Hypoxia and Hypoxemia

Jacob Lee

Background and Definitions 

  • Hypoxia: A condition where the oxygen supply is inadequate either to the body as a whole (general hypoxia) or to a specific region (tissue hypoxia)
  • Hypoxemia: low oxygen in arterial blood, as measured by PaO2 or SpO2
  • Can be both hypoxic without hypoxemia (i.e. anemia, cardiogenic shock) and hypoxemic without hypoxia (i.e. mild V/Q mismatch states) but severe hypoxemia will almost always cause hypoxia

Measuring Oxygenation 

  • Two major ways to measure oxygenation, which are inter-related:
    • SpO2 (oxygen saturation by pulse oximetry or "pulse ox") - the percentage of hemoglobin that's saturated with oxygen; ≥95% considered normal
    • PaO2 - partial pressure of oxygen in arterial blood; 75-100 considered normal
    • SpO2 and PaO2 can be interconverted using the oxygen-hemoglobin dissociation curve (sigmoidal curve)
      • PaO2 ~100 → SpO2 ~98-100%; PaO2 ~ 60 → SpO2 ~90%; Below PaO2 of 60, small decreases in PaO2 cause large drops in SpO2 (hemoglobin loses affinity for oxygen
      • The curve can shift to the right (hemoglobin has lower affinity for oxygen) due to elevated levels of CO2, low pH, and increased temperature/fever
  • A-a gradient: the difference in the partial pressure of oxygen as measured in the alveoli (A) and arterial blood (a); normal is (Age+10)/4; See 'Basics of Blood Gases' for more details

Mechanisms of Hypoxia 

  • Hypoxemic Hypoxia – low PaO2 leads to poor tissue oxygenation (examples below)
  • Anemic Hypoxia – normal PaO2 but reduced hemoglobin leads to reduced oxygen carrying capacity and thus decreased tissue oxygenation (i.e. anemia, CO poisoning, methemoglobinemia)
  • Circulatory Hypoxia – states of inadequate perfusion (shock) leading to poor tissue oxygenation (i.e. shock, heart failure, ischemia)
  • Histotoxic Hypoxia – inability of tissues to use oxygen (i.e. cyanide poisoning, mitochondrial dysfunction, sepsis)
  • Demand Hypoxia – oxygen requirements exceed oxygen delivery (i.e. hypermetabolic states such as thyrotoxicosis, sepsis, prolonged seizures, prolonged exercise)

Mechanism

Pathophysiology

Improvement with Supplemental O2

A-a Gradient

Examples
Low FiO2 Low fraction of inspired oxygen causes low PAO2 and thus low PaO2 Yes Normal High-Altitude
Hypoventilation Low oxygen delivery from low RR or TV to the alveoli reduces PAO2 and thus low PaO2 Yes, if ventilation (RR or TV) increase Normal Neuromuscular disease, obesity hypoventilation syndrome, opioid overdose
V/Q Mismatch
  1. V/Q >1 (more ventilation relative to perfusion) PAO2 is normal but inadequate perfusion limits gas exchange
  2. V/Q <1 (less ventilation relative to perfusion) blood oxygenation is impaired due to poor gas exchange
 Yes Elevated
  1. Pulmonary Embolism
  2. Pneumonia, ARDS, Pulmonary Edema
Right-to-left Shunt
  1. Anatomic: Blood bypasses the alveolarcapillary interface and does not participate in gas exchange
  2. Physiologic: Gas exchange is impaired
  1. Anatomic - no
  2. Physiologic - yes
 Elevated
  1. Heart defects, AV malformations
  2. Diffuse parenchymal disease
Diffusion Limitation Adequate PAO2 but oxygen cannot effectively cross into the bloodstream Yes Elevated ILD

Important to note that causes of hypoxia/hypoxemia are often multifactorial and may not fit neatly Into only one of the above categories

Differential diagnosis for hypoxia based on anatomical location

Anatomical Location

Differential Diagnosis
Airways COPD (chronic bronchitis), CF/bronchiectasis, bronchitis, severe asthma
Alveoli Blood (DAH), Pus (Pneumonia), Water (pulmonary edema) Protein/Cells/Other:(ARDS, pneumonitis), atelectasis, emphysema
Interstitium/Parenchyma Interstitial lung disease
Vascular/Cardiac Pulmonary Emboli, intra/extrapulmonary shunts
Pleural Space and Chest Wall Pleural effusions*, PTX, neuromuscular weakness*, tense ascites* *More likely to cause dyspnea, need to be severe to cause hypoxia

Evaluation

  1. For new or increasing oxygen requirements, evaluate patient at bedside with a focused physical exam, taking particular note of signs of respiratory distress
  2. Ensure pleth has good waveform – consider switching pulse ox probe to different anatomic location (earlobe, forehead) if poor circulation (vasculopathy, scleroderma)
  3. Labs: Blood gas (VBG vs ABG), Lactic acid, CBC; consider infectious workup with blood/sputum cultures, RPP, CMP, BNP, troponin, lipase. a
    1. D-Dimer rarely helpful in our patient population
  4. Imaging:

Study

Indications

Comments
CXR First study for hypoxia / hypoxemia
CT Indicated if CXR non-diagnostic or evaluating for pathology not well identified with CXR
  • Without contrast – best to evaluate lung parenchyma
  • High Resolution – best for ILD
  • With contrast – highlights the pleura and mediastinum
  • CTA/CTPE – CTA bronchial artery protocol for massive hemoptysis, CTPE for PE
US Evaluation for shunt TTE with bubble study great for evaluation of anatomic shunt; POCUS helpful for evaluation of lung slide/Kerley B lines as well as diaphragm paralysis

5. Outpatient PFTs if suspected obstructive or restrictive disease

Management 

  • Should be directed at underlying cause
    • For acute decompensation - bronchodilators, IV diuretics, IV antibiotics, anticoagulation, or steroids can be given depending on clinical picture
    • See ‘COPD Exacerbation, Heart Failure, Pneumonia, Pulmonary Embolism, Chest Tubes’ for more specific management strategies
  • Supplemental Oxygen Therapy
    • Goal SpO2 is 92-96% for most pts; 88-92%; for patients with chronic hypoxia from COPD (i.e., on home O2)
    • See ‘Modes of O2 Delivery’ for nuances in choosing the correct oxygen delivery system in patient
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