- The control of breathing involves both volitional and automatic elements and is far more complicated than merely reflecting a response to hypoxemia or hypercapnia.
- Hyperventilation describes breathing that is in excess of what is needed to meet the metabolic needs of the body, as reflected in the production of carbon dioxide.
- Hypoventilation describes breathing that is insufficient to meet the metabolic needs of the body, as reflected in the production of carbon dioxide.
- Hyperpnea refers to increased breathing that matches the metabolic needs of the body.
- Tachypnea signifies an increase in respiratory rate above the normal range.
- The neural structures responsible for the automatic control of breathing reside primarily in the medulla. Neurons in the pons may contribute to the transitions from inspiration to expiration.
- Minute-to-minute breathing in a normal person is the consequence of the automatic activity of neurons in the brainstem, which is referred to as the central pattern generator.
- Nerves that innervate the diaphragm exit the spinal cord between the third and fifth cervical vertebrae. The intercostal muscles are supplied by nerve roots emanating from the thoracic spinal cord.
- The breathing of children with congenital central hypoventilation syndrome suggests that in the awake state, breathing is not dependent on a functioning central pattern generator.
- Anxiety and discomfort affect the volitional control of breathing. Patients typically adopt breathing patterns that seem to reduce the discomfort of breathing.
- There are multiple sources of information from receptors throughout the respiratory system that affect the control of breathing.
- Mechanoreceptors in the upper airway, lungs, and chest wall are activated by mechanical distortion of their local environment.
- Stimulation of flow receptors in the airways has an inhibitory effect on ventilation.
- Inflation of the lungs, which stimulates SARs, has an inhibitory effect on the controller.
- Deflation of the lungs has a stimulatory effect on the controller, mediated via both slowly and rapidly adapting receptors (decreased activity of SARs; increased activity of RARs).
- Stimulation of J receptors (C fibers) by increased pulmonary vascular pressures or interstitial edema may contribute to the tachypnea seen in individuals with CHF.
- Information from Golgi tendon organs and muscle spindles in the chest wall may play an important role in load compensation.
- The peripheral chemoreceptors are located in the carotid bodies and are stimulated by low PaO2, high PaCO2, and low arterial pH.
- The central chemoreceptor is located in the medulla and is activated by high PaCO2 and low arterial pH.
- The differential permeability of the blood-brain barrier for carbon dioxide and hydrogen ions results in a counterbalancing role for the central chemoreceptor relative to the peripheral chemoreceptor when the latter is responding to acute changes in arterial pH.
- The ventilatory response to hypoxia is relatively flat until the PaO2 decreases below 60 mm Hg.
- The ventilatory response to hypercapnia is linear.
- The ventilatory response to exercise consists of three phases: neurological, metabolic, and compensatory. None of these depends on the presence of hypoxemia or hypercapnia.
- Patients with chronic hypercapnia do not depend on hypoxemia in order to breathe. Administration of oxygen to patients with acute respiratory problems superimposed on chronic respiratory failure will not cause the patients to stop breathing in most situations. PaCO2 increases under these circumstances as a result of a small decrease in ventilation, worsening ventilation/perfusion mismatch, and the Haldane effect.