Right Heart Strain on EKG

EKG is neither sensitive nor specific for PE, but there are some clues that can be another data point in your decision making. Remember, EKG stands for electrocardiogram, not pulmonary-artery-gram. The absence of these findings should not decrease your suspicion of PE. 

As we all know, EKG can be completely normal in PE; sometimes, it can have the following changes. Changes in EKG occur due to acute cor pulmonale, resulting in acute dilatation and partial failure of the right side of the heart and the resultant abnormal electrical activity. 

Rate & Rhythm findings: Sinus tach, new onset atrial fibrillation

Axis findings: Right axis deviation, S wave in lead I. Remember lead I is looking at the left side of the heart, so a pronounced S wave and thus overall negative deflection of lead I means there is right axis deviation

Interval findings: QRS complex: New right bundle branch block. Remember, the RV contains the right bundle and poor blood flow to the RV due to dilatation and resultant ischemia to the right bundle results in the block.

Ischemia findings: 

• Delayed R wave progression due to dilatation of the RV and resultant shift in electrical activity towards the right side

• ST segment changes: 

  • (S1)Q3T3 

  • Anterior T wave inversions (almost mimicking Wellens - apparently in Steve Smith’s book, there is a way to tell the difference from T wave inversions in Wellens/ACS vs T wave inversions from PE/pseudo-wellens, but they look identical to me)

  • Anterior ischemia along with inferior (lead III) inversions is more specific than just anterior ischemia (which can be Wellens/ACS) 

  • V1 ST-Elevation due to RV ischemia 

  • Diffuse ST depression with reciprocal STE in aVR due diffuse subendocardial ischemia in obstructive shock from a PE 

Hypertrophy findings: A dominant R wave in V1 and other evidence of right ventricular hypertrophy on EKG (right atrial enlargement) speaks against an acute process such as PE. The patient likely has chronic cor pulmonale.  

Those with more hemodynamically significant PEs are more likely to have these changes. Conversely, having some of these findings below in a patient with known PE such as anterior T wave inversions, ST depressions with reciprocal aVR elevation, & sinus tachycardia makes the patient at high risk or in RV failure (so maybe don’t overload that RV with 3L of fluids or cardiovert the compensatory atrial fibrillation). Don’t forget the differential for T wave inversions/depressions also includes other pathologies such as ACS. 

https://litfl.com/right-ventricular-strain-ecg-library/

https://litfl.com/ecg-changes-in-pulmonary-embolism/

Vanni, Simone & Polidori, Gianluca & Daviddi, F. & Ponchietti, Stefano & Curcio, M. & Conti, Alberto & Vergara, Ruben & Grifoni, S.. (2007). Right Ventricular Strain Pattern at ECG Predicts Early Adverse Outcome in Patients With Acute Pulmonary Embolism and Normal Blood Pressure. Journal of Emergency Medicine - J EMERG MED. 33. 336-336. 10.1016/j.jemermed.2007.08.043. 

https://emergencymedicinecases.com/ecg-cases-26-pulmonary-embolism-and-acute-rv-strain/

POTD: Droperidol

CODE WHITE AMBULANCE TRIAGE. The patient is at imminent risk of harming themselves and your staff. Verbal deescalation was attempted but has failed. Everyone is looking to you for your OK for chemical sedation. You dig your heels in and are about to mutter the first thing that comes to mind: "5 of haldol and 2 of ativan."

But hold up. Because this POTD is about droperidol.

Background: Droperidol is a dopamine antagonist, and is a first generation antipsychotic. It used to be a favorite of ED doctors to treat agitation in the ED and was used for more than 30 years for acute agitation. It was removed from market 20 years ago because of a black box warning due to QTC prolongation and risk of torsades/sudden cardiac death. This was based off a study looking at 273 case reports over a 4 year period. In the deaths reported, the doses used were 25mg-250mg per dose, doses MUCH higher than what we would typically give in the ED for agitation. Adverse cardiac events or death occurred in 10 patients who received a dose less than 2.5mg. From this study, the FDA placed a black box warning on droperidol. Upon further review of these cases by multiple authors, all of these cases had confounding factors that could have accounted for the adverse event. Overwhelming evidence after the FDA black box warning was issued has showed that droperidol is both safe and effective, especially when used at typical dosing for agitation.

