1. HYPERTENSION EMERGENCIES
and
HYPERTENSION URGENCIES
Case based approach and management

2. Introduction
• Hypertension is the most common modifiable risk factor for
cardiovascular diseases.
• Most common indication for adults to visit a physician.
• Its prevalence will continue to increase,both among the young
because of increasing obesity and in older adults because of longer
life expectancy.
• Despite being common, it is inadequately treated.

3. Epidemiology
• Approximately 1% hypertension pts may develop hypertensive
crises during their lifetime.
• Annual incidence of hypertensive emergencies being
1-2 cases/1,00,000 pts.
• Higher rates have been reported in African Americans,
low socioeconomic people, in developing countries.
• Incidence in men 2 times higher than in women
Curr Opin Cardiol 2006;
Curr Hypertens Rep 2003;

4. Joseph varon et al.Critical care 2008

5. Hypertensive Crises
• More generalised term .
• Not defined by a specific blood pressure reading, rather it is a
clinical syndrome that is associated with acute elevation of blood
pressure.
• It includes
– Hypertensive Emergency
– Hypertensive Urgency

6. • Characterised by severe increase in systolic and/or diastolic blood pressure
assosciated with signs or symptoms of acute end-organ damage.
 No blood pressure threshold for diagnosis.
• Usually,
– SBP > 180-220 mm Hg
– DBP > 120-130mm Hg
– MAP > 180 mm Hg
• Requires an immediate BP reduction in few minutes –hours.
• Requires an ICU care.
• IV drugs
Hypertensive Emergency

7. Hypertensive Emergencies
Hypertensive encephalopathy
Hypertension assosciated with acute cerebrovascular disease
Hypertension assosciated with pulmonary edema
Hypertension assosciated with acute coronary syndromes
Hypertension assosciated with dissecting aortic aneurysm
Pheochromocytoma
Hypertension associated with acute renal failure
Eclampsia
Microangiopathic anemia

8. What is the primary reason for hypertensive
emergencies ?
1. Renovascular Disease
2. Pheochromocytoma
3. Non-adherence to anti-hypertensive medication
4. Hyperaldosteronism
5. Erythropoeitin

9. Hypertensive Urgency
• Severe elevation in BP >180/120 mm Hg without
symptoms or signs of acute target organ involvement.
• Adequate treatment of these conditions, a BP lowering
within 24 hrs by administration of oral drugs.
• ICU admission is usually not required.

10. Hypertensive Urgency
Severe uncomplicated essential hypertension
Severe uncomplicated secondary hypertension
Postoperative hypertension
Hypertension assosciated with severe epistaxis
Drug induced hypertension
Rebound hypertension (i.e sudden withdrawal of clonidine)
Cessation of prior antihypertensive therapy
Anxiety ,panic attacks or pain

11. Why rapid reduction of BP not recommended
in absence of end organ damage??
An aggressive approach.
A precipitous and unpredictable BP fall
Harmful (esp . In pts with multiple risk factors)
Cardiol clinics 2006;24:135-46.

12. Accelerated - Malignant Hypertension
• Severe hypertension and presence of retinopathy .
• Exudates,hemorrhages – Accelerated hypertension.
• Papilledema – Malignant hypertension.

13. Acute target organ damage in hypertension
Target organ Complications
Brain Hypertensive encephalopathy
Cerebral infarction
Cerebral hemorrhage
Advanced retinopathy
Heart Acute coronary syndrome
Acute heart failure
Aorta Aortic dissection
Kidney Acute renal failure
Placenta Eclampsia

14. • Single organ inv. in approximately 83%.
• Two organ inv. found in 14%,multiorgan inv. in 3 % pts.
Most common clinical presentations
- cerebral infarction (24%)
- pulmonary oedema (22%)
- HTN encephalopathy (16%)
- Cong. HF (12%)
•Less common presentations – IC hemorrhage, Aortic dissection
and Eclampsia ESC/ESH 2013

15. Joseph varon et al.Critical care 2008

16. Etiology
• Essential hypertension : Inadequate blood pressure control and
noncompliance are common precipitants (MOST COMMON)
• Renovascular
• Eclampsia/pre-eclampsia
• Acute glomerulonephritis
• Pheochromocytoma
• Anti-hypertensive withdrawal syndromes
• Head injuries and CNS trauma
• Renin-secreting tumors
• Drug-induced hypertension
• Burns
• Vasculitis
• Post-op hypertension
• Coarctation of aorta (very rare)
2nd common

17. • Unclear, but some candidates
– ACE DD genotype
– Absence of the β and γ subunit of ENaC
– Elevated adrenomedullin levels
– Elevated natriuretic peptide level
– Abnormalities in oxidative stress markers and endothelial
dysfunction
Vaughan and Delanty Lancet 2000; 356:411
Why only some are affected?

