1. DR IMRAN GAFOOR
DR ASHOK ANAND
DEPTT OF CCEM ,
SIR GANGARAM HOSPITAL,N.DELHI

2. DEFINITIONS
HYPERTENSIVE EMERGENCY
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

3. DEFINITIONS
ACCELERATED HYPERTENSION
- keith wagener barker retinopathy grade 3
(constriction,sclerosis+hemorrhages,exudates)
- may be urgency or emergency
- presence of exudate more worrisome

4. DEFINITIONS
• MALIGNANT HYPERTENSION
- KWB grade 4 retino + papilledema
(neuroretinopathy)
- Always an emergency

5. 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

6. 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

7. 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

8. 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

9. PATHOPHYSIOLOGY
Increased SVR
Damage to endothelial lining
Leakage of plasma
Fibrinoid necrosis of arterioles(histo hallmark)
Local edema & sclerosis
Ischemia of brain ,heart, kidneys

10. 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.

11. 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

12. 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.

13. 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)

14. 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

15. 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)

16. 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
.

17. 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

18. PULMONARY EDEMA…
B) with poor systolic function
MYOCARDIAL ISCHAEMIA
-nitroglycerine is preferred(dilates collaterals)
MYOCARDIAL INFARCTION
- sedn/pain control
- DBP>100 - nitroglycr
- early β-blockade

19. 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

20. 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.

21. 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.

22. 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.

23. HTN ENCEPHAL..
Posterior leukencephalopathy syn.-
reversible vasogenic subcortical edema without
infarct
 MRI – white matter edema in post cerebral
hemispheres

24. 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

25. ISCHEMIC STROKE
Latest studies recommend modest reduction of BP
(10-27mmHg) improved outcomes but effect waned
with increasing age ,so,avoid >10% sudden drop

26. 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.

27. 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 recommends…decrease 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

28. HEAD TRAUMA
With trauma comes edema
With ICP monitoring –target MAP ≥90
Prefferd- lobet or nicardipine

29. POST OP PAIN
Early-(0-2hrs) : pain, hypoxemia, hypercabia,
shivering.
Intermed(12-36hrs) : fluid overload, reaction to
ET/FOLEYS.

30. 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

31. 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

32. ANTIPHOSPHOLIPID Ab SYNDROME
Microvasculopathy & emboli to renal artery
T/t – Na nitropru/lobet & anticoagn.

33. GBS
Dysreflexia (bladder/bowel distension below level of
lesion trigger massive sympatc discharge)
Symptoms – Htn,bradycardia, diaphoresis,headache.
T/t – Na nitroprus., phentolamine,lobet

34. RENAL TRANSPLANT RECEPIENT
Acute rejection
Obstructive uropathy
 Cyclosporine/steroid.
T/t oral CCB

35. NEW ONSET HYPERTENSION IN ICU
Pain
Anxiety
Hypoxemia
Hpercarbia
Shivering
Vol overload
Discontinuation syndrome

36. 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.

37. 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.

38. INTRAVENOUS MEDICATIONS
LABETOLOL : β > α (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,

39. INTRAVENOUS MEDICATIONS
ESMOLOL: cardioselective β1 blocker
Used in aortic dissection
Onset 60 seconds, duration 10-20 min.
Infusion 50-300 mic/kg/min.
Not dependant on hepatic/renal function

40. 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

41. 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)

42. INTRAVENOUS MEDICATIONS
PHENTOLAMINE: α – blockade
Used primarily in pheochromocytoma
Dose 5-15 mg
Always f/b β-blockade

43. 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

44. 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.

45. Thank you