Published online before print
April 9, 2007, 10.1097/PSY.0b013e3180417d04
Psychosomatic Medicine 69:256-261 (2007)
© 2007 American Psychosomatic Society
Tonic and Phasic Heart Rate as Predictors of Posttraumatic Stress Disorder
Meaghan L. O’Donnell, PhD,
Mark Creamer, PhD,
Peter Elliott, PhD and
Richard Bryant, PhD
From the Australian Centre for Posttraumatic Mental Health (M.L.O., M.C., P.E.), Victoria, Australia; Department of Psychiatry (M.L.O., M.C., P.E.), University of Melbourne, Melbourne, Australia; National Trauma Research Institute (M.L.O.); and School of Psychology (R.B.), University of New South Wales, Australia.
Address correspondence and reprint requests to Meaghan O’Donnell, Australian Centre for Posttraumatic Mental Health, P.O. Box 5444, West Heidelberg, Victoria 3091, Australia. E-mail: mod{at}unimelb.edu.au
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ABSTRACT
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Objective: To examine the relationship between acute measures of a) heart rate (HR) immediately after traumatic injury, b) tonic (resting) HR at 1 week post injury, c) phasic (aroused) HR at 1 week post injury, and d) somatic symptoms of arousal in the prediction of subsequent posttraumatic stress disorder (PTSD). Fear conditioning models propose that HR reactivity shortly after trauma may predict PTSD.
Method: In a longitudinal study, consecutive injury survivors (n = 197) admitted to a hospital trauma service were assessed within 1 week and at 12 months post injury. HR was assessed by paramedics at the site of the trauma and pulse oximetry technology at 1 week post trauma. Somatic symptoms of arousal were measured using the somatic scale on the Beck Anxiety Inventory (BAI). PTSD was assessed using the Clinician Administered PTSD Scale at 12 months.
Results: At 12 months post injury, PTSD was diagnosed in 10% of participants. Only HR change scores (phasic – tonic HR) and BAI scores significantly predicted later PTSD.
Conclusions: These findings question the clinical usefulness of tonic HR as a biological marker of later PTSD. The finding that HR reactivity (phasic – tonic) predicts later PTSD has theoretical importance. The strongest predictor of later PTSD was somatic arousal.
Key Words: posttraumatic stress disorder • heart rate • psychophysical arousal • fear conditioning
Abbreviations: HR = heart rate; PTSD = posttraumatic stress disorder; MTBI = mild traumatic brain injury; BAI = Beck Anxiety Inventory; CAPS = Clinician Administered PTSD Scale
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INTRODUCTION
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There is increasing interest in factors occurring immediately after trauma exposure that predict subsequent posttraumatic stress disorder (PTSD). Although the majority of individuals experience an initial fear response, most people seem to adapt to the traumatic experience in the ensuing months. This pattern has been observed in survivors of assault, motor vehicle accidents, and terrorist attacks (1–4). Although some evidence points to initial symptoms or cognitive factors that predict subsequent PTSD, these factors have limited predictive ability and require time-consuming measures (5).
Fear conditioning models have led to the exploration of early biological markers of PTSD. These models posit that exposure to a traumatic event (unconditioned stimulus) leads to a strong fear reaction (unconditioned response), which becomes conditioned to many stimuli associated with the traumatic event. Accordingly, when people are exposed to reminders of the trauma (conditioned stimuli), they experience a strong fear reaction (conditioned response) (6). Fear conditioning models propose that stress hormones (neuropeptides and catecholamines) released at the time of the trauma contribute to fear conditioning and overconsolidation of trauma memories (7–9). This proposal is consistent with animal studies that indicate that epinephrine administration after an aversive experience enhances fear conditioning (10). Increased heart rate (HR) after trauma represents a marker for this adrenergic activity.