18. Pathophysiology
Increase in
BP
Mechanical stress
Endothelial injury
Increased
permeability
ischemia
RAAS
Activation of
coagulation
cascade,platelets
Deposition
of fibrin
IL-6
PRESSURE
NATRIURESIS
End organ
hypoperfusion,
ischemia,
dysfunction
Increase in
SVR
Humoral
factors
Vaughan and Delanty Lancet 2000; 356:411
Fibrinoid
necrosis

19. Vaughan and Delanty Lancet 2000; 356:411

20. CASE 1
• A 65 yr old male, hypertensive, chronic smoker, driver by
occupation admitted in ED with c/o headache since 3 days,increased
in severity over the past one day, associated with vomitings and
altered sensorium.
• He has been noncompliant to drugs since 15 days.
• At presentation his pulse rate was 70/min,regular, BP recording was
240/140 mm Hg, CVS- being normal on auscultation, lungs b/l basal
crepts.
• What is the diagnosis ?What would you do ?
• Admit ? What would be BP goal in this patient?

21. CASE 2
• A 38 yr old male,daily labourer, hypertensive since past
6yrs,came for follow up at OPD.
• His BP was 180/100 mm Hg .
• ECG showed LV strain.
• No symptoms of SOB on exertion,angina.
• Admit ?/ OPD Rx ?
• IV drugs / oral?

22. CASE 3
• A 28 yr old female, primi (6 months amenorrhea) was referred to
physician with
c/o headache,vomitings,decreased urine output.
her BP was recorded to be 170/100 mm Hg
• CBP –leucocytosis,low platelets.
• CUE –pus cells,RBC
• LFT – mildly raised aminases,bilirubin being 2.8mg/dl
• ECG –sinus tachycardia ,LVH with strain.
• 2Decho – concentric LVH.
• What to do ?
• Admit ?
• Normalize BP ?

23. CASE 4
• A 54 yr old male was admitted in ED with c/o weakness of
right upper limb and lower limb since morning,
• Known hypertensive,diabetic.
• Alcoholic
• Was unconscious, BP was 190/100 mm Hg
• CT brain – large MCA territory ischemic infarct
• What to do ?
• Normalize BP?

24. CASE 5
• A 45 yr old male ,K/C/O CAD, hypertensive,diabetic, smoker
came with sudden onset of ripping pain, sharp sensation in the
back, along with SOB class IV.
• At presentation BP was 240/140 mm Hg
• Pulses discreprenancy on palpation.
• What to do ?
• Normalize BP ?

25. CASE 6
• A 23 yr old male,degree student, was brought to casualty with
sudden onset of SOB since 2 hours,saturations at room air
were normal.
• BP – 180/100 mm Hg
• CVS/RS –NAD
• What to do ?
• IV/oral/reassurance

26. Clinical assessment
• Complete history collection
• Detailed physical examination
• Duration and degree of pre existing hypertension
• Evidence of target organ damage
• Details of antihypertensive therapy
• Compliance with medications
• Use of the over counter drugs
• Illicit drugs usage

27. Symptom End organ damage

28. Examination of pt
• BP sitting and standing position (if possible) with an appropriate
size cuff in both arms(difference - aortic dissection).
• If peripheral pulses are markedly reduced (lower limb BP
required).
• RR,HR
• O2 saturation
• Fundoscopic examination.
• CVS – murmurs (aortic insufficiency, ischemic MR)
• S3,gallop,crackles in lung fields, raised JVP (signs of HF)
• Renal bruit (renovascular HTN)
• Abdominal mass (PCKD)
• Level of consciousness ,focal signs of ischemia

