Respiratory Alkalosis

Respiratory alkalosis is a condition where the blood pH is alkaline (pH>7.45) due to low levels of carbon dioxide. Recall that CO₂ is in equilibrium with carbonic acid. Hence, low levels of blood CO₂ will translate to low levels of carbonic acid, which in turn will raise pH. The body loses or sloughs off too much CO₂ primarily by means of hyperventilation.

Causes of Respiratory Alkalosis

Respiratory Alkalosis is caused primarily by hyperventilation. As a patient hyperventilates the the serum CO₂ comes into contact with the atmosphere. Intracellular CO₂ makes up approximately 5.2% of the partial pressure of venous blood. By contrast atmospheric CO₂ levels are much lower, making up only 0.04% of the concentration of the atmosphere^[8]. This incredible difference in concentration creates a concentration gradient which draws CO₂ out of the lungs and into the atmosphere through capillaries in alveoli – thus reducing serum CO₂ levels. The faster the patient breathes, the greater the volume of CO₂ comes in contact with the atmosphere, the faster the loss of CO2 from the body. As CO₂ levels drop so do carbonic acid levels, (remember our buffer system). The result is a reduction in proton availability in the serum resulting in an elevated pH.

Hyperventilation has many causes including psychological (e.g. panic attack) and physiological mechanisms. The body’s response to pain often manifests in a sympathetic response causing an increase in respiratory rate. Similarly, poor oxygenation of blood (hypoxemia) will also cause a sympathetic tachypnea. Obstruction in airways (severe pneumonia) or insufficient oxygen loading of blood (e.g. pulmonary embolism) will also lead to hypoxemia and hence hyperventilation.^[1]

Another cause of hyperventilation is damage to the respiratory centres or mechanical drive to hyperventilate (e.g. use of a ventilator in a health care setting).

Clinical Manifestation of Respiratory Alkalosis

Presentation of respiratory alkalosis will be increased respiratory rate alongside symptoms of the cause of the hyperventilation. If the cause is psychological in nature, a pronounced sympathetic response would be present (e.g. high heart rate, twitching muscles, sense of anxiety). If the cause is due to hypoxemia, a low O₂ saturation in peripheral blood may manifest as short of breath, fatigue, and weakness. An obstruction in airway causing the hypoxemia can be audible as crackles (e.g.. pneumonia) alongside the fast respiratory rate. Please note that hypoxemia caused by pulmonary embolism (i.e. blockage in pulmonary blood vessels) will NOT present with any audible lung sounds – but pain would be present.

Compensation

In order to lower the alkaline pH, the kidneys would have to play a role until the hyperventilation is dealt with. During compensation there will be a reduction in serum bicarbonate reflect a compensatory mechanism of the kidneys eliminating bicarbonate to lower the pH.^[4]

If there is no renal compensation evident, it may be reflective of a mixed alkalosis, resulting from both metabolic and respiratory conditions. Mixed alkalosis is beyond the scope of this text.

Complications of Respiratory Alkalosis

Alkalosis can lead to hypokalemia and hypocalcemia which can lead to life threatening arrhythmias.

Hypokalemia

Studies have shown that both respiratory and metabolic alkalosis result in the kidneys trying to retain H+ to lower the blood pH. However, to maintain electroneutrality, the kidneys will increase excretion of potassium, thus leading to hypokalemia ^[2].

Respiratory Alkalosis and Hypocalcemia

As pH rises, albumin, being a protein buffer, begins to undergo physical changes in response to the new environment. Hydrogen is removed from the albumin and calcium binds instead. This slowly leads to low serum calcium levels (hypocalcemia). Calcium is essential action potentials and neurotransmitter release (see Neurons: the Functional Unit of the Nervous System). It is likely that the removal of calcium raises the resting membrane potential bringing it closer to threshold, meaning less stimulus is required to achieve the electrical potential required for inciting an action potential. This may be the mechanism by which hypocalcemia increases nerve excitability. As nerves begin to fire unexpectedly a patient may begin experiencing tingling sensations. Once levels drop past a certain threshold the patient may begin to experience spontaneous muscle contraction, known as twitching that develops into tetany (sustained muscle contraction). This can cause additional panic and confusion in an already hyperventilating person.^[3][5]

References

1. 1. Rational Treatment of Acid Base Disorders
   2. Fluid, Electrolyte and Acid-Base Disorders: Clinical Evaluation and Management
   3. Membrane Potentials and Action Potentials
   4. Physiology, Acid Base Balance – StatPearls 4
   5. pH and smooth muscle