Low Heart Rate Variability is linked to Enhanced Stress Response in PTSD

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Key Points

  • PTSD patients have an elevated and prolonged stress response

  • Low baseline HRV is associated with an enhanced stress response in PTSD

  • Low parasympathetic tone might cause the heightened stress response in PTSD

The Breathing Diabetic Summary

In post-traumatic stress disorder (PTSD), physiological arousal is increased when a person is reminded of their traumatic experience.  This is somewhat expected.  However, the exact mechanisms behind this heightened physiological response are not well understood.

It is almost certain that an over activated sympathetic nervous system plays a role.  However, under activation of the parasympathetic nervous system, or “low vagal tone,” might be equally important. 

The parasympathetic nervous system acts to control heart rate increases: When the sympathetic branch ramps up, so does the parasympathetic branch to maintain balance.  Therefore, a weakened parasympathetic tone would weaken cardiovascular regulation in response to stress.  This could also explain the enhanced stress response in PTSD.

Therefore, the goal of this paper was to answer the following question: Is sympathetic over activation or parasympathetic under activation responsible for the enhanced stress response in PTSD?

Thirty-one patients with PTSD were studied.  They tested their baseline heart rate variability (HRV) as a predictor of their future stress response.  They predicted that patients with low HRV (and thus low parasympathetic tone) would have an increased stress response compared to those with relatively higher HRV.

The measurement of HRV that they used was respiratory sinus arrhythmia (RSA).  RSA is the increase of heart rate with inhalation and decrease of heart rate with exhalation.  It is thought to be a measure of high-frequency HRV (HF-HRV; frequencies above 0.12 Hz).  At these frequencies, the parasympathetic nervous system is able to respond to breathing and alter heart rate, but the sympathetic nervous system cannot.  Therefore, they used RSA as a measure of parasympathetic control. 

Subjects were instructed to lie down and listen to a relaxing audiotape for 2 minutes.  Then, they listened to a neutral tape for 2 minutes.  After this, they listened to a 2-minute script that reminded them of their traumatic experience (the scripts were developed individually based on each patient’s past traumatic event).  After this, they rested for 5 minutes and then repeated the relaxing and neutral scripts.

Measurements revealed that patients with a higher baseline RSA (and thus higher HRV) did not experience as much stress as those with lower RSA.  The subjects with lower RSA showed a higher heart rate peak, followed by a much slower deceleration of heart rate.  That is, they showed an elevated stress response.

Moreover, the researchers defined a parameter called the half-recovery time, which was the amount of time that each participant had a heart rate that was above the mid-point between their resting heart rate and their maximum heart rate achieved during the script.  For example, if they started with a baseline heart rate of 70, and the maximum heart rate they achieved during the trauma script was 130, then the half-recovery time would be the time spent with a heart rate above 100 ([130 + 70]/2).

The patients with lower baseline RSA had longer half-recovery times.  Moreover, the lower the RSA got during the trauma script, the longer the half-recovery time.

Because subjects with low baseline RSA had the greatest stress response, these findings indicate that low parasympathetic tone, not increased sympathetic activity, might be responsible.

Moreover, measurements of RSA (and hence HRV) in PTSD could provide physiological insight into the state of their condition and predict how that person will respond to stress. 

Finally, we know from several studies that slow breathing is one of the fastest ways to improve HRV, both immediately and long term.  If HRV predicts the stress response, and HRV can be increased via breathing exercises, it is conceivable that breathing practices could improve stress resiliency in PTSD.  (In fact, a 2013 study found that a yoga breathing program significantly improves PTSD symptoms in Australian Vietnam veterans.)

To summarize, low baseline RSA is associated with enhanced stress arousal in PTSD. Thus, it might be low parasympathetic tone, rather than excess sympathetic activity, that causes their heightened physiological arousal.

Abstract

BACKGROUND:

There is extensive evidence that the parasympathetic branch of the autonomic nervous system can modulate psychophysiological arousal. To date, no studies have investigated associations between cardiac vagal tone and the time course of arousal during exposure to trauma-related stimuli in posttraumatic stress disorder (PTSD).

METHODS:

Thirty-one subjects, 29 with PTSD and 2 with partial PTSD, had electrocardiograms recorded during baseline and 2-minute traumatic and neutral script-driven imagery periods. Heart rate, respiratory sinus arrhythmia (RSA), and heart rate half-recovery to the trauma script were quantified, and subjects were divided into low and high baseline RSA groups.

RESULTS:

Across all participants, heart rate significantly increased from the neutral to the trauma script and RSA significantly decreased from baseline to trauma script (p < .05). As predicted, low RSA subjects had more prolonged heart rate increases to the trauma script than high RSA subjects (p < .001), and heart rate half-recovery was negatively correlated to baseline RSA (r = -.50, p =.005).

CONCLUSIONS:

This study is the first to find decreased RSA in response to a traumatic reminder and an association between low baseline RSA and sustained conditioned arousal in PTSD. Low vagal tone may account for deficient arousal and emotion regulation capacities often observed in PTSD.

Journal Reference:

Sack M, Hopper JW, Lamprecht F. Low respiratory sinus arrhythmia and prolonged psychophysiological arousal in posttraumatic stress disorder: heart rate dynamics and individual differences in arousal regulation.Biol Psychiatry. 2004;55(3):284-290.