29. Joseph varon et al.Critical care 2008

30. ESC/ESH,2013

31. Keith-Wagener-Barker Classification
• Grade 1
– Mild narrowing of the arterioles
– “Copper Wire”
• Grade 2
– Moderate narrowing –
– Copper wire and AV nicking
• Changes associated with long
standing essential hypertension
Grade 3
Severe Narrowing -
Silver wire changes,
hemorrhage, cotton wool
spots, hard exudates
Grade 4
Grade 3 + Papilledema
Grade 3 and 4 highly
correlated with progression to
end organ damage and
decreased survival

32. Normal

33. Grade 1

34. Grade 2

35. Grade 3 KWB Retinopathy

37. Investigations
• Blood electrolytes
• Creatinine
• Urea nitrogen
• Cell count
• Smear (microangiopathic hemolysis)
• ECG
• CXR
• CT Brain
• CT chest/MRI

38. Management

39. Normalisation of BP is usually not
recommended*
How fast and how much BP to be lowered to be given importance.

40. Why ??
• Sudden fall in BP may cause acute hypoperfusion of vital organs
and results in myocardial ischemia or infarction, hemiplegia,or
acute renal failure.
• Older patients with long lasting hypertension and preclinical organ
involvement (LVH, atherosclerosis and arteriolar remodelling) are
at risk of these complications as the lower limit of autoregulation
shifted to right.

41. Appropriate treatment is dictated more by the
features of the acute syndrome and by the
patient’s characteristics than by a body of
scientific evidence.
• Controlled trials not available (extremely heterogenous population)
• Tailored on individual patient
– Organ at risk.
Varon J et al ;Crtical care 2003
ESC/ESH manual of Hypertension 2009

42. HYPERTENSIVE EMERGENCIES

43. Hypertensive Emergency
• Damage Heart - CHF, MI, angina
Kidneys - acute kidney
injury, microscopic
hematuria
CNS - encephalopathy,
intracranial hemorrhage, Grade
3-4 retinopathy
Vasculature - aortic
dissection, eclampsia

44. • GOAL reduce MAP by no more than 20-25%,
DBP to 100-110mm Hg within few minutes to 2 hours.
• More aggressive and rapid BP reduction (Acute Pulmonary
edema ,Aortic dissection)
• More slowly for acute cerebrovascular damages with
monitoring of neurological status.
• Constant infusion of intravenous agents required (no
intermittent IV boluses/oral/sublingual drugs- drastic BP
fall).

45. Ideal drug
 Fast acting
 Easily titratable
 Rapidly reversible and safe
 No single agent has these characteristics

46. Sodium nitroprusside
• Potent short acting arterial and venous dilator
(reduces pre- and after- load)
• Rapid onset of action.(seconds)
• Continuous intra-arterial BP monitoring required.
• Infusion chamber and tubing to be covered.
•  intracranial pressure (caution in intracerebral hemorrhage)
• Induces coronary steal (non selective coronary vasodilation)
• Increases mortality in pts with acute MI. (NEJM,1982)
• Thiocyanate toxicity (nausea,vomiting,lactic acidosis and altered mental
status)
– Usually rare, seen in pts with renal ,hepatic dysfunction.
Freiderich et al, Anesth Analo 1995:81:152-162

47. Fenoldopam
• A peripheral dopamine-1 receptor antagonist (DA1).
{highly specific}
• 10 –fold more potent than dopamine as a renal vasodilator.
• Antihypertensive effect by combined natriuretic and vasodilatory effect
(esp. intrarenal arteries)
• Not to be used as prophylactic agent for preventing CIN
(CAFCIN Trial)
• Agent of choice in hypertensive emergencies assosciated with renal
dysfunction.
• Adv effects – hypotension ,hypokalemia
Clin Invest 1993;72:60-64

48. Nicardipine
• Second generation DHP CCB.
• Strong cerebral and coronary vasodilation.
• Onset of action 5-15 min, Duration being 2-6 hrs.
• Increases both stroke volume and coronary blood flow with a favourable
effect on myocardial oxygen balance.
• CAD with Systolic HF. C/I in Aortic stenosis.
• Dosage independent of weight.
• Infusion rate of 5mg/h – 2.5 mg/h increments every 5 min –max being 15
mg/h.
• IV Nicardipine maintained BP in Treatment range > IV Labetalol
(CLUE trial) BMJ,2013
J Emerg Med 1987:5:463-473

