RE: Fwd: Mini-Journal Club

[Guest guest]

Mike,

That's an interesting stroke study. What journal did it come out of?

Questions for the group: Do you lower BPs pre-hospital in suspected CVA

patients?

Gene

[Guest guest]

Yes, through the use of drugs. 15 years ago it was common to treat all

hypertension pre-hospital aggressively. For example, when I first started in

the

business we carried labetalol and used it whenever we had a patient with

hypertension that exceeded the cutoff level, usually a systolic >200 and a

diastolic

of 130 or more.

Then nifedipine came into vogue and we carried nifedipine (Procardia) caps

and administered them by squeezing the contents under the patient's tongue or

having them chew them up and swallow them. Nifedipine can really do a number on

your BP, as in crashing it big time. So we stopped that. NTG will also

lower your BP, sometimes drastically.

So now we've become more interested in when and why we lower BPs pre-hospital

and what agents we use. Studies show conclusively, to me at least, that in a

patient with an emergent CVA lowering the BP is not the right thing to do.

The articles I read recommend that systolic BP not be lowered until CT is

done and the cause of the stroke can be determined, since the increased BP may

be

a compensatory action to maintain brain perfusion.

I am unaware of anyone who currently recommends that we use an

antihypertensive agent in the ambulance for a suspected CVA patient.

Further, the recommendation now is that when BP is lowered it should be done

slowly using an agent that can be titrated, such as sodium nitroprusside

(Nipride), liquid NTG (Tridil), or labetalol (Trandate), and the systolic BP

should be lowered no more than 10% per hour.

Perhaps there ARE situations where hypertension (not related to an ongoing

CVA) should be lowered, as in some of the cases Mike mentioned and where end

organ failure is a factor. So, guess what. We're back to labetalol for that.

In 25 years the treatment has come full circle.

Gene

In a message dated 10/30/2003 9:40:36 PM Central Standard Time,

cafr@... writes:

> Questions for the group: Do you lower BPs pre-hospital in suspected

> CVA

> patients?

>

> Gene

>

By the use of drugs or what? I certainly don't think you want to raise

it.

[Guest guest]

In a message dated 10/30/03 9:07:49 PM Central Standard Time,

wegandy1938@... writes:

Questions for the group: Do you lower BP pre-hospital in suspected CVA

Patients?

Gene

Train of thought used to be Yes. Train of thought now is NO. Increased BP

means Increased perfusion.

Danny L.

Owner/NREMT-P

Panhandle Emergency Training Services And Response

(PETSAR)

Office

FAX

[Guest guest]

Allright here is another question. Do we see any comeback for increased

ventilation for CVA?

Danny L.

Owner/NREMT-P

Panhandle Emergency Training Services And Response

(PETSAR)

Office

FAX

[Guest guest]

I don't. I don't know of any studies that now indicate it. Anybody else?'

G

In a message dated 10/30/2003 11:40:18 PM Central Standard Time,

petsardlj@... writes:

Allright here is another question. Do we see any comeback for increased

ventilation for CVA?

Danny L.

Owner/NREMT-P

Panhandle Emergency Training Services And Response

(PETSAR)

Office

FAX

[Guest guest]

The reason for the question of comeback for Increased ventilation is.....

Are we about to see a trend of treating differential diagnosis in CVA i.e.

Blockage vs Bleed?

Danny L.

Owner/NREMT-P

Panhandle Emergency Training Services And Response

(PETSAR)

Office

FAX

[Guest guest]

>Questions for the group: Do you lower BPs pre-hospital in suspected CVA

>patients?

>

>Gene

>

No certainly NO.

Jim<

[Guest guest]

> Questions for the group: Do you lower BPs pre-hospital in suspected

> CVA

> patients?

>

> Gene

>

By the use of drugs or what? I certainly don't think you want to raise

it.

[Guest guest]

An article in the Canadian Journal of Neuroscience (Can. J. Neurol. Sci.

2002; 29: 113-114) opened discussion regarding the treatment of hypertension

in acute CVA and addressed the issue of myth vs. fact with regards to the

same. Though, I do not see that EMS is the place to start lowering the BP

in acute stroke with marked hypertension, there is definite need for more

discussion. After reading this article, I feel that more physicians and

neuroscientists need to be on the same page before field treatment is

warranted.

" On the other hand, I have argued for many years7 that there are some

circumstances in acute stroke in which blood pressure must be treated,

so the argument is not about whether hypertension should be

treated in acute stroke, but how and when. Aortic dissection,

pulmonary edema with concomitant myocardial infarction,

hypertensive encephalopathy and worsening intracerebral hemorrhage

with very high pressures likely represent circumstances in which the

pressure must be treated. Furthermore, very high pressures probably

aggravate edema and hemorrhage, so that control of severe

hypertension may prevent worsening of the stroke itself.7,8 "

For further reading, the citations and references of this article are listed

below. But, recent literature also states that the blood glucose level is a

significant prognosticator of morbidity (I'll find the relevant studies when

I can).

1 Spence JD. Cerebral consequences of hypertension. In: Laragh JH, Brenner

B, eds. Hypertension: Pathophysiology, Diagnosis, and Management. New York:

Raven Press, 1995: 741-753.

