Regulation of Breathing Study Notes

Chapter 15: Regulation of Breathing

Medullary Respiratory Center

• Origin of Breathing Cycle:

  • The rhythmic cycle of breathing originates in the medulla.

• Modification of Medullary Output:

  • Higher brain centers, systemic receptors, and reflexes modify the output of the medulla.

• Neuronal Organization:

  • There are no distinct inspiratory or expiratory centers.

  • The medulla contains scattered groups of respiratory neurons forming:

  • Dorsal Respiratory Groups (DRG)

  • Ventral Respiratory Groups (VRG)

Dorsal Respiratory Groups (DRG)

• Composition:

  • Mainly composed of inspiratory neurons, bilaterally located in the medulla.

• Function:

  • DRG neurons send impulses to the motor nerves of diaphragm and external intercostal muscles.

  • DRG nerves extend into VRG (and not vice versa) and contain both inspiratory and expiratory neurons.

• Sensory Input:

  • The vagus and glossopharyngeal nerves bring sensory impulses to the DRG from:

  • Lungs

  • Airways

  • Peripheral chemoreceptors

  • Joint proprioceptors

  • This input modifies the breathing pattern.

Ventral Respiratory Groups (VRG)

• Composition:

  • Contains both inspiratory and expiratory neurons, located bilaterally in the medulla.

• Impulses Sent:

  • VRG sends inspiratory impulses via the vagal nerve to:

  • Laryngeal and pharyngeal muscles

  • Diaphragm and external intercostals

  • Additional VRG neurons send expiratory signals to:

  • Abdominal muscles

  • Internal intercostals.

• Inspiratory Ramp Signal:

  • The ramp signal starts low and gradually increases, promoting smooth inspiratory effort rather than a gasp.

Pontine Respiratory Centers

• Function:

  • The pons modifies medullary centers' output.

• Components:

  • Two pontine centers:

  • Apneustic Center

  • Pneumotaxic Center

• Apneustic Center:

  • Its function was identified by severing its connection to medullary centers.

  • Apneustic breathing is marked by long gasping inspirations interrupted by occasional expirations.

• Pneumotaxic Center:

  • Manages the "switch-off" mechanism, effectively controlling the inspiratory time (IT).

  • Increased signals from the pneumotaxic center can raise the respiratory rate (RR), while weaker signals can prolong IT and increase tidal volume (VT).

Reflex Control of Breathing

• Hering-Breuer Inflation Reflex:

  • Receptors: Located in smooth muscle of both large and small airways.

  • Mechanism: Lung distention activates stretch receptors that send inhibitory signals to DRG, halting further inspiration.

  • Activation: Primarily active in adults with large tidal volumes (>800 ml) and helps regulate the rate and depth of breathing during exercise.

• Deflation Reflex:

  • Sudden lung collapse triggers a strong inspiratory effort leading to hyperpnea, especially observable in conditions like pneumothorax.

• Head's Paradoxic Reflex:

  • Preserves large tidal volumes during exercise and encourages deep sighs.

  • Periodic sighs prevent alveolar collapse (atelectasis) and may facilitate newborns' first breaths at birth.

• Irritant Receptors:

  • Activated by inhaled irritants or mechanical factors, leading to:

  • Bronchospasm

  • Cough

  • Sneeze

  • Tachypnea

  • Narrowing of the glottis

  • Reflexes triggered during hospital interventions (e.g., suctioning, bronchoscopy, endotracheal intubation).

• J-Receptors (Juxtacapillary Receptors):

  • Found in lung parenchyma, stimulated by conditions such as pneumonia, congestive heart failure (CHF), and pulmonary edema.

  • Result in rapid, shallow breathing, dyspnea, and glottic narrowing during expiration.

• Peripheral Proprioceptors:

  • Located in muscles, tendons, joints, and pain receptors.

  • Movement stimulates hyperpnea as limb movement, pain, and cold water can induce breathing increases in patients with respiratory depression.

Chemical Control of Breathing

• General Mechanism:

  • The body maintains proper levels of O2, CO2, and pH via chemoreceptors affecting minute ventilation (VE).

