bleep.guide · Foundation Emergencies
Wednesday, 14 October 2026
Recognition of acute decompensated heart failure, oxygen and nitrate therapy, intravenous diuresis and assessment of response, indications for CPAP, and criteria for critical care referral.
Foundation Emergencies · Session 5 · 14 October 2026 · Oliver Devine
These notes come from a live recording, transcribed and written up using automated tools. Use them to recap, not as guidance. If something looks wrong, let us know.
All patient examples are hypothetical.
Hi guys, it's Ollie. Welcome back to Foundation Emergencies. I do try to make this weekly; night shifts have got in the way. We're doing things a little differently with the technology this week, so if there are any problems, just pop them in the chat.
For those who don't know me, I'm a medical registrar in Cambridge and one of the people behind Bleep Guide. Today we're talking about heart failure and acute pulmonary oedema, working through a fictional patient, Mr B. Any questions, let me know.
You're on call and Sam, the nurse in charge on ward 7, calls:
“Mr B is really short of breath. His saturations are 86% on 2 litres, his respiratory rate is 32, and his NEWS2 is 10.”
What do we know about him? He's 79, on day two after a hemiarthroplasty for a neck of femur fracture. He has known heart failure, and his latest echo shows an ejection fraction of 30%. His usual medicines include bisoprolol, ramipril, dapagliflozin and furosemide 40 mg every morning.
Pulmonary oedema has to be high on the list. But he's postoperative, so keep pneumonia, aspiration and PE in mind as well. Having heart failure doesn't stop somebody having something else.
Before you put the phone down, ask the team to sit him upright if tolerated, increase his oxygen, and stop any unnecessary IV fluid running. With saturations of 86% and this degree of distress, put him on a reservoir mask at 15 L/min while you're getting there, and check it's connected and the bag is inflated. Then titrate to 94–98%, or 88–92% if he's at risk of hypercapnic respiratory failure.1
Ask for a full set of observations, monitoring, an ECG and the blood-gas equipment. Some ward teams can obtain an ABG while you're on your way; elsewhere you'll be doing it yourself. Either way, don't let arranging investigations delay getting to the patient.
And get help involved. A NEWS2 of 10 and severe respiratory distress need an urgent response. Don't assume outreach has already been called because the score is high; make sure it has happened. If there's an immediate airway or breathing threat, or he is approaching arrest, use the emergency call.2
Five minutes later, Mr B is upright, sweating and speaking in short phrases. He's alert, but frightened. The slides fill in the observations:
His hands are warm, with a capillary refill time of about two seconds. The JVP is raised to the earlobe. There are fine crackles to both mid-zones, a little wheeze, pitting oedema to the knees and sacral oedema. The catheter has produced 20 mL/hour for four hours, and the fluid chart records a positive balance of 3.1 litres over two days.
That sounds like significant congestion with decompensated heart failure. Wheeze happens in pulmonary oedema too, so it doesn't make this an obstructive exacerbation.
But look at the breathing. He's still hypoxaemic on a high oxygen flow. Don't let warm hands and a high blood pressure make that look safe. Continue through A–E, including mental state, perfusion, urine output and a review of the medicines and fluid charts.
I always come back to this grid. Someone showed it to me at medical school, and I don't think I properly understood it at the time. It's useful because it asks two separate questions: is the patient congested, and are they adequately perfused?
!The session slide: two bedside questions, is he wet and is he warm, as a grid of warm and dry, warm and wet (Mr B), cold and dry, and cold and wet.
Is he wet, and is he warm? The grid from the session.
View figure at full size
“Cold” is shorthand for hypoperfusion, not just the temperature of one hand. Look for confusion, mottling, reduced urine output and a rising lactate. A normal blood pressure doesn't rule it out.3
On a failing heart's function curve, more filling pressure gives very little extra stroke volume and makes the congestion worse. Taking some of that pressure off relieves the congestion.
Sit him upright, review and stop unnecessary fluids, obtain IV access, and keep checking oxygenation, ECG and blood pressure. If a transfusion is running and you suspect a transfusion reaction, stop it and follow the transfusion-reaction pathway as well.
I'd want:
The chest X-ray supports the diagnosis and shows anything else going on, such as consolidation or an effusion.
