Shock: Back to basics, beyond the BP

Apologies to the smart ones reading this – but I have been trying to explain this concept to my students for a while – so I thought I would share.

Shock: this is defined by hypoperfusion of the tissues resulting in insufficient substrates (oxygen, sugar etc) for aerobic cellular respiration.

The good news is that evolution has supplied us with a back up plan in the event of “inadequate substrate for aerobic respiration” – namely anaerobic respiration – neat eh!  But there is a limit to this – you eventually need to get back to Aerobic metabolism, clear the toxic byproducts of anaerobic respiration and repay the oxygen debt.

Ok that is the technical bit done.  Now onto the clinical application of this science.

In order to maintain tissue perfusion (and fuel / oxygen supply) you need to have blood passing through those little terminal arterioles / capillaries at a rate fast enough to keep up with the demands of the tissue – this can vary also.

Here we meet the problem – we (clinicians) have got no good direct way of measuring the flow or demand in those little vessels.  At the bedside we can just guess as to what is going on.  Unfortunately our instincts for this “guess work” are a bit skewed and that is the point of this post – we need to develop better instincts here.  So this is how I do it.

The blood pressure is an important piece of information – very important – but it is not the only player when it comes to working out the perfusion of the important organs.

Problem is – we all cut our teeth on relatively stable, healthy patients who have good physiological reserve and are operating towards the centre of the comfort zone of perfusion.  In these patients the BP is probably a good proxy for “perfusion”.  BUT – in the patient who is sick (ie. the one where you really want to know what is going on ) the physics are not ‘normal’ – you need more info and here the instinct needs to be developed.

Ok, some boring mathematics now :-

Cardiac output (CO) =   HR   x   stroke volume (SV)                  and              BP   =   CO  x   systemic vascular resistance (SVR)  or  CO  = BP  / SVR

So therefore:     HR  x  SV    =     BP  /  SVR.    Yep, I just tried to reduce CV physiology to 4 numbers. Not always so simple – but its a start.

You can read HR and BP off of the monitor, or even do it manually!

The SV  – hard to measure clinically – you can palp the radial pulse and guess its ‘volume’, you can ask the patient if they have some chronic cardiac disease / cardiomyopathy / IHD.  Or you can pick up an ECHO probe and eyeball it, or ask an ECHO tech to give you a number (LVEF).  Knowing that the preload is good certainly helps – so look at the IVC – is it collapsing?

So that just leaves the SVR – and this is tough.  In a sick patient – you cannot interpret the BP or guess the cardiac output without having some idea about the SVR.  So how can we measure this?  Look at the patient – are they red, flushed or pale and white.  Feel the hands and radial pulse – are they cool and thready or bounding and warm?  Urine output – if this is low – there is a good chance the normotensive patient has a high SVR.  Or you can get a fancy monitor which gives you a number – SVV (stroke volume variation) or Oesophageal Doppler etc.  None of these are perfect.

So once you have guessed the patient’s SVR you are in a position to interpret the BP and make an estimate of the perfusing  cardiac output / cardiac index  (NB: the cardiac index sounds impressive, but it is just the CO divided by the patient’s body surface area.  ie. big people need more CO to perfuse their body than little people)

Confused yet?  Lets look at a few common clinical scenarios to illustrate these points.  Also to look at the uses and abuses of inotropic meds in the hypotensive patient.

If you give a decent slug of propofol to anybody over about 60 – they will probably crash their BP. Is this a bad thing? well yes, but not as bad as you might think.

The propofol causes a loss of SVR by relaxing all the peripheral vessels.  So both the BP and SVR have fallen – the CO is proabably not crashing as much as the BP would suggest.  Of course if the propofool renders the heart bradycardic and negative inotropy reduces the ability of the heart to compensate – this is not great.  But any Anaesthetic doc will tell you – if you give them a whiff od metaraminol / phenylepherine  – the BP comes up quick.  And as soon as the surgeon inflicts pain – they settle quickly.  So here is an example of ‘relative’ hypotension – sure it is low – but so is the SVR – so it isn’t so bad.

