Engage your brain when reading ECGs

Click on ECG to enlarge

Fast AF

An 80 year old presented with mild nausea and shortness of breath.  His vital signs were normal other than the tachycardia.

He had a history of chronic atrial fibrillation, moderate chronic kidney disease and type 2 diabetes.

This ECG was given to a doctor to interpret

The doctor correctly identified that there were no signs of an MI, signed off the ECG and left the patient in the queue to be seen.

An hour later the patient was seen by another doctor.  By this time the patient’s heart rate was still 170, his blood pressure was sagging and the was febrile.

10 minutes later the patient’s blood pressure was 80/60.

His lactate was 6.0

No septic source was found but the patient had a history of multiple abdominal surgeries and a colostomy and similar episodes which grew enteric bacteria.  It is presumed that he has episodic bacteraemia from his gut.  The surgeons understandably were not keen to go hunting for a surgical remedy.

He was started on broad spectrum antibiotics to cover gut flora (cefuroxime and metronidazole), given IV fluids and started immediately on a vasopressor.

We chose to use phenylephrine in the hope that it’s alpha receptor agonism would cause vasoconstriction and cause a reflex drop in heart rate (rather than using a mixed alpha and beta agonist such as noradrenaline).  You could equally argue that noradrenaline would give some Beta 1 mediated inotropy which may have increased cardiac output and thus led to a decreased heart rate.  Often it is trail and error to see what works for a particular patient.

A vasporessor was used straight away as it was thought an 80 year old heart would not tolerate sepsis and a HR of 170 for long.

This patient’s heart rate and BP improved fairly quickly but if they hadn’t we get into the tricky situation of needing a negative chronotrope (to reduce the rate) but most negative chronotropes also drop the blood pressure.  In this setting most clinicians will use diltiazem, though a beta blocker has as much evidence for it.  Some will use IV digoxin, though most argue this takes too long to work.

Moral of the story

Engage your brain when reading ECGs.

You are not only looking for myocardial ischaemia – ECGs can tell us a lot about other badness.

This ECG was screaming “This patient is sick, or is going to become sick very soon”

Old hearts can not tolerate going at 170/min for long.  This is an old cardiovascular system attempting to compensate for badness, maxed out and about to decompensate.

For someone in fast AF always looks for a driver eg sepsis, congestive heart failure, thyrotoxicosis (rare and it is debated whether we should look for it).

This ECG should have led to a fairly immediate bedside review of the patient.


Music (on the podcast:

Fire by Sol3 Mio https://itunes.apple.com/nz/artist/sol3-mio/id732813196

Health Professionals need to ensure TPPA / TTIP do not harm public health


A lot of this will have parallels with the European/US “trade deal” the TTIP.  This article specifically address the Pacific version, the TTPA, as this is the one that could effect my community.

The TPPA is opposed by

  • The World Medical Association
  • The World Federation of Public Health Associations
  • The NZ Association of Salaried Medical Specialists (ASMS, senior doctors’ union)
  • The NZ Nurses Organisation (nurses union) and
  • Multiple professors of public health policy. (1)
  • The Australian Medical Association (2)
  • Médecins Sans Frontières (3)

  • Consumer, Oxfam and Greenpeace (4)

The Trans Pacific Partnership Agreement is a “trade deal” with ominous implications for health.

Some of the most concerning implications would be the ability of corporations to sue governments, health boards, schools etc for what they see as anticompetitive practices eg buying a cheaper medicines, banning soft drinks in schools, requiring plain packaging of cigarettes, banning alcohol sponsorhip in sport.  The TPPA also proposes significantly longer patents on medications.(5)

Even if the legal arguements are spurious a wealthy multinational corporation and its lawyers  could bankrupt a school or a small country like New Zealand with legal costs, or just fatally slow any public health measure.

Health Professionals have a Duty to Advocate for Public Health

eg From the ACEM curriculum for emergency medicine specialists:  “a FACEM will be able to use their expertise and influence to protect and advance the health and well-being of any individual patients, communities and populations.”(6)

But What About the Benefits?

The US Department of Argiculture estimates the best case for New Zealand from lowered tarrifs is an increase GDP of 0.01%.(7)  The real benefits are likely to be a lot less.  Not worth the risk.

