Pacing in the ED

Authors: Daniel Haigh, Charlotte Davies, Jennifer Tremble, Ify Chika-Ezerioha, Dave McCreary / Editor: Swagat Mishra / Codes:  / Published: 08/02/2022

Our curriculum mentions pacing, and we all think that we know all about that as weve got ALS right? Some of our brief discussions on twitter highlighted that pacing can be more complicated than ALS implies, and actually isnt very common in ED. Were going to talk through some of the algorithm, with thanks to everyone who responded to the #RCEMBlogs post. 

What is Bradycardia?

Most people would define bradycardia as being a heart rate <60 bpm, and for more details on the physiology and causes of bradycardia do visit the RCEMLearning reference article, or for RCEM members the bradycardia module

ALS says extreme rates are those <40bpm, and certainly I would admit anyone with a heart rate of <40 whether the ECG is normal, and there are any other concerning steps points or not. Would you? 

Step One

Hiding away right at the top of the ALS algorithm is finding and correcting reversible causes eg. electrolytes, and I think were all pretty good at thinking hyperkalaemia when we see a bradycardic ECG – get the calcium in. 

More interesting are the drug overdoses, and how reversible are they. Sometimes it is clear and you know the patient has had an overdose, and our #RCEMblogs crew were clear at this point they would exit the bradycardia algorithm, and move on to the toxicology algorithm and treat the propanolol overdose.  

Have you had a chance to engage into our crowd sourced blogs yet? Here’s a new scenario? #rcemblogs

Its 3pm and 62y/o Semi’s turned up after an overdose of propanolol
Observations: RR 18, SpO2 99% RA, HR 32, BP 80/40,GCS 14
Do you pace him?How?
What sedation do you use, if any?

RCEMLearning (@RCEMLearning) September 9, 2020

What is less clear is the management of therapeutic beta blockade with adverse signs. It seems most people wouldnt exit the algorithm at this point, but would instead look for other adverse signs whilst they wait for the beta blockers to wear off in both Faisal and Swagats cases. We will come back to the borderline hypotension later. 

58 y/o Faisal has been feeling dizzy for a few days and pre-syncopal. He’s normally fit & healthy but takes atenolol for hypertension.
Heart rate: normal sinus rhythm
Observations: RR 18, SpO2 99% RA, HR 38, BP 120/80, GCS15
Do you pace him?how?
What sedation do you use, if any?

RCEMLearning (@RCEMLearning) September 3, 2020

81y/o Swagat’s been feeling dizzy for a few days and pre-syncopal. He’s normally fit and healthy but takes atenolol for hypertension.
Heart rate: complete heart block
Observations: RR 18, SpO2 99% RA, HR 38, BP 120/80,GCS 15.
Do you pace him?How?
What sedation do you use, if any?

RCEMLearning (@RCEMLearning) September 4, 2020

There are toxicological causes of bradycardia too – one of the most significant being Nerve Agents – covered in August 2018s podcast (it was topical back then). 

So, the other reversible causes. In hypothermia, atropine is unlikely to work until the patient is more than 30 degrees, but Bradycardia can occur at 33degrees and below. So what do you do in between 30 and 33? Atropine might work – so if they have adverse signs, Id probably give it whilst treating other potential causes for their cardiac arrest. 

Hypothyroidism is another reversible cause, but it takes a very long time for any TFTs. We might need to ring the lab and ask them to expedite the sample, especially if there are clinical signs of hypothyroidism.

Our endocrine team suggest not treating bradycardia with Levothyroxine on clinical symptoms/findings without the result of TFTs – except possibly if they have just had a total thyroidectomy or ablative radioiodine. Obviously if the patient is normally on Levothyroxine and says or you have evidence that they have not taken it for a week or more then you should restart it possibly with twice the usual dose as a start and then their usual dose. If the usual dose is not known then 1.6mcg per kg once a day would be a rough estimate of requirements. If the patient is in myxoedema coma the guidelines say thyroxine 300 – 500 mcg. We have been giving doses of a weeks worth of thyroxine at one time in our non compliant patients – which is over 1000 mcg – so it is safe in the well patient at least.  I note that guidelines do say IV thyroxine in myxoedema coma – I have never seen this used in the UK.  IV liothyronine (T3) is incredibly expensive – in the 1000 per vial range – so it is not stocked and if required has to be transferred from another hospital which usually takes around 24 hours. Monitoring it is incredibly difficult due to its long half life. Given how quickly thyroxine works orally (NG tube if unable to take orally) – I usually don’t use it.  

I’m sure you’re all wondering if the bradycardia is caused by significant blood loss in trauma, and a very unwell patient. No? Read about the Bezold-Jarisch reflex from St Emlyns here

The last reversible cause I could think of is vagal stimulation, or cervical shock.

