ambulance Charity Kent Surrey Sussex (KSS), a Helicopter Emergency Medical Service covering a large geographical area with a resident population of 4.5\u0026nbsp;million and a transient population of 8\u0026nbsp;million. The enhanced care team comprise a doctor (with at least five years of postgraduate experience and six months of hospital anaesthesia training) and a paramedic (with specialist training, including modules on prehospital anaesthesia).\u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003eStudy design\u003c/h3\u003e\n\u003cp\u003eWe performed a retrospective observational cohort study of all patients who received PHEA for suspected TBI by KSS between 6 January 2022 and 6 July 2024. IBP monitoring was introduced on 1 January 2022 and indicated for those receiving PHEA for suspected TBI.\u003c/p\u003e \u003cp\u003eStandard Operating Procedures (SOP) outline the indications, preparation and conduct of PHEA for patients with traumatic injuries, the indications for IBP monitoring, and the management of hypotension in TBI. The indications for PHEA include actual or impending airway compromise, ventilatory failure, reduced Glasgow Coma Scale (GCS), anticipated clinical course and humanitarian reasons (\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e). Preparation includes patient positioning, equipment readiness and monitoring. Preoxygenation is performed for at least three minutes. For trauma patients, the standard drugs and doses are Fentanyl 3 \u0026micro;g/kg, Ketamine 2 mg/kg, and Rocuronium 2 mg/kg (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e). Dose adjustments are made for hypovolaemic, frail, or elderly patients by reducing (\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e) or omitting (0-1-2) Fentanyl (\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e). Monitoring includes NIBP measured at three-minute intervals, and continuous IBP and other vital signs. The process for IBP monitoring is as follows: (\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e) an arterial catheter is placed in either the radial or femoral artery; (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e) the arterial catheter is attached to a saline-filled pressure transducer system; (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e) continuous monitoring is displayed on the patient monitor. In the context of brain injury, the recommended haemodynamic targets are SBP 110\u0026ndash;150 mmHg and a mean arterial pressure\u0026thinsp;\u0026gt;\u0026thinsp;80 mmHg with aggressive management of SBP\u0026thinsp;\u0026lt;\u0026thinsp;90 mmHg. The options available for management of hypotension include 0.9% sodium chloride, adrenaline, noradrenaline, ephedrine and metaraminol.\u003c/p\u003e \u003cp\u003eThe objective of this study was to determine the hypotensive response to PHEA in patients with suspected TBI monitored with IBP. The primary outcome was the incidence of post-PHEA absolute hypotension.\u003c/p\u003e \u003cp\u003eSecondary outcomes:\u003c/p\u003e \u003cp\u003e \u003col\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003eThe dose of post-intubation absolute hypotension\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003eThe incidence and dose of post-intubation \u0026lsquo;clinically important hypotension\u0026rsquo;, defined as SBP\u0026thinsp;\u0026lt;\u0026thinsp;110mmHg (\u003cspan citationid=\"CR23\" class=\"CitationRef\"\u003e23\u003c/span\u003e)\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003eThe timing and occurrence of absolute and clinically important hypotensive episodes following PHEA\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003eThe factors associated with the incidence and dose of post-intubation absolute hypotension\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003c/ol\u003e \u003c/p\u003e\n\u003ch3\u003eParticipants\u003c/h3\u003e\n\u003cp\u003eAdult (\u0026ge;\u0026thinsp;16 years) trauma patients who had IBP initiated at least three minutes before PHEA were included. The three-minute threshold was established by author consensus to balance the collection of sufficient pre-PHEA clinical data with the inclusion of eligible patients.\u003c/p\u003e \u003cp\u003ePatients were excluded if they had no presumed TBI on case review, a nontraumatic brain injury (including spontaneous intracranial haemorrhage, hanging/asphyxiation associated injury), had been in cardiac arrest, IBP was not cited pre-PHEA, if there were insufficient data points for analysis, or if there was an IBP malfunction. Interfacility transfers were also excluded, as were those with IBP monitoring but no PHEA or no documented time of PHEA. Children were not included as their physiology and expected normal haemodynamic parameters differ, which would have made interpretation complex. Similarly, the pathophysiology of nontraumatic intracranial lesions is sufficiently different as not to be included (\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e, \u003cspan additionalcitationids=\"CR13\" citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e).