Acute Hypertensive R Acute Hypertensive R e Response in Stroke: e - - PowerPoint PPT Presentation

Acute Hypertensive R Pathophysiology a Acute Hypertensive R Pathophysiology a

Adnan I. Q

Professor, Neurology, Neur President, International Societ

Adnan I. Q

Professor, Neurology, Neur President, International Societ President, International Societ

For the ATACH I Zeenat Qureshi Stro University of Minneso

President, International Societ

For the ATACH I Zeenat Qureshi Stro University of Minneso

e Response in Stroke: y and Management e Response in Stroke: y and Management

Qureshi MD

eurosurgery, and Radiology iety of Interventional Neurology

Qureshi MD

eurosurgery, and Radiology iety of Interventional Neurology iety of Interventional Neurology

H II Investigators troke Research Center sota, Minneapolis, MN

iety of Interventional Neurology

H II Investigators troke Research Center sota, Minneapolis, MN

Initial Systolic Blood Pressure the Emergency Room

(National Hospital Ambulatory

Initial Systolic Blood Pressure the Emergency Room

(National Hospital Ambulatory

60% 80% 100%

ients (%)

0% 20% 40% 60%

All stroke IS IC Proportion of patien

Adapted from: Qureshi AI, et al. A .

ure in Patients Presenting to m with Stroke in US

ry Medical Care Survey 2003)

ure in Patients Presenting to m with Stroke in US

ry Medical Care Survey 2003)

>220 mm Hg 1858219 mm Hg 1408184 mm Hg <140 mm Hg

ICH SAH

• l. Am J Emerg Med 2007;25(1):32#8.

Acute Hyperten Acute Hyperten

• Stroke specific
• Transient
• Prognostic significanc
• Stroke specific
• Transient
• Prognostic significanc
• Prognostic significanc
• Prognostic significanc

(Qureshi AI: Circulation 200

tensive Response tensive Response

ance ance ance ance

008 Jul 8;118(2):176#87)

Acute hyp

Stroke s aut

Acute hyp

Stroke s aut

Disrupt and/o Parasym acti Sympa act (Qureshi AI: Circulation 2008 Jul

ypertensive response:

e specific disruption of autonomic activity

ypertensive response:

e specific disruption of autonomic activity

uption: structural d/or functional ympathetic ctivity pathetic ctivity

BP

Adaptation: functional ul 8;118(2):176887)

Treatment of acut response in isch Treatment of acut response in isch response in isch response in isch

(Qureshi AI: Circula

cute hypertensive schemic stroke cute hypertensive schemic stroke schemic stroke schemic stroke

culation 2008 Jul 8;118(2):176887)

Reduction in cer SPECT Reduction in cer SPECT erebral blood flow CT scan erebral blood flow CT scan

Severe hypoperfus moderate hypoper alive but Severe hypoperfus moderate hypoper alive but fusion (core)8mild to erfusion (penumbra) but at risk fusion (core)8mild to erfusion (penumbra) but at risk

Cerebral blood flo Perfusion8Diffu Cerebral blood flo Perfusion8Diffu

Diffusion8weighted MRI

flow and cell death ffusion mismatch flow and cell death ffusion mismatch

Perfusion8weighted MRI

Hypoperfused but a salvageable8 Hypoperfused but a salvageable8

Diffusion8weighted MRI

t alive888potentially 888Penumbra t alive888potentially 888Penumbra

Perfusion8weighted MRI

Rapid collateral form intracranial occlusio

(Qureshi AI: J Vasc Interven

Rapid collateral form intracranial occlusio

(Qureshi AI: J Vasc Interven

• rmation during acute

sion888residual rCBF

ent Neurol 2008; 1(3):70872).

• rmation during acute

sion888residual rCBF

ent Neurol 2008; 1(3):70872).

