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Physiology of Gas Exchange

Overview of Hypercapnia

  • Definition of Hypercapnia
    • PaCO₂ is directly proportional to rate of CO₂ production (VCO₂)
    • PaCO₂ is inversely proportional to rate of CO₂ elimination by lung -- alveolar ventilation
  • Hypercapnia 2/2 increased CO₂ production (VCO₂)
    • Increased metabolic rate
      • Increased activity
      • Sepsis
      • Thyrotoxicosis
    • Metabolizing of carbohydrates
  • Hypercapnia 2/2 decreased alveolar ventilation (\(V_A\))
    • Decreased minute ventilation
    • Increased VD/VT (i.e. physiologic dead space) with stable minute ventilation
    • Rapid, shallow breathing
  • Clinical Effects of Acute Hypercapnia
    • Decreased level of consciouness
      • PaCO₂ >60-70 mmHg in normal individuals
      • PaCO₂ >90-100 mmHg in patients with chronic hypercapnia
    • Increased cerebral blood flow, ICP
    • Decreased myocardial contractility
    • Decreased diaphragmatic function
    • Shift oxyhemoglobin dissociation curve to the right
    • Signs & Symptoms

Etiology of Hypercapnic Respiratory Failure

  • Broken link in the chain of events
    • Central respiratory center → spinal cord → motor neurons → neuromuscular junction → respiratory muscles → chest wall → lung

Central Respiratory Drive

  • Decreased respiratory drive
    • Sedative
    • Opioid overdose
    • Encephalitis
    • Stroke
      • Cheyne-Stokes Respiration
        • Most common with heart failure, high altitude, and neurologic disease
      • Biot Respiration
        • Irregular clusters of breaths and apnea
        • Lesion of upper pons or lower medulla
    • Obesity hypoventilation syndrome
    • Sleep apnea (central sleep apnea & obstructive sleep apnea)
    • Congenital central alveolar hypoventilation
    • Hypothyroidism
      • Myxedema coma → depressed hypercapnic ventilatory drive & hypoxic ventilatory drive + respiratory muscle weakness & compromise of the upper airway
    • Metabolic Alkalosis

Spinal Cord, Nerves, Neuromuscular Junction

  • Disorders of Spinal Cord
    • Direct Spinal Cord Injury
      • Traumatic spinal cord injury -- 50% of motor vehicle accidents, neurologic progression over hours
      • Cervical spinal cord injury & respiratory muscles
        • Phrenic nerve to diaphragm: C3-C5
        • Scalene muscles: C4-C8
        • Sternocleidomastoid, trapezius: C1-C4; CN XI
      • Complete injury above C3 = ventilatory failure
      • Injury at C3, C4, C5 -- often wean from ventilator
    • Amyotrophic Lateral Sclerosis
    • Tetanus
      • Caused by toxin-producing anaerobe Clostridium tetani
      • Retrograde transport of exotoxin up axons to brainstem and spinal cord
      • Blocks inhibitory neurotransmitters
      • Results in: spastic paralysis especially laryngeal muscles and respiratory muscles
      • Treatment: tetanus immune globulin, muscle relaxants, supportive (debridement, antibiotics, mechnical ventilation)
  • Disorders of Peripheral Nerves
  • Disorders of Neuromuscular Junction

Respiratory Muscles & Chest Wall

  • Respiratory Muscle Weakness
    • Etiology
      • Pre-existing
        • Neuromuscular junction
        • Malnutrition
        • Hyperinflation
        • Endocrine
          • Hyperthyroidism
          • Hypothyroidism
      • New-onset
        • Metabolic
          • Hypokalemia
          • Hypophosphatemia
          • Acidosis
        • ICU-Acquired Weakness
        • Mechanical ventilation
    • Clinical features
      • Decreased vital capacity
      • Increased residual volume
        • expiratory muscles → decreased expiratory reserve volume
      • Decreased total lung capacity
        • inspiratory muscles → decreased inspiratory capacity
      • Further decrease in vital capacity when supine
      • Decrease in maximum expiratory peak flow and maximum inspiratory peak flow
      • Results in hypercapnia when strength is <40% predicted
      • Desaturation, hypercapnia during REM sleep & in supine position
  • Disorders of the Chest Wall
    • Results in decreased chest wall compliance & reduced tidal volume (increased VD/VT)
    • Hypercapnia exacerbated by
      • reduced ventilatory drive
      • muscle weakness
    • Kyphoscoliosis
      • Most patients with angle >90 degrees have hypercapnia
    • Obesity Hypoventilation Syndrome
      • Management of hypercapnic respiratory failure in morbid obese patients
        • Identify and manage precipitating causes
        • Non-invasive positive pressure ventilation
          • improves ventilation → reduces work of breathing
          • recruits atelectatic lung → improves V/Q matching → better oxygenation
          • improves upper airway patency
        • Head up (reverse Trendelenburg) position

