There are many ways to classify pulmonary embolism, but the best clinical definition would depend on the hemodynamic consequences. For example, massive pulmonary embolism can be defined as systemic hypotension (SBP < 90 mmHg or a drop in SBP of at least 40mmHg for at least 15 min) or shock (tissue hypoperfusion, hypoxia, altered mental status, oliguria, or cool clammy extremities.) There is a second subset is submassive pulmonary embolism. These patients are defined as lack of systemic hypotension (<90mmHg), but have right ventricular dysfunction/hypokinesis. RV dysfunction tells us that there is severe pulmonary artery obstruction and impending hemodynamic failure. Submassive PE is the most common event we see in healthcare.
How is Submassive PE defined: in the Literature:
- Acute PE without hypotension (SBP <90mmHg) but with any of the following:
- RV dysfunction
- Elevated BNP (>500pg/mL)
- Elevated Troponin
- New ECG Changes (Complete or Incomplete RBBB, ST-Segment Elevation/Depression, or T-Wave Inversion)
Why is it Important to Identify Patients with Massive and Submassive PE?
Reviewing large registry trials, 30 day mortality for PE is about 3%. Hypotension and RV dysfunction in the setting of acute pulmonary embolism are both associated with an increasing mortality.
Acute obstruction to of the right heart causes circulatory failure which is the leading cause of death in patients with PE. Therefore, initial stabilization should focus on hemodynamic support. We also should not the following:
- Hypoxia and Hypercarbia: We want to avoid hypoxia and hypercarbia as these can result in pulmonary vasoconstriction. In patients with PE the clot in pulmonary arteries can create shunt blood due to poor gas exchange resulting in elevated C02 levels and decreasing 02 levels. Supplemental oxygen and even intubation maybe required
- Volume Expansion: Patients will usually will have IVs started fluid fluids infusing, however in the critical PE patient this may cause further increased RV pressure resulting in ischemia and failure. In these patients we really want to limit the amount of fluids we are infusing.
- Initial Resuscitation Summary: Escalating Therapy – Start with gentle hydration (500 mL), then consider the addition of a vasopressor early, followed by an inotrope. If the patient is still hemodynamically unstable, consider adding inhaled NO.
- Vasopressors and Inotropes: Early use of vasopressors and inotropes can help enhance heart function. Some meds can help improve RV function and cardiac output while decreasing pulmonary vascular resistance.
- Pulmonary Vasodilators: Inhaled nitric oxide (NO) is very promising in the management of RV failure. Physiologically, it decreases pulmonary vascular resistance without reducing systemic pressures. It also appears to improve ventilation-perfusion mismatch
Massive PE: Thrombolytics are supported by several international organizations as first line therapy (ACCP, AHA, EHA, & ACEP)
Submassive PE: Thrombolytic therapy controversial and confusing. The reason for the controversy is mortality benefits have been mixed amongst studies while there is a real 2 – 3% intracranial hemorrhage rate with thrombolysis. Also, there have been no head-to-head comparisons of thrombolytic agents conducted, to help select one over another.
Clinical Take Home Points:
- Be careful with too much volume resuscitation as this can cause hemodynamic decompensation in patients with acute submassive/massive PEs
- Consider starting vasopressors/inotropes sooner than later
- In massive PE thrombolytics is the standard of care
- Submassive PE is a spectrum of disease. Not all patients will require thrombolytics.
- The only role for inferior vena cava filters is contraindications to anticoagulant treatment
- Sekhri V et al. Management of Massive and Nonmassive Pulmonary Embolism. Arch Med Sci 2012.
- Meyer G et al. Recent Advances in the management of Pulmonary Embolism: Focus on the Critically Ill Patients. Ann Intensive Care 2016.
- Jaff MR et al. Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension: A Scientific Statement form the American Heart Association. Circulation 2011.