What about PE? He's had a hip operation, so this matters. If PE is possible, investigate it alongside treating the congestion. Don't give heart-failure treatment for a few hours as a test of whether you need to think about PE. Use the Wells score: PE likely means imaging, and D-dimer only helps when PE is unlikely (it's usually raised after surgery anyway). If imaging is delayed, discuss interim anticoagulation with your senior, given the recent operation.4
The ECG shows new atrial fibrillation at about 130/min, with no ST elevation on this tracing. That may be the precipitant, a consequence of the acute illness, or both. We'll come back to that in the questions.
The first results slide gives pH 7.31, PaCO₂ 6.3 kPa, PaO₂ 8.1 kPa and lactate 2.4 mmol/L, still on 15 L/min through the reservoir mask.
He's acidaemic and the CO₂ is up, while he's breathing at 32 and still hypoxaemic on 15 litres. That's a worrying gas. Check the bicarbonate and base excess for a metabolic component too, and note the raised lactate.
At this point, I'd already be discussing non-invasive respiratory support with the senior and critical-care teams. Severe breathlessness with acidaemia in cardiogenic pulmonary oedema warrants that discussion now, alongside the diuretic and the rest of the treatment.5
His troponin is 64 ng/L. Is he having an MI? Not necessarily: heart failure, fast AF and renal dysfunction all raise troponin. Repeat it and look at the trend; calling it an infarction needs evidence of ischaemia as well, on symptoms, serial ECGs or imaging. Equally, don't dismiss evolving ischaemic changes as “just strain”.6
His creatinine is 138 µmol/L, from a baseline of 110: a rise of 28, which is an AKI if it happened within 48 hours. With a urine output of 20 mL/hour, watch the trend closely.7
His potassium is 4.9 mmol/L and haemoglobin is 92 g/L. Anaemia adds to the strain on the heart, so look at the trend and for any bleeding.
Lots of people send a natriuretic peptide in acute heart failure. It's most useful when heart failure is a new suspicion.
Heart failure is unlikely with a BNP below 100 ng/L or an NT-proBNP below 300 ng/L: different tests, different thresholds. A high result doesn't tell you how many litres someone is overloaded. Age, AF and renal function raise it; obesity lowers it.8
In Mr B, with an EF of 30% and obvious congestion, it adds little tonight. Don't wait for it before treating.
I want to spend a little time on the physiology, because it explains both the examination and the treatments.
In cardiogenic pulmonary oedema, left-sided filling pressures rise, increasing pulmonary venous and capillary hydrostatic pressure. More fluid is filtered into the lung interstitium than can be cleared. With further accumulation, fluid reaches the alveoli, lung compliance falls, and gas exchange deteriorates.
Hydrostatic pressure pushes fluid out of the capillaries, oncotic pressure draws it back, and the lymphatics drain the excess. When the pressure rises faster than the lymphatics can cope, the lungs fill.
!The session slide: hydrostatic pressure pushes fluid out of the pulmonary capillary, oncotic pressure draws it back and lymphatics drain the excess, with the three stages of rising left atrial pressure.
Why the lungs fill.
View figure at full size
Mr B has a substantial positive balance and peripheral oedema. But not every episode of acute pulmonary oedema means somebody has gained several litres. Marked hypertension and vasoconstriction can redistribute blood centrally and raise filling pressures very quickly.9
The term pulmonary artery wedge pressure comes from a pulmonary artery catheter. It's intensive-care monitoring, not something you'll see on the ward.
The catheter passes through the right atrium and ventricle into the pulmonary artery. Inflating its balloon briefly occludes a small pulmonary arterial branch. With no flow beyond the balloon, the pressure at the tip reflects the pressure downstream, so it estimates left atrial pressure.10
!Pulmonary artery catheter passing through the right atrium and ventricle, with its balloon wedged in a small pulmonary artery branch.
What the wedge pressure measures.
View figure at full size
The traditional pressure bands explain the progression:
These are rough bands that overlap; you can't read a wedge pressure off a chest X-ray.11
!AP portable chest radiograph showing bilateral perihilar and interstitial shadowing in acute pulmonary oedema.
Acute pulmonary oedema on an AP portable film. Dr Jeremy Jones, Radiopaedia.org, via Wikimedia Commons, CC BY-SA 3.0.
