Michael Patterson FCICM FANZCA
Mike is an intensivist anaesthetist in Melbourne. He has spent years thinking about disasters seen in anaesthetics and ICU–most of them are hemodynamic ones. His original interest in this problem stemmed from the death of a young lady having elective gynae surgery, in the setting of anaphylaxis. She had an easily palpable central pulse and reassuring EtCO2 throughout. He was involved late due to issues with arterial access. She died of a hypoxic brain injury solely because her pressure was too low for too long. He has been reflecting on this over the last few years and building up a picture of the problems and the solutions. Subsequently, he had been involved in one patient that died in the setting of a POCUS pulse but inadequate pressure and another young lady who lived despite nearly the same problem occurring as the lady that died.
Central pulses are almost meaningless
- We are mostly just feeling a change in pressure
-
Hence 50/10 might feel similar to 120/80
Central pulses are particularly dangerous in distributive shock where the pulse will be felt strongly below 50/-. This has been my repeated experience. It is easily palpable even in hypovolaemic shock with BP < 60 on occasion – You can’t measure pressure from a central pulse until you place an arterial line
POCUS Pulse as a Representation of Adequate Pulse
The use of POCUS to confirm flow in the femoral artery or palpation of a femoral artery pulse is problematic, as you discussed. In your hands (and proper resuscitationists), there will be an arterial line in place very quickly so it is a non-issue. Obviously, those involved in resuscitation should fix their system to achieve this but for lots of reasons that is a problem in many parts of the world (including most Melbourne ED’s/ICU’s).
The problems with ROSC in the setting of PEA or profound hypotension in general are:
POCUS pulse has the same problems as a central pulse unless applied to the brachial artery where you can place a manual cuff and visualize the occlusion pressure
Normal EtCO2
A normal EtCO2 is not reassuring that the pressure is adequate, as you mention – It is useful to suggest ROSC when it kicks up – It is dangerous as any reassurance in distributive shock where pulmonary perfusion is maintained and EtCO2 often doesn’t drop at all despite BP’s < 50/- – In the cardiac arrest setting, PaCO2 has often risen significantly so an EtCO2 in the 30’s may still represent inadequate perfusion let alone pressure I like your step-wise summary of the progression to ROSC. It is brilliant.
The yellow zone is where all the badness is happening in the anaesthetic world and I wonder if that is true in ED and ICU but we just don’t recognize it (as the patients are sick beforehand so any bad outcome isn’t attributed to the haemodynamic management).
You explained the problems with this zone excellently but I wonder if people will appreciate the dangers of a POCUS pulse or a palpable central pulse for that matter. I am concerned they will be misused and prolong periods of hypotension. I know you were only talking PEA but the issues are the same in profound hypotension.
My approach is as follows in the setting of profound hypotension = POCUS pulse:
Radial Pulse?
Identify that the radial pulse is rapidly and easily felt before you have a problem – This is obviously irrelevant for those presenting in cardiac arrest – In most other circumstances, if you knew it was strong and easily palpable prior, you can’t end up with confirmation bias – convincing yourself there is no problem. Occasionally it is difficult to locate prior, in which case, if they are sick you better put in an arterial line while the going is good as you are hosed with no endpoint. – It is essential in anaesthesia where patients are well before we start.
Peri-Intubation A-Line
But it is useful for peri-intubation management in ED and ICU when there is no arterial line – If it disappears – you have a problem until you get it back. No denial. – Once you have it – you can measure a manual BP rapidly – I agree that people don’t feel pulses well in cardiac arrest. It needs to match the ECG rhythm and disappear with cuff inflation. This probably is not useful in ROSC after cardiac arrest and points 2 or 3 are required.
Start thinking POCUS Blood Pressure
The only useful POCUS pulse is the brachial and it needs to disappear when a manual cuff is inflated – then you know the blood pressure – To be honest – unless you have practiced looking at brachial pulses with ultrasound regularly and recently I don’t know I recommend this one – If this was thought to be a useful end-point then we would need to practice it – I don’t have enough experience with this (in a resus setting) as I haven’t had the opportunity since I thought of it but it isn’t that hard in well patients – Is pulsation enough or should colour doppler be the only endpoint we accept? I don't know. All sorts of things go wrong in this area. I think pulsation is fair and accommodates all skill levels probably…..
