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 Hyperventilation Syndrome 2

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عدد الرسائل : 197
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تاريخ التسجيل : 27/07/2008

مُساهمةموضوع: Hyperventilation Syndrome 2   الخميس مارس 15, 2012 3:01 am

Pathophysiology
Hyperventilation syndrome occurs in acute and chronic forms. Acute hyperventilation syndrome accounts for only 1% of cases but is more easily diagnosed. Chronic hyperventilation syndrome can present with a myriad of respiratory, cardiac, neurologic, or GI symptoms without any clinically apparent overbreathing by the patient. Hypocapnia can be maintained without any change in the absolute minute volume if the patient exhibits frequent sighs interspersed with normal respirations.

Because of the subtlety of hyperventilation, many patients with chronic hyperventilation syndrome are admitted and undergo extensive and expensive testing in an attempt to discover organic causes of their complaints.

The underlying mechanism by which some patients develop hyperventilation is unknown. One theory suggests that certain stressors provoke an exaggerated respiratory response. Several such stressors have been identified, including emotional distress, sodium lactate, caffeine, isoproterenol, cholecystokinin, and CO2. Predisposition to hyperventilation syndrome may also be rooted in childhood. Patients with hyperventilation syndrome were shown to have a higher percentage of overprotective parents when they were children. A sudden stressful situation later in life can then incite the first episode of hyperventilation syndrome.[1]

Infusion of lactate provokes symptoms of panic in 80% of patients with panic disorder but in only 10% of controls. Approximately one half of the lactate responders develop acute hyperventilation as part of the panic reaction. Lactate levels are higher and remain elevated longer in patients with panic disorder than in controls, suggesting that abnormal metabolism of lactate is involved in the pathogenesis, although the exact abnormality has not been characterized. Whether the same abnormality is operant in pure hyperventilation syndrome is unknown. In addition, elevated levels of carbon dioxide have been shown to induce panic symptoms in a majority of patients with panic disorder. Those patients who panicked with increased carbon dioxide had significantly greater baseline respiratory variability, which is also found in patients with hyperventilation syndrome, further suggesting a connection between the two.[2]

The explanation of hyperventilation syndrome lies partially in the mechanics of breathing. Normal tidal volumes range from 35-45% of vital capacity at rest. The elastic recoil of the chest wall resists hyperinflation of the lungs beyond that level, and inspiratory volumes beyond this level are perceived as effort or dyspnea. Patients with hyperventilation syndrome tend to breathe by using the upper thorax rather than the diaphragm, resulting in chronically overinflated lungs. When stress induces a need to take a deep breath, the deep breathing is perceived as dyspnea. The sensation of dyspnea creates anxiety, which encourages more deep breathing, and a vicious cycle is created.

Another common theory is that patients with panic disorder have a lower threshold for the fight or flight response. In patients who are susceptible, even minor stresses can trigger the syndrome, which then tends to manifest with primarily psychiatric complaints, such as fear of death, impending doom, or claustrophobia. In contrast, it is believed that patients with hyperventilation syndrome tend to focus on somatic complaints related to the physiologic changes produced by hyperventilation. The initiating stimulus and the abnormal stress response may be identical in each group but are expressed differently.
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Hyperventilation Syndrome 2
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