Hypertensive Crisis

dr Putra Hedra SpPD

UNIBA
 Hypertension: A Significant
CV and RenaKomplikasil
Disease Risk Factor
Retinopati
CHF
Stroke LVH

Hypertension
Renal disease
Morbidity
Disability
Peripheral vascular
disease

National High Blood Pressure Education Program Working Group. Arch Intern Med. 1993;153:186- 2
208.
 JNC-7 HTN
Prehypertension
SBP 120-139 mmHg or DBP 80-89 mmHg

Stage I HTN
SBP 140-159 mmHg or DBP 90-99 mmHg

Stage II HTN
SBP >160 mmHg or DBP >100 mmHg
 Crisis: What is it?
SBP >180 or DBP >120
Urgency = no signs of end-organ damage
Days to Weeks
Emergency = signs of end-organ damage
Minutes to Hrs

Need to know pts baseline before crisis

Incidence: only <1%

But >50 million have HTN!
 What Causes Crisis?
Failure of normal autoregulation & Abrupt rise in SVR
Endovascular injury: fibrinoid necrosis w/i Arterioles
Ischemia, Platelet deposition, Further autoregulatory dysfunction

4 major organ systems affected: CNS, CV, Renal & Gravid uterus
1 Organ: 83%
2 Organ: 14%
Multi-Organ: 3%

Most Common Clinical Presentations:

cerebral infarction (24.5%)
pulmonary edema (22.5%)
hypertensive encephalopathy (16.3%)
CHF (12.0%)
less common: intracranial hemorrhage, Ao dissection, eclampsia,
epistaxis
 Ask the Patient
Meds
AntiHTN meds & Compliance
OTC meds i.e.
sympathomimetic agents
Use of illicit drugs such as
cocaine
Duration/Severity of
preexisting HTN, Degree of BP
control
Previous End-Organ Damage
renal and cerebrovascular
disease
Date of last menstrual period
Co-morbidities
h/o HTN, thyroid dz, Cushing dz,
SLE, renal dz
Evidence of End-Orgna Damage:
Chest pain - Myocardial ischemia
or infarction
Back pain - Aortic dissection
Dyspnea - Pulmonary edema,
congestive heart failure
Neurologic symptoms - Seizures,
visual disturbances, altered level of
consciousness (hypertensive
encephalopathy)
 Work-Up
Labs:
Ureum, creatinin: evaluate for renal impairment
CBC/Smear
U/A with Microscopy: hematuria/proteinuria or RBCs/Casts
Other : Pregnancy, Endocrine

Imaging Studies:
CXR:
Cardiac enlargement , Pulmonary edema, Widened mediastinum
Head CT and/or brain MRI: abnormal neuro exam or concern for
Intracranial bleeding, Cerebral edema, Cerebral infarction
CT Chest, Angiography: Aortic dissection suspected

EKG: evidence of MI/LVH

 Definitions
Emergencies
Symptomatic
Acute End-Organ Damage
Diastolic B.P. usually >130 mmHg

Urgencies
Asymptomatic
NO Acute End-Organ Damage
Diastolic B.P. usually >110 mmHg; Systolic
B.P. usually >180 mmHg
Hypertensive Urgency
BP Elevation
w/o
End-Organ Damage
 BP Goals
No proven benefit to rapid reduction
can induce Ischemia: CVA/MI

1-2hrs: dec MAP by 20-25% or

DBP to <120 mmHg
2-6hrs to Days: reduce to <160/100

Remember the Pts Baseline!!

