(P62) Velocity Time Integral in Pulmonary Embolism

Chief Complaint : Shortness of breath, dyspnea on exertion, and mild chest pain

History of Present Illness : Patient A is a 59-year-old Hispanic male with a past medical history of hypertension, hyperlipidemia, polycythemia vera, heart failure with preserved ejection fraction, and a history of myocardial infarction status post stent placement who presented to his primary care clinic for follow up following a 6-day hospital admission for a heart failure exacerbation one week prior with complaints of increasing fatigue, worsening shortness of breath, and diaphoresis. Additional history was gleamed from his wife which corroborated the patient’s worsening dyspnea and decompensating status. Notably, during his prior admission he underwent a nuclear medicine stress test with myocardial perfusion study which was normal but noted an incidental retroperitoneal mass. Subsequent work up including a biopsy with interventional radiology revealed an adrenocortical neoplasm. Given the patients clinical status, low grade fever (100.4F), tachycardia (120) and hypoxia (percent oxygen saturation of 93%) he was sent to the emergency department for further work up.

Pertinent Physical Exam: Patient was tachycardic with a heart rate of 120, febrile with a maximum temperature of 100.6F and tachypneic with a respiratory rate of 36, and blood pressure was 135/90. On examination, the patient was conversationally dyspneic and in acute distress, with diffuse bilateral lower extremity pitting edema; cardiopulmonary auscultation revealed a regular tachycardic heart rate with no murmurs, bibasilar diminished breath sounds and inspiratory fine crackles.

Pertinent Laboratory Data: High sensitivity troponin I value was 67 ng/L (reference value < 15 ng/L), a Brain-type natriuretic peptide value of 67 pg/mL and venous blood gas with a pH of 7.49, partial pressure of venous carbon dioxide of 35 mmHg, and mixed venous bicarbonate of 27 mmHg which was most consistent with a primary respiratory alkalosis without metabolic compensation.

He subsequently underwent a bedside transthoracic echocardiography with phased array (cardiac) probe, and diagnostic computed tomography (CT) pulmonary angiography.

Case Discussion: Left ventricular outflow tract velocity time integral (LVOT VTI) is a well-validated, rapid measure that has no danger due to its noninvasive nature of obtainment.(1) It has been shown that emergency physicians, including medical trainees and residents, can rapidly obtain VTI without extensive training with veracity and validity that correlates well with subsequent cardiologist evaluation. (1) Additionally, LVOT VTI has been shown to predict outcomes in select populations, including patients with acute decompensated heart failure and pulmonary embolism. (2,3) Yuriditsky et al. demonstrated that a low VTI, defined as less that 15 cm, was significantly associated with worse outcomes, specifically in-hospital death or cardiac arrest and shock or need for reperfusion in patients with acute PE. (4) Current prevailing theory posits that a low LVOT VTI correlates with left ventricular dysfunction and hemodynamic instability and subsequent poor clinical outcomes. (4)

In our case, the patient had a VTI of 12.9cm and a TAPSE of 1.9cm, indicating no evidence of right heart strain, but an abnormally low VTI, well below the cutoff defined by Yuriditsky.

This case described here shows conflict between the LVOT VTI and TAPSE values in the diagnosis and prognostication of PE. We therefore propose that LVOT VTI could augment all bedside echocardiographic evaluation of patients with suspected acute PE given its strong association with adverse short-term outcomes in acute pulmonary embolism and utility for risk stratification. Additional studies need to be performed to better compare VTI and TAPSE to determine which is the most appropriate initial measure in these patient populations.

The patient was initiated on intravenous continuous heparin therapy and was subsequently transitioned to oral direct anticoagulation with apixaban for three months for treatment of an acute provoked pulmonary embolus in the setting of a hypercoagulable state secondary to malignancy.

References and Acknowledgements (Optional): 1. Christopher William Parker, Amie Marie Kolimas, Pavitra Kotini-Shah,Velocity-Time Integral: A Bedside Echocardiography Technique Finding a Place in the Emergency Department, The Journal of Emergency Medicine, Volume 63, Issue 3, 2022, Pages 382-388, ISSN 0736-4679, https://doi.org/10.1016/j.jemermed.2022.04.012. (https://www.sciencedirect.com/science/article/pii/S0736467922002864)

2. Blanco, P. Rationale for using the velocity–time integral and the minute distance for assessing the stroke volume and cardiac output in point-of-care settings. Ultrasound J12, 21 (2020). https://doi.org/10.1186/s13089-020-00170-x

3. Tan, C., Rubenson, D., Srivastava, A. et al. Left ventricular outflow tract velocity time integral outperforms ejection fraction and Doppler-derived cardiac output for predicting outcomes in a select advanced heart failure cohort. Cardiovasc Ultrasound 15, 18 (2017). https://doi.org/10.1186/s12947-017-0109-4

4. Yuriditsky E, Mitchell OJ, Sibley RA, Xia Y, Sista AK, Zhong J, Moore WH, Amoroso NE, Goldenberg RM, Smith DE, Jamin C, Brosnahan SB, Maldonado TS, Horowitz JM. Low left ventricular outflow tract velocity time integral is associated with poor outcomes in acute pulmonary embolism. Vasc Med. 2020 Apr;25(2):133-140. doi: 10.1177/1358863X19880268. Epub 2019 Nov 10. PMID: 31709912.