Category Archives: Podcast

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

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

Calming the Hulk: Sedating and Restraining Aggressive Patients



Take home points

  • Always try to find the cause of agitation and talk the patient down if possible.
  • Call for security or police early.  Better to over-call than under-call.
  • Sometimes it is good just to step back and wait.  Sometimes you need to intervene early before things escalate further.
  • You have a responsibility to restrain / sedate unwell or injured patients who may be a risk to themselves or others.
  • Ketamine is a great sedative but it is not generally accepted for behaviour control yet, especially by unsupervised junior doctors.  If you are in a small hospital with no seniors on site – phone a senior for advice, if time allows.  Once you have given someone ketamine you are committed to finding the cause of the agitation and to keeping them sedated, usually overnight, until the precipitant has worn off.  You don’t want them waking up from a bad ketamine trip on your shift.
  • Haloperidol is a good sedative and doesn’t cause airway or respiratory depression.  This is particularly useful when the patient has a large quantity of airway depressant on board eg alcohol ie most aggressive people in Australasian EDs
  • Benzodiazepines are good sedatives but may cause loss of airway control and respiratory depression especially for patients with lots of alcohol onboard.  Benzodiazepines are the drug of choice for alcohol withdrawal and for agitation due to stimulants such as methamphetamine.
  • Often we use haloperidol and midazolam – probably without good reason
  • If you need to take a patient down get as many people to help as possible – preferably 5 + one ready with sedative medication.  Failing that a rugby tackle may work.
  • Don’t restrain patients face down – they may suffocate.
  • If you have given the patient lots of sedative put them in the recovery position and monitor their oxygen saturation continuously.  They will need one-on-one nursing until you are happy the patient can safely maintain their own airway.
  • If using physical restraints (eg leather wrist and ankle straps) use chemical sedation as well to ensure the patient isn’t straining against the restraints (which could make them more agitated and may rarely lead to rhabdomyolysis).  In many hospitals use of physical restraint needs to be recorded on particular forms and obs documented regularly.
  • It is acceptable to leave physical restraints on a patient overnight if you consider them to be high risk.
  • RSI is not good for first line behaviour control.  Sedate the person then, if needed to a “delayed sequence intubation” or DSI


Sometimes we have to restrain and sedate the crap out of aggressive patients.

In some hospitals we have little or no security assistance and doctors will be expected to take control of an aggressive patient.

The question is often asked: can we sedate or restrain a patient against there will if they don’t have a psychiatric problem? The answer is usually yes.

If you believe the patient may have a medical problem that’s putting themselves or others at risk, be it intoxication, head injury, sepsis, hypoxia or psychiatric disorder, you have a responsibility, also called a “duty of care”, to do what is needed to keep the patient and/or others safe.

If they are bad rather than sick or mad, you need to get police or security to deal with them.  If in doubt assume the patient is unwell.


The cases

Case One


A gang member in his 50s, 160kg of lard and muscle, was in ICU on BiPAP for an exacerabation of COPD.  I was called into help at 6am.  He was in the ED waiting room when I arrived.  We tried reasoning with him to no avail.  He was mildly agitated and sick of being in hospital.  The police sent one 60kg unarmed officer to help.

Another gang member arrived to collect the and we elected to allow him to leave – for our safety and so as not to inflame the situation.  We asked the associate to try and convince the patient to return.

The patient and associate returned 20 minutes later as the patient had become more short of breath.  He tolerated BiPAP and an IV line and we transferred him to ICU.

He was seen by the duty anaesthetist who wanted to place an arterial line but quickly backed off when the patient became stroppy.

He was given a small prophylactic dose of 3mg haloperidol.  A short time later he became agitated again, ripped off his BiPAP and was thrashing around and being quite scary.  His associate tried to calm him down.  We kept our distance and waited.