Do you know where your nearest speculum is? Mentally rehearse this scenario. Remember other things can cause vagal stimulation and bradycardia like constipation triggering autonomic dysreflexia. A speculum and a manual evacuation could be life saving procedures. 

Step Two

ALS talks about worrying when adverse signs are present: shock, myocardial ischaemia, syncope, and heart failure. Simples right? 


Defined by RCEMLearning in their shock module as the state that results when circulatory insufficiency leads to inadequate tissue perfusion and thus delivery of oxygen to the tissues of the body. 

But how do you know someone is shocked? Well, in most cases you look for tachycardia which clearly isnt in existence here. So, is blood pressure a useful surrogate marker? In the case of Faisal above, his BP was 120/80 but he was normally on antihypertensive treatment – normal for him, or lower than his baseline ? Its clear  shock is more subjective than it could be, and brain perfusion is a useful surrogate. Treat the patient, not the numbers. 


So when does pre-syncopal become syncopal? And when is a faint with vagal stimulation a syncopal event? 

Well, Id expect a faint to resolve quickly – so if the patient is still symptomatic, its not a faint. Id expect the 3Ps to be present – and if theyre not, its not a faint. If my patient collapsed and called an ambulance and is now fine, Id say they may have been syncopal, but are no longer. If every time they stand they feel woozy- Id say theyre still syncopal. 

Does dizziness count as pre-syncope? Im not sure, but if in doubt, I think Id treat the bradycardia and see if the dizziness improved. 

Myocardial Ischaemia

Classically, chest pain is a convincing sign of myocardial ischaemia, but as good historians we know the signs are more subtle than that. 

So youre going to take a history, and see how you go. 

What about ECG changes? Is the subtle ST depression a sign of myocardial ischaemia or normal for the patient, or because of their digoxin? If the patient looks well and wants to leave to run home – its probably normal for them! But if theyre crashingly unwell maybe they have myocardial ischaemia! 

Would you give GTN and see what happens? I always feel a little reluctant to do this as if their BP drops I dont know whether its GTN related or deterioration related, and I feel that if I really think the pain is due to ischaemia, I should pace, and if I dont why am I giving GTN, especially when the response isnt predictable. What do you do? 

Heart Failure

Pitting oedema to their ankles – would you pace? What about to their umbilicus? I think more of the patient with crashing heart failure here – the diaphoretic dyspnoeic ones that look like theyre going to crash any second. Its a sign of shock – theyre not perfusing anything. They need treatment ASAP. 

Treatment One 

If one of these adverse signs are present we first give 500mcg IV atropine. The vials are normally 600mcg – giving 600mcg instead of 500mcg. Atropine is a muscarinic receptor antagonist (an anti-muscarinic), so it essentially blocks the vagal nerve. The vagal nerve affects heart muscle. This hopefully reverses your bradycardia – even if the bradycardia is due to vagal nerve stimulation. The anti-muscarinic receptors are a specific subtype of the anticholinergic receptors, so atropine can cause anticholinergic effects, although the possible resulting urinary retention may help the bradycardia or it may worsen it! Atropine can also make the elderly confused – but so can the bradycardia. You can repeat the atropine up to 3mg in total if needed (six doses). Giving doses more than this is unlikely to be helpful as youve reached atropinisation.  Giving atropine in a patient with cardiac transplant associated bradycardia might also be unhelpful and cause sinus arrest

You could consider giving glycopyrolate instead – its in the next box of the guideline and works a lot slower, but as it doesnt cross the blood brain barrier may help prevent cholinergic agitation. 

So, if none of those four adverse signs are present, we next move onto assessing the risk of asystole. Asystole seems a very end stage condition, and Id rather worry about patients who might develop shock etc. but I guess its all part of a spectrum. 

We assess for:

* Recent asystole: well how do we know this? Our patients in ED may or may not have been on a monitor, and if they were on a monitor and had asystole did anyone notice? I suspect this comes down to clinical suspicion and if someone has collapsed, and is now bradycardic, assume they have worrying signs. 

* Mobitz II AV block: do your cardiologists always agree with your ECG interpretations or do they sometimes think what you think is Mobitz II is complete heart block? 

* Complete heart block with broad QRS: personally, I admit and worry about all patients with complete heart block regardless of the QRS width, but now Ive re-read this, maybe I can save some admissions (or not). 

* Ventricular pause > 3s: just one or every time? Symptoms probably guide you

Treatment Two 

If there are any of these risk of asystole features, you should move onto interim measures like more drugs or pacing. The pictorial algorithm strongly encourages this, but the accompanying ALS text says consider. 

Generally, if patients are stable, I keep them in the department on a monitor. Ive only ever given isoprenaline in the ED once, and it took us a long time to work out how to prescribe it (if you use Cerner iCare search for critical care and it comes up in the bundle!) – and from my discussions with colleagues, it seems Im not alone. 


