HYPERTENSIVE

EMERGENCY
 Content.
Definition
Pathophysiology
Diagnosis
Management
 Definition
HYPERTENSION = persistent elevation
of SBP 140 mmHg and/or DBP 90
mmHg
 Severe Hypertension

Defined as BP > 180/110 mmHg

with/without TOD

Hypertensive urgency without TOD

Hypertensive emergency with TOD
 These patient may presented with:
Incidental findings, asymptomatic patient
Non-specific symptoms: headache,
dizziness, lethargy
Symptoms/signs of TOD: acute heart
failure, ACS, ARF, hypertensive
encephalopathy, stroke
 Risk Factor
Uncontrolled essential hypertension
Cigarette smoking
Central obesity
Sedentary lifestyle
Diabetes mellitus
Dyslipidaemia
Family hx of premature cardiovascular
disease (men < 55 y/o, women < 65
y/o)
 Pathophysiology
The renin-angiotensin-aldosterone
system
 Hypertensive Emergency
Failure of normal autoregulatory
function
Leads to a increase in systemic vascular
resistance
Endovascular injury with arteriole
necrosis
Ischemia, platelet deposition and
release of vasoactive substances
Further loss of autoregulatory
mechanism
Exposes organs to increased pressure
 Management
It depends on:
History
Physical examination
Lab investigations
Thorough evaluation of patient,
particularly looking for signs of acute
TOD and causes of secondary HPT
 Manifestation of TOD
ORGAN SYSTEM MANIFESTATION
CARDIOPULMONARY Acute pulmonary oedema, ACS,
acute aortic dissection, heart
failure

CEREBROVASCULAR Hypertensive encephalopathy,

stroke, subarachnoid
haemorrhage

RENAL Acute renal failure

RETINOPATHY Haemorrhage/exudates with/

without papilloedema
APPROACH
TO PATIENT
 Approach to patient
Recheck blood pressure
Appropriate size cuff.
Cuff not over clothing
History
Prior crises
Renal disease
Medications
Compliance
 Approach to patient

cont
Physical examination focus on TOD
Neurology
Cardiac
Renal
Neurology
Hypertensive encephalopathy
Fundoscopy: Papilloedema
Seizures
Ischaemic vs haemorrhagic CVA
Focal Neurological Deficits
 Approach to patient
cont
Cardiac:
Cardiac ischemia
ECG - for ischaemic changes
Acute left ventricular failure
Pulmonary oedema
CXR
 Approach to patient
cont
Renal
Electrolytes
Urea/creat
Chronic failure/insufficiency @ acute failure
UFEME haematuria, proteinuria, casts
 Approach to patient
cont

Patient are then categorised as having:

Asymptomatic severe HPT
HPT urgencies
HPT emergencies
MANAGEMENT
 Asymptomatic severe
HPT
Admission may be necessary in the
newly dx or
Compliance may be a problem
Pt already on tx need to have their
medication reviewed
 HPT urgencies

Include pt with grade III or grade IV

retinal changes, without TOD
May need admission
Initial tx should aim for 25% reduction
of BP over 24h but no lower than
160/90 mmHg
 HPT emergencies

