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EKG Contributor: Massoud Kazzi, MD
Resident Author: Jennifer Rabjohns, MD
Faculty Mentor: Massoud Kazzi, MD
Date of Presentation: 7/1/19

60yoF presents with syncope.

EKG is below:

As noted in the previous post, this patient had digoxin toxicity. From that post, Take-home points for digoxin toxicity (part 1):

  • Toxicity can be acute or chronic. Look for presents GI symptoms, altered mental status, and visual changes (e.g., yellow halos).
  • Antibiotics, calcium channel blockers, beta-blockers, amiodarone, and spironolactone decrease digoxin protein binding -> higher digoxin levels.
  • Hypokalemia enhances effects of digoxin on myocardium.
  • The elevated intracellular calcium in toxicity raises the resting membrane potential in the myocardium -> higher risk of spontaneous dysrhythmias.

EKG Findings with Digoxin
This patient doesn't have it, but the digitalis effect doesn't relate necessarily to toxicity. It's prolonged PR and scooping ST segments in lateral precordial leads. Below is an example from Goldfrank's (1):

The ST segments are described as like Salvador Dali's mustache (2).

Digoxin can cause a variety of EKG changes, though. These range from extra beats to tachydysrhythmias to varying AV blocks.

Besides the reasons mentioned in the earlier post and the reasons above, one of the reasons for such varying presentations is digoxin can increase parasympathetic (vagal) or sympathetic tone.

You can also see U waves caused by excess Ca 2+ being spontaneously released from cells.

Bidirectional ventricular tachycardia is "nearly pathognomonic" for digoxin toxicity per Goldfrank's.

These are from Goldfrank's. ABC's first, of course.

Early and delayed activated charcoal could be helpful to reduce enterohepatic circulation (1g/kg q2-4h, max of 4 doses).

Hyperkalemia is poor prognostic indicator; in one study, 50% of patients with K of 5-5.5 died. But treating hyperkalemia doesn't improve survival.

Digoxin levels don't necessarily correlate with toxicity. However, consider Digifab if:

Digifab dosing varies depending on acute or chronic poisoning. Most relevant for us is empiric dosing. Expect a clinically unimportant increase in total digoxin serum levels after Digifab due to binding to digoxin in tissues and then going into the plasma. Also expect potassium to go down.

If you *don't* have digifab, phenytoin may reverse digoxin-induced AV blocks and suppress digoxin-induced tachydysrhythmias. Options for phenytoin dosing are:

  • Start phenytoin at 50mg/min drip or
  • 100mg q5 min until dysrhythmia is controlled or
  • total of 1000mg adult dose (15-20mg/kg in pediatric total dose).

Lidocaine is another option. By this point, you should be, of course, talking with your pharmacist.

Careful with pacing, it can induce dysrhythmias. But you would not be faulted for following ACLS for unstable VT or VF.

Dialysis isn't helpful for removal because so much plasma digoxin is protein-bound and the majority (90%) is in tissues anyway.

Goldfrank's dodges the calcium-stoneheart controversy. In a retrospective review published in JEM in 2011, of 23 patients with digoxin toxicity who received calcium, none had life-threatening dysrhythmias within 4 hours of receiving calcium (3). But the jury is still out.

Take-home points for digoxin toxicity (part 2):

  • EKG's can vary, but look for brady or tachydysrhythmias (including bidirectional ventricular tachycardia), AV blocks.
  • K is important - hypoK can enhance digoxin effect, K of 5-5.5 is a poor prognostic indicator.
  • ABC's, of course.
  • Consider early and delayed activated charcoal.
  • Work with your pharmacist for Digifab.
  • Phenytoin and lidocaine are options if you don't have Digifab.