Balloon inflation

Hypoperfused but alive— BP change888impaired au are BP de Hypoperfused but alive— BP change888impaired au are BP de

SBP=100 mm

—vulnerability to systemic autoregulation—collaterals dependant —vulnerability to systemic autoregulation—collaterals dependant

mm Hg SBP=160 mm Hg

Current guidelines are

• f avoiding further

Current guidelines are

• f avoiding further
• f avoiding further
• f avoiding further

re based on the policy her ischemic injury re based on the policy her ischemic injury her ischemic injury her ischemic injury

Intravenous Nim European St

(Ahmed et al. Cerebrovasc

Intravenous Nim European St

(Ahmed et al. Cerebrovasc Total anterior circulation infarction (n=106) (n=106) Placebo IV nimodipine 1 or 2 mg/h No difference in

• utcome

Within 24

Nimodipine West Stroke Trial

sc Diseases 2003;15:235#43)

Nimodipine West Stroke Trial

sc Diseases 2003;15:235#43) Partial anterior circulation infarction (n=62) (n=62) Placebo IV nimodipine 1 or 2 mg/h Diastolic BP reduction associated with neurological deterioration and outcome 24 hours

BP reduction harmful? BP reduction no effect?

Courtesy of David S. Liebeskind MD, UCLA Stroke Center, LA

Acute hypertensiv not be treated in

Qureshi AI: Circulation 2

Acute hypertensiv not be treated in

Qureshi AI: Circulation 2 A subgroup of patients may deteriorate

sive response should in ischemic stroke

n 2008 Jul 8;118(2):176#87

sive response should in ischemic stroke

n 2008 Jul 8;118(2):176#87 Benefit of acute blood pressure reduction unclear

American Heart As 2007 u American Heart As 2007 u

Pending more data, emerg antihypertensive agents s the diastolic blood pressu the systolic blood pressur Pending more data, emerg antihypertensive agents s the diastolic blood pressu the systolic blood pressur The panel remains concern aggressive lowering of blo patients may cause neurol goal is to avoid overtreati until definitive data are a The panel remains concern aggressive lowering of blo patients may cause neurol goal is to avoid overtreati until definitive data are a

American S

• Council. Str

Association Guidelines updates Association Guidelines updates

rgency administration of s should be withheld unless sure is >120 mm Hg or unless sure is >220 mm Hg. rgency administration of s should be withheld unless sure is >120 mm Hg or unless sure is >220 mm Hg. erned by the evidence that blood pressure among rological worsening, and the ating patients with stroke available. erned by the evidence that blood pressure among rological worsening, and the ating patients with stroke available.

n Stroke Association Stroke

• Stroke. 38(5):1655#711, 2007 May.

Treatment of acu response in pat Treatment of acu response in pat response in pat thromb response in pat thromb

(Qureshi AI: Circulat

acute hypertensive atients receiving acute hypertensive atients receiving atients receiving mbolysis atients receiving mbolysis

ulation 2008 Jul 8;118(2):176887)

Acute hypertensive re the risk of post8throm hemorr Acute hypertensive re the risk of post8throm hemorr

Impaired Reperfus (Qureshi AI: Circula Impaired autoregulation +SBP Reperfus +coagulo

response may increase rombolysis intracerebral

• rrhage

response may increase rombolysis intracerebral

• rrhage

rfusion ulation 2008 Jul 8;118(2):176887) rfusion ulopathy

SBP and post8th

Studies Patients wit acute ischem stroke ECASS II

(Stroke. 2001; 32(2):438#41)

793

(Stroke. 2001; 32(2):438#41)

Multicenter rt8PA stroke survey

(Circulation 2002;105:1679#1685)

1205

EPITHET

(Stroke. 2010; 41(1):72#7)

97

thrombolytic ICH

ith emic Intracranial hemorrhage rate Predictor

60 (8%)

Baseline SBP

158 (13%)

Pre8 treatment SBP

15 (15%)

Weighted SBP 1824 h

American Heart Ass Thromb American Heart Ass Thromb

• Systolic blood pressure is

diastolic blood pressure is Level of Evidence B) befor started.

• Systolic blood pressure is

diastolic blood pressure is Level of Evidence B) befor started.