About 30 minutes later the patient was asleep or unconscious.  I snuck into his room and gave him a massive dose of IV ketamine.  I would normally give a patient 1mg/kg of IV ketamine to completely flatten them.  I gave this 400mg of ketamine.  I wanted to be sure he was dissociated quickly and completely.  He quickly woke up and looked like a sterotypical zombie: arms stretched out in front of him staring into space and looking confused.   We were able to get the BiPAP on him. 5 minutes later he was still moving.  I gave him another 200mg of IV ketamine and started a ketamine infusion at 200mg an hour, 5 mg IV haloperidol. He settled briefly.  5 minutes later he was getting agitated again and I gave him 5mg of midazolam.  Then he finally stopped moving and tolerated the BiPAP

We converted him slowly to fentanyl for sedation.  Fentanyl and/or propofol are probably the best medium term sedatives once you have the patient under control.  There is less chance the patient will wake up delerious than with ketamine or even benzodiazepines.

The patient needed to be heavily sedated for behaviour control and probably needed to be intubated as he was going to need ventilatory support for days.  The patient was in ICU so I needed to run this past an anaesthetist.   I spoke to the anaesthetist who had seen the patient earlier who suggested we needed to wake the patient up and have that discussion with the patient.  I invited him to have that discussion with the patient and went home to bed.

When I arrived for my shift a few hours later the patient was intubated.

I saw the pateint a few days later.  He recognised me, thanked me for caring for him.  He had no recollection of a bad ketamine trip.

Bottom line: some patients need massive doses of anaesthetics and sedatives to control their agitation so they can be safely managed.  For patients like this get senior help early.


Case Two

Later that day a man in his late 20s was brought in by ambulance and police, drunk after putting his arm through a window.  His father said the patient had only used alcohol.  The patient was handcuffed, agitated and abusive and bleeding quite a bit from a forearm laceration.  A CAT tourniquet was applied.  The patient was given 10mg IM haloperidol and 5mg IM midazolam with little effect.  10 minutes later he was given another 10mg IM haloperidol and settled.  He was kept on oximetry without supplemental oxygen.  He was restrained with leather wrist and ankle restraints.  IV access was obtained and further boluses of 10mg haloperidol or 2.5 midazolam were given as required.  A nasophyaryngeal airway was inserted.  His wound was loosely sutured then dressed to control the bleeding.  He was kept sedated and restrained overnight and then taken to theatre for definitive management the next day.

Case two could have been controlled with ketamine but I think it would have been overkill.  Case one needed to be immobilised completely, very quickly.  Partial sedation may have left him still able to inflict serious harm to staff.  I wanted an agent that worked quickly, totally immobilised him but wouldn’t stop him breathing.  Ketamine was ideal.


Case Three

A chap in his late 30s was in ICU with a delirium of unknown cause: toxicology screen, CT, LP, bloods were normal.  Formal toxicology and a brain MRI was pending.  He heard someone talking about the psychiatric unit and thought he was going to be sent there and went ballistic.  He hit 3 staff, made many holes in the walls and smashed a window with a drip pole.  Luckily the was a visitor in the unit his 50s who had been a rugby player in his younger days.  He did what was reported as a stunning tackle on the patient.

A bit like this one by one of my daughter’s friends:


I arrived a minute later.  The patient was being restrained by the visitor and a couple a male nurse.  The patient still had an IV line in place.  He was given 10mg of IV haloperidol, 5mg of IV midazolam which settled him well.  He was bound with leather restraints and charted PRN haloperidol and midazolam and a security guard was assigned to watch him.


Case Four

A 93-year-old was in an orthopaedic ward post hip replacement.  He was delirious and whacking everything and everybody in site with his crutches.

