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A retrospective observational study examining the admission arterial to end-tidal carbon dioxide gradient in intubated major trauma patients.

Airway and ventilatory support are cornerstones of trauma management and are commonly instituted in the field by ambulance personnel. Indications for intubation include cardiac and respiratory arrest, and a Glasgow Coma Score (GCS) of less than 10 associated with absent airway reflexes, traumatic and non-traumatic brain injury, hypoxic brain injury and status epilepticus (1). Both hyperventilation and hypoventilation may worsen clinical outcomes and early control of arterial carbon dioxide partial pressure (PaCO2) is desirable (2-5). While blood gas analysis remains the gold standard of gauging optimal ventilation, sampling and assessment of this variable is only practical in a hospital setting(6). Conversely, non-invasive end-tidal carbon dioxide measurement (PetC[O.sub.2]) may be used in almost all environments to provide an estimate of PaC[O.sub.2] via its approximation of alveolar carbon dioxide tension7-9. Multiple factors may impact on the relationship between PaC[O.sub.2] and PetC[O.sub.2]. We sought to describe the pattern of PaC[O.sub.2] and PetC[O.sub.2] as well as the frequency of hypoventilation in head-injured patients in the intubated major trauma population arriving at our institution.

MATERIALS AND METHODS

The study was approved by the Human Research Ethics Committee at the Alfred Hospital. The Alfred Hospital in Victoria is a state service hospital for trauma patients, receiving 45,000 emergency patients per year (10). One hundred consecutive major trauma patients who were intubated and admitted to the Alfred Hospital Trauma Centre were identified from the Alfred Trauma Registry. Major trauma was defined as death after injury, injury severity score (ISS) greater than 15 or need for admission to the intensive care unit for ventilation, or major intracranial, intra-abdominal, pelvic or spinal surgery (11). Patients were excluded if admission blood gas was not obtained within 60 minutes of arrival, PetC[O.sub.2] was not recorded on arrival (edPetC[O.sub.2]), patients were transferred from another hospital, patients suffered a cardiac arrest in transfer or if the time of the accident occurred more than eight hours prior to presentation.

Confidential, de-identified data were collated from the registry and medical records that included patient demographics, accident profile, ISS, emergency department blood gas (partial pressures of arterial oxygen [edPa[O.sub.2]] and carbon dioxide [edPaC[O.sub.2]], arterial pH [edpH] and arterial bicarbonate concentration [edHC[O.sub.3.sup.-]]), and biochemistry profile, as well as retrieval parameters and emergency department vital signs. The edPetC[O.sub.2] was measured using calibrated inline infrared capnography.

Descriptive statistics of the data are presented as a mean and standard deviation. We introduced arbitrary definitions for extrapolation to clinical scenarios. Severe traumatic brain injury was defined as a patient's scene GCS of less than nine. Hypotension was defined as a systolic blood pressure less than 90 mmHg. Hypoxia was defined as a pulse oximeter recording less than 90%. Hyperventilation and hypoventilation were defined as an edPaC[O.sub.2] <35 mmHg and an edPaC[O.sub.2] >45 mmHg respectively. Using univariate and multivariate analysis we determined factors significantly associated with an increased gradient between edPaC[O.sub.2] and edPetC[O.sub.2] (the edPa-etC[O.sub.2] gradient).

RESULTS

Seventy-five male and 25 female patients were included with a mean (standard deviation) age of 37 (18). The scene time was 36 minutes (21) and transit time 67 minutes (32). The mean scene GCS (ambGCS) was 6 (3.2) and ISS was 32 (13.2). Baseline statistics of the study population are shown in Table 1.

