This fine paper published not very long ago in the journal Psychosomatic Medicine is an excellent explanation of why an integrated view of heart rate variability (HRV) and Pco2 (for hypocapnia = abnormally low carbon dioxide in the blood; measured as end-tidal Pco2 by capnography) are so valuable for assessment and treatment for post-traumatic stress disorder and panic disorder. The authors first state that:

“Posttraumatic stress disorder (PTSD) and panic disorder (PD) are two anxiety disorders with prominent psychophysiological symptoms. The PTSD criterion of persistent hyperarousal suggests autonomic dysregulation, and the disorder has been associated with elevated heart rate. In contrast, PD has been associated with respiratory abnormalities such as low end-tidal Pco2.”

They note that there is little written about an integrated analysis of both autonomic and respiratory function (the type of analysis we perform here) in regard to these two anxiety disorders. So they set out to investigate the connections:

“Electrodermal, cardiovascular, and respiratory psychophysiology was examined in 23 PTSD patients, 26 PD patients, and 32 healthy individuals at baseline and during threat of shock.”

Their data painted the exactly the same picture that we see in the clinic here:

“At baseline, the PTSD patients, in contrast to the other two groups, were characterized by attenuated parasympathetic and elevated sympathetic control, as evidenced by low respiratory sinus arrhythmia (a measure of cardiac vagal control) and high electrodermal activity. They also displayed elevated heart rate and cardiovascular sympathetic activation in comparison with healthy controls. PD patients exhibited lower Pco2 (hypocapnia) and higher cardiovascular sympathetic activation compared with healthy controls.”

Remember that sympathetic (nervous system) dominance (loss of parasympathetic tone in comparison to sympathetic activity) is a characteristic of most chronic degenerative diseases and increasing neurodegeneration with age. For the vast majority of people we endeavor to recover and support parasympathetic function. The authors also noted:

“The elevated cardiovascular and electrodermal activity among PTSD patients is also consistent in suggesting particularly high levels of sympathetic arousal in this clinical group. Thus, sympathetic hyperarousal and profound parasympathetic withdrawal may be characteristic of PTSD and may contribute to a failure to downregulate from the state of hyperarousal caused by the trauma.”

Both PTSD and PD patient groups exhibited respiratory dysregulation:

“Two theories emphasize a respiratory abnormality in PD patients: the hyperventilation theory and the suffocation false alarm theory. The hypocapnia of about 3 torr found in our PD patients is consistent with both theories and previous research. However, the PTSD group also showed abnormal breathing patterns (high sigh rate, more abdominal breathing, and only slightly less hypocapnia than the PD group). This…stresses the importance of including respiratory measures in the study of anxiety disorders, in general.”

And they made an additional curious observation:

“PTSD patients, but not PD patients, sighed more frequently than controls.”

It’s helpful to understand that these are very powerful phenomena. The autonomic nervous system (ANS; sympathetic and parasympathetic, measured by HRV) regulates all our internal functions and expresses our arousal state. Breathing has a potent effect on the ANS, and excess ventilation (overbreathing) of CO2 sharply reduces oxygen perfusion in the brain. This applies to general health, not just PTSD and PD. But if you do suffer from either of these conditions, by all means keep their conclusion in mind and bring it to the attention of your doctor:

“To conclude, this study supports the idea of autonomic dysregulation in PTSD. Elevated sympathetic activity…and profound cardiac vagal [= parasympathetic] withdrawal may represent psychophysiological markers for PTSD and may predict long-term cardiovascular risk. Hypocapnia once again characterized PD patients, but elevated frequency of sighing was unexpectedly only found among the PTSD group, who also showed depressed levels of Pco2, compared with HC [healthy controls].”

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Healthy brain function requires oxygen which depends on good cerebral blood flow (among other factors). As I see from measuring oxygen saturation and end-tidal CO2 (ETCO2 as measured by capnography; too little CO2 in the bloodstream impairs oxygen dissociation from hemoglobin), suboptimal perfusion and oxygenation of brain tissue occurs all too often. This welcome study published not long ago in the American Journal of Clinical Nutrition offers evidence that resveratrol can help.

“In this randomized, double-blind, placebo-controlled, crossover study, 22 healthy adults received placebo and 2 doses (250 and 500 mg) of trans-resveratrol in counterbalanced order on separate days…Cerebral blood flow and…concentration changes in oxygenated and deoxygenated hemoglobin, were assessed in the frontal cortex…”

Their data painted this picture:

“Resveratrol administration resulted in dose-dependent increases in cerebral blood flow…There was also an increase in deoxyhemoglobin after both doses of resveratrol, which suggested enhanced oxygen extraction…”

Other studies have shown how resveratrol may support insulin dynamics, combat inflammation and help accelerated degeneration. Your doctor may suggest, with good reason, that you take resveratrol if impairment of brain perfusion is contributing to your cognitive, emotional or physical problems.

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