Old man scowls, leans forward and shakes his cane

We formed a 5 person team.   A sixth person was standing by with 3mg of IM haloperidol.  I was at the point of the chevron shaped formation, armed with a pillow to take the blows from the crutches.  The person on my left and right were assigned to an upper limb each, the people behind them were assigned to a lower limb each.  We heroically over powered the old gentleman and lowered him onto his bed.  The people on upper limbs grab a shoulder and a wrist.  The people on lower limbs hold a knee and ankle.  People are best held down on their backs as they have less purchase.  Avoid face down due to risk of suffocation.  If the patient is given lots of chemical sedatives it is best to have the patient in the recovery position if possible. The lead person quickly changes position and restrains the head to prevent biting.

We then did a thorough assessment to see if there was a cause for his agitation: hypoxia, fever, fluid overload inadequate analgesia, excess analgesia, full bladder.  Often it is just post operative delirium.

Post script

There has been a belief, which I have believed, that antipsychotics are slow acting in acute agitation.  This paper, discussed in Life in the Fast Lane Research and Reviews, argues otherwise:

“Calver L et al. Droperidol v. haloperidol for sedation of aggressive behaviour in acute mental health: randomised controlled trial. Br J Psychiatry 2014. PMID: 25395689

  • Although not widely available, droperidol is often used for the management of agitated delirium. This paper compares droperidol (10mg IM) in 118 patients vs. haloperidol (10mg IM) in 100 patients. Appropriate sedation within 120 seconds occurred in 92% of patients without differences between agents. While sedation with droperidol required less rescue doses, it also had higher adverse events (5% vs 1%).” [emphasis mine]


See also

Behavioural Emergencies by Kane Guthrie in Life in the Fast Lane


Grumpy old man image from

Meningococcal sepsis – lest we forget



Meningococcal sepsis and meningococcal meningitis

Meningococcal infections are something we don’t see often but we need to know about.  There was an outbreak in Suva, Fiji while I was there.

They may present with meningococcal sepsis, meningitis or both.  They may or may not have a rash.  They may or may not have neck stiffness.  They may or may not look sick.

When I was a young doc I almost sent a child home because who had a fever and purpura, but had no neck stiffness and was walking around looking fine.  Luckily the paediatrician I consulted decided to come in and see the child himself.

Papura can be easy to miss, especially in dark-skinned people: looks at the palms and soles for pupura and look at the conjunctivae and in the mouth, especially on the soft palate, for petechiae.

I treated one of the Suva patients myself.  She was a 22-year-old student from Vanuatu who had mild fever and myalgias the day before.  On the day of presentation she was found confused and hot and brought to hospital.  Her temperature was 38.5, HR 130, no palpable pulse, no BP, no sats reading, her neck was rigid and she had widespread purpura – but this was missed by a good local doctor.  She was alert but confused.  She did not vocalise or responding to questions.

She was given IV penicillin while we waited for ceftriaxone to arrive from pharmacy (consultant order required!).  Cefotaxime is the empiric therapy in some centres.  Neonates required different antibiotics (eg amoxycillin and cefotaxime) to cover maternal vaginal flora and those over 50 usually have ampicillin or amoxycillin added to cover Listeria.  Where there is a high incidence of penicillin resistant penumococcus vancomycin is usually added to the empiric antibiotics.


After 2L of IV fluid the local doc ultrasounded her: her IVC was not changing with respiration but her cardiac contractility was reduced.  He used M mode of the anterior leaflet of the mitral valve, see for example Minimum distance between the tip of the anterior leaflet of the mitral valve and the septum < 7mm represents good contractility, > 1cm shows poor contractility. She was started on an adrenaline (1mg in 1L of saline, running freely) while a noradrenaline infusion was prepared.  The noradrenaline quickly went up to 20mcg/minutes but the adrenaline wasn’t slowed for several hours.

She was also given intravenous steroids.  Hydrocortisone 50mg.  Starship Children’s Hospital recommends Dexamethasone 0.15 mg / kg 6 hourly for 2 days for children with presumed bacterial meningitis.

After about 4.5L of fluid she became tachypnoic and agitated – I thought we were going to have to ventilate – but there was no ventilator in ICU and no ventilator in ED and no ketamine. Fluids were slowed right down and luckily she settled.