Lung

  • Hypercapnic respiratory failure in patients with airflow obstruction
  • Acute hypercapnic respiratory failure 2/2 COPD
    • Advanced COPD patients have a difficult time overcoming new infections like pneumonia
    • Fever causes increased VCO₂ and/or increased VD (due to pneumonia) → increased minute ventilation (by increasing RR) → decreasing expiratory time and increasing air trapping → increased work of breathing, fatigue → acute respiratory failure
    • Goal: rest, relief of air trapping
      • Non-invasive positive pressure ventilation
  • Acute hypercapnic respiratory failure 2/2 status asthmaticus
    • Development of dynamic hyperinflation
      • Bronchospasm, airway inflammation, mucous plugging → airflow obstruction → prevents gas emptying
      • New breath initiated before previous breath empties → increasing functional residual capacity
      • Dynamic hyperinflation develops when the time needed to deflate the lung to normal FRC between breaths is insufficient
        • i.e. auto-peep
    • Effects of dynamic hyperinflation
      • Moves diaphragm downward and at a mechanically disadvantageous position
      • Incomplete alveolar gas emptying → elevated alveolar volume & alveolar pressure (intrinsic PEEP or auto-PEEP)
      • Auto-PEEP represents a threshold pressure that must be overcome before inspiratory flow can occur → increasing work of breathing
    • Ventilator adjustments for airflow obstruction
      • Deliver adequate oxygenation
      • Primary goal = increase expiratory time (i.e. time needed to exhale)
      • Sedate patient to slow the respiratory rate
      • Set lower RR -- most effective method
      • Set lower tidal volume → less volume to exhale
      • Increase inspiratory flow rate to deliver air more rapidly thus more time for exhalation

Capnography

  • Monitoring exhaled CO₂
  • Phases in measurement of exhaled CO₂
    • Phase 1: no exhaled CO₂ -- end inspiration to early exhalation of dead space gas from proceeding breath
    • Phase 2: rise in exhaled CO₂ during the mixing of dead space gas and emptying of alveoli with transition to
    • Phase 3: reflects the alveolar plateau as alveoli empty, reaching a maximum exhaled CO₂ immediately prior to
    • Phase 4: the rapid fall in CO₂ during inspiration
  • Angles
    • The α angle represents the angle formed between Phase 2 and Phase 3; normally 110 degrees
      • Variations in this angle is linked to variations in time constants within the different alveolar units and thus overall V/Q status
      • Other factors that affect this angle: cardiac output, airway resistance, and changes in FRC
  • Clinical Utility of Capnography
    • Confirmation of endotracheal tube placement
    • Continuous monitoring (loss of exhaled CO₂ = displaced ETT)
    • Perfusion during CPR -- effectiveness of resuscitation, ROSC
    • Detection of hypoventilation, bradypnea, apnea, and reverse I:E ventilation (shorter time during exhalation)
    • In Asthma/Chronic Obstructive Pulmonary Disease → uneven alveolar emptying and V/Q mismatch → "Shark-Fin" contour representing airflow obstruction
    • Gap between arterial and end-tidal CO₂ is usually negligible in healthy nonintubated patients (usually around 2 to 5 mmHg) - P(a-ET)CO₂
      • Cardiac and respiratory pathologies can increase this gap and this can be used to estimate alveolar dead space ventilation
      • In conditions such as acute pulmonary embolism, a precipitous drop of end-tidal CO₂ will happen and if the PaCO₂ remains constant, this leads to a significant increase in P(a-ET)CO₂
      • Normalization of this gap has been shown as a positive prognostic sign when seen after re-perfusion from tPA
      • Other causes of increased P(a-ET)CO₂
        • Hypovolemia
        • Hemorrhage
        • Excessive PEEP
        • Early ARDS -- independent risk factor for death
      • Negative P(a-ET)CO₂
        • Uncommon → verify the validity of the values from capnopgraph and ABG
        • Etiologies:
          • low frequency and high tidal volume ventilation
          • post CABG
          • post exercise
          • pregnant
          • pediatric patients

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