THE MANY EFFECTS OF ANXIETY ON YOUR BREATHING

MINDRISE CLIFFNOTES

• During hyperventilation, less oxygen is actually delivered to the brain despite increased quantity of it in the blood.
• Even a brief period of fast breathing induces panic and suffocation alarm among individuals with panic disorder and social anxiety disorder
• Preventing too much carbon dioxide from accumulating in the blood is more essential than increasing its quantity, which explains why after a panic attack or an anxiety attack symptoms such as sluggishness, headaches, shortness of breath linger for a little bit, which further exacerbates anxiety.
• The respiratory system is susceptible to moment to moment changes in emotions and cognitions. For example, a fleeting thought of an anxious event can influence your breathing pattern, so it is important to be mindful of your thoughts and internal dialogue.
• Frequent sighing reflects irregular respiratory pattern and is often present in individuals with anxiety
• Respiration is a mechanism that evolved to supply the body with oxygen (i.e., O2) and rid it of carbon dioxide (i.e., Co2). This apparent simplicity belies an intricate set of redundant and asymmetrical systems that govern one of the most essential machines for man.
• In fact, respiration is rarely completely regular, except during NREM states (i.e.,  stage of deep sleep) and anesthesia. Notably, oxygen absorption in the body is regulated by the amount of available O2 in the air, the temperature and the blood’s pH level. Hemoglobin has a high affinity with O2 (i.e., O2 binds easily to hemoglobin) which assures a stable supply of oxygen even under difficult conditions, such as physical exercise. However,  when there is an overabundance of oxygen, the molecule does not detach easily from hemoglobin to reach target organs and nourish them.

THE ROLE OF CARBON DIOXIDE (CO2)

Hyperventilation is one such instance where the supply of oxygen is so excessive that the actual amount that is carried to the organs is low in comparison.

Contrary to common belief, carbon dioxide is not a waste gas, but rather an essential element of the respiratory system. The Bohr effect, for example, is a physiological phenomenon that emphasizes the crucial role that carbon dioxide plays in respiration. It describes the mechanism by which the affinity of hemoglobin for oxygen is decreased when there is too much carbon dioxide in the blood (i.e., carbon dioxide partial pressure, PCo2).

Similarly, when PCo2 is reduced during diffusion of carbon dioxide from the blood to the alveoli (i.e., tiny sacs in the lungs) raising blood pH, the quantity of oxygen binding with hemoglobin is considerably increased, which contributes to oxygenation of the lungs. Thus, carbon dioxide is crucial in driving oxygenation of the blood in the lungs, and then again in enhancing the release of oxygen from the blood to the tissue cells.

Hyperventilation, on the other hand, appears to disrupt respiratory homeostasis, as it is associated with an array of unpleasant symptoms, such as dizziness, trembling, a feeling of unreality, and palpitations.

HYPERVENTILATION

Those symptoms arise because over-breathing results in alkalosis (i.e., loss of acidity due to a drop in carbon dioxide) which in turn provokes constriction of the cerebral arteries. As a consequence, less O2 is actually delivered to certain brain regions, possibly jeopardizing certain brain functions.

Interestingly, the system regulating PCo2 levels reveals a certain asymmetry. Indeed, it appears that preventing a build-up of carbon dioxide in the blood is more essential than increasing its levels, which explains why hypocapnia (i.e., low blood levels of carbon dioxide) is more likely than hypercapnia (i.e., high blood levels of carbon dioxide). Furthermore, because of this asymmetry, under states of extended stress or during high anxiety, PCo2 may not normalize for a long time.

For example, slow recovery of PCo2 after voluntary hyperventilation has been consistently documented among patients with panic disorder (PD). What happens is that if the increase in ventilation is not followed by sufficient physical activity, PCo2 levels simply falls, which explains why hypocapnia occurs during anxiety states.

More evidence is provided in a study consisting of six cycles of 1 minute of fast breathing alternating with 1 minute of recovery, followed by 3 minutes of fast breathing and 10 minutes of recovery for 14 patients with PD, 24 patients with social phobia (SP), and 24 controls (i.e., healthy participants). Results reveal that during fast breathing SP and PD patients experienced an increase in anxiety, feelings of shortness of breath and suffocation compared to controls.

At the end of the last recovery period, however, PD patients reported being more aware of their breathing and shortness of breath, which indicates that their symptoms take longer to dissipate.

In addition, the large number of cortical (i.e., in the cortex of the brain) and subcortical (i.e., under the brain cortex) projections (i.e., brain cells) that are located in the brain stem, which is the brain’s respiratory center, is believed to contribute to the moment-to-moment changes in respiration.

As a result of this intricate system, a fleeting thought of a stressful or anxious event could potentially influence the ongoing breathing pattern profoundly.

For example, a cognitive intervention (i.e., involves working with your thoughts) designed to reassure panic disorder patients about experiencing bodily symptoms during a panic provocation experiment is sufficient to reduce the panic response, but it has no effect on the respiratory irregularities (i.e., hyperventilation, sighing, etc…).

SIGHING

Frequent sighing is a type of respiratory instability that appears to occur in the background of already unstable respiration. Furthermore, studies show that it is not a homeostatic response, as it does not help compensate for the rise in PCo2. Although, we do not know whether frequent sighing is a cause or effect of hypocapnia, it is a consistent and frequent process in hypocapnia in PD patients along with increased depth of sighing and slower recovery of PCo2 after sighing.

Sporadic sighing, by contrast, is an adaptive mechanism that functions to prevent collapsing of alveoli in some parts of the lungs. Interestingly, investigations reveal that sighing could be a conditioned behavior (i.e., learned) that was adopted because it is reliably followed by a positive reinforcement of increased positive mood and symptom reduction.

Albeit brief, sighing induces relief by causing lung expansion, decreased heart rate and reduced respiratory drive. Subsequently though, arterial PCo2 goes back to pre-sigh levels again, triggering breathlessness and hyperventilation.

However, the mental association between sighing and relief, even temporary, is so strong that it becomes an automatic behavior. Consequently increased sighing occurring in the background of anxiety is likely to be maintained or worsened.