Hypocapnia: Description, Causes and Risk Factors:

Abnormally decreased arterial carbon dioxide tension.

Hypocapnia is defined as a deficiency of carbon dioxide (CO2) in the arterial blood. Most medical sources define hypocapnia as less than 35 mmHg for partial CO2 pressure in the arterial blood. The arterial CO2 value for normal breathing at rest is 40 mmHg (or about 5.3% CO2 partial pressure at sea level).


Hypocapnia is the result of overbreathing behavior, the mismatch of breathing rate and depth. Its consequence is an increased level of pH, or respiratory alkalosis, which may have profound immediate and long-term effects that trigger, exacerbate, and/or cause a wide variety of emotional, perceptual, cognitive, attention, behavioral, and physical deficits that may seriously impact health and performance. Although the fundamental importance of CO2 in body chemistry regulation, pH, and electrolyte balance, is common knowledge to any pulmonary or acid-base physiologist, it remains virtually unknown by most healthcare practitioners, health educators, breathing trainers, and laypeople.

Hypocapnia may be the result of the nervous system, cardiovascular (e.g., low blood pressure), respiratory (asthma), and metabolic disorders (e.g., diabetes), including challenges such as drugs, hormone changes (e.g., in pregnancy), altitude, heat, lung irritants, severe exercise, and others. In many of these cases, it plays an adaptive role, where it serves to compensate for pH deregulation, such as in the cases of lactic acidosis during severe exercise and ketoacidosis in diabetes.

Another term "alveolar hypocapnia" describes low CO2 levels in the alveoli of the lungs. Severe alveolar it generally leads arterial it, which causes respiratory alkalosis. (People with lung conditions often have arterial hypercapnia (elevated CO2) caused by alveolar is since alveolar hypocapnia immediately causes bronchospasm). These studies show that alveolar hypocapnia is very common for many chronic diseases. Most of these patients (with heart disease, diabetes, cancer, and so forth) have arterial hypocarbia as well.

Hypocapnia is caused by chronic hyperventilation (or an automatic deep breathing pattern) leading to alveolar it (lack of CO2), and if there is no ventilation-perfusion mismatch, to arterial CO2 deficiency. Normal breathing is imperceptible or unperceivable since it is small and light (10-12 breaths/min, 500 mL for tidal volume, and 6 L/min for minute ventilation at rest for a 70-kg person). In contrast, hypocapnic patients and even most normal subjects breathe over 10 L/min and have over 18 breaths/min for respiratory frequency.

Among lifestyle factors that cause hyperventilation and hypocapnia are physical exercise with mouth breathing, meals (eating and especially overeating), stress, anxiety, overheating, attempts to breathe deeply, deep breathing exercises (except slow ones, like Pranayama), supine sleep and being in the horizontal position, poor posture and many other factors.


General symptoms may include:

Visual disturbances.

  • Anxiety.
  • Transient dizziness in the person.
  • Muscle cramps.
  • Blackouts.

Since it is based on chronic hyperventilation, its symptoms are the same as the symptoms of hyperventilation. They are very wide and range from chronic coughing and nasal congestion to constipation, coughing and muscle cramps. Among other common symptoms of this disease are bronchospasm, cold extremities, mouth breathing, exacerbations of asthma, angina pain, and many others.

The key pathological effect of both, alveolar and arterial it is reduced levels of oxygen in body cells (tissue hypoxia).This promotes virtually all chronic diseases. These and other physiological effects associated with low CO2 and low oxygen levels in body cells, with numerous medical studies, are provided below (in CO2-related links).


A physician will typically start with a physical examination to determine the cause of hypocapnia. He or she may ask a series of questions regarding the type of symptoms, characteristics of the hypocapnia, medications being taken, medical conditions, feelings of anxiety or stress and other questions that can help determine the cause of the condition.

The following tests can also help diagnose episodes of hypocapnia:

Arterial Blood Samples.

  • Other Blood Tests.
  • Chest X-rays.
  • Ventilation/Perfusion Scans.
  • Chest CT Scans.
  • ECG (Heart Tracing).


Since hypocapnia is based on overbreathing, successful treatment of hypocapnia is based on addressing the cause: chronic hyperventilation. Therefore, treatment of hypocapnia is the same as treatment of hyperventilation.

The widely held view that hypocapnia poses a little risk to health under most conditions is no longer considered accurate. In fact, substantial hypocapnia in hospitalized patients, whether it is spontaneous or deliberately induced, may result in transient or permanent damage in the brain as well as in the respiratory and cardiovascular system.

Furthermore, rapid correction of severe hypocapnia leads to vasodilation of ischemic areas, resulting in reperfusion injury in the brain and lung. Consequently, severe hypocapnia in hospitalized patients must be prevented whenever possible, and if it is present, abrupt correction should be avoided. Severe alkalemia caused by acute primary hypocapnia requires corrective measures that depend on whether serious clinical manifestations are present. Such measures can be directed at reduction of plasma bicarbonate concentration, increase of PaCO2 or both. Even if baseline plasma bicarbonate concentration is moderately decreased, reducing it further can be particularly rewarding in this setting, as this maneuver combines effectiveness with relatively little risk. For patients with the anxiety-hyperventilation syndrome, in addition to reassurance or sedation, re-breathing into a closed system might prove helpful by interrupting the vicious circle that can result from the reinforcing effects of the symptoms of hypocapnia.

NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.


  1. Dr. Kushal kumar. A

    thank you for a detailed, comprehensive and neatly written article, it was of immense help for me to prepare my presentation on hypocapnea.

  2. Donald N.S. Wilson

    I am curious if you have observed a connection between Hypocapnia and seizures. This morning after a swim workout I was sitting in the sauna doing deep-breathing exercises. I breathed deeply, held my breath, and “stretched out” my lungs. I do this often as it induces a pleasant, even blissful, fainting feeling and associated “high”. However, this morning on my third such breath in I fainted for a moment (not uncommon) then as I “awoke” began convulsing for 4-7 seconds. I was sitting upright, and the convulsions were “mild” – in the sense I was able to remain sitting upright even just half “awake” – but it was a very weird experience as I have no history of seizures whatsoever. I feel great after (if a little embarrassed), but definitely a little concerned at the strange result.

    • editor-m

      Thank you for sharing your expirience with us. It is believed that the reduction in carbon dioxide tension and emerging with alkoloz and electrolyte shifts may affect certain neural structures, increasing their excitability, in connection with what hypertonus and convulsions are often observed in skeletal muscles.


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