49. Clevidipine
• Third generation, intravenous, dihydropyridine caclium channel
antagonist.
• FDA approval (2008)
• Ultra short half life of about 1 min.
• Potent arterial vasodilation (no effect on venous capacitance,
myocardial contractility)*
• No significant adverse effect on heart rate’.
• Injectable emulsion.
• 99.9% bound to protein.
• Safe in pts with renal,hepatic dysfunction.
• C/I –allergies to soy products,eggs and egg products,defective lipid
metabolism.
*Rivera et al .,2010,Polly et al 2011.
50mg/100ml

50. Dosage
•An IV infusion at 1–2 mg/hour is recommended for initiation and
should be titrated by doubling the dose every 90 seconds.
• As the blood pressure approaches goal, the infusion rate should be
increased in smaller increments and titrated less frequently.
•The maximum infusion rate for Cleviprex is 32 mg/hour.
•Most patients in clinical trials were treated with doses of 16 mg/hour
or less.
No more than 1000 mL (or an average of 21 mg/hour) of Cleviprex
infusion is recommended per 24 hours..
Am J Cardiovascular Drugs 2009;9;117-134

51. Clevidipine
• ESCAPE1(pre op),ESCAPE 2(post op) plaebo controlled trials –
15% reduction in SBP within 6 min post infusion.
Rivera et al.,2010.
Levy et al .,2007.
• ECLIPSE – Clevidipine maintained BP within target range with
minimal excursions.
Singla et al .,2008
• VELOCITY study for hypertensive crises.
Pollack et al .,2009
• ACCELERATE trial –management of severe HTN with ICH
Graffagnino et al., 2009

52. Labetalol
• Combined selective 1 adrenergic and non selective β adrenergic
receptor blocker (1:7).
• Hypotensive effect – in 2-5 min after IV admin.
• Maintains cardiac output (unlike other BB).
• Reduces SVR, but does not decrease PBF.
• Cerebral,renal,coronary blood flow maintained.
• Less placental transfer can be used in pregnancy induced HTN
emergency.
• Metabolised by liver.
• Oral/IV. Drugs 1984,Suppl 2 :35-50.

53. Esmolol
• Ultrashort acting cardioselective β adrenergic blocking agent.
• Ideal β blocker in critical cases.
• Useful in severe postoperative HTN.
• Onset of action is within 60 sec
• Duration of action being 10-20min.
• Rapid hydrolysis of ester linkages by RBC esterases(metabolism),
not dependent on renal or hepatic function.
• 0.5 to 1mg/kg loading dose over 1min,followed by an infusion -
50ug/kg/min.(max 300ug/kg/min)
Chest 1988;93:398-403

54. Not to use
Sublingual Nifedipine
• Drug is poorly soluble, not absorbed through buccal mucosa
• Sudden uncontrolled and severe reductions in BP,may precipitate
cerebral,renal and myocardial ischemic events.
• Lack of clinical documentation attesting to a benefit from its use.
• The Cardiorenal Advisory Committee of the FDA has concluded
“that the practice of administering SL/oral nifedipine should be
abandoned because this agent is not safe nor efficacious”.
Anaesth Clin North Am.1999.

55. SPECIAL SCENARIOS

56. Myocardial ischemia/infarction
• may be assosciated with HTN at presentation
(usually in a previously HTN pt).
• High BP exacerbated by pain and agitation.
• IV Nitrates reducing systemic vascular resistances,LVpreload,
improves coronary perfusion.
• B blockers may contribute to a fall in BP (reduces myocardial O2
consumption)
• BP control mandatory before thrombolysis (BP<180/100 mmHg).
Vaughan et al Lancet 2000;356:411-7

57. Acute Cardiogenic Pulmonary Edema
• Ventilation
• Reduction of LV preload and afterload.
• IV nitrate, loop diuretics.
• Others – urapidil, nicardipine,sodium nitroprusside.
• {Urapidil is a sympatholytic antihypertensive drug. Peripheral α1-
adrenoceptor antagonist and a central 5-HT receptor agonist, does not
elicit reflex tachycardia(weak β1adrenoceptor antagonist activity, effect on
cardiac vagal drive). Not approved by the USFDA, but it is available
in Europe}.
• Bolus 12.5-25 mg (50 mg),infusion 5-40mg/h,onset 3-6 min,duration 4-6
hr .
Salgado et al.Annals of intensive care 2013;3:17