View figure at full size
The film shows pulmonary oedema, a big heart (remember an AP film magnifies it) and probably a small left effusion.
We've identified new AF, but don't stop looking there. CHAMPIT is a useful reminder of important precipitants:
On the ward, also look at what we've done or haven't done: ongoing IV fluids, a recent transfusion, diuretics held and never restarted, worsening renal function, a new NSAID, or heart-failure medicines omitted during medicines reconciliation. Look at what was actually administered, not just the usual medication list.
Mr B's precipitant slide adds that his furosemide has been held for three days and that he had one unit of blood the day before. Along with the positive balance and new AF, those are useful clues. A recent transfusion also raises transfusion-associated circulatory overload (TACO).
One more thing about his dapagliflozin: SGLT2 inhibitors are stopped during major surgery or serious illness. If a postoperative patient on one is acidotic, check the ketones, even if the glucose is normal.12
There are a few causes worth keeping firmly in mind:
Just a quick interlude: Bleep Guide has an acute pulmonary oedema checklist that takes you through assessment, treatment and reassessment. Have a look.
There's also arrest scribe mode, for recording events during an arrest call, and the hospital directory, where you can save and share useful local numbers. If your hospital is recruiting a directory moderator, you can put your name forward through the app. Appointed moderators receive Unlimited access free for as long as they moderate.
All right—back to Mr B.
Imagine Mr B on the flatter part of a failing-heart function curve: high filling pressure, with relatively little extra output from adding more filling.
!Ventricular function curves showing a congested failing heart at A, less filling at B and lower afterload at C.
How each treatment helps.
View figure at full size
Furosemide offloads salt and water and lowers the filling pressure, moving him from A to B: less congestion and better oxygenation, for much the same output. The heart is no stronger; it just isn't flooding the lungs.
Lowering the afterload lets the ventricle eject against less resistance, moving from A to C. GTN dilates the veins at low doses, reducing preload, and the arteries at higher doses, reducing afterload. That's why it helps when the pressure is high, and why it's dangerous when the pressure is low.
Mr B normally takes 40 mg orally each day. So give 80 mg IV: in someone already on a loop diuretic, start at about twice their usual oral dose, given intravenously.15
Give it slowly, no faster than 4 mg a minute, so 80 mg takes about 20 minutes.16
Then find out whether it has worked. Look at urine output, breathing, oxygen requirement, congestion, blood pressure, renal function and electrolytes. A functioning catheter and an accurate chart help; check for blockage if the apparent response is poor.
Early response measures described in the current ESC guidance include urine output of at least 100 mL/hour during the first six hours, or a spot urine sodium of at least 70 mmol/L at about two hours. If he isn't reaching those, review the dose with your senior.15
Nitrates aren't routine. NICE keeps them for myocardial ischaemia, severe hypertension or regurgitant aortic or mitral valve disease, with close blood-pressure monitoring in a level 2 setting; ESC uses a systolic above 110 mmHg.17
Mr B's pressure of 172/96 makes a GTN infusion worth discussing. In someone hypotensive and poorly perfused, nitrates make things worse.
Morphine used to be standard for pulmonary oedema. We don't routinely give it now, and midazolam isn't the substitute: both depress breathing and consciousness. If somebody is frightened because they can't breathe, treat the breathing.18
There's now 150 mL in the catheter bag. The reassessment slide shows a respiratory rate of 30/min and SpO₂ 91% on 15 L/min. Those numbers have improved a little, but he looks exhausted. The repeat gas is pH 7.28 with PaCO₂ 6.7 kPa: worsening acidaemia and rising CO₂.
The furosemide is working; the respiratory failure isn't. Giving furosemide and walking away isn't enough.
Critical care should already be on their way; a worsening gas and exhaustion make it urgent. He needs non-invasive ventilation now, and a decision about whether he's heading for intubation.5
CPAP is a form of non-invasive ventilation. It supplies a continuous positive airway pressure, including at the end of expiration. That end-expiratory effect is central to why it helps here.
!The session slide: CPAP reopens flooded air sacs, reduces venous return to the right atrium and reduces the load on the left ventricle.
How CPAP helps: three effects.