The mean edPaC[O.sub.2] was 47 mmHg (11), the mean edPetC[O.sub.2] was 31 mmHg (6) and the mean edPaetC[O.sub.2] gradient was 15 mmHg (10). Nearly half (49%) of the patients had an edPaC[O.sub.2] >45 mmHg. Frequency tabulation of edPaC[O.sub.2] by severity of head injury (Table 2) demonstrated that in patients with a scene GCS <9 (80% of the study group), 42 out of the 80 (52.5%) had an edPaC[O.sub.2] >45 mmHg. This was no less frequent (P=0.55) than in the group with a GCS >9.

A comparison between the baseline characteristics of the hypoventilated and combined hyperventilated/ normoventilated (edPaC[O.sub.2] 45 mmHg) groups is shown in Table 3. In the hypoventilated group there was a statistically significant decrease in the ambSp[O.sub.2] and edPa[O.sub.2]. Although highly statistically significant, there was only a 5 mmHg difference between the two groups' edPetC[O.sub.2]. This suggests that the large 11 mmHg difference between the groups' edPa-etC[O.sub.2] gradients is due mainly to the 16 mmHg edPaC[O.sub.2] difference. A significant decrease in edpH and increase in edPaC[O.sub.2] in the absence of a significant difference in edHC[O.sub.3]-suggests a largely respiratory-based acidosis. There was no difference in ISS scores between the groups.

Univariate regression modelling patient factors that might predict a larger edPa-etC[O.sub.2] gradient showed significance in ambulance hypoxia (P <0.0001), arrival hypotension (P <0.012) and ISS (P <0.004). There was no evidence that ambGCS as a continuous or as a dichotomous variable was a significant predictor of either a larger edPa-etC[O.sub.2] gradient or edPetC[O.sub.2].

Under multivariate analysis, adjusting for confounding factors, only ambSp[O.sub.2] (r=-0.56, CI -0.81 to -0.31, P <0.001) and [edP.sub.a][O.sub.2](r=-0.02, CI -0.03 to -0.01, P <0.002) maintained statistical significance as predictors of an increased edPa-etC[O.sub.2] gradient. As continuous variables however, these measurements are not clinically useful in the early prediction of an increased edPa-etC[O.sub.2] gradient. Hence when repeating the analysis using dichotomised data, only scene hypoxia, scene non-hypotension (SBP >90 mmHg) and arrival hypotension were predictors of an increased edPa-etC[O.sub.2] gradient. These three dichotomised parameters had an adjusted r2 of 0.44 indicating their ability to explain 44% of the observed variability in the edPa-etC[O.sub.2] gradient. Overall, 14 patients had scene hypoxia (mean edPa-etC[O.sub.2] gradient of 28 mmHg), and this was associated with an edPa-etC[O.sub.2] gradient of almost 15 mmHg higher than those with an ambSp[O.sub.2] greater than 90% (mean edPa-etC[O.sub.2] of 13 mmHg).

DISCUSSION

Early blood gas analysis (within one hour of arrival) of the study population showed that half of the intubated major trauma patients arriving at the hospital's trauma centre had a PaC[O.sub.2] >45 mmHg. This is of concern, as over 80% of these patients had a scene GCS <9: a potentially head-injured population in which PaC[O.sub.2] control is a key management principle (12). Overall, the mean Pa-etC[O.sub.2] gradient was 15 mmHg, and up to 55 mmHg in one case.

Physiological deadspace limits the approximation of PaC[O.sub.2] by PetC[O.sub.2] manifesting as the Pa-etC[O.sub.2] gradient. Physiological deadspace is the sum of all parts of the tidal volume that do not participate in gas exchange (anatomical deadspace and alveolar dead space) (9). While a negligible gradient exists in health, it is an increase in alveolar deadspace in the hypovolaemic trauma patient that contributes to regional ventilation-perfusion mismatch and the observed Pa-etC[O.sub.2] gradient. The data from our study confirm earlier comments on the potential for PetC[O.sub.2] to be a misleading guide for adequacy of Ventilation (6,13,14). This is relevant as ventilation (via a self-inflating Laerdel [TM] or Ambu [TM] bag) in the pre-hospital setting is typically titrated to PetC[O.sub.2] and not with a ventilator with spirometry analysis.

