Hypoxemia!

Approach to Hypoxemia

Recap on a few things...

A-a oxygen gradient — a common measure of oxygenation (“A” denotes alveolar and “a” denotes arterial oxygenation). It is the difference between the amount of the oxygen in the alveoli (ie [PAO₂]) and the amount of oxygen dissolved in the plasma (PaO₂)

 A-a oxygen gradient = PAO₂ - PaO_2. 

PaO₂ is measured by ABG and the PAO₂ is calculated using the alveolar gas equation:

 PAO₂  =  (FiO₂  x  [Patm  -  PH₂O])  -  (PaCO₂  ÷  R)

·       FiO₂ is the fraction of inspired oxygen (0.21 at room air), Patm is the atmospheric pressure (760 mmHg at sea level),  PH₂O is the partial pressure of water (47 mmHg at 37 degrees C), PaCO₂ is the arterial carbon dioxide tension (obtain from the ABG) and R is the respiratory quotient (~0.8 at steady state), but varies according to the relative utilization of carbohydrate, protein, and fat.

NOTE: The normal A-a gradient varies with age and can be estimated, assuming the patient is breathing room air

A-a gradient = 4 + age/4

PaO2/FiO2 ratio — The PaO₂/FiO₂ ratio is another common measure of oxygenation. A normal PaO₂/FiO₂ ratio is 300 to 500 mmHg, with values <300 mmHg indicating abnormal gas exchange

MECHANISMS OF HYPOXEMIA — Hypoxemia is defined as a decrease in the partial pressure of oxygen in the blood. 

Causes: Hypoventilation, ventilation-perfusion mismatch, right-to-left shunt, diffusion impairment, or reduced inspired oxygen tension

1.Hypoventilation — arterial (PaCO₂) and alveolar (PACO₂) carbon dioxide tension increase during hypoventilation, which causes the alveolar oxygen tension (PAO₂) to decrease. As a result, diffusion of oxygen from the alveolus to the pulmonary capillary declines. The net effect is hypoxemia.

Hypoxemia due to pure hypoventilation can be identified by 2 clues:

·       A) It readily corrects with a small increase in FiO₂

·       B) The A-a gradient is usually normal, EXCEPT, when the hypoventilation is prolonged because atelectasis can occur, which will increase the A-a gradient. Examples that can cause hypoventilation:

o   CNS depression (i.e. drug overdose- narcotics, structural CNS lesions, ischemic CNS lesions affecting the respiratory centre)

o   Obesity hypoventilation (Pickwickian) Syndrome

o   Impaired neural conditions (i.e. ALS, GBS, high C-spine injury, phrenic nerve paralysis)

o   Muscular weakness (i.e. myasthenia gravis, muscular dystrophy, polymyositis, severe hypothyroidism)

o   Poor chest wall elasticity (i.e. flail chest or kyphoscoliosis)

2.V/Q mismatch — an imbalance of blood flow and ventilationà composition of alveolar gas varies among lung regions:

Lung regions with low ventilation compared to perfusion will have a low alveolar oxygen content and high CO₂ content

 Lung regions with high ventilation compared to perfusion will have a low CO₂ content and high oxygen content

NOTE: In the normal lung, there is V/Q mismatch because perfusion and ventilation are heterogeneous. Both ventilation and perfusion are greater in the bases than in the apices. However, the difference between apical and basilar ventilation is smaller than the difference between apical and basilar perfusion. This causes the V/Q ratio to actually be higher in the apices compared to the bases. This V/Q mismatch is responsible for the normal A-a gradient.

In the diseased lung, V/Q mismatch increases because heterogeneity of both ventilation and perfusion worsen. This results in hypoxemia.

Clues for V/Q mismatch: correction with low to moderate flow supplemental oxygen and characterized by an increased A-a gradient.

o   i.e. obstructive lung diseases (asthma, COPD), pulmonary vascular diseases (PE), alveolar (CHF), interstitial diseases.

3.Right-to-left shunt —exists when blood passes from the right to the left side of the heart without being oxygenated. There are 2 types to keep in mind

·       Anatomic shunts, where alveoli are bypassed!

o   i.e. intra-cardiac shunts, pulmonary AVMs, hepato-pulmonary syndrome

·       Physiologic shunts: where non-ventilated alveoli are perfused.

o   i.e. atelectasis and diseases with alveolar filling (i.e. pneumonia, ARDS).

NOTE: Right-to-left shunts cause very extreme V/Q mismatch, with a V/Q ratio of zero in some lung regions. The net effect is hypoxemia, which is difficult to correct with supplemental oxygen. True anatomical shunts DO NOT correct with supplemental oxygen!!!!

4.Diffusion limitation — where the movement of oxygen from the alveolus to the pulmonary capillary is impaired, often as a result of alveolar and/or interstitial inflammation and fibrosis (i.e. interstitial lung diseases). In such diseases, diffusion limitation usually coexists with V/Q mismatch.

o       Clues: characterized by exercise-induced or -exacerbated hypoxemia.

o   During rest, blood traverses the lung relatively slowly allowing for sufficient time for oxygenation to occur even if diffusion limitation exists.

o   During exercise, cardiac output increases and blood traverses the lung more quickly. As a result, there is less time for oxygenation.

o   In healthy pts, compensatory mechanisms occur

o   Pulmonary capillary dilatation (increase in surface area available for gas exchange)

o   PAO₂ increasesàpromotes oxygen diffusion by increasing the oxygen gradient from the alveolus to the artery

o   In diffusion limitation (i.e. IPF, anemia): there is insufficient time for oxygenation to occur & most have parenchymal destruction (impossible to even recruit additional surface area!!!)

5.Reduced inspired oxygen tension 

Reduction of the PiO₂ will decrease the PAO₂. This impairs oxygen diffusion by decreasing the oxygen gradient from the alveolus to the artery. The net effect is hypoxemia. A common example is living at high altitude.

Complications of Hypoxemia: Dyspnea, reduction in exercise tolerance and functional capacity. Over time,  Pulmonary HTN can arise in the setting of chronic alveolar hypoxemia