Rhythm Nation returns with another ECG from University Hospital of Brooklyn at SUNY Downstate Medical Center.

 

Case: 52-year-old man with past history of of Hypertension, Diabetes mellitus, and Hyperlipidemia who presented with chest pain.

 

HPI: The patient’s chest pain started two days ago, has been intermittent, and is present upon arrival in the Emergency Department. The pain is described as pressure, located substernally, and radiates to the left chest. At onset, the pain was severe but has been improving since the patient arrived. His symptoms are exacerbated by exertion and relieved by rest. He has experienced prior episodes, but they were shorter in duration, and the pain was less intense. He denies nausea, vomiting, shortness of breath, diaphoresis, abdominal pains, or history of trauma.

While in the ED, the patient has a second episode of chest pain, associated with nausea, vomiting, and diaphoresis.

ROS: No fever, chills, syncope, headache, sore throat, blurred vision, bloody or black stools, dysuria, rash, joint pains, lower extremity edema, or lymphadenopathy.

PMHx: As in HPI

SH: Denies Alcohol, Tobacco, and Illicit Drug Use.

 

Physical Exam:

Vital Signs: 98.2°F, 102/81 mm Hg, 90 bpm, 18 resp, 99% on RA.

General: Well Developed Male, Appears Stated Age, NAD

Eyes: PERRLA, EOMI, Normal Conjunctiva

Neck: Supple, No JVD

CVS: RRR, S1S2; No Murmurs, Rubs, or Gallops

Resp: CTA, No Wheezes, Rales, or Rhonchi, No Tenderness

Abd: Soft, NTND, No Guarding or Rebound

Back: Normal Inspection, No CVA Tenderness

Skin: No Rashes, Warm, Well Perfused

Ext: Normal ROM, No Calf Tenderness, No LE Edema

Neuro: AAOx3, CN II-XII Intact, Strength 5/5, Sensations Intact to Light Touch, No Dysmetria or Dysdiadochokinesia, Normal Gait

 

As the strong emergency physician that you are, you create a differential diagnosis of concerning cardiopulmonary, GI, and musculoskeletal pathology. With your differential in mind you order tests with the following results:

 

Labs:

CBC: 8.45>12.8/38.9<236

BMP: 139/4.3/109/23/18/1.03<280

PT/PTT/INR: 11.2/26.9/0.9

Trop I: 0.12 (Ref: <=0.15)

 

CXR: “Impression: No evidence of acute pleural or parenchymal pathology.”

 

ECG:

 

This is Rhythm Nation after all, and the money is likely within the above ECG. To help crystalize your diagnosis, test your knowledge with the following questions.

 

Questions:

  • What ECG finding can be identified, and what is its pathophysiologic basis?
  • What are the next steps in the treatment of this patient?
  • What testing would be contraindicated given this presentation?
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bmweissman

Combined EM/IM PGY-1 resident at SUNY Downstate/Kings County Medical Center. Graduate of St. George's University School of Medicine, Grenada. Alumni of Dickinson College, '08. Recent transplant from Los Angeles, but hoping to slowly develop into a true New Yorker over the next 5 years.

Latest posts by bmweissman (see all)


bmweissman

Combined EM/IM PGY-1 resident at SUNY Downstate/Kings County Medical Center. Graduate of St. George’s University School of Medicine, Grenada. Alumni of Dickinson College, ’08. Recent transplant from Los Angeles, but hoping to slowly develop into a true New Yorker over the next 5 years.

1 Comment

Kylie Birnbaum · November 16, 2017 at 4:45 pm

Looks like Wellen’s Syndrome to me. Type A – biphasic T waves starting positive and ending negative in precordial leads with some ST elevation in the precordial leads (V2-3). Although pain free now, he had recent angina and normal troponin.

The pathophys I’m just gonna steal this explanation from Life in the Fast Lane:

The following sequence of events is thought to occur in patients with Wellens’ syndrome:
1. A sudden occlusion of the LAD, causing a transient anterior STEMI. The patient has chest pain & diaphoresis. This stage may not be successfully captured on an ECG recording.
2. Re-perfusion of the LAD (e.g. due to spontaneous clot lysis or prehospital aspirin). The chest pain resolves. ST elevation improves and T waves become biphasic or inverted. The T wave morphology is identical to patients who reperfuse after a successful PCI.
3. If the artery remains open, the T waves evolve over time from biphasic to deeply inverted.
4. The coronary perfusion is unstable, however, and the LAD can re-occlude at any time. If this happens, the first sign on the ECG is an apparent normalisation of the T waves — so-called “pseudo-normalisation”. The T waves switch from biphasic/inverted to upright and prominent. This is a sign of hyperacute STEMI and is usually accompanied by recurrence of chest pain, although the ECG changes can precede the symptoms.
5. If the artery remains occluded, the patient now develops an evolving anterior STEMI.
6. Alternatively, a “stuttering” pattern may develop, with intermittent reperfusion and re-occlusion. This would manifest as alternating ECGs demonstrating Wellens’ and pseudonormalisation/STEMI patterns.

https://lifeinthefastlane.com/ecg-library/wellens-syndrome/

This patient should go for cath and PCI given an imminent LAD stenosis and STEMI that may happen in the next hours to days. Get him on a monitor, give him aspirin and plavix and call cardiology! Do not stress test him as it can awaken the beast and precipitate the MI.

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