Resus: What is the Ideal Hemodynamic Resuscitation for High Risk PE?
Case Presentation
Patient was a 33-year-old male with a medical history significant for prior PE in 2013, HIV, hypertension, and Crohn’s colitis, who was brought into the Emergency Department by EMS for syncope. Patient reported that when the syncopal episode occurred, he was bending down to reach for an object, and it lasted 1 to 2 mins. He was recently diagnosed with a LLE DVT for which he was prescribed Apixaban. Per EMS, patient’s blood pressure was 70’s over palp initially. On arrival to the ED, patient reported feeling mildly confused and lightheaded, and experiencing a headache with shortness of breath and mild nausea.
Initial vitals were significant for hypotension at 97/70, mild tachycardia with heart rate ranging between 90s -100s, and SpO2 of 91 – 92% on room air, which increased to 94% on 3 L NC. Physical exam was significant for mild diaphoresis and tachycardia, but otherwise it was unremarkable. A point of care cardiac ultrasound showed evidence of right heart strain. EKG showed S1 and T3 with no Q3. CT Angio chest for PE was conducted and it showed an extensive acute saddle pulmonary embolism with large clot burden involving multiple pulmonary arterial branches bilaterally, RV to LV ratio more than 1 and subtle flattening of basilar portion of interventricular septum suggestive of right heart strain. Patient was given 1 liter of normal saline which improved systolic blood pressure to low 100s. A heparin infusion was initiated. PERT was called and they recommended continuation of systemic anticoagulation with heparin and monitoring in the CICU, with a low threshold for re-conference to discuss catheter directed thrombolysis vs tPA if patient decompensates. An echocardiogram was completed on admission, and it showed mild to moderate RV enlargement with dysfunction, and a normal ejection fraction of 55-60%. Troponin was elevated at 0.24 which increased to 0.43 and decreased to 0.38 on hospital day 2.
If the patient loses hemodynamic stability, should IV fluids or vasopressors be considered as the next step?
In patients who present with high risk PE, defined as a patient with suspected/confirmed PE with hypotension, controversy still exist on the proper use of fluids and vasopressors in the management of hypotension. Traditionally, patients presenting with hypotension in the presence of a PE are initially resuscitated with 500-1000 ml of normal saline. Although fluids may initially increase cardiac output, early experimental studies by Ghignone et al [1], Belenkie et al [2], and Molloy et al [4] showed that the use of fluids in hypotensive PE patients with moderate to severe RV dysfunction can result in further increased RV end diastolic pressure, and decreased RV coronary perfusion pressure which intensifies ischemia of the right ventricle, and ultimately, further decrease in function. Fluid administration in the presence of RV dysfunction also causes further interventricular septal shift towards the left ventricle, resulting in worsened left ventricular compliance and filling, which further decreases cardiac output.
A review article by Sekhri et.al suggested that in cases were the central venous pressure is high, greater than 12-15 mmHg, or when severe RV dysfunction is documented, fluids should be used with extreme caution, and early consideration should be given to use of vasopressors [9]. The 2019 European Society of Cardiology Guidelines for the Diagnosis and Management of Acute Pulmonary Embolism recommend that in patients with right ventricular failure in acute high-risk pulmonary embolism, cautious volume loading with fluids less than or equal to 500 mL over 15 -30 mins can be considered in patients with normal to low central venous pressure [6]. It may be reasonable to start with vasopressors instead of fluids in order to prevent further exacerbation of hemodynamic instability, especially since the adequate amount of fluids to administer is difficult to accurately determine.
The vasopressors commonly utilized are norepinephrine, epinephrine and vasopressin. Norepinephrine is an inoconstrictor that functions by increasing both cardiac output and systemic vascular resistance, while minimally affecting the pulmonary vascular resistance [6,9,12]. Epinephrine functions as a vasoconstrictor which helps to increase systemic vascular resistance. Vasopressin can be utilized due to its effects on increasing systemic vascular resistance only and no effect on pulmonary vascular resistance, as shown in a study by Sarkar et al.[7,8]. Some practices use vasopressin as either a first line agent instead of norepinephrine or epinephrine, or as a second line agent if norepinephrine or epinephrine are ineffective at elevating blood pressure.
Inodilators such as dobutamine and milrinone can increase RV function and cardiac output, and decrease pulmonary vascular resistance, but they are also potent vasodilators which can worsen systemic hypotension [9,13]. As a result, they are utilized in conjunction with vasopressors. Dopamine, an inoconstrictor, can also help increase cardiac output and systemic vascular resistance, but it results in tachycardia that causes low cardiac output, and ultimately further exacerbates the hypotension [9,13].
Conclusion
On hospital day 3, patient was initiated on Apixaban 10 mg BID for 7 days with a transition to 5 mg BID. He remained hemodynamically stable and SpO2 ranged between 94-98% on room air. Patient was discharged on hospital day 4 while on Apixaban with close follow-up with vascular medicine.
Take Home Conclusion
In high risk PE patients presenting with hypotension, it is advisable to start with vasopressors instead of fluids due to the increased risk of further right ventricular dysfunction, and ultimately, exacerbated hemodynamic instability.
POST BY: LORADO MHONDA (MS4)
FACULTY EDITING BY: DR. COLIN MCCLOSKEY (EM-INTENSIVIST)
References
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