In this ECG Cases blog we review 8 cases of patients with prehospital ECGs. Can you avoid the pitfalls and spot the pearls that help to make the diagnosis?

Written by Jesse McLaren; Peer Reviewed and edited by Anton Helman. June 2022

8 patients presented with acute symptoms, with prehospital ECGs and interpretations. Were they correct, and what were the diagnoses?

Case 1: 60 year old with chest pain, STEMI positive with paramedics

Case 2: 70 year old with one hour of chest pain, STEMI positive with paramedics

Case 3. 55 year old with diabetes, presenting with shortness of breath and sugar reading ‘high’, treated by paramedics with calcium, then ECG repeated in ED

Case 4: 75 year old short of breath, presyncope and brief confusion, atrial fibrillation reported by paramedics, then ECG repeated in ED

Case 5: 60 year old with 6 hours of chest pain and nausea, STEMI negative on serial prehospital ECGs then ECG repeated in ED

Case 6: 55 year old with one hour of chest pain, STEMI positive with paramedics then ECG repeated in ED

Case 7: 80 year old with 2 hours of chest pain, STEMI positive with paramedics then ECG repeated in ED

Case 8: 60yo with chest pain, STEMI positive with paramedics but cancelled by cardiology, ECG repeated in ED

Prehospital ECGs

Paramedics play a crucial role in the early diagnosis and treatment of acute coronary occlusion, arrhythmias and other emergencies based on ECG. Prehospital ECGs are associated with reduced reperfusion time and reduced mortality [1], and ECG education of paramedics is associated with greater use of STEMI bypass [2]. Some paramedics have developed advanced ECG interpretation (see, and a recent study has tested the feasibility of paramedic point of care troponin and echo [3].

Serial prehospital ECGs improve identification of STEMI[4], and can be combined with emergency department ECGs to detect serial changes—including early changes of Occlusion MI which are more obvious on subsequent ED ECGs, or transient STEMIs which are more obvious on initial prehospital ECGs.

As with any transfer of patients between health providers, paramedic ECG acquisition and interpretation should be reassessed in the emergency department. There’s significant variation in the placement of prehospital precordial leads [5], especially V1-3, which can result in lead misplacement errors. Paramedics have higher rates than cardiologists of false cath lab activation [6], and it is challenging to interpret EMS ECGs that truncate the QRS amplitude and make it difficult to judge proportional ST changes (which is crucial for diagnosing acute coronary occlusion in the presence of LVH or LBBB).

While the problem of false positive STEMI (ie. ECG meets STEMI criteria but patient does not have acute coronary occlusion) is widely known, the opposite problem of false negative STEMI (ie ECG does not meet STEMI criteria but patient does have acute coronary occlusion) is not. In fact, the STEMI paradigm rules out this possibility, because such patients are diagnosed as “non-STEMI” even if they have a totally occluded coronary artery (and resulting higher mortality). For example, a study of “inappropriate cath lab activations” (defined as those activated by paramedics or emergency physicians and cancelled by cardiology) found that 6.5% required emergent reperfusion for acute coronary occlusion but all were diagnosed as “non-STEMI” [7]. But these are more appropriately termed false negative STEMI, or STEMI(-) Occlusion MI, with false cath lab cancellation.

So prehospital ECGs showing “STEMI” should be reassessed for the possibility of false positive STEMI to avoid false cath lab activation; prehospital ECGs which are “STEMI negative” should be reassessed for the possibility of STEMI(-) OMI to avoid delayed cath lab activation; and prehospital cases with cath lab cancellation by cardiology should be reassessed for the possibility of false cath lab cancellation.

Back to the cases

Case 1: false positive ST elevation from truncated EMS ECG

  • Heart rate/rhythm: sinus, borderline tach
  • Electrical conduction: LBBB
  • Axis: left in context of LBBB
  • R wave progression: delayed in context of LBBB
  • Tall/small voltages: voltages cut off by EMS ECG
  • ST/T changes: discordant ST changes, can’t tell proportionality due to voltages being cutoff

Impression: LBBB with discordant ST changes but can’t assess proportionality because voltages cut off

Patient was taken as code STEMI because of anterior ST elevation. But when a full 12-lead ECG was done this ST elevation is proportional to large voltages, and cath was negative

Case 2: STEMI(-)OMI diagnosed by paramedics

  • H: normal sinus rhythm
  • E: normal conduction
  • A: normal axis
  • R: loss of R wave in V2 and small Q in V3
  • T: normal voltages
  • S: upgoing ST depression rising into hyperacute T wave in V2-3 (deWinter T wave) and hyperacute T wave in V4, hyperacute T wave in I/aVL with reciprocal inferior ST depression. (note height of hyperacute T wave in V2 is truncated)

Impression: proximal LAD occlusion

Patient taken directly to cath lab, where repeat ECG showed evolving Q in V3 and anterior ST elevation now ECG meeting STEMI criteria. Cath: 100% proximal LAD occlusion, first trop I was 1,000 ng/L and peak was 35,000.

Case 3. hyperkalemia diagnosed and treatment initiated by paramedics

  • H: EMS ECG regular wide complex tachy without visible P waves, ED ECG sinus tachy
  • E: first degree AV block appeared on ED ECG, LBBB morphology
  • A: from left axis to borderline left axis
  • R: delayed R wave progression
  • T: voltages cutoff on EMS ECG, normal on ED ECG
  • S: peaked T waves

Impression: wide complex tachycardia with peaked T waves, with appearance of P waves and normalizing axis after initiation of calcium, diagnostic of hyperkalemia

After more calcium and insulin the first degree AV block and LBBB resolved and the axis normalized. Initial potassium was 6.8.