• Maintained below 180/105

first 24 hours after intra

• Blood pressure recommend

in patients undergoing intr (Class I, Level of Evidence

• Maintained below 180/105

first 24 hours after intra

• Blood pressure recommend

in patients undergoing intr (Class I, Level of Evidence

American S

• Council. St

ssociation Guidelines8 mbolysis ssociation Guidelines8 mbolysis

is <=185 mm Hg and their is <=110 mm Hg (Class I, fore lytic therapy is is <=185 mm Hg and their is <=110 mm Hg (Class I, fore lytic therapy is 05 mm Hg for at least the ravenous rtPA treatment. ndations should be followed ntra8arterial thrombolysis nce C). 05 mm Hg for at least the ravenous rtPA treatment. ndations should be followed ntra8arterial thrombolysis nce C).

n Stroke Association Stroke

• Stroke. 38(5):1655#711, 2007 May.

Post8hoc analysis of

• Stroke. 29(8):15

Post8hoc analysis of

• Stroke. 29(8):15

Acute ischemic stroke and SBP >180 mm Hg (3824 h Antihypertensive treatment (N=65) 32% Clinical improvement at 24 hours

• f NINDS rt8PA trial

150489, 1998 Aug.

• f NINDS rt8PA trial

150489, 1998 Aug. nd received rt8PA hours after symptom onset) No antihypertensive treatment (N=112) 52%

Post8hoc analysis of

• Stroke. 29(8):15

Post8hoc analysis of

• Stroke. 29(8):15

Acute ischemic stroke and SBP >180 mm Hg (3824 h Antihypertensive treatment (N=65) 32% Clinical improvement at 24 hours

• f NINDS rt8PA trial

150489, 1998 Aug.

• f NINDS rt8PA trial

150489, 1998 Aug. nd received rt8PA hours after symptom onset) More severe hypertension No antihypertensive treatment (N=112) 52% More severe hypertension More abrupt decline of BP in response to antihypertensive medication

Post8hoc analysis of

• Stroke. 29(8):15

Post8hoc analysis of

• Stroke. 29(8):15

Acute ischemic stroke and SBP >180 mm Hg (3824 h Antihypertensive treatment (N=65) 32% Clinical improvement at 24 hours Occlusion BP high

• f NINDS rt8PA trial

150489, 1998 Aug.

• f NINDS rt8PA trial

150489, 1998 Aug. nd received rt8PA hours after symptom onset) More severe hypertension More abrupt decline of BP in response to antihypertensive No antihypertensive treatment (N=112) 52% response to antihypertensive medication (recanalization is associated with spontaneous BP decline) Recanalization Reocclusion BP normal BP high

Special cons post thrombol Special cons post thrombol

• Greater level of suscep

pressure decline/fluctua related to recanalizatio #Mattle HP, et al. Stroke. Fe

• Greater level of suscep

pressure decline/fluctua related to recanalizatio #Mattle HP, et al. Stroke. Fe #Mattle HP, et al. Stroke. Fe

• First 6 hours is the per

fluctuations in blood pr thrombolytic treatment #Aiyagari V, et al. Stroke. O #Mattle HP, et al. Stroke. Fe

• First 6 hours is the per

fluctuations in blood pr thrombolytic treatment #Aiyagari V, et al. Stroke. O

nsiderations8 bolytic patients nsiderations8 bolytic patients

eptibility to blood tuations (presumably tion).

Feb 2005;36(2):264#268.

eptibility to blood tuations (presumably tion).

Feb 2005;36(2):264#268. Feb 2005;36(2):264#268.

period of maximum pressure following nt.

. Oct 2004;35(10):2326#2330. Feb 2005;36(2):264#268.

period of maximum pressure following nt.

. Oct 2004;35(10):2326#2330.

Treatm acute hypertens intracerebral Treatm acute hypertens intracerebral intracerebral intracerebral

Re: Qureshi AI

tment of nsive response in ral hemorrhage tment of nsive response in ral hemorrhage ral hemorrhage ral hemorrhage

AI: Lancet 2009;373:1632844.

