A cardiac arrest alert sounded on the orthopedic surgery ward. When you arrived, CPR was already started by the intern and nursing staff with the 3rd cycle underway. You ask "what was the rhythm?" and the nursing supervisor recording the events responded "PEA!". The intern runs to you saying "this is a 77-year-old lady, who is hypertensive, diabetic and had PCI to the RCA 3 months ago who is post op day 3 after total hip replacement" and she shows you this ECG (done between cycles when ROSC was briefly achieved before she arrested again!)
Sorry! I forgot the references:
References:
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Thank you for all your comments. You all raise important and relevant points for discussion!
The ECG demonstrates and ectopic focus for atrial depolarization (P wave being negative in II, III and aVF). This 'ectopic' atrial rhythm is firing at a rate of ~150/min. The ST changes are a little unusual in the following points:
1. There is STE in III and aVF but not in II
2. There is STE in V1 and V2
3. There is incomplete RBBB pattern and in that context. The S waves seen in I could be due to the iRBBB pattern but also the infamous McGinn-White sign.
4. STE in aVR is also noted but unlike the classic pattern of diffuse subendocardial ischemia, we don't see much ST depressions in the other leads.
5. The distribution of ST elevation don't fit one arterial territory (one may argue that there is nothing that is a 100% in medicine!)
Therefore, and based on the ECG findings; one cannot definitely rule out an acute thrombotic occlusion of the RCA with the patient being off dual antiplatelet therapy for his surgery and by the same token, one cannot completely ignore that the fact that the clinical context is very attractive for a massive pulmonary embolism as another differential diagnosis.
The ECG is an important tool in evaluating patients in emergencies. Acute pulmonary embolism, however, is associated with a whole host of changes that that are can be helpful but not all that accurate for diagnosis:
- 10-25% of patients have a completely normal ECG.1 The most commonly quoted ECG sign is the S1Q3T3 sign (also known as the McGinn-White sign). This indicates acute RV strain. This pattern is found in only 20% of patients with pulmonary embolism.
- The most common ECG finding is sinus tachycardia
- Other reported findings include
** Electrical alternans2
** ST elevation in aVR and ST depression in leads 1, V4-V63
- Some ECG features are associated with poor prognosis: RBBB, STE in V1 are associated with cardiogenic shock4
- Additional findings associated with bad prognosis include: Atrial tachyarrythmias, complete RBBB, peripheral low voltages, pseudo-infarction pattern in the inferior leads (Q waves) and ST segment changes over the left precordial leads are commonly associated with fatal outcomes.
- The most common finding in confirmed massive PE was T wave inversion in the precordial leads with an earlier onset in more severe cases5
- In patients with RV dysfunction, T wave inversion in V1-V3 had greater sensitivity and diagnostic accuracy compared with S1Q3T3 and RBBB, which had good specificity but only moderate accuracy.5
- Atrial tachyarrythmias as AF, AFL and atrial tachycardia is seen in up to 8% of patients with acute PE.
- Simultaneous T wave inversions in inferior II, III and aVF and right precordial leads (V1-V4) is the most specific finding in favour of PE, with reported specificity of up to 99% in one study.
- Simultaneous T wave inversions in III and V1 are observed in only 1% of patients with ACS compared with 88% of patients with acute PE. “Negative T waves in leads III and V1 were observed in only 1% of patients with ACS compared with 88% of patients with Acute PE (p less than 0.001). The sensitivity, specificity, positive predictive value, and negative predictive value of this finding for the diagnosis of PE were 88%, 99%, 97%, and 95%, respectively. In conclusion, the presence of negative T waves in both leads III and V1 allows PE to be differentiated simply but accurately from ACS in patients with negative T waves in the precordial leads” Kosuge M et al. Am J Cardiol 2007
- A few case reports describe ST elevation in patients with massive pulmonary embolism but the exact mechanism is unclear7-9. Possible mechanisms include:
** Acute ischemia in an acutely pressure overloaded RV confounded by hypoxia and hypotension
** Possible paradoxical embolism through a PFO which opened up due to pressure variation in the left and right side of the heart
** Possible compression of the proximal segment of an anomalous right coronary artery (especially when vessel is coursing between the pulmonary trunk and aorta) as shown below (variant 3B and 3C)
-Inferior ST elevation is rare. Some possible causes include:
- Severe right ventricular dilation with significant increase in wall tension and oxygen consumption.
- Sudden coronary hypoperfusion caused by the sudden drop in the right and left ventricular output
- Hypoxia caused by the massive PE and finally
- Possible coronary spasm caused by hypoxia and increased right heart pressure might all have contributed to inducing the acute right ventricular ischemia which showed as ST-segment elevation in the inferior leads and an elevation in cardiac enzymes.
- There is also the possibility of proximal RCA compression between the PA and aorta especially with anomalous RCA origin from the left coronary cup or
- embolic occlusion of an RCA with anomalous origin from the main pulmonary artery.
- Paradoxical embolism through a PFO always remains a possibility.
To differentiate the two definitively, as the treatment may be fundamentally different (depending on your local resources) and quick look echo will likely be helpful. This is one clip that is diagnostic and allows us to administer the correct treatment:
As seen on the echo clip, the RV is enlarged with a severely depressed systolic function. The LV is underfilled with compressed. The septum is flattened in systole due to RV pressure overload. Moreover, the inferior wall is contracting normally. All the above findings confirm the diagnosis of acute massive pulmonary embolism.
orthopedic surgery by itself has an intermediate risk factor for MI in patient with known CAD.
with the history of PCI 3 months back and surgical intervention within less than one year carry high risk of recurrent MI.
in view of the ECG finding of STE in the inferior lead and reciprocal changes in the high lateral leads I would think about recurrent RCA MI.
Well
it seems that she’s having a diffuse ST changes with ST elevation in aVR and se can not ign the right sided ST changes with changes in the rhythm , so there is involvement of both sides right and left side
possible diagnosis is in stent thrombosis or new MI
PE is a possibility as mentioned previously
my question is did the patient got anticoagulation for dvt prophylaxis ?
I agree with what ahmed said regarding PE for this patient giving his risk and some ecg findings . But on the other hand i can not ignore those ugly ischemic ST segments.
He underwent a major surgery which i guess demanded the stop of his DAP. His PCI is recent and this will put him at risk of stent thrombosis most probabbly at RCA. Which also may explain his non SA node p waves in lead II due to ischemic SA node which is supplied by SA nodal branch of RCA.
2 main possibilities here:
1- PE. this possibility is supported by:
- the patient rythum during arrest was PEA.
- S1Q3T3 in the ECG
-Dominant R wave in V1.
-atrial tachycardia ( p wave is negative in lead 2 , suggesting the pacemaker is somwhere in the atrium rather than sinus node).
-post hip replacement.
2- inferior STEMI.
this is supported by STE in the inferior leads with reciprocal changes in the lateral leads.
but those changes can also occur in PE due to RV strain and demand ischemia in massive P.E.
so as a conclusion i think the possibility of P.E is higher in this patient.