\u003c/p\u003e\n\u003ch3\u003eData collection\u003c/h3\u003e\n\u003cp\u003eInvasive arterial blood pressure readings were recorded every minute from three minutes pre-PHEA until 15 minutes post-PHEA, with the time of PHEA marked as 0 minutes. We then removed spurious blood pressure readings, defined as any of: SBP\u0026thinsp;\u0026gt;\u0026thinsp;280mmHg, SBP\u0026thinsp;\u0026lt;\u0026thinsp;30mmHg, SBP \u0026lt;(DBP\u0026thinsp;+\u0026thinsp;5mmHg), DBP\u0026thinsp;\u0026lt;\u0026thinsp;10mmHg, or DBP\u0026thinsp;\u0026gt;\u0026thinsp;150 mmHg (\u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e). As described by Spaite et al. previously, the dose of absolute hypotension was calculated by combining the depth (magnitude of BP below 90mmHg) with the duration (time with BP below threshold) and expressed as a single value (mmHg*min; Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e) (\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e).\u003c/p\u003e \u003cp\u003ePhysiological data is stored on our patient monitor (Tempus Pro ALS, Philips\u0026reg;), and the device uploads patient information to a dedicated electronic patient clinical record system (HEMSbase V.2.0, Medic One Systems, UK), allowing for numeric and visual trend analysis.\u003c/p\u003e\n\u003ch3\u003eStatistical methods\u003c/h3\u003e\n\u003cp\u003eCategorical data are presented as frequency (\u003cem\u003en\u003c/em\u003e) and percentage (%). Continuous data are reported as mean and standard deviation (SD) for normally distributed data or median and interquartile range (IQR) for non-normally distributed data. The distribution of numerical data was assessed using visual inspection of histograms and Q-Q plots, with normality evaluated using the one-sample Kolmogorov-Smirnov test.\u003c/p\u003e \u003cp\u003eFor the primary analysis, patients were categorised based on whether they had an incident of absolute hypotension post-PHEA or not. Categorical data were compared between groups using Fisher\u0026rsquo;s exact test. For continuous variables, comparisons were performed using either the Mann-Whitney U test or t-test, depending on the normality of the data. To identify the doses, the magnitude and duration of abnormal SBP were calculated for each endpoint and expressed as a single figure (mmHg*min). This was measured from the first to the fifteenth minute post-PHEA.\u003c/p\u003e \u003cp\u003eA binary logistic regression model was used to analyse the association between predictor variables and whether a patient would have an episode of absolute hypotension post-PHEA. A linear regression model was used to analyse the association between predictors and dose of hypotension. Predictors were identified before analysis and included the patient's age, weight (kg), time-to-PHEA (defined as the time from 999 call-to-PHEA in minutes) and pre-PHEA BP category: absolute hypotension (SBP\u0026thinsp;\u0026lt;\u0026thinsp;90mmhg), clinically important hypotension (SBP 91mmhg\u0026ndash;110mmhg), normotension (111\u0026ndash;179mmhg) or hypertension (\u0026gt;\u0026thinsp;180mmhg). 95% confidence intervals (CI) for regression estimates were calculated to indicate precision.\u003c/p\u003e \u003cp\u003eStatistical significance was set at \u003cem\u003ep\u003c/em\u003e\u0026thinsp;\u0026lt;\u0026thinsp;0.05 for all analyses. All statistical analyses were performed using R Statistical Software 4.4.2 (\u003cspan citationid=\"CR25\" class=\"CitationRef\"\u003e25\u003c/span\u003e). R packages included: \u003cem\u003etidyverse\u003c/em\u003e, \u003cem\u003egtsummary\u003c/em\u003e, \u003cem\u003ediptest\u003c/em\u003e, and \u003cem\u003elme4\u003c/em\u003e for modelling.\u003c/p\u003e"},{"header":"Results","content":"\u003cdiv id=\"Sec9\" class=\"Section2\"\u003e\n \u003ch2\u003eBaseline characteristics\u003c/h2\u003e\n \u003cp\u003eBetween 6 January 2022 and 6 July 2024, 305 cases were identified. 165 cases were excluded, leaving 140 (45.9%) for analysis (Fig. \u003cspan class=\"InternalRef\"\u003e2\u003c/span\u003e). Table \u003cspan class=\"InternalRef\"\u003e1\u003c/span\u003e provides a summary of the included patients: the median age was 58 years (IQR 42\u0026ndash;73), most were male sex (\u003cem\u003en\u003c/em\u003e\u0026thinsp;=\u0026thinsp;108, 77%) and the median GCS was 6/15 (IQR 4.0\u0026ndash;7.5).\u003c/p\u003e\n \u003cdiv class=\"gridtable\"\u003e\u0026nbsp;\u0026nbsp;\u003ctable id=\"Tab1\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e\n \u003cdiv class=\"CaptionContent\"\u003e\n \u003cp\u003eBaseline characteristics, mechanism and time-interval descriptors for included patients.\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eVariable\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003en\u0026thinsp;=\u0026thinsp;140\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAge (years) (Median, IQR)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e58 (42, 73)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eSex (n, %)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eFemale\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e32 (23%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMale\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e108 (77%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eWeight (kg) (Median, IQR)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e80 (70, 80)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMOI (n, %)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAccidental injury\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e87 (62%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAssault\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7 (5.0%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eExposure\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1 (0.