Evolution of our unde hypertensiv

Phase I (198581997) Phase II (199882003) DONOT TREAT BP IN ACUTE ICH# EXPERIMENTA REDUCE BP – MODESTLY# CASE SERIES ICH# EXPERIMENTA L/CLINICAL RESEARCH CASE SERIES PERI# HEMATOMA ISCHEMIA HIGH BP ~ HEMATOMA EXPANSION

nderstanding of acute sive response

Phase III (200482009) Phase IV (2010888) AGGRESSIVE BP REDUCTION EXPLORED# PILOT AGGRESSIVE BP REDUCTION CONFIRMED# PHASE III EXPLORED# PILOT STUDIES CONFIRMED# PHASE III STUDIES BP REDUCTION~ HEMATOMA EXPANSION BP REDUCTION ~ PATIENT OUTCOMES

Evolution of our unde hypertensiv

Phase I (198581997) Phase II (199882003) DONOT TREAT BP IN ACUTE ICH# EXPERIMENTA REDUCE BP – MODESTLY# CASE SERIES ICH# EXPERIMENTA L/CLINICAL RESEARCH CASE SERIES PERI# HEMATOMA ISCHEMIA HIGH BP ~ HEMATOMA EXPANSION

nderstanding of acute sive response

Phase III (200482009) Phase IV (2010888) AGGRESSIVE BP REDUCTION EXPLORED# PILOT AGGRESSIVE BP REDUCTION CONFIRMED# PHASE III EXPLORED# PILOT STUDIES CONFIRMED# PHASE III STUDIES BP REDUCTION~ HEMATOMA EXPANSION BP REDUCTION ~ PATIENT OUTCOMES

Acute Hypertensive Respons

(Powers WJ. Neurolog

Acute Hypertensive Respons

(Powers WJ. Neurolog

Perihematoma ischemia is a serious concern

• nse Should Not Be Treated

logy 1993;43:461#467)

• nse Should Not Be Treated

logy 1993;43:461#467)

Hematoma expansion is uncommon

rCBF Hibernation stage (082 days) Reperf stage Metabolism

Qureshi AI, et al. Neurosu

erfusion e (2814 days) Normalization stage (>14 days)

surg Clin N Am 2002;13:3558370.

Evolution of our unde hypertensiv

Phase I (198581997) Phase II (199882003) DONOT TREAT BP IN ACUTE ICH# EXPERIMENTA REDUCE BP – MODESTLY# CASE SERIES ICH# EXPERIMENTA L/CLINICAL RESEARCH CASE SERIES PERI# HEMATOMA ISCHEMIA HIGH BP ~ HEMATOMA EXPANSION

nderstanding of acute sive response

Phase III (200482009) Phase IV (2010888) AGGRESSIVE BP REDUCTION EXPLORED# PILOT AGGRESSIVE BP REDUCTION CONFIRMED# PHASE III EXPLORED# PILOT STUDIES CONFIRMED# PHASE III STUDIES BP REDUCTION~ HEMATOMA EXPANSION BP REDUCTION ~ PATIENT OUTCOMES

Hematoma E

(From: Qureshi: N Engl J M

Hematoma E

(From: Qureshi: N Engl J M Baseline

Enlargement

Med; 344.: 2001.1450#1460)

Enlargement

Med; 344.: 2001.1450#1460) 6 hours

Elevated systolic blood pr hematoma e

Kazui: Stroke, Volume 28(12)

Elevated systolic blood pr hematoma e

Kazui: Stroke, Volume 28(12)

patients (%) 30 40 50 Proportion of pa 10 20 30 Hematoma enlargement

pressure may predispose to enlargement

2).December 1997.237082375

pressure may predispose to enlargement

2).December 1997.237082375

SBP>200 mm Hg

No hematoma enlargement

Acute Hypertensive Resp

(Qureshi et al.: Lancet

Acute Hypertensive Resp

(Qureshi et al.: Lancet

Is there perihematoma ischemia?

sponse Should be Treated

cet 2009;373:1632844)

sponse Should be Treated

cet 2009;373:1632844)

Hematoma expansion is a reality

Guidelines for the Mana Intracerebral Hemorr

Guideline From the American St

Guidelines for the Mana Intracerebral Hemorr

Guideline From the American St

• Until ongoing clinical trials of

for ICH are completed, physi pressure on the basis of the p

• Suspect elevated intracranial
• Until ongoing clinical trials of

for ICH are completed, physi pressure on the basis of the p

• Suspect elevated intracranial
• Suspect elevated intracranial

pressure <180 mm Hg.

• Do not suspect elevated intrac

blood pressure <160 mm Hg.

• Suspect elevated intracranial

pressure <180 mm Hg.