Patient presented with TOD

It may occur in patients with BP <
180/110 mmHg, particularly if BP has
risen rapidly
Patient must be admitted
BP should be reduced by 25% over 3-
12h but no lower than 160/90 mmHg
 DRUGS DOSE ONSET OF DURATION REMARKS
ACTION
Sodium 0.25 10 g/kg/min Seconds 1-5 min Caution in renal
Nitroprusside failure
Labetalol Iv bolus 25-50mg 5 min 3-6 hrs Caution in heart
(over at least 1min) failure, asthma
rpt if necessary at 5
min intervals (max
300mg), then 0.5-
2mg/min ivi
Nitrates 5 100 g/min 2-5 min 3-5 min Preferred in ACS
and APO
Hydralazine Iv 5-10mg, maybe 10-20 min 3-8 hrs Caution in ACS,
rpt after 20-30 min CVA and dissecting
IVI 200-300 mcg/min 20-30 min aneurysm
initially. Maintenance
50-150 mcg/min
Nicardipine IV bolus 10-30 5-10 min 1-4 hrs Caution in acute
mcg/kg over 1 min, heart failure and
IVI 2-10 mcg/kg/min coronary
ischaemia
Esmolol Iv bolus 250-500 1-2 min Used in peri-
mcg/kg over 1min, operative
IVI 50- 3-10 min situations and
200mcg/kg/min for 4 tachy-arrhythmias
min
PHARMACOTHERA
PY
 1.Sodium nitroprusside
MOA: potent vasodilator in arterioles and venules
Decreases afterload and preload by reduces peripheral
vessel resistance and venous return
No direct negative inotropy or chronotropy
Kinetics
Onset: seconds
Duration: 1-2 min
1/2 life: 3-4 min
Side effect: hypotension
Relative contraindication:
Hepatic dsfxn - hepatic enzyme is involved in metabolism of
nitroprusside
Renal impairment
Hepatic encephalopathy it will further increased ICP
 2. Nitroglycerin
(nitrates)
Vasodilator
At high doses dilates arteriolar smooth muscle
Better dilation of coronary conductance
arteries
Kinetics
Onset: 1-2 min
Duration: 3-4 min
Indication:
myocardial ischemia,
moderate HTN complicating USA
pulmonary oedema
 3. Labetalol
Mixed selective alpha-1 & non-selective beta blocker
(ratio : = 1:7)
Advantages:
Maintains cardiac output
Decreased PVR without reflex tachycardia
Maintains cerebral, renal & coronary blood flow
Kinetics
Onset: 2-5 min
Peak: 5-15 min
Duration: 4-8 hrs
Indication:
PIH associated with pre-eclampsia
Acute HPT of pheochromocytoma & HPT crisis
Contraindication: asthma, COPD, bradycardia (2nd and
3rd degree heart blocks)
 4. Esmolol
Cardioselective 1 receptor blocker with:
rapid onset of action
very short duration of action
Rapidly metabolized by plasma esterase
Negative chronotropy/inotropy
Kinetics
Onset: 1-5 min
Duration: 10-20 min
Indication: SVTs, tachycardia and HPT
perioperatively, MI, USA and thyrotoxocosis
Contraindication: asthma, COPD
 5. Nicardipine
Dihydropyridine Ca2+ channel blocker
More selective on vascular smooth
muscle than cardiac muscle
produces relaxation of coronary vascular
smooth muscle and cause little or no
negative inotropic effect
useful in the management of CCF
Kinetics
Onset: 5-15 min
Duration: 4-6 hrs
 SPECIFIC
TREATMENT
 HPT encephalopathy
Pathophysiology:
Loss of cerebral autoregulation of blood
flow, resulting in cerebral hyperperfusion,
loss of BBB integrity and cerebral oedema
reversible
Symptoms: headache, lethargy,
confusion, visual disturbance, seizures
Signs: hypertensive retinopathy,
papilloedema, decrease level of
consciousness, coma
 Aim: to reduce MAP by 25% and to
lower the DBP to 100-110 mmHg
Excessive BP reduction may result in
cerebral infarction, blindness & cardiac
ischaemia
Labetalol, nicardipine are the preferred
medications
Cerebral Infarction/Haemorrhage
Pathophysiology: thrombosis, embolism
or hypoperfusion
Symptoms: depending on location of
insult
Signs: focal neurologic deficits
Ix: CT brain urgent!!
 Tx should started when SBP > 220
mmHg @ DBP > 120 mmHg
BP should be cautiously reduced by no
more than 15% over the initial 24-hour
period
Recommended antihypertensive:
nicardipine, labetalol, esmolol
These medications are relatively short
acting
Medications contraindicated :
nitroprusside can cause sudden drops in
BP and the possibility of increasing ICP
through venodilatation
 TABLE 1. Approach to Elevated Blood Pressure
in Acute Stroke
Clinical Situation Recommendation
SBP <220 mm Hg, Observe BP unless there is other TOD involvement (eg:
DBP <120 mm Hg aortic dissection, renal failure, or AMI) that would
mandate emergent treatment.

SBP >220 mm Hg or Labetalol 1020 mg IV over 12 min. May repeat or

DBP 121140 mm Hg double every 10 min to a maximum dose of 300 mg OR
Nicardipine 5 mg/h IV infusion as initial dose; titrate to
desired effect by increasing by 2.5 mg/h every 5 min to
maximum of 15 mg/h (target 10%15% reduction)

DBP >140 mm Hg Sodium nitroprusside 0.5 m/kg per min IV with

continuous BP monitoring (target 10%15% reduction)

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 Acute Aortic Dissection

Pathophysiology: intimal tear resulting

in blood flow into the media
Symptoms: anterior chest pain
(ascending aorta)/ interscapular pain
(descending aorta), tearing/sharp in
nature
Signs: bounding pulses, wide pulse
pressure, diastolic murmurs, raised JVP
 Ix:
Cxr: widening mediastinum, pleural
effusion, tracheal deviation to the right,
depression of left main stem bronchus
ECHO
 Aim to reduce cardiac contractility
(beta blocker) and systemic arterial
pressure (vasodilator)
Goal is to lower SBP to 90 120 mmHg
Medication preferred: Labetolol,
esmolol, sodium nitroprusside,
nicardipine
Contraindication: hydralazine
 Acute Myocardial
Ischaemia / Infarction
Pathophysiology:
Increased afterload, cardiac workload,
myocardial oxygen demand
Decreased coronary artery blood flow
Symptoms: chest pain, SOB,
nausea/vomiting, profuse sweating
Signs:
Heart failure signs
ECG changes
 Aim:
Immediate BP reduction to prevent
myocardial damage
Preferred medication:
Nitroglycerin iv @ sublingual
Nitroprusside
Beta-blocker
 Congestive Heart Failure
Pathophysiology: increased afterload
with reduced cardiac output
Symptoms: SOB, cough, bilateral leg
swelling
Signs: raised JVP, hepatomegaly,
bibasal crepts, gallop rhythm, bilateral
pedal oedema
Preferred anti-HPT:
Nitroprusside @ iv nitroglycerin
(vasodilator) in addition to diuretics
THANK YOU