Pathophysiology: Airway and Ventilation

Anatomy and Physiology Review

• The upper and lower airways
  

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• The muscles of ventilation

Normal Respiratory Physiology

• The medulla oblongata (brainstem) is the center of respiratory control and uses input from chemoreceptors and other nervous system receptors to adjust breathing to meet metabolic demand.
• The airway must be patent to maintain oxygenation and ventilation. That means air must be capable of traveling from the mouth and nose to the alveoli and back out again in order to sustain normal physiologic requirements.
• Ventilation is the movement of air in and out of the body.
• Minute ventilation (MV) is a product of tidal volume (TV) multiplied by rate (MV = TV × RR)
• Alveolar ventilation is the amount of oxygen delivered to the alveoli during one breath.
• Respiratory physiology is maintained by changing pressures within the chest.
  • Negative pressure is created by dropping the diaphragm and expanding the chest wall. This causes inhalation.
  • Positive pressure is caused by relaxation of the diaphragm and chest wall. This causes exhalation.
  • Movement of the diaphragm and thoracic muscles required for chest expansion.
• External respiration occurs when gases are transferred by diffusion at the level of the alveoli.
  • O₂ moves from inhaled air into the blood in the pulmonary capillaries, and CO₂ moves from the bloodstream into the air in the alveoli for removal during exhalation.
• For external respiration to occur there must be a ventilation/perfusion match (otherwise known as V/Q matching).
  • Red blood cells must be present in the pulmonary capillaries outside the alveoli. There must also be a sufficient quantity of them to carry oxygen.
  • Air must be able to reach the alveoli and also be able to be exhaled following diffusion.
  • V/Q matching occurs when both air and blood are matched and the ratio of each one to the other is proper.
• Internal respiration occurs when gases are diffused from the blood to the cells of the body.
  • O₂ diffuses from the blood in the capillaries into the cells.
  • CO₂ diffuses from the cells into the bloodstream.
  • Adequate delivery of blood to the cells is referred to as perfusion.

Pathophysiology of Breathing

• Minute ventilation can be disrupted in several ways:
  • Control of breathing can be impaired.
    • Injuries to and alterations in the brain can lead to impaired mental status.
    • Altered mental status can cause loss of airway patency.
  • Nervous system messaging can be disrupted (as with a spinal injury).
    • Loss of messaging capabilities can eliminate the stimulus for breathing.
  • The ability to change pressure within the chest can be disrupted.
    • Holes in the chest wall and holes in the lung tissue can reduce the ability to create negative and positive pressure and thus impair breathing function.
    • Air and blood in the pleural cavity can reduce the lungs’ capability to expand during the breathing process.
  • Alveolar ventilation changes with minute volume changes.
    • Slower rates reduce the amount of air that reaches the alveoli.
    • Reduction in tidal volume can decrease the amount of air that reached the alveoli.
  • Damage to lung tissue can impair breathing.
  • V/Q mismatching disrupts pulmonary function:
    • If blood does not reach the pulmonary capillaries (as in hypovolemic shock), external respiration will not occur.
    • If red blood cells are not present in sufficient quantity, oxygen cannot be transported.
    • If air does not reach the alveoli, external respiration will not occur.

Respiratory Compensation

• The brain’s chemoreceptors sense chemical changes in the blood and cerebral spinal fluid.
  • Chemoreceptors are sensitive to changes in oxygen and carbon dioxide levels and to changes in pH.
• The sensation of dyspnea occurs when the respiratory system is incapable of meeting metabolic demands.
  • The brain senses that supply does not equal demand.
• When demands are not met, the medulla attempts to adjust minute volume, resulting in:
  • respiratory rate increases.
  • adjustments to tidal volume.
  • recruitment of the accessory muscles (those of the neck, back and shoulders) to help improve tidal volume.
    • The person adjusts his or her body position (e.g., the tripod position) to help improve breathing.
  • When demands are not met, the body attempts to increase perfusion, resulting in increased cardiac output:
    • The heart rate increases.
    • Contractility (the strength of contraction) increases.
    • Blood vessels constrict.
  • Compensation has a cost:
    • The muscles of compensation’s increased use of O₂ and energy means that compensation is a limited capability that can fail.

Signs and Symptoms of Respiratory Compensation (Respiratory Distress)

• The sensation of dyspnea
• The sensation of anxiety
• Tachypnea
• Tachycardia
• Accessory muscle use, including sternal, superclavicular and intercostal retractions
• Pale skin
• Increased capillary refill time
• NOTE: Metabolic needs are met during respiratory distress, which typically means that the patient is not yet hypoxic and that mental status is reasonably normal.

Signs and Symptoms of Failed Compensation (Respiratory Failure)

• Altered mental status secondary to hypoxia and hypercapnia (high CO₂)
• Hypoxia, especially hypoxia despite supplemental oxygen
  • Signs of hypoxia include cyanosis, altered mental status, and low pulse oximetry.
• Increasing tachypnea (the worsening of respiratory distress as compensation fails)
• Eventual respiratory fatigue as compensation fails
• Slowed and/or irregular breathing
• Poor tidal volume/poor air movement (diminished lung sounds) and silent chest
• Increasing tachycardia and eventual bradycardia
• Increasing accessory muscle use and work of breathing