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eIntentional self-harm\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1 (0.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eRTC\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e44 (31%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCode Red\u003csup\u003e\u0026dagger;\u003c/sup\u003e (n, %)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7 (5%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eVasopressor administration\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e65 (46.4%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eInitial GCS (Median, IQR)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e6.00 (4.00, 7.50)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eUnreactive pupil (n, %)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e55 (39%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eTime-to-HEMS activation (min) (Median, IQR)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e10 (\u003cspan class=\"CitationRef\"\u003e5\u003c/span\u003e, \u003cspan class=\"CitationRef\"\u003e22\u003c/span\u003e)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eTime-to-scene arrival (min) (Median, IQR)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e33 (24, 41)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eTime-to-PHEA (min) (Median, IQR)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e28 (23, 36)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eTime-to-first IBP (min) (Median, IQR)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e20 (\u003cspan class=\"CitationRef\"\u003e15\u003c/span\u003e, \u003cspan class=\"CitationRef\"\u003e26\u003c/span\u003e)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003c/table\u003e\n \u003c/div\u003e\n \u003cp\u003e\u003cstrong\u003eLegend table 1.\u0026nbsp;\u003c/strong\u003eKg, kilograms; MOI, mechanism of injury; RTC, road traffic collision; GCS, Glasgow Coma Scale; HEMS, Helicopter Emergency Medical Services; PHEA, prehospital emergency anaesthesia; IBP, invasive arterial blood pressure; \u0026dagger; patients suspected to have major haemorrhage.\u003c/p\u003e\n \u003cp\u003eThirteen patients (9.3%) were found to have an episode of absolute hypotension pre-PHEA, increasing to 53 (37.9%) post-PHEA. There were 25 patients (17.9%) who had clinically important hypotension pre-PHEA, increasing to 80 post-PHEA (57.1%).\u003c/p\u003e\n \u003cp\u003eThe dose of absolute hypotension was highest in patients classified as having pre-PHEA absolute hypotension, with a median dose of 144 mmHg*min. A wide IQR (3.75\u0026ndash;1675.5) indicated a significant spread in absolute hypotension severity within this group. In comparison, pre-PHEA clinically important hypotensive patients experienced a median dose of 19.5 mmHg*min (IQR 0\u0026ndash;450.75), while pre-PHEA normotensive patients experienced a median dose of 0 mmHg*min (IQR 0\u0026ndash;23.75). As shown in Fig. \u003cspan class=\"InternalRef\"\u003e3\u003c/span\u003e, 89 (63.5%) patients did not have a dose of absolute hypotension post-PHEA, these were predominantly those without pre-PHEA absolute or clinically important hypotension. Patients with a higher dose of hypotension were typically from the pre-PHEA hypotension patients.\u003c/p\u003e\n \u003cp\u003eOf the 53 patients who experienced post-PHEA absolute hypotension, over half (\u003cem\u003en\u003c/em\u003e\u0026thinsp;=\u0026thinsp;28, 52.8%) experienced their first episode within the first five minutes post-PHEA (Fig. \u003cspan class=\"InternalRef\"\u003e4\u003c/span\u003ea). The remaining 25 patients (47.2%) had their first absolute hypotensive episode occur after five minutes post-PHEA. In this latter cohort, the median duration of these episodes was three minutes (IQR 1.0\u0026ndash;4.5). One patient experienced an absolute hypotensive episode at minute 15. This case was reviewed and the patient returned to normal blood pressure at minute 16 and remained stable.\u003c/p\u003e\n \u003cp\u003eFigure \u003cspan class=\"InternalRef\"\u003e4\u003c/span\u003eb presents the distribution of the duration of absolute hypotension following PHEA. Most patients experienced hypotension lasting less than six minutes (\u003cem\u003en\u003c/em\u003e\u0026thinsp;=\u0026thinsp;29, 54.7%) and of these, 12 (22.6%) had episodes lasting less than one minute, while 22 (41.5%) experienced episodes lasting less than three minutes. The distribution showed a steep decline after the first minute, with progressively fewer patients experiencing longer durations and only a small number having episodes lasting up to 15 minutes.