It is difficult to interpret the cardiovascular parameters that predicted an increased Pa-etC[O.sub.2] gradient. Arrival hypotension contributing to physiological deadspace would understandably predict the increased gradient, however no metabolic marker of hypoperfusion showed a similar correlation. Furthermore, scene hypertension actually predicted the increased gradient. As only 14 patients had scene hypotension, this statistic may represent a Type I error or may be the influence of hypercapnic mediated sympathetic stimulation. A greater sample size would have better delineated these variables. The most clinically useful predictor of an increased Pa-etC[O.sub.2] gradient (and tendency for hypoventilation) was scene hypoxia which predicted a Pa-etC[O.sub.2] gradient 16 mmHg greater than those patients with a scene oxygen saturation greater than 90%.

Variable guidelines for target PaC[O.sub.2] exist for the ventilatory management of patients with traumatic brain injury. The Association for Anaesthetists of Great Britain and Ireland's guidelines state that the target PaC[O.sub.2] should be 33 to 37 mmHg (15). In the absence of evidence, The Brain Trauma Foundation's Guidelines for Prehospital Management of Traumatic Brain Injury suggest aiming for normal ventilation defined as 10 breaths per minute in adults (12). The Brain Trauma Foundation, The American Heart Association's Advanced Cardiac Life Support Guidelines and the Australian College of Surgeons all caution hyperventilation (PaC[O.sub.2] <30 mmHg) in the absence of signs of cerebral herniation, emphasising the importance of avoidance of hypoxia and hypoventilation (12,16,17). We have dichotomised data on the basis of hypoventilation defined as a PaC[O.sub.2] >45 mmHg, but as the above guidelines suggest a lower target range is not unreasonable in this population. Had we used 40 mmHg as a cut-off, 75% of all patients and 74% of patients with a GCS <9 would have been 'hypoventilated'.

Our study's results have shown that an alarming number of intubated trauma patients may be under-ventilated during the acute care phase as evident by the key end-point of ventilation: the PaC[O.sub.2]. We can speculate upon the reasons for the hypoventilation. Neither the ventilatory modes nor respiratory parameters are of great concern because inherent across the acute care phase would have been the intent to provide adequate ventilation. The early management of severe trauma is a dynamic and changing environment. The patients would have had a sequence of (scene) manual ventilation possibly followed by a period of mechanical ventilation, then again a period of manual ventilation during the transport phase of care. Further, again in the emergency department, they would have had another period of mechanical ventilation. The ventilatory parameters during these phases are not easily measurable or retrievable and in the end, the key point remains. That is, in the early management of severely injured patients ventilation as measured by arterial carbon dioxide was inadequate in a significant percentage of patients. This is a significant learning point.

Given the challenge of interpreting PetC[O.sub.2] in the face of physiological deadspace, targeting a lower PetC[O.sub.2] is potentially deleterious to the patient as our study has shown such wide-ranging Pa-etC[O.sub.2] gradients. For example, targeting a PetC[O.sub.2] of 30 mmHg may lead to iatrogenic hyperventilation, hypocapnia and associated cerebral hypoperfusion in a potentially head-injured population where brain perfusion is critical. However, the subgroup of patients who are found by ambulance paramedics to be hypoxic have a predictably larger Pa-etC[O.sub.2] gradient, and a lower PetC[O.sub.2] could be targeted in this group for optimal ventilation.

The retrospective nature of this study is a limitation on the application of its results. Furthermore, contrary to expectation, patients with more severe injuries and indicators of shock (increased heart rate, hypotension and low pH) did not consistently show evidence of greater physiological deadspace manifesting as a larger Pa-etC[O.sub.2] gradient. This may be due to confounding errors, documentation and data collection errors, the study population size not capturing a representative subgroup, or because we required higher fidelity markers of shock. A prospective study addressing these issues and one that focuses on the subgroup of hypoxic trauma patients might lead to targeted, pre-hospital and emergency department ventilatory management in these patients.