View figure at full size
There are three useful effects to think about:
The same effects can drop the blood pressure, so watch it, especially in someone who is preload-dependent or has a struggling right heart.
Bilevel NIV adds a higher inspiratory pressure above the expiratory pressure. That pressure difference assists ventilation and can help CO₂ clearance. So the distinction is CPAP versus bilevel NIV, not CPAP versus NIV.20
If he's vomiting, can't protect his airway, is getting drowsier or has an untreated pneumothorax, a mask is the wrong answer: get the anaesthetist. A mask trial mustn't delay intubation.
The large 3CPO trial found no difference in seven-day mortality, but breathlessness, acidosis and CO₂ improved faster on CPAP or NIV. Across the trials it reduces intubation, and ERS/ATS recommend CPAP or bilevel NIV in cardiogenic pulmonary oedema.21
As an FY1 or FY2, your job is to recognise the respiratory failure, start the treatment and get the right people. Nobody expects you to choose the settings.
Suppose instead the blood pressure is 82/50, the knees are mottled, he's newly confused, the lactate is 4.8 mmol/L, and almost nothing is coming into the catheter. That's cold and wet: cardiogenic shock.
This needs immediate senior, cardiology and critical-care involvement. Look for the cause, including ischaemia, an arrhythmia or a mechanical complication, and discuss circulatory support. He may need inotropes or vasopressors in critical care. Don't give something that lowers the pressure further simply because it helped the hypertensive pulmonary-oedema patient.22
We'll skip the worked SBAR slide and go to the questions.
Yes: these notes include the diagrams from the slides.
The two can coexist, and the relationship can go both ways. AF may worsen filling through loss of coordinated atrial contraction and, when the ventricular rate is rapid, less time for diastolic filling. Acute illness and raised filling pressures can also trigger AF.
The immediate question is whether the arrhythmia is causing or materially worsening the instability. If a tachyarrhythmia is producing life-threatening features such as severe pulmonary oedema, shock or myocardial ischaemia, urgent synchronised cardioversion is appropriate, with experienced help and the necessary anaesthetic or sedation support. Don't delay a genuinely unstable patient for prolonged debate about which problem started first.
But AF in someone with heart failure doesn't mean emergency cardioversion. Treat the congestion and the triggers, and decide about rate or rhythm control in that light.23
We record the sessions, but the material we publish for this series is the lecture notes, including relevant diagrams and slide content, rather than putting the recording online.
Yes—check electrolytes and renal function when assessing a new arrhythmia. Potassium and magnesium abnormalities can contribute, and calcium is relevant where indicated. Magnesium often needs requesting separately from routine U&Es.
Correct what you find, bearing his kidney function in mind.24
Use a physiology source you find clear and work back through filling pressure, ventricular function and the effects of positive intrathoracic pressure. Life in the Fast Lane has useful critical-care explanations, and Radiopaedia can help with imaging examples.
Either works: the DOSE trial found no difference between them. What matters is the total dose and the response.
If repeated doses aren't working, don't keep giving another forty; agree a plan with your senior, which may mean a higher dose or a second diuretic.25
CPAP is already NIV, and in pulmonary oedema its effects on the lungs and the heart make it very useful. When the CO₂ is climbing and he's tiring, he needs help to ventilate as well, which is where bilevel NIV comes in, and critical care to decide whether he needs intubating.20
Because urine in the bag doesn't instantly clear the lungs or rest tired respiratory muscles. A rising CO₂ means he isn't ventilating enough. Look for other causes too, such as opioids, underlying lung disease or a second diagnosis, and get him the respiratory support he needs.5
Yes. Treat the pulmonary oedema first, but watch the sodium from the start. In congested heart failure, low sodium is usually dilutional, and diuresis can make it rise too quickly, particularly with a brisk water diuresis.
Check it six-hourly while things are stable, and two-hourly if he starts passing large volumes or the sodium is climbing fast, with specialist advice. Keep the rise to no more than 10 mmol/L in the first 24 hours and 8 mmol/L in each 24 hours after that. Severe neurological symptoms need immediate specialist treatment.26
All right, that's everything. Next session is acute severe asthma, Wednesday 21 October at 19:00. Thanks very much, and I'll see you then.