A brief discussion on Hypertensive Emergencies including - Definition, Classification, Etiology, Pathophysiology, Assessment & Evaluation, Clinical characteristics, Treatment goals, Management

1. HYPERTENSIVE EMERGENCIES
DR BODHISATWA CHOUDHURI
MBBS, MD(MED), MRCEM(UK), MEM(USA), MRCP ACUTE MEDICINE, DIP RHEUMATOLOGY(UK), FCCS, CCEBDM
CONSULTANT, EMERGENCY MEDICINE & CRITICAL CARE, ILS HOSPITAL HOWRAH

2. DEFINITION
 There is a continuous relationship between the level of blood pressure and
the risk of complications.
 Starting at 115/75 mmHg, CVD risk doubles with each increment of 20/10
mmHg throughout the blood pressure range.
 According to API: Hypertension in adults age 18 years and older is
defined as systolic blood pressure (SBP) of 140 mm Hg or greater and/or
diastolic blood pressure (DBP) of 90 mm Hg or greater or any level of
blood pressure in patients taking antihypertensive medication.

3. CLASSIFICATION

4. HYPERTENSIVE CRISIS
 Hypertensive crises are classified as hypertensive emergencies or urgencies.
 HYPERTENSIVE EMERGENCIES are characterized by severe elevations in BP (>180/120 mm
Hg) complicated by evidence of impending or progressive target organ dysfunction. They
require immediate BP reduction (not necessarily to normal) to prevent or limit target organ
damage. Examples include hypertensive encephalopathy, intracerebral hemorrhage, acute
myocardial infarction, acute left ventricular failure with pulmonary edema, unstable angina
pectoris, aortic dissection, or eclampsia.
 HYPERTENSIVE URGENCIES are those situations associated with severe elevations in BP
without progressive target organ dysfunction. Examples include upper levels of stage II
hypertension associated with severe headache, shortness of breath, epistaxis, or severe
anxiety. The majority of these patients present as noncompliant or inadequately treated
hypertensives, often with little or no evidence of target organ damage.

8. HYPERTENSIVE EMERGENCIES
 Although hypertensive emergencies can lead to significant morbidity and
potentially fatal target-organ damage, only 1%–3% of patients with
hypertension will have a hypertensive emergency during their lifetime
(Deshmukh 2011).
 Despite the low incidence, hospitalizations because of hypertensive
emergencies have increased since 2000 (Deshmukh 2011), possibly because of
the heightened awareness, recognition and subsequent diagnosis of
hypertensive emergency.
 However, even though more hospitalizations are secondary to hypertensive
emergencies, mortality remains low, with an in-hospital mortality of around
2.5% and 1- and 10-year survival greater than 90% and 70%, respectively
(Deshmukh 2011; Lane 2009; Webster 1993).

12. ETIOLOGY
 Essential hypertension : Inadequate blood
pressure control and noncompliance are most
common precipitants
 Renovascular – Renal artery stenosis
 Eclampsia/pre-eclampsia
 Acute glomerulonephritis
 Pheochromocytoma
 Anti-hypertensive withdrawal syndromes
(clonidine, beta blockers)
 Head injuries and CNS trauma
 Renin-secreting tumors
 Toxins (cocaine, amphetamines, phencyclidine)
 Drug-induced hypertension
 Drug-drug/drug-food interactions (e.g., MAO
inhibitors and TCA, antihistamines or tyramine)
 Vasculitis, Connective tissue disrorders
 Idiopathic hypertension
 Post-op hypertension
 Coarctation of aorta
 Severe pain

13. PATHOPHYSIOLOGY
 Autoregulatory changes in vascular resistance through the
autocrine/paracrine system occur in response to the production of
endogenous vasoconstrictors (e.g., catecholamines) or endogenous
vasodilators (e.g., nitric oxide).
 During a hypertensive emergency, acute elevation in blood pressure
overwhelms the autoregulation of the endothelial control of vascular tone,
leading to mechanical vascular wall stress with subsequent endothelial
damage and vascular permeability.
 This permeability leads to the leakage of plasma into the vascular wall,
resulting in activation of platelets, initiation of the coagulation cascade,
deposition of fibrin, and recruitment of inflammatory mediators.
 This inappropriate vasoconstriction and microvascular thrombosis leads to
hypoperfusion and end-organ ischemia with subsequent target-organ

18. TREATMENT GOALS
 Hypertensive urgency often requires initiating,
reinitiating, modifying, or titrating oral therapy and
usually does not require ICU or hospital admission. The
treatment target for hypertensive urgency is a gradual BP
reduction over 24–48 hours.
 Overaggressive correction needs to be avoided.
 Particularly important in patients with chronic
hypertension because their end organs adapt to
chronically elevated BP, setting a new physiologic “norm”
of autoregulation. This new “norm” leads to optimal
organ perfusion at a higher baseline BP.
 If this autoregulatory shift is unrecognized during a
hyper-tensive emergency, patients may be at risk of harm
from overcorrection or over-normalization of blood
pressure.

20. BP TREATMENT GOALS FOR HYPERTENSIVE EMERGENCY
 Exceptions: Aortic dissection, acute stroke (ischemic and hemorrhagic) and pregnancy-
associated severe hypertension (preeclampsia/eclampsia and hypertensive emergency in the
pregnant patient).
 Each of these populations has unique treatment targets, considerations for subpopulations
within them or additional considerations during treatment.

