Renal failure, hyperkalaemia, tachycardia. What’s going on?

A 67-year-old with a Hx of dilated cardiomyopathy, atrial fibrillation and obstructive uropathy presented after a collapse at home.  He said his urine has been white recently.

His temperature was 37.9 in the ambulance, 37.4 in ED.

He was tachycardic at 125, BP 90/60 (it had been 69/49 in the ambulance, in dropped again 81/60 again in ED).  He was euvolaemic.  He had no chest pain.

He had a large bladder and he was catheterised, he drained frank pus then clear urine.




A flutter name erased

He was treated for urosepsis with IV cefuroxime and IV fluids and his BP improved.

What did the ED doctors miss?

Dig level

The patient was digoxin toxic.

This was picked up by the medical RMO.

Think about digoxin toxicity in any patient with AF who is unwell.  The ED doctor did not get a medication history for this patient.

Patients on digoxin who develop renal failure (in this case probably obstructive and secondary to urosepsis) often become digoxin toxic.

The combination of hyperkalaemia (digoxin blocks the ATPase Na-K pump causing hyperkalaemia) , a very high digoxin level and a supraventricular tachycardia with AV block (atrial flutter with variable block, misread as atrial fibrillation) is very suggestive of digoxin toxicity.

Probably anyone with a supratherapeutic digoxin level should be treated with digoxon FAB (antibodies that bind digoxin) eg digifab.  This patient definitely needed it.  He was prescribed digoxin FAB by ED (2 vials).  The admitting general physician cancelled the prescription as the patient wasn’t symptomatic, but was able to be convinced that treatment was a good idea.

Digoxin FAB is very expensive, but failure to treat may be life threatening and results in longer admissions – costing more than the digoxin FAB.

Keep the patient on telemetry for 6 hours.

Don’t retest the digoxin level – the test measures bound and free digoxin and so is meaningless and confusing after digoxin FAB


It is very easy to miss digoxin toxicity as elderly patients often have other good reasons for their hyperkalaemia and arrhythmias.


By the way, a posterior ECG didn’t show any posterior ST elevation.


Further reading:

Why I don’t like digoxin

Why Billy Mallon doesn’t like digoxin



Toxicology Handbook.  2nd edition.  Murray et al



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Burn this ECG into your brain

63-year-old male with 5 hours of central chest pain


Posterior inferior STEMI

What is the diagnosis?



This is a posterior and probably inferior STEMI.

Anterior ST depression is a posterior STEMI (or a Sgarbossa +ve STEMI in the presence of LBBB) till proved otherwise.

To confirm that the anterior ST depression is the reciprocal changes from the posterior ST elevation, do a posterior ECG.

Move V4,5,6 to the posterior chest so they become V7-9 with V8 at the tip of the scapula.

Posterior leads posterior STEMI

The amplitude of the ST elevation on the posterior leads is not impressive – because there is lung between the heart and the posterior chest wall. Life in the Fast Lane says only 0.5mm of ST elevation is required to diagnose STEMI.

This patient was thrombolysed and did well.

And a reminder to document on the ECG the time your read it, your interpretation and your name legibly. DJM (the IIIrd) is not adequate.  Remember that the nurses need you to document the time you read the ECG to prove that they put it under your nose immediately after it was taken.



Life in the Fast Lane. Posterior Myocardial Infarction


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The crashing intubated patient: DOTTS

R main stem intubation

Whenever a patient you have just intubated deteriorates, or a patient on a ventilator deteriorates quickly:


Disconnect and let them exhale:

This gets the ventilator out of the equation and simplifies things / reduces our cognitive load: we understand BVMs (bag-valve-mask), ventilators and circuits confuse and scare us.  It also stops ventilation for a few seconds and lets the patient exhale which will help with over inflation / breath stacking.  This is especially important in patients with asthma (see Pop goes the wheezer)

O2 via BVM, slow:

Ventilate the patient slowly with a bag-valve-mask.  Look at the chest movements, listen to the breath sounds.

Is only one side of the chest moving?  Is it a bronchial intubation (check tube depth, see below), a mucus plug (suction the tube, see below) or a pneumothorax (usually unlikely, we’ll check for this later, see below, but if it’s a trauma patient ultrasound and/or perform a finger thoracostomy now)?

