In this ECG Cases blog we look at the role of the ECG in pre-arrest, arrest and post-arrest care

Written by Jesse McLaren; Peer Reviewed and edited by Anton Helman, February, 2024

10 patients presented pre-arrest, arrest or post-arrest. What do their ECGs show and how does this help guide management?

Case 1. 60 year old with lethargy and shortness of breath. RR20, sat 86%, HR 90, BP 150/40

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Patient 2: 80yo with palpitations. R20 sat 93%, HR 50, BP 200/100

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Patient 3: 90 year old with generalized weakness, R 18 sat 94%, HR 70, BP 90/50

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Case 4: 45 year old with weight loss and progressive shortness of breath. HR 140 BP 110

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Case 5: 70 year old with 1 hour chest pain radiate to arms, with diaphoresis. R18 sat 99% HR 70 BP 130/80.

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Case 6: 40 year old with severe chest pain radiating to the back, hypotensive

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Case 7: 80 year old with 2 weeks SOB, then syncope. EMS found tachycardic and hypotensive then developed PEA arrest, achieved ROSC and taken directly to cath lab as inferior STEMI

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Case 8: 70 year old with witnessed collapse, GCS 3 with agonal respirations, then PEA arrest. ROSC with no regional wall motion abnormalities on POCUS

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Case 9: 75 year old with chest pain. Normal vitals at triage, then VF arrest. Post-ROSC ECG

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Case 10: 80 year old witnessed collapse, bystander CPR, VF defibrillated by EMS, arrived ROSC.

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ECG in cardiac arrest, pre-arrest and post arrest

ACLS simplifies ECG interpretation into rhythm analysis, dichotomized by shockable (VT/VF) vs non-shockable (asystole, PEA) with a list of reversible causes (‘Hs and Ts’). The STEMI paradigm simplifies ECG interpretation to ST segments, with emergent reperfusion dichotomized by the presence vs absence of ST elevation. While it’s important to rapidly identify shockable rhythms and acute coronary occlusion that meets STEMI criteria, there’s much more information provided by the 12-lead ECG beyond rate/rhythm and ST changes, which can guide cardiac arrest and peri-arrest care.

Pre-arrest ECG: empiric care to prevent arrest and guide resuscitation

The first role of the 12-lead ECG in peri-arrest care is identifying conditions that could lead to cardiac arrest, and guiding empiric treatment to prevent it. For example, the ECG can often identify patients with severe hyperkalemia at risk of arrest [1] and guide treated with empiric calcium, long QT can be treated with magnesium to prevent torsades, and acute coronary occlusion can be treated with reperfusion.

A pre-arrest 12-lead ECG can also be helpful if a patient’s condition deteriorates into cardiac arrest. This includes identifying ECG signs of acute coronary occlusion prior to VF arrest, or signs of PE prior to PEA arrest. While undifferentiated patients in cardiac arrest don’t benefit from thrombolytics [2], this doesn’t apply to patients with pre-arrest ECG or POCUS findings of acute coronary occlusion or PE. Similarly, a pre-arrest ECG for patients who develop PEA can help narrow the long list of reversible “Hs and Ts” and guide treatment.

Arrest ECG: ACLS vs pseudo-PEA

There’s no role for the full 12-lead ECG in cardiac arrest from VT/VF, asystole or true PEA: these patient need high quality CPR with as little interruption as possible, basic rhythm analysis to guide defibrillation for VT/VF, and identification of the underlying cause. There was a suggestion that PEA could theoretically be simplified into narrow-complex mechanical causes and wide-complex metabolic causes, which could guide resuscitation [3]. But a study of PEA patients found no association between rhythm analysis and cause of PEA [4]. This is not surprising considering the limited information provided by rhythm analysis. For example, hyperkalemia can cause narrow complex brady-asystole or wide complex tachycardia, and MI or PE can be narrow or wide complex (if complicated by bundle branch block).

