Chest
Volume 121, Issue 3, March 2002, Pages 877-905
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Major Pulmonary Embolism: Review of a Pathophysiologic Approach to the Golden Hour of Hemodynamically Significant Pulmonary Embolism

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Major pulmonary embolism (PE) results whenever the combination of embolism size and underlying cardiopulmonary status interact to produce hemodynamic instability. Physical findings and standard data crudely estimate the severity of the embolic event in patients without prior cardiopulmonary disease (CPD) but are unreliable indicators in patients with prior CPD. In either case, the presence of shock defines a threefold to sevenfold increase in mortality, with a majority of deaths occurring within 1 h of presentation. A rapid integration of historical information and physical findings with readily available laboratory data and a structured physiologic approach to diagnosis and resuscitation are necessary for optimal therapeutics in this “golden hour.” Echocardiography is ideal because it is transportable, and is capable of differentiating shock states and recognizing the characteristic features of PE. Spiral CT scanning is evolving to replace angiography as a confirmatory study in this population. Thrombolytic therapy is acknowledged as the treatment of choice, with embolectomy reserved for those in whom thrombolysis is contraindicated.

Section snippets

Circulatory Model

The care of the critically ill hemodynamically unstable patient often proceeds along the following two parallel paths: physiologic resuscitation and differential diagnosis investigation. Frequently, the initial physiologic characterization and the subsequent physiologic response to therapy contribute to establishing the definitive diagnosis and initiating optimal treatment. Accordingly, the utilization of a universally applicable physiologic model of the circulation that allows for the

Mechanism of Cardiac Failure

Cardiac failure from MPE results from a combination of the increased wall stress and cardiac ischemia that comprise RV function and impair left ventricular (LV) output. Research from animal models and evidence from clinical investigations clearly demonstrate that the impact of embolic material on the pulmonary vascular outflow tract precipitates an increase in RV impedance. This initiates the vicious pathophysiologic cycle depicted in Figure 4. The degree of increase in RV impedance is

Incidence and Presentation

It has been estimated that hemodynamically unstable MPE constitutes 10% of all PE presentations, although this percentage may be higher given the aforementioned selection bias issues.22 In the UPET,35 the Urokinase-Streptokinase Embolism Trial (USPET),96 and the ICOPER,12 9% (14 of 160 patients), 7% (12 of 167 patients), and 4.2% (103 of 2,454 patients) of all patients, respectively, initially presented in shock. In the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED), 10% of

Basic Diagnostic Findings

The early generation of a differential diagnosis in hemodynamically unstable patients is usually dependent on elements derived from their medical histories and associated risk factors, physical findings, and the basic but readily available diagnostic studies (ie, ECG, chest radiograph [CXR], and arterial blood gas measurement). Definitive studies for PE are rarely available in the first hour of clinical presentation, therefore, recognizing the manifestations of MPE from the preceding is crucial

Shock as a Discriminator

The most consistent operational definition of shock in the PE literature is the presence of hemodynamic instability. With a literature span of 30 years and data predominately derived from case series and subsets of patients from various trials, there is no standard definition. At a minimum, this pragmatic definition requires the presence of hypotension (ie, systolic BP ≤ 90 mm Hg) and/or the use of vasopressor therapy. The presence of shock in patients with acute PE, either as a consequence of

Emboli-in-Transit

Right heart emboli-in-transit have been echocardiographically documented in up to 17% of patients with acute PEs.172 Given the widespread availability and increasing application of ECHO, it is likely that clinicians will be challenged increasingly to define their significance and treatment. The European Cooperative Study304 of 119 patients classified emboli-in-transit into two major categories with different morphologies, etiologies, and clinical significance. Type A thrombi are long, thin,

Conclusion

MPE is dominated by the pathophysiology of the disease, which often defines outcome in the first golden hour. Similar to the golden hour of trauma or myocardial infarction, MPE demands expediency. A pathophysiologic approach to recognition, resuscitation, and treatment provides the greatest opportunity to optimally impact on this lethal disease.

ACKNOWLEDGMENT

The author gives sincere appreciation and gratitude to Doug Coursin, MD, for his review of the manuscript, and to Julie Wardwell for its preparation.

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