bleep.guide · Foundation Emergencies
Wednesday, 16 September 2026
Volume status and perfusion, differentiating hypovolaemic, distributive, cardiogenic and obstructive shock, the fluid challenge and assessment of response, and criteria for escalation.
Foundation Emergencies · Session 2 · 16 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 It may contain transcription errors or clinical inaccuracies, and information may become out of date.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. Welcome back to session two of our Foundation Emergencies teaching. These sessions go through the emergencies section of bleep.guide in a bit more detail than we can on the app itself.
Today we're doing hypotension and the shocked patient. I'm Ollie, a medical registrar in Cambridge. We'll make a start and leave some time for questions at the end.
Imagine you're carrying the ward-cover bleep and you're called about Mrs K. She's 72, with fever, urinary symptoms and poor intake for 48 hours. She has an ejection fraction of 35%, is normally independent, and takes bisoprolol, ramipril and furosemide.
The nurse tells you that she's not producing much urine and isn't feeling herself. Her blood pressure is 102/58 mmHg, but she normally runs a systolic pressure of about 150. Her pulse is 106, respiratory rate 28, and her saturations are within target. She's newly confused.
Are you concerned? And if you aren't, at what point do you become concerned?
People sometimes wait for the magic systolic of 90 before calling someone shocked. But this is a substantial change from her baseline, and shock can be present before the blood pressure reaches that number.
NEWS2 doesn't directly score the fall from her usual blood pressure. It would, however, flag this particular patient: new confusion and a respiratory rate of 28 score three each, and her systolic pressure and pulse score one each. That's at least eight before adding temperature and oxygen scores. She already needs emergency assessment; don't wait for the pressure to fall further.1
The point is to look at perfusion and the change in the patient alongside the number on the machine.
There are three particularly useful places to look for evidence of poor perfusion: the brain, the skin and the kidneys.
Is she confused or drowsy? Is that a change from baseline? What's her capillary refill like? Is there mottling? We already know that her urine output has fallen. Check catheter patency and compare her renal function with previous results.
Those findings matter even if the blood pressure doesn't initially look dramatic. A reasonably preserved pressure can conceal poor flow.
When you go to see her, start the A–E assessment you've practised at medical school. Suppose she's communicating, but confused, with a GCS of 14.
Look at her work of breathing, check the saturations against her target, and listen to the chest. Are the breath sounds reduced on one side? Are there crackles suggesting infection or pulmonary oedema?
Repeat the blood pressure at the bedside. Check the pulse and capillary refill. Have a look at the JVP, which can give you useful information about the venous side of the circulation. Get an ECG and, if it's available, telemetry. I would usually ask for a gas and routine bloods as well.
And don't forget glucose. You've identified a change in consciousness, so check it.
You're also looking for an explanation. In this scenario, sepsis sounds quite plausible, but don't stop thinking once you've found one possibility. Look for bleeding, a rash, and other infection sources. Examine the chest and abdomen, think about fluid balance, and consider a bladder scan. If there's a catheter, look at whether it's draining and what is in the bag.
Now suppose the repeated pressure is 82/44 mmHg. You should already have senior help on the way for this patient. If she appears at imminent risk of arrest, use the emergency call rather than waiting for a routine review.2
You know the relationship from medical school: mean arterial pressure is approximately cardiac output multiplied by systemic vascular resistance. That's a useful simplification, leaving out right atrial pressure.
Then we have the four broad mechanisms of shock: cardiogenic, obstructive, distributive and hypovolaemic. The equation helps, but I think a diagram makes it easier to picture what's going wrong.
!Schematic showing pump failure, obstruction, loss of vascular tone and reduced circulating volume.
Slide illustration: four mechanisms of shock. The pulmonary circuit is omitted from this simplified diagram; more than one mechanism can coexist.
With cardiogenic shock, you're thinking about pump failure—for example, an MI. There may be chest pain, pulmonary oedema or a raised JVP. Those signs aren't present in every case, and an MI isn't the only possible cause.
With obstructive shock, something is preventing filling or forward flow. Think about a large PE, tamponade or tension pneumothorax.
With distributive shock, think about sepsis and anaphylaxis. Loss of vascular tone is important, and capillary leak can also move fluid into the tissues.
With hypovolaemic shock, think about bleeding and other significant fluid losses. If there's major haemorrhage, you need the haemorrhage pathway and control of the bleeding, not just repeated bags of crystalloid.
JVP can help you put those possibilities together. A clearly raised JVP points you in a different direction from a clearly low one. But if you can't assess it reliably, don't make it the deciding factor.
