Hypertensive emergencies management

1. Management of hypertensive
Emergencies and Urgencies
DR VISHNU
RS

2. Blood Pressure Measurement
 Stephen Hales 1733
 Hollow glass tube in
neck artery of horse
 Blood rose 9 feet in
glass tube
Medicine, an Illustrated History 1987

3. Malignant hypertension
 The term malignant hypertension first appeared in 1928 to describe
patients with very high blood pressure (BP) values.
 “Malignant” was used to compare the prognosis of these patients with that
of most cancers because they had such rapid target organ deterioration,
such as retinal hemorrhages or exudates and papilledema, usually
associated with encephalopathy, acute renal failure, and microangiopathic
hemolytic anemia.

5.  Dramatic advancements of both in-hospital and outpatient treatment of
hypertensive emergencies have led to an improved prognosis.
 Decrease in 1-year mortality from 80% in 1928 to 50% in 1955 and 10% in
1989.
 Terms such as malignant and accelerated hypertension have been replaced
by the terms hypertensive emergency and hypertensive urgency.

6. Hypertensive emergency
 A hypertensive emergency is defined as marked elevation in BP
complicated by evidence of acute life-threatening target organ damage,
such as coronary ischemia, dissecting aortic aneurysm, pulmonary edema,
hypertensive encephalopathy, cerebral hemorrhage, and eclampsia.
 In this clinical condition, BP should be reduced by at least 20 to 40 mm Hg
within 10 to 30 minutes with parenteral drug therapy in an intensive care
unit.

7. Hypertensive urgency
 Hypertensive urgency is a clinical setting of significant BP elevation,
generally above 180/110 mm Hg, without life-threatening target organ
dysfunction (i.e., papilledema, evidence of early heart failure, acute renal
failure), although some evidence of target organ damage is usually present
(hemorrhages and exudates in fundi, headaches).
The approach to hypertensive urgency is a gradual BP reduction within hours,
usually with oral medications

8.  In a study with more than 14,000 emergency department visits during 12
months showed that hypertensive urgencies accounted for 76% and
emergencies for 24% of hypertension-related visits.12
 The most common presentations of hypertensive emergencies were
associated with cerebral infarction (24.5%), acute pulmonary edema (22%),
hypertensive encephalopathy (16%), and acute heart failure (14%),
myocardial infarction (12%), cerebral hemorrhage (5%), eclampsia (5%),
and aortic dissection (2%).

9. PATHOPHYSIOLOGY
 Hypertensive Emergency
 Failure of normal autoregulatory function
 Leads to a sharp 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

10. MECHANISM OF HYPERTENSIVE CRISIS
Sudden severe increase in
blood pressure
Endothelial
injury/dysfunction
Pressure
natriuresis
Increase vasoconstrictors
and decrease in
vasoldilators
Activation of
procoagulation cascade
and inhibition of
fibronolytic mechanism
Release of
inflammatory
markers and reactive
oxygen species
Volume depletion and
positive feedback to
reninangiotensin system
Fibroinoid necrosis and
myo-proliferation
Further increase in blood
pressure

12. General Principles for Management
 Therapy with parenteral antihypertensive agents should be initiated in
the emergency department.
 patients with a hypertensive emergency should be admitted to an
intensive care unit for continuous BP monitoring, clinical surveillance, and
continued parenteral administration of an appropriate agent
 Specific BP levels do not determine the severity and the emergency of the
situation .
 Autoregulatory structural and functional changes may vary between
individuals, such that some individuals may develop target organ damage
at lower BP.

13.  Understanding of autoregulation is crucial for therapeutic decisions;
sudden lowering of BP into a “normal” range could lead to inadequate
tissue perfusion.
 There is evidence that abrupt lowering of BP is harmful.
 The use of sublingual nifedipine may precipitate stroke or shunt blood
away from the penumbra of the brain, resulting in cognitive dysfunction.
 The goal of antihypertensive therapy is not to rapidly normalize BP .
 To prevent target organ damage by gradually reducing BP while
minimizing the risk of hypoperfusion.

14.  The mean BP should be reduced by no more than 20% to 25% within the
first few minutes to an hour.
 A diastolic BP target between 100 and 110 mm Hg or a reduction of 25%
compared with the initial baseline, whichever is higher, is appropriate to be
achieved within the next 2 to 6 hours.
 Reduction of BP diastolic pressure to less than 90 mm Hg or by 35% or
more of the initial mean BP has been associated with major organ
dysfunction, coma, and death.

15.  If the level of BP reduction is well tolerated and the patient clinically stable,
further gradual reductions toward levels below 140/90 mm Hg should be
implemented within the next 24 to 48 hours.
 Typically, a long-acting oral calcium channel blocker (CCB) is given along
with either an α- and β-blocker like carvedilol or nebivolol or RAS blocker,
and the intravenous medication is gradually reduced during 1 to 2 hours
 An important consideration before initiation of intravenous therapy is
assessment of the patient’s volume status.
 Because of pressure natriuresis, patients with hypertensive emergencies
may be volume depleted, and restoration of intravascular volume may help
restore organ perfusion and prevent a precipitous fall in BP.

