Hypocapnia, also known as respiratory alkalosis, is a condition defined by abnormally low levels of carbon dioxide (CO2) in the blood, specifically a partial pressure of carbon dioxide (PaCO2) below 35 millimeters of mercury (mmHg). This imbalance results from hyperventilation, where rapid or deep breathing causes the lungs to “wash out” CO2 faster than the body produces it. The primary goal of treatment is to restore normocapnia, a normal PaCO2 level maintained between 35 and 45 mmHg. The specific approach depends heavily on the underlying cause of the hyperventilation, whether temporary or physiological.
Physiological Effects and Measurement
A low PaCO2 level triggers physiological changes, manifesting as distinct physical symptoms. The most immediate effect is cerebral vasoconstriction, where blood vessels supplying the brain narrow. This narrowing reduces blood flow, leading to neurological symptoms such as dizziness, lightheadedness, confusion, or fainting.
The drop in carbon dioxide leads to a rise in blood pH, known as respiratory alkalosis. This pH shift affects electrolyte balance, particularly calcium ions, increasing nerve and muscle excitability. Patients often experience paresthesia, a tingling or pins-and-needles sensation, typically in the hands, feet, and around the mouth. In severe cases, this hyperexcitability can progress to muscle cramps, spasms, and tetany.
The definitive way to measure hypocapnia is through an arterial blood gas (ABG) analysis, which determines the PaCO2 level in arterial blood. Readings below 35 mmHg indicate hypocapnia. A significantly low PaCO2, especially with an elevated pH, confirms the severity of respiratory alkalosis and guides management decisions.
Immediate Correction for Acute Causes
Hypocapnia resulting from acute, transient causes, such as anxiety or panic attacks, is addressed with non-medical interventions controlling the breathing pattern. The goal is to consciously reduce minute ventilation—the total volume of air breathed per minute—allowing CO2 levels to slowly rise toward the normal range. This is achieved by encouraging a slower, more deliberate rate of respiration.
Controlled breathing exercises are the primary self-management technique. Patients focus on diaphragmatic breathing, involving slow, deep inhalations followed by a prolonged exhale. The emphasis is on slowing the respiratory rate and ensuring the exhale is longer than the inhale to help retain carbon dioxide. This measured control counters the rapid, shallow breathing characteristic of hyperventilation.
While rebreathing into a paper bag was historically suggested, this method is generally no longer recommended by medical professionals. The concern is that rebreathing can inadvertently cause hypoxemia, or low oxygen levels, which is potentially dangerous. Focusing on conscious, controlled breathing remains the preferred and safest first-line intervention for acute, anxiety-induced hypocapnia.
Clinical Management of Severe Hypocapnia
For severe or sustained hypocapnia, especially in a hospital setting, management focuses on adjusting respiratory support to ensure a stable PaCO2. In intubated patients receiving mechanical ventilation, hypocapnia often occurs when ventilator settings are too aggressive, delivering minute ventilation higher than the patient’s metabolic need. The primary strategy involves manipulating the mechanical ventilator to reduce the amount of air moved in and out of the lungs.
This adjustment is achieved by decreasing the respiratory rate (breaths per minute) or by reducing the tidal volume (the size of each breath). Both actions decrease minute ventilation, allowing metabolic CO2 to accumulate until the PaCO2 returns to the target range of 35 to 45 mmHg. Careful monitoring using repeated ABG analysis or continuous end-tidal CO2 monitoring is necessary after adjustment to ensure gradual and precise correction.
In certain contexts, such as managing severe traumatic brain injury, temporary mild hypocapnia may be intentionally induced to reduce elevated intracranial pressure. This therapeutic hypocapnia utilizes the cerebral vasoconstrictive effect of low CO2, but it must be tightly controlled to prevent excessive reduction of cerebral blood flow. Beyond ventilator adjustments, overall clinical management requires identifying and treating the underlying cause driving hyperventilation, such as pain, fever, or sepsis.