Some would argue that once we saw her IVC was full we should of stopped the IV fluids and just used pressors, thus reducing the risks of volume overload such as ARDS.

A central line was placed.

Within 3 hours of arrival she was sitting up talking and saying thank you.

She was transferred to ICU.

She was transferred out of ICU approximately 24 hours after her arrival in hospital with no sequelae.

Last I heard there were 3 other meningococcal cases in the 6 bed ICU.

Here is some photos from one of them courtesy of Dr Krisneel Krishna




Typically this is a disease of the young – preschoolers and young adults, but my mother-in-law had it in her 60s.  She was found confused at home, and had no fever, no rash.

In New Zealand we do blood cultures and meningococcal PCR to confirm the diagnosis.  LP in this setting is controversial. There is little utility to doing a lumbar puncture and there are concerns that the patient could “cone” if they have raised ICP from the meningitis. Starship Children’s Hospital says that an LP is contraindicated in a child with meningitis who is “sick or has a rapidly evolving rash” or “haemodynamically unstable” or “GCS < 13”.

CSF can be sterilised within an hour of giving IV antibiotics, so by the time your patient has had their CT to rule out raised ICP it is not that useful to do a LP.  Administration of antibiotics should not be delayed till after the LP.

PCR can not give antibiotic sensitivities.

We didn’t do an LP on the young woman.





Monach by Shapeshifter

A Beginner’s Guide to STEMI Thrombolysis: 5 Minutes Door to Needle

The Case

A 57-year-old man was brought in by ambulance with 1 hour of left shoulder pain, nausea and feeling faint.

He had a history of obstructive sleep apnoea and recurrent low back pain.

Paramedics had given aspirin and clopidogrel, obtained IV access and called us saying probable inferior STEMI.

He goes into a resus bay and the team pounce on him: monitoring, ECG, a second IV line, bloods including a troponin, a very focused history and examination.

He is pale but his obs are normal.

These was his first ECG in ED.

Inferior STEMI

It shows an inferior STEMI.  Note the reciprocal ST depression in aVL which helps to support the diagnosis.

See STEMI criteria.

We don’t have PCI so he needed thrombolysis.  Generally we will thrombolyse anyone who meets ECG criteria, has had pain for less than 12 hours and doesn’t have contraindications.

As always, if you are alone at night (or any other time) trying to make this big decision, scan and email, or text a photo of the ECG to someone else for a second opinion.

Contraindications to Thrombolysis

We quickly checked that he didn’t have any contraindications to thrombolysis. You can use a check list for this:

Absolute contraindications
History of any intracranial hemorrhage
History of ischemic stroke within the preceding three months, with the important exception of acute ischemic stroke seen within three hours, which may be treated with thrombolytic therapy
Presence of a cerebral vascular malformation or a primary or metastatic intracranial malignancy
Symptoms or signs suggestive of an aortic dissection
A bleeding diathesis or active bleeding, with the exception of menses; thrombolytic therapy may increase the risk of moderate bleeding, which is offset by the benefits of thrombolysis
Significant closed-head or facial trauma within the preceding three months
Relative contraindications
History of chronic, severe, poorly controlled hypertension or uncontrolled hypertension at presentiaton (blood pressure >180 mmHg systolic and/or >110 mmHg diastolic; severe hypertension at presentation can be an absolute contraindication in patients at low risk)
History of ischemic stroke more than three months previously
Any known intracranial disease that is not an absolute contraindication
Traumatic or prolonged (>10 min) cardiopulmonary resuscitation
Major surgery within the preceding three weeks
Internal bleeding within the preceding two to four weeks or an active peptic ulcer
Noncompressible vascular punctures
Current warfarin therapy – the risk of bleeding increases as the INR increases
For streptokinase or anistreplase – a prior exposure (more than five days previously) or allergic reaction to these drugs


So key screening questions to ask your patient:  Are you prone to excessive bleeding, have you ever had anything unusual happen to your brain like a stroke or head injury, does your pain radiate to your back, is it tearing, was it most severe at onset, have you been in hospital in the last 3 months, what medications are you on, could you be pregnant?