Why would our policiticans support the TPPA if is potentially harmful?

A generous answer is that they want to maintain a strong Western alliance against the threat of Chinese economic power.  Other answers are so that they can keep playing golf with the US president, and of course the multinational corporations have huge amounts of money to lobby politicians with meetings in exotic locations, dinner, wine and promises of well paid jobs when they retire.

 What you can do

Educate yourself eg read the references below.

Financially support the legal challenge to the secrecy of the TPPA documents.  https://givealittle.co.nz/cause/tppnosecrecy

Join Doctors for Healthy Trade https://www.facebook.com/DrHealthyTrade?ref=ts&fref=ts

Support / encourgage your union to advocate for public health.

Email your minister of health and local member of parliament and professionally express your concerns.

Stay uptodate with protest action eg https://www.facebook.com/groups/TPPActionGroup/?fref=ts

Join a protest:

TPPA wellington march

I’m the guy in the red scrubs.

Who knows if it will work, but sitting on the couch won’t stop this menace.

Dr Chris Cresswell

Emergency Physician and Whanganui Branch President ASMS


New Zealand




1  Freeman et al.  Call for transparency in new generation trade deal. Lancet. 2015 Feb 14;385(9968):604-5  http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2815%2960233-1/fulltext?rss%3Dyes

2 https://www.mja.com.au/insight/2015/4/trade-deal-health-concerns

3 http://www.msfaccess.org/spotlight-on/trans-pacific-partnership-agreement


5 eg http://www.theguardian.com/australia-news/2015/feb/23/medicines-forecast-to-cost-taxpayers-millions-more-in-secret-tpp-trade-deal

6 https://www.acem.org.au/getmedia/a5e86d4e-3c85-4307-bcf0-c6162ea1c340/ACEM_CurriculumFramework_V2_FINAL-17-February-2015.pdf.aspx  page 42



DSI for Respiratory Failure



Delayed Sequence Intubation should be well-known by now, but it isn’t.  I was interviewing an emergency physician who was applying for a job here and took him through the case that follows – the applicant wanted to do a crash RSI.  So last decade!  :-(

The Case

A 64-year-old male with a history comes to ED with SOB and wheeze, like his usual COPD but worse.

His usual level of functioning is OK: he is able to walk around he supermarket, is independent for ADLs and isn’t on home O2.

He has markedly high work of breathing: he is tripoding, using accessory muscles +++.  He has generalised wheeze with reasonable air entry.

He is given continuous oxygen driven nebulisers, his sats are 94%, band he is getting worse not better.  200mg IV hydrocortisone is also given.

He is tried on BiPAP at various settings starting at 10/4.  He is getting excellent tidal volumes but is getting more agitated.

We are starting to get nervous.  Are we missing something?  Is some thing else going on?  Most people at least feel a little better on BiPAP.  We discuss as we are going and we think it’s probably just COPD, either way this guy needs ventilatory support.

He is given 0.5mg IV lorazepam to calm him (and therefore us) down but he becomes more restless and wanting to pull the mask off, sats drop to 86%.

A quick chat with his partner: “Would he want to have a machine breath for him for a few days?”  Answer: “Yes” (The patient is no longer competent to answer this question.  The partner can not make the decision for him, but she can help inform our decision of what action is in the best interests of the patient.

It’s DSI time

Delayed Sequence Intubation is sedating a patient so they can be prepared for, then safely intubated.  We use DSI rather than RSI (rapid sequence intubation) when the patient is not in optimal condition for RSI because of poor compliance with preoxygenation / preventilation or because of behavioural challenges (see Calming the Hulk).  In these situation a “crash RSI” may mean the patient crashes due to poor preoxygenation / ventilation, or we are just too rushed and don’t have all our gear ready, or our team is just too busy holding the patient down.

So this patient was given 100mg of ketamine (a little over 1mg/kg for this patient), he then “dissociated” (some where in there is an awake human – but he isn’t aware of what is going on around him), he keeps breathing spontaneously and now tolerates the BiPAP.  Everyone in the room calms down and there is less chance of error.

We put a nasal cannulae on under the BiPAP mask and turn that up to 10L/minute.  After about 3 minutes his sats have climbed up to 100% and we are confident we have denitrogenated his lungs.

