Hyperventilation syndrome pathophysiology

Hyperventilation syndrome Microchapters
Home
Patient Information
Overview
Historical Perspective
Pathophysiology
Causes
Differentiating Hyperventilation syndrome from other Diseases
Epidemiology and Demographics
Risk Factors
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
Chest X Ray
CT
Echocardiography or Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Hyperventilation syndrome pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Hyperventilation syndrome pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Hyperventilation syndrome pathophysiology
CDC on Hyperventilation syndrome pathophysiology
Hyperventilation syndrome pathophysiology in the news
Blogs on Hyperventilation syndrome pathophysiology
Directions to Hospitals Treating Hyperventilation syndrome
Risk calculators and risk factors for Hyperventilation syndrome pathophysiology

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.

Psychopathology

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.

Basis of Neurologic Symptoms

With decreasing arterial Carbon Dioxide levels (PaCO₂), cerebral blood flow decreases in a linear fashion. Raichle and 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 in combination with 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, the reticular activating system, are important in the 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 such as the hippocampus, medial prefrontal cortex, amygdala and its brain stem projections, also some times called “Fear Center,” have been associated with hyperventilation syndrome. Increased sensitivity to carbon dioxide has also been proposed as a mechanism for 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 occur as part of a panic attack. Despite the stigma, most patients are exaggerating symptoms but are in true distress.

Patients with HVS feel as though they cannot get enough air, but the opposite is true: they have too much oxygen and too little carbon dioxide in their blood. Hyperventilation is self-promulgating as rapid breathing causes carbon dioxide levels to continue to fall, and respiratory alkalosis (high blood pH) develops. This makes the symptoms worse, which causes the patient to try breathing even faster, perpetuating the cycle.