There is much more information provided by the full 12-lead ECG, and this is where the identification of pseudo-PEA is important. This is a profound shock state with blood pressure so low that pulses aren’t palpable, but with organized cardiac activity and femoral/carotid pulsation on POCUS, and cardiac output detected by arterial line and end-tidal CO2. In pseudo-PEA the focus shifts from CPR to resuscitation of severe shock and identifying the underlying cause – including with 12-lead ECG and POCUS.

Post-arrest ECG: false positive STEMI and false negative STEMI

The post-arrest ECG can be difficult to interpret because of the impact of the ischemic and metabolic derangements of the arrest itself, regardless of the cause. For example, diffuse ST depression with reciprocal ST elevation in aVR is not a “STEMI equivalent” but a nonspecific sign of subendocardial ischemia which can be seen in any post-arrest state including from subarachnoid hemorrhage. [5] While serial ECGs reduce the rate of false positive STEMI [6], the first post-arrest ECG is still valuable especially when considering signs of Occlusion MI beyond STEMI criteria. [7] This includes massive ‘sharkfin’ ST elevation that can be mistaken for wide QRS. [8]

STEMI criteria misses a significant proportion of patients with acute coronary occlusion, and this is especially important to consider for if the pretest likelihood is high. A significant minority of post-arrest patients without STEMI criteria have acute coronary occlusion [9], especially those presenting with shockable rhythms [10]. While a couple of trials have suggested no benefit to immediate angiography for post-arrest patients without STEMI criteria, these included patients with non-shockable rhythms at lower likelihood of occlusion[11] or had exclusion criteria resulting in low prevalence of occlusion [12]. Like other NSTEMI trials, these excluded patients with refractory ischemia or electrical/hemodynamic instability, who require immediate angiography regardless of the ECG.

Back to the cases

Case 1. 60 year old with lethargy and shortness of breath. RR20, sat 86%, HR 90, BP 150/40. Pre-arrest hyperkalemia treated empirically with calcium

  • Heart rate/rhythm: extremely wide idioventricular rhythm with sine-wave pattern
  • Electrical conduction: no PR, very wide QRS, long QT
  • Axis: extreme
  • R-wave progression: delayed
  • Tall/small voltages: normal
  • ST/T changes: discordant ST/T

Impression: sine wave from pre-arrest hyperkalemia. Treated with empiric calcium and ECG repeated:

Regular wide complex tachycardia, wider than is typical for VT, consistent with VT + hyperkalemia. Treated with more calcium, insulin/dextrose and electrical cardioversion:

Sinus bradycardia with PAC, RBBB, left axis with LAFB. Potassium 7.9 Taken for emergent dialysis.

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Patient 2: 80yo with palpitations. R20 sat 93%, HR 50, BP 200/100. Very long QT at risk for polymorphic VT.

  • H: sinus bradycardia
  • E: normal PR/QRS, long QT vs QU
  • A: normal axis
  • R: normal R wave
  • T: normal voltages
  • S: down-up ST depression

Impression: Long QT vs QU, with bradycardia that increases the risk of torsades. This was not recognized and 2 hours later the patient became unresponsive:

polymorphic VT that spontaneously resolved, with long QT. Treated with magnesium. Follow up ECG

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Patient 3: 90 year old with generalized weakness, R 18 sat 94%, HR 70, BP 90/50. Severe hypokalemia at risk of electrical instability

  • H: normal sinus, with P waves fusing with U waves
  • E: long PR and long QU
  • A: normal axis
  • R: normal R wave
  • T: normal voltages
  • S: diffuse ST depression, flat T waves

Impression: diffuse ST depression with flat T waves and long QU, consistent with hypokalemia. Not initially recognized and patient developed palpitations:

PVCs with bigeminy. Potassium level returned at 1.6, and was replaced, with improvement

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Case 4: 45 year old with weight loss and progressive shortness of breath. HR 140 BP 110. Tamponade at risk of PEA arrest.