Suppose the ECG shows sinus tachycardia, the JVP appears low and the chest is initially clear. She has fever and flank tenderness, with very little intake and low urine output. Her lactate is 4.2 mmol/L, and her creatinine is 180 micromol/L, compared with a previous result of 90.
This sounds like a possible combination of distributive and hypovolaemic shock, with limited cardiac reserve. You would be concerned about an acute kidney injury, while checking the timing of the creatinine change.
Treat the suspected sepsis alongside the resuscitation: bloods and cultures, prompt antibiotics and a search for the source. For a high-risk ward patient like this, current NICE guidance calls for IV antibiotics within an hour of the first NEWS2 assessment on deterioration. Take cultures first if you can do so without delaying treatment.3
Urinary infection seems likely in this example. Given the poor urine output, I would have a low threshold for checking for retention with a bladder scan. If you haven't used one before, ask someone to show you; it's a useful bedside skill.
Let's talk about a fluid challenge, and then a way of challenging preload without leaving extra fluid in the patient.
For this suspected-sepsis scenario, start with 250 mL of isotonic crystalloid over about 10–15 minutes, then reassess promptly before prescribing more. Recheck the pressure, but also look at capillary refill, consciousness, breathing and signs of congestion.3
Don't write up the next bolus without finding out what the first one did. In this patient, with poor ventricular function and clear signs of hypoperfusion, I would want senior involvement early.
Suppose she starts at 82/44, gets 250 mL and shows very little improvement. After another 250 mL, any improvement is transient. Her capillary refill is still four seconds, she's still confused, and now you can hear crackles. She's also needing more oxygen.
At that point, continuing to fill her might produce a small change in pressure, but she's showing signs that she may not tolerate more fluid. Stop further routine boluses, reassess the cause of the respiratory deterioration, and get urgent critical care input. She may need vasopressor support.
The trigger isn't simply that you've reached two boluses. It's the combination of ongoing poor perfusion and possible harm from more fluid. You don't have to complete a predetermined volume before escalating.
This brings us to the Frank–Starling relationship. Within limits, more ventricular filling can increase stroke volume. As the relationship flattens, additional filling may produce much less extra forward flow and more congestion.
!Qualitative Frank–Starling curve showing different stroke-volume responses to the same increase in preload.
Slide illustration: the Frank–Starling relationship. This is a qualitative curve, not a measurement of where Mrs K's circulation sits.
We can't look at a cuff pressure and say that we've found the exact limit of her myocardial fibres. What we can say is that she's still poorly perfused and is developing signs of congestion. That's the bedside problem we need to act on.
There are two questions here: will more preload increase stroke volume, and can the patient tolerate the extra volume? They aren't the same question. Someone with heart failure may have much less tolerance for additional volume.
A passive leg raise can provide a reversible preload challenge. In a suitable patient, moving from semi-recumbent to a horizontal trunk with the legs raised transfers blood towards the chest; returning to the original position reverses the manoeuvre. It isn't reliably equivalent to a fixed 500 mL bolus.
To use it as a test of fluid responsiveness, you need to assess the rapid change in cardiac output or stroke volume. A repeat cuff pressure on its own isn't a reliable substitute. It's useful when the appropriate assessment is available, but it shouldn't delay help for someone who's deteriorating.4
And remember that a low urine output isn't always a request for more fluid. Venous congestion can also impair kidney function.5
They may consider a vasopressor such as noradrenaline. It's the usual first-line vasopressor in septic shock; the choice of circulatory support needs individual assessment, particularly when cardiac dysfunction is also present.6
The basic idea is alpha-mediated vasoconstriction. On the arterial side, that supports pressure. On the venous side, reducing capacitance can recruit blood towards the heart and increase the pressure driving venous return. You're changing where the blood is and the pressures around it, rather than adding fluid.7
!Dilated and constricted veins illustrating recruitment of venous blood towards the heart.
Slide illustration: venous tone and stressed volume. Vessel size and red-cell density are illustrative; this does not guarantee an increase in cardiac output.
So Mrs K's lactate is 4.2. We talk about lactates a lot on the medical take: two, three, four—when should you be worried?
You need to think about what the number represents. Lactate is produced, and lactate is cleared. Hypoperfusion can increase production, but so can adrenergic stimulation. Impaired clearance—for example with significant liver dysfunction—can contribute to a lactate staying high even after you've addressed the circulation.8
I would repeat it according to how unwell the patient is and pay attention to the trend. If it's rising, reassess what's happening. Think about drugs, including recreational drugs, as well as the other possible explanations.
The number needs to make sense alongside the patient. It isn't, on its own, an instruction to keep giving fluid.
