Intrapulmonary Shunt and Hypoxemia Relationship

Pathophysiological Mechanism

The American Thoracic Society notes that hypoxemia caused by intrapulmonary shunt results from the passage of venous blood through non-ventilated alveolar units, creating a venous mixture that directly reduces arterial PaO2 1, 2
In normal conditions, the intrapulmonary shunt represents less than 5% of the total cardiac output, according to the European Respiratory Society 1, 2
When the shunt exceeds 25% of cardiac output (as in ARDS), hypoxemia becomes severe and refractory to supplemental oxygen, as stated by the Society of Critical Care Medicine 1
Blood perfusing collapsed or fluid-filled alveoli cannot be oxygenated, regardless of the administered FiO2, as noted by the American College of Chest Physicians 1

The Society of Critical Care Medicine states that in ARDS associated with sepsis, extensive right-to-left intrapulmonary shunt is the primary cause of hypoxemia, resulting from persistent perfusion of atelectatic and fluid-filled alveoli 1, 3
The shunt can consume more than 25% of the total cardiac output in ARDS, according to the European Society of Intensive Care Medicine 1
Hypoxic pulmonary vasoconstriction, which normally compensates by limiting perfusion to poorly ventilated units, may be absent or ineffective in lung damage, as noted by the American Thoracic Society 1

The American College of Chest Physicians notes that hypoxemia in hepatopulmonary syndrome is specifically due to intrapulmonary shunt, manifested by late appearance of contrast in the left heart (after 3-5 cardiac cycles) and limited response to 100% oxygen 4
Patients demonstrate low saturations breathing room air and do not increase saturation as expected with 100% oxygen, according to the European Respiratory Society 4
They present with increased calculated shunt fraction, as stated by the Society of Critical Care Medicine 4

The Society of Critical Care Medicine states that mixed venous oxygen concentration significantly modifies the ability to compensate for intrapulmonary shunt, where low SvO2 values exacerbate the resulting hypoxemia from the same percentage of shunt 1
Differences in mixed venous oxygen concentration among patients result from differences in cardiac output or tissue oxygen consumption, as noted by the American College of Chest Physicians 1
A low SvO2 amplifies the hypoxemic effect of any given amount of shunt, according to the European Society of Intensive Care Medicine 1

The American Association for the Study of Liver Diseases recommends screening for intrapulmonary shunt in patients with unexplained hypoxemia with pulse oximetry <97% on room air in the upright position 5, 6
The European Association for the Study of the Liver suggests screening for intrapulmonary shunt in patients with digital clubbing, facial telangiectasia, dyspnea, wheezing, or syncope in patients with liver disease or portal hypertension 5, 6
Platypnea-orthodeoxia (worsening hypoxemia when upright) is a symptom that warrants screening for intrapulmonary shunt 7

The American Heart Association recommends contrast echocardiography (bubble study) as the primary diagnostic modality for confirming intrapulmonary shunt 5, 6, 7, 8
The American College of Cardiology suggests that microbubbles appearing in the left atrium within 3-6 cardiac cycles confirm intrapulmonary shunt (hepatopulmonary syndrome pattern) 5, 6, 7
The Society of Critical Care Medicine recommends quantitative assessment with 99mTechnetium-macroaggregated albumin (MAA) perfusion lung scan to quantify the degree of intrapulmonary shunting 5, 6

The American College of Cardiology states that intrapulmonary shunt is characterized by bubbles appearing 3-6 cardiac cycles after injection, whereas intracardiac shunt is characterized by bubbles appearing immediately or within 1-3 cardiac cycles 5, 6, 7, 9

The American Association for the Study of Liver Diseases recommends screening all liver transplant candidates with pulse oximetry in upright position for intrapulmonary shunt 5, 6
The American College of Chest Physicians suggests screening for intrapulmonary shunt when evaluating patients with elevated RVSP >45 mmHg for pulmonary hypertension 8
The Society of Critical Care Medicine states that intrapulmonary shunt in ARDS is due to persistent perfusion of atelectatic and fluid-filled alveoli, and normal intrapulmonary shunt is <5% of cardiac output; in ARDS it may exceed 25% 10, 11