32.2f Regulation of Ventilation

The lower portions of the brainstem, specifically the medulla, control ventilation.

This area of the brain sends a constant, repetitive signal to the lungs to initiate inspiration.

The medulla contains both an inspiratory and an expiratory center.

However, because expiration is generally a passive process, the inspiratory center plays a more active role in the rhythm of breathing.

The resting rate of respiration varies between 12 and 20 breaths per minute in an adult.

The medullary signal is transmitted through the phrenic and intercostal nerves to the primary muscles of ventilation—that is, to the diaphragm and the intercostal muscles, respectively.

The medullary signal can be modified by input from voluntary centers in the cerebral cortex, from other centers in the hypothalamus and brainstem (pons), and from other areas of the medulla.

Other receptors throughout the body also provide input to the respiratory center.

This allows tight control of ventilation in response to the body’s physiologic needs.

Stretch receptors, located on the visceral pleura and on the walls of the bronchi and bronchioles, are important body structures that provide input to the medulla’s respiratory center.

As the patient continues to inhale, signals from these receptors become stronger until they completely inhibit impulses transmitted from the medulla.

As the lungs begin to recoil, the signals become less intense, allowing the medulla to begin another inspiratory phase.

This mechanism called the Hering-Breuer reflex prevents overinflation of the lungs.

The medulla also receives input to increase the ventilatory rate from receptors that are stimulated by irritants in the lung and bronchial tree and from receptors that detect increased activity in muscles and joints.

The most important determinant of the ventilatory rate is the arterial partial pressure of carbon dioxide (PCO2).

An increase in the patient’s arterial PCO2 results in a decrease in the pH of the blood.

An increase in carbon dioxide in the blood also results in an increase in carbon dioxide in cerebrospinal fluid (the fluid that bathes the brain and spinal cord).

Carbon dioxide (CO2) and water combine to produce an acid, resulting in a lowering of the pH (increasing the concentration of hydrogen ions) in the cerebrospinal fluid.

Chemical receptors in the area of the medulla detect this decrease in the pH, producing an increase in the ventilatory rate, which helps the body eliminate excess CO2 and return the pH to a normal level.

There are also chemical receptors in the carotid artery and aorta that are directly sensitive to the arterial PCO2.

Stimulation of these receptors by an increase in arterial PCO2 will also stimulate respiration.

Remember that there is instantaneous feedback through these chemical receptors to the medulla so that, once changes in cerebrospinal fluid pH and arterial PCO2 are corrected, the stimulus to increase respiration ceases.

Unfortunately, regulation of ventilation in patients with COPD does not take place as described.

In patients with this disorder, the body becomes less responsive to changes in arterial PCO2.

Instead, the major breathing stimulus comes from the level of oxygen detected in arterial blood by receptors in the aortic arch.

As a result, patients with COPD will achieve a delicate balance in the partial pressure of oxygen (PO2), with the level being low enough to continually stimulate the medulla’s respiratory center while having enough oxygen to maintain normal body functions.

Measured PO2 levels of between 50 and 60 mmHg are not uncommon in this patient population.