Check their blood pressure, check both radial pulses, listen for aortic regurgitation from a thoracic aortic dissection

Treatment Agreement

Discuss the risks and benefits with the patient.

Benefit: one life saved for every 43 people treated within 6 hours of onset of pain  (there are likely to be more who have no or reduced heart failure or angina due to treatment).

Harm: One in 250 recipients will have a haemorrhagic stroke – usually fatal.  2 of the patients I have thrombolysed have bled into their brains and died.  It isn’t pleasant.  There is also risk of other serious bleeding.  If the patient has any of the relative contraindications their risk of bleeding may be highter.


We usually use tenectoplase.  Some recommend streptokinase for the elderly as it is associated with a lower rate of intracranial bleeding.

For tenectoplase:


Inject the 10 ml of water from the syringe into the bottle with the powder then mix.

tenectoplase gear connected verticle

Tip the bottle and syringe upside down and draw out the required volume of the mixture.  The weight-adjusted dose is on the syringe. Our patient was over 90kg so he got the full 10ml = 50mg.

tenectoplase syringe verticle


Weight (kg) tenecteplase (IU) tenecteplase (mg) Volume of reconstituted solution (mL)
< 60 6,000 30 6
60 to < 70 7,000 35 7
70 to < 80 8,000 40 8
80 to < 90 9,000 45 9
90 and up 10,000 50 10

Give it as an IV push over 5 seconds

Other treatments

Give aspirin and clopidogrel if not already given.  Dose of clopidogrel with thrombolysis is controversial.  We currently use 300mg.

Give 30mg IV enoxaparin (omit if > 75 years old or known GFR < 30). Then 1mg/kg SC enoxaparin (0.75mg/kg if patient over 75, max 75mg).

Then we gave him small boluses of fentanyl.  I’m a little cautious with the opioids with inferior ventricular infarcts. They might have right ventricular infartion as well (see below).  I don’t want to venodilate the patient too much.  That would decrease his right ventricular preload and therefore his left ventricular preload.

After 40mcg of fentanyl he was painfree and back to a normal colour.  About 15 minutes post tenectoplase his inferior ST elevation had reduced to ~ 1mm.

Treatment Failure

If his pain persisted and 60-90 minutes post tenectoplase his ST elevation was still > half of what it had been at its largest this would count as failed thrombolysis.  Patients with failed thrombolysis are candidates for urgent transfer for PCI.  Some argue that all STEMIs in peripheral hospitals should be thrombolysed and flown urgently to a PCI capable centre so that they can receive PCI if thrombolysis fails.  This is not the practice in our region.

Door to Needle Time

I was a little disappointed our door to needle time was 5 minutes. We can do better,  eg we could have had the tenectoplase at the bedside before the patient arrived.

Supplementary ECGs

For interest, after thrombolysis, we also did a right-sided and posterior ECG.

We always do right-sided leads if there is inferior ST elevation looking for a right ventricular infarct. We do a posterior ECG when there is anterior ST depression looking for a posterior STEMI

His right-sided ECG (V4, V5 and V6 put on to the R side of the chest) showed ST elevation in V4R and V5R showing right ventricular infarction

RV infarct

The posterior ECG didn’t show any posterior ST elevation.  So this is an inferior and right ventricular STEMI.

Delayed ST Elevation

One last point:  If your patient has chest pain and a normal ECG, then develops ST elevation in front of you: thrombolyse, no matter how long they have had the pain.



Thrombolysis contraindications from UpToDate

Tenectoplase dose

Risks and benefits of thrombolysis from the NNT

Whanganui Hospital ACS Guideline.


