Tasty Morsels of EM 039 BradyDysrhythmias

[Featured image via LITFL]

Approach to BradyDysrhythmias

EB Medicine Article [free via EMRA if you’re a member. About 70 dollars a year. Well worth it.]


On a FOAMed note, it’s interesting that all the ECGs in the article are taken from LITFL. Another sign that FOAMed is not providing a marginal, niche resource, but a highly curated and high quality resource for all.

  • while usually thought benign, first degree block are more likely to develop AF and have a (moderately) increased rate of death [Cheng S, Keyes MJ, Larson MG, et al. Long-term outcomes in individuals with prolonged PR interval or first-degree atrioventricular block. JAMA. 2009;301(24):2571-2577. (Prospective analysis; 7575 patients)]
  • in sinus node dysfunction and in particular, tachy-brady syndrome most of the tachycardias will be AF (but not all)
  • sinus node dysfunction is seen in the oldies
  • pathological bradycardias in the context of ACS are typically associated with RCA occlusions. I have a vivid memory as a 1st year doc of seeing a bradycardic, diaphoretic guy with chest pain and the more senior doc coming down saying “what do you think? a nice big inferior?” with a grin on his face.
  • Some of the more interesting and esoteric causes of a pathological brady
    • hypothyroid
    • hyperkalemia
    • chagas disease (common world wide but not here)
    • Lyme disease
    • parvovirus or coxsackie (in the context of myocarditis)
    • syphillis (so it turns out that Amal Mattu might be wrong and it’s not just Hyperkalemia that is the syphilis of electrocardiography but syphilis itself is the syphilis of electrocardiography)
    • some chemo regimens (not in the article but I saw this last month…)
  • atropine is of course recommended but no surprise that it’s rarely effective. Given that most of the nasty bradys I see are third degree blocks then I find that it’s rarely helpful.
  • dopamine is also recommended but along with some other smart people I just use adrenaline for virtually all vasoactive situations as I actually know how to use it 😉

Tasty Morsels of EM 037 – Heart Transplants

I keep a little, ever-expanding note on my phone where I jot down little morsels of goodness that I pick up while listening to or reading one of the many excellent sites/podcasts in the useful resource section. They’re useful in a kind of “board review” way. I tend to skip the really basic stuff and try and focus on what I didn’t know.

I’ll try and transfer them here for your enlightenment.

  • 5 year survival about 75%
  • most common ED complaints are fever, SOB, GI probs, chest pain
  • baseline tachycardia is normal as no vagus innervation to the transplanted heart
  • patient has no pericardium but due to scarring clinical tamponade can still develop
  • chest pain is rarely related to ischaemia as heart is denervated (most anginal pain is probably sympathetically mediated and the sympathetic plexi around the heart would have been disconnected at transplant)
  • however ischaemia is common as atherosclerosis is accelerated in the graft. Often presents as CHF or arrhythmia.
  • CMV is a risk factor for accelerated atherosclerosis.
  • ECG Often demonstrates two p waves. One is from native sinus node (which is often left in place as it lies in the post RA) and the other is from the donor SA node. The donor p wave is the one that should conduct.
Via Wikipedia

Via Wikipedia

  • rarely a heterotropic transplant is done where the the native heart remains in entirety in the chest. The ECG in this scenario is understandably bizarre.


Rosen 7th Edition p2369-70

The ECG in the poisoned patient

Most patients presenting to the ED with either accidental or intentional drug ingestion will get an ECG. In most departments I’ve worked in, the senior doctor looks at all the ECGs, primarily for STEMI, but for other findings too. The juniors will come to me later discussing the case and when I ask about the ECG, they frequently say it’s normal. This always starts me on a bit of a rant as when I ask them, it turns out they have no idea what they’re actually meant to be looking for in the ECG of a poisoned patient. [The same goes for syncope patients…]

So, after considering what I look for on the ECG, here’s my list of things to check in the poisoned patient.

What to look for on the ECG

  • long QT

    • all kinds of drugs

    • results from prolonged K efflux

  • wide QRS

    • Na Channel blockade

      • TCA

      • propanolol

      • cocaine

      • lots of other unexpected drugs too

  • dominant R aVR

    • Na channel blockade

  • scooped ST segments

    • digoxin

  • bradycardia

    • digoxin

    • beta blockers

  • AV block

    • beta blockers

    • digoxin

Or can be expressed as 5 main cardiac toxicities if you’re into the pathophysiology of it

  1. Na channel blockade [depolarisation]

    • wide QRS (>100ms is the cut off here)

    • prolongation of the last 40ms of the QRS which produces a right axis on ECG

    • dominant R aVR [PMID 7618783]

  2. potassium efflux blockade [repolarisation]

  3. Na/K/ATPase pump blockade

    • all about digoxin here

    • can produce almost any rhythm

    • tachys with AV blocks are a big clue

  4. beta blockade

    • brady

    • AV blocks

  5. calcium channel blockade

    • brady

    • AV blocks


If you know of any other interesting ECG patterns in tox patients please let me know in the comments.