\u003c/p\u003e\n \u003cp\u003eWe further evaluated the timing of the first clinically important hypotensive episode (Fig. \u003cspan class=\"InternalRef\"\u003e4\u003c/span\u003ec); a peak was observed within the first minute post-PHEA. The distribution then tapers off, with fewer patients encountering their first absolute hypotensive episode beyond this time and a small proportion extending to minute 10.\u003c/p\u003e\n \u003cp\u003eFigure \u003cspan class=\"InternalRef\"\u003e4\u003c/span\u003ed illustrates the distribution of clinically important hypotensive episode durations post-PHEA. The duration of hypotensive episodes varied with the median duration of clinically important hypotension being 10 minutes (IQR 7\u0026ndash;14).\u003c/p\u003e\n\u003c/div\u003e\n\u003ch3\u003ePrediction of post-PHEA absolute hypotension\u003c/h3\u003e\n\u003cp\u003eVariables were then explored to determine their relationship with predicting post-PHEA absolute hypotension (supplementary Table\u0026nbsp;1). In the univariate analysis pre-PHEA clinically important hypotension emerged as a significant predictor with a substantial positive association. Pre-PHEA absolute hypotension also demonstrated a strong association, although this did not reach statistical significance. Other variables did not show significant associations in the univariate analysis; however, females exhibited a trend towards a higher risk of post-PHEA absolute hypotension. In the multivariate model, pre-PHEA clinically important hypotension remained a significant independent predictor of post-PHEA absolute hypotension. None of the other variables reached statistical significance in the multivariable model.\u003c/p\u003e\n\u003cp\u003eSeveral variables were associated with the post-PHEA dose of absolute hypotension in the univariate analysis (supplementary Table 2). Pre-PHEA clinically important hypotension emerged as a significant predictor, associated with an increase of 858 mmHg*min (95% CI: 564\u0026ndash;1152, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;\u0026lt;\u0026thinsp;0.001) when compared with pre-PHEA normotensive patients. Similarly, pre-PHEA absolute hypotension was associated with a higher dose, contributing an additional 464 mmHg*min (95% CI: 13.6\u0026ndash;915, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.044). Weight and initial GCS were also significant, with increases of 501 mmHg*min (95% CI: 18.4\u0026ndash;984, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.042) and 352 mmHg*min (95% CI: 120\u0026ndash;585, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.003), respectively. Meanwhile, MOI, age and time-to-PHEA did not show statistically significant associations.\u003c/p\u003e\n\u003cp\u003eIn the multivariable analysis, pre-PHEA clinically important hypotension remained a strong independent predictor, associated with an increase of 802 mmHg*min (95% CI: 504\u0026ndash;1100, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;\u0026lt;\u0026thinsp;0.001). Similarly, pre-PHEA absolute hypotension was independently associated with an increase of 573 mmHg*min (95% CI: 55.9\u0026ndash;1090, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.030). Female sex was a significant predictor, associated with an additional 327 mmHg*min (95% CI: 120\u0026ndash;534, \u003cem\u003ep\u003c/em\u003e\u0026thinsp;=\u0026thinsp;0.002) compared to male sex. Other factors, including age, weight, initial GCS, time-to-PHEA, and MOI were not significantly associated.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eTo our knowledge this is the first study to utilise IBP monitoring to analyse post-PHEA absolute hypotension in suspected TBI patients. We observed a high incidence of absolute hypotension following PHEA (\u003cem\u003en\u003c/em\u003e\u0026thinsp;=\u0026thinsp;53, 37.9%) compared to previous studies (\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e, \u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e, \u003cspan citationid=\"CR26\" class=\"CitationRef\"\u003e26\u003c/span\u003e). Notably, in a previous study conducted by our service (\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e) the incidence of absolute hypotension was less than a quarter (9%) of the rate we observed. This discrepancy likely reflects differences in frequency of BP measurement. In the previous study, two consecutive NIBP readings (at least three minutes apart) were required to meet the definition of absolute hypotension, whereas we included any single episode of absolute hypotension which was recorded every minute.\u003c/p\u003e \u003cp\u003eMeidart et al. found that continuous BP monitoring identified nearly four times as many hypotensive episodes as intermittent NIBP (\u003cspan citationid=\"CR27\" class=\"CitationRef\"\u003e27\u003c/span\u003e), while Wijnberge et al. (2022) demonstrated that intermittent NIBP missed 8% of hypotensive events (\u003cspan citationid=\"CR28\" class=\"CitationRef\"\u003e28\u003c/span\u003e). Although these studies are hospital based and their results are therefore not directly generalisable to prehospital care, they underscore the broader issue of missed hypotension with infrequent measurements, a phenomenon likely mirrored in previous prehospital studies using NIBP only.\u003c/p\u003e \u003cp\u003eOur study suggests that continuous IBP captures episodes of hypotension that would otherwise be missed, both clinically and in the published literature. Given a single episode of prehospital absolute hypotension has been associated with a doubling of mortality in TBI patients (\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e, \u003cspan citationid=\"CR24\" class=\"CitationRef\"\u003e24\u003c/span\u003e) these occult episodes of hypotension might be considered clinically relevant. However, direct comparison with prior studies that used NIBP values is difficult because the duration of a single episode of hypotension is unknown, likely variable and potentially prolonged. A deeper understanding of the impact of both the magnitude and duration of hypotension on outcomes is therefore required (\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e, \u003cspan citationid=\"CR29\" class=\"CitationRef\"\u003e29\u003c/span\u003e, \u003cspan citationid=\"CR30\" class=\"CitationRef\"\u003e30\u003c/span\u003e). Spaite et al. demonstrated a linear relationship between the dose of absolute hypotension and mortality, with a 19% increase in mortality risk for every doubling of hypotension dose (\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e). Their findings suggest that depth and duration, rather than just incidence, may be a more relevant measure. This is in-keeping with a large body of evidence from elective surgery that injury to end organs is a function of both depth and duration of hypotension (\u003cspan citationid=\"CR31\" class=\"CitationRef\"\u003e31\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eInterestingly, although we observed a high incidence of absolute hypotension compared to previous studies, the duration of these episodes was generally brief, with a significant proportion (54.7%) lasting less than six minutes post- PHEA. Of these episodes, 12 (22.6%) had absolute hypotension lasting less than one minute, and 22 (41.5%) experienced absolute hypotension lasting less than three minutes. This further supports our hypothesis that these episodes may have been missed in studies using intermittent NIBP and demonstrates the importance of considering duration alongside depth of hypotension. These short episodes of hypotension may also represent early recognition and intervention by the treating team because of continuous IBP monitoring (\u003cspan citationid=\"CR32\" class=\"CitationRef\"\u003e32\u003c/span\u003e) which would be in-keeping with previous work by Maheshwari et al. who found that continuous monitoring significantly reduced the duration of intraoperative hypotension (\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eWe found that in most cases the peak incidence (\u003cem\u003en\u003c/em\u003e\u0026thinsp;=\u0026thinsp;28, 52.8%) of absolute hypotension occurred within the first five minutes post-PHEA, coinciding with the hemodynamic effects of induction agents and positive pressure ventilation. This finding, in keeping with our clinical experience and previous studies (\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e, \u003cspan citationid=\"CR26\" class=\"CitationRef\"\u003e26\u003c/span\u003e), strongly supports siting arterial access prior to PHEA when possible. Not only does this allow the prompt detection and treatment of post-PHEA hypotension but also ensures the team is not task-fixated on arterial line insertion during a period of patient care associated with a heightened risk of hypotension. Furthermore, accurate and reliable pre-PHEA IBP monitoring may aid with the choice of induction drug and dose. When siting an arterial line, it therefore seems prudent to maximise clinical benefit by achieving this prior to PHEA whenever possible.\u003c/p\u003e \u003cp\u003eOur results show that patients with both absolute and clinically important hypotension were more likely to experience a single episode of post-PHEA absolute hypotension. Conversely, we found patients without pre-PHEA absolute or clinically important hypotension were largely spared from post-PHEA absolute hypotension, a finding similar to Price et al (\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e). These findings raise the question of whether proactive management to achieve a SBP\u0026thinsp;\u0026gt;\u0026thinsp;110 mmHg before PHEA and a careful induction regimen may mitigate some of the hemodynamic risks of PHEA, a question that warrants further investigation.\u003c/p\u003e \u003cp\u003ePre-PHEA clinically important hypotension was the only variable associated with the post-PHEA absolute hypotension in both univariate and multivariate analyses. Perhaps surprisingly, we did not observe an association of age with hypotensive episodes as others have reported (\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e, \u003cspan citationid=\"CR26\" class=\"CitationRef\"\u003e26\u003c/span\u003e, \u003cspan citationid=\"CR33\" class=\"CitationRef\"\u003e33\u003c/span\u003e), potentially due to the higher frequency of brief absolute hypotensive episodes in our cohort. This may also explain why pre-PHEA absolute hypotension was not significantly associated with post-PHEA absolute hypotension, however this may also be due to the team selecting a more reserved induction regimen.\u003c/p\u003e \u003cp\u003eAnalysis of hypotensive dose on the other hand identified lower initial GCS, heavier weight and female sex as significant predictors in univariate analysis, with female sex remaining significant in multivariate analysis. Heavier patient weight was not retained in multivariate analysis, which may have been due to the variability and inaccuracy associated with clinician estimation of weight (\u003cspan citationid=\"CR31\" class=\"CitationRef\"\u003e31\u003c/span\u003e). Lower GCS scores were similarly associated with higher doses in univariate analysis but not in multivariate models, potentially reflecting impaired compensatory mechanisms in patients with severe brain injury.\u003c/p\u003e \u003cp\u003eOur finding that female sex predicts an increased dose of post-PHEA absolute hypotension is novel and has not previously been reported. Whilst this result should be interpreted with caution due to the retrospective nature of the study and low proportion of female sex (\u003cem\u003en\u003c/em\u003e\u0026thinsp;=\u0026thinsp;32, 23%), it is not an isolated observation in prehospital trauma management (\u003cspan citationid=\"CR33\" class=\"CitationRef\"\u003e33\u003c/span\u003e) and merits further investigation.\u003c/p\u003e \u003cdiv id=\"Sec12\" class=\"Section2\"\u003e \u003ch2\u003eLimitations\u003c/h2\u003e \u003cp\u003eThere are several limitations to this study which we should acknowledge. Firstly, the absence of patient outcome data such as mortality or neurological recovery limited our ability to correlate hypotensive dose with clinical endpoints. We have described that most patients who experience absolute hypotension post-PHEA have a relatively low dose, however without patient outcome data we are unable to describe the clinical significance of this. Previous work would suggest that these low doses are not associated with poor patient outcomes (\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e), but these data were based on infrequent NIBP measurements. Large, in-hospital, peri-operative datasets suggest a linear relationship between the duration of hypotension and end-organ damage with evidence of renal and/or cardiac harm even with very brief exposure (1\u0026ndash;5 minutes). As the injured brain is arguably more sensitive to hypotensive episodes (\u003cspan citationid=\"CR34\" class=\"CitationRef\"\u003e34\u003c/span\u003e) even very short episodes of hypotension (i.e. those with low doses) may be clinically relevant. A prospective prehospital study utilising continuous IBP measurements and clinical outcomes is required to better understand this relationship.\u003c/p\u003e \u003cp\u003eSeveral factors influence the accuracy of SBP as measured by IBP monitoring. Changes in the position of the transducer relative to the patient in the vertical axis can lead to significant under or overestimates of the true BP, a significant risk in the dynamic environment of prehospital care. To mitigate this all clinicians at KSS secure the transducer with tape to the regimental badge area of the lower deltoid for radial arterial lines and upper thigh for common femoral arterial lines. Nevertheless, unrecognised movement of the transducer may have led to erroneous readings. Similarly, underdamping and overdamping can lead to overestimation and underestimation of the true SBP respectively. KSS utilise the same transducer set up for every patient, minimising but not eliminating the risk of these artifacts.\u003c/p\u003e \u003cp\u003eSeventeen (5.57%) cases were excluded from this study due to arterial line malfunction identified by clinicians on scene. This may be due to discontinuity at any point from the artery to the transducer or failure of the mechanical and/or electrical components within the system. It\u0026rsquo;s possible that in this cohort of patients, arterial line placement was technically more challenging leading to subsequent displacement or a markedly damped trace. We cannot elucidate the aetiology of malfunction for each case from documentation but recognise this may be an important group of patients who were excluded from this study.\u003c/p\u003e \u003cp\u003eRegarding diagnosis of TBI, this was a retrospective study in which patients were included based on the teams\u0026rsquo; suspicion of TBI, as opposed to a confirmed diagnosis following diagnostic imaging. It is therefore possible that some patients included in this study did not have intracranial pathology, however this reflects the limitations of current prehospital diagnostics and allows extrapolation of results to clinical practice.\u003c/p\u003e \u003cp\u003eThe times of induction and intubation were recorded by the enhanced care team manually using recorded electronic patient record time stamps. Although cases were reviewed to address any apparent timing issues, this may mean the recorded time of PHEA and the actual time were not identical. Therefore, a pre-PHEA hypotensive event occurring one minute before the documented induction time could be related to the PHEA rather than the underlying pathology.\u003c/p\u003e \u003cp\u003eSeveral patients had their arterial line placed post-PHEA which may represent those who were clinically deteriorating, whose need for clinical intervention outweighed the benefit of real-time monitoring or those in whom arterial line placement was technically more challenging and abandoned pre-PHEA. This exclusion may bias our results towards underestimating the overall risk of post-PHEA hypotension.\u003c/p\u003e \u003cp\u003eWe recognise our assumption that the increased incidence of absolute hypotension in this study compared to prior published literature reflects increased frequency of measurement as opposed to a true increased incidence. Whilst it is possible that there was a lower true incidence of absolute hypotension in previous studies this is not in-keeping with prior work comparing IBP and NIBP (\u003cspan citationid=\"CR27\" class=\"CitationRef\"\u003e27\u003c/span\u003e, \u003cspan citationid=\"CR28\" class=\"CitationRef\"\u003e28\u003c/span\u003e) nor have there been any substantial changes in our service that would explain such a finding.\u003c/p\u003e \u003cp\u003eConstraints of our data collection software meant we were unable to evaluate continuous IBP recordings and instead relied on single entries at one-minute intervals. While this is more frequent and reliable than NIBP, there still exists the risk of missed hypotensive episodes, albeit very brief.\u003c/p\u003e \u003cp\u003eThe reliance on estimated weights introduced variability into our data. While weight was a borderline predictor of hypotensive dose in univariate analysis, this was based on clinician estimation of weight, which is known to be inaccurate (\u003cspan citationid=\"CR35\" class=\"CitationRef\"\u003e35\u003c/span\u003e) undermining the validity of this finding.\u003c/p\u003e \u003cp\u003eFinally, it was not possible to review the impact of vasopressor drugs such as adrenaline, noradrenaline, ephedrine or metaraminol on hypotensive episodes, as these are most often documented as the total amount given and not time-stamped at the exact time of administration. As such, clinical teams may have seen a hypotensive episode occur and treated it immediately with a vasopressor in less than a minute, hiding an incidence of hypotension.\u003c/p\u003e \u003c/div\u003e"},{"header":"Conclusion","content":"\u003cp\u003eTo our knowledge this is the first study to utilise IBP monitoring to analyse post-PHEA absolute hypotension in patients with suspected TBI. We report a high incidence of absolute hypotension compared to previous studies utilising NIBP, likely reflective of the increased frequency of measurements. We demonstrate the potential value of considering dose when analysing IBP measurements, as despite an increased incidence of absolute hypotension, most of these episodes were of short duration and low dose. These findings also suggest benefit in pre-PHEA IBP monitoring. Further studies utilising continuous IBP monitoring to analyse dose of hypotension and its association with clinical outcome measures such as mortality and long-term neurological function are required.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003eBP\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Blood pressure\u003c/p\u003e\n\u003cp\u003eCI\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u0026nbsp;Confidence interval\u003c/p\u003e\n\u003cp\u003eDBP\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u0026nbsp;Diastolic blood pressure\u003c/p\u003e\n\u003cp\u003eGCS \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u0026nbsp;Glasgow Coma Scale\u003c/p\u003e\n\u003cp\u003eIBP\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u0026nbsp;Invasive arterial blood pressure\u003c/p\u003e\n\u003cp\u003eIQR\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Interquartile range\u003c/p\u003e\n\u003cp\u003eKg\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Kilogram\u003c/p\u003e\n\u003cp\u003eKSS\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u0026nbsp;Air Ambulance Charity Kent Surrey Sussex\u003c/p\u003e\n\u003cp\u003eNIBP\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Non-invasive blood pressure\u003c/p\u003e\n\u003cp\u003ePHEA\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Prehospital emergency anaesthesia\u003c/p\u003e\n\u003cp\u003eSBP\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u0026nbsp;Systolic blood pressure\u003c/p\u003e\n\u003cp\u003eSD\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u0026nbsp;Standard deviation\u0026nbsp;\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eSOP\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u0026nbsp;Standard operating procedure\u003c/p\u003e\n\u003cp\u003eTBI\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u0026nbsp;Traumatic brain injury\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthical approval and consent to participate\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe project met the National Institute for Healthcare Research (NIHR, UK) criteria for service evaluation and formal ethical approval was waived.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and materials\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe datasets used and/or analysed during the current study are available from the corresponding author on reasonable request.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare that they have no competing interests.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAll authors fulfilled the ICMJE criteria for authorship. SHB conceived the study. LB provided supervisor oversight. SC retrieved the data. SHB/SC/JB/JG analysed the data and performed the statistical analysis. SHB/NH/JB/JG drafted the manuscript. All authors read and approved the final manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgements\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWe are grateful for the support of our clinical and operational support colleagues at Air Ambulance Charity Kent Surrey Sussex for providing both clinical governance and operational experience to support the implementation of invasive arterial blood pressure monitoring at our service.\u0026nbsp;\u003cstrong\u003e\u003cbr\u003e\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eLee JW, Wang W, Rezk A, Mohammed A, Macabudbud K, Englesakis M, et al. Hypotension and Adverse Outcomes in Moderate to Severe Traumatic Brain Injury: A Systematic Review and Meta-Analysis. 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QJM. 2012;105(8):769\u0026ndash;74.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"Non-invasive blood pressure, Invasive arterial blood pressure, Absolute hypotension, Clinically important hypotension, Dose of hypotension, Traumatic brain injury, Prehospital emergency anaesthesia, Helicopter emergency medical service, Critical care","lastPublishedDoi":"10.21203/rs.3.rs-6229140/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-6229140/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cb\u003eBackground\u003c/b\u003e\u003c/p\u003e \u003cp\u003eThe prehospital management of moderate/severe traumatic brain injury (TBI) centres on the prevention of secondary brain injury. In some cases, prehospital emergency anaesthesia (PHEA) may be required to provide optimal neuroprotective care. Continuous invasive arterial blood pressure (IBP) monitoring is increasingly utilised in this cohort. PHEA can result in significant blood pressure changes, particularly around induction. IBP allows for a more targeted approach to blood pressure management in these patients. The aim of this study was to analyse hypotension frequency, depth and duration in suspected TBI patients monitored with IBP before PHEA.\u003c/p\u003e\u003cp\u003e\u003cb\u003eMethods\u003c/b\u003e\u003c/p\u003e \u003cp\u003eA retrospective analysis of suspected TBI patients attended by Air Ambulance Charity Kent Surrey Sussex who received IBP prior to PHEA between the 6 January 2022 and the 6 July 2024. The magnitude and duration of \u0026lsquo;absolute hypotension\u0026rsquo; (systolic blood pressure (SBP)\u0026thinsp;\u0026lt;\u0026thinsp;90mmHg) were combined to establish a \u0026lsquo;dose\u0026rsquo; of absolute hypotension (mmHg*min). The primary endpoints were the incidence and dose of absolute hypotension.\u003c/p\u003e\u003cp\u003e\u003cb\u003eResults\u003c/b\u003e\u003c/p\u003e \u003cp\u003e305 patients were identified, of which 140 (45.9%) were included. Median age was 58 years (interquartile range (IQR) 42\u0026ndash;73), predominant sex was male (\u003cem\u003en\u003c/em\u003e\u0026thinsp;=\u0026thinsp;108, 77%) and median Glasgow Coma Scale (GCS) was 6/15 (IQR 4.0\u0026ndash;7.5). Thirteen patients (9.3%) were found to have an episode of absolute hypotension pre-PHEA, increasing to 53 (37.9%) post-PHEA. Twenty-five patients (47.2%) had an initial absolute hypotensive episode occur after five minutes post-PHEA, with a median duration of three minutes (IQR 1.0\u0026ndash;4.5). The median dose of absolute hypotension was 144 mmHg*min (IQR 3.75\u0026ndash;1675.5). Twenty-five patients (17.9%) had \u0026lsquo;clinically important hypotension\u0026rsquo; (SBP\u0026thinsp;\u0026lt;\u0026thinsp;110mmHg) pre-PHEA, increasing to 80 post-PHEA (57.1%). Pre-PHEA absolute and clinically important hypotension were found to be associated with both the incidence and dose of post-PHEA absolute hypotension.\u003c/p\u003e\u003cp\u003e\u003cb\u003eConclusion\u003c/b\u003e\u003c/p\u003e \u003cp\u003eThis study highlights a higher incidence of absolute hypotension using IBP compared to previous studies utilising intermittent non-invasive blood pressure monitoring. While post-PHEA absolute hypotension was common, over half of these events were brief (less than five minutes). These findings highlight the importance of analysing depth and duration of hypotension and suggest the need for prehospital outcome-based studies utilising continuous IBP.\u003c/p\u003e","manuscriptTitle":"Invasive arterial blood pressure monitoring to detect post-intubation hypotension in patients who receive a prehospital emergency anaesthetic for suspected traumatic brain injury","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-03-27 05:33:51","doi":"10.21203/rs.3.rs-6229140/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"7df3c330-fd8b-4cf9-8138-2893b974323d","owner":[],"postedDate":"March 27th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2025-04-13T03:53:26+00:00","versionOfRecord":[],"versionCreatedAt":"2025-03-27 05:33:51","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-6229140","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-6229140","identity":"rs-6229140","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}