bleep.guide · Foundation Emergencies
Wednesday, 9 September 2026
Structured A–E assessment of the acutely unwell patient, recognition of deterioration, escalation and the call for help, and the immediate priorities on arriving at a cardiac arrest.
Foundation Emergencies · Session 1 · 9 September 2026 · Oliver Devine
Caution: live-session transcript
This is an edited version of an automated transcript of a live teaching session. It may contain transcription errors or clinical inaccuracies, and information may become out of date. Check current guidance and local protocols before using it in clinical practice.
All patient examples are hypothetical.
Hey guys. I'm Ollie, and welcome to the first of our Foundation Emergencies talks.
When we did the foundation preparation webinars, a lot of the feedback was that you'd quite like us to talk through emergencies. We have a big section of bleep.guide that focuses on emergency checklists, and these sessions are a chance to go through them in a bit more detail.
Tonight, I want you to imagine that you're the first doctor through the door when a patient deteriorates. I'll keep it suitable for medical students and foundation doctors, but try to build in some additional detail as we go.
Imagine you're carrying the ward-cover bleep on a night shift. A nurse calls about Mr H, who's 76: “He says something is wrong.”
You have a look through the electronic notes. He's on day two of IV furosemide for heart failure, he's had a previous anterior MI, and his latest echo gives an ejection fraction of 30%. The nurse tells you he was chatting and eating supper a couple of hours ago. Now he's got central chest pressure, he's clammy and he's breathless.
One of the first things I would ask is: what's changed, and when was he last well? As with most pathology, knowing the timescale gives you a good indication of what might be going on.
This sounds like an acute deterioration. I wouldn't spend too long asking questions on the phone. I would go and see what's happening. The nurse's concern and the patient's trajectory matter, and you can call for help while you're assessing him.1
Think about what this might actually look like. It's dark, the ward lights are off, and people are moving around. It's a little different from an OSCE: quite a lot of the information is available as you walk in, and things happen at the same time.
I would usually say, “Can someone please sort out the observations so we've got live information coming in?” Then I would get on with the A–E assessment.
Suppose Mr H is speaking to you. His airway is patent at that moment, but you're watching whether that changes. He's breathing at about 30 a minute, his saturations are 90% on air, and there are crackles at the bases. You might be thinking: is this chap fluid overloaded? Get oxygen going, ask for a full set of observations, and get an ECG. If telemetry is available, use it.
You can see a big difference between how he looks now and how the nurse describes him a couple of hours earlier. Something is very wrong. When you feel his pulse, it's very fast.
Let's say it's 190 and regular. The blood pressure reading looks reasonably reassuring, but his peripheries are shut down and his capillary refill is four seconds. The ECG is being done, and you're looking at the tracing on the machine rather than waiting for the paper copy. It shows a regular broad-complex tachycardia. My immediate concern would be ventricular tachycardia with a pulse.
He might still be awake, but now he's confused, saying less and looking pale. His finger-prick glucose is 7.1 mmol/L. Ask for the blood pressure to be repeated. Suppose there's no obvious bleeding, fever or other clear sign of infection. Ask for a gas and bloods, including electrolytes. Given the chest pain, previous MI and poor ventricular function, you would also be thinking about myocardial ischaemia. A troponin result mustn't hold up urgent treatment.
The number you've got is a single reading. The patient in front of you looks unwell.
Pressure can be preserved while perfusion is getting worse. The faster the heart beats, the less time there is for ventricular filling and diastolic coronary perfusion, while myocardial oxygen demand increases.
He's got chest pain, and the breathlessness and crackles raise concern about acute pulmonary oedema. Those are adverse features. With this unstable tachyarrhythmia, I would be thinking about urgent synchronised cardioversion, with expert help and appropriate sedation or anaesthesia if he's conscious. Bring the crash trolley in. You should already be asking for the emergency call to go out.2
The point is that a previously reasonable blood pressure doesn't outweigh what you can see happening in front of you.
Now suppose that, before you get the gas or repeat the blood pressure, he slumps back and stops responding. He's making occasional gasps. The monitor still shows a fast rhythm.
The old blood pressure is no longer evidence of circulation. Those gasps aren't normal breathing. If he's unresponsive with absent or abnormal breathing, assess for cardiac arrest; if you're uncertain whether there's a pulse, start CPR without delay.3
Put out the arrest call—2222 in most UK hospitals, or your local emergency number—and start managing the situation while the arrest team is coming.