Why Droperidol: Comparatively to other sedatives, namely haloperidol, droperidol is more potent, is faster onset, and has a shorter duration. According to Cressman et. al who examined absorption, metabolism, and excretion of droperidol, absorption via IM is near equivalent to IV administration. Onset of action is 3-10 minutes, and peaks at 30 minutes. Duration of effect is 2-4 hours, and effects may last up to 12 hours. Undergoes hepatic metabolism.

In the DORM study, 10mg droperidol IM was compared to 10mg IM Midazolam. Droperidol, compared to Midazolam, reduced the duration of violent behavior (20 min vs 24 min), required less additional sedation (33% vs 62%), and has less respiratory distress among intoxicated agitated patients.

If single agent droperidol is not enough, it was found in a study authored by Taylor et al that combination 5+5 droperidol and midazolam was more effective at sedation than droperidol or olanzapine alone.

Uses: Typical dosing ranges between 5mg -10mg for agitation, and can be administered IM or IV.

In addition, it can be used to treat headaches, vertigo, nausea, and pain, usually at half the agitation dose.

Side effects: Sedation, extrapyramidal effects, hypotension, prolongation of QT interval. Obtain an EKG if possible before administration, but if not possible, can be obtained after if the patient is agitated. Be mindful of using droperidol in the setting of patients with known prolonged QT interval and patients at risk given their medication history (e.g. methadone).

Sources:

https://vimeo.com/180991859

https://pubmed.ncbi.nlm.nih.gov/4707581/

http://www.emdocs.net/droperidol-use-in-the-emergency-department-whats-old-is-new-again/

http://www.emdocs.net/the-art-of-the-ed-takedown/

https://www.tamingthesru.com/blog/2019/4/20/the-return-of-droperidol

https://pubmed.ncbi.nlm.nih.gov/12707137/

https://dailymed.nlm.nih.gov/dailymed/fda/fdaDrugXsl.cfm?setid=147e033d-d997-4ef6-8bb5-a9ba372590b2&type=display

Pacemakers for the ER Physician

Pacemakers

Or, like, the most complicated things ever 

Holy fish-balls, these things are crazy complicated.

Lucky for you all, I have no life – AND DESPITE THIS ENTIRE DOCUMENT ALREADY HAVING BEEN DELETED ONCE – I have (re)gone through a ton of resources to help you, a baller-life-saving-ER-provider, make some sense of these damn things.

We’re going to go over WHY people get pacemakers, WHAT they actually are, HOW they work (barely), and their corresponding EKGs.

If I haven’t thrown my computer out the window, we’ll cover just a couple of pacemaker-malfunction emergencies.

Let’s get started.

CHAPTER 3:

Pacemaker EKGs

EKG#1 - Atrial Pacing

o Note the tiny lines, or “pacer spikes,” on the EKG that precede P waves

o The pacemaker is triggering atrial beats, depolarizing the atria – the current continues down and appears to depolarize the ventricles through the normal conduction pathway

o This patient may still have a dual chamber pacemaker, but only requires atrial pacing during this EKG

EKG#2 - Ventricular Pacing

o Like we talked about above, the pacing lead is in the RV – the left ventricle relies on the current from the RV, so it looks like a LBBB

o Use modified Sgarbossa, but know that it is not perfect in these patients

EKG#3 - Dual Chamber Pacing

o This patient is having their atria and ventricles triggered by separate impulses

EKG#4 - Bi-Ventricular Pacing

o   I’m not going to give you an EKG for this one – in theory you have a RBBB combined with a LBBB, but the patterns are highly variable and non-essential for your knowledge

o   Just know you can have two spikes in a QRS… or not…

o   If it looks like LBBB, treat it like LBBB

CHAPTER 4:

Pacemaker-Malfunction Emergencies

Lastly, this website has a great algorithm for “ED Approach to Pacemaker ECGs” and the rest of their site is fantastic.

https://canadiem.org/pacemaker-essentials-interpret-pacemaker-ecg/

REFERENCES:

https://litfl.com/pacemaker-rhythms-normal-patterns/

https://johnsonfrancis.org/professional/single-chamber-pacemaker-and-aortic-prosthetic-valve/

https://www.ecgmedicaltraining.com/the-basics-of-paced-rhythms-part-1/

https://canadiem.org/pacemaker-essentials-interpret-pacemaker-ecg/

https://canadiem.org/pacemaker-essentials-need-know-ed/

https://litfl.com/pacemaker-malfunction-ecg-library/