Perhaps the best comment came from Domhnall:

Succinctly summarised as the “horizontal” ECG as opposed to the “vertical” ECG of IHD….


Critical Decisions in Emergency and Acute Care Electrocardiography. Brady and Truwit 2009 Wiley


Liebelt, E L, P D Francis, and A D Woolf. “ECG Lead aVR Versus QRS Interval in Predicting Seizures and Arrhythmias in Acute Tricyclic Antidepressant Toxicity..” Annals of Emergency Medicine 26, no. 2 (August 1995): 195–201. PMID 7618783


Tasty Morsels of EM 031 – Retrograde p waves

I keep a little, ever-expanding note on my phone where I jot down little morsels of goodness that I pick up while listening to or reading one of the many excellent sites/podcasts in the useful resource section. They’re useful in a kind of “board review” way. I tend to skip the really basic stuff and try and focus on what I didn’t know.

I’ll try and transfer them here for your enlightenment.

From K Wang on HQMEDED

The basics on retrograde p waves

  • a junctional beat is one occurring from the AV node

  • normally narrow with no preceding p wave

  • the impulse travels down from av node causing the narrow complex qrs

  • an impulse also goes up from the av node and depending on whether the atrium is refractory or not will result in a retrograde (usually inverted p wave)

Example here from LITFL of an accelerated junctional rhythm with retrograde p waves(inverted p waves in II, III and aVF)

Accelerated Junctional Rhythm

Standing Test for Long-QT syndrome

This was all brand new to me. I was reviewing a syncope patient left over from the night shift before. The hand over was: recent change in anti-hypertensives, now feeling weak and dizzy about 1 week. Syncopal episode at dinner table last night.

She’d been in the department overnight, got some fluids, bloods and an ECG. The ECG was said to be normal.

I went and chatted to the patient and yes indeed it did sound all very like postural hypotension. I went back and looked at the ECG and did my usual syncope ECG review looking for the following:

  • Brugada
  • HOCM
  • WPW
  • intervals – QT and PR

And there it was – a nice big QTc of 550ms staring at me.

I still suspect that postural hypotension was the main cause of her symptoms but it would be a tad on the risky side to call it that in the context of a long QT. K+ and Mg++ were on the low side (3.5 and 0.6) so she got a bit of both and admitted for ECG monitoring.

The interesting bit came in the discussio with admitting doctor who was (for once) interested, enthusiastic and asked about the standing test for Long QT. This was all news to me but effcetively people with a long QT syndrome (LQTS) have an abnormal response in QTc with standing.

In healthy people on standing the heart rate goes up with corresponing shortening of the QT interval. Due to the fact that heart rate goes up more than the QT comes down, the QTc actually goes up slightly,

In LQTS the QTc often goes up substantially.

This paper addresses this concept and while it’s in now waty perfect (ie it examined it in people known to have LQTS which undermines its use as a diagnostic test in undiagnosed QT problems) it suggests that in healthy people an increase in QTc on standing of about 10-15ms is allowed but in LTQS is likely to be in the range of 90-100 ms.

Viskin, Sami, Pieter G Postema, Zahurul A Bhuiyan, Raphael Rosso, Jonathan M Kalman, Jitendra K Vohra, Milton E Guevara-Valdivia, et al. “The Response of the QT Interval to the Brief Tachycardia Provoked by Standing: a Bedside Test for Diagnosing Long QT Syndrome..” Journal of the American College of Cardiology 55, no. 18: 1955–1961. doi:10.1016/j.jacc.2009.12.015. PMID 20116193



  • the normal response to standing after lying is an increase in HR. This would normally be accompanied by a shortedned QT. In LQTS this apparently isn’t the case
  • The intervention was standing and recording QT changes.
  • they did this on high risk LQTS (lots of features but no diagnosis as yet) and those who actually had it genetically documented. The controls were healthy relatives of those pts or volunteers (the vast majority)
  • took them off Beta blockers for a day then lay them flat 10 mins and stood them up for 5 mins with telemetry.
  • blinded investigator performed the measurement had a set part of the trace. Bazzett’s  formula was the main one used.
  • excluded the obviously normal and obviously prolonged



  • 68 LQTS; 82 controls
  • the baseline QTs were 380 v 450 – not diagnositcially different but borderline
  • the QT went down in all the normals but less than the RR interval therefore the QTc goes up slightly.
  • the QT of those with LQTS didn’t change at all. In some it went up. Or put another way the QTc of the control group went up 13ms while the LQTS patients the QTc went up 89ms

Not something I’m going to be doing every day, but it’s a fairly nice, bedside test that we can apply in the ED.