**16. Submassive pulmonary embolism**

**Massive Sub-massive Low-Risk**

hypotension Acute PE without systemic hypotension Low-risk PE

Systolic blood pressure > 90 mm Hg but with either RV dysfunction or myocardial

RV dysfunction defined as the presence

∙RV dilation (apical 4-chamber RV diameter divided by LV diameter 0.9) or RV systolic dysfunction on

Acute PE and the absence of the clinical markers of adverse prognosis that define massive or

necrosis

submassive PE Hypotension not due to a cause

of at least 1 of the following:

echocardiography

0.9) on CT

( 500 pg/mL); or

wave inversion)

the following:

ng/mL)

ng/mL)

Myocardial necrosis is defined as either of

∙Elevation of troponin I (0.4

∙Elevation of troponin T ( 0.1

**Table 4.** Definitions of massive, submassive and low risk of pulmonary embolism (based on 2011 American Heart

The mainstay of treatment for low risk PE is prompt initiation of anticoagulation. Importantly, if there is a high clinical suspicion for PE, anticoagulation should be initiated prior to confir‐ mation of the diagnosis (Tapson 2012). The 2012 American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (Kearon 2012) for Venous Thromboembolism

∙RV dilation (4-chamber RV diameter divided by LV diameter

∙Elevation of BNP ( 90 pg/mL) ∙Elevation of N-terminal pro-BNP

∙Electrocardiographic changes (new complete or incomplete right bundle-branch block, anteroseptal ST elevation or depression, or anteroseptal T-

Acute PE with sustained

Systolic blood pressure < 90 mm Hg for at least 15 minutes or requiring

> ∙Including but not limited to arrhythmia, hypovolemia, sepsis, or LV dysfunction, pulselessness, or persistent profound bradycardia

◦Heart rate 40 bpm with signs or symptoms of shock.

Association Scientific Statement)

**15. Low risk pulmonary embolism**

inotropic support

130 Pulmonary Hypertension

other than PE

The treatment of submassive PE remains controversial. Patients with submassive PE carry an increased risk of adverse outcomes and early mortality (Piazza 2013); however, there is no clear evidence that thrombolysis in addition to heparin in this subset of patients improves mortality. In 2002, Konstantinides et al (Konstantinides 2002) evaluated 256 patients with submassive PE who were randomly assigned to receive heparin plus alteplase versus heparin plus placebo. Treatment with heparin plus placebo was associated with more frequent clinical deterioration requiring an escalation of treatment (11% versus 25%); however, no change in mortality was detected (Konstantinides 2002). Further study is required to determine appro‐ priate management of this patient population. Currently, comprehensive evaluation weighing risks and benefits of anticoagulation with heparin versus thrombolysis is the usual approach.