1. Hack, J. B., & Lewin, N. A. (2006). Goldfrank's Toxicologic Emergencies(Vol. 8). New York, NY: McGraw-Hill. Retrieved June 26, 2019, from Ch 62: Cardioactive Steroids

2. Burns, E. (2019, March 16). Digoxin Effect • LITFL Medical Blog • ECG Library Toxicology. Retrieved June 26, 2019, from

3. Levine, M., Nikkanen, H., & Pallin, D. J. (2011). The Effects of Intravenous Calcium in Patients with Digoxin Toxicity. The Journal of Emergency Medicine,40(1), 41-46. doi:10.1016/j.jemermed.2008.09.027

EKG Contributor: Massoud Kazzi, MD
Resident Author: Jennifer Rabjohns, MD
Faculty Mentor: Massoud Kazzi, MD
Date of Presentation: 6/30/19

60yoF presents with syncope.

EKG is below:

How would you describe this EKG?
Narrow complex bradycardia without P waves. Rate is in the 20s, don't see P waves, but normal intervals. Peaked T's in the leads with tall R waves (V4-V6). No A-V blocks.

What is the differential diagnosis?
NEJM has a nice review article on bradycardia here. The list of causes is pretty long... (1).

On getting further history, this patient had a digoxin overdose.

Digoxin is a cardioactive steroid from the foxglove plant (2, 3).

Onset of action for oral digoxin is 1.5-6 hours; for intravenous, it's 5-30 minutes. It's cleared mostly renally, with some hepatic clearance.

Toxicity can be acute or chronic, and presents with gastrointestinal symptoms, altered mental status, the visual changes we've all seen on test questions (e.g., yellow halos around lights), and EKG changes (we'll review some below).

Antibiotics (especially macrolides), quinidine, verapamil, diltiazem, carvedilol, amiodarone, and spironolactone can all cause decreased digoxin protein binding to elevate digoxin levels up to two-fold.

Hypokalemia enhances the effects of digoxin on the myocardium, possibly because digoxin doesn't have to compete with as much potassium - remember the mechanism of action here (2):

Digoxin causes increased intracellular Na -> increased intracellular Ca 2+ -> ionotropy.

In toxicity, that high intracellular Ca 2+ -> higher resting membrane potential -> possible dysrhythmias and arrest.

Take-home points for digoxin toxicity (part 1):

  • Toxicity can be acute or chronic. Look for presents GI symptoms, altered mental status, and visual changes (e.g., yellow halos).
  • Antibiotics, calcium channel blockers, beta-blockers, amiodarone, and spironolactone decrease digoxin protein binding -> higher digoxin levels.
  • Hypokalemia enhances effects of digoxin on myocardium.
  • The elevated intracellular calcium in toxicity raises the resting membrane potential in the myocardium -> higher risk of spontaneous dysrhythmias.

1. Mangrum, J. M., & Dimarco, J. P. (2000). The Evaluation and Management of Bradycardia. New England Journal of Medicine,342(10), 703-709. doi:10.1056/nejm200003093421006

2. Hack, J. B., & Lewin, N. A. (2006). Goldfrank's Toxicologic Emergencies(Vol. 8). New York, NY: McGraw-Hill. Retrieved June 26, 2019, from Ch 62: Cardioactive Steroids

3. Foxglove: Toxic to the Heart. (n.d.). Retrieved June 26, 2019, from

EKG Contributor: Allen Wang, MD
Resident Author: Jennifer Rabjohns, MD
Faculty Mentor: Massoud Kazzi, MD
Date of Presentation: 5/24/19

40yoF presents after taking extra verapamil 2 hours ago. Her systolic blood pressure is persistently in the 70s but she's mentating well.


How would you describe this EKG?
Rate is about 75 and normal sinus. Normal axis. First degree AVB. Borderline long QT.

What is the differential diagnosis?
Goldfrank's has an extensive list of medications that can cause conduction abnormalities, included here because there are some medications that are surprising (1).

But back to the more common scenario - calcium channel blocker vs beta-blocker overdose. Goldfrank's notes it is very hard to distinguish based on EKG. But they note a few principles:

Beyond EKG's and looking more generally at the patient, Goldfrank's notes:

For this patient, her glucose was 140.

As alluded to above, verapamil and diltiazem (non-dihydropyridines) are associated with more myocardial effects.

Regular release formulations of calcium channel blockers have onset of signs and symptoms at 2-3 hours post-ingestion. Patients who take sustained release formations usually have onset of symptoms at 6-8 hours (1).

Goldfrank's has specific recommendations.