Fear conditioning models posit two general predictions in trauma-exposed populations. First, the adrenergic increase after trauma may be reflected in increased resting HR (tonic HR), which may represent a marker of fear conditioning that leads to chronic PTSD. Eight longitudinal studies published to date have shown a relationship between acute tonic HR and the subsequent development of PTSD in survivors post injury (11–18) (Table 1). In the first study, Shalev and colleagues reported a prospective study that identified significantly higher tonic HR measurements obtained in the emergency department (ED) in trauma patients who developed PTSD by 4 months compared with those who did not develop PTSD (16). Bryant and colleagues found that tonic HR at 1 week after trauma exposure was higher in those who developed PTSD than those who did not develop PTSD at 6 months post trauma exposure (13). Using the same sample, Bryant and Harvey (12) found that those who developed delayed-onset PTSD also had higher acute tonic HRs, as did those who developed PTSD at 2 years post trauma exposure (19). Increased tonic HR shortly after trauma has also been associated with subsequent PTSD in samples of survivors of traumatic injury (15,18), severe traumatic brain injury (11), and also in injured children (14). This relationship has led some researchers to adopt HR cut-offs as a screening criterion for both pharmacological (20,21) and psychological (22) early intervention trials, and others to suggest that the relationship between tonic HR and PTSD has public health implications (18). It should be noted, however, that this pattern has not been observed in all research samples (23,24) or has been only partially replicated (17). Although the study by Blanchard et al. (23) had some methodological flaws (such as its retrospective methodology and nonrepresentative sample), some research does not support a clear relationship between early HR increase and PTSD development.
The second proposition of fear conditioning models is that there will be hyperreactivity (conditioned responses) to conditioned stimuli. Robust evidence demonstrates that people with PTSD are strongly reactive when they are thinking about their traumatic experience (25–30). This research has been conducted on samples of individuals with chronic PTSD. There is also evidence that people with acute stress disorder within a month of trauma do display physiological reactivity during the narration of their trauma (31). To date, there is no research determining the extent to which reactivity during the acute phase is predictive of subsequent PTSD.
The current study had a number of aims. First, we aimed to replicate the findings of earlier studies that suggest that those who develop PTSD will show significantly increased tonic HR in the early aftermath of trauma. We recorded two measurements of tonic HR: the first HR measurement was recorded at the scene of the injury by paramedics before analgesic medication was administered; the second measurement occurred at 1 week post trauma and was conducted by trained researchers using specialized equipment. The second aim of the study was to compare the relative predictive abilities of tonic HR and phasic arousal HR (HR measured during recounting the trauma). On the basis of fear conditioning models, we predicted that phasic HR (conditioned response) would be a stronger predictor of PTSD than tonic HR. This prediction was based on the following: a) we hypothesized that conditioned responses would elicit greater sympathetic activation than unconditioned responses, and b) whereas there is modest evidence for increased tonic HR after trauma, there is strong evidence for increased phasic HR in response to trauma cues (7). We also predicted that HR reactivity (phasic HR relative to tonic HR) would be a better predictor of PTSD than tonic or phasic HR alone. The final aim of the study was to identify the most useful arousal measure in predicting later PTSD. To do this, we assessed the participants’ somatic symptoms of arousal and indexed this as a predictor of subsequent PTSD.
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METHOD
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Participants
This study was nested within a previously described larger investigation of psychiatric prevalence and vulnerability to PTSD after traumatic injury (32,33). A total of 226 adults consecutively admitted to a Level 1 trauma service during 2001 participated in the current study. The study was approved by the Research and Ethics Committee at the recruiting hospital. The study participants had experienced a physical injury resulting in hospitalization for at least 24 hours, were aged between 18 and 70 years, and had either no brain injury or a mild traumatic brain injury (MTBI) as defined by the American Congress of Rehabilitation Medicine (34). Participants who received ß blockers or hypertensive medications were excluded from the study (n = 7). Acute assessments were conducted only after opioid analgesia was ceased. Assessments were conducted before discharge from the acute hospital setting and at 12 months post injury.
Of the 226 participants assessed in the acute hospital setting, 190 (84.1%) were assessed at 12 months. Those who did not complete the study were similar to those who completed the study on demographic variables except for age. Completers were significantly older than were noncompleters (completers versus noncompleters: 35.97 ± 13.17 (mean ± standard deviation, SD) years versus 29.22 ± 9.33 years; t(64.68) = 3.70; p < .001).
Of those who completed the study, three quarters (78%) of participants were male, aged 18 to 69 years. Injury severity was measured by the Injury Severity Score (ISS) (35). The ISS was 13.41 ± 9.28, indicating a moderate level of injury, with 55% experiencing MTBI. Participants spent on average 1.34 ± 3.48 days in an intensive care unit. An individual’s primary injury site was most likely to be the trunk (46%), then lower limb (32%), upper limb (16%), and head (6.0%). Fractures occurred in 75% of cases. The length of stay in hospital was on average 10.12 ± 10.54 days.
