esc to dismiss

Physiology of Gas Exchange

Overview of Hypoxemia

  • Impairment of perfusion and the matching of ventilation and perfusion results in Hypoxemia

  • Principle mechanisms of hypoxemic respiratory failure can be separated into intrapulmonary and extrapulmonary factors
    | Mechanisms | PaO2 | PaCO2 | A-a on RA | A-a on 100% | Intrapulmonary vs Extrapulmonary |
    | --------------------------------------------------------------- | ------ | -------------------- | --------- | ----------- | -------------------------------- |
    | Low Cardiac Output → Low O₂ delivery | ↓ | ↑ | N | N | Intrapulmonary |
    | High Altitude | ↓ | ↓ | N | N | Intrapulmonary |
    | Alveolar Hypoventilation | ↓ | ↑ | N | N | Extrapulmonary |
    | VQ Mismatch | ↓ | ↓, N, or ↑ | ↑ | Corrects | Extrapulmonary |
    | Diffusion Block | ↓ | N or ↓ | ↑ | Corrects | Extrapulmonary |
    | Right-to-Left Shunt | ↓ | N or ↓ | ↑ | ↑ | Extrapulmonary |

  • Extrapulmonary Factors

    • High Altitude
      • Low partial pressure of inspired oxygen (PIO₂) which reduces oxygen content (e.g. high altitude -- above 8000 feet) → results in hyperventilation → lower PaCO₂
      • A-a gradient is normal and therefore the lung function is normal
        • \(P_{AO_{2}} - P_{aO_{2}} = F_{IO_{2}}(P_{atm}-P_{H_{2}O})-P_{aCO_{2}}/R - P_{aO_{2}}\)
        • R = the respiratory exchange ratio \((\dot{V}_{O_{2}}/\dot{V}_{CO_{2}})\)
          • \(\dot{V}_{O_{2}}\) = Oxygen consumption
          • \(\dot{V}_{CO_{2}}\) = Carbon dioxide production
      • Decrease in \(F_{IO_{2}}\) or \(P_{atm}\) via travel to altitude will functionally decrease \(P_{AO_{2}}\) and lead to hypoxemia despite normal lung function
    • Low Cardiac Output
      • Low oxygen delivery to the tissues as a result of low cardiac output resulting in tissue hypoxia → generation of lactic acid (supply/demand mismatch)
        • normal oxygen content
        • due to the tissues wanting more oxygen, it will be extracted by the tissues more and the amount of deoxygenated blood returning to the lung is higher
          • If normal lungs then this is rapidly re-oxygenated
          • If impairment in lung oxygenation, blood leaving the lungs may not be fully oxygenated
        • DO₂  Cardiac Output x Carrying Capacity
          • = Cardiac Output x {(Hb x %saturation of Hb x 1.34  PaO₂ x 0.003
          • Carrying capacity is equivalent to oxygen content
  • Intrapulmonary Factors
    • Shunt
      • Perfusion without accompanying ventilation -- can be structural or physiological
      • Structural Shunt
        - Intracardiac
        - right-to-left communication -- PFO, PDA, ASD, VSD
        - Intrapulmonary
        - abnormal connection between pulmonary arteries and pulmonary veins -- AVM
        - Differentiate between intracardiac and intrapulmonary shunts
        - Contrast echo w/ air bubbles injected into the venous circulation and visualized in the left atrium
        - Timing differentiates between intracardiac and intrapulumonary
        - Intracardiac -- within 1 to 3 cardiac cycles
        - Intrapulmonary -- within 6 to 8 cardiac cycles
      • Physiologic Shunt
        • Found in states of dense alveolar filling or collapse
          • atelectasis or compresive atelectasis (due to abdomen or pleural effusion)
          • Pneumothorax
          • Central airway obstruction
        • In these conditions, hypoxic vasoconstriction reduces much of the blood flow through the nonaerated lung zones but not completely leaving areas of perfusion without ventilation
    • V/Q Mismatch
      • Spectrum of diseases
      • Most common cause of Hypoxemic Respiratory Failure
      • Optimal gas exchange is based on maximally matching ventilation and perfusion that is, a V/Q ratio equal to 1
      • In a healthy patient, V/Q ratio is not uniform in the lung but the summation of the 300 million alveoli in a normal distribution around a V/Q ratio equal to 1
      • In disease states, regional mismatching of ventilation and perfusion leads to ineffective gas exchange
        • Regional vascular dropout
          • Emphysema or large pulmonary embolism → high V/Q (nearing dead space physiology) → hypercapnia
        • Patchy alveolar filling → low V/Q state (nearing shunt physiology)
      • Common conditions associated with abnormal V/Q matching
        • Pneumonia
          • Alveoli fill with purulent material over time → disrupt basement membrane and cellular tight junctions → disruption in alveolar ventilation → low V/Q → hypoxia
        • Cardiogenic pulmonary edema and congestive heart failure
          • Fluid accumulation in the interstitium and alveolus due to disruption in the direction and rate of fluid exchange due to left heart issues
          • Left heart issues → elevated left atrial pressure → capillary hydrostatic changes → fluid accumulation in the interstitium
          • Hypoxemia in CHF = multifactorial
            • Early on the interstitial fluid causes a diffusion abnormality & low V/Q
              • Diffusion abnormality
                • interstitial fluid → diffusion abnormality → hypoxemia
              • Low V/Q
                • interstitial fluid → decrease in lung compliance → regional decline in ventilation → Low V/Q
                • interstitial fluid → narrowing of the airways surrounding this region → decline in ventilation → Low V/Q (classic cardiac wheeze on physical examination)
            • Later → alveolar flooding → low V/Q areas convert to shunt physiology → progressive hypoxemia
        • Noncardiogenic pulmonary edema and Acute Respiratory Distress Syndrome
          • Fluid accumulation in the interstitium and alveolus due to disruption in the direction and rate of fluid exchange due to changes in oncotic pressure and/or capillary permeability
          • Oncotic pressure changes and/or capillary permeability changes → leak of protein and fluid accumulation in the interstitium
          • Appearance of classic hyaline membranes lining the alveoli
          • Hypoxemia in ARDS = multifactorial
            • Early → increased permeability & fluid extravasation → low V/Q
            • Later → atelectatic lungs from low ventilation in dependent lungs & overdistention in anterior portions of lungs
              • Chest wall restrictions of posterior ribs → decreased compliance
              • Pooling of fluid and exudate in posterior lungs → decreased ventilation
    • Diffusion block
      • Pulmonary Hypertension
      • Interstitial Diseases
      • These patients only become hypoxic when they exert themselves as this decreases the time the red blood cell spends in the capillary → decreased time for diffusion to occur
        • normally, exertion causes an increase in cardiac output and recruitment of pulmonary vascular units → decreasing pulmonary vascular resistance
        • These patients are unable to recruit pulmonary vascular units therefore the flow rates through the capillary bed increase, leading to a decrease in time for uptake of oxygen in the capillary unit
    • Alveolar Hypoventilation
      • Final common pathway for all causes of respiratory distress
    • Alveolar filling processes caused by pneumonia, ARDS, alveolar hemorrhage, CHF usually affect the lung in a heterogenous fashion therefore have both shunt and V/Q mismatch contributing to the hypoxemia

Acute Respiratory Distress Syndrome

Backlinks