ECG of the Week – 22nd May 2017 – Interpretation

The following ECG is from a 67yr old male who presented with a 36 hour history of central chest pain and diaphoresis. He has a history of CABG. 

Click to enlarge


  • Ventricular rate 36 bpm
  • Atrial rate ~ 60 bpm
  • Regular ventricular and atrial rhythms
  • Complete heart block
  • Normal
  • PR - AV dissociation with no relation between P and QRS
  • QRS - Normal
  • ST Elevation leads II (1mm), III and aVF (3mm) V5-6 (1mm)<1mm avf="" font="" iii="" mm="" v5-6="">
  • ST Depression leads V2 - flat morphology
  • ST Depression leads I, aVF

  • Infero-lateral STEMI
    • Likely posterior extension
    • Complete heart block
    • Ventricular bradycardia with narrow complex escape rhythm
What happened ?

The patient was taken for urgent angiography which showed:
  • LMCA: 80% Stenosis
  • LAD: Patent LIMA (left internal mammary artery) and SVG (saphenous vein graft)
  • Cx: Patent SVG
  • RCA: Subacute thrombotic occlusion with severe ostial and proximal vessel stenosis.
The RCA lesion was stented but the patient's recovery was complicated by repeated PEA, VT and VF cardiac arrests necessitating placement of an Intra-Aortic Balloon Pump (IABP).

A bit on IABPs

Check out the following LitFL pages for a nice overview of IABPs:

A bit on CABG anatomy and techniques

This is outside of the scope of this blog but I found the following links useful refreshers on CABG techniques and post CABG angiography / intervention:

References / Further Reading

Life in the Fast Lane

  • Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P. ECG in Emergency Medicine and Acute Care. Elsevier Mosby 2005.

Homer’s Hepatic Board Review – Hepatic Encephalopathy

By Surriya Ahmad and Kylie Birnbaum


It’s a busy night in the Springfield ED. You’ve just treated Lisa for a pneumothorax after she played her sax too hard, and you’ve treated her brother Bart for a laceration from skating too hard. You also treated Mr. Burns for narcissistic personality disorder! Oh, is that untreatable? Just as you are about to go out to the Kwik-e-Mart for some snacks and time with Apu, you get called to see an altered patient.

Homer, a 45 year-old man with alcohol abuse and a donut fetish, lies before you confused and very jaundiced (you start to realize that all of your patients this evening have been quite yellow, actually). His wife called EMS for his acting strange for a few days, ever since they visited Kansas where Homer ate a lot of BBQ and drank some Duff beer. He is delirious and unable to answer your questions appropriately. Upon chart review, you discover Dr. Grock has treated him before.


Vitals: BP 106/70, HR 98, RR 26, rectal temp 99.0, FS 105

You notice lethargy, scleral icterus, a distended abdomen, and gynecomastia.


We can tell Mr. Simpson has the history and stigmata to suggest liver failure. What is your differential?
  • Intracranial hemorrhage (subdural hematomas are more common given the associated coagulopathy)
  • Alcohol intoxication or withdrawal
  • Sepsis
  • Spontaneous bacterial peritonitis
  • Anemia / GI bleed
  • Nutritional encephalopathy (Wernicke-Korsakoff Syndrome)
  • Uremia / Renal failure
  • Hepatic encephalopathy


While your incredible nurse is getting the IV, O2, monitor, and labs, what other exam finding do you want to assess for?

Asterixis. Sure, we all know to have Mr. Simpson hold out his arms extended at the wrists and notice his hands flap. To be really slick, you can have Homer stick out his tongue and you will notice it move back and forth when extended (doesn’t count if he is imagining a donut).


You really want to nail the diagnosis of hepatic encephalopathy. How do you diagnose it?

Trick question! Hepatic encephalopathy is a diagnosis of exclusion, and can often be caused by those other problems on your differential. It occurs from nitrogenous waste build up, which can be precipitated by:

  • Large, protein-laden meals (Kansas City BBQ, anyone?)
  • Occult GI bleed
  • Transjugular intrahepatic portosystemic shunt (TIPS)
  • Opioid or benzodiazepine accumulation (in the setting of impaired metabolism)


The symptoms of hepatic encephalopathy lie on a spectrum from fatigue to coma. The increased ammonia in blood can also contribute to cerebral edema and increased intracranial pressure, therefore exacerbating symptoms.

Patients will often have elevated serum ammonia levels, but the severity of encephalopathy and altered mental status does not reliably correlate with ammonia levels. It is imperative you consider the differential diagnoses in entirety and treat the inciting cause.


What is your ED management?

First: stabilization! These patients often require critical care and can decompensate quickly. Have a low threshold for intubation.

Treatment involves removal of nitrogenous waste and suppression of intestinal bacterial that produce this waste.

Lactulose is the main treatment and your board answer. It becomes lactic acid in the colon, making the colon acidic and trapping the ammonia for excretion. It can be given PO or PR. Why don’t we ask Mr. Simpson which he would prefer? Although lactulose has been the standard treatment for hepatic encephalopathy, the HELP trial suggests that polyethylene glycol may lead to more rapid hepatic encephalopathy resolution than standard therapy.[2]


What is your dispo? Can you ever send home patients with hepatic encephalopathy?

You may assess severity and trend AMS changes with the West Haven Criteria, but ultimately use your clinical judgment.

  • Grade I: Apathy, change in behavior without change consciousness
  • Grade II: Lethargy, drowsiness, asterixis, disorientation
  • Grade III: Marked confusion, incoherent speech, hyperreflexia
  • Grade IV: Comatose, unresponsive to pain, decorticate or decerebrate posturing

Generally, Grade 1 and 2 may be able to go home in the absence of other co-morbidities and after consultation with the patient’s gastroenterologist.

Grades 3 and 4 should be admitted. Consider consultation with the ICU.


Bonus Question! What is the name of Lisa Simpson's sax-y mentor, and what disease does he obviously have?

Bleeding Gums Murphy. He has scurvy! Or just bad gingivitis…. Get that man some oranges and a toothbrush.



[1] O’Mara SR, Gebreyes K. Hepatic Disorders. In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e New York, NY: McGraw-Hill; 2016.

[2] Rahimi R et al. Lactulose vs Polyethylene Glycol 3350-Electrolyte Solution for Treatment of Overt Hepatic Encephalopathy: The HELP Randomized Clinical Trial. JAMA Intern Med. 2014;174(11):1727-1733. doi:10.1001/jamainternmed.2014.4746

The post Homer’s Hepatic Board Review – Hepatic Encephalopathy appeared first on The Original Kings of County.

EM Nerd-The Case of the Tardy Delegate

We have discussed the dangers of surrogate outcomes at length, but none are more evident to an Emergency Physician than the time-based metrics we are subjected to on a daily basis. The latest of these temporal surrogates forced upon us is the 3-hour bundle of care in patients presenting to the Emergency Department with symptoms […]

EMCrit by Rory Spiegel.