Approach Considerations
Upon a first attack of acute hyperventilation syndrome (HVS), the diagnosis depends on recognizing the typical constellation of signs and symptoms and ruling out the serious conditions that can cause the presenting symptoms.
Acute coronary syndrome (ACS) and pulmonary embolism (PE) are two of the most common serious entities that may present similarly to HVS. Usually, clinical assessment is sufficient to rule out these entities. Depending on that assessment, more specific testing is sometimes warranted.
A standard workup for atypical chest pain, including pulse oximetry, chest radiography, and electrocardiography (ECG), may still be warranted depending on the clinical picture.
Laboratory Studies
Patients with a history of HVS who have undergone an appropriate workup at some earlier time may not need any further laboratory evaluation in the setting of a recurrence. Recognition of the typical constellation of dyspnea, agitation, dizziness, atypical chest pain, tachypnea and hyperpnea, paresthesias, and carpopedal spasm in a young, otherwise healthy patient with an adequate prior evaluation is often sufficient to establish the diagnosis.
A low pulse oximetry reading in a patient who is hyperventilating should never be attributed to HVS. These patients should always be evaluated for other causes of hyperventilation. A normal pulse oximetry reading is not helpful, because a severe defect in gas exchange can be masked by hyperventilation. A fraction of patients with chronic PE will have compensated chronic hyperventilation that may mimic primary chronic hyperventilation.
Arterial blood gas (ABG) measurement is indicated if any doubt exists as to the patient’s underlying respiratory status. Arterial blood gas analyses may be helpful when HVS-induced alkalosis is suspected, or when shunting or impaired pulmonary gas exchange is being considered.
In chronic HVS, ABG sampling confirms a compensated respiratory alkalosis in a majority of cases. The pH is typically near normal, with a low PaCO2 and a low measured serum bicarbonate level. ABG sampling is also useful in ruling out toxicity from carbon monoxide poisoning, methemoglobinemia, and sulfhemoglobinemia, which may present similarly to HVS. [8]
Drug toxicology screening is often indicated. If acute PE is being considered, a quantitative enzyme-linked immunosorbent assay (ELISA) D-dimer assay may be helpful in young patients who are free from comorbid illnesses.
Imaging studies
Imaging studies are not indicated when the diagnosis of HVS is clear. In less obvious cases of HVS, imaging studies are typically normal. Chest radiographs may reveal hyperinflation.
Because PE can present with findings identical to those of HVS, a first-ever episode of acute HVS may warrant ventilation/perfusion scanning or computed tomography (CT) pulmonary angiography to rule out perfusion defects. Chest radiography is indicated for patients who are at high risk for cardiac or pulmonary pathology. Chest radiography is also indicated when the diagnosis is not clear.
Electrocardiography
ECG changes are common and may include the following:
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ST depression or elevation
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Prolonged QT interval
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T-wave inversion
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Sinus tachycardia
Orthostatic respiratory rate changes
In a normal individual, the respiratory rate typically increases when the person moves from a supine to a standing position. Patients with HVS have an accentuated increase in minute ventilation. End-tidal carbon dioxide is significantly lower in patients with HVS, and ventilatory equivalents for oxygen and carbon dioxide are significantly higher. Thus, noninvasive measurements of gas exchange during orthostatic testing are useful in the diagnosis of HVS. [1]
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Trousseau sign.