• Do not suspect elevated intrac

blood pressure <160 mm Hg.

• Stroke. 3

nagement of Spontaneous

• rrhage in Adults. 2007

Stroke Association Stroke Council

nagement of Spontaneous

• rrhage in Adults. 2007

Stroke Association Stroke Council

• f blood pressure intervention

ysicians must manage blood e present incomplete evidence. al pressure8keep systolic blood

• f blood pressure intervention

ysicians must manage blood e present incomplete evidence. al pressure8keep systolic blood al pressure8keep systolic blood racranial pressure8keep systolic . Regular clinical evaluation. al pressure8keep systolic blood racranial pressure8keep systolic . Regular clinical evaluation. . 38(6):2001823, 2007 Jun.

BP reduction and he BP reduction and he

No sta

Jauch E

37%

180 mm Hg Sing IV

Q J

17% 37%

hematoma enlargement hematoma enlargement

standard management practices

h EC, Stroke. 2006 Aug;37(8):2061#5.

ingle center8AHA guidelines IV nicardipine 5815 mg/hr

Qureshi AI, Crit Care Med. Jul 2006;34(7):197581980.

Intracerebral Hemorrhage Quality Metrics8 An algorithm that evaluates "best available" evidence in

Variable Quality param Treatment of acute hypertensive response (SBP ≥180 Time interval b consecutive SB AND first SBP response (SBP ≥180 mm Hg) AND first SBP recording Re: Qureshi AI.

26 quality indicators relat ge Specific Intensity of Care 8BP management es principles of care using the in a semi#quantitative manner

ameter 1 points if YES or not applicable l between two SBP≥180 mm Hg BP<180 mm Hg Achieved target range with 2. 5 hours of second of BP<180 mm Hg hours of second of the two consecutive measurements OR not applicable

• I. Neurocrit Care 2011;14:291#317

lated to 18 facets of care

50 70 90 110 130 150 170 190 210 230 1 2 3 4 5 6 7 8 9 10 11 1 Systolic blood pressure (mm Hg) Tim

Intravenous calcium c blocker infusion initia

Figure 3

Effective and timely reduc

Achieved target range with 2.

Baseline 2 hours

Tim 12 13 14 15 16 17 18 19 20 21 22 23 24 25 Time (hours)

um channel itiated

uction of SBP:

• 2. 5 hours =1 point

24 hours

Time (hours)

Intracerebral Hemorrhage Quality Metrics8VA Score on performance m patients

Low Re: Qureshiu AI. J Stroke Cerebr [Epub ahead of print] Low performance

17 ge Specific Intensity of Care VALIDATION STUDY metrics and survival in 50 s with ICH

High ebrovasc Dis. 2012 May 24. High performance

26

Intracerebral Hemorrhage Quality Metrics826 Score on performance urvival

Re: Qureshiu AI. J Stroke Cerebr [Epub ahead of print]

% surv ge Specific Intensity of Care 26 quality indicators nce metrics and survival

ebrovasc Dis. 2012 May 24.

Evolution of our unde hypertensiv

Phase I (198581997) Phase II (199882003) DONOT TREAT BP IN ACUTE ICH# EXPERIMENTA REDUCE BP – MODESTLY# CASE SERIES ICH# EXPERIMENTA L/CLINICAL RESEARCH CASE SERIES PERI# HEMATOMA ISCHEMIA HIGH BP ~ HEMATOMA EXPANSION

nderstanding of acute sive response

Phase III (200482009) Phase IV (2010888) AGGRESSIVE BP REDUCTION EXPLORED# PILOT AGGRESSIVE BP REDUCTION CONFIRMED# PHASE III EXPLORED# PILOT STUDIES CONFIRMED# PHASE III STUDIES BP REDUCTION~ HEMATOMA EXPANSION BP REDUCTION ~ PATIENT OUTCOMES

Intensive blood pressure re haemorrhage trial (INTERACT

Variables Intensive SBP<140mmHg (n=203) Hematoma expansion (>33%

• r 12.5 ml)

15% Variables SBP reduction ≥60 mmHg (n=32) Hematoma expansion(>33%) 19%

Antihypertensive Treatm Hemorrhage (ATACH) Stud reduction in acute cerebral CT) Lancet Neurology 2008;7:3918399

Hg AHA8guideline SBP<180mmHg (n=201) p8value 23% 0.05 ion SBP reduction <60 mmHg (n=28) RR (95% CI) 33% 0.6 (0.2, 1.4)

tment of Acute Cerebral

• udy. Arch Neurol 2010: 67(5):57086.