Procedure
The first measurement of tonic HR was recorded at the scene of the injury by paramedics (initial HR) using radial, brachial, or carotid pulse palpation measured over a minimum of 60 seconds. Our use of routinely collected HR data are similar to the majority of studies that have found a relationship between tonic HR and PTSD (Table 1). We used HR recorded at the scene for two reasons. First, given its immediacy to the traumatic event, we hypothesized that it represented the best marker of the fear conditioning environment. Second, this HR measurement was taken before the administration of opioid analgesia, which may confound the HR response. The second measurement of tonic HR was obtained under controlled conditions at 1 week post injury (7.85 ± 6.78 days post injury). Phasic HR data were also collected at this time. Two trained mental health researchers measured and recorded the tonic HR and phasic HR data using a pulse oximeter (PROFOX Oximetry software, PROFOX Associates, Inc., Escondido, CA). The handheld HR monitor sampled and recorded average HR every 4 seconds via a finger electrode. Tonic HR data were collected with the participant in a resting supine position for 15 to 20 minutes. Phasic HR was collected during the participant’s trauma narrative. The trauma narrative was elicited using a structured approach. The participant was asked to describe what he/she remembered happening and was encouraged during the narrative by asking "and then what happened?" In both the tonic and phasic cases, HR was recorded every 4 seconds for the duration of the period (with the participant resting in supine position or during the trauma narrative), then averaged to create a single score for each period. An HR change score was then calculated as the mean tonic HR was subtracted from the mean phasic HR. The participant’s somatic symptoms of arousal were assessed using the somatic scale of the Beck Anxiety Inventory (36). The somatic scale is made up of 12 arousal symptoms including numbness or tingling, feeling hot, wobbliness in legs, dizzy or lightheaded, heart pounding or racing, unsteady, hands trembling, feeling shaky, feeling scared, faint, face flushed, and sweating.
Participants were contacted via telephone at 12 months post injury and were assessed for PTSD severity using the Clinician Administered PTSD Scale (CAPS) (37). The CAPS has excellent reliability and validity conducted face-to-face (38) or over the telephone (39). A PTSD diagnosis was obtained if a participant met the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria for PTSD: criterion A (exposure to a life-threatening event; a response of fear, helplessness, or horror); one reexperiencing symptom; three avoidance symptoms; and two arousal symptoms; and criterion F (clinical level of impairment or distress). Subsyndromal PTSD was diagnosed if a participant met the criteria for criterion A, criterion F, and reexperiencing, and either the avoidance or the arousal symptoms. Approximately 30% of all interviews were audiotaped, of which one third were randomly subjected to interrater reliability analysis. 
for categorical diagnostic agreement was 1.00 (p < .001) and total severity score correlation was 0.99 (p < .001).
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RESULTS
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At 12 months post injury, 19 (10%) participants met the diagnostic criteria for PTSD and 30 (16%) participants met the criteria for either PTSD or subsyndromal PTSD. The PTSD severity score was 16.97 ± 20.53. There was no significant difference in the incidence of PTSD or subsyndromal PTSD between those with and without an MTBI. There was also no significant difference in the HR measurements or somatic arousal as a function of MTBI or gender. ISS was significantly correlated with tonic HR (r (147) = 0.25, p = .002) and phasic HR (r (147) = 0.25, p = .002) but not with the other HR or somatic arousal measurements. Table 2 presents the mean scores for the HR measurements, somatic arousal, and CAPS scores according to diagnostic status. There were significantly higher HR change scores and somatic arousal scores in trauma patients who developed PTSD at 12 months compared with those who did not develop PTSD. There were no significant between-group differences in the other HR measurements.
Table 3 presents the bivariate correlation coefficients for the relationships between the 12-month CAPS scores, HR scores, and somatic arousal. Twelve-month PTSD severity was found to positively correlate significantly with the somatic symptoms of arousal and with the HR change score. No significant correlations, however, were observed between PTSD severity and either the initial HR, phasic HR, or tonic HR conditions. There were no significant relationships between the somatic symptoms of arousal and any of the objective HR measurements.
A regression of measurements predicting PTSD severity at 12 months indicated that both somatic arousal and the HR change score explained 15% of the variance in PTSD scores, F(2, 145) = 12.834, p < .001 (Table 4). Somatic symptoms of arousal uniquely explained 10.82% of the variation in PTSD severity scores whereas HR change score uniquely explained 3.24%. Thus, somatic arousal was a stronger predictor of later PTSD severity than the HR change score. Nevertheless, the observation that both were making significant unique contributions to predicting the 12-month PTSD score suggested that they were explaining different aspects of PTSD.
