Diagram Omitted. Please refer to source for complete article.
Since the original descriptions in soldiers, it is now recognized that hyperventilation occurs in many persons under stresses of daily living. It is manifest not only in those overtly stressed, anxious and depressed but also in those who appear outwardly calm as they "bottle up" their feelings, often because of undeveloped or lack of acceptable emotional outlets. Physicians and lay persons alike readily recognize acute hyperventilatory attacks occurring under acute stress. However, chronic or recurrent hyperventilation problems often are unrecognized probably for a variety of reasons, including the frequent lack of obvious overbreathing, a tendency to focus on one or two complaints that alone are not particularly suggestive of hyperventilation, minimal discussion of the topic in medical school and cursory coverage in medical textbooks.
Respiratory alkalosis increases the avidity of oxygen binding to hemoglobin such that oxygen becomes less readily released to tissues (the Bohr effect). Hypophosphatemia develops rapidly and persists for the duration of respiratory alkalosis, probably related to intracellular shifts of phosphorus. With persistent hyperventitation, hypophosphatemia would impair generation of 2,3-diphosphoglycerate (2,3- DPG), further reducing oxygen availability for tissue utilization.
It is estimated that a 2 percent reduction in cerebral blood flow occurs for every decline of 1 mm of mercury in arterial carbon dioxide tension. This, along with the Bohr effect, leads to reduced cerebral oxygenation. Cerebral hypoxia, however, produces a vasodilatory response that may compensate for the initial reduction in cerebral perfusion.
Cardiovascular responses are variable and seem to be in large part related to the duration of hyperventilation. The initial response is a reduction in systemic vascular resistance and blood pressure with an increase in heart rate and cardiac output. Within four to seven minutes of sustained hyperventilation, however, this response diminishes or disappears.
Finally, several investigators have shown coronary vasoconstriction induced by hyperventilation in some patients with Prinzmetal's angina and others with fixed coronary occlusive disease.
PSYCHIATRIC Anxiety, depression, phobias, feeling far away, sensations of unreality
NEUROLOGIC Paresthesias in extremities or periorally, lightheadedness, dizziness, disorientation, impaired thinking, seizures, syncope, headaches
CARDIOLOGIC Palpitations, chest pain
RESPIRATORY Dyspnea often without provocation characterized as being unable to take a satisfying deep inspiration, exaggerated thoracic breathing, sighing, yawning
GASTROINTESTINAL Dry mouth, bloating, belching, flatulence
MUSCULAR Cramping, spasm, musculoskeletal chest wall pain (chest wall syndrome)
The dizziness of hyperventilation may be described as lightheadedness or an unsteady, giddy feeling, similar to drunkenness or vertigo. In one review of 104 patients who presented to a specialty clinic for the evaluation of dizziness, 23 percent had hyperventilation as the sole or prominent contributing factor. There may also be some degree of disorientation and mental impairment.
Breathlessness is a common complaint and is usually described as the inability to inhale a satisfyingly deep breath. It may be manifested by periodic, predominantly thoracic deep breaths, sighing and yawning. Sighing dyspnea is not a manifestation of cardiac failure. Although the hyperventilation syndrome rarely is associated with an obvious increase in respiratory rate, astute observers usually will note an increase in thoracic respiratory efforts. Paradoxically, whereas many people take deep breaths in an effort to relax, they may be provoking the very state they wish to avoid. The dyspnea of the syndrome may arise from fatigued respiratory muscles, overworked from chronic, excessive respiratory efforts. Since this type of dyspnea rarely occurs in the absence of other related symptoms, it is important that other manifestations of the hyperventilation syndrome be sought in all cases of otherwise unexplained dyspnea.
Gastrointestinal manifestations include dry mouth, bloating, belching and flatulence, related to aerophagia associated with overbreathing. Depression with attendant anorexia and weight loss may mimic systemic disease.
Cardiovascular symptoms of the syndrome are primarily palpitations and chest pain, which may mimic angma. Continuous ambulatory electrocardiographic monitoring of hyperventilators has shown frequent sinus tachycardia and supraventricular arrhythmias, even during sleep. Hyperventilatory symptoms without apparent provocation may occur during these times.
The chest pain of hyperventilation is variably described. It may be sharp and stabbing, thought to be related to pressure on the diaphragm from gastric distention or diaphragmatic hypertonicity related to a generalized hypertonic muscular contractile state. Other types of chest pain have features that may strongly suggest angina including location and radiation patterns. The pain may be described as dull, gnawing, burning or constricting and localized to the precordial or retrosternal area but is often rather diffuse and of greater duration than is typical of angina pectoris. It is not predictably associated with events that usually provoke angina, frequently occurring at rest or after exertion, and is not reliably relieved by nitroglycerin. Occasionally, "pseudoischemic" electrocardiographic patterns may be seen in patients with chest pain from hyperventilation. It currently remains uncertain whether hyperventilation- induced coronary vasospasm and myocardial ischemia contribute to the chest pain associated with the hyperventilation syndrome. Unfortunately, a diagnosis of noncardiac chest pain, while initially gratifying, usually does not result in a significant reduction in outpatient clinic or emergency room visits as symptoms often persist. Therefore, in evaluating chest pain, the historical data base should include questions directed toward the possibility of hyperventilation lest the etiologic basis of the chest pain be dismissed as noncardiac, yet unrecognized as hyperventilatory.
Other symptoms of hyperventilation are usually present but rarely offered voluntarily. Apart from other disorders the patient may have, the physical examination is often normal. Patients often do not appear overtly anxious though they are frequently depressed. Obvious hyperventilation is usually lacking although occasional deep breaths, sighing or yawning and palpable chest wall tenderness may be noted. The diagnosis of chest wall syndrome requires exclusion of the hyperventilation syndrome which may be its basis.
It is critical to recognize that the presence of the syndrome does not exclude the presence of an organic disease. In fact, reaction to the symptoms of an organic disease may be a prime factor provoking hyperventilation.
After provocation of symptoms .during a hyperventilatory trial, breathing into a lunch bag-sized brown paper bag will result in resolution of those symptoms that are directly related to hypocapnea. Dyspnea and chest pain, however, may persist in that they are not caused by hypocapnea, but more likely by the excessive use of thoracic musculature.
Because many patients have experienced substantial adverse effects on their employment and social interactions it is beneficial for a spouse or a friend to be present during a hyperventilation trial. Family and friends may be highly skeptical that something as simple as overbreathing can be having such devastating effects on the patient and indirectly upon them as well. Convincing both the patient and others provides support for the patient as he or she attempts to regain control.
Although some believe bag rebreathing is of little value, we have found it to be useful, allowing patients an escape from symptoms. Initially, we encourage patients to attempt bag rebreathing, relax and get away from the situation that may have triggered the response. As a result, patients appreciate a newfound control. This greatly reduces the anxiety and stress that fuel the hyperventilation cycle.
Long-term control may be achieved by relaxation therapy and retraining patients to become diaphragmatic rather than thoracic breathers. Referral to behavior modification experts may be of value in particularly difficult patients with long-standing symptoms. In anxious and depressed persons with chronic hyperventilation we have rarely seen substantial benefit from the use of anxiolytic or antidepressant medications when the hyperventilatory component was unrecognized or being inadequately addressed. in conjunction with therapeutic measures directed toward the hyperventilatory tendency these drugs may be of additional benefit though we often find them unnecessary.
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