DR IMRAN GAFOOR

DR ASHOK ANAND
DEPTT OF CCEM ,
SIR GANGARAM HOSPITAL,N.DELHI
HYPERTENSIVE EMERGENCY
DEFINITIONS
BP elevation is associated with ongoing
neurological, myocardial, hematological or renal TARGET ORGAN
DISEASE (TOD)

HYPERTENSIVE URGENCY
- potential for TOD is great & likely to occur if BP is not controlled.
- occurs on chronic stable complication
. Stable angina
. Old MI
. CCF,CRF
. TIA,old CVA
 DEFINITIONS
ACCELERATED HYPERTENSION
- keith wagener barker retinopathy grade
3

(constriction,sclerosis+hemorrhages,exudates)
- may be urgency or emergency
- presence of exudate more worrisome
 DEFINITIONS
MALIGNANT HYPERTENSION
- KWB grade 4 retino +
papilledema
(neuroretinopathy)
- Always an emergency
MALIGNANT
HYPERTENSION.
MALIGNANT HYPERTENSION
- Increased BP + neuroretinopathy
- Fundus : flame shaped hemmorhags,
cotton wool spots, papilledma
- Assoc with : encephalopathy, LV failure,
micro angio hemolytic anemia,
renal fibrinoid necrosis with
endarteritis.
Risk factors : 30-50ys, male, smoking
MALIGNANT
HYPERTENSION.
Renal failure is most common cause of
death(fibrinoid necrosis+prolif endarteritis)
espc if assoc with glomerulonephritis.
Recovery predicted if combined length of
both kidneys >20.2cm & highly unlikely if
<14.2 cm.
Presenting creatinine >4.5 - dialysis
Treatment-sod nitroprusside
(0.3microg/kg/min) also-
labetolol, nicardipine,fenoldopam
BP CLASSIFICATION(Chobanian et
al/JNC 7)
sys(mm Hg) dias(mm
Hg)

NORMAL <120 & <80

Pre Htn 120-139 or 80-89

Stage I Htn 140-159 or 90-99

Stage II Htn 160 or 100

Iso sys Htn 140 &<90

MANIFESTATIONS OF TARGET
ORGAN DISEASE
LARGE VESSELS Aneurysmal dilations , Acc atheroscl.,
Aortic dissection

CARDIAC Acute - pulm edema , MI

Chronic - LVH , CAD

CEREBROVASCULAR Intracereb bleed, TIA, seizures, mental

status change, stroke

RENAL Hematuria, azotemia, Cr>1.5,

proteinuria>1+

RETINOPATHY Papilledema, Hemorrhages,

Exudates, Arterial nicking
PATHOPHYSIOLOGY
Increased SVR

Damage to endothelial lining

Leakage of plasma

Fibrinoid necrosis of arterioles(histo hallmark)

Local edema & sclerosis

Ischemia of brain ,heart, kidneys

PATHOPHYSIOLOGY
Patients with antecedent Htn can tolerate

higher fluctuations due to shift of autoreg

threshold.
Patients with no antecedent Htn organ

specific changes occur with DBP>100.

Most sensitive vascular bed is CEREBRAL.
 INITIAL EVALUATION
Cardinal points in history-
- TOD symptoms (most imp)
- prior Htn
- Medical Renal Disease
- medicine with compliance
- cocaine, amphetamine
-Htn from any cause may enter emergent phase.
-Usually occurs on background of essential hypertn.
- Imp secondary causes- renovascular(fibromuscular dys-
plasia/atheresclerosis)
- chronic GN
- reflux nephropathy
- analgesic nephropathy

 SYMPTOMS OF HYPERTENSIVE
CRISIS
MC is - headache (usually worse in morning)
- visual (scotoma, diplopia, hemianopia, blindness)

- neuro (focal deficits, stroke, TIA, somnolence)

- ischemic chest pain
- renal (polyuria, nocturia, hematuria)
- back pain (aortic aneurysm)
- nausea ,vomiting
- wt loss.

PATIENTS OFTEN HAVE INTRAVASCULAR VOLUME

DEPLETION.
 EXAMINATION
Verify BP recordings in diffn position(if possible)

Fundus exam arterio thickng, Incr light reflex, vascular

tortuosity, AV nicking

retinal hemmorhages, lipid leakage (hard

exudates)

nerve ischemia, papilledema

(cotton wool spots)
ABDOMEN
masses(PCKD),bruits(aneuyrsm)
 ANCILLARY TESTS
Sr Na, K, bicarb, BUN, Cr, CBC (with P/S for
schitocytes)

PT/aPTT, tox screen, pregnancy test, ECG,

urinanalysis

USUALLY - hypoNa and matabolic alkalosis

- incr BUN, Cr
- proteinuria, hematuria
- marked proteinuria suggets GN
 PSUDOHYPERTENSION
Overestimation of true BP due to stiff artery

OSLERS MANOEUVRE. : inflate BP cuff to

greater than brachial systolic, a palpable
radial artery but pulseless.