Music on podcast:  Release by Afro Celt Sound System

A Beginner’s Guide to Procedural Anaesthesia in ED

Procedural anaesthesia is providing IV anaesthesia to allow a painful procedure to be performed.  Very rarely it will be performed to rapidly control dangerous behaviour.

It has also been called conscious sedation or procedural sedation but usually we don’t want our patient to be conscious and we want them to be anaesthetised, not just sedated.  These terms are largely hangovers from the past when we had to pretend we weren’t really doing anaesthesia in ED.

We don’t usually count giving up to 70% nitrous oxide within the realms of procedural anaesthesia as there is very low risk of loss of airway with just nitrous oxide.

Generally the procedure is very similar to performing a rapid sequence intubation (RSI) just smaller doses of drugs are used, we don’t use paralytics and we don’t stick a tube in the trachea.  Otherwise the set up and monitoring is very similar.  This is a bit of over kill for procedural anaesthesia, but it ensures you have all the equipment, staff and drugs you need if anything goes wrong, and it’s good practice for the set up for RSIs so it keeps the team slick.  You can even use the first part of your RSI check list to set up for procedural anaesthesia, modifying it as required.

part RSI checklist

This will make sure you remember all the equipment and steps and will keep everyone familiar with your RSI checklist.

Written Treatment Agreement

Unless this is an emergency procedure eg unstable tachyarrhythmia, procedural anaesthesia requires a written treatment agreement or treatment request form (commonly know as a Consent Form).

You need to disuss and document the risks and benefits of the procedure and the anaesthesia. Risk of anaesthesia are: experiencing of pain, nausea, vomiting, inhaling vomit, confusion, hallucinations (depending on the agent used), allergic reaction to drugs, stopping breathing.  With any anaesthesia there is a tiny chance of death.   The benefits of anaesthesia is that it usually a pleasant, pain free experience with no recollection of the painful procedure.

You may want to make a pre printed treatment agreement form with all of the above alreay on it.


Any bay with suction, oxygen and monitoring could be used.  In our hospital we use a resus bay as has all the gear in it already, and again it helps with team familiarisation with RSI procedures.


Generally we like to have at least 3 staff for procedural anaesthesia.  An appropriately qualified doc to perform the anaesthesia and watch the patient.  A nurse as super can do everything person, helping with preparation, advocating for the patient and monitoring the patient.  They can help with the procedure being performed while keeping an eye on the patient.  The third staff member is usually a doctor performing the procedure itself.  You will need to check what your institutions rules are regarding how many staff are required and what the skill level required is. Generally the doctor performing the anaesthesia will be senior ED registrar (resident) level or above. ACEP allows just 2 staff members to be present, it does not require that 2 doctors are present.

If a consultant is performing the anaesthesia they may briefly help with the procedure while still closely watching the patient.


The choices of medication(s) varies with every consultant and often will vary depending on the patient and procedure.  Ask the team leader what they want.

For procedural anaesthesia we are aiming for that sweet spot where the patient is maintaining their airway, breathing spontaneously has a good cardiac output yet has no or minimal experiece of pain.

All medications need to be double checked and labeled (prefilled, prelabeled syringes of medication are ideal) and placed tidally in a tray.

Medication is administered by the doctor performing anaesthesia or by a nurse following the doctor’s direct instruction.

Some docs will push the whole predicted dose of anaesthetic, others prefer to titrate slowly eg asking patients to keep their eyes open or to hold one arm up in the air and stopping drug administration when the eyes close or the arm drops.  I prefer to push the predicted dose. Generally we will have more than the predicted dose drawn up in the syringe to allow for top up doses.  Doctor’s must make themselves aware of what is in the syringe.  We have had 2 episodes of doctors getting over excited and just pushing a whole syringe of the white stuff thinking the syringe contained the predicted dose only.