Intensive blood pressure re haemorrhage trial (INTERACT

Variables Intensive SBP<140mmHg (n=52) Hematoma expansion (>33%

• r 12.5 ml)

12%

after onset

Variables SBP reduction ≥60 mmHg (n=11) Hematoma expansion(>33%) 18%

Antihypertensive Treatm Hemorrhage (ATACH) Stud Treated <3 hrs a reduction in acute cerebral CT) Lancet Neurology 2008;7:3918399

Hg AHA8guideline SBP<180mmHg (n=52) p8value 27% 0.08 ion SBP reduction <60 mmHg (n=9) RR (95% CI) 38% 0.5 (0.1, 2.3)

tment of Acute Cerebral

• udy. Arch Neurol 2010: 67(5):57086.

Intensive blood pressure re haemorrhage trial (INTERACT

Variables Intensive SBP<140mmHg (n=52) Hematoma expansion (>33%

• r 12.5 ml)

12%

after onset

Attenuation of hematoma e Variables SBP reduction ≥60 mmHg (n=11) Hematoma expansion(>33%) 18%

Antihypertensive Treatm Hemorrhage (ATACH) Stud Treated <3 hrs a

Attenuation of hematoma e

• reduction. Attenuation m

recruited

reduction in acute cerebral CT) Lancet Neurology 2008;7:3918399

Hg AHA8guideline SBP<180mmHg (n=52) p8value 27% 0.08 expansion with intensive SBP ion SBP reduction <60 mmHg (n=9) RR (95% CI) 38% 0.5 (0.1, 2.3)

tment of Acute Cerebral

• udy. Arch Neurol 2010: 67(5):57086.

expansion with intensive SBP most prominent in patients ed within 3 h

Evolution of our unde hypertensiv

Phase I (198581997) Phase II (199882003) DONOT TREAT BP IN ACUTE ICH# EXPERIMENTA REDUCE BP – MODESTLY# CASE SERIES ICH# EXPERIMENTA L/CLINICAL RESEARCH CASE SERIES PERI# HEMATOMA ISCHEMIA HIGH BP ~ HEMATOMA EXPANSION

nderstanding of acute sive response

Phase III (200482009) Phase IV (2010888) AGGRESSIVE BP REDUCTION EXPLORED# PILOT AGGRESSIVE BP REDUCTION CONFIRMED# PHASE III EXPLORED# PILOT STUDIES CONFIRMED# PHASE III STUDIES BP REDUCTION~ HEMATOMA EXPANSION BP REDUCTION ~ PATIENT OUTCOMES

Primary hypothe

Intensive SBP reduction1 red death or disability at 3m2 aft greater when compared with reduction. reduction.

1. SBP≤140 mmHg using IV nicar within 3.5 h of onset of ICH 2. Defined by mRS score of 4#6 3. SBP≤180 mmHg

hesis: ATACH II

educes the likelihood of after ICH by 10% or th standard SBP

cardipine with treatment initiated and continued for the next 24h 6

Trial design:

• re. Qureshi AI, Palesch YY. Neu

Trial design:

• re. Qureshi AI, Palesch YY. Neu

SBP<180 mm Hg

Baseline

SBP<140 mm Hg

: ATACH II

eurocrit Care. 2011;15(3):559876.

: ATACH II

eurocrit Care. 2011;15(3):559876.