Seen in - atherosclerosis,
- monckebergs medial calcification,
- metastatic calcification(ESRD)
 TREATMENT
Initial therapy should terminate ongoing TOD, not return
of BP to normal.
Generalized goal : decrease MAP by 20-25% within one
hour
f/b decr to ~160/100 by 2-6 hrs
and towards normal over 1-2 days
EXCPTNS : . ischemic stroke
. aortic dissection
. active unstable angina or CCF

More gradual reduction in elderly with carotid stenosis

.
SPECIFIC HYPERTENSIVE
CRISIS
1 . PULMONARY EDEMA
a) with preserved systolic function(LVH)-
- abrupt increase in afterload with poor
diastolic
relaxation leads to pulmn HTN and edema.
- Treatment is with Na-nitropru (it prefrnn
dilates
resistance vessels)
- less emergnt condn ACEI/CCB
 PULMONARY EDEMA
B) with poor systolic function
MYOCARDIAL ISCHAEMIA
-nitroglycerine is preferred(dilates
collaterals)

MYOCARDIAL INFARCTION
- sedn/pain control
- DBP>100 - nitroglycr
- early -blockade
SPECIFIC HYPERTENSIVE
CRISIS
2) AORTIC DISSECTION

BP lowered rapidly to lowest clinically

acceptable level

Agents used lobet or esmolol, later on

nitropru added

Alternative agent-trimetaphan
SPECIFIC HYPERTENSIVE
CRISIS
3) HYPERTENSIVE ENCEPHALOPATHY
When high perfusion pressure overwhelms
cerebral autoregulation.
Can lead to blindness, seizures, coma, gradually
worsening headache.
Pathologically-cerebral edema, petechial
hemorrhg,
microinfarcts.
Immed Neuroimagng - to rule out ischemic
stroke/hemorrhage
Hallmark is improvement in 12-24 hrs of BP redn.
HTN ENCEPH
Treatment
short acting parenteral agents used.
MAP should decrease by 15-20% over 2-3 hrs.
D/d : cerebral infarct,
ICH/SAH,
subdural hematoma,
brain tumor, seizures,
vasculitis/meningoenceph.
 HTN ENCEPH
DIFFN POINTS :
1) Focal neurological deficit is unusual without
cerebral bleed
2) Papilledema is almost always assoc with Htn
enceph
3) Mental staus improves by 24-48hrs-delayed
in CNS bleed
4) Brain dysfunction develops by 12-24 hrs in
Htn but more acutely with ischemic
stroke/bleed.
 HTN ENCEPHAL..
Posterior leukencephalopathy syn.-
reversible vasogenic subcortical edema
without infarct

MRI white matter edema in post cerebral

hemispheres
 ISCHEMIC STROKE
For every 10 mmHg incr in pressure >180 a 40%
incr in worsening neurological status.
Area of stunned but viable tissue(ischemic
penumbra)may need higher perfusion
pressures, so
ASA/AHA-recommends (after excluding pain,
nausea, full bladder, hypoxia, incr ICP)
BP redn. If sys>220 or dias > 120
Also, for thrombolysis BP<185/110.
And post reperfusion use lobet or nicardipine for
sys>180 or dias>105 & Na nitro for sys >230
ISCHEMIC STROKE
Latest studies recommend modest reduction

of BP

(10-27mmHg) improved outcomes but effect

waned with increasing age ,so,avoid >10%
sudden drop
SUBARACHNOID
HEMORRHAGE
SAH incr ICP & decr cerebral perfusion causing
global
ischemia
Induces intense vasospasm in neighbouring vessels
(4- 12 days) after initial bleed.
Goal-dec 20-25% of MAP over 6-12 hrs but not
<160/100.
If vasospasm occurs later-inc BP with 3H(not proven)
Preffred - lobet
Avoid- nitrodilators
No data to support oral nimodip dec vasospasm.
 INTRACRANIAL
HEMORRHAGE
Major risk factor is Htn.
Most rapid decline in BP occurs in first 24 hrs but
may remain elavated for 7-10 days (while in ischemic
stroke BP dec to normal in 24-48 hrs)
AHA/ASA recommendsdecrease BP if-
Sys>200 or MAP>150,
ICP incr suspected sys>180 or map>130
ICP incr not suspec-target MAP~100 or
BP~160/90

