Current Management of

Hypertensive Crisis
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DR. Dr. H. DJOKO TRHAD, 8p.PD, FCCP
R8UD Kota 8emarang - 8MF Penyakit Dalam
pidemiology of Hypertensive
mergency (H
First described by Volhard and Fahr (1914
who saw patients with severe hypertension
accompanied by signs of vascular injury to the
heart brain retina and kidney.
Prior to the introduction of antihypertensive
medications 7% of hypertensive pts had H.
Currently, 1 to 2% of pts with hypertension will
have a HE at some time in their life.
Marik Paul Varon Joseph CHST 2007;131:1949-62
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efinitions
Hypertensive Crisis
BP > 180/120
Hypertensive Urgency Hypertensive Emergency
MarkedIy eIevated BP MarkedIy eIevated BP
without severe symptoms or with acute or progressing
progressive target organ damage. target organ damage.
BP shouId be reduced within hours. BP shouId be reduced immediate.
OraI agents. ParenteraI agents.
Kaplan NM Hypertensive Crises in : Clinical hypertension 9 th d
Lippincott Williams & Wilkins 2006:609-630
efinitions (cont'd
Accelerated malignant hypertension represents
markedly elevated BP with papiledema (grade 4
Keith-Wagener retinopathy and/or hemorrhages
and exudates (grade 3 Keith-Wagener retinopathy.
The Clinical features and prognosis are similar with
grade 3 or 4 retinopathy (Ahmed et al. 1986
Hypertensive encephalopaty is a sudden marked
elevation of BP with severe headache and altered
mental status reversible reduction of BP.
Kaplan NM Hypertensive Crises in : Clinical hypertension 9th
d Lippincott Williams & Wilkins 2006:609-630
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Keith-Wagner Classification System
Grade : Change in ratio of arteriole-venule
diameter.
Grade : Arteriovenous nicking "copper wire"
appearance.
Grade : Focal or diffuse arteriolar spasm
flame hemorrhages cotton wool spots
exudate silver wire appearance right-angle
deviation.
Grade V: Papilledema vessel obstruction.
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Pathophysiology:
Mechanism of malignant hypertension
CriticaI degree of hypertension
Increase in vasoconstrictors
EndotheIiaI damage
(renin-angiotensin, vasopressin,
cathecoIamines)
PIateIet and fibrin deposition
Further BP increase
IntravascuIar hemoIysis
Pressure natriuresis
Fibrinoid necrosis and
IntimaI proIiferation HypovoIemia
Further reIease of vasoconstrictors
Increase in BP and ischemia
tiology
ssential hypertension
Renal parenchymal etiologies: Glomerulonephritis
tubulointerstitial nephritis
Systemic disorders with renal involvement: SL
vasculitides.
Renovascular: atheroma fibromuscular dysplasia
ndocrine: pheocromocytoma Conn's syndrome
Cushing syndrome
rugs : cocain amphetamine clonidine withdrawal etc
Tumor related
Coarctation of the aorta
Pre-eclampsia/ eclampsia Kitiyakara C Guzzman NJ.J Am Soc Nephrl 1998:133-42
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Clinical Presentation
0%
25%
25%
2%
20%
16%
14%
15%
12%
10%
5%
5%
2%
0%
CerebraI ICH or SAH Hypertensive Acute Acute CHF AMI or UAP Aortic
Infarction encephaIopathy puImonary dissection
edema Zampaglione B Pascale C et al. Hypertension
1996;27:144-7
nitial valuation of Patients with
a Hypertensive mergency
History :
- Prior diagnosis and treatment of HT
- ntake of pressor agents : street drugs
sympathomimetics
- Symptoms of cerebral cardiac and visual dysfunction
Physical exam.
-
BP
-
Funduscopy
-
Neurologic status
-
Cardiopulmonary status
-
Body fluid volume assessment
-
Peripheral pulses
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nitial valuation of Patients with
a Hypertensive mergency
Lab. evaluation
-
Hematocrit and blood smear
-
Urine analysis
-
Automated chemistry : creatinine glucose electrolytes
-
Plasma renin activity and aldosterone (if primary aldosteronism
is suspected
- Plasma renin activity before and 1 h after 25 mg captopril (if
renovascular hypertension is suspected
CXR (if heart failure or aortic dissection is suspected
CG
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Autoregulation mechanism
CBF
Normal
Mean Arterial Pressure (mmHg
Chronic Hypertension
11
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Management of
Hypertensive mergency
Patients should be admitted to an CU for
continuous monitoring of BP and parenteral
administration of an appropriate agent
nitial goal therapy is to reduce MAP by no more
than 25% (within min. to 1 hour.
Then if stable to 160/100 to 110 mmHg within
the next 2 to 6 hours.
xcessive falls in pressure that may precipitate
renal cerebral or coronary ischemia should be
avoided.