The two diagnostic classifications of PTSD used in this study (12-month PTSD status, and 12-month PTSD and subsyndromal PTSD status) were regressed on somatic arousal and HR change score (Table 5). For both diagnostic classifications, somatic arousal and HR change scores were significant predictors, with higher levels of somatic arousal and HR change scores predicting greater likelihood of PTSD and subsyndromal PTSD at 12 months.
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DISCUSSION
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This study contrasts with those studies that found that subsequent PTSD is associated with increased tonic HR (13,14,16,19), but is in accord with other studies (17,23,24). It is important to question if methodological differences between our study and other studies contributed to our findings. First, the most notable difference between our study and others is that our participants were more severely injured (Table 1). Our study’s finding that there was a significant relationship between tonic HR/phasic HR and ISS questions the notion that the relationship between simple measurements of HR and PTSD has public health applications, at least in the more severely injured. Second, the majority of studies that found a significant relationship between early HR and later PTSD recorded HR in the ED whereas we used HR recorded at the scene of the injury. Although our measurement of HR was not confounded by opioid analgesia (as would have been the case if we had used HR measured in the ED), it may have be confounded by other factors such as blood loss or pain.
Importantly, we found that the increase in phasic HR relative to tonic HR was a stronger predictor of subsequent PTSD than tonic HR alone. That is, the extent to which an individual’s HR increased from a resting state during the recall of his/her traumatic event was indicative of the likelihood of subsequent PTSD development. This finding is consistent with the large body of evidence that people with PTSD produce heightened physiological responses to trauma-related cues (25–30) If one adopts a fear conditioning conceptualization of PTSD, this pattern may indicate that the initial conditioned response is a marker for subsequent conditioned responses (i.e., PTSD). Tonic HR immediately after trauma may not be the optimal predictor of PTSD. Consistent with this interpretation, Shalev and Friedman (17) found increased tonic HR in all survivors of terrorist attacks (regardless of PTSD development) relative to motor vehicle accident survivors. Focusing on phasic HR in response to trauma cues relative to tonic HR may provide a more accurate predictor of later PTSD.
An individual’s perception of his/her somatic symptoms of arousal was the strongest predictor of later PTSD. That is, the extent to which an individual perceived that he or she experienced acute somatic symptoms of anxiety determined his/her risk to later PTSD. This finding is strongly supported by studies that have demonstrated the importance of the relationship between early subjective arousal and later PTSD (40,41). It is noted that somatic arousal and CAPS scores were both based on self report and that this may have, in part, contributed to their strong relationship. This relationship, however, may also reflect that individuals at risk for PTSD are hypersensitive to interoceptive cues. Our results may suggest that the sensitivity to arousal cues make individuals highly conditionable, contributing to their risk for PTSD.
This study is limited by several factors. First, comparability of HR measurements across studies is difficult because HR assessment is variable across studies. We did not use tightly controlled experimental paradigms for measuring HR. Although our approach is more relevant for public health applications, more rigorous measurement is needed to advance our understanding of theoretical models of trauma response. Second, we did not assess tonic or phasic HR at the 12-month follow-up. These data would clarify the role of the relationship between fear conditioned responses in the acute and chronic phases after trauma. Third, we did not index HR variability, which may also provide a more accurate predictor of subsequent PTSD. Finally, we did not measure pain levels before collecting HR data. It is likely that high pain levels would increase HR especially in the immediate aftermath of the injury and, therefore, pain severity may have acted as a potential confounding factor in our study.
These limitations notwithstanding, this study questions the clinical usefulness of HR measurements as a marker for PTSD vulnerability. Using HR as an early predictor of PTSD requires sufficient sensitivity and specificity, which is not adequate in any reported studies (42). The finding that phasic HR in response to trauma cues relative to tonic HR is predictive, however, points to the need for more research on this topic. This response may lead to better prediction and may also improve our understanding of fear conditioning models of PTSD.
We gratefully acknowledge the assistance provided by patients and staff at the Alfred Trauma Service.
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NOTES
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Received for publication May 21, 2006; revision received November 21, 2006.
This study was supported by the Victorian Trauma Foundation, Grant V-11, a National Health and Medical Research Council Australian Clinical Research Fellowship (359284), and National Health and Medical Research Council Program Grant 300304.
DOI:10.1097/PSY.0b013e3180417d04
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ABSTRACT
INTRODUCTION