We then go through our RSI check list to make sure we have everything ready.

We give the patient some extra anaesthetic to make sure the endotracheal tube doesn’t distress him.  We could use more ketamine.  The doctor running this case chose to give the patient 20mg of etomidate.  He was then given 100mg of suxamethonium (100mg of rocuronium would have been equally as good), the BiPAP mask was left on and the patient was gently ventilated by the BiPAP machine at it’s back up rate, then when the relaxant has had 20 -30 seconds to work, the BiPAP mask is removed, he is still being oxygenated via the nasal prongs, and he was intubated easily and quickly.

Hold on,  don’t run away.  The job is only half done.

Post Intubation Management


Check the tube: fogging, chest movement, bilateral air entry and good square waves on the capnography, O2 sats and request a CXR

Secure the tube, suction down the tube, place an NG tube.


Vent settings: for this guy TV of 6ml/kg ideal body weight, RR say 8 (this is called a lung protective stratergy as it reduces the risk of barotrauma, yes his CO2 will stay high, or may even climb = this is called permissive hypercapnia and is acceptable), minimum PEEP, in our case 5cm (but we might remove the PEEP if BP drops too much),   Check the X-Ray: position of tubes (tip of ETT below the bottom of the clavicles and above the carina), rule out pneumothoraces


Will probably need some fluids, may need some pressors.  Usually aiming for MAP > 65mmHg


Analgesia.  Fentanyl eg 1 mcg/kg/hour titrated to keep him comfortable and chilled.  A sedative like propofol may be necessary as well, but lead with opioid.


Ensure he is not too hot or cold


Check the NG tube is in the right place.  Ensure the belly isn’t distending.  Check the blood glucose if not already done.


Refer to a medical or respiratory team and a critical care physician or anaesthetist.


He was extubated a few days later and is doing well.



References and resources



Funky Rhythm II

Slow and irregular

Click here for the first Funky Rhythm post.

A 46-year-old male presented with shaking, sweating, general malaise, near syncope and one episode of foul diarrhoea.

He had Type 1 Diabetes with every complication and was on haemodialysis with his last dialysis session 3 days prior, next session due in several hours … in a different city.  We don’t have a dialysis unit in our town.

His obs at triage were normal other than a blood sugar of 12mmol/L.

It was a crazy busy day and he didn’t get hooked up to a monitor straight away.

Some 40 minutes later he complained of feeling faint and his RN noted his HR was 25.

She notified the RMO who rightly requested an ECG

Slow and irregular

Click on the image to enlarge


What is the diagnosis?

He correctly assumed that this was severe hyperkalaemia: slow, no p waves, slightly widened QRS and pointy T waves.


How would you assess and manage this patient


Resus bay, IV access, urgent blood gas to get K+ level.

Stabilise the membrane

Adult 2.25–4.5 mmol calcium (10–20 mL calcium gluconate 10% injection) with plasma-calcium and ECG monitoring (risk of arrhythmias if given too rapidly), and either repeated as required or, if only temporary improvement, followed by a continuous intravenous infusion.

Move Potassium intracellularly

Salbutamol 10mg nebulised

100 mL of 50% glucose (dextrose) IV over 15-30 minutes plus 10 units actrapid insulin IV

and / or

100 mL of 8.4% sodium bicarbonate (100 mmol) over 4 hours if metabolic acidosis and provided patient is not fluid overloaded (HCO3 probably only works if acidotic – most dialysis patients are chronicly acidotic)

Remove the potassium:


Forced diuresis (ie give IV fluids) if the patient makes urine and isn’t over loaded.  Some people give frusemide if the patient is able to make urine.

Resonium is seldom used now due to concerns re safety and efficacy.




Back to the case

We gave him 2.25g =  10ml of calcium gluconate over a minute which did nothing. We moved him to a resus bay (not for any good reason – just a bit more room and a few more toys).  We considered if there was another diagnosis.  He was on diltiazem but he was adamant he hadn’t had excess of these.

The patient had a huge smelly diarrhoea which was expertly cleaned up by super RN Kim then she was back doing drugs and ECGs without missing a beat.

We gave another 10ml 2.25g =  10ml of calcium gluconate over a minute and his rhythm normalised, he felt hot all over but much better.