SpO2 Blood Pressure
Occasionally the SpO2 probe on the finger maintains an excellent trace despite horrible blood pressures (<35/- is my most impressive example to date) – In this setting, you can inflate the manual cuff and note when it disappears to measure the BP 4. In the absence of 1, 2 or 3, you best hope you get an arterial line in efficiently because you are in no man’s land –
Repeatedly we see prolonged efforts at placing an arterial line only to find the pressure disastrously low once it is transduced. –
Central vs. Peripheral Arterial Lines
Treatment
I think escalating boluses/infusions of adrenaline/noradrenaline/vasopressin +/- fluids or blood depending on the circumstances. Basically, I have no idea what the right thing to do is and I suspect it depends on the case, likely aetiology and experience (which is a frighteningly unreliable approach). 1, 2 and 3 are the EtCO2 of the circulation as I see it. The measures you can’t argue with. If you don’t have them – you have a problem and there is no point denying it. They are the hard end-points that are needed to avoid loss of situational awareness and the passage of time trying to place arterial lines. Anyway, that is lengthy. Hopefully I’m not saying something really stupid. I think that very few ED’s and ICU’s work as well as yours. I have worked at most hospitals in Melbourne including an ICU fellowship at the Alfred. Very few clinicians have exposure to enough of these patients to be super slick with them – it requires a whole system to work (which is the point of your ED ICU’s but you’re a super specialised crew currently…..). Relying on speed to femoral arterial line placement doesn’t seem robust enough to me. Happy to discuss if it is of any use. I’m truly passionate about this problem as I feel the young lady that died deserves some system change. The yellow zone is a nightmare without an arterial line……
Additional New Information
- (Crit Care 2014;18:719)
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Using vascular doppler, may be another way to obtain information at least about systolic BP. In the veterinary small animal field BP have been assessed with such devices for decades. Technic: Place the probe over a finger or radial artery area until you have nice sound of blood flow. Fix it by tape. Using appropriate BP cuff and sphygmomanometer, blood pressure could be evaluated extremely easy. We could get BP as low as in the range of 40’s and small animals arteries are tiny compared to humans. Animals are having similar pathophysiology of shock as well. Truly like the podcast.… Read more »
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Hi Scott. Enjoyed this episode. The podcast made me think that it should be easy to objectively prove the utility/lack there of central pulses. As a cardiac surgeon twice a day I have access to pts who have arterial lines. Quick PubMed search however showed its already been published proving the points made in this episode.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC27481/#!po=16.6667
Cheers
Hossein
This episode was absolutely brilliant. The concept of measuring pulse pressure, and not adequate perfusion with central pulse checks just makes too much sense. The unreliability of ETCO2, and SPO2 in distributive shock states is the most important thing I’ve heard all year. Also the nod to confirmation bias, and the extreme ownership shown by Mike in the telling of his case study made this a very well rounded episode. 10/10
This episode was absolutely brilliant. The concept of measuring pulse pressure, and not adequate perfusion with central pulse checks just makes too much sense. The unreliability of ETCO2 and SPO2 in distributive shock states is the most important thing I’ve heard all year. Also the nod to confirmation bias, and the extreme ownership shown by Mike in the telling of his case study made this a very well rounded episode. 10/10
Very thought provoking case – I wish I had heard it 5 years ago! – I had a similar case 4 years ago young pregnant woman anaphylaxis to suxamethonium at induction of general anaesthesia for insertion of cervical suture. My patient was very unstable and actually arrested initially – needing adrenaline and CPR but after 10min or so we had a fairly easily palpable carotid pulse (must admit at the time I falsely assumed that this meant her BP was probably not terrible – obviously as you eloquently explianed this logic is false). We then went onto to put in… Read more »
Hey Roger!
Sounds like a frightening case. I think this is a really big issue in anaesthetics – we have the opportunity to define our haemodynamic endpoint before we have a problem which isn’t always the case in ED/ICU.
I’d be thrilled to discuss on your podcast – I’ll take any opportunity to get this message out there! I’ll shoot you an email.
Awesome. Just want to make a general comment. The presence of a mere pulse( palpable or POCUS ) should not assure anyone that all is well. It just means that there is definitely some circulation going on but that may or may not be enough to provide the perfusion to end organs. The same holds true for ETCO2 and oxygen saturation. Thanks for the great post.
Hey, I’m an anaesthetic registrar in Wellington NZ. I want to put together a brief talk with the evidence around correlation of pulse, etCO2 and BP for our monthly departmental education session. I would like to summarise your case @Michael Patterson.
Haven’t managed to find a contact for you otherwise.
I am wondering;
1. would you mind if I presented a summary of your case to our department?
2. Is there a formal write up of what took place available to the public?
Thanks and thanks for a thought provoking podcast.
Strong insight with respect to central pulses/pulse pressure. With regard to the consistent CO2, were there any other patient factors or even positioning factors with this? The hypothesis seems to be: there was enough cardiac output to see a normal CO2, and enough blood pressure for there to be runoff to enough tissue that CO2 production was fairly normal, but there was insufficient MAP for brain perfusion. I can imagine this being a salutory lesson on the sensitivity of brain tissue vs the rest of the human to hypoxia.
I know this podcast is from >1yr ago……. As a respiratory therapist, THIS podcast hit me the hardest. It’s about airway for us, but no BP=no PP (pee), but no BP is no cerebral perfusion. It means no ventilation/oxygenation. it’s killed me to hear “the BP will cycle again…….” =====mind you i just listened to your APRV podcast (i’ve only been listening for a year -so it’s all catch up) BP= cardio, cerebral, nephro PERFUSION…….. toooooooo much relies on the BP & to rely on NIPB (esp when iffy) is tragic….. God bless you Scott……i email you about wanting a… Read more »