16. Major exceptions to these treatment recommendations
 patients with acute stroke, in whom there is no clear evidence to support
immediate BP lowering and a more cautious approach is needed.
 patients with aortic dissection, who should have their systolic BP lowered
to below 100 mm Hg if tolerated
 patients in whom BP should be lowered to enable the use of thrombolytic
agents

17. IDEAL IV ANTI- HYPERTENSIVE
 IDEAL IV ANTI- HYPERTENSIVE” Lower the BP without compromising
blood flow to critical organs
 Vasodilators generally considered first because they preserve organ
blood flow in the face of reduced perfusion and also tend to increase CO.

18. Profile of an ideal IV antihypertensive
 Preserves GFR and renal blood flow
 Few or no drug reactions
 Little or no potential for exacerbation of co-morbid conditions
 Rapid onset and offset of action
 Minimal hypotension
 Minimal need for continuous BP monitoring and frequent dose titration
 No acute tolerance
 Ease of use and convenience
 Safe and no toxic metabolites
 Multiple formulations for short and long term use
 Minimal symphathetic activation

19. Sodium Nitroprusside
 MoA: Direct smooth muscle dilator (art + ven) Nitric oxide compound
Potent preload and afterload reducer
 Causes cerebral vasodilation
 Ultra short acting
 Immediate onset –
 DoA : 10min
 Dose: 0.1-0.5mcg/kg/min IV infusion titrate to desired effect rates
 >10mcg/kg/min – cyanide toxicity

20.  Adverse affects/Precautions: Cyanide and thiocyanate toxicity (pts with
liver/renal dysfunction)
 Can cause precipitous drop in BP (hypotensive effects unpredictable)
 Ideally Art.line with continuous BP monitoring
 Causes significant reflex tachycardia ( incr Oxygen demand) (angina/aortic
dissection/cerebral oedema)
 Nausea and vomiting
 Increased ICP
 Drug of choice: Perioperative HPT Cocaine toxicity Aortic
dissection(combination) Neurologic syndromes

21. Nitroglycerin
 MoA: Potent vasodilator (nitric oxide compound)
 Primary affects the venous system, decrease preload Decreases coronary
vasospasm
 Dose: cont infusion start 5mcg/min, incr by 5mcg/min every 3-5min to
20mcg/min
 If NO Response increase by 10mcg/min every 3-5min,up 200mcg/min
 Onset : 2-5min/
 DoA : 5-10min

22.  Adverse effects/precautions: Constant monitoring is essential Tolerance
from uninterrupted use (12hr withdrawal)
 Headache, tachycardia, flushing
 Contra ind: Concurrent use with PDE-5 inhibitors - causes significant
hypotension
 Head trauma/cerebral haemorrhage Severe anaemia
 Drug of choice: Acute HF ACS

23. Nicardipine
 Ca channel blocker – selective arterial vasodilator
 Onset: 1-5min
 DoA: 15-30min
 Dose: start 5mg/hr IV infusion, titrate every 15min to max 15mg/hr.
 Advantages: Cause cerebral and coronary vasodilatation
 Precautions: can worsen/cause HF liver failure can exacerbate renal insuff.
 Ideal for CNS emergencies

24. Fenoldopam
 MoA: Peripheral dopamine agonist (high vs low doses) causes selective
neuro vasodilatation mesenteric vasodilatation increases renal blood flow
and sodium excretion
 Onset – <5min, but more gentle, lasts for 30min (titratable, predictable
and stable) Standard BP monitoring is sufficient, no toxic metabolites
 Dosing: Start at 0.1-0.3mcg/kg/min IV infusion May be increased in
increments of 0.05- 0.1mcg/kg/min every 15min, until target BP reached
 Precautions: Pts with glaucoma or intraocular hypertension Dose related
tachycardia can occur – angina Close BP monitoring Close K monitoring
Caution with raised ICP
 Drug of choice Renal insuffiency Strokes ( combination with nicardipine)

25. Hydralazine
 MoA: Decreases systemic resistance by direct vasodilation of arterioles
 Dose: 5-20mg IV bolus or 10-40mg IV repeat every 4-6hrs
 Adverse effects/Precautions tachycardia, flushing, headache sodium and
water retention increased ICP adjust dose in severe renal dysfunction
response may be delayed and unpredictable
 drug of choice in pregnancy(Eclampsia), but B-blocker/Labetalol

26. Enalapril
 The active component of Enalapril (hydrolyzed in liver and kidney) MoA:
ACE inhibitor
 Dose: 0.625-2.5mg every 6hr IV Not titratable Onset – within 30 min +
long half life
 Adverse effects/Precautions Contra-indicated – volume depletion, renal
vascular disease Prolonged ½ life