24. PHARMACOLOGICAL THERAPY
 Vasodilators: Sodium nitroprusside, Nitroglycerin, Hydralazine
 Beta blockers: Esmolol, Labetalol, Metoprolol
 Calcium channel blockers: Nicardipine, Nifedipine
 ACEI: Enalaprilat, Captopril
 α-Antagonist: Phentolamine
 D1 receptor antagonist: Fenoldopam
 α2-Agonist: Clonidine

25. SODIUM NITROPRUSSIDE
 Arteriolar and venous dilation
 Predictably effective in lowering BP, Rapid onset & offset
 Usual dosage 0.25-10 mcg/kg/min, Titrate by 0.1-0.2 mcg/kg/min q5min
 Potential cyanide (in liver failure) or thiocyanate (in renal failure) toxicity with
prolonged infusion(>72 hrs)/high doses (>3 mcg/kg/min)
 May result in coronary steal
 Increases ICP
 Used in most indications (excluding ICP elevations and coronary
infarction/ischemia)
 Require continuous IV infusion, constant patient monitoring

26. NITROGLYCERIN
 Predominant venodilation at low infusion rates; significant arteriolar dilation
at higher dosages
 Effective in management of hypertension complicated by CHF or cardiac
ischemia or pulmonary edema
 Usual dosage 5-200 mg/min, Titrate by 5–25 mcg/min q5–10min
 Tachyphylaxis occurs rapidly, requiring frequent dose titrations
 Adverse effects: Flushing, headache, erythema, often dose limiting
 Require continuous IV infusion, constant patient monitoring

27. HYDRALAZINE
 Unpredictable hypotensive effect, can result in prolonged hypotension, given
longer half-life
 Delayed onset compared to other parenteral agents
 Reflex increase in HR and CO
 Largely outmoded for acute therapy except in pre-eclampsia/eclampsia,
where it is “traditional” therapy
 Adverse effects on cerebral autoregulation
 Headaches, lupus like syndrome (more likely with long-term use)

28. NIFEDIPINE
 Peripheral and coronary arteriolar vasodilation
 Rapid onset of antihypertensive effect: 5-20 minute onset, peak effect in 30-
60 min, duration 4-5 hr
 Potential hypotension and/or reflex cardiac stimulation
 Several case reports of cerebral or myocardial ischemia after rapid decrease in
BP
 Treatment of choice in Prinzmetal angina
 Also used in severe hypertension in pregnancy and in premature labour

29. LABETALOL
 Combined α+β adrenergic blockade
 Rapidly effective when given IV; Onset <5 min, peak 5-10 min, duration 2-6 hr
(sometimes longer)
 Usual dosage 20 mg IV, then 40-80 mg IV q 10-15 min until achieving desired
effect, or total of 300 mg
 Indicated in acute ischemic or hemorrhagic stroke, aortic dissection, coronary
ischemia/infarction, pregnancy
 Contraindicated in acute decompensated heart failure, asthma, heart block
 Prolonged hypotension may occur with overtreatment

30. CLONIDINE
 Central α-agonist; ↑sympathetic tone to heart and peripheral
vessels
 Usual regimen: 0.1-0.2 mg po, then 0.1 mg po q hr until desired BP
achieved
 Onset 30-60 min, peak 2-4 hr, duration 6-12 hr
 Sedation may interfere with neurologic assessment of patient
 Rarely a first-line agent

31. ACE INHIBITORS
 IV Enalaprilat, oral Captopril potentially useful for acute BP reduction
 Enalaprilat dose: IV bolus: 1.25 mg q6hr, Titrate no more than q12–24hr; max
dose: 5 mg q6hr
 Cautious dosing; prolonged duration of action
 Little clinical experience in patients with hypertensive emergencies
 Difficult to titrate (sometimes ineffective, sometimes excessive BP↓)
 Positive effects on cerebral autoregulation
 Indicated in Acute left ventricular failure
 Contraindicated in pregnancy

32. FENOLDOPAM
 Peripheral Dopamine-1 receptor agonist
 Direct vasodilation, Renal artery vasodilation
 Can be used in most indications
 IV 0.03–1.6 mcg/kg/min, Titrate by 0.05–1 mcg/kg/min q15min
 Natriuresis
 Caution with increases in ICP or intraocular pressure
 Risk of reflex tachycardia
 Can cause hypokalemia, flushing; can worsen glaucoma

33. PHENTOLAMINE
 Used in catecholamine-induced hypertensive emergency
(Pheochromocytoma)
 If used for cocaine-induced HTN crisis – Use in conjunction with
BZDs
 IV bolus: 1–5 mg PRN; max 15 mg
 Onset of action – in seconds

40. CONCLUSION
 Hypertensive emergencies are commonly encountered in emergency departments wordwide.
 The most important factor that limits morbidity & mortality from this disorders is prompt and
carefully considered therapy.
 They are among the most misunderstood & mismanaged medical problems today.
 Clinicians dealing with hypertensive emergencies should be familiar with pathophysiology the
disease.
 The treating clinician needs to rapidly assess target-organ damage to differentiate
hypertensive emergency from hypertensive urgency.
 In addition, the clinician must consider whether a patient qualifies as an exception to the
general treatment principles of hypertensive emergency.
 Each patient will need continuous monitoring to assess for achievement of target goal(s) and
avoidance of overaggressive, unintentional correction.