Post Ca


Calcium can be repeated until the QRS duration normalises (<120ms)

We gave him 50mmol of Na HCO3 over a few minutes.

We gave him IV glucose and insulin (I elected for 10% dextrose at our hospitals standard rate for most things of 80ml/hour as he was going to be dialysed soon and so I wasn’t too concerned about volume) and insulin infusion – we didn’t give him a 10 unit load as he had already had some long and short acting insulin that morning.  Probably would have been more useful to give him the 10 units – we could always give more glucose if needed.


His K was 8.6.

His bloods and CXR and his physical exam didn’t show  a focus of infection other than the diarrhoea.

We then arranged for the 1 hour road transport to dialysis.

If we had a dialysis unit upstairs I would have just given the salbutamol and the calcium and then transferred him up. for urgent dialysis

And later that evening he was discharged home.  The dialysis unit was not too concerned about his symptoms or his K level – they see this sort of thing all day every day, usually due to eating a lot of potassium rich foods.

Thresholds for Treatment

Widened QRS (> 120ms) (unless this is old) or K > 7.5

=> Calcium and salbutamol and all the following

K 6-7.5

  • Stop renal toxins or K supplements esp ACEI, NSAID, KCL, K sparing diuretics
  • Rehydrate if dry.  Be cautious if patient anuric
  • Ifoliguric or not reversible cause found
    • 100 mL of 50% glucose (dextrose) IV over 15-30 minutes plus 10 units actrapid insulin IV, or
    • 100 mL of 8.4% sodium bicarbonate (100 mmol) over 4 hours if metabolic acidosis and provided patient is not fluid overloaded.

Top Tip

If a dialysis patient comes in mildly unwell: do an ECG

References / Resources

NZ Formularly http://nzf.org.nz/nzf_5278#prepg

Management Guidelines for Common Medical Conditions  “The Blue Book”  15th Edition 2013  http://bluebook.streamliners.co.nz/

ECG features of Hyperkalaemia http://lifeinthefastlane.com/ecg-library/basics/hyperkalaemia/

Hyperkalaemia Management http://lifeinthefastlane.com/ccc/hyperkalaemia-management/

Music on podcast

Te Rau Arohoa by Ihirangirangi / Te Amakura http://teamokura.nz/

Audio from the podcast

Headspace Meditation app

One of our doctors recommended this app for one of my friends who is a nurse and is a bit … frenetic.

Here’s the introduction video

Here is an excerpt from session three of Take 10.

If you want some help to cope with the stress of work, or of life in general, or you want to boost your performance in your work, try meditation.  Headspace is a great place to start.

Get the app here

Other resources

Mindfulness for Health Professionals

Contagious Calmness: Mindfulness at Work

It is normal for BHCG to fall in early pregnancy

A woman was seen in ED with bleeding in early pregnancy.

Her ßHCG had fallen from 95,000 to 50,000 over 2 weeks.

On the basis of this she was told she had miscarried.

The next day she had an ultrasound which showed a viable pregnancy.

It is normal for ßHCG to fall in early to mid pregnancy.


In our shop if a woman presents with threatened miscarriage we will rule out a life threatening miscarriage or ectopic pregnancy:

  • Haemodynamically normal
  • No foul-smelling discharge or fever to suggest a septic miscarriage
  • No peritonism
  • Pain not localised to one side or the other
  • Not bleeding lots – eg bleeding able to be controlled by hourly changes of pads
  • Patient lives within say 30 minutes of hospital

If she passes all of the above we will usually discharge with advice to return if she is gushing blood, feeling faint or has severe pain.  Give paracetamol and a weak to moderate opioid for pain (not a NSAID in early pregnancy)

She will be asked to return in the morning to Early Pregnancy Clinic (EPC)

Our EPC and ultrasound doesn’t run on the weekends so often one of the ED senior docs will do a bedside ultrasound to try to confirm an intrauterine pregnancy.  If we can’t we might get the woman to return to ED or EPC in 2 days for repeat ßHCG and repeat scan.