58. Aortic Dissection
• Most dramatic and rapid fatal complication in HTN emergencies.
• Acute BP reduction reduces shear forces on damaged aorta.
• Aim of treatment to reduce SBP as rapidly as possible down to
100-110 mmHg, simultaneously control tachycardia resulting form
the sympathetic activation.
• B blocker + vasodilator to be given
• Esmolol + nitroprusside would be a better combination.
• Hydralazine is C/I Circulation 2006;114:1384-89

59. Ischemic stroke
• BP elevations can occur in previously hypertensive and in
normotensive pts.
• BP declines to pre stroke values within 3-4 days after an ischemic
stroke.
• Severe HTN Rx controversial issue.
Lesions in
cerebral area
Impaired
neurogenic
control of CVS
HIGH BP
Arch Intern Medicine 2003;163:211-216

60. Shift to right in case of chronic HTN

61. AHA recommendation
• Threshold for treatment BP > 220/120 mmHg
• Target BP should be a 10-15% lowering of BP.
• Raised ICP – MAP<130 (1st 24hrs)
• No raised ICP – MAP<110
• IV Labetalol or Nicardipine .
• IV tPA (if to be given) BP <185/110mm Hg.
Stroke 2003;34:1056-83

62. IC bleed
• To prevent rebleeding and reduce edema formation.
• BP >180/105 mmHg ,may benefit from gradual 20-25%
reduction in BP.
Nimodipine, a dihydropyridine calcium blocker,is effective
(antagonist effects on cerebro vasospasm).
AHAguidelines;Critical care Med 2006;34:1975-1980

63. Hypertensive Encephalopathy
• Potential lethal complication of severe or abrupt BP elevation.
• Previously HTN/normotensive pts.
• Acute glomerular nephropathy, Eclampsia, TTP, Pheochormocytoma,
Erythropoietin administration, immunosupressive drugs
HIGH
BLOOD
PRESSURE
Excessive
increase
in
cerebral
blood flow
HYPERFILTRATION
LOCALISED
OR
WIDESPREAD
EDEMA
Hinchey J et al,NEJM 1996;334:494-500

64. • Cerebral ischemia resulting from arteriolar spasm*.
• Severe headache,vomitings,visual disturbances,confusion, focal or
generalized seizures.
• Fundoscopic examination(key role)
• Mean BP should be reduced by 20% within first hour.
• IV sodium nitroprusside is DOC (rapid onset of action)
ESC/ESH 2003
• IV labetalol,nicardipine,hydralazine .
Circulation,2004;110:2241-5

65. Eclampsia
• Hypertension complicates 12% pregnancies, 18% maternal deaths.
• Volume expansion,MgSo4 for seizure prophylaxis.
• MgSo4 4-6 g in 100ml 5%D over 15- 20 min - 1-2g/h infusion
(hourly DTR,urine output).
• Antihypertensive therapy (to prevent complications in mother).
• SBP :155-160 mmHg,DBP>105mm Hg.(initiation of Rx)
• ICH is a devastating complication.
• Methyl dopa,Hydralazine DOC,
• Others being IV labetalol,nicardipine.
• Avoid sublingual or oral nifedipine.
• Nitroprusside,ACEI – C/I
Am J Obst 2000:183:S1-S22

66. HTN emergencies due to catecholamine excess
Abrupt increase in alpha adrenergic tone.
• IV labetalol
• Pheochromocytoma crisis (IV alpha blocker phentolamine)
followed by B blocker(for tachycardia or VPCs).
Withdrawal of centrally acting anti HTN drugs (clonidine)
Pheochromocytoma
Cocaine intoxication
Abuse of sympathomimetics
Post operative Hypertension

72. ORAL DRUGS FOR HTN URGENCIES
Drug Initial dose Onset duration Adverse effects

73. Acute and transient BP elevations
• Anxiety
• Panic attacks
• Pain
Rx - Administration of anxiolytic or analgesic drugs.
• Refractory nose bleeding
– IV drugs to be used sometimes

74. TAKE HOME MESSAGE
• Most common cause for HTN crises is
UNDIAGNOSED/UNTREATED/
INADEQUATELY TREATED HYPERTENSION
• Differentiation of emergency from urgency is absence of target organ
damage in the later.
• Clevidipine is the new drug approved for hypertensive emergencies.
• IV Nicardipine , IV Labetalol are preferred for most of emergency
situations.
• SL/oral nifedipine not to be used..

75. THANK YOU