Overview of Respiratory Acidosis

With respiratory acidosis, “acidosis” refers to a process that lowers blood pH below 7.35, and “respiratory” refers to the fact that it’s a failure of the respiratory system carrying out its normal pH- balancing job.

Normally, during an inhalation, the diaphragm and chest wall muscles contract to pull open the chest and that sucks in air like a vacuum cleaner. Then, during an exhalation, the muscles relax, allowing the elastin in the lungs to recoil, pulling the lungs back to their normal size and pushing that air out. Ultimately, the lungs need to pull oxygen into the body and get rid of carbon dioxide CO2. CO2 binds to water H2O in the blood and forms H2CO3 carbonic acid, which then dissociates into hydrogen H+ and bicarbonate ions HCO3-. So, in order to prevent pH fluctuations, the CO2 concentration, or the partial pressure of CO2, called PCO2, needs to be kept within a fairly narrow range. For this reason, lungs maintain the ventilation rate they need to get rid of CO2 at the same rate that it’s created by the tissues. If PCO2 levels starts to rise and pH starts to fall, chemoreceptors that are located in the walls of the carotid arteries and in the wall of the aortic arch start to fire more, and that notifies the respiratory centers in the brainstem that they need to increase the respiratory rate and the depth of breathing. As the respiratory rate and depth of each breath increase, the minute ventilation increases - that’s the volume of air that moves in and out of the lungs in a minute. The increased ventilation helps move more carbon dioxide CO2 out of the body, reducing the PCO2 in the body, which raises the pH.

In respiratory acidosis, the normal mechanism of ventilation is disturbed, and minute ventilation becomes inadequate to balance the pH. This could be due to a number of problems. Sometimes, the problem is not in the lungs themselves, but in the respiratory centers of the brainstem. After a stroke or a medication overdose, like with opioids or barbiturates, the respiratory centers can slow their rate of firing, so breathing becomes extremely slow or stops entirely.

It may also be due a neuromuscular disorder like myasthenia gravis, where the nerves don’t effectively stimulate the muscles to contract. Sometimes the diaphragm or chest wall muscles didn’t work properly, which can happen after severe trauma, or due to obesity when the chest wall is too heavy for the muscles to lift.

Another reason is airway obstruction, which might happen if a child swallows an object like a peanut and it lodges in the right mainstem bronchus, preventing that lung from fully ventilating.

Finally, there might be impaired gas exchange between the alveoli and the capillary. That might happen if alveoli are damaged from chronic obstructive pulmonary disease, or if fluid accumulates within the alveoli like in pneumonia, or if fluid collects between the alveoli and the capillary walls like in pulmonary edema.

In all of these situations, the result is that the lungs can’t efficiently get rid of CO2. The CO2 accumulates in the blood, so PCO2 rises, usually above 45 mmHg. This causes a decrease in blood pH, often reducing it below 7.35. To compensate for this decrease, the body has designed several mechanisms. If the respiratory centers are working, then they try to increase the rate and depth of ventilation. If that doesn't work, then some of the excess CO2 diffuses across cell membranes, especially into red blood cells, where it reacts with water H2O molecules and forms H2CO3 carbonic acid, which eventually gets converted into hydrogen H+ and bicarbonate ions HCO3-. The key here is that this HCO3- can quickly escape to the circulation, trying to counteract the increased PCO2 and keeping the pH from getting too low. At the same time, though, free hydrogen H+ ions are generated, which could very well make the intracellular environment acidic. Fortunately, they can be bound and neutralized by various basic molecules within the cells, mainly exposed —NH2 amine groups in proteins like hemoglobin. However, the concentration of these proteins is too low compared to the amount of excess carbon dioxide molecules floating through the blood. What this means is that if all of these carbon dioxide molecules tried to hide inside the cells, they would give rise to a whole lot of hydrogen H+ ions that have no spare protein to bind to and thus, mess with the intracellular pH. So, essentially, only a small amount of carbon dioxide molecules find their way into the cells. As a result, the amount of HCO3- that is generated is too little- about 1 mEq/L for each 10-mmHg increase in PCO2, to have a substantial effect on pH. For example, if PCO2 has an acute rise of 20 mmHg, let’s say it moved from 40-mmHg to 60-mmHg, then this mechanism could only result in a rise of plasma bicarbonate by 2 mEq/L from its reference value of 24 mEq/L up to 26 mEq/L, which can’t have a big impact on the pH. Therefore the pH remains very low during this acute phase of the disorder.

Fortunately, if minute ventilation hasn’t decreased to life-threatening levels, then within about three to five days, the kidneys start sensing that pH is too low and step up to help correct the imbalance. More specifically, the cells of the proximal convoluted tubule begin generating and reabsorbing more HCO3- into the bloodstream. In fact, the kidneys are pretty effective in doing so, as they manage to increase the concentration of HCO3- about 4 mEq/L for each 10-mmHg increase in PCO2. So if PCO2 went up from 40-mmHg to 60-mmHg, a 20 mm-Hg increase, plasma bicarbonate HCO3- would increase by 8 mEq/L, going from its reference value of 24 mEq/L up to 32 mEq/L. This can lead to a substantial increase in the pH, bringing it closer to its normal range again.

All right, as a quick recap, respiratory acidosis occurs when the lungs fail to eliminate excess CO2, which builds up in the blood, causing blood pH to fall below 7.35. It is divided into an acute and a chronic phase according to the absence or presence of renal compensation, respectively, which raises HCO3- concentration in blood.