Accepted for publication on September 20, 2009.

REFERENCES

(1.) Metropolitan and Rural Ambulance Service. Clinical Practice( Guidelines (Version 7- 200906) 2006.

(2.) Davis DP, Dunford JV, Poste JC, Ochs M, Holbrook T, Fortlage DB et al. The impact of hypoxia and hyperventilation on outcome after paramedic rapid sequence intubation of severely head injured patients. J Trauma 2004; 57:1-10.

(3.) Diringer MN, Videen TO, Yundt K, Zazulia AR, Aiyagari V, Dacey RG. Regional cerebrovascular and metabolic effects of hyperventilation after severe traumatic brain injury. J Neurosurg 2002; 96:103-108.

(4.) Muizelaar JP, Marmarou A, Ward JD, Kontos HA, Choi SC, Becker DP et al. Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial. J Neurosurg 1991; 75:731-739.

(5.) Chestnut RM, Marshall LF, Klauber MR, Blunt BA, Baldwin N, Eisenberg HM et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma 1993; 34:216-222.

(6.) Kerr ME, Zempsky JR, Sereika S, Orndoff PR, Rudy EB. Relationship between arterial carbon dioxide and end-tidal carbon dioxide in mechanically ventilated adults with severe head trauma. Crit Care Med 1996; 24:785-790.

(7.) Carlon GC, Cole R, Miodownik S, Kopec I, Groeger JS. Capnography in mechanically ventilated patients. Crit Care Med 1988; 16:550-556.

(8.) Mackersie RC, Karagianes TG. Use of end-tidal carbon dioxide tension for monitoring induced hypocapnia in head-injured patients. Crit Care Med 1990; 18:764-765.

(9.) Lumb AB. In: Nunn's Applied Respiratory Physiology, 6th ed. Philadelphia, Pennsylvannia: Elsevier/Butterworth Heinemann 2005. p. 120-121.

(10.) Alfred Health Emergency and Trauma Centre. From http:// www.alfred.org.au/Department.aspx?ID = 141 Accessed December 2008.

(11.) Acute Health Division, Department of Human Services. Review of Trauma and Emergency Services 1999. Formal Report, Victoria 1999.

(12.) The Brain Trauma Foundation. Guidelines for Prehospital Management of Traumatic Brain Injury. New York 2000.

(13.) Russell GB, Graybeal JM. End-tidal carbon dioxide as an indicator of arterial carbon dioxide in neurointensive care patients. J Neurosurg Anesthesiol 1992; 4:245-249.

(14.) Isert P. Control of carbon dioxide levels during neuroanaesthesia: current practice and an appraisal of our reliance upon capnography. Anaesth Intensive Care 1994; 22:435-441.

(15.) Recommendations for the Safe Transfer of Patients with Brain Injury, Working party for The Association of Anaesthetists of Great Britain and Ireland, London 2006.

(16.) Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 6: advanced cardiovascular life support: section 8: postresuscitation care. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation 2000; 22:102 (8 Suppl):166-171.

(17.) The Management of Acute Neurotrauma in Rural and Remote Locations: A Set of Guidelines for the Care of Head and Spinal Injuries. J Clin Neurosci 1999; 6: 85-93.

J. HILLER *, A. SILVERS [[dagger]], D. R. McILROY [[double dagger]], L. NIGGEMEYER [[double dagger]], S. WHITE [[section]]

Department of Anaesthesia and Perioperative Medicine, Alfred Hospital, Melbourne, Victoria, Australia

* M.B., B.S (Hons.), Anaesthesia Fellow.

[[dagger]] M.B., B.S (Hons.), F.A.N.Z.C.A., Specialist Anaesthetist.

[[double dagger]] Trauma Program Manager.

[[section]] Trauma Registry.