Image from http://www.glowm.com/section_view/heading/Development%20and%20Physiology%20of%20the%20Placenta%20and%20Membranes/item/101

Defibrillation with paddles – Old Style Shocking

One day you may find yourself working somewhere with a defibrillator that uses paddles instead of adhesive pads, because the health system of that country cannot afford the cost of single-use defibrillator pads.



You may also find that your team takes an awfully long time to first shock because they are mucking around trying to read the rhythm through the monitor or defibrillator leads, rather than through the paddles.

So key points to using an old school defib:

You need to familiarise yourself with the machine(s) in use in your setting.

All defibrillators should default to reading through the paddles or pads.  If not you will need to change the lead to “paddles” or “pads” on the defibrillator

Some defibrillators have a single button (the yellow button in the photo above) which charges the defibrillator. Some defibrillators are charged by depressing the same two buttons used to deliver the shock.  Alternatively you can ask someone else to push the “charge” button on the defibrillator machine.

Put gel on the paddles.

Put the paddles on the patient’s chest.

Charge the defibrillator as soon as the paddles are on the chest.

While charging read the rhythm (via the paddles) on the defibrillator screen.

Stop CPR briefly while you read the rhythm.

If it is a shockable rhythm, deliver the shock as soon as charging is complete.

Recommence CPR as soon as the shock is delivered.

Here is a video of some Fijian doctors resuscitating our old friend Annie with an old-school defibrillator with paddles.

By getting them to change to reading the rhythm through the paddles rather than via the leads, time to defibrillation was reduced from about 2.5 minutes to 40 seconds.

At 0300 the next morning some of the doctors were able to put this into practice and got ROSC (return of spontaneous circulation) on the second shock.

Productive Cough and Right Lower Zone Dullness

A 30-year-old indigenous Fijian male presented to a Fijian emergency department with several days of productive cough and lethargy.  He had normal vital signs and had decreased air entry and dullness to percussion at the right base.

This is his CXR



I thought this was a right lower lobe pneumonia and would have treated his as such.

One of the good local docs, Vivek, put an ultrasound on the patient’s chest and found the real cause.

He then went on to CT.  This is a video of the CT captured by phone (this is known as “mobile PACS” (picture archiving and communication system): there are no computers in that ED for viewing images, clinicians go to radiology and take images on their phones and take them back to ED to share with the team).



Scroll down




This is a massive liver abscess with a small pleural effusion.  The productive cough was a red herring.  Liver abscess in Fiji are usually seen in young adult males and are believed to be due to amoebic infection from contaminated water used to prepare kava.  Kava is prepared from a local plant appears to have anaesthetic properties causing tingling of the lips and tongue and sedation.  It tastes like mud and probably should be tried once to keep your hosts happy.

A couple of times a week in this ED young men were diagnosed with liver abscesses.   They usually presented due to jaundice (this patient was not jaundiced) +/- mild right upper quadrant pain +/- fever.

Patients are treated with antibiotics eg oral metronidazole. Ultrasound is used to see if the abscess is fluctuant (ie changes shape with pressure).  If it is fluctuant the abscess is drained percutaneously.  If the abscess is not fluctuant the patient is treated with antibiotics for a few days until the abscess becomes fluctuant.

UpToDate says aspiration or drainage of amoebic liver abscesses is not usually required, but drainage of pleural effusions is recommended.  I don’t know why the practice in Fiji differs from this.  Maybe someone from Fiji can let us know in the comments.  Perhaps they have some with bacterial superinfection.  UpToDate recommends subsequently treating with paromomycin to eliminate intraluminal (within the gut) cysts.  UpToDate also reminds us that oral metronidazole has excellent bioavailability and there is little to be gained by IV treatment if the patient is able to take oral meds – and oral metronidazole is much cheaper.

So keep liver pathology in mind with a patient with right lower zone dullness / opacity, especially if they have recently travelled to a Pacific Island.

Approach to the CXR

When viewing a right lower zone opacity our radiologist recommends considering:

  • above the diaphragm eg pneumonia, pleural effusion, subpulmonary effusion
  • the diaphragm itself eg eventration, phrenic nerve palsy
  • below the diaphragm: eg hepatomegaly, liver abscess, subprenic abscess.

This CXR does not particularly suggest something subdiaphragmatic is going on, our radiologist had his money on a subpulmonary pleural effusion.

Tutorials for junior ED docs