Regulation of Breathing Study Notes

Chapter 15: Regulation of Breathing

Medullary Respiratory Center

  • The rhythmic cycle of breathing originates in the medulla.

  • Outflow from the medulla is modified by:

    • Higher brain centers

    • Systemic receptors

    • Reflexes

  • There are no distinctly separate inspiratory and expiratory centers; rather:

    • The medulla consists of several widely dispersed groups of respiratory-related neurons.

    • These neurons form dorsal and ventral respiratory groups (DRG and VRG).

Dorsal Respiratory Groups (DRG)

  • Primarily composed of inspiratory neurons located bilaterally in the medulla.

  • Functionality:

    • Neurons send impulses to motor nerves of the:

    • Diaphragm

    • External intercostal muscles.

  • These DRG nerves connect to the VRG, which contains both inspiratory and expiratory neurons.

  • Sensory input comes from:

    • Vagus and glossopharyngeal nerves that relay signals from:

    • Lungs

    • Airways

    • Peripheral chemoreceptors

    • Joint proprioceptors.

  • Input from these receptors modifies the breathing pattern.

Ventral Respiratory Groups (VRG)

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

  • Sends inspiratory impulses through the vagal nerve to:

    • Laryngeal and pharyngeal muscles

    • Diaphragm

    • External intercostals.

  • Other VRG neurons send signals for expiration to:

    • Abdominal muscles

    • Internal intercostals.

  • Inspiratory ramp signal creates a smooth inspiratory effort (gradually increasing signal rather than a gasp).

Pontine Respiratory Centers

  • The pons modifies the output from the medullary centers through two pontine centers:

    • Apneustic Center:

    • Identified mainly by cutting connections to the medulla.

    • Characterized by long gasping inspirations interrupted by occasional expirations, known as apneustic breathing.

    • Pneumotaxic Center:

    • Controls the switch-off mechanism, regulating inspiratory time (IT).

    • Increased signals elevate the respiratory rate (RR), whereas weak signals extend inspiratory time and increase tidal volume (VT).

Reflex Control of Breathing

  • Hering-Breuer Inflation Reflex:

    • Stretch receptors located in the smooth muscle of large and small airways.

    • Lung distention activates these stretch receptors to send inhibitory signals to the DRG, stopping further inspiration.

    • Active in adults primarily with large tidal volumes (>800 ml).

    • Helps regulate the rate and depth of breathing during moderate to strenuous exercise.

  • Deflation Reflex:

    • Triggered by sudden lung collapse, stimulating a forceful inspiratory effort, resulting in hyperpnea (seen with conditions like pneumothorax).

  • Head’s Paradoxic Reflex:

    • Maintains large tidal volumes during exercise and contributes to deep sighs, preventing alveolar collapse (atelectasis).

    • Potentially responsible for initiating a baby’s first breaths at birth.

  • Irritant Receptors:

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

    • Bronchospasm

    • Coughing

    • Sneezing

    • Tachypnea

    • Narrowing of the glottis.

    • These reactions are classified as vagovagal reflexes, prominent during medical interventions like suctioning and bronchoscopy.

  • J-Receptors (Juxtacapillary):

    • Located in lung parenchyma, stimulate in response to conditions such as:

    • Pneumonia

    • Congestive Heart Failure (CHF)

    • Pulmonary edema.

    • Result in rapid, shallow breathing, dyspnea, and expiratory narrowing of the glottis.

  • Peripheral Proprioceptors:

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

    • Movement stimulates hyperpnea; responses include movement of limbs or exposure to pain or cold water.

Chemical Control of Breathing

  • The body regulates proper levels of Oxygen (O2), Carbon Dioxide (CO2), and pH via chemoreceptor mediation to affect ventilation (VE).

  • Central Chemoreceptors:

    • Positioned bilaterally within the medulla.

    • Respond directly to H+ ions and indirectly to CO2.

    • Given the blood-brain barrier's impenetrability to H+ and HCO3-, CO2 can cross easily; once in the cerebrospinal fluid (CSF), CO2 is hydrolized, releasing H+ ions, causing increased ventilation to normalize pH and CO2 levels.

    • Ventilation increases approximately 2–3 L/min for each 1 mm Hg increase in PaCO2.

  • Peripheral Chemoreceptors:

    • Located in the aortic arch and the bifurcations of the common carotid arteries.

    • React to reductions in arterial O2 levels:

    • Increased hypoxemia enhances receptor sensitivity for H+.

    • PaO2 affects VE inversely; hypoxemia is the most common cause of hyperventilation.

    • Significant response does not occur until PaO2 falls to approximately 60 mm Hg, after which a sharp increase in VE can occur.

  • Receptors are less responsive to changes in PaCO2 than central chemoreceptors but respond quickly to changes in [H+].

  • In chronic hypercapnia, sudden rises in PaCO2 prompt immediate VE increases, while slow rises in patients with severe Chronic Obstructive Pulmonary Disease (COPD) lead to kidney retention of HCO3-, maintaining CSF pH and blunting increased ventilation response.

  • Oxygen-Induced Hypercapnia:

    • Oxygen therapy in patients with severe COPD may unexpectedly raise PaCO2 due to:

    • The removal of the hypoxic drive.

    • Potential worsening of ventilation/perfusion (V/Q) mismatch.

    • Risk of absorption atelectasis.

Abnormal Breathing Patterns

  • Cheyne-Stokes Respiration (CSR):

    • Characterized by cyclic waxing and waning ventilation, alternating between apnea and hyperpnea.

    • Common in low cardiac output states like CHF due to lag in CSF CO2 affecting arterial PaCO2.

  • Biot’s Respiration:

    • Similar to CSR, but with a constant tidal volume interrupted by apneic periods.

    • Observed in patients with elevated intracranial pressure (ICP).

  • Apneustic Breathing:

    • Indicates damage to the pons.

  • Central Neurogenic Hyperventilation:

    • Can be caused by head trauma, severe brain hypoxia, or lack of cerebral perfusion.

  • Central Neurogenic Hypoventilation:

    • Medulla respiratory centers fail to respond adequately, often linked to:

    • Head trauma

    • Cerebral hypoxia

    • Narcotic suppression.

CO2 and Cerebral Blood Flow (CBF)

  • CO2 important in the autoregulation of CBF via its H+ formation.

  • Increased levels of CO2 lead to dilation of cerebral vessels, while decreased levels do the opposite.

  • In cases of Traumatic Brain Injury (TBI), brain swelling can elevate ICP beyond cerebral arterial pressure, stopping perfusion and causing hypoxia/ischemia.

    • Mechanical hyperventilation can lower PaCO2 and ICP, but this is controversial given potential reductions in O2 and CBF to the injured brain.

  • It is crucial to avoid hypoventilation in patients with TBI.

RRxTV=MV

Minute volume can be Ve,V, or MV