This is usually a vasoplegic state – all those inflammatory cytokines cause a decrease in SVR,  the vascular bed expands – making the patient “relatively hypovolemic”.  There is a fall in CO due to poor venous return – so the BP drops as does the perfusing pressure – and shock occurs.  In some (maybe 15%) they get myocardial depression form the toxins of sepsis and also therfore suffer from “pump failure as well as the other mechanisms of shock at play.

So – for sepsis the rule of thumb is :-  give a heap of fluids – more than you think.  Give 2 litres and ask questions later.  If they remain hypotensive / acidotic / high lactate then you might need to give inotropes.  BUT you have to “prime the pump first” – check the IVC / SVV (or CVP if you believe in it) to ensure they are fluid loaded adequately.  So which fluid?   The SAFE trial – no difference between saline and albumin, though there was a trend towards benefit in giving albumin in the septic subgroup.  To me, in a small place Hartman’s (Ringer’s) seems to make sense – it is chaep, easy and doesn’t screw with your acidosis too much?

Then, and only then give inotropes…which one?    I think the answer is noradrenaline – it is widely used for sepsis and makes sense as it has good alpha agonism – so combats the low SVR.  You could also use phenylepherine if you cannot get a CVC.  If htere is evidence of myocardial depression – then you might need to get smarter and use adrenaline or call a friend for help! Having said that Myburgh et al (Aussie ICU crew) showed no difference between norad and epi – so it is a bit theoretical.

This is not the same as the septic patient.  In my mind this is the opposite of sepsis in a way.  Consider a 30 yo. motorcyclist with crush chest and pelvic fracture.  The BP is lowish, you guess he is bleeding into his chest, pelvis, ?abdo… and his endogenous adrenaline is surging – so he has a massive SVR.  So here – a lowish BP equals a crappy CO and his perfusion of the terminal vessels is terrible.  This is not a place to use vasopressors – you will make his SVR go higher and kill the perfusion further.

The patient with hypovolemic shock needs volume +++ – see recent post on Massive transfusion in trauma.  Blood, clotting factors, keep them warm and manage acidosis.  And acidosis is the result of the anaerobic metabolism in the O2-starved tissues – muscles, livers etc.

So here what you want to do is open up the vascular bed, get the perfusion happening ASAP – you actually want to drop the SVR – the catch phrase is “sympatholytic resuscitation”.  You do this by filling them up with volume, then giving fentanyl (or your favourite alternative) to reduce the endogenous sympathetic drive and allow the red cells you are pumping in to get to the areas that need the oxygen.

Remember – target MAP is 65 initially – so if your patient has a comfy MAP of 85, yet you know they have bleed a lot – your BP is giving you a seriously false sense of goodness. The best guide here is the pH, or lactate or base deficit or the temp of the hands – these are the markers of poor perfusion – not the BP so much!

This is pretty uncommon… unless you are an Obstetric Anaesthetic doc – then you come across it everytime you do a C-section. So I will use this as an example.

When you do a spinal – the first nerves to go ofline are those little sympathetic fibres – so you lose your peripheral vascular tone and the SVR drops quick – and your patient vomits, looks very grey and sweaty.  If the spinal goes higher, you lose the sympathetic fibres to the cardiac plexus – and your patient gets bradycardic, maybe some aorto-caval compression = a problem (CO = HR x SV), a double whammy – SVR crash, then CO crash – not good at all. {pray there isn’t a big bleed mid-op!}

So how to manage this – well it depends on the level of the cord lesion / block.  Lower levels, without bradycardia – maybe just a phenylepherine infusion.  Higher blocks with slow heart – you might need some chronotropy to help – good old adrenaline is my choice (ephedrine is an option – though a bit weak)  The high-spinal is the one emergency that goes C, B, A  – not A, B, C in real time!

So that is my super-simple and pragmatic approach to SHOCK.  In my experience – the big problem with SHOCK is recognizing it.  Once you have made the diagnosis he management is easier – but just remember – the BP is just part of the story.

If you don’t think about the other players – CO, SVR etc then it is a bit like walking into a movie theatre half way through a good “who-dun-it” murder mystery.  You might never guess who the killer was!

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