  • Continuous cardiac monitoring
  • EKG q1-2 hours
  • Fluid bolus PRN hypotension
  • Because of the significant danger of calcium channel blocker overdose, strongly consider orogastric lavage; recognize patients may have vagal response to it (worsening bradycardia and hypotension)
  • Activated charcoal
  • Whole bowel irrigation, especially if sustained-release ingestion

Pharmacologically, evidence for efficacy is lacking but you can try to work around the calcium channel blockage. Goldfrank's recommends the following sequence:

  • Atropine (ACLS dosing); anticipate treatment failure
  • Calcium: 10–20 mL of 10% calcium chloride or 30–60 mL of 10% calcium gluconate), repeat q15–20 minutes up to 3–4 doses or start continuous infusion
  • Catecholamine such as norepinephrine,
  • High-dose insulin infusion: if glucose is <250 mg/dL, give 25–50 g of dextrose (0.5–1 g/kg) followed by a dextrose infusion of 0.25–0.5 g/kg/h. Then give insulin bolus of 0.1 U/kg, followed by an insulin infusion (0.5 U/kg/h).
  • Glucagon, 3-5mg given over 1-2 minutes
  • Phosphodiesterase inhibitor (e.g., milrinone), using standard CHF dosing

Take-home points for calcium channel overdose:

  • ABC's first
  • Early decontamination is critical
  • Serial EKG's (q1-2h)
  • Pharmacologic sequence is atropine, calcium, catecholamine, high dose insulin/glucose, glucagon, and phosphodiesterase inhibitor


  1. Flomenbaum, N. & Goldfrank, L. & Hoffman, R. & Howland, M. & Lewin, N. & Nelson, L. (2006). ELECTROCARDIOGRAM DISTURBANCES. Goldfrank's Toxicologic Emergencies. Retrieved May 24, 2019 from

EKG Contributor: Massoud Kazzi, MD
Resident Author: Jennifer Rabjohns, MD
Faculty Mentor: Massoud Kazzi, MD
Date of Presentation: 3/28/19

30 year old female presents with alcohol intoxication and suicidal ideation. You're unable to get much history because she is obtunded, but she's protecting her airway. You order psych labs and screening EKG:

You notice her QTc is long, but as soon as you get her on the cardiac monitor, you see this:

How would you describe this EKG?
Sinus beat followed by tachycardia.

What is the differential diagnosis?
This is a wide tachycardia. It's either supraventricular with a bundle branch block or ventricular. Deciding between the two is a whole other discussion; for this case, we'll assume it's ventricular tachycardia (VT). VT can be monomorphic or polymorphic (1).

In this case, there are different morphologies, so it's polymorphic VT.

There are two different kinds of polymorphic VT; those associated with long QT (torsades de pointes) and those that aren't.

Polymorphic VT without long QT is most often associated with cardiac ischemia.

In contrast, polymorphic VT with long QT usually is acquired (not congenital), from electrolyte abnormalities like hypokalemia and hypomagnesemia, and/or a long list of medications. Then an R-on-T starts torsades.

A normal QTc in men is <450mS; in women, it's <460mS (2). Courtesy of LITFL (3), once your actual (not corrected) QT goes above this nomogram line (~500mS), you're more likely to go into torsades. Remember that principle, but you can also see Dr. Smith's blog for an explanation of how QTc can throw you off (4).


This patient has polymorphic ventricular tachycardia with a documented long QT; she is in Torsades. Luckily, most Torsades resolves quickly and spontaneously; episodes usually are <90 seconds long, but you may have up to 30 episodes before they go away completely (5)! Here's how you escalate if you need to (1, 5, 6)):

  • If unstable with a pulse, cardiovert. Rosen's recommends not synchronizing, which makes sense; your machine never be able to because of the twisting points.
  • If unstable without a pulse, defibrillate. Torsades can degenerate into ventricular fibrillation anyway, and often VF is mistaken for torsades (2,3).
  • Replete K, even to mildly supranormal levels
  • Give Magnesium sulfate 2-4g, regardless of level
  • Give isoproterenol if assumed acquired torsades; use beta-blocker if congenital since it's usually triggered by catecholamines.
  • Overdrive pace (100-120 bpm).
  • Consider lidocaine.