Squeezing the bag lets us get a feel for what is going on: is the patient easy or hard to ventilate.  If the bag collapses easily but the chest doesn’t move the tube probably isn’t in the trachea or is disconnected from the bag.  If it is hard to squeeze the bag: it might be a problem with the tube or the patient.  In the above X-Ray the patient has a R main bronchus intubation with R lung hyperinflation and L lung collapse (which happens amazingly rapidly).


Is it in the ETT in right place, is it blocked, is there a big leak (tube too small or has the cuff deflated)?  Check the capnography trace:  Is there a good wave form?  Is the tube at the right depth (around 22cm at the teeth for an adult or ~ 3 times tube diameter (actually 30 times), or black mark on ETT just through the cords in kids)?

Suction the tube.  If the suction catheter goes right down, the tube is patent.   You may suck out a big mucus plug or piece of broccoli.

Tubes is also for a nasogastric or orogastric tube.  If you haven’t got one in get someone to put one in while you continue to trouble shoot, otherwise make sure that is working (aspirate stomach contents, or insufflate air and listen to it gurgle in the stomach.

In the above X-Ray the ETT is down the R main stem bronchus (it was at 19cm at the teeth in a 3 year old) and the NG tube is curled up in the upper airway and has not decompressed the stomach.  Kids especially can be difficult to ventilate, be hypoxic or hypotensive due to gastric distension increasing intrathoracic pressure

Tweak the vent:

Do you need to reduce the tidal volume or respiratory rate if the patient has stiff lungs?  We usually start with a tidal volume of 6ml/kg ideal body weight.

If the patient is ventilating OK but is still hypoxic you probably need to increase the PEEP.


Ultrasound to look for pneumothorax.  This is last because it is relatively rare.

Get a chest X-Ray as well, but hopefully you will have fixed the problem using the above mnemonic before the radiographer arrives.


If the above hasn’t worked (it will sort the problem 99% of the time) get senior help! (if you haven’t already)

Next steps will depend on whether it appears to be a ventilation problem (hypoxia, difficult to ventilate) or a circulatory problem (easy to ventilate but hypotensive).  eg see


The above patient apparently tolerated the misplaced tubes very well and the only clue was an end tidal CO2 in the hundreds.  With repositioning of tubes the patient quickly improved.





Music (on podcast)

Nga Hau e Wha by Hui-a


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LBBB and Sgarbossa


Left bundle branch blocks cause a lot of confusion.

People often mistake the normal anterior ST elevation of LBBB as an MI

Less frequently people miss significant concordant ST segment changes which may be a STEMI (by Sgarbossa Criteria)

The Law of Discordance or the Law of Appropriate Discordance

In a normal LBBB the ST segments should be isoelectric or go be in the opposite (discordant) direction from the dominant part of the QRS


So typically in V1 the QRS is mainly negative and the ST segment in elevated.  This is normal for LBBB

In V6 the QRS is mainly positive and the ST segment is down.  This is normal for LBBB

Modified Sgarbossa Criteria for diagnosing STEMI in the presence of a LBBB

If there is concordant ST changes (ST segments in the same direction as the dominant part of the QRS) or a discordant ST elevation of greater than 1/4 of the amplitude of the S wave.

A: Concordant STE ≥ 1mm (in any lead) = Most specific for MI

B: Concordant STD ≥ 1mm in V1, V2, or V3 = Specific for MI

C: Discordant STE > 0.25 R or S wave

So, for example the ECG below shows a concordant ST depression in V3 (circled).  This only needs to be in a single lead. Therefore this meets Sgarbossa criteria for diagnosing a STEMI.



All of this applies to patients who have ventricular pacing as well (which usually causes a LBBB pattern on ECG)

This patient was not diagnosed as a STEMI, did not receive reperfusion therapy and died 9 hours later (but to keep this in perspective, in that hospital the patient would have had to be thrombolysed and there is only around a 1 in 43 chance that thrombolysis would save the average patients life even if given within 6 hours).


This ECG shows Sgarbossa +ve concordant changes in I, aVL and V3 (so Sgarbossa A + B)

Sgarbossa from Mattu


Here are some examples of Modified Sgarbossa C +ve complexes:


Modified Sgarbossa c from mattu

Most of us regard Sgarbossa as an indication for revascularisation (PCI or thrombolysis) because it has greater specificity for MI than standard STEMI criteria, but it is not in black and white as a criteria in the latest definition of MI.