Also known as Jackson Juice.  For a very brief procedure eg cardioversion, shoulder or hip relocation, often just propofol will be used.  eg 1mg/kg for a young person, down to 20mg for a 90 year old.

Propofol and Ketamine

For longer or very painful procedures often a combination of ketamine and propofol are used.  This may be in a fixed mg:mg ratio (know as ketafol) or titrated separately.


These drugs work well synergistically.  Propofol gives good anaesthesia and is antiemetic, it’s down side is that it can cause loss of airway reflexes, hypoventilation and hypotension.  Ketamine is very analgesic and dissociative anaesthetic usually with maintained airway, breathing and circulation but can cause unpleasant hallucinations and nausea and vomiting.  The combination allows lower doses of each agent and they negate each others negative effects.

As always doses need to be reduced in the elderly.  Good anaesthesia for cardioversion for an 89-year-old can be achieved with 20mg of ketamine and 20mg of propofol.

For a young person for a quite painful, longer procedure, eg MUA and plastering of a fracture, I will typically give 0.8 mg/kg of propofol and 0.8 mg/kg of ketamine.  If further doses of anaesthetic are needed I will usually just give boluses of propofol alone eg 0.2mg/kg, rather than giving further doses of ketamine to reduce recovery time and to reduce the adverse effects of ketamine.  But every patient is different and you need to be flexible titrating against respirations and response to pain.  It is reassuring that even when patients appear to be experiencing pain they only occassionally remember cardioversions but it seems they never remember the MUAs or I+Ds

I am not in favour of ketamine only anaesthesia.  I have had too many patients, even ones who said as they woke up “Wow, that was amazing”, stop me in the supermarket a week later and say “Hey doc, that drug was awful.”  One of our anaesthetists tells us of having ketamine only anaesthesia then spending the whole night hallucinating he was being repeatedly run over by cars.  A tad unpleasant.

I do rarely use ketamine only anaesthesia for rapid control of dangerous (to themself or others) patients eg ketamine 5mg/kg IM.


Especially when ketamine is used it is good to add an antiemetic eg ondansetron 4mg or 0.15mg/kg.

Other medications

There are many other drug cocktails used.


AMPLE history

Allergies (especially to anaesthetic medication)


Past medical history (yes, I know that is redundant) especially anaesthetic history, family history of anaesthetic problems, obesity and reflux



In my opinion this patient is not a candidate for ED procedural anaesthesia.  I gave him 100µg IV fentanyl and 70% nitrous but we couldn’t get his shoulder relocated.  He went upstairs.  (Turned out an anaesthetist with large gonads just gave him a truck load of propofol and face mask ventilated him while a very good ortho reg struggled for 15 minutes to relocate it).

Obese patients are our nemisis.  They occlude their airways at the drop of a hat, they are difficult to ventilate or intubate and they are high aspiration risks.  Just don’t go there for procedural anaesthesia unless it is emergent eg haemodynamically unstable arrhythmia.  Let someone else take that risk.

Last ate or drank, the patient does not need to be fasted according to ACEP, but we may modify things if we know he’s just had 10 beers.

Events: make sure you know the full story about this patient before you put them to sleep.  Is that dislocated shoulder actually attached to a broken neck?

Airway exam

Feel the neck, identify the cricothyroid just in case it all turns to custard.  Assess neck mobility and thyromental distance.  We want4 of the patients fingers (guestimate with your own fingers) between the top of the thyoid cartilage and the bottom of the front of the mandible with the neck extended.  Make sure the patient can protrude their lower teeth infront of their upper teeth and that the mouth opens wide (at least 3 of their fingers (again guestimate with yours if necessary), how much of the oropharynx can you see:

See Mallampati score

Is their anything on their face that would make them hard to ventilate with a BVM?


If the patient is obese ramp them so their tragus is higher than their manubrial-sternal joint (blue line in the picture below)

If you are dealing with a lesion on the patient’s back put the patient on their side, not face down.