Congratulations! You've successfully gotten this patient out of torsades, but you may not be out of the woods yet. Magnesium is poorly absorbed by cardiac myocytes and drugs that induce long QTc usually have a longer half-life then the magnesium that you gave; start a magnesium drip. A case series in Circulation showed success (no recurrence) with magnesium 3-20mg/min until QT < 500mS (5, 8).

Take-home points:

  • Polymorphic VT can be Torsades (requires long QT) or not (most often due to cardiac ischemia).
  • Once actual (not corrected) QT >500mS, there's a higher risk of Torsades.
  • Most Torsades is brief and episodic...
  • but give magnesium bolus and drip, and be ready to escalate care if needed: unsynchronized cardioversion/defibrillation, potassium, isoproterenol, overdrive pace, consider lidocaine.


  5. Rosen's:!/content/book/3-s2.0-B9780323354790000696?scrollTo=%23hl0001640
  6. Tintinalli's:

EKG Contributor: Brett Linowes
Resident Author: Jennifer Rabjohns
Faculty Mentor: Massoud Kazzi
Date of Presentation: 2/25/19

A 9 year old girl presents with chest pain a week ago.

How would you describe this EKG?
Regular rate, rhythm, and left axis. PR is short (see lead II and V1, <120), QRS has normal interval but has upsloping.

What is the differential diagnosis?
The short PR makes you think of an accessory pathway, which usually means either Wolff-Parkinson-White (WPW) or Lown-Ganong-Levine (LGL) syndrome.

We talked a little bit about pre-excitation syndromes in the AVRNT and AVNT challenge. WPW and LGL are both associated with supraventricular tachycardias. In particular, WPW is associated with atrial fibrillation, atrial flutter, and then ultimately ventricular tachycardia or fibrillation. LGL is so rare and the accessory tract is so elusive that some people don't think it exist, but it seems to have similar risks (1).

Discriminating features of the two are below (2, 3).

Avoid sympathomimetics; they might enhance conduction through the AV node and lead to dysrhythmias (4). Some say if the patient is tachycardic with a narrow QRS that adenosine is ok, but the safest approach in known WPW or LGL would be to avoid AV-nodal blockers (3). AV-nodal blockers can lead to increased fast pathway conduction and ventricular fibrillation. If stable, use procainamide; otherwise, use synchronized cardioversion. Definitive treatment is ablation (5).

Take-home points:

  • Consider pre-excitation syndromes in syncope, palpitations, and episodic chest pain.
  • Lack of delta wave doesn't exclude a pre-excitation syndrome.
  • Avoid sympathomimetics.
  • Avoid AV-nodal blockers - use procainamide or synchronized cardioversion.
  • Talk w/ cardiology - definitive treatment is ablation.


  1. Cadogan, M. (2019, February). PR Interval.
  2. Zhang, G. (2019, February). Lown–Ganong–Levine syndrome.
  3. Burns, E. (2019, February). Pre-excitation Syndromes.
  4. Podrid, P. (2017, November). Lown-Ganong-Levine syndrome and enhanced atrioventricular nodal conduction.
  5. Biase, L. (2018, September).Treatment of symptomatic arrhythmias associated with the Wolff-Parkinson-White syndrome.

Resident Author: Jennifer Rabjohns
Faculty Mentor: Massoud Kazzi
Date of Presentation: 1/24/2019

40yoM, h/o EtOH abuse, found unresponsive at home.

EKG is below (@ 1030):

How would you describe this EKG?
Rate is about 80. It's hard to see P waves, but they're there, and they're all different; rhythm is irregularly irregular (atrial fibrillation). EKG machine reads a LBBB (however, does not meet LBBB criteria because aVL is down). QRS has an extra notch at the end. Deep inferolateral T wave inversions.

What is the differential diagnosis?
This extra notch at the end of the QRS is right before the J point. See examples here from LITFL:

(For a review of J points, see the last blog post.)

From this review article, J waves (also known as Osborn waves) are associated with hypothermia but can also be seen in vasospastic angina, idiopathic ventricular fibrillation, cardiopulmonary arrest from oversedation, hypercalcemia, brain injury, and subarachnoid hemorrhage.

According to Dr. Smith's ECG Blog, the differential includes the above plus Brugada syndrome and benign early repolarization.

From Tintinalli's, J waves usually are seen at temperatures <32C.

For this patient, we don't have an initial core temperature. For his second EKG (@ 1045), his core temperature was 28C (82F). The Osborn waves are smaller, which is to be expected as patients become warmer.

Second EKG (@ 1045):

The patient was still being rewarmed during his third EKG (@1530, as inpatient):

Patient was normothermic for his fourth EKG (@ 430am the next day):

Tintinalli's notes that atrial fibrillation and flutter are expected. Other things you should know about hypothermia and EKG's - hypothermic J waves also have an arrhythmogenic potential that is proportional to the size of the J wave and not fully understood. Hypothermia can also cause any type of heart block or atrial/ventricular arrhythmias; be careful handling patient to minimize triggering them!

Take-home points:

  • Use your history and physical if you see J waves, since the differential diagnosis includes hypothermia and other processes.
  • J (Osborn) waves are usually seen at <32; as you warm your patients, their amplitude should go down.
  • Be careful moving your hypothermic patients; rough handling can trigger arrhythmias.


  • Links as above.
  • Brown D. Hypothermia. In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8eNew York, NY: McGraw-Hill; 2016. Accessed January 26, 2019.

Resident Author: Jennifer Rabjohns
Faculty Mentor: Massoud Kazzi
Date of Presentation: 12/27/2018

70yoM p/w exertional fatigue, altered mental status, and BP 80s/50s. Hx significant for head and neck cancer complicated by recent CSF leak.

EKG is below:

How would you describe this EKG?
Inferolateral ST segment elevations with aVR depression.

What is the differential diagnosis?
When seeing AMS and hypotension, remember your causes of shock: hypovolemic, distributive (sepsis, anaphylaxis), obstructive, neurogenic, and cardiogenic. The recent CSF leak with concern for sepsis was a red herring! EKG showed STEMI.

Background on Ischemic EKG Changes:
In August of 2018, the Fourth Universal Definition of Myocardial Infarction was published, which included EKG changes suggestive of ischemia (Thygesen 2018):

We'll talk about ST elevation here.

A review: The J-point is the start of the ST segment. Compare it to the T-P segment (ST Morphology).

Some sources (including the above) recommend comparing the J-point to the P-R segment, but pericarditis (PR depression) can make things confusing, and T-P is generally isoelectric.

Now, ST elevation suggestive of ischemia is defined as 1 of 2 things:

1.) 1mm in 2 contiguous leads except for V2 and V3. Remember our example from this case:


2.) Specific ST elevations in V2 or V3

(STEMI and STEMI Equivalents 2015).

In the next example, the STE actually extends beyond V2 and V3.

However, STEMI's only account for 25% to 40% of presentations of MI (Tamis-Holland 2014). This is consistent with the table above, which mentions ST depression and TW inversion as possible evidence of ischemia. But from the 2017 European Society of Cardiology Guidelines for the Management of STEMI, patients may have coronary artery occlusion or global ischemia without ST-elevation if there is:

  • bundle branch block
  • ventricular pacing
  • hyperacute T waves
  • isolated ST-depression in anterior leads, and/or
  • universal ST-depression with ST-elevation in aVR.

Those ESC guidelines state that in patients without ST elevation, but who have "the  [above] mentioned electrocardiographic (ECG) changes and clinical presentation compatible with ongoing myocardial ischemia, a primary percutaneous coronary intervention (PCI) strategy (i.e., urgent angiography and PCI if indicated) should be followed" (Kala 2017).

Take-home points:

  • Look for the ST elevation criteria if you have suspicion.
  • Keep an eye out for MI without ST elevations and consult cardiology as needed.

Case Resolution:
Cath attack was called. Cath showed 3-vessel disease: 100% occlusion in LAD, 99% in circumflex (received BMS), 99% in RCA (received BMS). Pt transiently had IABP, RV Impella, and was on multiple pressors; he was successfully weaned off of these and discharged home.


  • Kala, P., Mates, M., Zelizko, M., Rokyta, R., & Ostadal, P. (2017). 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Summary of the document prepared by the Czech Society of Cardiology. Cor Et Vasa, 59(6). doi:10.1016/j.crvasa.2017.10.008
  • ST Morphology. (n.d.). Retrieved December 27, 2018, from
  • STEMI and STEMI Equivalents, i.e. Who Needs the Cath Lab Now! (2015, August 31). Retrieved December 27, 2018, from
  • Tamis-Holland, J. E., & Ogara, P. (2014). Highlights From the 2013 ACCF/AHA Guidelines for the Management of ST-Elevation Myocardial Infarction and Beyond. Clinical Cardiology,37(4), 252-259. doi:10.1002/clc.22258
  • Thygesen, K., Alpert, J. S., Jaffe, A. S., Chaitman, B. R., Bax, J. J., Morrow, D. A., & White, H. D. (2018). Fourth Universal Definition of Myocardial Infarction (2018). Journal of the American College of Cardiology, 72(18), 2231-2264. doi:10.1016/j.jacc.2018.08.1038

Resident Author: Evan Kuhl
Resident Editor: Jennifer Rabjohns
Faculty Mentor: Massoud Kazzi
Date of Presentation: 11/29/2018

65yoM p/w palpitations for 2 days.

How would you describe this EKG?
The EKG above shows a regular, narrow complex tachycardia.

What is the differential diagnosis?
A narrow complex tachycardia is supraventricular, meaning it originates above the ventricles before the His-Purkinje system.

If this was an irregular rhythm, then atrial fibrillation, variable flutter, or multifocal atrial tachycardia would be more likely.

Regular supraventricular tachycardias (SVT) include sinus tachycardia, atrial flutter, AV nodal reentrant tachycardia (AVNRT) and AV reentrant tachycardia (AVRT)1.

NEJM has a good review2 of these, and this is their ddx algorithm:

AVNRT is more common, is typically rapid in onset, with regular palpitations. Generally, AVNRT is well tolerated without hemodynamic instability. AVNRT occurs when there are two pathways through the AV node, a slow and fast conducting pathway. Normal sinus rhythm is conducted through the fast pathway, however if a stimuli arrives to the AV node while the fast pathway is still in a refractory state, the slow pathway is activated, which may lead to the reentry phenomena.

AVRT is less common, occurs when a reentry circuit is present in an accessory pathway outside the AV node, and may have several different EKG morphologies3. Wolff-Parkinson-White is an example of one AVRT.

Schematics are from the same NEJM review article2:

On closer examination of this EKG, you can also see retrograde P-waves (blue arrows, below).

This EKG is a case of AVNRT.

How would you treat this patient?

If this patient became unstable, you would immediately cardiovert the patient using the synchronized cardioversion setting. Since he was stable, modified vagal maneuvers were attempted without success4. A single dose of 6mg of adenosine was then used to chemically terminate the arrhythmia. A second dose of 12mg adenosine could be attempted if the first dose fails.

Our illustrious resident on the case recorded the continuous EKG showing the cardioversion.


  1. Tintinalli JE, Stapczynski JS, Ma OJ, Cline D, Meckler GD, Yealy DM. Chapter 18, Tintinalli's emergency medicine : a comprehensive study guide: New York : McGraw-Hill Education, 2016. Eighth edition.; 2016.
  2. Link, M. Evaluation and Initial Treatment of Supraventricular Tachycardia. NEJM;367:1438-1448. DOI: 10.1056/NEJMcp1111259.
  3. Supraventricular Tachycardia - Life in the Fast Lane ECG Library. @sandnsurf, 2018. at
  4. Appelboam A, Reuben A, Mann C, et al. Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): a randomised controlled trial. Lancet 2015;386:1747-53.

End-tidal CO2 monitoring is a measure of metabolism, perfusion, and ventilation - although we usually use it for the latter two.

The waveform is really well-explained in this JEMS article, which is where this schematic is from. The main point is the EtCO2 number is at the peak of expiration.