27. Labetolol
 MoA: selective alpha blocker – will reduce vascular smooth m. resistance
non-selective Beta blocker – decrease cardiac inotropic and myocardial
O2 consumption, will prevent reflex tachycardia
 Dose: Bolus: effect in 5-10min,max effect at 20min. (DoA: 2-6hrs) 1st dose
20mg then every 10-20min 2nd dose 40mg, 3rd dose 80mg. Cont.
infusion: 0.5 – 2mg/min – titrate to response,max 300mg total dose
Difficult to titrate due to very wide dose range
 Advantages: smooth onset Transition to oral Rx easy (dose equivalent)
Improve cerebral blood flow – stroke pt No need for ICU/Arterial line

28.  Adverse effects/precautions Relative CI – Heart failure, heart block, Asthma
(bronchoconstriction) Vomiting, scalp tingling Impaired hepatic function
Elderly patients
 Contraindicated in HPT secondary to Cocaine use/Phaeochromocytoma (B-
blocker effect outway the alpha effect, thus unapposed alpha constriction)
 Drug of choice: Aortic dissection Hypertensive emergencies

29. Esmolol
 MoA: highly selective beta blocker
 Dose: (titratable) bolus: 250-500mcg/kg IV over 1-3min infusion: 50-
100mcg/kg/min may repeat bolus after 5min or increase infusion rate to
300mcg/kg/min Onset 1-2min / short acting
 Adverse effect/Precautions Hypotension common nausea Asthma 1st
degree AV block heart failure
 Contraindications Sinus bradycardia Heart block Cardiogenic shock
Bronchial asthma Uncompensated CF Pregnancy
 Drug of choice: Aortic dissection ( with nitrate)

30. Phentolamine
 MoA: alpha adrenergic receptor blocker
 Dose: load 5-20mg IV every 5min or infusion 0.2-0.5mg/min Onset 1-
2min
 Adverse effect/precautions tachycardia flushing/headache MI
cerebrovascular spasm
 Contra-indications renal impairment Concurrent use with PDE-5 inhibito
coronary or cerebral arterioscleros
 Drug of choice Cocaine associated HPT crisis Pheochromocytoma HPT
crisis

33. Special situations
 Neurological emergencies Acute ICH/SAH Treatment based on
clinical/radiographic evidence of raised ICP Raised ICP – MAP<130 (1st
24hrs) No raised ICP – MAP<110
 Drug of choice: Sodium Nitroprusside Labetalol Nicardipine

34.  Cardiovascular emergencies ACS treat if SBP>160 and/or DBP>100
Reduce MAP by 20 -30% of baseline nitrates should be given till
subside or until DBP<100
 Drug of choice: Nitroglycerine Labetalol Nicardipine

35.  Acute HF (pulmonary edema) treat with vasodilator (additional to
diuretics) Sodium Nitroprusside in conjunction with morphine, oxygen
loop diuretic Enalaprilat also an option
 CVS emergencies Aortic dissection anti-hypertensive Rx is aimed at
reducing the shear stress on aortic wall (BP and Pulse) immediate
of BP – lifesaving maintain SBP<110, unless signs of end organ
hypoperfusion
 preferred Rx is combination of Morphine, B-blocker and vasodilator
Nitroprusside + Labetalol

36.  Cocaine toxicity/pheochromocytoma Hpt and tachycardia rarely require
 specific Rx Alpha adrenergic blockers – preferred B – blockers can be
added, but only after alpha blockade.
 Drug of choice Phentolamine Labetalol Diazepam

37.  Pre-eclampsia/Eclampsia Goal SBP<160 and DBP<110 in pre-and-
intrapartum periods. Platelets < 100 000, BP should be maintained <
150/100
 IV Magnesium to prevent seizures
 Drug of choice: Methyldopa Hydralazine

38. Perioperative hypertension target BP to within 20% of baseline, except if
potential for life threatening arterial bleeding typically related to
catecholamine surge post-op.
Drug of choice : B-blocker Labetalol

39. Treatment of Hypertensive Urgencies
 There is no proven benefit from rapid BP reduction in
asymptomaticpatients without evidence of acute target organ damage;
 BP lowering should occur during a longer time than for a hypertensive
emergency.
 BP reduction to levels within the range below 160/100 mm Hg may be
accomplished within 2 to 4 hours in the emergency department with
orally administered drugs.
 the most important aspect of treatment of a hypertensive urgency is not
achievement of BP goal but ensuring adequate follow-up, within a week
generally.

40.  The choice of drugs for treatment of hypertensive urgency is much
broader than for emergencies
 Almost all antihypertensive drugs lower BP effectively in a reasonable time.
 Captopril, clonidine, labetalol, and other shortacting antihypertensive
drugs have been mostly used for this .
 Short-acting nifedipine once commonly used, is now contraindicated
secondary to a higher incidence of stroke, myocardial infarctions, and
deaths related to precipitous hypotensive episodes

42. .