RCP 100 Ch 15 Regulation of breathing

Regulation of Breathing

• Breathing regulation is covered in chapter 15.
• A rhythmic breathing cycle begins in the medulla.
• Higher brain centers, systemic receptors, and reflexes can modify the medulla's output.
• The medulla contains diverse groups of respiratory-related neurons instead of separate inspiratory and expiratory centers.
• These neurons form dorsal and ventral respiratory groups.

Medullary Respiratory Center

• The dorsal respiratory groups (DRG) consist mainly of inspiratory neurons bilaterally in the medulla.
• DRG neurons send impulses to the motor nerves of the diaphragm and external intercostal muscles.
• DRG nerves extend into the Ventral respiratory groups , containing both inspiratory and expiratory neurons.
• Vagus and glossopharyngeal nerves relay sensory impulses to the DRG from the lungs, airways, peripheral chemoreceptors, and joint proprioceptors.
• This input modifies the breathing pattern.
• Ventral respiratory groups (VRG) contain both inspiratory and expiratory neurons bilaterally in the medulla.
• VRG sends inspiratory impulses via the vagal nerve to laryngeal and pharyngeal muscles, the diaphragm, and external intercostals.
• Other VRG neurons send expiratory signals to abdominal muscles and internal intercostals.
• The inspiratory ramp signal starts low and gradually increases.
• This produces a smooth inspiratory effort instead of a gasp.

Pontine Respiratory Centers

• This modifies the output of medullary centers.
• The pontine centers are apneustic and pneumotaxic
• The apneustic center identifies its function by cutting connection to medullary centers.
• Apneustic breathing has long gasping inspirations interrupted by occasional expirations.
• The pneumotaxic center controls the "switch-off," thus controls I₁ (inspiratory time).
• Increased signals increase RR, and weak signals prolong I₁ and large V₁.

Reflex Control of Breathing

• The Hering-Breuer inflation reflex has receptors in the smooth muscle of large and small airways.
• Lung distention causes stretch receptors to send inhibitory signals to the DRG, stopping further inspiration.
• In adults, the Hering-Breuer inflation reflex is active only on large V₁ (>800 ml).
• It regulates the rate/depth of breathing during moderate to strenuous exercise.
• Deflation reflex: Sudden lung collapse stimulates a strong inspiratory effort, causing hyperpnea as with pneumothorax.
• Head's paradoxic reflex may maintain large V₁ during exercise and deep sighs.
• Periodic sighs help prevent alveolar collapse, or atelectasis.
• It is considered possible for babies' first breaths at birth.
• Irritant receptors are stimulated by inhaled irritants or mechanical factors.
• They cause bronchospasm, cough, sneeze, tachypnea, and narrowing of the glottis.
• These are vagovagal reflexes.
• In a hospital, they are triggered by suctioning, bronchoscopy, and endotracheal intubation.
• J-receptors (juxtacapillary) are located in the lung parenchyma.
• They are stimulated by pneumonia, CHF, and pulmonary edema.
• They cause rapid, shallow breathing and dyspnea with expiratory narrowing of the glottis.
• Peripheral proprioceptors are found in muscles, tendons, joints, and pain receptors.
• Movement stimulates hyperpnea.
• Moving limbs, pain, and cold water all stimulate breathing in patients with respiratory depression.

Chemical Control of Breathing

• The body maintains O2, CO2, and pH levels via chemoreceptors' mediation, affecting Vᴇ.
• Central chemoreceptors are located bilaterally in the medulla.
• Central chemoreceptors are directly stimulated by H+ ions and indirectly by CO₂.
• The blood-brain barrier is almost impermeable to H+ and HCO₂- yet CO₂ freely crosses.
• In CSF, CO₂ is hydrolized, releasing H+.
• Increased CO₂ increases H+ in CSF, causing increased ventilation to restore normal levels pH and CO2.
• V increased 2-3 L/min for every 1 mm Hg rise of PaCO2 in the medulla.
• Peripheral chemoreceptors are located in the aortic arch and bifurcations of common carotid arteries.
• They are oxygen-sensitive cells that react to reductions of oxygen levels in the arterial blood.
• Hypoxemia boosts receptors' sensitivity to H+.
• ↓PaO2 causes ↑ Vᴇ for any pH, and vice versa.
• In severe alkalosis, hypoxemia has little affect on V.
• There is no significant response until PaO2 falls to ~60 mm Hg.
• Then, a further PaO2 fall results in sharp increase in Vᴇ.
• Even under normal circumstances, oxygen plays no role in drive to breathe.
• Hypoxemia the most common cause of hyperventilation.
• Peripheral chemoreceptors' response is less responsive than central chemoreceptors (CCRs).
• CCRs account for ⅓ the hypercapnic response, reacting more rapidly to changes in [H+]. Carotid bodies are directly exposed to arterial blood, helping the ventilatory system quickly respond to metabolic acidosis, even with the H+ ions cross the BBB with difficulty.
• In hyperoxia, PCRs are almost totally insensitive to changes in PaCO2; therefore, any response results from CCRs.
• Coexisting acidosis, hypercapnia, and hypoxemia maximally stimulate peripheral chemoreceptors.
• Hypercapnic COPD patients depress the respiratory response to ↑CaO₂.
• In slow-rising PaCO2 (severe COPD), kidneys retain HCO3-, which maintains CSF pH, so there is no increased ventilation response.
• Hypoxemia with hypercapnia becomes the minute-to-minute breathing stimulus via an altered response to [H+].
• Hypoxemia is always present in severe COPD, causing mismatches in V/Q.
• An increased FIO₂ raises PaO₂, which makes the PCR less sensitive to [H+], raising PaCO2.
• O2 therapy may cause a sudden rise in Paco₂ in severe COPD with chronic hypercapnic.
• Hypoxic drive is traditionally removed.
• ↑FIO₂ may worsen V/Q mismatch.
• Hypoxic pulmonary vasoconstriction is reversed to poorly ventilated alveoli.
• An ↑FIO₂ may make a patient susceptible to absorption atelectasis.
• O₂ should NEVER be withheld in hypoxemic COPD patients.

Oxygen-induced Hypercapnia Key Points

• “COPD” does NOT signify chronic hypercapnia, or that O2 therapy will induce hypoventilation.
• The characteristics only occur in end-stage disease and are present in small percentage of COPD patients.
• Concern about O₂-induced hypercapnia and acidemia is not warranted in most COPD patients.
• Preparation is necessary to provide mechanical ventilation for rare COPD patents experiencing severe hypoventilation because of oxygen therapy.

Abnormal Breathing Patterns

• Cheyne-Stokes respirations (CSR) are characterized by cyclic waxing/waning ventilation with apnea, gradually causing hyperpnea.
• CSR is seen with low cardiac output states (CHF)
• There is a lag of CSF CO₂ behind arterial Paco₂ and a characteristic cycle follows.
• Biot's respiration is similar to Cheyne-Stokes with constant Vᴛ except during apneic periods.
• Biot's Respiration is seen with patients with elevated ICP.
• Apneustic breathing indicates damage to the pons.
• Central neurogenic hyperventilation may be caused by head trauma, severe brain hypoxia, or lack of cerebral perfusion.
• Central neurogenic hypoventilation occurs when the medulla respiratory centers are not responding to appropriate stimuli.
• It can be associated with head trauma, cerebral hypoxia, and narcotic suppression.

CO2 and Cerebral Blood Flow

• CO₂ plays an important role in autoregulation of CBF mediated through H+ formation.
• Increased CO₂ dilates cerebral vessels, and a decrease causes the vessels to narrow.
• In traumatic brain injury (TBI), the brain swells, raising ICPs beyond cerebral arterial pressure.
• This results in cerebral hypoxia/ischemia.
• Mechanical ventilation lowers PaCO2 and ICP
• It is controversial because it reduces O₂ and CBF to the injured brain.
• Hypoventilation in TBI patients must be avoided.