Chobanian AV et al The JNC 7 report JAMA 2003;389-2560-70
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Management of
Hypertensive mergency (cont'd
f this level of BP is well tolerated and the
patients is clinically stable further gradual
reductions toward a normal BP can be
implemented in the next 24 to 48 h.
xceptions :
1. schemic stroke
2. Aortic dissection SBP should < 100 mmHg
3. Patients whom BP is lowered to enable the use of
thrombolytic agents
Chobanian AV et al The JNC 7 report JAMA 2003;389-2560-70
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Parenteral rugs for Treatment of
Hypertensive mergencies based on JNC 7
ose Onset uration of
Action
Sodium Immediate 1-2 minutes after
nitroprusside infusion stopped
NTG 5-500 ug/min 1- minutes 5-10 minutes
LabetaIoI HCI 20-80 mg every 10-15 min 5-10 minutes -6 minutes
or 0.5-2 mg/min
FenoIdopam HCI 0.1-0. ug/kg/min <5 minutes 0-60 minutes
Nicardipine HCI 5-15 mg/h 5-10 minutes 15-90 minutes
EsmoIoI HCI 250-500 ug/kg/min IV 1-2 minutes 10-0 minutes
boIus, then 50-100
ug/kg/min by infusion;
may repeat boIus after 5
min or increase infusion
to 00 ug/min
Chobanian AV et al The JNC 7 report JAMA 2003;389-2560-70
Parenteral rugs for Treatment of
Hypertensive mergencies based on
ASA Guideline
rug I.V. BoIus ose Continous Infus
Rate
5 - 20 mg every 15'
LabetaIoI 2 mg/min (max 00mg/d)
Nicardipine NA 5-15 mg/h
EsmoIoI 250 ug/kg IVP Ioading dose 25-00 ug/kg/m
EnaIapriI 1,25-5 mg IVP every 6 h NA
5 - 20 mg IVP every 0'
HydraIazine 1,5-5 ug/kg/m
Nipride NA 0,1-10 ug/kg/m
NTG NA 20-400 ug/m
This parenteraI drugs are approved for hypertensive emergency
15
in acute ischemic stroke and ICH
AHA/ASA GuideIine, 2007 update. Stroke. 2 007;8: 2001-2.
Parenteral rugs for Treatment of
Hypertensive mergencies based on CHST 2007
Acute P / Systolic Nicardipine fenoldopam or nitropruside combined with
dysfunction NTG and loop diuretic
Acute P/ iastolic smolol metoprolol labetalol verapamil combined with
dysfunction low dose of NTG and loop diuretics
Acute schemia Coroner Labetalol or esmolol combined with diuretics
Hypertensive encephalopaty Nicardipine labetalol fenoldopam
Acute Aorta issection Labetalol or combined Nicardipine and esmolol or combine
nitropruside with esmolol or V metoprolol
Preeclampsia eclampsia Labetalol or nicardipine
ARF / microangiopathic Nicardipine or fenoldopam
anemia
Sympathetic crises/ cocaine Verapamil diltiazem or nicardipine combined with
overdose benzodiazepin
Acute postoperative smolol Nicardipine Labetalol
hypertension
Acute ischemic stroke/ CH Nicardipine labetalol fenoldopam
Marik Paul Varon Joseph CHST 2007;131:1949-62
Actions to increase organ blood flow
Pharmacodynamic action
Nicardipine: ? g/kg/min ? 20 min
( ? %)
(Hypertensive patients, n = 9)
Mean BP VertebraI RenaI Coronary
artery bIood fIow bIood fIow
BIood
fIow
chang
e rate
60
bIood fIow
Baseline value
40
103 ? 11 mmHg
Mean blood pressure
20
Vertebral artery
183 ? 65 mL/min
blood flow
Renal artery
563 ? 29mL/min
0 blood flow
Mean
bIood
pressu
re
Coronary artery
121 ? 42 mL/min
chang
e rate
blood flow
-10
- 20
( ? %)
(Shoji Suzuki et al. The 20th Annual Scientific Meeting of the Japanese Society of Hypertension: 1997
Special Condition: Stroke
To recent consensus decreasing BP in acute
phase of ischemic stroke is allowed only if :
-
schemic Stroke with BP >220/120.
-
Candidate of rtPA therapy : BP >185/110.
-
Hemorrhage stroke with BP >180/100.
-
Acute stroke in hypertensive patients with hypertensive
encephalopathy aortic dissection acute MC acute
lung edema and ARF.
Choose parenteral antihypertensive drugs and do
the BP control cautiously
Labetalol and Nicardipine has been
demonstrated to be an effective agent for the
control of BP in patients with schemic Stroke
and CH.
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Special Condition:
Preeclampsia and clampsia
nitial therapy of preeclampsia includes volume
expansion Mg SO4 for seizure prophylaxis and
BP control.
elivery is definite treatment for preeclampsia
and eclampsia
Based on current data suggest that hydralazine
and nifedipine not be used as first line treatment
of severe hypertension in pregnancy.
V labetalol or nicardipine which are easier to
titrate and appear to be safe and effective.
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Special Condition: ARF
EIevated BP causes deterioration of renaI
function, therefore Iowering BP is required
Therapy shouId reduce BP without
compromising the RBF or GF
Preferred agents : Nicardipine or
fenoIdopam, because of it has been show to
reduce BP, but stiII maintain and increase
bIood fIow to renaI artery.
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SpeciaI Condition:
LV faiIure and PE
Acute heart failure occurs as a result of an acute
rise in systemic vascular resistance and reduced
LV compliance.
Acute P / Systolic dysfunction : Nicardipine
fenoldopam or nitropruside combined with NTG
and loop diuretic
Acute P/ iastolic dysfunction : smolol
metoprolol labetalol verapamil combined with
low dose of NTG and loop diuretics
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Special Condition:
Post operative hypertension
Acute postoperative hypertension has been
defined as a significant elevation in BP during
the immediate postoperative period that may
lead to serious neurologic cardiovascular or
surgical site complications.
Pain and anxiety are common contributors to BP
elevations and should be treated before
administration of antihypertensive therapy.
Labetalol esmolol nicardipine and clevedipine
have proven effective in the management of
APH.
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Conclusion
Patients with hypertensive emergencies require
the immediate reduction of the elevated BP to
prevent and arrest progressive end organ
damage.
The best clinical setting to achieve this control is
in the CU .
There are several antihypertensive agents
available including esmolol nicardipine
labetalol and fenoldopam.
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