EtCO2 in CPR
In 2014, two Norwegians published a great way to remember the uses of EtCO2 in CPR: PQRST. Look familiar? 😉 

Let's walk through these...

Position of the endotracheal tube (PQRST)
ACEP's policy is that direct visualization is great, and bilateral breath sounds are not reliable. As we know, we can't pause CPR to do a portable chest x-ray, which ACEP also notes is not reliable. They do recommend, however, ultrasound in the hands of an experienced operator and EtCO2.

Waveform EtCO2 (vs. colorimetric) can be helpful because you may still get color change with the first few breaths of an esophageal intubation, which can be misleading. But the waveform does not lie (this schematic and the others were taken from this great JEM article).

Quality of CPR (PQRST)
We normally assess quality of CPR by palpable pulses (which can be challenging and even unreliable) or arterial diastolic pressure >25 (which is great if we have an arterial line). EtCO2 provides the same information in an objective, reliable way. We aim for EtCO2 of at least 10, with a goal of 20. (This is the official AHA guideline.) Why 10? CPR provides ~1/4 of normal cardiac output, and normal EtCO2 is 35-45.


Return of spontaneous circulation (PQRST)
Getting ROSC can be detected on EtCO2 prior to a scheduled pulse check. An increase of EtCO2 to normal values (35-45) or an increase of 10 is 97% specific. (Unless you give bicarb right before, which artificially increases it.) (Source: this JEM article.)

Strategies for treatment (PQRST)
Different waveform morphologies can help us decide what our next steps should be.

For example, movement of a LUCAS device or ETT dislodgement:

Or the appearance of two smooshed EtCO2 waveforms, indicating a cuff leak, supraglottic intubation, or right mainstem intubation (basically, one part of the lungs ventilates before another):

Or, the waveform looks like a sharkfin, indicating expiratory obstruction (as in bronchospasm, kinked or blocked ETT or circuit):

Termination (PQRST)
Lastly, EtCO2 can provide one data point (of many) for when to terminate CPR. Chance of ROSC is significantly higher if EtCO2 >20 at 20 minutes, and significantly less if EtCO2 <10. (Also per the AHA guidelines.)

I couldn't find much data on EtCO2 with bagged patients or patients with LMA's; using EtCO2 pretty much requires intubated patients. This is a touchy topic, as intubation can, as we know, decrease compression fraction by increasing time off the chest. There is also very little data on correlation of blood values of PCO2 vs EtCO2; animal studies do not show much correlation, and as you would expect with CPR, there will likely be some dead space and/or V/Q mismatch.

Take-home points
That said, there are some really great uses for EtCO2 in CPR: evaluating position of ETT, judging CPR quality, seeing ROSC quicker, adjusting strategies for treatment, and providing one data point for when to terminate resuscitation - some important things to keep in mind the next time your callbox goes off with a CPR in progress. Especially since it can be so quick to set up! (See video of me setting one up on an Alaris IV pump below).

Resident Author: Jennifer Rabjohns, MD
Faculty Mentors: Randy Myers, Massoud Kazzi
Date of Presentation: 10/31/2018

Introduction: 34yoM, h/o DM, p/w chest pain.
EKG at 7:10pm:

What's the differential? 
We discussed big T waves in a prior challenge, here.

Note this is likely not a pericarditis given the inferior ST/TW reciprocal changes.

Serial EKG's were obtained. EKG at 7:25pm:

EKG at 7:31pm:

What is the management?
Have a high suspicion and follow your ACLS guidelines for ACS.

What happened to this patient?
Cardiology was contacted after the first EKG, so they could be ready to activate the cath lab if needed. After the third EKG, a cath attack was called. This patient was shown to have diffuse disease, w/ stent placed to LAD and CABG scheduled for the next day.

Take Home Points

  • STEMI's happen in 34 year olds.
  • Get in touch with cardiology early if you have a high suspicion and/or want a second opinion for EKG's.
  • If you're at all suspicious, get serial EKG's (q5-10min or continuous). This is the recommendation in the ACC/AHA Guidelines for the Management of Patients with STEMI.


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