As an aside, imagine being called to another patient in the next bay while you're dealing with Mrs K. Mr T is 68, has melaena, looks faint and clammy, and has a blood pressure of 80/50 mmHg. His haemoglobin is 132 g/L.
That haemoglobin doesn't reassure me that he isn't bleeding. It's a concentration. Acute blood loss can initially leave it looking normal because red cells and plasma are being lost together. The subsequent result depends on fluid shifts and resuscitation; there isn't a fixed number of hours before it must fall.9
You need to act on the clinical picture of possible major bleeding, not wait for the haemoglobin to catch up.
Suppose instead that Mrs K has just received penicillin, you find a recorded penicillin allergy, and she develops wheeze and swelling around her mouth. That would point you towards anaphylaxis and its emergency treatment pathway, including IM adrenaline. It isn't the same adrenaline route and dose as cardiac arrest.10
Chest pain and pulmonary oedema might point towards cardiogenic shock. Sudden breathlessness, syncope and haemodynamic instability should make you consider a high-risk PE. That needs urgent expert assessment for possible reperfusion treatment. Thrombolysis isn't a routine treatment for a haemodynamically stable PE, even if there is right ventricular strain.11
Don't forget tension pneumothorax. If you suspect it in someone with haemodynamic instability or severe respiratory compromise, call for emergency help and arrange decompression by someone with the required skills. Don't wait for a portable chest X-ray in an unstable patient with suspected tension pneumothorax.12
Coming back to Mrs K, your handover might sound like this:
“Mrs K is shocked. Her BP is 86/46, she's confused and her capillary refill is prolonged. Five hundred millilitres gave only transient improvement. She's now got crackles and a new oxygen requirement. We've treated her for suspected urinary sepsis and stopped further fluids. We'd like urgent review for circulatory support.”
You should expect questions about her baseline function, her wishes and any treatment escalation plan. Have that information ready where you can, alongside the immediate clinical picture.
There is also the very common overnight call about a patient with a low blood pressure while asleep. Blood pressure normally falls during sleep, so context matters.
But don't assume sleep is the explanation without assessing the patient and checking the reading. Are they appropriately rousable? Is this their usual pressure? Are there signs of poor perfusion, fever, chest pain or another change?
If they're comfortable, appropriately responsive and well perfused, you may be reassured. The timing of repeat observations should follow the findings, NEWS2 and local policy. A blanket instruction to wait four hours isn't appropriate for every sleeping patient with a low reading.12
That's the sort of distinction the hypotension-overnight section in bleep.guide is trying to help you make.
Think about three hypothetical situations.
First, a blood pressure of 94/60 in someone who normally runs at 94/60, is comfortable and alert, and has normal perfusion. That may simply be their baseline.
Second, a pressure of 112/70, which sounds reasonable, but the patient is newly confused, mottled and making less urine. That still worries me. Look beyond the pressure, and remember that new confusion also contributes to NEWS2.
Third, someone who remains poorly perfused after a bolus and now has signs of pulmonary congestion and an increasing oxygen requirement. That's a reason to stop and get urgent help, rather than reflexively give another bolus.
Who needs fluid, who needs urgent help, and who can be reassessed on a less urgent plan? Those are the questions I want you to be asking.
How do you identify a low JVP? We know what a raised one looks like, but what about a low one?
First, don't assume that a JVP you can't see is necessarily low. It can be difficult to identify. Adjust the patient's position and look for the venous waveform; lowering the head of the bed may bring a low venous column into view. If you still can't assess it, say that it's not assessable rather than declaring it low.13
I would recommend watching good demonstrations on real people and practising with someone who can show you the waveform. It's much easier to understand when you've seen it than from a textbook description alone.
What would you classify as peri-arrest?
I'm thinking about a patient who's deteriorating and appears at imminent risk of cardiac arrest. Chest pain, severe breathlessness, hypotension and altered consciousness are warning signs, particularly when they're a clear departure from baseline.
There is still circulation, but the breathing may already be severely abnormal. If the patient becomes unresponsive with absent or abnormal breathing, assess for arrest and start resuscitation when indicated. Peri-arrest shouldn't imply that they're breathing normally.2
Could vasoconstriction put more strain on the heart and worsen the shock?
Yes, it can. It depends on the patient's physiology and the agent you're using. Increasing afterload can make it harder for a failing ventricle to eject, while improved arterial and coronary perfusion pressures may be helpful.
I'm not going to profess to being an expert in choosing a particular agent for every situation. That's why this needs critical care input and reassessment of the response. Vasopressors aren't interchangeable simply because they all raise blood pressure.6
We'll leave it there. These sessions are deliberately short and bite-sized, rather than me talking at you for an hour. Next time, we're looking at urine output, retention and AKI. Thanks very much for coming along.