 Urgent Approach
Put pt in a quiet room
10-20mmHg

Already on Meds
Inc existing meds vs. Add another agent
Restart non-compliant meds
Add diuretic & reinforce Low-salt diet

No Meds
Oral meds Add longer agent & f/u few days
Start 2 Agents: thiazide + 2nd
Keep in mind co-morbid conditions
 Treatment Options - Oral
Captopril
action may be potentiated w/concurrent use of a loop diuretic
s/e: reflex tachycardia; ARF (b/l RAS)

Clonidine
-adrenergic agonist
s/e: sedation, rebound hypertension

Labetalol
-/-adrenergic antagonist
s/e: bradycardia, bronchospasm not if heart block, asthma, CHF

Prazosin:
-adrenergic antagonist
Tx pheochromocytoma
s/e: syncope, palpitations, tachycardia, orthostatic hypotension, 1st dose syncope
 Watch & Wait
Observe for a few hours

Titrate meds as outpt to goal <140/90 (<130/80

in select groups)

Most do not need admission:

Does not improve long-term

morbidity/mortality
Hypertensive
Emergency
BP Elevation
+
End-Organ Damage
 Mechanism of Vascular Injury
MAP Arterial Vasoconstriction
Inc
Damage to Vascular Wall
Plasma constituents enter vascular wall
Narrow/Obliterate lumen

Brain: Breakthrough vasodilation

Cerebral edema
 Neuro
Cerebral Autoregulation:
maintain a constant cerebral blood flow despite changes in BP
Chronic HTN: tolerate higher MAPs before disruption BUT
Inc CVR & more prone to cerebral ischemia when flow decreases

Malignant HTN
Retinal hemorrhages, Hard Exudates, Papilledema
Ischemia & Leakage of blood/plasma

HTN Encephalopathy
Signs of Cerebral Edema 2/2 breakthrough hyperperfusion from
severe/sudden rise in BP
HA, AMS, Blurred vision, N/V, Seizures/Focal changes
HPT retinopathy
 Cardiac
HTN affects structure/function of coronary
vasculature & LV

Activates RAAS Inc SVR

Inc LV wall tension/LVH Inc O2 demand

HTN Emergency: LV cant overcome SVR LV

failure, Pulmonary Edema or AMI/Arrythmias
 Renal - Nephrosclerosis
HTN: pathologic changes to small arteries
Endothelial dysfunction & Impaired vasodilation
(alters renal autoregulation) Intraglomerular
pressure varies w/systemic art pressure

HTN Crisis: acute renal ischemia

Acute Renal Failure or Oliguria
Hematuria or Erythrocyte cast formation
Proteinuria
 Treatment Options - IV
Nitroprusside Infusion
Arteriolar/Venous dilator via
cGMP
Onset: sec, Durn: 2-5 min,
use no >10min
s/e: CN toxicity (met to CN)
NTG Infusion
Venous>Arterial dilation
Good for CAD or s/p CABG
s/e: tachycardia, HA
Nicardipine
Arteriolar dilator
Labetalol
Alpha/beta-adrenergic blocker
Avoid: COPD, CHF, Brady or
1st AVB, Cocaine use
Fenoldopam
Peripheral dopamine-1
receptor agonist
Increases renal perfusion
while lowering BP
c/i: glaucoma
Others:
Esmolol, Hydralazine, Lasix,
Enalaprilat, Phentolamine
 When to Use What
Aortic dissection CVA & SAH
-blkr then sodium Sodium nitroprusside
nitroprusside Nicardipine
Labetalol
Trimethaphan Hypertensive encephalopathy
-blkr
CHF Trimethaphan
Furosemide Sodium nitroprusside
Morphine sulphate
Nitroglycerin Pheochromocytoma
Labetalol
MI/ischemia Phentolamine
ACE inhibitors Sodium nitroprusside
-blkr
Nitroglycerin
 Emergency Approach
End-Organ Damage:
Admit to ICU

BP Lowering: IV meds

cont infusion, short-acting, titratable, parenteral

antihypertensive agent

Goal:
Prevent further end-organ damage

Lower progressively

Precipitous decrease Ischemia

cerebral, cardiac, renal

 Goal of Therapy
Lower DBP to 100-105mmHg: IV
Over 2-6hrs
No > 25% reduction
Gradual healing of necrotizing vascular lesions

Lower DBP to 85-90mmHg: Oral

Over 2-3 months
Often associated with modest worsening Cr
 Prognosis
1 yr mortality for untreated HTN Emergency
90% !!!

Mod-Severe chronic/acute vascular damage

Riskof Coronary, Cerebrovascular or Renal

disease cont.
TERIMA KASIH