Blood Pressure in Stroke

Today’s discussion: Why and How do you control the blood pressure in both ischemic and hemorrhagic stroke?


To know the rationale behind the need to lower the blood pressure in stroke and the limitations, we have to review the cerebral physiology and cerebral autoregulation.

Where CBF: cerebral blood flow
CPP: cerebal perfusion pressure
CVR: cerebral vascular resistance



The issue in ischemia is that it disrupts that cerebral autoregulation, so the CVR does not respond to changes in CPP.

Another thing to consider is that the impact of decreased cerebral blood flow (CBF) is related to both the magnitude and duration , therefore:
- CBF <10-15 mL for more than a short time = neuronal death. Labeled as “infarct”
- CBF 15-20 mL = neuronal functional impairment. Labeled as “penumbra”

The “Penumbra” is an area of high CBF, high O2 consumption, and preserved metabolic rate. This area is seen by PET, and sometimes with MRI. It’s ischemic, but not infarcted. It is very vulnerable to any decrease in blood pressure.

On the other hand, leaving the blood pressure too high predisposes the patient to more bleeding and hematoma formation in hemorrhagic stroke, and to more edema and hemorrhagic transformation in ischemic stroke. However, clinical data supporting this theory is sparse.

A few pointers to keep in mind:

- Patients with chronically uncontrolled HTN have “reset” their “normal” CPP to a higher level, so their CBF decreases at a relatively higher MAP. Therefore, lowering their blood pressure too much can be detrimental.

- Patients with carotid stenosis will have even more compromised cerebral blood flow with acute reduction in blood pressure.

Now that we’re done with the logic behind it, here’s the most consistent data for management of BP in stroke (according to Rosen’s 6th Edition); most of it was reached by consensus:

As for ischemic strokes;

As for hemorrhagic strokes, these are the latest AHA guidelines:

A few pointers to remember:
- MAP= 1/3 SBP + 2/3 DBP
- Labetalol should be avoided in asthma, acute heart failure, or severe cardiac conduction abnormalities.
- In refractory HTN, other agents may be considered. However, drugs that cause precipitous decrease in bp should be avoided, such as sublingual nitroglycerin and calcium channel blockers (CCB)

So to sum it up:
- If the blood pressure is too high, the patient will rebleed (especially in hemorrhagic strokes).
- If the pressure is too low, the patient will infarct his penumbra (especially in ischemic stroke)
- Therefore, blood pressure must be controlled in acute stroke; in hemorrhagic stroke more than ischemic, and in patients managed with tPA more than non-thrombolytic candidates

Arterial vs Venous Lactate

The other day, the supervising Consultant asked me to look up the difference between arterial and venous lactate. This was a direct result of my big mouth as I was the one who raised this point, since a lot of the articles that talked about lactate made a point to mention that it was “arterial” lactate, whereas some articles just said “lactate”.


The question is, are they really any different?

To answer this question, I googled it! (sorry pubmed lovers, I’m a “google” chick!)

And Here is what I got:

There are 3 studies that compare arterial and central venous lactate in patients in shock/cardiac arrest (J Resuscitation 2008;03:055 , Emerg Med J 2006;23:622-624, Crit Care 2005;9:44). They all came to the same conclusion; the levels are closely correlated. The first one even added that the levels more closely correlated if arterial lactate value was >5mmol/L.

I also came across a nice website (that is Google’s benefit  ), called www.emedmag.com , in which there’s an article discussing the most important differences in values of ABGs and VBG, AGs, and finally, lactate.

This website came to the conclusion that since an elevated venous lactate (1.6 mmol/L or greater) is 100% sensitive and 89% specific in predicting elevated arterial lactate level, then a normal venous lactate should be enough, but an elevated venous lactate necessitates that an arterial lactate should be obtained. It cites a 1996 study by Younger of 48 ED patients as a basis for this conclusion. These results were bolstered by a 2000 study by Lavery on 375 hypovolemic patients.

While discussing the findings of my mini-search with my colleagues and seniors, we came to a discussion; is lactate higher in arterial blood or venous blood?

Logic says that it should be higher in venous blood than in arterial, as it is always a result of poor tissue perfusion, and is cleared by the liver, right?

NOT EXACTLY!

According to “The ICU Book” by Paul Marino; Lactate level is not indicative of poor tissue perfusion, but rather is a method of detecting global dysoxia. However, it sometimes indicates other things, such as hepatic insufficiency, thiamine deficiency, severe sepsis (as a direct result of endotoxins rather than O2 deprivation) and, finally, intracellular alkalosis.

It’s interesting how a discussion can clarify some of your most basic concepts!