Crisis Hypertension:

Management to
Prevent Complication
AGUS SUBAGJO, dr.SpJP, FIHA,FAsCC
 EPIDEMIOLOGY
 Hypertensive crisis is 27% of all medical
emergencies, consists of 76% urgencies and 24%
emergencies (Zampaglione et al, 1996)

 Higher incidence among the elderly and African –

Americans, Man : Woman = 2:1
(Potter et al,1995)

 Significant improvement in 5-year survival from 32%

(1977) to 91% ( 1997 – 2006)
(Lane et al, 2009)

 At present, it’s estimated that only 1-2%

hypertensive patient will have hypertensive
emergency
 Definition...

Emergency

urgency

Hipertensive Crisis
 Definitions

Hypertensive Crisis
Acute increasing of BP
>180/120 mmHg
Need immediate treatment

Hypertensive Urgency Hypertensive Emergency

Markedly elevated BP Markedly elevated BP

Without severe symptoms or With acute or progressing
progressive target organ damage target organ damage
BP should be reduced within hours BP should be reduced immediate
ORAL AGENTS PARENTERAL AGENTS

Kaplan NM ,Hypertensive Crises in : Clinical hypertension 9th Ed, Lippincott Williams & Wilkins 2006:609-630
 Epidemiology

Hypertensive crisis occurred in 500,000 American

population or 1% of the adult population

16%
23%

19 42%

Maria AR. et al. Cardiology in review. 2010

RISKESDAS
Tahun 2013 2018
Pravelensi HTN (%) 25,8 34,1

Kalimantan Selatan = 44,1 %

Papua = 22,2 %
 ETIOLOGY
 Medication non-  Collagen vascular
compliance disease (SLE)

 Antihypertensive drugs  Cushing disease

withdrawal (ie. Clonidin)
 Pheochromocytoma
 Renal parenchymal
disease  Preeclampsia and
eclampsia
 Renovascular disease
 Postoperative state
 Drugs (ie.cocaine,etc)
 Etiology
Causes of hypertension emergencies :
Essenstial hypertension
Renal disease
chronic pyelonephritis
Primary glomerulonephritis
Vascular/ glomerular disease : SLE,systemic sclerosis, renal vasculitides (microscopic
polyarteritis nodosa, Wegener’s granulomatosis)
Tubulointerstitial nephritis
Renovascular disease
Renal artery stenosis : fibromuscular dysplasia
Atherosclerotic renovascular disease
Drugs
Abrupt withdrawal of centrally acting α1 adrenergic agonist (clonidin, methyldopa)
Phencyclidine, cocain or other sympathomimetic drug intoxication
Interaction with monoamine oxidase inhibitors (tranylpromine, phenelzine, and selegiline)
Pregnancy : eclampsia/ severe pre-eclampsia
Endocrine : Pheochromocytoma,primary aldosteronism,glucocorticoid excess, renin secreting tumors
Central nervous system disorders : CVA infarction/ hemorrhage, head injury
Kaplan et al. 2010
 PATOPHYSIOLOGY

Critical degree of HT or rapid rate of rise

& ↑ vascular resistance

Endothelial Damage Spontaneous natriuresis

EDCF (Endothelin, ATII,superoxide anion) Intravascular vol depletion

↑ vasocontriction, ↑ vasoconstrictors
Platelet and fibrin deposition
Mitogenic and migration fc
SEVERE BP ↑ Further increase in BP

Myointimal proliferation &

fibrinoid necrosis TISSUE ISCHEMIA
Kitiyakara C, Guzman NJ.
Malignant hypertension
and hypertensive emergencies. J
END ORGAN DYSFUNCTION Am Soc Nephrol 1998
 Severe hypertension
Endocrine disorder
Essential hypertension

pregnancy
Renal disorder
Critical degree of HT or
Drug
rapid rate of rise & ↑
vascular resistance

Local effects (PG, free radical) Spontaneous

natriuresis
Endothelial damage Intravascular vol depletion

↑ endothelial permeability ↑ vasoconstrictors

Platelet & fibrin deposition Vasodilators ↓

Further increase in BP
Mitogenic & migration fc Severe BP ↑
Myointimal proliferation &
Tissue ischaemia End organ dysfunction
fibrinoid necrosis
 DIAGNOSIS

 ANAMNESIS
 PHYSICAL EXAMINATION
 ADDITIONAL EXAMINATION
 DIAGNOSIS OF CRISIS HYPERTENSION

SYMPTOMS  TARGET
ORGAN DAMAGE
PHYSICAL EXAMINATION ECG  ACS / ARRYTHMIA
Chest Pain, Dyspneu,
Palpitation

ECHO:
CXR  CONGESTIVE - DYASTOLIC DYSFUNCTION
PULMONUM, AORTA LABORATORY FINDINGS & LV REMODELLING
ELONGATION - AORTIC ROOT
FORMATION

ESC, 2013
 ANAMNESIS
 History of duration, antihypertensive drugs, and
compliance

 Use of drugs ( Cocain, NSAID, oral

contraception,ect) and alcohol

 Renal system disorder (Oliguria, history of renal

disease)
 Neurological disorder ( headache, vomit, seizure,
mental state changing)

 Cardiovascular disorder (chestpain, dypsneu,

epistaxis,ect)
ANAMNESIS
 PHYSICAL EXAMINATION
 Blood pressure measurement
 Pulse palpation in all extremities
 Auscultation of the carotid arteries,renal
arteries and abdominal aorta
 Cadio pulmonary : rales , gallop,
murmur
 Neurologic examination
 ADDITIONAL EXAMINATION

