History
Patients with acute hyperventilation syndrome (HVS) may present with great agitation and anxiety.
Most commonly, the history is of sudden onset of dyspnea, chest pain, or neurologic symptoms (eg, dizziness, weakness, paresthesias, near syncope) following a stressful event.
Patients with chronic hyperventilation syndrome present with similar symptoms, including recurrent chest pain, dyspnea, and neurologic deficits, and usually have many similar presentations in the past.
Acute hyperventilation
Patients often present dramatically with agitation, hyperpnea and tachypnea, chest pain, dyspnea, wheezing, dizziness, palpitations, tetanic cramps (eg, carpopedal spasm), paresthesias, generalized weakness, and syncope.
The patient often complains of a sense of suffocation. An emotionally stressful precipitating event often can be identified.
An emotionally stressful precipitating event can often be identified.
Cardiac symptoms
The chest pain associated with hyperventilation syndrome usually has atypical features, but, on occasion, it may closely resemble typical angina. It tends to last hours rather than minutes, and is often relieved rather than provoked by exercise.
It is usually unrelieved by nitroglycerin.
The diagnosis of hyperventilation syndrome should be considered in young patients without cardiac risk factors who present with chest pain, particularly if associated with paresthesias and carpopedal spasm. However, this diagnosis should be reached cautiously, because many other potentially lethal conditions can cause young patients to present with chest pain (eg, pulmonary embolism, spontaneous pneumothorax).
ECG changes are common in patients with hyperventilation syndrome. Abnormalities may include prolonged QT interval, ST depression or elevation, and T-wave inversion.
In patients with subcritical coronary artery stenosis, the vasospasm induced by hypocarbia may be sufficient to provoke myocardial injury.
The incidence of hyperventilation syndrome is high among patients with mitral valve prolapse (MVP), and the chest pain associated with MVP may be due to hyperventilation.
Prinzmetal angina (ie, coronary angiospasm) is triggered by hyperventilation syndrome, but the chest pain associated with this syndrome normally would be expected to respond to nitrates or calcium channel blockers.
Central nervous system symptoms
CNS symptoms occur because hypocapnia causes reduced cerebral blood flow (CBF). CBF decreases 2% for every mm Hg decrease in pCO2.
Symptoms of dizziness, weakness, confusion, and agitation are common.
Patients may report feelings of depersonalization and may experience visual hallucinations.
Syncope or seizure may be provoked by hyperventilation.[4]
Paresthesias occur more commonly in the upper extremity and are usually bilateral.
Perioral numbness is very common.
GI symptoms
GI symptoms (eg, bloating, belching, flatus, epigastric pressure) may result from aerophagia.
Metabolic changes
Acute metabolic changes result from intracellular shifts and increased protein binding of various electrolytes during respiratory alkalosis.
Acute secondary hypocalcemia can result in carpopedal spasm, muscle twitching, prolonged QT interval, and positive Chvostek and Trousseau signs.
Hypokalemia tends to be less pronounced than hypocalcemia but can produce generalized weakness.
Acute secondary hypophosphatemia is common and may contribute to paresthesias and generalized weakness.
Chronic hyperventilation
The diagnosis of chronic hyperventilation syndrome is much more difficult than that of acute hyperventilation syndrome because hyperventilation is usually not clinically apparent.
Often, these patients have had extensive medical investigations and have been assigned several misleading diagnoses.
Two thirds of patients with chronic hyperventilation syndrome have a persistently slightly low pCO2 with compensatory renal excretion of HCO3, resulting in a near-normal pH level. These patients tend to have more prominent CNS symptoms than patients who maintain normal pCO2 during attacks. These patients usually present due to dyspnea and chest pain.
The respiratory alkalosis can be maintained with occasional deep sighing respirations, which are observed often in patients with chronic hyperventilation syndrome.
When faced with an additional stress that provokes hyperventilation, the physiologic acid-base reserve is less, and these patients become symptomatic more readily than patients without hyperventilation syndrome.
Other
Dry mouth occurs with mouth breathing and anxiety.
Many of these patients suffer from obsessive-compulsive disorders, experience sexual and marital difficulties, and have poor adaptations to stress.
Patients with chronic hyperventilation syndrome may have symptoms that mimic virtually any serious organic disorder, but they usually have atypical features of these diseases.
Patients with acute hyperventilation syndrome (HVS) may present with great agitation and anxiety.
Most commonly, the history is of sudden onset of dyspnea, chest pain, or neurologic symptoms (eg, dizziness, weakness, paresthesias, near syncope) following a stressful event.
Patients with chronic hyperventilation syndrome present with similar symptoms, including recurrent chest pain, dyspnea, and neurologic deficits, and usually have many similar presentations in the past.
Acute hyperventilation
Patients often present dramatically with agitation, hyperpnea and tachypnea, chest pain, dyspnea, wheezing, dizziness, palpitations, tetanic cramps (eg, carpopedal spasm), paresthesias, generalized weakness, and syncope.
The patient often complains of a sense of suffocation. An emotionally stressful precipitating event often can be identified.
An emotionally stressful precipitating event can often be identified.
Cardiac symptoms
The chest pain associated with hyperventilation syndrome usually has atypical features, but, on occasion, it may closely resemble typical angina. It tends to last hours rather than minutes, and is often relieved rather than provoked by exercise.
It is usually unrelieved by nitroglycerin.
The diagnosis of hyperventilation syndrome should be considered in young patients without cardiac risk factors who present with chest pain, particularly if associated with paresthesias and carpopedal spasm. However, this diagnosis should be reached cautiously, because many other potentially lethal conditions can cause young patients to present with chest pain (eg, pulmonary embolism, spontaneous pneumothorax).
ECG changes are common in patients with hyperventilation syndrome. Abnormalities may include prolonged QT interval, ST depression or elevation, and T-wave inversion.
In patients with subcritical coronary artery stenosis, the vasospasm induced by hypocarbia may be sufficient to provoke myocardial injury.
The incidence of hyperventilation syndrome is high among patients with mitral valve prolapse (MVP), and the chest pain associated with MVP may be due to hyperventilation.
Prinzmetal angina (ie, coronary angiospasm) is triggered by hyperventilation syndrome, but the chest pain associated with this syndrome normally would be expected to respond to nitrates or calcium channel blockers.
Central nervous system symptoms
CNS symptoms occur because hypocapnia causes reduced cerebral blood flow (CBF). CBF decreases 2% for every mm Hg decrease in pCO2.
Symptoms of dizziness, weakness, confusion, and agitation are common.
Patients may report feelings of depersonalization and may experience visual hallucinations.
Syncope or seizure may be provoked by hyperventilation.[4]
Paresthesias occur more commonly in the upper extremity and are usually bilateral.
Perioral numbness is very common.
GI symptoms
GI symptoms (eg, bloating, belching, flatus, epigastric pressure) may result from aerophagia.
Metabolic changes
Acute metabolic changes result from intracellular shifts and increased protein binding of various electrolytes during respiratory alkalosis.
Acute secondary hypocalcemia can result in carpopedal spasm, muscle twitching, prolonged QT interval, and positive Chvostek and Trousseau signs.
Hypokalemia tends to be less pronounced than hypocalcemia but can produce generalized weakness.
Acute secondary hypophosphatemia is common and may contribute to paresthesias and generalized weakness.
Chronic hyperventilation
The diagnosis of chronic hyperventilation syndrome is much more difficult than that of acute hyperventilation syndrome because hyperventilation is usually not clinically apparent.
Often, these patients have had extensive medical investigations and have been assigned several misleading diagnoses.
Two thirds of patients with chronic hyperventilation syndrome have a persistently slightly low pCO2 with compensatory renal excretion of HCO3, resulting in a near-normal pH level. These patients tend to have more prominent CNS symptoms than patients who maintain normal pCO2 during attacks. These patients usually present due to dyspnea and chest pain.
The respiratory alkalosis can be maintained with occasional deep sighing respirations, which are observed often in patients with chronic hyperventilation syndrome.
When faced with an additional stress that provokes hyperventilation, the physiologic acid-base reserve is less, and these patients become symptomatic more readily than patients without hyperventilation syndrome.
Other
Dry mouth occurs with mouth breathing and anxiety.
Many of these patients suffer from obsessive-compulsive disorders, experience sexual and marital difficulties, and have poor adaptations to stress.
Patients with chronic hyperventilation syndrome may have symptoms that mimic virtually any serious organic disorder, but they usually have atypical features of these diseases.
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