Some foundation doctors will have ALS training early on; others won't. Either way, if you're first through the door, you may have to take some leadership until help arrives.
You might not know everyone's name. What matters is making it clear who you're asking, what you need them to do, and that they should come back to you when it's done.
I would use wording such as:
“Can you please put out the arrest call, tell them exactly where we are, and then tell me when it's been done?” “Can you take over compressions while I coordinate?” “Can you take the gas, run it, and come back to me with the result?”
You're closing the loop. Asking for something doesn't tell you whether it has actually happened.
You might start compressions yourself, then realise you need someone else to take over. You might look around and find that you're the person best able to manage the airway, so you move to the head of the bed and begin bag-mask ventilation while a colleague compresses.
That may be necessary, but think about the human factors. If you ask someone to do compressions, they may keep going until they're exhausted. If you're absorbed in a technical task yourself, it's difficult to notice that they're tiring or to anticipate the next step.
My advice is to get yourself into a position where you can keep an overview, often at the foot of the bed, as soon as the team has enough people with the right skills. Start the task that needs doing, then hand it over explicitly when someone suitable is available. Don't abandon a necessary task just to stand back.
We're taught 100–120 compressions a minute, to a depth of 5–6 cm on the lower half of the sternum. Full recoil matters: release the pressure completely between compressions while keeping the heel of your hand in contact with the chest. Don't lean on it.3
Coronary blood flow during CPR is limited, so we need to make the compressions as effective as possible. That means minimising gaps and allowing recoil. Leaning on the chest and excessive ventilation can increase intrathoracic pressure and impair venous return.
Good compressions are fundamental. Effective ventilation is also part of resuscitation: use 30 compressions to two breaths before an advanced airway, with someone competent managing the airway and bag-mask seal.2
Attach the pads, with the lateral pad below the armpit. Use the defibrillator in a mode you're trained and competent to use. If you're using an AED, follow its prompts. If it advises a shock, give it safely and resume CPR immediately.2
Let's suppose you're an ILS-trained F1 and the arrest team arrives after the first shock. Your handover could be:
“Mr H is 76, with heart failure and a previous MI. Chest pain and VT preceded a witnessed arrest at 22:17. We started CPR immediately. One shock has been given, no drugs have been given, and IV access is in place. Bloods have been taken but the results aren't back.”
Then identify yourself and make the leadership transfer clear. The people arriving don't necessarily know who you are, what training you've had, or whether you're comfortable continuing to lead.
I would say:
“I'd like you to take over as leader. What would you like me to do?”
That leaves everyone clear about who's leading and what your next job is.
People can become very focused on memorising the flowchart. I want to make the shockable and non-shockable sides a little more intuitive, while keeping the priorities clear: good CPR, early defibrillation when indicated, and treatment of reversible causes.
In the shockable pathway, the rhythm is VF or pulseless VT. After each shock, you resume CPR for two minutes before the next scheduled rhythm check. If the rhythm remains shockable, you give the next shock.
In the standard adult pathway, after the third shock you give adrenaline 1 mg and amiodarone 300 mg. After the fifth shock, give a further 150 mg of amiodarone. In a non-shockable arrest—PEA or asystole—give adrenaline 1 mg as soon as possible. Repeat adrenaline every 3–5 minutes while resuscitation continues. These are IV/IO arrest doses; follow the current algorithm and team leader.2
Why the different timing? In a shockable rhythm, early defibrillation is a priority: you're trying to terminate disordered electrical activity so that an organised rhythm can resume. In a non-shockable rhythm, there isn't a rhythm for a shock to treat. You're supporting circulation and addressing the cause.
That distinction helps explain the algorithm, but it isn't a reason to improvise the drug timing. Follow the sequence rather than deciding to give the drugs early because they're available.
This brings us to coronary perfusion pressure.
Think back to the coronary arteries coming off the aortic root. Blood has to flow through the coronary circulation and ultimately return through the venous side to the right atrium. It's the pressure difference across that circulation that matters.
During the relaxation phase of CPR, a useful approximation is:
Coronary perfusion pressure = aortic pressure − right atrial pressure.
If aortic pressure is low, or right atrial pressure is high, that gradient is reduced. Adrenaline's alpha-mediated vasoconstriction helps raise aortic pressure. Full chest recoil and avoiding excessive ventilation also matter because of their effects on filling and pressure.4
!Diagram of the pressure gradient from the aorta through the coronary circulation to the right atrium.
Slide illustration: coronary perfusion pressure during CPR relaxation. A conceptual diagram, not an anatomical drawing or measured flow.
This is why I want you to understand the physiology rather than only remember the drug names. Adrenaline isn't a switch that restarts the heart. We're trying to improve the conditions for recovery while treating the cause of the arrest. That applies to both sides of the algorithm.
You might then ask: why give amiodarone acutely when it's a drug associated with a very long half-life?
Its long half-life and the time taken to reach steady state during ongoing treatment don't mean that an IV dose has to wait weeks to have an effect. Acute IV effects and chronic effects are different.5
Adrenaline acts at both alpha and beta receptors. We want the vasoconstrictor effect, but beta stimulation can also make the heart more prone to arrhythmia—what you might think of as making it more “twitchy”. Amiodarone has anti-adrenergic effects, but it also acts on several ion channels. It isn't simply given to cancel out the beta effects of adrenaline. Its role here is as an antiarrhythmic adjunct in persistent or recurrent VF/pulseless VT.52
!Schematic action potentials illustrating a longer refractory period with chronic amiodarone treatment.
Slide illustration: refractoriness with chronic amiodarone treatment. This does not show the immediate mechanism of an IV arrest dose, and the traces are illustrative.
Nor is it a panacea. In the overall population of the ALPS trial of out-of-hospital shock-refractory arrest, amiodarone did not significantly improve survival to discharge or favourable neurological outcome compared with placebo. That doesn't establish that it can never help, and it remains in the ALS algorithm. The practical point is that a drug mustn't distract us from good resuscitation.6
Back to Mr H. Suppose the potassium comes back at 2.8 mmol/L and the magnesium at 0.55 mmol/L. Both are low and may promote arrhythmia, particularly in an already vulnerable, ischaemic ventricle. The team needs to recognise and treat those deficits using the appropriate monitored protocols.
This is where the four Hs and four Ts help organise the search for reversible causes. They're relevant in both shockable and non-shockable arrest.7
Now suppose that after three shocks you see a more organised rhythm on the monitor. It looks compatible with a pulse, but at the assessment there isn't one. That's pulseless electrical activity: you can't diagnose it from the ECG alone.
A tidy-looking rhythm doesn't prove circulation. Resume CPR, don't give a shock for PEA, and move to the non-shockable pathway. The team leader will want to know when adrenaline was last given. Changing pathway doesn't mean forgetting the doses already administered.
If you're using an AED, “No shock advised” doesn't mean that resuscitation has finished.
Let's say a definite pulse returns. It's weak, and the repeat blood pressure is 94/61 mmHg. That's a return of spontaneous circulation, but the patient is still critically unwell.
Go through A–E again. Reassess the airway, breathing and circulation, obtain a 12-lead ECG, and arrange critical care. The team may now have secured the airway with a tracheal tube or a supraglottic device.
Treat the hypotension according to its cause. In someone with poor ventricular function and possible pulmonary oedema, a further fluid bolus isn't automatic; the senior and critical care team need to assess what circulatory support is appropriate.8
Scribing is a very common foundation-doctor job at an arrest. You can learn a lot about how an arrest is led by keeping an accurate record, but it's harder than it looks.
First, have something to write with. If you're going to an arrest, take a pen and paper rather than assuming they'll appear when you need them.
Keep communicating with the team leader. They may ask: when was the last adrenaline given? How many cycles have we done? How many shocks has the patient had? You want to be able to answer without reconstructing the whole event.
That's the thinking behind Arrest Scribe Mode, which is part of the Bleep Guide app. It gives you a running, timestamped log: airway and IV access, gases, rhythm checks, pauses, shocks, drugs and the Hs and Ts. You can record the rhythm found and what happened next.
There are other tools that do similar things. The attraction is having the information organised while everyone is working under pressure. Whatever record you use, distinguish a drug that's been requested from a drug that's actually been given. Use locally approved arrangements for recording and transferring any clinical information.
Question: When considering hypoxia, do you mentally go through hypoxic, anaemic, circulatory and histotoxic causes? The overlap with the other Hs and Ts can make it feel as though you're bouncing back and forth.
If I'm honest, this is one reason I think prompts and checklists can be useful. There's a lot to hold in your head, particularly when you're relatively inexperienced and the situation is stressful.
You don't need to make using a prompt into something to be embarrassed about. Use an appropriate aid to organise what you're considering and what the team has already checked. It should support the team and the resuscitation, rather than distract from what's happening in front of you.
We'll leave it there. Next time, we're looking at hypotension and the shocked patient, in the same short, case-based format. Thanks very much for coming along.