 Blood test  Funduscopic

 Urinalysis  Renal function test
 ECG  Intracerebral
examination (CT
 Echocardiography scan, MRI)
 Chest x-ray
Evidence of Target Organ Damage
Evidence of Target Organ Damage
MANAGEMENT OF CRISIS HYPERTENSION

HYPERTENSIVE EMERGENCY

 Intravenous agents are generally preferred

 To avoid cerebral, coronary and renal ischemia, mean BP levels should be reduced
approximately by 25% MAP within few minutes, reaching the goal of 160/100 mmHg within
2-6 hours
 Transition to oral agent within 6-12 hours, with titrate down of intravenous agent
 BP should then be normalized in the following 24-48 hours

HYPERTENSIVE URGENCY

 Generally oral medications are used for gradual reduction of blood pressure
 mean BP levels should be reduced approximately by 25% MAP within the first 24 hours
 Loading dose of anti HTN cause accumulation by the time patient is home
 Rapid onset of action
 Predictable dose response
 Titratable to desired BP
 Minimal dosage
adjustments
 Minimal adverse effects
 Easy conversion to oral
agents
 Acceptable cost-benefit
ratio

21
AUTOREGULATION

22
Acute Intracerebral Acute Subarachnoid
Hemorrhage Stroke Hemorrhage Stroke

BP : monitored & controlled to balance the risk of stroke,

hypertension-related re-bleeding,& maintenance of CPP (Class
I, LoE B).

SBP 150 to 220 mm Hg 

acute lowering of SBP to To prevent recurrent SAH
140 mm Hg is “probably” : SBP <140 -160 mmHg
safe (Class IIa; LoE).

Suggested Agents for Stroke : Nicardipine

Consider : Ultra short acting  Nitroprusside or
labetalol/esmolol
 Neurological Emergencies:

Ischemic stroke:
•Dont decrease BP rapidly: hypoperfusion of the peri-infarct area 
infarct expansion
•Usually antiHT is held unless DBP >120 mmHg or SBP >220 mmHg
•Permissive HT for 24-28 hr is allowed
•If px need thrombolytic: aggresive BP control (SBP <180 mmHg,
DBP<110 mmHg) to prevent hemorrhagic conversion

Drugs:
Labetalol or Nicardipine  first choice, minimal effect on
cerebral blood flow and dont lead to hypoperfusion
Nimodipine  subarachnoid hemorrhage  prevent
cerebral arteriolar vasospasm
 Hypertensive Emergency…
Acute Aortic Dissection
 Therapeutic goal :
Reduction of shear stress by reduction of BP &
HR
 Mortality increases 1% to 2% / hour during the
first 24 hours after the onset of symptoms

 Acute  reduce BP within 15-30 minutes

 Target : HR< 60bpm & SBP 100-120 mmHg

 Suggested agents : iv labetalol  iv ß blocker
Nitroprusside Ramos AP et al,
2014
 Hypertensive Emergency…
Acute Myocardial Infarction
Therapeutic goal : Reduction of BP & Decrease myocardial O2
demand
IV nitroglycerin :
Coronary dilatation, improve coronary perfusion, & reduce
symptoms
Used as needed to reduce BP (reduce preload and afterload)

IV β-blockers :
 Reduce HR & myocardial oxygen consumption
 Useful in combination with nitrates unless ventricular function is
compromised
 Reduces mortality associated with ventricular arrythmia

o BP goal : reduce max 25% from baseline

o Avoid : nicardipine & hydralazine  tachycardia
effect
 Hypertensive Emergency…

Acute Pulmonary Oedema

Theraupetic Goal : Preload & afterload

reduction
• Nitrates (e.g nitroglycerin)  effective
reduce preload (venodilatory effects)
• IV ACE inhibitors  Afterload reducers
• Promotes diuresis

Sodium Nitroprusside  best agent

 decreases both preload & afterload
BP Goal  Reduce 15% from MAP
within 15-30 minutes
Avoid  Beta Blockers iv line
Mehta Y et al, 2016
 Hypertensive Emergency...
Acute Renal Injury
Therapeutic goal :
Reduction of BP & increases creatinin clearance

Suggested agents :
 Fenoldopam :
Reduce BP and increases creatinin
clearance
 the best choice
 Nitroprusside
 Labetalol
Caution : ACE-I & Diuretic in hypovolemic pts  worsen renal
failure
 Hypertensive Emergency...

ECLAMPSIA

- Anticonvulsant Agent should be administered 

MgSO4
- Drug of choice: Hydralazine iv, Labetalol iv, Nicardipine
iv (negative teratogenic effect)
- Avoid : ACE inhibitor iv
- Therapeutic goal: anti hypertensive is needed when
TDS ≥ 100 mmHg  adequate uteroplacenta perfusion
HYPERTENSIVE URGENCY

Avoid more than 25% reduction

within the first 24 hours

Most commonly due to poorly

controlled chronic hypertension

REMEMBER: START LOW AND GO SLOW

 RELATED TO AUTOREGULATION

Loading dose of of oral anti

hypertension  accumulation effect!

Drug of choice: Captopril, Clonidine

 HYPERTENSIVE URGENCY

THE KEYS…

•Optimize (or restart) their current treatment regimens

•Consider oral short-acting agents (e.g. Captopril, Labetalol,
Clonidine)
•Do not treat aggressively with i.v. drugs or oral loading
•Ensure the patient has good follow up within a few days
WHAT’S THE RECOMMENDATION
•In the first hour there was no
significant difference
between sublingual and oral
captopril to reduce the blood
pressure.
•There wasn’t any difference
between oral and sublingual
group at any time.
 SUMMARY

Crisis Hypertension
1. Treatment not blood pressure
2. Short acting drug and Minimal adverse effects
3. Autoregulation
4. Decrease MAP 10-25 % accept stroke and
aorta dissection
THANK YOU