Gordon had a 69yo patient who presented to ED following a pre-syncopal event while visiting family at the Children's. He had a PHx of IHD, CCF, moderate pulmonary HT.
The patient had had a syncopal event 2/52 ago. Today, he felt faint and was lowered to the ground. Nil LOC. Nil SOB or CP. Hypotensive and bradycardia on MAS arrival and noted to be plethoric and "purple" in the face.
In ED, plethoric, BP 90/50 HR 55 SR sats 96% on RA. Chest bibs crackles.
ED echo was done to look for reversible causes.
PLAx showing moderate LV systolic dysfunction, dilated RV (>3cm diameter) with relatively preserved contractility. Also a small pericardial effusion.
In comparison PLAx in patient with acute PE, the RV free wall does not move at all.
PSAx in this patient showing dilated RV, bowing of the IV septum into the LV. Pericardial effusion.
So is his collapse due to a massive PE?
He has known elevated pulmonary pressures (from a previous echo) which would cause a dilated, hypertrophied RV.
Subcostal 4C shows he does has RV hypertrophy consistent with chronic RV P overload (RV free wall >6mm).
CTPA was done and showed 2x LLL PE.
In this patient with a Ddx of ?acute PE causing collapse, the ED cardiac US was confusing because he had pre-existing pulmonary HT and RV dysfunction secondary to this.
In acute PE, the RV is dilated (normal RV is 60% of LV), thin walled, with poor contractility. The RV may show McConnell's sign (RV apical preserved contractility with poor free wall contractility). McConnell's sign was initially reported to have a high PPV for acute PE (1). However, recent studies have shown that it is also present in patients with chronic pulmonary HT (2,3). So it can't be relied on to tell the difference between acute and chronic pulmonary HT. In this patient looking closely at the RV free wall in PLAx, there is pretty good contractility which you wouldn't expect from acute RV P overload.
At the same time, the LV in acute PE should be contracted and hyper dynamic. This patient has moderate LV systolic dysfunction, so you can't rely on the absence of hyper dynamic LV to differentiate acute from chronic.
In the end, Gordon and I decided because the RV free wall was still working, he doesn't have a saddle PE and could wait for CT. In the end his collapse was probably a combination of CCF, bradycardia +/- PE.
Importantly, echo is only helpful for massive PE (i.e. the unstable patient). The European Society of Cardiology 2014 PE guidelines does not recommend the use of echo in the stable patient with a suspected PE. However, if the patient is unstable and there is a high risk of PE, bedside echo will show signs of RV dysfunction in 80% of patients (5).
McConnell MV, Solomon SD, Rayan ME, et al. Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism. Am J Cardiol. 1996; 78:469–473. [PubMed: 8752195]
2. Mediratta, A, Addetia, K, Medvedofsky D et al. Echocardiographic Diagnosis of Acute Pulmonary Embolism in Patients with McConnell’s Sign. Echocardiography. 2016 May ; 33(5): 696–702. doi:10.1111/echo.13142.
3. Walsh BM, Moore CL. McConnell's Sign Is Not Specific for Pulmonary Embolism: Case Report and Review of the Literature. J Emerg Med. 2015 Sep;49(3):301-4. doi: 10.1016.
4. Konstantinides SV, Torbicki A, Agnelli G et al. 2014 ESC Guidelines on the diagnosis and management of acute pulmonary embolism. Eur Heart J. 2014 Nov 14;35(43):3033-69, 3069a-3069k.
5. Kearon, C. (2003) Diagnosis of pulmonary embolism. Canadian Medical Association Journal, 168, 183-194