The clot CAUSES Dead space; which does not cause hypoxia/hypoxemia on its own.
ALWAYS ASK ABOUT:
- Resp Rate (PE creates dead space, reduced alveolar ventilation, CO2 increases and patient attempts to blow off CO2)
- Blood pressure (?Obstructive shock from large saddle PE)
- Tachycardia (Left heart trying to increase cardiac output because stroke volume low)
Mechanisms by which a PE might cause Hypoxia/Hypoxemia:
Significant V/Q Mismatch (though usually dead space ventilation, but impaired pulmonary oxygen transfer can occur due to vascular re-distribution and release of vaso-active inflammatory molecules such as: serotonin, histamine, prostaglandins, bradykinin etc.)
Pain -> Splinting and atelectasis [caused by loss of surfactant and alveolar hemorrhage]
Inflammation causing infarction [however may be a matched defect] +/- superimposed pneumonia
Increased pulmonary vascular resistance; potentiating right heart strain and cardiac stunting if (i.e PFO)
- Huet Y, Lemaire F, Brun-Buisson C, Knaus WA, Teisseire B, Payen D, Mathieu D. Hypoxemia in acute pulmonary embolism. Chest. 1985 Dec;88(6):829-36.
- Santolicandro A, Prediletto R, Fornai E, Formichi B, Begliomini E, Giannella-Neto A, Giuntini C. Mechanisms of hypoxemia and hypocapnia in pulmonary embolism. Am J Respir Crit Care Med. 1995 Jul;152(1):336-47.
- Torbicki A, Perrier A, Konstantinides S, Agnelli G, Galiè N, Pruszczyk P, Bengel F, Brady AJ, Ferreira D, Janssens U, Klepetko W, Mayer E, Remy-Jardin M, Bassand JP. Guidelines on the diagnosis and management of acute pulmonary embolism: the Task Force for the Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC). Eur Heart J. 2008 Sep;29(18):2276-315.