Chest
ReviewsMajor Pulmonary Embolism: Review of a Pathophysiologic Approach to the Golden Hour of Hemodynamically Significant Pulmonary Embolism
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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