Reflex Control of Breathing

• The medulla houses both inspiratory and expiratory neurons that interact to regulate breathing.
• Dorsal Respiratory Groups (DRGs) contain primarily inspiratory neurons.
• Ventral Respiratory Groups (VRGs) contain both inspiratory and expiratory neurons.
• DRG neurons are mainly inspiratory neurons located on both sides of the medulla.
• The vagus and glossopharyngeal nerves transmit sensory impulses to the DRGs from the lungs, airways, peripheral chemoreceptors, and joint proprioceptors.
• VRG neurons are located bilaterally in the medulla in two different nuclei and contain inspiratory and expiratory neurons.
• The pons contains the apneustic center and the pneumotaxic center.
• The apneustic center's function is evident when its connections to the pneumotaxic center and vagus nerves are severed.
• Severing these connections causes prolonged inspiratory gasps interrupted by occasional expirations, called apneustic breathing.

Reflex Control of Breathing

• The Hering-Breuer inflation reflex is generated by stretch receptors in the smooth muscle of large and small airways.
• Sudden lung collapse stimulates strong inspiratory effort.
• The Head paradoxical reflex may be responsible for the first breaths of a newborn.
• Rapidly adapting irritant receptors in the epithelium of larger conducting airways have vagal sensory nerve fibers.
• Stimulation of irritant receptors causes reflex bronchoconstriction, coughing, sneezing, tachypnea, and narrowing of the glottis.
• Hydrogen has a proportional relationship with PaCO2.
• J-receptors are C-fibers in the lung parenchyma near the pulmonary capillaries.
• Alveolar inflammatory processes, pulmonary vascular congestion, and pulmonary edema stimulate J-receptors.
• Proprioceptors in muscles, tendons, joints, and pain receptors send stimulatory signals to the medullary respiratory center.
• CO2 stimulates the medullary chemoreceptors by forming H+ in the cerebrospinal fluid (CSF).
• The blood-brain barrier is almost impermeable to H+ and HCO3 − but is freely permeable to CO2.
• Peripheral chemoreceptors are located in the aortic arch and bifurcations of common carotid arteries.
• Peripheral chemoreceptors are oxygen-sensitive cells that react to reductions of oxygen levels in the arterial blood.
• Hypoxemia increases receptors sensitivity for hydrogen H+.
• Decreased PaO2 causes an increase in VE for any pH, and vice versa.
• Oxygen is not a significant response until PaO2 falls to 60 mmHg. A further fall results in a sharp increase in VE.
• Under normal circumstances, oxygen plays a role in drive to breath.
• Hypoxemia is the most common cause of hyperventilation.
• Peripheral chemoreceptors respond to increased PaCO2 and H+ but are less responsive to CO2 and hyperemia.
• Coexisting acidosis, hypercapnia, and hypoxemia maximally stimulate peripheral chemoreceptors.
• In hypercapnic COPD patients there is a depressed respiratory response to increased CaO2.

Control of Breathing in Chronic Hypercapnia

• A sudden rise in PaCO2 causes an immediate rise in VE.
• In slow-rising PaCO2 (severe COPD), kidneys retain HCO3, which maintains pH.
• Oxygen therapy may cause a sudden rise in Paco2 in severe COPD with chronic hypercapnia due to removal of hypoxic drive.
• Absorption atelectasis can occur with FiO2 > 60%.
• COPD does not always signify chronic hypercapnia or that O2 therapy will induce hypoventilation and is only present in end-stage COPD.
• Oxygen should never be withheld in hypoxemic COPD patients as tissue oxygenation is an overriding priority.

Abnormal Breathing Patterns

• Cheyne-Stokes respirations (CSR) are characterized by cyclic waxing and waning ventilation with apnea.
• CSR is seen with low cardiac output states in CHF.
• Biot’s respiration occurs with CNS problems similar to Cheyne-Stokes but VT is constant except during apnea periods.
• Central neurogenic hyperventilation may be caused by head trauma, severe brain hypoxia, or lack of cerebral perfusion.
• Central neurogenic hypoventilation means the medulla respiratory centers are not responding to appropriate stimuli.
• Central neurogenic hypoventilation is associated with narcotic suppression, head trauma, and increased ICPs.
• Increased CO2 will dilate cerebral blood vessels and vice versa, and perfusion stops with acute ICP.
• Mechanical hyperventilation lowers PaCO2 and ICP but is controversial as it reduces O2 and CBF to the injured brain.
• Central chemoreceptors are the primary drive to breath in healthy humans and operate off of increased levels of CO2 (PaCO2 levels > 45).
• COPD patients' drive to breathe is when PaO2 is < 60.