  • H: sinus tach (P waves upright in II, biphasic in V1)
  • E: normal conduction
  • A: normal axis
  • R: normal R wave progression
  • T: small voltages limb (all <5mm) and precordial (all <10mm) leads
  • S: nonspecific T wave changes

Impression: sinus tach and small voltages in patient with shortness of breath. POCUS confirmed large pericardial effusion with tamponde, and patient received pericardiocentesis. Patient also diagnosed with malignancy. Follow up ECG had normal voltages precordial leads:

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Case 5: 70 year old with 1 hour chest pain radiate to arms, with diaphoresis. R18 sat 99% HR 70 BP 130/80. LAD occlusion with electrical instability at risk for VF arrest

  • H: NSR with PVC in bigeminy
  • E: normal
  • A: normal
  • R: loss of R waves V2-3
  • T: normal voltages
  • S: hyperacute T waves anteroapical, with inferior reciprocal STD

Impression: STEMI(-)OMI proximal LAD occlusion with electrical instability. Shortly after the patient developed VF arrest, which was refractory to multiple defibrillation attempts. Because of pre-arrest chest pain and ECG hyperacute T waves the patient was given thrombolytics and achieved ROSC. Post-arrest ECG:

New RBBB and persisting lateral ST elevation. Cath lab activated: 80% mid LAD occlusion (partially reperfused after thrombolytics) with residual thrombus in the distal LAD. First trop 10 ng/L (normal) and peak 10,000, with antero-apical dyskinesis on echo. Patient was discharged with good neurological function, and ECG showing resolution of RBBB and reperfusion T wave inversion.

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Case 6: 40 year old with severe chest pain radiating to the back, hypotensive – from aortic dissection progressing to PEA arrest

  • H: NSR
  • E: normal
  • A: normal
  • R: normal
  • T: normal
  • S: diffuse primary ST depression with reciprocal ST elevation in aVR/V1

Impression: significant but nonspecific subendocardial ischemia, in 40 year old with severe chest pain radiating to the back. POCUS showed good LV function but possible aortic flap. Stat CT chest confirmed acute aortic dissection type A. Patient then developed PEA arrest without other reversible causes (including no pericardial effusion) and could not be resuscitated.

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Case 7: 80 year old with 2 weeks SOB, then syncope. EMS found tachycardic and hypotensive then developed PEA arrest, achieved ROSC and taken directly to cath lab as inferior STEMI – but diagnosed with massive PE

  • H: sinus tach, high lead placement chest leads (fully negative P wave in V1 and biphasic P wave in V2)
  • E: RBBB
  • A: normal axis
  • R: normal
  • T: low voltages limb leads
  • S: secondary STD/TWI in leads with RsR’

Impression: sinus tach and RBBB without signs of occlusion MI, in PEA arrest preceded by SOB. Cath lab found no acute coronary occlusion but a massive PE was diagnosed and treated with thrombectomy. Discharge ECG had resolution of RBBB:

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Case 8: 70 year old with witnessed collapse, GCS 3 with agonal respirations, then PEA arrest. ROSC with no regional wall motion abnormalities on POCUS – found to have massive SAH

  • H: NSR
  • E: normal conduction
  • A: right axis
  • R: normal R wave
  • T: normal voltages
  • S: inferolateral primary STD with reciprocal STE-aVR

Impression: PEA arrest with subendocardial ischemia on ECG and no regional wall motion abnormalities on POCUS. Cath lab activated but coronaries were normal, then diagnosed as massive SAH.

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Case 9: 75 year old with chest pain. Normal vitals at triage, then VF arrest. Post-ROSC ECG – LAD occlusion

  • H: wide complex tachycardia, with some of the width representing ST change
  • E: no PR, wide QRS/QT
  • A: left axis from LAFB
  • R: early R wave in V2
  • T: low voltages chest leads
  • S: massive anterolateral STE and inferior STD

Impression: wide complex tachycardia with features of anterolateral STE. Repeat ECG showed sinus rhythm and a clearer delineation between end of QRS and massive ‘sharkfin’ ST elevation

Cath lab activated: 100% prox LAD occlusion. First troponin 500 ng/L and peak 255,000. Follow up ECG showed narrow complex QRS with antero-lateral Q waves

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Case 10: 80 year old witnessed collapse, bystander CPR, VF defibrillated by EMS, arrived ROSC. Posterior Occlusion MI

  • H: atrial fibrillation
  • E: RBBB
  • A: right axis from LPFB
  • R: early R wave from RBBB
  • T: normal voltages
  • S: primary ST depression V3-4 and hyperacute T wave in V6

Impression: VF arrest with ECG sign of posterolateral occlusion MI. 15 lead ECG showed ongoing significant ST depression in V3 but falsely negative posterior leads

Stat cardiology consult led to cath lab activation: 100% circumflex occlusion, which was stented. Patient then re-arrested and could not be resuscitated.

