Pulmonary embolism (PE) represents a clinical diagnostic dilemma. About 650 000 patients are diagnosed with PE each year in the USA and up to one-third die as a result of PE [1,2]. Pulmonary embolism is most commonly due to blood clots that travel through the venous system and lodge in the pulmonary arterial tree. Alternatively, embolism may be due to gas (i.e., air or carbon dioxide [CO2]) , tumor, fat, or even bone cement . Findings in large autopsy studies showed that PE was not identifi ed premortem in up to 70% of patients who die as a direct result of this condition [1,2,5,6]. Presenting symptoms, i.e., tachypnea and shortness of breath , or alterations in arterial oxygen content [8–10] are non-specifi c. In actuality, these fi ndings are more commonly due to an alternative diagnosis, such as postoperative atelectasis or pneumonia. Th e majority of deaths from PE occur within the first hour of the embolic event. For patients who survive beyond the fi rst hour, appropriate therapy decreases the death rate from 30% to 2.5–10% [1,11]. Conversely, since only 20–40% of patients with clinically suspected PE actually have PE, empirical therapy may unnecessarily subject patients to a risk of bleeding. Unfortunately the common diagnostic techniques of V /O Q O scanning, pulmonary angiography, or computed tomography (CT) angiography, are cumbersome, invasive, require transportation of potentially critically ill patients, or involve the use of radiation or nephrotoxic agents. A simple, rapid bedside method to screen, or more importantly, diagnose PE would be of great benefit. To this end, several investigators have assessed respiratory deadspace-based parameters derived from capnography to detect the presence of pulmonary emboli. Advances in technology have brought capnography to the bedside. This chapter describes the pathophysiologic basis and use of capnography in the detection of PE from a variety of causes.
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