24 hrs 3 m

Overview of the study

Patient screened Patient meets eligibility criteria Randomize subjects 1:1 Intensive treatment SBP≤140mmHg Standard tre SBP≤180mmH IV nicar treatment SBP≤140mmHg using IV nicardipine ±labetalol SBP≤180mmH IV nicar ±labeta mRS and Euro8QOL

udy design8ATACH II

ED personnel Site investigator WebDCUTM system at MUSC treatment mHg using ardipine Site investigator mHg using ardipine talol Blinded neurological evaluation by site investigator FDA#IND#exempt # 107804

INTERACT II

• Onset <6

hours

• SBP 1508220

mm Hg mm Hg SBP#66% in 6h SBP 90% in 2 ATACH II

• Onset <4.5

hours

• SBP >180 mm

Hg

• Hematoma

vol.<60 cc vol.<60 cc SCORE IT

• CT spot sign

BP# 0% 2h Intensity

• f care

INTERACT II

• Onset <6

hours

• SBP 1508220

mm Hg mm Hg SBP#66% in 6h SBP 90% in 2 ATACH II

• Onset <4.5

hours

• SBP >180 mm

Hg

• Hematoma

vol.<60 cc vol.<60 cc SCORE IT

• CT spot sign

BP# 0% 2h Intensity

• f care

Integration: additive Integration: additive

ATACH II INTERACT II SBP reduction <140 mm Hg <140 mm Hg Time window Patient subset Time to reach SBP goals Intens

• f car

ive OR synergistic? ive OR synergistic?

STICH II Surgical evacuation

• f lobar ICH

ensity care IVH8CLEAR Intraventricular hemorrhage+ thrombolytics

Treatm acute hyperten Choosing th antihyperten Treatm acute hyperten Choosing th antihyperten antihyperten antihyperten

Re: Qureshi AI: Circulat

tment of ensive response: the right IV rtensive agent tment of ensive response: the right IV rtensive agent rtensive agent rtensive agent

ulation 2008 Jul 8;118(2):176#87.

The search for t The search for t

• Treats underlying patho
• Rapid onset of action
• Predictable dose respon
• Titratable to desired B
• Treats underlying patho
• Rapid onset of action
• Predictable dose respon
• Titratable to desired B
• Titratable to desired B
• Minimal dosage adjustm
• Minimal adverse effect
• No increase in ICP
• No coronary or cerebra
• Easy transition to oral
• Titratable to desired B
• Minimal dosage adjustm
• Minimal adverse effect
• No increase in ICP
• No coronary or cerebra
• Easy transition to oral

r the ideal regimen r the ideal regimen

thophysiology ponse BP thophysiology ponse BP BP tments cts bral steal al formulation BP tments cts bral steal al formulation

Systolic blood pressure recor

IV Labetalol+ Hydral

Systolic blood pressure recor

IV Labetalol+ Hydral

125 150 175 200 225 250 275 d pressure (mm Hg) 25 50 75 100 125 2 4 6 8 10 Time after initiation of a Systolic blood p From: Qureshi AI. Journa

cordings for 24 hrs in ICH pts

ralazine± Nitroprusside

cordings for 24 hrs in ICH pts

ralazine± Nitroprusside

12 14 16 18 20 22 24 f antihypertensive treatment (hrs) rnal of Intensive Care: 2005;20:34842

Systolic blood pressure recor

IV Labetalol+ Hydral

Systolic blood pressure recor

IV Labetalol+ Hydral

125 150 175 200 225 250 275 d pressure (mm Hg)

IV bolus IV bolus

25 50 75 100 125 2 4 6 8 10 Time after initiation of a Systolic blood p From: Qureshi AI. Journa

cordings for 24 hrs in ICH pts

ralazine± Nitroprusside

cordings for 24 hrs in ICH pts

ralazine± Nitroprusside

• lus

IV bolus IV bolus

12 14 16 18 20 22 24 f antihypertensive treatment (hrs) rnal of Intensive Care: 2005;20:34842

Goals not met Prominent fluctuations

Hourly mean arterial pressu hour period in ICH pts (

From: Qureshi AI. Critical C

ssure recordings for the 248 s (IV nicardipine infusion)

l Care Medicine 2006;34:1975#80

Hourly mean arterial pressu hour period after initiatin

Infusion ba

From: Qureshi AI. Critical C

Infusion ba effective tha

ssure recordings for the 248 ting IV nicardipine infusion

based regimens are more

l Care Medicine 2006;34:1975#80

based regimens are more than bolus based regimens

Antihypertensive medication Antihypertensive medication

Intracranial mass lesion+ Cerebra Antihypertensive meds→ Cerebral

ion and intracranial pressure ion and intracranial pressure

ral blood volume [venous]=ICP ral venous dilation→ CBV [venous]↑↑

Comparison of IV anti Comparison of IV anti

Agent Mechanism of action C b Labetolol α & β#adrenergic blockers Hydralazine Direct relaxation

