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.