aka Cardiovascular Curveball 003
As leader of the MET team you were called to a ‘Code Blue’ to resuscitate a 57 year-old man who arrested on the ward post-operatively. The initial rhythm was ventricular fibrillation. Following defibrillation (1 x 200J biphasic), 1 mg adrenaline IV and 2 minutes of CPR he had an idioventricular rhythm with a rate of 40 but remained pulseless. CPR was continued for a further 2 minutes and 1.2 mg atropine was administered. The patient then had return of spontaneous circulation and was intubated as he remained unconscious.
This was his ECG post-intubation:
Post-resuscitation ECG (click to enlarge)
Q1. Describe this ECG.
This is an unusual ECG!
- There is an underlying sinus rhythm with normal axis.
- The QRS complexes are high voltage with markedly prolonged QT intervals (although the ends of many of the T waves are not easily seen).
- There is a broad complex (~120 msec) QRS occurring on every second T wave… This is consistent with bigeminal ventricular premature contractions (VPBs) with recurrent R-on-T phenomenon.
Q2. Can you guess what happened next?
He arrested again – this time the ECG monitor was suggestive of torsades de pointes (‘twisting of the points’) – presumably because of the barn-door R-on-T phenomenon seen in the above ECG.
He reverted to sinus rhythm following 1 x 200J biphasic defibrillation. However, the ECG monitor showed that he soon returned to the rhythm shown in his post-intubation ECG.
He was not in torsades de pointes long enough to capture a 12-lead ECG – but this is what it looks like:
An R-on-T phenomenon leading to Torsades des Pointes (click to enlarge)
The features of torsades de pointes are:
- polymorphic ventricular tachycardia with a rate of >200/min.
- The axes of the QRS complexes undulate with the polarity of the complexes appearing to shift about the baseline.
- often occurs in short episodes (<90 seconds) but prolonged episodes can occur.
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His arterial blood gas post-intubation showed:
| pH | 7.403 | [7.350 - 7.450] |
| pCO2 | 48.6 mmHg | [36.0 - 45.0] |
| pO2 | 176 mmHg | [85.0 - 110] |
| Bicarbonate | 29.7 mmol/L | [21.0 - 28.0] |
| Sodium | 130 mmol/L | [134 - 146] |
| Potassium | 2.6 mmol/L | [3.4 - 5.0] |
| Chloride | 98 mmol/L | [98- 108] |
| Glucose | 8.6 mmol/L | [3.0 - 5.4] |
| Lactate | 1.8 mmol/L | [<1.3 mmol/L] |
Q3. Describe the arterial blood gas.
The patient is ‘over-oxygenated’. pH is normal with a mild respiratory acidosis and mild metabolic alkalosis. There is mild hyponatremia, hyperglycemia and a mild hyperlactemia.
Overall this is a great gas for someone who just had a cardiac arrest!
The key abnormality though is the presence of hypokalemia, which is likely to have a causative role in this patient’s predilection for torsades.
Q4. What further management is necessary?
Correction of moderate hypokalemia (1.5 – 3.5 mmol/L) with potassium and administration of magnesium for impending torsades de pointes.
The patient was administered 20 mmol of KCl IV over 5 minutes via a central line and was administered 10 mmol MgCl2 IV.
Following the further management given in Q4, the patient had another ECG:
ECG following further management
Q5. Describe the ECG findings. Is the ECG suggestive of an underlying diagnosis?
The ECG findings are:
- Atrial fibrillation (irregularly irregular with absent P waves) with a heart rate of ~ 100/min.
- Normal axis
- QRS complexes meets voltage criteria for left ventricular hypertrophy
(Sokolow and Lyon criteria: S(V1) + R(V5 or V6) > 35 mm; Framingham criteria: S(V1 or V2) + R(V5 or V6) > 35 mm)- Prolonged QT interval (QTc ~500)
- ST depression (up to 2-3 mm) predominantly in anterolateral leads (I,II, aVL and V3-V6)
- Widespread biphasic T waves
Review of this patient’s notes showed that a coronary angiogram 1 year previously has excluded coronary artery disease. However an echocardiogram was also performed at this time, the findings were consistent with severe hypertrophic obstructive cardiomyopathy (HOCM).
Emergency and critical care doctors need to look for the classic features of HOCM on the ECGs of patients presenting with syncope or arrhythmias. The ECG is abnormal in about 90% of HOCM cases and features include:
- non-specific findings such as increased QRS voltage, QRS widening, ST segment and T waves changes consistent with hypertrophy.
- deep narrow Q waves in the lateral leads (I, II, aVL, V5, V6) with high voltage QRS’s in a younger patient with syncope is considered a specific finding highly suggestive of HOCM (not present in this patient’s ECG).
Check out the free ‘EMRAPTV episode 65: Syncope‘ to hear Amal Mattu discussing the “not-to-miss” ECG findings in the patient presenting with syncope.
Q6. What does ST elevation in aVR mean?
Never forget to scrutinize aVR for ST elevation (STE) in a patient who may be having an acute coronary syndrome:
It is 95% specific for left main coronary artery (LMCA) occlusion when there is evidence of ischemia in other leads (typically widespread ST depression).
Patients with significant STE in aVR due to an acute coronary syndrome have a 70% chance of developing cardiogenic shock or dying – and medical treatment (including thrombolysis) does nothing to change this… They need to go to the cath lab STAT!
The post-treatment ECG shown above has features consistent with an LMCA occlusion, however:
- the patient had atrial fibrillation and structural heart disease (HOCM) which may account for the ECG findings.
- the patient had a recent ‘normal’ coronary angiogram and an ECG at that time (although sinus rhythm was present) had a similar pattern of ST segment changes.
Finally, here are some more scary things to know about acute coronary syndromes with ST elevation in aVR (these do not apply in the absence of evidence of ischemia in other leads, nor in the presence of supraventricular tachycardias):
- STE in aVR and aVL is highly specific for LMCA stenosis.
- STE in aVR and V1 is specific for proximal left anterior descending (LAD) or LMCA stenosis. If the STE in aVR is greater than the STE in V1 this indicates LMCA stenosis (81% sensitivity, 80% specificity, and 81% accuracy) rather than LAD stenosis.
- STE in aVR >1.5mm has ~75% mortality!
References
- Williamson K, Mattu A, Plautz CU, et al. Electrocardiographic applications of lead aVR. Am J Emerg Med 2006;24:864-874. PMID: 17098112.
About Chris Nickson
ECG-Bigeminal rythm one sinus complex and the next a PVC
PVCs R wave shows a R on T phenomenonPVCs in V1 show a RBBB pattern so they r of left ventricular origin
sinus QRS is suggestive of LVH.
the P-R INTERVAL and P wave mprphology of SINUS COMPLEXES IS NORMAL.
Good reminder of the Corey Slovis mantra “hypo-K = hypo-Mag” -- reminder to treat both if you’re treating low K, (and the Mg is the specific Rx for torsades/long QT). And don’t forget to speed the rate up in bradycardic patients going in/out of torsades (eg atropine,adrenaline, isporenaline, pacing), as the risk of torsades is higher if the rate is slow.