When a standard blood test, often part of a comprehensive metabolic panel, shows a low level of carbon dioxide (\(\text{CO}_2\)), it signals an underlying disturbance in the body’s acid-base balance. This reading, typically reported as Total \(\text{CO}_2\) or Bicarbonate, measures the components circulating in the bloodstream that regulate acidity, not the gas you exhale. A significantly reduced value indicates the body is struggling to maintain its internal chemical equilibrium, a condition known as acidemia or a compensatory state for acid loss. This imbalance requires prompt medical attention to identify the root cause, but it can often be successfully treated once diagnosed.
Understanding Carbon Dioxide’s Role in Blood
The \(\text{CO}_2\) measurement on a metabolic panel represents the total concentration of all forms of carbon dioxide in the blood. The majority of this total \(\text{CO}_2\) (approximately 90 to 95 percent) exists as bicarbonate (\(\text{HCO}_3^{-}\)), a negatively charged electrolyte. Bicarbonate functions as the body’s primary chemical buffer, neutralizing acids produced through normal metabolic processes.
The body requires a narrow and slightly alkaline \(\text{pH}\) range to function optimally, maintained by the bicarbonate-carbonic acid buffer system. The kidneys and lungs work together to regulate bicarbonate levels and the partial pressure of \(\text{CO}_2\) gas to keep the blood \(\text{pH}\) stable. A normal adult reference range for Total \(\text{CO}_2\) or bicarbonate generally falls between 23 and 29 milliequivalents per liter (\(\text{mEq/L}\)). A value below this range suggests the buffering capacity is depleted, leading to an overly acidic state called metabolic acidosis, or an attempt to compensate for another imbalance.
Underlying Causes of Low Blood CO2 Levels
Low Total \(\text{CO}_2\) levels are primarily caused by two distinct physiological mechanisms: metabolic acidosis (accumulation of too much acid) or respiratory alkalosis (compensation for excessive \(\text{CO}_2\) loss). In metabolic acidosis, the bicarbonate buffer is consumed while neutralizing an overproduction of acid from other sources. A common example is diabetic ketoacidosis (\(\text{DKA}\)), where a lack of insulin generates acidic ketone bodies that quickly deplete the available bicarbonate.
Failure to excrete acid waste is another cause of metabolic acidosis, frequently seen in advanced chronic kidney disease. Kidneys normally remove non-volatile acids and regenerate bicarbonate, but impaired function allows these substances to build up, consuming the buffer. Severe gastrointestinal losses, such as prolonged diarrhea, can also cause a direct loss of bicarbonate. Lactic acidosis, caused by conditions like sepsis or severe organ failure leading to low tissue oxygen, produces large amounts of acid that overwhelm the system.
The second primary mechanism is respiratory alkalosis, where low total \(\text{CO}_2\) is a compensatory response. This occurs when a person hyperventilates, breathing too quickly or deeply, causing excessive \(\text{CO}_2\) gas to be exhaled from the lungs. This rapid removal of \(\text{CO}_2\) gas lowers the acid component, prompting the body to excrete bicarbonate in the urine to correct the resulting alkaline state. Triggers for hyperventilation include anxiety, panic attacks, high fever, or exposure to high altitudes.
Recognizing the Physical Signs of Low CO2
The symptoms of low blood \(\text{CO}_2\) relate directly to the resulting acid-base imbalance and its severity. In metabolic acidosis, milder cases may present with fatigue, nausea, and headache. As acid levels increase, symptoms often progress to include confusion, lethargy, and weakness.
A physical sign of severe metabolic acidosis is Kussmaul breathing, a distinct pattern involving deep, rapid, and labored breaths. This occurs as the respiratory system attempts to compensate for the acid buildup by expelling more \(\text{CO}_2\) gas. Individuals with respiratory alkalosis may experience dizziness, lightheadedness, or numbness and tingling in the hands and feet due to hyperventilation.
Medical Approaches to Correcting Low CO2
Treatment for low blood \(\text{CO}_2\) focuses on identifying and resolving the underlying condition causing the imbalance, rather than just the numerical result. For patients with metabolic acidosis due to \(\text{DKA}\), immediate intervention includes administering insulin to halt ketone production and providing intravenous fluids to restore fluid and electrolyte balance. In cases of severe acidemia (e.g., blood \(\text{pH}\) below 7.1), intravenous sodium bicarbonate may be given to rapidly replenish the depleted buffer.
Fluid and electrolyte management is necessary to correct volume depletion and address abnormalities like low potassium. For chronic conditions like kidney disease, oral alkali therapy (such as sodium bicarbonate tablets or citrate solutions) is often prescribed to help maintain the serum bicarbonate level above 22 \(\text{mEq/L}\). If the low \(\text{CO}_2\) is caused by respiratory alkalosis from anxiety or pain, the approach involves calming the patient, using breathing techniques to slow the respiratory rate, and treating the source of the hyperventilation.