1. Hypertensive Emergencies
Alyssa Morris, R3
March 5, 2009
Thanks to Dr Gant!

2. Definitions Hypertensive Emergency
Acute, life threatening, usually a BP> 180/120
Target organ damage
Hypertensive Urgency
Asymptomatic, severe HTN, usually >180/120
NO target organ damage
These are not absolute numbers
- nb to treat the patient and not the number

3. Hypertensive Emergencies
Neurological
Hypertensive Encephalopathy
CVA
SAH
ICH
Cardiovascular
MI/ischemia
Acute LV dysfxn
Ao dissection
Pulmonary
Acute edema
Other
Acute renal failure/insufficiency
Retinopathy
Eclampsia
MAHA

4. Components of BP BP= CO x SVR CO= HR x SV Think of the components as:
CO= heart
BP= arteries
SVR= arterioles
- Other systems impact these factors. The RAAS system and the ANS play a role.

5. CPP=MAP-ICP
-throughout the normal range of BP, cerebral blood flow is maintained by fluctuation in the vascular tone of the cerebral resistance vessels (which are have ability to constrict to prevent too much pressure). So they dilate to increase flow at the bottom of curve and then constrict to prevent to much flow in the upper portion of the curve.
- In patients with HTN, cerebral autoregulation is reset at a higher level
Lower part of curve, you won’t perfuse brain
In upper part of brain you can get brain edema because previously constricted vessels reach a critical level and then suddenly dilate, leading to leakage of fluid thru BBB

6. Secondary causes of HTN
Conn’s is primary hyperaldosteronism: increase aldo leads to increase Na therefore increase volume
- RAS- bilateral increases RAAS but can’t filter voume like you can with unilateral , therefore, bilat is volume HTN and unilat is constriction HTN
- mineralcorticoids increase Na retention
- catecholamines increase vasoconstriction

7. CASE 1

8. Hypertensive Encephalopathy
Uncommon syndrome
Acute and reversible
Results from an abrupt, sustained rise of BP that exceeds the limits of cerebral autoregulation of the small resistance arteries in the brain
Arises from “breakthrough” hyperperfusion and leakage of fluid thru BBB

9. Flow diagram of pathophys

10. Clinical Presentation
Severe h/a
Drowsiness
ALOC
Vomitting
Seizures
Focal neuro deficits
Blindness
Focal neuro do not follow a specific territory or anatomic pattern

11. Tx Various recommendations 25% over 3-4hrs
10% in first hour, 15% in next 2-3 hours
*will not be able to perfuse brain if you drop it too fast or too much
-various recommendations but basically 25% over 3-4 hours
EMR suggested 10% in first hour, then 15% in next 2-3 hours
- will not be able to perfuse brain b/c will drop off curve and then get ischemia

12. CPP=MAP-ICP
-throughout the normal range of BP, cerebral blood flow is maintained by fluctuation in the vascular tone of the cerebral resistance vessels (which are have ability to constrict to prevent too much pressure). So they dilate to increase flow at the bottom of curve and then constrict to prevent to much flow in the upper portion of the curve.
- In patients with HTN, cerebral autoregulation is reset at a higher level
Lower part of curve, you won’t perfuse brain
In upper part of brain you can get brain edema because previously constricted vessels reach a critical level and then suddenly dilate, leading to leakage of fluid thru BBB

13. Drug Options VASODILATORS Nitroprusside Nitroglycerin Fenoldopam
Hydralazine
BETA BLOCKERS
Labetalol
Esmolol
CALCIUM CHANNEL BLOCKERS
Enalaprilat/enalipril
ALPHA BLOCKERS
Phentolamine
Clonidine

14. Nitroprusside Potent smooth muscle relaxing agent
Reduces both preload and afterload
Rate of onset rapid, duration very short
Also a cerebral vasodilator
Can increase ICP secondary to increased cerebral blood flow
Unstable in UV light, therefore wrapped in tinfoil
Infusion at ug/kg/min -then increase by 0.5mcg/kg/min
Max of 10 mcg/kg/min
This is an excellent choice in hypertensive crisis for these reasons
- b/c of reduction in preload by venous dilation, the CO often improves if CHF or bad LV fxn is present
- can get hypotension and get a reflex tachycardia as a result

15. Nitroglycerine Activates guanylate cyclase Accumulation of cGMP
Sequestration of Ca into SR
Relaxation of Vascular smooth muscle
Dose dependent
Low dose: venodilator (preload)
High dose: veno and arteriodilator (afterload)
Therefore, usually reduce BP by reducing preload and CO
Start with 10-20ug/min infusion
Titrate up 5-10ug/minQ3-5min
Doses as high as ug/min may be needed for maximal antihypertensive effect
- reduction in preload and CO might not be desirable in pts with poor cerebral and renal perfusion
- careful when using it in patients with RV dysfxn to avoid hypotension (preload dependent)
- best used in pts with cardiac ischemia or pulmonary edema

16. Hydralazine Direct arteriolar vasodilator
Used to be used as first line in pregnancy htv emergencies
Starting dose is 5mg IV
Repeat doses of 5-10mg IV every 20 mins to maintain desired BP
Complications:
Marked hypotension
Reflex tachycardia (can give angina)
Flushing and nausea
H/a
- Now using labetolol or nicardipine

17. Labetalol Selective α-1 blocker and nonselective β-blocker
α:β blockade ratio between 1:3 and 1:7
Not a significant drop in CO like other βB
Does not affect cerebral blood flow or renal fxn
BP starts to fall in 5-10m, max effect at 30m
How much do you guys give?

