Hyperventilation syndrome pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1],Farman Khan, MD, MRCP [2]

Pathophysiology

The pathophysiology of hyperventilation syndrome can be divided into psycopathology, abnormalities of regulatory system, mechanism of pulmonary, and neurologic symptoms.

Psycopathology

There is an association between hyperventilation syndrome and psychological conditions such as panic disorder, but whether the psychological condition is primary or secondary is often unclear. Somatic and respiratory symptoms are common in patients with psychological distress. “Disproportionate breathlessness" is associated with depression, anxiety, bereavement, and resentment.

Basis of Pulmonary symptoms

Imbalance between sensory signals from pulmonary and chest wall stretch receptors and motor signals from the motor cortex result in feelings of dyspnea.The greater the imbalance, the greater the severity of dyspnea. Patients with hyperventilation syndrome may have an imbalance in these signals leading to a sensation of dyspnea that then precipitates a voluntary increase in minute ventilation.

Basis of Neurologic symptoms

With decreasing PaCO2 Cerebral blood flow decreases in a linear fashion. Raichle Plum has shown that a decrease of 1 mmHg of PaCO2 is associated with a 2 percent decrease in cerebral blood flow. Reduction in cerebral blood flow in the setting of hyperventilation, respiratory alkalosis may explain the neurologic symptoms such as paresthesias, headache, and light-headedness. In Hyperventilation syndrome respiratory alkalosis leads to acute changes in ionized serum calcium levels, which could result in paresthesias and/or tetany.

Regulating system dysfunction

Abnormalities in control system for ventilation (Reticular activating system) are important in development of symptoms in some patients with hyperventilation syndrome.Under normal conditions, healthy individuals demonstrate regular breathing with no voluntary effort.Hypersensitivity of certain parts of the brain like hippocampus, medial prefrontal cortex, amygdala and its brainstem projections also some times called “Fear Center” have been associated with hyperventilation syndrome .Increased sensitivity to carbon dioxide has also been proposed as mechanisms for the hyperventilation syndrome and its association with psychological symptoms.An activated hypersensitive fear network leads to increased central respiratory drive, causing low PaCO2 levels.

HVS can be part of a panic attack but, despite all the stigma, most patients are not putting on a show but are in true distress.

People with HVS feel like they can't get enough air, but the opposite is actually true: they have too much oxygen and too little carbon dioxide in their blood. The hyperventilation is self-promulgating as rapid breathing causes carbon dioxide levels to fall, and respiratory alkalosis (high blood pH) develops. This makes the symptoms worse, which causes the patient to try breathing even faster, which further exacerbates the problem.