Take home points for ECG interpretation in cardiac arrest

  • Pre-arrest ECG: identify high risk ECGs requiring empiric treatment – like calcium for hyperkalemia, magnesium for long QT, or reperfusion for Occlusion MI
  • Arrest ECG: follow ACLS guidelines for cardiac arrest, but identifying pseudo-PEA puts more focus on 12-lead ECG and POCUS to find the underlying cause
  • Post-arrest ECG: serial ECGs can reduce false positive STEMI, POCUS can help with the differential of diffuse ST depression with reciprocal ST elevation in aVR, and signs of Occlusion MI can identify those with false negative STEMI

* For interactive online and live ECG interpretation courses for medical students, residents, paramedics, and emergency physicians, visit heartsECGcourse.com

References for ECG Cases 48: ECG interpretation in cardiac arrest

  1. Durfey N, Lehnhof B, Bergeson A, et al. Severe hyperkalemia: can the electrocardiogram risk stratify for short-term adverse events? West J Emerg Med 2017 Aug;18(5):963-971
  2. Wang Y, Wang M, Ni Y, et al. Can systematic thrombolysis improve prognosis of cardiac arrest patients during cardiopulmonary resuscitation? A systematic review and meta-analysis. J Emerg Med 2019 Oc;57(4):478-487
  3. Littman L, Bustin DJ, Haley MW. A simplified and structured teaching tool for the evaluation and management of pulseless electrical activity. Med Princ Pract 2014;23(1):1-6
  4. Bergun D, Skjeflo GW, Nordseth T, et al. ECG patterns of early pulseless electrical activity – associations with aetiology and survival of in-hospital cardiac arrest. Resusc 2016 Jul:104:34-9
  5. Kim YJ, Min SY, Lee DH, et al. The role of the post-resuscitation electrocardiogram patients with ST-segment changes in the immediate post-cardiac arrest period. JACC Cardiovasc Interv 2017 Mar 13;10(5):451-459
  6. Baldi E, Schnaubelt S, Caputo ML, et al. Association of timing of electrocardiogram acquisition after return of spontaneous circulation with coronary angiography findings in patients with out-of-hospital cardiac arrest. JAMA Netw Open 2021 Jan 4;4(1):e2032875
  7. Sharma A, Miranda D, Rodin H, et al. Do not disregard the initial 12 lead ECG after out of hospital cardiac arrest: it predicts angiographic culprit despite metabolic abnormalities. Resusc Plus 2020 Oct 1:4:100032
  8. Escabi-Mendoza J, Diaz-Rodriguez PE, Silva-Cantillo RD. Shark fin occlusive myocardial infarction ECG pattern post-cardiac arrest misinterpreted as ventricular tachycardia. Cureus 2023 May;15(5):e38708
  9. Staer-Jensen H, Nakstad ER, Fossum E, et al. Post-resuscitation ECG for selection of patients for immediate coronary angiography in out-of-hospital cardiac arrest. Circ Cardiovasc Interv 2015 Oct;8(10):e002784
  10. Dumas F, Bougouin W, Geri G, et al. Emergency percutaneous coronary intervention in post-cardiac arrest patients without ST-segment elevation pattern: insights from the PROCAT II Registry. JACC Cardiovasc Interv 2016 May 23;9(10): 1011-8
  11. Lemkes JS, Janssens GN, van der Hoeven NW, et al. Coronary angiography after cardiac arrest without ST segment elevation. N Engl J Med 2019 Apr 11;380(15):1397-1407
  12. Desch S, Freund A, Akin I, et al. Angiography after out of hospital cardiac arrest without ST elevation. N Engl J Med 2021 Dec;385(27):2544-2553