• f arteriolar

smooth muscle smooth muscle Nitroprusside Releases nitric

• xide

Nicardipine Calcium channel blocker Esmolol∗∗ β#adrenergic blocker Re: Qureshi AI: Cir

ntihypertensive agents ntihypertensive agents

Cerebral blood flow

ICP

Onset of action … … 5#10 min ++ ++ 10#20 min ++ ++ Within seconds + … 5#10 min … … 5 min Circulation 2008 Jul 8;118(2):176#87

Comparison of IV anti Comparison of IV anti

Agent Mechanism of action C b Labetolol α & β#adrenergic blockers Hydralazine Direct relaxation

• f arteriolar

smooth muscle smooth muscle Nitroprusside Releases nitric

• xide

Nicardipine Calcium channel blocker Esmolol∗∗ β#adrenergic blocker Re: Qureshi AI: Cir

ntihypertensive agents ntihypertensive agents

Cerebral blood flow

ICP

Onset of action … … 5#10 min ++ ++ 10#20 min ++ ++ Within seconds + … 5#10 min … … 5 min Circulation 2008 Jul 8;118(2):176#87

Summ Summ

Re: Qureshi AI: Circulat

mmary mmary

ulation 2008 Jul 8;118(2):176#87.

Stroke subtype spe recommen

American Stroke Assoc

Stroke subtype spe recommen

American Stroke Assoc Acute ischemic stroke Not a candidate for thrombolysis Candidate for thrombolysis Acute Suspect high Acute intracerebral hemorrhage Suspect high ICP Do not suspect high ICP Acute subarachnoid hemorrhage Aneurysm not secured Aneurysm secured

pecific BP treatment endations:

sociation, Stroke Council

pecific BP treatment endations:

sociation, Stroke Council SBP<220 mm Hg SBP<160 mm Hg SBP<180 mm Hg SBP<180 Hg SBP<180 Hg SBP<160 mm Hg SBP<160 mm Hg Depends upon presence of vasospasm Depends upon presence of vasospasm

Stroke subtype spe recommen

American Stroke Assoc

Stroke subtype spe recommen

American Stroke Assoc Acute ischemic stroke Not a candidate for thrombolysis Candidate for thrombolysis Acute Suspect high Acute intracerebral hemorrhage Suspect high ICP Do not suspect high ICP Acute subarachnoid hemorrhage Aneurysm not secured Aneurysm secured

Early diagnosis an into stroke sub

pecific BP treatment endations:

sociation, Stroke Council

pecific BP treatment endations:

sociation, Stroke Council SBP<220 mm Hg SBP<160 mm Hg SBP<180 mm Hg SBP<180 Hg SBP<180 Hg SBP<160 mm Hg SBP<160 mm Hg Depends upon presence of vasospasm Depends upon presence of vasospasm

and differentiation ubtypes is key!!

Conclus Conclus

Treatment of acute hyp patients with stroke rep applicable and cost effe improve patient outcome improve patient outcome However such benefit is appropriate interpretatio integration of results of

lusions lusions

ypertensive response in represents a widely ffective intervention to mes. mes. is contingent on ation, implementation, and

• f on8going clinical trials.

Thank

Zeenat Qureshi Stroke Re

ank you

Research Center 2012

INTERACT II

• Onset <6

hours

• SBP 1508220

mm Hg mm Hg SBP#66% in 6h SBP 90% in 2 ATACH II

• Onset <4.5

hours

• SBP >180 mm

Hg

• Hematoma

vol.<60 cc vol.<60 cc SCORE IT

• CT spot sign

BP# 0% 2h Intensity

• f care

INTERACT II

• Onset <6

hours

• SBP 1508220

mm Hg mm Hg SBP#66% in 6h SBP 90% in 2 ATACH II

• Onset <4.5

hours

• SBP >180 mm

Hg

• Hematoma

vol.<60 cc vol.<60 cc SCORE IT

• CT spot sign

BP# 0% 2h Intensity

• f care