If in Doubt

… get a second opinion.  If you don’t have senior support (eg smaller hospitals overnight) email (or take a photo on your phone and text or email, or fax) the ECG to the relevant specialist then phone them to get their interpretation.


Time ECG read

Your interpretation

When repeat ECGs are needed (if they are)

Your name (get a stamp)



Audio only



Sgarbossa Criteria.  Life in the Fast Lane
Thrombolytics given for Major Heart Attack (STEMI).  The NNT.



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The future funding of FOAM

Free Open Access Medical Education or FOAM has been free to users and producers largely due to the generosity of this man


the Godfather of FOAM, Mike Cadogan.

When I last spoke to him over a year ago, he was pouring over $75,000 a year of his own money to pay for technical support, Word Press fees and bandwidth to make FOAM happen.

A lot of us, me included (probably one of the narcissists he refers to), have taken this philanthropy for granted.

I have recently looked to getting funding from my employer to start another FOAM project, thus not putting more financial burden on Mike, but was quite happy to let him keep funding this website, leaving me only paying US$ 20/month for the audio hosting.

In the last few days we have had a wake up call from Mike in his post 5 Lessons Learned  This post is partly about self-care, valuing real life family and friends over a virtual life, and saying no, but it is also about the financial cost of FOAM.

We the FOAM producers need to find alternative, sustainable funding streams for FOAM.  I’m sure many already are eg EMCRIT’s CME option. Others of us need to obtain funding.  5 years from creation, FOAM has proved itself as one of, if not the of the best forms of medical education and practice improvement.  Now we need to get our employers and institutions to recognise this and fund FOAM.

We each need to go to our employers and say FOAM is the best thing in Continuous Quality Improvement (or what ever the latest buzz word is) since sliced bread and they need to contribute to it.

I have asked The Frontier Group, who provides a lot of the technical support for FOAM, for the true monetary cost of EM Tutorials (and for my next FOAM project), and I have started negotiations with my employer to get it to pay those costs.

In New Zealand each District Health Board gets tens of thousands of dollars a year per junior doctor of government funding for training.  This money largely just disappears into the hospitals’ coffers.  We need to claim some or all of that money and actually use it for education.  I’ve started negotiations at my hospital to have at least a good chunk of this money ring-fenced for education, managed by an education committee, and some of that will go to funding this website and podcast.

I suggest other FOAM producers start similar negotiations with their employers so that there is Learning and Development money  being used to ensure the amazing educational resource, that Mike has largely created and funded himself, is sustainable without draining his pocket anymore.






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Trauma: Lessons from the Military. Wing Commander Dr Paul Nealis



Key points

Stop bleeding!

Tourniquets are great.

Pack bleeding wounds firmly.  A roll of gauze works well. “Haemostatic dressings” eg quik clot, don’t seem to make much difference.  It appears the pack needs to be absorbent probably because they absorb water out of the blood in the wound thereby increasing the concentration of clotting factors.

Don’t get hung up on big IV lines.  The difference in flow rate between a 18 and 16 gauge is not that great.  If the patient is bleeding out that fast they aint going to make it, and sometimes 18s are just easier to get in especially in a shocked patient.

Permissive hypotension: aim for a systolic of 80 (90 if head injury).  Don’t rely on mental status (BP 60 systolic but compensating and still conscious… 60 and compensating  still conscious …. 60 and still conscious … dead).

For massive haemorrhage transfuse and give tranexamic acid early.  For us this may mean sending an “unknown patient” label down to get some O-negative blood from the lab before the patient arrives.  Get FFP thawing ASAP. Get platelets ASAP.

Use ketamine rather than fentanyl in major trauma -> lives saved,  presumably by avoiding the sympatholytic effects of fentanyl

Ketamine appears to reduce the incidence of Post Traumatic Stress Disorder by 60%!  This may be by reducing the patients’ experience of pain and mutilation.

ED teams (in the military ED docs and nurses and military medics) resuscitate the patient, others behind the red line.  When the external bleeding has been stopped and the patient resuscitated, then the anaesthetist and surgeon are invited to take the patient to theatre/operating room

Some of the slides:

Audio only:

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