Preffred agent : lobet

 HEAD TRAUMA
With trauma comes edema

With ICP monitoring target MAP 90

Prefferd- lobet or nicardipine

 POST OP PAIN
Early-(0-2hrs) : pain, hypoxemia, hypercabia,

shivering.
Intermed(12-36hrs) : fluid overload, reaction

to ET/FOLEYS.
 Pheochromocytoma
Very rare cause of hypertension
Headache,palpitations,Htn,anxiety,abd pain
diaphoresis
Orthostatic changes in BP
Paroxsysmal symptoms
T/t : i/v phentolamine f/b b-blockade
 GESTATIONAL
HYPERTENSION
After 20 wks in normotensive.
SBP>140 & DBP>90 on two separate occasions
6 hrs apart.
Pre-eclampsia gestn htn + 300 mg in 24 hrs
proteinuria
Eclampsia- +seizures
T/t bed rest & parenteral Mg
Use (lobet,hydralazine) if SBP>160 or DBP>100
 ANTIPHOSPHOLIPID Ab
SYNDROME
Microvasculopathy & emboli to renal artery
T/t Na nitropru/lobet & anticoagn.
 GBS
Dysreflexia (bladder/bowel distension below
level of lesion trigger massive sympatc
discharge)

Symptoms Htn,bradycardia,
diaphoresis,headache.

T/t Na nitroprus., phentolamine,lobet

 RENAL TRANSPLANT
RECEPIENT
Acute rejection
Obstructive uropathy
Cyclosporine/steroid.
T/t oral CCB
NEW ONSET HYPERTENSION
IN ICU
Pain
Anxiety
Hypoxemia
Hpercarbia
Shivering
Vol overload
Discontinuation syndrome
 INTRAVENOUS
MEDICATIONS
Sodium nitoprusside : nitric oxide compound
-arterio-veno dilator
-useful in most Htn crisis
dose 0.25mic/kg/min(max 8)
C/I high output cardiac failure, cong optic atrophy.
Cyanide toxicity anemia & liver d/e
-acidosis, tachycardia, almond smell,
change in mental status.
Thiocyanate tox. renal d/e
-psychosis, hypereflexia,seizure,tinnitus
-thiocyanate>10 should be avoided.
Avoiod infusion>48 hrs.
INTRAVENOUS
MEDICATIONS
NITROGLYCERINE- predom. Veno dilator,

decreases preload.
Use : cardiac ischemia

Dose : 5mic/min(max 100)

C/I : incresed ICP, angle closure glaucoma

Most useful in cadiac compromise(MI,LV

failure,pulm edema),,not recommnded > 48 hrs.

INTRAVENOUS
MEDICATIONS
LABETOLOL : > (7 : 1) adrenergic blockade

Onset 2-5 min, durn 3-6 hrs

Bolus 20 mg (max 300 mg)

Infusion 0.5-2mg/min ,used in pregnancy along

with hydralazine.
Avoid in bronchospasm, bradycardia, CCF,

>first degree heart block,

INTRAVENOUS
MEDICATIONS
ESMOLOL: cardioselective 1 blocker

Used in aortic dissection

Onset 60 seconds, duration 10-20 min.

Infusion 50-300 mic/kg/min.

Not dependant on hepatic/renal function

INTRAVENOUS
MEDICATIONS
FENOLDOPAM : post synaptic dopamine agonist.

-primarily arterial dilator,rapid

onset/offset of effect.
Advantageous in kidney d/e, increases renal

blood flow,natriuresis.
Dose : 0.1 mic/kg/min.

C/I : glaucoma,hypotension,,check K+ every 6 hrs

INTRAVENOUS
MEDICATIONS
HYDRALAZINE : direct arteriolar dilator.

Used in pregnancy/eclampsia

Dose 10 mg every 60 min (max 20 mg)

Duration of action 2-4 hrs

Reflex tachycardia, exacerbates angina,BP

lowering response is less predictable(depends

on renin&volume status)
INTRAVENOUS
MEDICATIONS
PHENTOLAMINE: blockade

Used primarily in pheochromocytoma

Dose 5-15 mg

Always f/b -blockade

INTRAVENOUS
MEDICATIONS
NICARDIPINE : dihydropyridine CCB
Onset 10-20 min,duration 1-4 hr
Dose 5 mg/hr (max 15 mg/hr)
Avoid in CCF,cardiac ischemia.

CLEVIDIPINE : short acting dihydropyridine

CCB.
Reduces BP without affecting cardiac filling
pressures or reflex tachycardia
INTRAVENOUS
MEDICATIONS
ENALAPRILAT : only parenteral ACE-I.
Dose 1.25-5 mg every 6 hr.
Response not predictable, hyperkalemia in
reduced GFR.

TRIMETHAPHAN : nondepolarizer ganglionic

blocker.
Dose : 0.5-5mg/min
Used in aortic dissection
Disadvntges : paralytic ileus, bladder atony,
tachyphyl.
Thank you