Case 4: AF misdiagnosed by paramedics, and diagnostic momentum in ED

  • H: sinus rhythm with premature atrial contraction in both EMS and ED ECG
  • E: normal conduction
  • A: normal axis
  • R: normal R wave
  • T: low voltages limb leads
  • S: no ST/T changes

Impression: sinus rhythm and PAC misdiagnosed as AF, which led to a presumptive diagnosis of TIA as an explanation for shortness of breath, presyncope and transient confusion. In Stroke Clinic a CTA of the head/neck found bilateral upper lobe PE.

Case 5: dynamic STEMI(-)OMI visible on serial prehospital ECGs

  • H: normal sinus rhythm
  • E: normal conduction
  • A: normal axis
  • R: normal R wave
  • T: normal voltages
  • S: prehospital ECGs show dynamic inferior/lateral hyperacute T wave and reciprocal change in aVL, which persist on ED ECG; V1-2 are too high on prehospital ECG (inverted P wave in V2), and not corrected on ED ECG

Impression: inferior/lateral STEMI(-)OMI and high V1-2 placement. Cath lab activated: 100% circumflex occlusion, first trop negative and peak 50,000. Discharge ECG had inferior Q wave and reperfusion T wave inversion, and normalization of lateral T waves; V1-2 are now correctly placed

Case 6: LAD occlusion migrating from mid to distal vessel with evolving ECG changes

  • H: sinus tach
  • E: normal conduction
  • A: normal axis
  • R: delayed R wave progression
  • T: normal voltages
  • S: antero-inferior ST elevation and hyperacute T waves, with ST elevation more obvious in anterior leads on prehospital ECG and inferior leads on ED ECG

Impression: antero-inferior STEMI(+)OMI

Cath lab activated: 100% distal LAD occlusion, with haziness in mid LAD from site of prior occlusion. First trop 500 and peak 5,000. Discharge ECG had anterior reperfusion T wave inversion.

Case 7: STEMI(+)OMI on prehospital ECG and STEMI(-)OMI on ED ECG

  • H: sinus bradycardia
  • E: normal conduction
  • A: normal axis
  • R: normal R wave
  • T: normal voltages
  • S: inferior hyperacute T waves with reciprocal change in aVL and ST Depression in V2, with inferior ST elevation on EMS ECG that resolved with ED ECG

Impression: transient STEMI with persisting OMI.

Repeat ECG: STEMI(+)OMI again, now also in lateral leads

Cath lab activated: 100% proximal RCA occlusion, first trop 6 and peak 50,000. Dicharge ECG had infero-lateral reperfusion T wave inversion:

Case 8: LAD occlusion diagnosed by paramedics, false cancellation by cardiology

  • H: normal sinus rhythm
  • E: normal conduction
  • A: normal axis
  • R: normal R wave
  • T: normal voltages
  • S: prehospital ECG had anterior ST elevation and hyperacute T waves with reciprocal ST depression inferiorly and in V6. ED ECG had resolution of ST elevation but ongoing hyperacute T waves and reciprocal change.

Impression: proximal LAD occlusion. ECG labeled as early repolarization by cardiology and cath lab cancelled. Patient had ongoing chest pain, first troponin 280, anterior regional wall motion abnormality on bedside echo, and a repeat ECG showing a run of VT

Cath lab activated: 100% LAD occlusion, peak troponin 100,000 but diagnosed as “NSTEMI”. Discharge ECG had loss of anterior R waves and reperfusion T wave inversion.

Take home points for Prehospital ECG Pearls and Pitfalls

  1. Scrutinize prehospital ECGs: they provide valuable information including dynamic ischemic changes and early evidence of Occlusion MI or transient STEMI, as well as dysrhythmias and metabolic emergencies
  2. Prehospital ECGs can have truncated voltages, making it difficult to determine proportional ST changes
  3. Every transition of care requires a reassessment of ECG acquisition and interpretation, to avoid diagnostic momentum
  4. EDs should reassess prehospital “STEMIs” for the possibility of false positive STEMI, and “STEMI negative” ECGs (including cath lab cancellations) for the possibility of STEMI(-) Occlusion MI

References for ECG Cases 32 Prehospital ECG Pearls and Pitfalls

  1. Ducas RA, Labos C, Allen D, et al. Association of pre-hospital ECG administration with clinical outcomes in ST-segment myocardial infarction: a systematic review and meta-analysis. Can J of Cardiol 2016;32:1531-1541
  2. Mahadevan K, Sharma D, Walker C, et al. Impact of paramedic education on door-to-balloon times and appropriate use of the primary PCI pathway in ST-elevation myocardial infarction. BMJ Open 2022 Feb 24;12(2):e046231
  3. Jacobsen L, Grenne B, Olsen RB, et al. Feasibility of prehospital identification of non-ST-elevation myocardial infarction by ECG, troponin and echocardiography. Emerg Med J 2022 Jan 21;emermed-2021-211179
  4. Verbeek PR, Ryan D, Turner L, et al. Serial prehospital 12-lead electrocardiograms increase identification of ST-segment elevation myocardial infarction. Prehosp Emerg Care 2012 Jan-Mar;16(1):109-14
  5. Gregory P, Kilner T, Lodge S, et al. Accuracy of ECG chest electrode placements by paramedics: an observational study. Br Paramed J 2021 May 1;6(1):8-14
  6. Huitema AA, Zhu T, Alemayehu M, et al. Diagnostic accuracy of ST-segment elevation myocardial infarction by various healthcare providers. Int J Cardiol 2014 Dec 20;177(3):825-9
  7. Shamim S, McCrary J, Wayne L, et al. Electrocardiographic findings resulting in inappropriate cardiac catheterization laboratory activation for ST-segment elevation myocardial infarction. Cardiovasc Diagn Ther 2014 June;4(3):215-223