Hypoxia – Henry Brems |
Background
- Two major ways to measure oxygenation, which are similar but distinct:
- SpO2 or "pulse ox" - most common measurement in the hospital or clinic, which measures the O2 saturation of Hgb at capillary level
- <95% is abnormal, but may not need supplemental O2 until <90-92% in most pts
- PaO2 -- the partial pressure of oxygenation measured on an ABG
- <80 mmHg is abnormal
- SpO2 or "pulse ox" - most common measurement in the hospital or clinic, which measures the O2 saturation of Hgb at capillary level
- The relationship between SpO2 and PaO2 is the classic S-shaped curve.
- Below an SpO2 of ~88%, PaO2 begins to fall off dangerously fast thus necessitating quick intervention for pts with SpO2 below this level
Mechanisms of Hypoxia:
Mechanism |
Pathophysiology |
Decreased barometric pressure |
- Normal A-a gradient - This is unlikely to be seen except at high altitudes |
Hypoventilation |
- Normal A-a gradient - Hypoxia easily correctable with supplemental O2 |
V/Q Mismatch |
- Increased A-a gradient - Processes that lead to areas of lung where V/Q <1, i.e. where there is relatively less ventilation than perfusion. - Common examples include PNA, ARDS, pulmonary edema |
Right-to-left Shunt |
- Increased A-a gradient - Can be anatomic (e.g intracardiac, AVMs) or physiologic (water/pus/blood filling alveoli) - Classically does not easily correct with supplemental O2 |
Diffusion Limitation |
- Increased A-a gradient - Often related to diseases affecting interstitium -- e.g., ILD |
Differential diagnosis for hypoxia based on anatomical location:
Anatomical Location |
Differential Diagnosis |
Airways |
- COPD most common, Asthma in very severe cases - CF, bronchiectasis in patients with appropriate history |
Alveoli |
- Any process that fills the alveoli with:
|
Interstitium/Parenchyma |
- Interstitial Lung Diseases (see section) |
Vascular |
- Pulmonary Emboli - particularly suspect these in patients with significant hypoxia and a clear CXR |
Pleural Space and Chest Wall |
- Pleural Effusions, Pneumothorax, Neuromuscular weakness, tense ascites - These are more likely to cause significant dyspnea and usually need to be quite severe to cause hypoxia |
Evaluation
- Confirm true hypoxia with good pleth. Can press pulse-ox on pt’s finger for better transmission
- CXR is almost always the first step
- Other common initial workup: CBC, BMP, BNP, troponin, EKG, ABG/VBG
- TTE -- particularly useful if suspected new pulmonary edema or pulmonary HTN
- Obtain with 'bubble study' if any concern for shunt
- Obtain “limited” if patient had recent “complete” TTE
- Chest CT
- Order CTA ('CTA PE' in Epic) if concerned for PE
- V/Q scan if unable to receive IV contrast
- CT Chest without contrast otherwise generally preferred for evaluation of lung parenchyma
- Order CTA ('CTA PE' in Epic) if concerned for PE
- PFTs are useful if there is suspected obstructive (e.g. COPD) or restrictive disease (e.g. ILD), or if the cause remains otherwise unknown after initial workup
- These are almost always done as an outpatient
Management
- Should be directed at underlying cause. See other sections for information relevant to particular diagnoses
- If acutely decompensating, Duonebs, IV lasix, Antibiotics depending on clinical picture
- Supplemental O2 for goal SpO2:
- >90-92% for most patients (There is generally no need to make SpO2 100%)
- Between 88-92% for patients with chronic hypoxia from COPD (i.e., on home O2)