Carbon Dioxide and pH

Ventilation

Respiration (the exchange of CO2 for O2) depends on adequate ventilation (the movement of air into and out of the lungs) and an adequate interface between the air and the surface area of the alveoli).

Two things drive the mechanical act of ventilation:

1. Higher-than-normal CO2 (primarily)
2. Lower-than-normal O2

Chemoreceptors that Drive Ventilation

The control of respiration is via neural and chemical receptors in the upper airway, lungs, and pulmonary vessels and the vagus nerve to affect the breathing pattern to increase respiration or stimulate cough, bronchoconstriction, and mucus production. Respiratory muscles move the diaphragm and manipulate respiratory muscle tone to maintain airway patency.

Central chemoreceptors in the central nervous system (CNS) adjust ventilation to maintain acid-base homeostasis, responding to pH changes. This surveillance is done at the medulla in the brainstem, via assessing acidity (lower pH) of cerebrospinal fluid (CSF). Acid production in the CSF is from CO² which crosses freely across the blood-brain barrier, proportionately to the higher CO² in the blood. 

There are also peripheral chemoreceptors in the carotid and aortic bodies to sense low O2 concentration primarily and, to a lesser extent, high CO².

The parasympathetic nervous system (PNS) responds to increased CO².

Stimulation of ventilation can occur with a small rise in CO², but requires a relatively larger fall in PO2.

Central respiratory centers receive stimulatory input from central respiratory pacer cells, central and peripheral chemoreceptors, upper airway receptors, other areas of the brain, and volitional pathways. Central respiratory centers integrate these signals into a combined output to the muscles of respiration. Thus breathing occurs autonomously, adjusting on the fly, but can also be controlled voluntarily.

TRANSLATED: You take in oxygen by inhaling, your body exchanges carbon dioxide for oxygen, you exhale and blow out the carbon dioxide from your body, and the whole process adjusts on the fly via central and peripheral chemoreceptors with involvement of the PNS (parasympathetic nervous system, vagus nerve). 

Chemoreceptors Summarized:

• Carotid body peripheral chemoreceptors: for O² and CO² (O² > CO²).
• Aortic body peripheral chemoreceptors: O² and CO², but mainly in infancy and childhood.
• CNS chemoreceptors: for pH.
• PNS: for CO².

 

CO2 is Associated with Acidosis

In contributing to acidosis, in order of magnitude, there are:

1. Carbonic acid (H²CO³), from the CO² produced with each breath combining with water.
2. Organic acids (lactic acid, citric acid) from reactions in day-to-day metabolism.
3. Nonvolatile acids, such as sulfuric acids from metabolism of sulfur-containing amino acids in the diet. They are excreted by the kidneys.

Of these, carbon dioxide is "respiratory acid," and it contributes the most acidity to the physiologic processes due to its conversion to carbonic acid.

When you're not breathing adequately, you are not getting rid of this "respiratory acid" and it builds up in the tissues, which can lower the pH (respiratory acidosis). Excess CO2 molecules combine with water in your body to form carbonic acid which makes your pH go down. This can begin a serious cascade of unfortunate events if not corrected.

Acidosis is a slippery slope--acidosis impairs systems which makes more acidosis--unless corrected.

HYPERCAPNIA: an increase in retained CO2. Acute and chronic respiratory failure cause hypercapnia, and when it is acute, it is always accompanied by acidosis; when it is chronic, acidosis can be absent or only slightly evident.

The worst-case scenario is an acute-on-chronic hypercapnia, in which the hypercapnia and acidosis is worse than in either alone.

Causes of Hypercapnia:

• Patient won't breathe: decreased respiratory drive due to impaired respiratory control center in the brain (opioid or benzodiazepine overdose, encephalitis, stroke, sleep apnea, hypothyroidism, and hypothermia).
• Patient can't breathe: neuromuscular disorders (infection, dehydration, cervical spine injury, ALS, polio, Guillain-Barré, phrenic nerve injury, myasthenia gravis, muscular dystrophy, and polymyositis; also some emphysema (COPD); also drugs, toxins, and poisons.
• Thoracic cage disorders (kyphosis, scoliosis, etc.)
• Increased dead space (non-gas-exchanging parts of the lung).

Anatomical dead space: if the inspiratory effort cannot move air all the way from the mouth/nose to the alveoli, it will only go in-and-out in the upper airways and CO2/O2 respiration cannot take place.

Alveolar dead space: If there is destruction to alveoli such that less surface area is available for respiration, at some point it becomes critical, creating alveolar dead space.

Examples of alveolar dead space:

• COPD,
• pneumonia,
• interstitial fibrosis, and
• pulmonary vascular disease.