2. SHEP ative Research Group. Prevention of stroke by anti-

hypertensive drug treatment in older persons with isolated

systolic hypertension. Final results of the Systolic Hypertension in the

Elderly Program (SHEP). JAMA1991;265:3255-3264.

3. Forette F, Seux M-L, Staessen J, Thij L, et al. Prevention of

dementia in the Syst-Eur trial. Lancet 1998;352:1347-1351.

4. Spence JD. Antihypertensive drugs and prevention of athero-

sclerotic stroke. Stroke 1986;17:808-810.

5. Barnett HJ, DW, Eliasziw M, et al. Benefit of carotid

endarterectomy in patients with symptomatic moderate or severe stenosis.

North American Symptomatic Carotid Endarterectomy Trial Collaborators. N

Engl J Med 1998 339(20):1415-1425.

6. PROGRESS Collaborative Group. Randomised trial of a

perindopril-based blood pressure-lowering regimen among 6105 individuals

with previous stroke or transient ischemic attack. Lancet

2001;358:1033-1041.

7. Spence JD, Del Maestro RF. Hypertension in acute ischemic

strokes: Treat. Arch Neurol 1985;42:1000-1002.

8. Tietjen CS, Hurn PD, Ulatowski JA, Kirsch JR. Treatment

modalities for hypertensive patients with intracranial pathology: options

and risks. Crit Care Med 1996;24:311-322.

9. Kanji S, Corman C, Douen AG. Blood pressure management in acute

stroke: comparison of current guidelines with prescribing patterns. Can J

Neurol Sci 2002;2:125-131. 10. Spence JD, Zarnke KB. Stroke and

Hypertension. In: Oparil S, Weber MA, eds. Hypertension: A Companion

to Brenner and Rector's The Kidney. Philadelphia: W.B. Saunders

Company, 2000:266-286.

11. Spence JD, son OB, Strandgaard S. Hypertension and Stroke. In:

Messerli FH, ed. The ABCs of Antihypertensive Therapy. New York:

Lippincott & Wilkins, 2000:279-296. 12. Schrader J, Rothemeyer

M, Luders S, Kollmann K. Hypertension and stroke - rationale

behind the ACCESS trial. Basic Res Cardiol 1998;93(Suppl 2):69-78.

13. Schrader J, Luders S, Kulchewski A, et al. [Acute Candesartan

Cilexitil Evaluation in Stroke Survivors: a double-blind

randomised comparison of candesartan cilexitil and placebo in the

control of blood pressure after an acute stroke.] Hochdruck und

Nierenkrankheit 2002; (abstract) in press

14. Spence JD. Stepped Care for Hypertension is dead but what

will replace it? CMAJ 1989;140:1133-1136.

15. Spence JD. Management of resistant hypertension in patients with

carotid stenosis: high prevalence of renovascular hypertension.

Cerebrovasc Dis 2000;10:249-254. 16. Spence JD. Physiologic

tailoring of therapy for resistant hypertension: 20 years

experience with stimulated renin profiling. Am J Hypertens

1999;12:1077-1083. 17. Eastwood JD, Provenzale JM, Hurwitz LM, Lee

TY. Practical injection-rate CT perfusion imaging:

deconvolution-derived hemodynamics in a case of stroke.

Neuroradiology 2001; 43(3):223-226.

18. Nabavi DG, Cenic A, Craen RA, et al. CT assessment of cerebral

perfusion: experimental validation and initial clinical experience.

Radiology 1999;213(1):141-149.

19. Bath P, Boysen G, Donnan G, et al. Hypertension in acute stroke: what

to do? Stroke 2001; 32(7):1697-1698.

Schadone, NREMT-Paramedic

City of Austin

Austin/ County EMS

Medic 12 / Medic 24

@...

[Guest guest]

>An article in the Canadian Journal of Neuroscience (Can. J. Neurol. Sci.

>2002; 29: 113-114) opened discussion regarding the treatment of hypertension

>in acute CVA and addressed the issue of myth vs. fact with regards to the

>same. Though, I do not see that EMS is the place to start lowering the BP

>in acute stroke with marked hypertension, there is definite need for more

>discussion. After reading this article, I feel that more physicians and

>neuroscientists need to be on the same page before field treatment is

>warranted.

>

Also interesting study in this weeks Neurology, Vol 61, Number 8, 10/28/03

www.neurology.org

Pg 1047 " Detrimental Effect of Blood Pressure Reduction in the First

24 Hours Following a Stroke. "

Jim<

[Guest guest]

I believe that most of the literature that I have been presented states (or,

leans towards) ventilating for SaO2 / SpO2 greater than 93% (except where

carboxyhemoglobin or methemoglobin are present or suspected to be present).

Interesting article that tells about the differences between PaO2, SaO2,

SpO2, and co-oximetry:

http://www.mtsinai.org/pulmonary/noninvasive/pulseoximetry.htm

Schadone, NREMT-Paramedic

City of Austin

Austin/ County EMS

Medic 12 / Medic 24

@...

[Guest guest]

Yes. I think that we will eventually see differing treatment modalities

regarding strokes (block v. bleed).

Schadone, NREMT-Paramedic

City of Austin

Austin/ County EMS

Medic 12 / Medic 24

@...