A prehospital cath lab activation for STEMI came through with the information that the 40-something woman had chest pain and a pulse of 140.
We were immediately skeptical that the patient had a STEMI because of the high heart rate. She would have to be in cardiogenic shock with a massive STEMI for that. Certainly possible, but when the heart rate is so high, be skeptical.
The patient arrived with this ECG:
Here the heart rate is obviously no longer 140
What do you think?
ECG: it certainly appears to be an anterior STEMI, but it is important to realize that right ventricular ischemia from either inferior and RV STEMI or from pulmonary embolism can manifest with STE in V1-V3.
On arrival, she immediately lost pulses. Due to body habitus, an adequate transthoracic echo could not be done. There was no ventricular fibrillation recorded, but in the rush of action, she did get defibrillated. Most involved agree there was never any ventricular fibrillation.
This turned out to be a pulmonary embolism (on autopsy).
Massive PE can have Right Ventricular ischemia resulting in RV ST Elevation. When there is sudden loss of pulse but no ventricular fibrillation, then STEMI is an unlikely etiology of arrest. In this series of 1246 cardiac arrests, 60 of which were from PE, only 3 had ventricular fibrillation.
In contrast, the vast majority of initial rhythms in cardiac arrest from acute coronary syndrome are shockable rhythms, and the vast majority are ventricular fibrillation.
This case was particularly confusing because CPR was very effective: good pulses, good O2 saturations, good arterial line waveform, non low end tidal CO2. CPR is generally not very effective in pulmonary embolism because of obstruction of the pulmonary vasculature. Additionally, transesophageal echo (TEE) was placed and did not show a particularly enlarged RV.
Unfortunately, in spite of administration of 100 mg of tPA, the patient could not be resuscitated.
See this case:
Learning Points:
1. When there is chest pain and ST elevation in the right precordial leads, think of pulmonary embolism.
2. When there is extreme sinus tachycardia, ACS becomes less likely unless there is:
A. Another simultaneous pathology
B. Pre-existing poor ventricular function or
C. Cardiogenic shock caused by the ACS, and confirmed by poor LV function on bedside cardiac echo.
3. Corollary to Learning point #2.: Cardiac ultrasound and volume assessment is essential to interpreting the ST Elevation on the ECG.
4. If a patient has cardiac arrest witnessed to be PEA, then ACS is very unlikely to be the etiology.
5. If a patient is found in PEA after a significant down time, the arrest may have started as ventricular fibrillation and degenerated to PEA. Such arrests may be due to any etiology.
https://pubmed.ncbi.nlm.nih.gov/12804925/
ReplyDeleteQR in V1--an ECG sign associated with right ventricular strain and adverse clinical outcome in pulmonary embolism
Excellent reference! Thank you!
DeleteQR in V1 – an ECG sign associated with right ventricular strain and adverse clinical outcome in pulmonary embolism.
Aims: To test the hypothesis that Qr in V(1)is a predictor of pulmonary embolism, right ventricular strain, and adverse clinical outcome.
Methods and results: ECG's from 151 patients with suspected pulmonary embolism were blindly interpreted by two observers. Echocardiography, troponin I, and pro-brain natriuretic peptide levels were obtained in 75 patients with pulmonary embolism. Qr in V(1)(14 vs 0 in controls; p<0.0001) and ST elevation in V(1)> or =1 mV (15 vs 1 in controls; p=0.0002) were more frequently present in patients with pulmonary embolism. Sensitivity and specificity of Qr in V(1)and T wave inversion in V(2)for predicting right ventricular dysfunction were 31/97% and 45/94%, respectively. Three of five patients who died in-hospital and 11 of 20 patients with a complicated course, presented with Qr in V(1). After adjustment for right ventricular strain including ECG, echocardiography, pro-brain natriuretic peptide and troponin I levels, Qr in V(1)(OR 8.7, 95%CI 1.4-56.7; p=0.02) remained an independent predictor of adverse outcome.
Conclusions: Among the ECG signs seen in patients with acute pulmonary embolism, Qr in V(1)is closely related to the presence of right ventricular dysfunction, and is an independent predictor of adverse clinical outcome.
thank you, Steve. Sad case, but very enlightening. interesting that TEE was not terribly helpful, and that full dose tPA ineffective.
ReplyDeleteSteve... there wasn't just ST elevation V1-3. there was significant ST depression inferior and laterally. thus, global ischemia? Is this simply RV injury pattern with reciprocal changes elsewhere, or ischemia elsewhere?
What a lovely reminder of PE in this ECG very suspicious for ischemia.
ReplyDeleteSome salient notes,
Thank you from ZA
Dr.Smith,thanks for this excellent but challenging ECG of 40 something woman with chest pain, ST elevation and tachycardia ( 30th JAN 2021 ) I fully agree with your very valid point on tachycardia
ReplyDeletein suspected ACS. Also, I think the diagnostic thinking in this emergency case would have included PTE had the refering team looked at patient's SPO2. Ofcourse, the ECG is arguably compelling enough to rush towards ACS.
with regards, Dr.R.Balasubramanian. PONDICHERRY, INDIA
SPO2 was excellent during chest compressions (for a cardiac arrest case), as was pulse, which made us think that there could not be pulmonary artery obstruction, as we were getting good flow and
DeleteHi Dr Smith, with this particular ECG , wouldn’t you consider the possibility of old ASMI( poor R IN V1-V3 with residual ST ELEVATION) with now ST elevation in aVR due to left main disease or severe TVD.. severe ischemia leading to tachycardia later leading to asystole
ReplyDeleteCertainly would consider it, but in the context of Non-shockable rhythm, PE climbs higher on the differential diagnosis.
Deletenice
ReplyDelete