Cerebral Perfusion

[Matthew Reeds]

As we have discussed at great length on this list, I would not be distracted
by the systolic blood pressure for a number of reasons:-

 

 

1) The brain has an excellent in-built mechanism to autoregulate cerebral
perfusion (controlled mainly by pCO2 and, to a lesser extent, pO2).

 

Increases in pCO2 (e.g. caused by cellular hypo-perfusion secondary to
trauma/haemorrhage) increases cerebral blood flow due to marked cerebral
vasodilatation (CO2 is a vasodilator metabolite which acts on the arteriolar
smooth muscle via myogenic autoregulation.) This is why head injury patients
are ventilated to low-normal pCO2 rather than low pCO2 as low pCO2 causes
vasoconstriction with potential cerebral ischaemia. Too much vasodilatation
on the other hand increases the risk of raised ICP (Monroe-Kellie Doctrine)
which we know is bad as this reduces the cerebral perfusion pressure CPP
(CPP = MAP - ICP). An important balance must therefore be maintained. As you
will see, this mechanism is mainly influence by pCO2 and not pO2 (pO2 only
plays a role at pO2 < 8kPa whereby cerebral blood flow may increase
dramatically below this point.)

 

The autoregulation works over a wide range (CPP range of between 60-160mmHg)
Indeed we now accept lower CPPs than we used to do as we may have previously
been overly aggressive in treating patients to their own detriment by aiming
for too high CPPs. 

 

These mechanisms are affected to varying degrees by a number of factors
(e.g. neurotrauma).

 

2) An excellent crude indicator of cerebral perfusion is conscious level. It
is used daily in neurosurgery and frequently by the military (the crude
correlation of carotid pulse/blood flow present = cerebral perfusion
present.) The military regularly apply the principle that if the patient can
state name, rank and number then they are OK and receive no fluid -
regardless of their other injuries/haemorrhage. Obviously if there is
inadequate cerebral perfusion then this must be addressed expeditiously;

 

3) At a systolic BP of 90mmHg in a head injured patient then cerebral
autoregulation may well still be present. It would depend entirely upon the
diastolic BP and ICP as well but many patients with a low BP have still been
able to maintain cerebral perfusion and consciousness;

 

4) Aiming for too high a CPP pressure will predispose to cerebral oedema
with raised ICP. This will ultimately have a detriment effect on CPP. This
can be counteracted with hypertonic saline (7.2% or 7.5% which also have an
osmotic diuresis effect and therefore reduce cerebral oedema and ICP as
well.) Hypertonic saline is therefore, in my opinion, the best fluid to give
if you have to give any fluid at all;

 

5) A much simpler reason is that C comes before D. If the patient is
haemorrhaging then there is no point trying to continually maintain cerebral
perfusion with fluids if the patient is exsanguinating to death without
correcting the underlying problem. Correct the haemorrhage and you will be
more likely to restore cerebral perfusion to normal physiological levels.
Naturally if the patient has no carotid or vertebral flow then the patient's
autoregulatory mechanisms have failed and fluid boluses (e.g. hypertonic
saline) may be required to increase the cardiac output in order to
re-establish cerebral flow and induce cerebral output!!

 

 

Although the above regulatory feedback mechanisms work to compensate and
maintain cerebral perfusion in adverse situations, the key is to stop the
haemorrhage and correct the problems rapidly - as these compensatory
mechanisms will eventually fail and the aim is to correct the problems
before this decompensation happens. For the aforementioned reasons, I think
we need to appreciate not to be too over-focused on increasing the cerebral
perfusion pressure, because it will more likely than not be sustained by the
body's autoregulation. This allows you to concentrate on the major
haemorrhage rapidly first and foremost - which is your more immediate
priority.

 

As you will see, like many others, I therefore don't focus on blood
pressure.

 

 

 

Matthew

 

 

-----Original Message-----
From: Anthony Caruso [mailto:medic541 at hotmail.com] 
Sent: 26 May 2008 19:53
To: Trauma &amp; Critical Care mailing list
Subject: RE: Delayed healing as reason for delaying definitive surgery

 

 

 

Mike, interesting to say the least.  I have a question however.  I have done
a bit of reading on this, as well as have seen it on this list from time to
time.  What do you do if the pressure drops below 90 systolic with a head
injured patient?  I believe that if a pressure drops below 90 systolic that
the patient has a 60% chance of the injury to be fatal. (Keeping in mind
that the near hypotension is related to blood loss and not necessarily a
neurogenic issue).  Do we infuse crystalloid's to keep the presure up?  We
have discussed on this list that infusing a large amount of crystalloids has
a worse outcome than holding off on giving them.  I suppose this would be a
question for one in the pre hospital arena as well as in the EW.  Any
thoughts?

 

Anthony M. Caruso EMT-P