This document defines various types of hypertensive crises and emergencies and provides treatment guidelines. It discusses malignant hypertension, hypertensive encephalopathy, ischemic stroke, subarachnoid hemorrhage, and other specific conditions. It also defines various intravenous antihypertensive medications and their usages, doses, and cautions. The document is intended to guide physicians in diagnosing and treating different hypertensive emergencies.

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