• Central Chemoreceptors (CCR):

  • Location: Bilaterally in the medulla.

  • Stimulation: Directly by H+ ions and indirectly by CO2.

  • H+ and HCO3- cross the blood-brain barrier poorly, while CO2 diffuses freely.

  • In the cerebrospinal fluid (CSF), CO2 hydrolizes, releasing H+, which leads to increased ventilation to restore normal pH and CO2 levels.

  • Functionally, for every 1 mm Hg rise in PaCO2, the tidal volume (VA) can increase by 2-3 L/min.

• Peripheral Chemoreceptors (PCR):

  • Location: Aortic arch and carotid artery bifurcations.

  • Sensitivity: Oxygen-sensitive cells react to lowered arterial blood oxygen levels.

• Response of PCR to PaO2:

  • Hypoxemia increases receptors' sensitivity to H+.

  • PaO2 influences VE for given pH; severe alkalosis diminishes hypoxemia's impact on VE.

  • Significant response from PCR is observed when PaO2 drops to approximately 60 mm Hg; any further decrease sharply increases VE.

  • Under normal circumstances, O2 plays a minimal role in the urge to breathe.

• Response of PCR to PaCO2 and [H+]:

  • Less responsive than central chemoreceptors for hypercapnia, accounting for roughly one-third of hypercapnic response.

  • However, they respond rapidly to changes in [H+].

  • The carotid bodies, being directly exposed to arterial blood, allow for this faster response in metabolic acidosis despite H+ ions crossing the blood-brain barrier with difficulty.

• Simultaneous Acidosis, Hypercapnia, and Hypoxemia:

  • These three conditions can synergistically stimulate peripheral chemoreceptors.

• Impact of Chronic Hypercapnia:

  • In cases of severe COPD, renal retention of bicarbonate (HCO3-) stabilizes CSF pH, dampening the typical ventilation response to rising PaCO2 levels.

• Hypoxemia and Breathing Stimuli:

  • Hypoxemia associated with hypercapnia can become the primary minute-to-minute inspiration stimulus by altering responses to H+ levels.

• Oxygen-Induced Hypercapnia:

  • Supplemental oxygen can unexpectedly elevate PaCO2 levels in patients with chronic hypercapnia associated with COPD.

  • Potential mechanisms for this include:

  • Removal of hypoxic drive (traditional view).

  • FIO2 exacerbating ventilation/perfusion (V/Q) mismatches by reversing hypoxic pulmonary vasoconstriction in poorly ventilated regions.

  • Increased susceptibility to absorption atelectasis due to oxygen therapy.

Abnormal Breathing Patterns

• Cheyne-Stokes Respirations (CSR):

  • Characterized by a cycle of waxing and waning ventilation interspersed with apneic periods, commonly seen with low cardiac output states such as CHF.

  • Results in a lag of CSF CO2 behind arterial PaCO2, leading to the characteristic respiratory cycle.

• Biot's Respiration:

  • Similar to CSR, but with consistent tidal volumes except during apneic episodes.

  • Typically observed in cases of elevated intracranial pressure (ICP).

• Apneustic Breathing:

  • Previous noted response indicating pons damage.

• Central Neurogenic Hyperventilation:

  • Possibly caused by head trauma, significant brain hypoxia, or deficient cerebral perfusion.

• Central Neurogenic Hypoventilation:

  • Reflects a lack of response from medullary respiratory centers to stimuli, often linked to head trauma, cerebral hypoxia, and narcotic suppression.

CO2 and Cerebral Blood Flow (CBF)

• CO2 Regulation Mechanism:

  • CO2 is crucial for autoregulation of CBF by mediating its conversion to H+.

  • Increased CO2 leads to cerebral vessel dilation, whereas decreased CO2 causes constriction.

• Impact of Traumatic Brain Injury (TBI):

  • Acute brain swelling raises ICP to levels exceeding cerebral arterial pressure, inhibiting perfusion and causing hypoxia/ischemia.

  • Mechanical hyperventilation decreases PaCO2 and ICP, although this practice is controversial since it may reduce O2 and CBF to the injured brain.

  • Consensus remains on avoiding hypoventilation in TBI patients.