Hypocarbia, also known as hypocapnia, is a decrease in alveolar and blood carbon dioxide (CO2) levels below the normal reference range of 35 mm Hg. CO2 is a metabolic product of the many cellular processes within the body when processing lipids, carbohydrates, and proteins. The primary organ systems responsible for regulating CO2 homeostasis are the pulmonary system and the renal system. Additionally, CO2 is regulated through the CO2/HCO3 pH buffering system. Aberrations that lead to hypocarbia typically also result in respiratory alkalosis.
At its root, hypocarbia is induced by either a decrease in CO2 production or an increase in CO2 loss. Since metabolic demand does not typically decrease in a way that meaningfully adjusts CO2 levels into hypocarbic levels, the primary occurrence is a loss of CO2 via the pH buffering system or changes in the pulmonary system. The pulmonary system is highly efficient in its removal of CO2 from the body through gas diffusion. This requires a diffusion gradient from the high concentration arteriolar blood into the relatively low concentration environmental air. This gradient is maintained through continually washing away CO2 from the alveolar space, regardless of the absolute PACO2 concentration. As such, the CO2 gradients are developed and maintained where PaCO2 in arterial blood is directly proportional to the rate of CO2 metabolic production and inversely related to the rate of CO2 elimination by the lung via increased alveolar ventilation. Alveolar ventilation is the removal of alveolar air into the environment, defined as the expired minute volume that reaches the alveoli and is determined by minute ventilation and the ratio of dead space to tidal volume. Mathematically, this relationship is determined as:
Where VCO2 is the metabolic production of CO2, VA is alveolar ventilation, VE is minute ventilation, VD is dead space ventilation, RR is the respiratory rate, and TV is tidal volume.
Through these relationships, one can conclude that respiratory rate and tidal volume are the 2 components of ventilation that are physiologically or artificially controlled to moderate CO2 elimination. Subsequently, the etiologies that induce hypocarbia are any disease which increases ventilation rate or tidal volume. More commonly, the increased respiratory rate is the culprit. A wide variety of illnesses may induce this. In almost every scenario, hypocarbia is synonymous with respiratory alkalosis as they are both induced by a process involving hyperventilation. These include central causes, hypoxemic causes, pulmonary causes, and iatrogenic causes. Central sources are a head injury, stroke, hyperthyroidism, anxiety-hyperventilation, pain, fear, stress, drugs, medications such as salicylates, and various toxins. Hypoxic stimulation leads to hyperventilation in an attempt to correct hypoxia at the expense of a CO2 loss. Pulmonary causes include pulmonary embolisms, pneumothorax, pneumonia, and acute asthma or chronic obstructive pulmonary disease (COPD) exacerbations. Iatrogenic causes are primarily due to hyperventilation in intubated patients on mechanical ventilation.
The frequency and distribution of illness is variable dependent on the exact etiology of the disease. Likewise, the morbidity and mortality are linked to the exact etiology of the inciting disease. In general, younger patients have better outcomes.
Hypocarbia is a result of hyperventilation. Increased ventilation to the alveolar space quickly removes gaseous CO2. This increases the diffusion gradient of CO2 from blood to alveoli. Subsequently, CO2 is more readily removed from the body. There are virtually no mechanisms outside of decreasing respiratory rate to regulate this loss.
Since the primary cause of all hypocapnia etiologies is hyperventilation, many patients present with complain to shortness of breath. The exact history and physical exam findings are highly variable as many pathologies induce the respiratory change. These may include acute onset dyspnea, fever, chills, peripheral edema, orthopnea, weakness, confusion, light-headedness, dizziness, anxiety, chest pain, wheezing, hemoptysis, trauma, history of central line catheter, recent surgery, history of thromboembolic disease, history of asthma, history of COPD, acute focal neurological signs, numbness, paresthesia, abdominal pain, nausea, vomiting, tinnitus, or weight loss.
Physical exam findings may be just as varied depending on etiology to include fever, tachycardia, tachypnea, diaphoresis, hyper or hypotension, altered mental status, productive or non-productive cough, wheezing, rales, crackles, cardiac murmur or arrhythmia, jugular venous distension, meningeal signs, focal neurological loss, Trousseau sign, Chvostek sign, jaundice, melena, hematochezia, hepatosplenomegaly, or there may be no definitive signs at all beyond hyperventilation.
With a wide preliminary differential diagnosis list, evaluation should always begin with a thorough history and physical exam to focus diagnostic considerations. In all cases, arterial blood gas is necessary to diagnose any pH imbalances. Serum electrolytes should be measured with attention to sodium, potassium, and calcium levels as aberrations in these may lead to further complication. Magnesium and phosphate are also essential to measure. In hypoxic patients, it is important to calculate the A-a gradient to determine the etiology and further diagnosis. If the A-a gradient is wide, be suspicious of pulmonary embolism and appropriately work up the patient. A chest x-ray is important in all patients as it helps discern an anatomical or infectious cause and may rule in/out pulmonary edema. If there is a clinical reason for it, chest CT can play a vital role in achieving a diagnosis. If there is appropriate clinical suspicion for neurological insult, CT or MRI of the head may be appropriate along with lumbar puncture for WBC, glucose, and protein analysis.
Treatment of hypocapnia is targeted at treating the underlying pathology to reduce the respiratory rate if possible. Historically treatment involved rebreathing into a paper bag to increase alveolar CO2. However, this has been shown to increase undesirable outcomes including mortality and is no longer recommended. In anxious patients, anxiolytics may be necessary. In infectious disease, antibiotics targeting sputum or blood cultures are appropriate. In embolic disease, anticoagulation is necessary. Ventilator support may be necessary for patients with acute respiratory failure, acute asthma, or acute COPD exacerbation if they show signs of respiratory fatigue. In ventilator controlled patients, it may be necessary to reevaluate their ventilator settings to reduce respiratory rate. If hyperventilation is intentional, monitor the arterial or venous blood gas values closely. In severe cases, pH may be directly reduced using acidic agents; however, this is not routinely performed.
Hypocapnia is relatively benign and well tolerated by patients, as such the prognosis is linked to the underlying etiology and response to treatment.
Hypocarbia is typically resultant to hyperventilation.
Hyperventilation typically occurs in response to an insult such as hypoxia, metabolic acidosis, pain, anxiety, or increased metabolic demand.
Hypocarbia results in respiratory alkalosis.
Respiratory alkalosis is not life-threatening. However, the underlying etiology may be. Always look for and treat the source of the illness.
Interventions to reduce pH directly are typically not necessary.