18. Esmolol Selective β-1 blocker Very short acting
Elimination ½ life of 9 minutes
No intrinsic sympathomimetic activity
-b/c the half life is 9 mins, you get substantial recovery from B blockade in mins

19. Phentolamine α-blocking agent
Used for the Mx of catecholamine-induced HTV crisis
MAOI, Pheo, Cocaine
Immediate effect
Effect lasts up to 15 mins
1-5mg IV boluses
MAOI
- pheo
Cocaine

20. CASE 2
Head CT demonstrates multiple, bilateral, patchy foci of hypoattenuatin within subcortical white matter in the occipital regions
- MR shows hyperintensity within the subcortical white matter of the bilateral occipital and anterior parietal lobes.

21. PRES Posterior reversible encephalopathy syndrome Pathophysiology
Cerebral vasospasm leading to cytotoxic edema
Vasodilattion leading to vasogenic edema
- again, disorder of cerebral autoregulation with two theories.

22. CASE 3 - What kind of stroke is this? L MCA
- Given this, would you treat the blood pressure? (200/110)

23. HTN Mx in Ischemic Stroke
Consensus guidelines published in the journal of stroke.
Stroke. 2007;38:

24. - Want to monitor BP after giving TPA as well. Same goals.

25. HTN Mx in Ischemic Stroke
HTN common in 1st hours after stroke
SBP>160 found in 60% pts with acute ischemic stroke
For every 10mmHg raise >180, risk of neurologic deterioration increases by 40% and risk of poor outcome by 23%
In these patients, htn is usually the physiologic response to the stroke itself and is not the immediate cause
- can try to reduce modifiable factors that could be contributing to the htn

26. HTN Mx in Ischemic Stroke
Theoretical reasons for lowering BP in stroke
Decrease formation of brain edema
Lessening risk of hemorrhagic transformation of infarction
Preventing further vascular damage
Forestalling early recurrent stroke
BUT remember aggressive tx of BP may lead to neurologic worsening by decreasing perfusion pressure to ischemic areas of brain

27. CPP=MAP-ICP
-Do not want to get them too low or won’t perfuse brain and the penumbra is depending on flow to deliver O2 and reduce the ischemic area

28. CASE 4 - What kind of stroke is this? L MCA
- Given this, would you treat the blood pressure? (200/110)

29. HTN Mx in Ischemic Stroke
A lot of studies showing harm with reduction of BP
Most pts have a decrease in BP a few hours post- stroke w/o intervention
Oliveira-Filho et al. Neurology. 2003;61:
Found >90% pts had a decrease in SBP by 28% in 24hrs post-stroke with no intervention
Outside TPA window
- DO NOT want to decrease pressure to much b/c penumbra dependant on perfusion pressure

30. Consensus Statement
“ emergency administration of antihypertensive agents should be withheld unless DBP>120 and SBP>220”
“reasonable goal to decrease blood pressure by % within 24 hours”
This is a case-by-case decision
More research needs to be done
-typically recommend labetalol 10mg IV over 1-2 minutes with rpt doses as needed unless there is a contraindication to BB then use nicardipine infusion
- Stated that the CHIPPS trial might be able to give more evidence

31. Case 4

32. Stroke, 2007;38:

33. HTN Mx in Hemorrhagic Stroke
Primary rational for reducing BP is to avoid hemorrhagic expansion from potential sites of bleeding
BP is correlated with increased ICP and volume of hemorrhage
Difficult to determine whether increased BP is a cause of hemorrhage growth or an effect of increased volumes of ICH and increased ICP

34. HTN Mx in Hemorrhagic Stroke
Summary of studies
Isolated SBP<210 is not clearly related to hemorrhagic expansion or neurologic worsening
Decrease in MAP by 15% does not result in decreased CBF
Baseline BP was not associated with growth of ICH in largest prospective study
Hemorrhage enlargement occurs more frequently in pts with increased SBP but it is not clear if this is an effect of increased growth of ICH with associated increase in ICP or a contributing cause to the growth of ICH
Evidence supports maintaining CPP >60mmHg
WE DON’T KNOW

35. Not a strong stand on the subject
- State that much more research needs to be done and could be answered by the ATACH study and the INTERACT study.

36. HTN Bleeds Where do you get HTN bleeds in the brain? Cerebellum Pons
Basal ganglia
Thalamus
- Areas in brain affected by chronic htn are the perforating arteries which serve these areas
-what about BP in the setting of hemorrhagic stroke??

37. Case 4
With nipride can get increased SV and a reflex tachycardia so you want to avoid it first
- go by R arm b/c flap flapping over is falsely lowering L arm BP
- remember to check leg BP if arms normal and you are thinking about dissection
- want to reduce shear force and pulse pressure
- Use a BB to reduce BP (labetalol or esmolol) for a goal of SBP<110 or
- if becoming too brady, can switch to nipride because you have sufficiently BB her and will blunt reflex tachycardia and

38. HTN Mx in Ao Dissection
Remember to check BP in legs if you are thinking dissection b/c the flap can give you falsely low BP in arms
Want to avoid shear stress and wide pulse pressures
Reduce the LV ejection force
Goal is to get SBP but just do what you can
Use labetalol or esmolol
Can use nipride after have sufficiently BB b/c will blunt the reflex tachycardia and increased SV

39. Case 6
- Discuss who would treat an urgency with risk factors and who would not

40. Drug Summary Nitroprusside Nitro Labetalol 0.25-0.5ug/kg/min
Inc by 0.5ug/kg/min quickly
Nitro
10-20ug/min
Inc by 5-10ug/min Q3-10min
Labetalol
10-20mg IV Q5-10min
Infusion at 1-2mg/min