ECG Cases 44 ECG Interpretation in Epigastric pain, Vomiting

Case 6: 35 year old with nausea and vomiting, glucose high. Old then new ECG

–

Case 7: 50 year old with vomiting and weakness

–

Case 8: 80 year old with epigastric pain and nausea

–

Case 9: 80 year old with epigastric pain

–

Case 10: 50 year old with epigastric pain

–

ECG interpretation in epigastric pain, vomiting

We might not think of the ECG as an initial test for patients presenting with epigastric pain, nausea and vomiting. But ECG interpretation is crucial for identifying cardiac and metabolic emergencies presenting with gastrointestinal symptoms, and to differentiate them from GI emergencies with secondary or incidental ECG findings.

1. Cardiovascular emergencies

Epigastric pain, nausea and vomiting can be anginal equivalents, like shortness of breath.[1,2] A lower index of suspicion and lack of STEMI criteria can lead to providers missing Occlusion MI (OMI), including subtle occlusions or those in the presence of LBBB or RBBB. Patients may also have delayed presentations, with subacute occlusions that have developed Q waves and T wave inversion.

Severe epigastric pain and vomiting can also be symptoms of rarer conditions like aortic dissection – but ECGs diagnostic of STEMI or OMI are highly unlikely to be secondary to aortic dissection.

2. Metabolic emergencies

Vomiting can also be associated with electrolyte emergencies, including both high and low potassium levels resulting in ECG changes. Hyperkalemia often presents with vomiting[3], and the ECG is crucial for the early diagnosis and treatment of severe cases.[4] In this situation it’s important to differentiate the peaked T waves of hyperkalemia (narrow, sharp peak, look pinched) from the hyperacute T waves of OMI (wide based, broad, look inflated); or the ST elevation of hyperkalemia-induced Brugada phenocopy from the ST elevation of OMI.

Conversely, vomiting can lead to severe hypokalemia which is often undertreated despite ECG changes.[5,6] ECG signs include ST depression, which can be differentiated from other causes of ST depression by its diffuse distribution and association with flat/inverted T waves, prominent U waves, and QT prolongation from associated hypomagnesemia.

3. GI emergencies

On the other hand, GI emergencies can present with secondary or incidental ECG changes that might be mistaken for cardiac emergencies. Diffuse ST depression with reciprocal ST elevation in aVR is a nonspecific sign of subendocardial ischemia that can be seen in GI emergencies including massive upper GI bleeds.

There are many case reports of patients with GI emergencies and ST elevation.[7] Some of these are true mimics (or GI emergencies complicated by coronary spasm, takosubo, or type 2 MI), but others reflect the limits of STEMI criteria and the importance of more advanced ECG interpretation. For example, a case report of pancreatitis mimicking “inferior STEMI” shows no reciprocal changes in aVL (making inferior OMI highly unlikely), and likely lead reversal.[8]

Back to the cases for ECG interpretation in epigastric pain, vomiting

Case 1: 70 year old with epigastric pain and vomiting, from STEMI(-) LAD occlusion, which was rapidly diagnosed

• Heart rate/rhythm: normal sinus rhythm
• Electrical conduction: normal conduction
• Axis: normal axis
• R-wave progression: small Q waves V2-3
• Tall/small voltages: normal voltages
• ST/T: anterior hyperacute T waves, mild ST elevation aVL with reciprocal inferior ST depression

Impression: proximal LAD occlusion. Cath lab activated: 100% proximal LAD occlusion, anterolateral hypokinesis, first troponion 45,000 ng/L (normal <26 in males and <16 in females) and peak 105,000. Discharge ECG showed anterolateral Q waves and reperfusion T wave inversion:

–

Case 2: 70 year old with epigastric pain and diaphoresis, from STEMI(-) RCA occlusion, which was rapidly diagnosed

• H: normal sinus rhythm
• E: normal conduction
• A: physiologic left axis
• R: borderline delayed R wave progression
• T: normal voltages
• S: Q wave in III, mild inferior convex ST elevation and hyperacute T waves with reciprocal change in aVL, and mild anterior ST depression

Impression: inferoposterior OMI. Cath lab activated: 100% RCA occlusion, inferolateral hypokinesis, first troponin 13,000 and peak 74,000 ng/L. Discharge ECG showed infero-postero-lateral reperfusion T wave inversion:

–

Case 3: 90 year old, no cardiac history, with two days of epigastric pain, from subacute LAD occlusion, with delayed presentation and delayed diagnosis

• H: junctional bradycardia with artifact, vs AF with complete heart block
• E: RBBB
• A: left axis from inferior Q waves
• R: early R wave from RBBB, delayed S wave
• T: normal voltages
• S: anterior Q wave, concordant convex ST elevation and T wave inversion

Impression: subacute LAD occlusion. Patient initially diagnosed as gastritis until troponin returned at 170,000 ng/L, then referred to cardiology as non-STEMI. Admitted as late STEMI. Cath lab: LAD occluded by 90% proximally and 100% mid vessel, peak trop 260,000, and echo showing antero/apical/inferior akinesis with EF of 25%. Then developed bradycardia in the 30s. Discharge ECG ventricular pacing with appropriate discordance:

–

Case 4: 50 year old with 4 days of chest/epigastric pain and vomiting, from RCA occlusion, with delayed presentation and delayed diagnosis

• H: sinus bradycardia
• E: LBBB
• A: normal axis
• R: normal R wave progression
• T: normal voltages
• S: concordant ST depression V2-3

Impression: bradycardia and anterior ST depression from posterior Occlusion MI. Referred to cardiology as “non-STEMI” with troponin 8,000 ng/L. Cath lab activated: 100% RCA occlusion, peak troponin 10,000 ng/L. Discharge ECG had normalization of anterior ST segments:

–

Case 5: 80 year old with two days of epigastric pain, BP differential without pulse deficit, from RCA occlusion with delayed reperfusion because of CT scan

• H: normal sinus rhythm
• E: normal conduction
• A: normal axis
• R: new early R wave progression with R>S in V2
• T: normal voltages
• S: new STE in III/aVF with Q in III, reciprocal STD in I/aVL and STD in V2-3

Impression: infero-posterior OMI. CT chest done because of BP difference: no dissection. Cath lab activation, with prolonged ECG-to-Activation time: 99% RCA occlusion. First trop 250 and peak 14,000 ng/L. Discharge ECG had inferior Q wave and reperfusion T wave inversion: