Acid Base Balance
Respiratory Acidosis
Carter Allen and Jennifer Kong
Learning Objectives
By the end of this section, you will be able to:
- Define respiratory acidosis.
- Explain the relationship between respiration and blood pH.
- Identify causes of respiratory acidosis.
Respiratory Acidosis
Respiratory acidosis is a condition where the lungs cannot remove enough CO2. As a result, the retained CO2 will be converted to carbonic acid, leading to increased acidity in the blood.
Causes of Respiratory Acidosis
Respiratory Acidosis is caused primarily by hypoventilation which means insufficient CO2 is being exhaled. CO2 is normally a byproduct of aerobic respiration to create ATP in order to meet metabolic demands. If the CO2 is not excreted in the lungs, then it begins to build up in the bloodstream. If we look back to our bicarbonate buffer equilibrium equation we will remember that, as CO2 levels rise the amount of carbonic acid made by carbon anhydrase will also increase, more protons will be released into the serum, and pH will lower (more acid).
Hypoventilation can be caused by CNS depression that affects the respiratory centres causing slow and/or shallow breathing (e.g. brain injury or medication/drug use).
Hypoventilation can also be caused by inefficient ventilation causing CO2 retention. Any condition which impairs the diaphragm from fully expanding or contracting will lead to insufficient CO2 being exhaled (e.g. obesity). Similarly, anything which prolongs exhalation – whether due to obstruction or lack of lung compliance as is the case of chronic obstructive pulmonary disease – will lead to hypoventilation
CO2 retention can also be a result of a physical blockage of CO2 leaving the respiratory system. Exudates in the alveolar space physically prevent alveolar gas exchange thus making it difficult for CO2 from being eliminated (e.g. Pulmonary edema, Pneumonia).
Clinical Manifestations of Respiratory Acidosis
As the root cause of respiratory acidosis is CO2 retention and hypoventilation, the signs and symptoms will be predominantly respiratory in nature. In the case of hypoventilation, an abnormally low respiratory rate will be seen with possible shallow breaths. In the case of alveolar exudates causing CO2 retention, coughing would be present. Upon auscultation, exudate manifest as audible crackles. Inefficient ventilation may also be heard as wheezes as exhalation is passing through a narrowed and/or blocked airway.
Consequences of Acidosis
Decreased Hemoglobin Affinity for Oxygen
Acidosis causes hypoxemia by reducing hemoglobin binding affinity for oxygen through what is known as the Bohr effect. As the environment around hemoglobin becomes saturated in hydrogen ions the hydrogen ions begin to cause conformational changes in hemoglobin. The hemoglobin that exists in these conditions is known as ‘taut hemoglobin’. When taut hemoglobin goes through a capillary in the alveoli the O2 concentration is so great that often it will bind some oxygen. When it reaches the tissues however it readily disassociates the oxygen in favour of binding to protons. This poses a barrier to proper perfusion.[1][3]
Acidotic Changes to Vessel Tone
Acidotic state often causes increased sympathetic tone – possibly as a way for the body to promote excretion of acid. The end result is increased cardiac output and vasoconstriction in peripheral vessels. Conversely, acidosis will cause vasodilation of cerebral capillaries which can lead to increased intracranial pressure. [2]
Compensation
The renal system should attempt to compensate by reabsorption of HCO3– at the proximal convoluted tubule to balance pH. [3] . In the distal tubule, H+ and NH4+ are excreted by increasing action of the sodium hydrogen antiporter: sodium is reabsorbed out of the solute in exchange for protons which are then excreted to compensate for the acidity. Urinary excretion of HCO3– under normal conditions is negligible.[2]