Administer centrally (ideally) at a rate of 1 – 4 mcg a minute, until a satisfactory heart rate is achieved. Isoprenaline stimulates the B1 & 2 receptors. Most patients on an isoprenaline infusion can be managed on the coronary care unit.

In Australia (or at least in the places Ive worked) it is pretty much our first line for significant bradyarrhythmia (once atropine inevitably hasnt worked). We give it through a good peripheral line if central isnt immediately available (just like we do for starting adrenaline and noradrenaline). Its generally well tolerated, though I have seen a couple of patients have the odd cheeky VT with it, particularly at the higher doses or with the older guidelines that had an initial bolus.

I like to hold off unless its really needed, but I probably wouldnt wait for a patient with significant bradycardia (say <40-45 bpm – plucking numbers entirely out of the air) to declare themselves as unstable as I think thats just asking for trouble. I know it doesnt often feel like it, and that critical care space is always at a premium, but the ED is a safe place to get treatments like this started and its nice to have the patient and their required dose stabilised before we send them upstairs.



Aminophylline has a narrow therapeutic index, and we use it more for bronchodilation than in treatment of bradycardia but the ERC guidelines say it is useful in bradycardia caused by inferior MI, cardiac transplant or spinal cord injury at 100 – 200mg slow IV infusion. EMCrit says it is useful for, amongst other things, ticagrelor induced bradycardia – but I think Id be on the phone to toxbase before using it. 


Dopamine might be available in pre-mixed bags, which might influence your decision to use it. 

Treatment Three

You can either use drugs, or pacing and I think most of us are more comfortable with transcutaneous pacing than aminophylline. 

Pad Position: AP is considered better, although ALS advises the standard positon- but if you cant sit the patient up to get the posterior pad on, standard pad position is fine. A recent study says AP is no better for cardioversion – well see if the evidence changes for pacing. 

Most machines also need the three lead ECG leads on to pace properly! 

Sedation: Pacing can cause some chest discomfort, so some sort of sedation might be needed. These patients are likely to be haemodynamically unstable, so care needs to be taken before choosing your agent. A single agent with no side effects will be ideal, but also an agent that will last for as long as your patient needs the pacing. This is a temporary measure until a transvenous pacer and then a permanent pacemaker can be inserted – but the patient is likely to be paced for at least six hours. 

Morphine is probably bad because it has a slow onset and offset of action, releases histamine and has direct cardiac effects – Fentanyl is probably better if youre used to using it. 

Midazolam at a very small dose – 0.25 to 0.5mg at a time titrating at most every 2 minutes or so before giving more could be useful, with the added advantage of if youre delayed giving it, the amnesic effects should kick in anyway. 

Remember, these are unwell patients, so it will take a long time for any drugs to be distributed. 

Pacing: Make sure you know how to use your device (and have the three lead attached). Most ED defibrillators will require you to turn them into manual mode, which will then enable you to access the pacing controls. The first one to adjust is the pacing rate – which enables you to choose the heart rate you want.

Then adjust the energy output. This is the amount of mA you need to obtain capture – or for the pacemaker to work. If your patient is unwell, some sources say to start at the maximum energy and titrate down but general guidelines are start at 70mA and increase until 10mA above capture. If there is no capture at 130mA, re-site the pads, and re-try. 

You know when capture has been achieved when you see a vertical pacing spike followed immediately and every time by a complex.

If your patient has arrived with pacing already in progress, how do you swap over pads? Have a look at twitters thoughts.

Transvenous Pacing

Our Australian correspondent stated that people should familiarise themselves with transvenous pacing – if you can place an IJ CVC, you can float a pacing wire – the tricky bit is being familiar with the pacing box and even that is easy when youve had a play. Im now looking to see if my department has a pacing box I think it is a good thing to be able to do – for more instructions, have a look at LITFL here.

And What about Children?

Similar principles apply to pacing children as well as pacing adults. Start by thinking of the cause – and only pace if its a cardiac trigger, not if its post arrest. The principles are the same – but youll need to use paediatric pads to make sure they fit on.

Hopefully this has been a useful discussion around the ALS bradycardia algorithm. Wed love to hear from you if you disagree with anything, or have some further comments and thoughts.

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Further RCEMLearning Links

Other References 

  1. Bradycardia algorithm. ALS Course.
  2. Siar J, Bo ttiger BW, et al. European Resuscitation Council Guidelines 2021: Adult advanced life support. European Resuscitation Council. Elsevier, 2021 (115-151).

About the Authors

Charlotte Davies is an ED Consultant, and one of the RCEMLearning blogs team.

Daniel Haigh is an anaesthetist and contributed especially to the inotrope sections.

Jennifer Tremble and Ife Chika-Ezerioha are endocrinologists, and contributed especially to the hypothyroidism section. 

Dave McCreary is one of the RCEMLearning Australia correspondents. 

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