Address for correspondence: Dr A. Silvers, Department of Anaesthesia and Perioperative Medicine, The Alfred Hospital, Commercial Road, Prahran, Vic. 3181.
Table 1
Baseline characteristics of study population

                           Mean (SD)     Median   Range

Scene time (min)           36 (21)       33       8-180
Transit time (min)         67 (32)       61       10-220
ambSBP (mmHg)              125 (34)      125      50-210
ambHR (bpm)                103 (27)      102      50-160
ambRR (bpm)                19 (8)        18       3-40
ambSp[O.sub.2] (%)         95 (7         98       56-100
ambGCS                     6 (3)         6        3-14
edpH                       7.31 (0.11)   7.33     6.81-7.50
edPaC[O.sub.2] (mmHg)      47 (11)       45       26-83
edPa[O.sub.2] (mmHg)       315 (152)     313      54-617
edHC[O.sub.3]-(mmol/l)     22.8 (3.3     23       8-29
edPetC[O.sub.2] (mmHg)     31 (6)        32       17-46
edPa-etC[O.sub.2] (mmHg)   15 (10)       13       0-55
edSBP (mmHg)               146 (36)      151      62-240
edHR (bpm)                 108 (22)      107      60-170
edTemp ([degrees] C)       35.1 (1.5)    35.3     30.6-37.9
Injury severity score      32 (13.2)     33       1-66

First recorded scene vital signs heart rate (ambHR), respiratory
rate (ambRR), systolic blood pressure (ambSBP) and oxygen
saturation (ambSp[O.sub.2]). Emergency department arrival systolic
blood pressure (edSBP), temperature (edTemp) and heart rate
(edHR). GCS=Glasgow Coma Score.

Table 2
edPaC[O.sub.2] frequency compared with ambGCS

edPaC[O.sub.2]   ambGCS <9   ambGCS [greater than or equal to] 9  Total

25-29            2           0                                     2
30-34            4           1                                     5
35-39            15          3                                     18
40-44            17          5                                     22
45-49            19          2                                     21
50-59            14          7                                     21
>60              9           2                                     11
Total            80          20                                    100

GCS=Glasgow Coma Score

Table 3
Comparison of hyper/normoventilated and hypoventilated groups.
Mean (SD)
                          Normal/           Hypoventilated   P value
                          Hyperventilated

Age                       38 (20)           35 (16)          0.40
Scene time (min)          35 (26)           37 (15)          0.62
Transit time (min)        67 (35)           68 (29)          0.89
ambSBP (mmHg)             124 (33)          127 (35)         0.61
ambHR (bpm)               101 (26)          105 (29)         0.56
ambRR (bpm)               18 (7)            19 (9)           0.55
ambSp[O.sub.2] (%)        97 (5)            93 (8.5)         0.004
edpH                      7.38 (0.06)       7.24 (0.10)      <0.0001
edPaC[O.sub.2] (mmHg)     39 (4.4)          55 (9.5)         <0.0001
edPa[O.sub.2] (mmHg)      371 (134)         258 (149)        0.0001
edHC[O.sub.3]-(mmol/l)    22 (3.3)          23 (3.2)         0.61
edPetC[O.sub.2] (mmHg)    29 (4.5)          34 (6.4)         <0.0001
edPa-etC[O.sub.2]         10 (5.1)          21 (10.6)        <0.0001
edSBP (mmHg)              144 (34)          148 (39)         0.64
edHR (bpm)                102 (19)          114 (25)         0.009
edTemp ([degrees] C)      35.1 (1.5)        35.0 (1.4)       0.55
Injury severity score     30.4 (13.3)       34.4 (13)        0.13


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Author:Hiller, J.; Silvers, A.; McIlroy, D.R.; Niggemeyer, L.; White, S.
Publication:Anaesthesia and Intensive Care
Article Type:Report
Geographic Code:8AUST
Date:Mar 1, 2010
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