Presented by: Dr. Luke Donnelly
Summarized by: Drs. Wendy Chan and Yonatan Yohannes
Reviewed by: Dr. Ian deSouza
The Case:
27 year-old male no PMH BIBEMS for syncopal episode in bathroom. + significant family Hx of PE. Initial vitals: HR 138, RR 33, BP 87/64, 91% 02 on room air. Pt was placed on 5L NC and given a small fluid bolus with some improvement of vitals. On physical exam, patient was alert, but tachypneic and diaphoretic. There was a high index of suspicion for massive PE, which was confirmed on bedside sono. Heparin therapy was begun while patient underwent CT head for possible traumatic ICH and CTA of pulmonary arteries. Scans showed no ICH and large bilateral PEs, respectively. Heparin was then held while alteplase was given. The patient was admitted to the MICU. The patient improved clinically and was discharged from the hospital on day #6 on warfarin.
Ultrasound: dilated RV on apical four-chamber view
EKG: 1) sinus tachycardia 2) P pulmonale (P >2.5mm in inferior leads , P > 1.5mm in V1,V2). prominent R in AVR, RV strain pattern (T inversion V1,V2), and right axis deviation
Pathophysiology
Hemodynamic “death spiral” of PE
The hemodynamic collapse is primarily a result of increasing pulmonary vascular resistance. This is a result of physical obstruction (i.e. clot burden), hypoxic vasoconstriction, and humoral mediator induced vasoconstriction within the pulmonary vasculature. This causes an abrupt and disproportionate increase in pulmonary vascular resistance, leading to RV strain, dilatation, and ischemia. This is the beginning of a downward spiral, which ends with reduced LV preload, decreased cardiac output and perfusion, further ischemia, and ultimately cardiogenic shock.
Hypoxemia
Hypoxemia initially results from V/Q mismatch and shunting. In addition, decreasing cardiac output leads to increased oxygen extraction in peripheral tissue. This further reduces the partial pressure of oxygen in the blood to abnormally low levels. This is also the mechanism for the large A-a gradient seen in PEs .
Shunting
Shunting occurs when there is reduced ventilation to perfused lung units or when the lungs are bypassed altogether.
Intracardiac shunt- Right to left intracardiac shunting may occur in the presence of PE if there is a patent foramen ovale present (up to 25-34% of people in the first 8 decades of life) due to tricuspid regurgitation and increasing right atrial pressure causing deoxygenated blood to flow across the pathological pressure gradient from right to left atrium. This results in deoxygenated venous blood entering arterial circulation.
Intrapulmonary shunt (V/Q mismatch of PE)– Particular areas of the lung will be overperfused to compensate for both the embolus and grossly vasoconstricted portions of the pulmonary vascular bed. The level of ventilation in these areas may not be sufficient to fully oxygenate the increased blood flow. In this scenario, the ratio of ventilation to perfusion falls to < 1.0. (in normal lung, ratio is approximately 1.0)
Managing Massive PE
-Don’t rush to intubate as this can hasten hemodynamic collapse. If you must intubate, use a norepinephrine drip or push dose epinephrine to maintain adequate blood pressure. To treat significant hypoxemia, high-flow nasal oxygen may be preferred as it does not involve positive pressure ventilation; PPV can precipitate hemodynamic collapse in RV failure.
-There is no data to support giving > 500CC fluid bolus to patient. Fluids may initially improve cardiac output, however with increasing RV end-diastolic pressure and decreasing RV contractility, additional fluids will likely cause further RV dilation, thus propagating the downward hemodynamic spiral. If you want to improve pressures, jump to pressors!
-tPA is the definitive treatment for massive PE. A recent meta-analysis of acute PE (both massive and submassive) showed when compared to anticoagulation, thrombolytic therapy is associated with lower all-cause mortality. However because the NNT (the number of patients who need to be treated to prevent one death) is high even in subgroup analysis stratifying high risk and intermediate risk PEs, this has minimal mortality benefits. However, tPA has been shown to reduce pulmonary hypetersion (16% vs 57% in submassive PEs with evidence of right heart strain. Moreover, in the under 65 age group, the high NNH (number needed to harm) suggests for massive PE in this age group, the benefits of tPA may outweigh the risks.
| Outcome of interest | No. needed to treat or harm | P value |
| All-cause mortality | NNT= 59 | .01 |
| ICH | NNH= 78 | .002 |
| Major Bleed | NNH= 18 | <.001 |
| Major Bleed age < 65 | NNH= 176 | >.05 |
| ICH age < 65 | NNH = 883 | >.05 |
-Contraindications to tPA include: brain mass, AVM, recent stroke, trauma or hemorrhage; active bleed; or recent “major” surgery or trauma. In patients where systemic thrombolysis is not an option, consider catheter-directed thrombolysis or embolectomy. Initial results show 86% clinical success without any major complications or bleeds.
-In cardiac arrest secondary to massive PE, consider half-dose tPA as a bolus. Ongoing CPR is not an absolute contraindication for fibrinolysis!
-Submassive PEs are different animals. Per PEITHO and MOPPET studies, consider tPA if +trops, BNP>300, or evidence of right heart strain. MOPPET used half-dose (50mg tPA)
In Summary:
-Have pressors ready, if not already running, when intubating in massive PE.
-Do not reflexively give IV fluids for hypotension as it could significantly worsen hemodynamics.
-If no contraindications are present, management with thrombolytics can save lives. The complication of thrombolytics of greatest concern is ICH, however with a significant reduction in all-cause mortality and a NNT < NNH, the benefit of thrombolytics in massive PE outweigh the risk of ICH, especially for our <65 year old population.
References
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Neumar, R. et al. “Part 8: Adult Advanced Cardiovascular Life Support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.” Circulation122.18_suppl_3 (2010): n. pag. Web.
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