While you are positioning the patient refresh you memory regarding the bed controls: work out how to tip the patient head down if they vomit

IV Access

One good IV or IO line is enough for procedural anaesthesia.  Make sure it is well secured.

Cautionary tale: beware the IV line in the foot. Some of my colleagues in a land big and red were anaesthetising an elderly patient for a cardioversion.  They gave some propofol, then some more propofol, then some more.  Eventually all the propofol made it to her heart and brain and she had a PEA arrest.  They had the good sense to cardiovert her and give good CPR till the propofol wore off and she made a full recovery.

Some people have IV fluids running (which reassures us the IV line is working and can be used to flush drugs) others find this to be another tube that gets in the way and is probably unneccessary.  Ask your team leader.


It’s OCD overkill time.

Size and have out on top of the resus trolley (or under the pillow) all of your airway equipment:

Suction – tested


Oropharyngeal airway

Nasopharyngeal airway

Supraglottic device (eg intubating LMA)

Scalpel (I always keep one in my pocket while at work too)



Bag-Valve-Mask (BVM)

Capnography tubing (we don’t routinely use this in our hospital for procedural anaesthesia as the powers that be have decided the consumables are too expensive, but have it out and ready to be used)

Laryngoscopes – tested

On the patient:

Nasal prongs oxygen running at 2L a minute till they are asleep then crank it up to 15L/min.

Non-rebreather oxygen mask with high flow O2.  3 minutes of preoxygenation.

Monitoring x 3 or 4  (depending on whether your hospital uses capnography (see above)

Audible oximetry (“the beeps”)

BP set to go every 2.5 minutes

ECG monitoring

+/- capnography depending on your hospital’s policy

The above rigmarole sounds complicated but takes very little time for a well trained team.

Push or titrate drugs

It’s finally sleepy time.

The anaesthesing doctor, or delegated nurse, pushes or titrates the anaesthetic drugs (see above)

Further top up doses may be required

Procedure, monitoring and apnoeas.

The patient is closely monitored and the procedure is performed.

Have a decent amount of chest and belly exposed so that you can watch the respirations.

Don’t panic if the patient stops breathing.  With the above preparation they will be able to tolerate a long period of apnoea.  If needed you can ask the doctor performing the procedure to inflict some pain or you can do a firm jaw thrust and the patient will usually start breathing again.  If not grab your BVM and start ventilating.  Use other airway adjuvants as needed.  Nasopharyngeal airways are very well tolerated and will sort out most airway occlusions.


The anaesthetic is not necessarily over when the procedure is finished.  Especially if opioids or benzodiazepines are used this can be the most dangerous time for apnoeas – the pain has stopped but the drugs are still onboard.

The patient must have one-on-one observation until they are talking clearly.  Once they are talking take the oxygen mask off just in case they vomit.  Have a vomit bowl handy.  Once the patient is talking they should be kept on monitoring (reduce the BP frequency to  q 15 minutes) and watched by reliable family.

The patient is fit for discharge when they can walk independently (or the equivalent for their age and abilities).

Give them verbal and written advice not to drive or operate dangerous machinery until after a full nights sleep and to phone ED if they have any problems.


Ketafol evolution

Facial piercings

Ramped patient

Contagious Calmness. Mindfulness at Work

By practicing mindful meditations we can find calmness within us and then bring this into our work.

We may find that the calmness starts to spread and appears in unexpected places.

Be the calmest person in the room no matter what is going on.

Focus on the people around you, patients, family, workmates, as a way to stay focused on the here and now, rather than lost in thoughts and worries.

Be patient with yourself. It takes time and practice to master these techniques.

Power of Now

The Power of Now is a great book for you, colleagues and / or patients.

Mindfulness for beginners

Some short guided mindfulness meditations from Prof Kabat-Zinn’s book Mindfulness for Beginners are here


Music from podcast: Lydia by Fur Patrol

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


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.



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: