HTN Crises (Final)
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HYPERTENSIVE CRISESFaris Mahmud
Provisionally Registered Pharmacist
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DEFINITION
Hypertensive crisis is defined as a severe
elevation in blood pressure (BP>180/110 mmHg)
If these conditions are not treated promptly, a
high rate of morbidity and mortality will ensue
These conditions are divided into two general
categories:Hypertensive urgencies
Hypertensive emergencies
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CLASSIFICATION OF
HYPERTENSIVE CRISES
Hypertensive urgencySeverely elevated BP above 180/110 mmHg without
evidence of end organ damage
Not immediately life threatening
Reduction of BP to a safe level may be done more slowly(over 24 to 48 hours)
Hypertensive emergencySeverely elevated BP with evidence of end organ damage
Usually occur when BP>180/110 mmHg, but may occur
at even lower level
Immediately life threatening
BP needs to be lowered to a safe level within minutes to
hours
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Hypertensive Emergency Hypertensive Urgency
Severely elevated blood pressure
(BP >180/110 mmHg)
Severely elevated blood pressure
(BP>180/110 mmHg)
Overt symptoms of end organ
damage present:
• CNS (encephalopathy,
intracranial/subarachnoid
hemorrhage, stroke)
• Heart (left ventricular failure,
pulmonary edema, MI, aortic
dissection)
• Renal failure/insufficiency
• Eyes (ocular hemorrhage,funduscopic changes, blurred
vision, loss of sight)
No evidence of end-organ damage
Requires immediate pressure
reduction
May be treated over several
hours (or even days)
Requires IV therapy May use oral or IV therapy
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COMMON CAUSES OF
HYPERTENSIVE CRISES
Renal parenchymal
diseaseChronic pyelonephritis
Primary
glomerulonephritisTubulointerstitial
nephritis
Systemic disorders with
renal involvementSystemic lupus
erythematosus
Systemic sclerosis
Vasculitides
Renovascular
Atherosclerotic disease
Fibromuscular disease
Polyarteritis nodosa Endocrine
Phaeochromocytoma
Conn syndrome
Cushing syndrome Recreational drugs Coarctation of aorta
Pre-eclampsia/eclampsia
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HYPERTENSIVE URGENCY
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GOAL OF THERAPY
Initial goal is BP reduction of up to 25% over
several hours (generally, 24-48 hours)
If the patient is then stable, BP can be further
reduced toward 160/100 mmHgPrecipitous drop in BP may lead to end-organ
ischemia or infarction
If patients tolerate this reduction well, additional
gradual reductions toward target BP values can
be attempted
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APPROACH OF TREATMENT
If the patient is already on maintenance therapy,
hypertensive urgencies are best managed by
optimizing the therapy, byadding a new antihypertensive
increasing the dose(s) of the present medication(s)
restart the medications (if the therapy was defaulted
or interrupted)
If acute BP reduction is necessary, short-acting
oral antihypertensive may also be administeredfollowed by careful observation for several hours – to
assure a gradual reduction in BP
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ORAL SHORT-ACTING ANTI-HTN FOR
HYPERTENSIVE URGENCIES
Drug Dose Onset ofaction (hr)
Duration (hr) Frequency(prn)
Maximumdaily dose
Captopril 25 mg 0.5 6 1-2 hrs 450 mg
Nifedipine 10-20mg 0.5 3-5 1-2 hrs 120-180 mg
Labetalol 200-400 mg 2.0 6 4 hrs 2400 mg
Adapted from CPG for Management of Hypertension 3rd ed. 2008
Available at HKB:• T. Capropril 25 mg
• T. Nifedipine 10 mg• T. Labetalol 100 mg
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USE OF NIFEDIPINE IN
HYPERTENSIVE URGENCIES
Oralnifedipine was commonly used as a rapid-acting
therapy in the acute management of hypertension
However, its use has been associated with life-
threatening adverse events such as ischemia, MI, and
stroke(Psaty BM et al. 1995; Schwartz M et al. 1990; Fami MJ et al. 1998)
Prompt absorption of rapidly acting CCB is followed by a
precipitous decrease in BP due to peripheral vasodilation
This reduces coronary perfusion, induces a reflex tachycardia,
and increases myocardial oxygen consumption(Grossman E et al. 1996)
Decreased cerebral blood flow has also been reported with
sublingualnifedipine (Gemici K et al. 2003)
Elderly patients with underlying coronary or
cerebrovascular disease, volume depletion, or concurrent
use of other anti-HTN drugs are at increased risk for
significant adverse events(Summers K et al. 2009)
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USE OFCAPTOPRILIN
HYPERTENSIVE URGENCIES
Oralcaptopril is as effective asnifedipine in acutely
reducing BP in both urgent and emergent conditions(Misra A et al. 1993; Kosuoglu B et al. 1991)
Captoprilhas been reported to increase cerebral blood
flow to a greater extent in patients with BP >180/120mmHg compared tonifedipine (Gemici K et al. 2003)
First-dose hypotension is a common limiting factor with
captopril use(Summers K et al. 2009)
Most likely to occur in patients with high renin levels – such
as those who are volume depleted or those receiving diureticsUnder these circumstances, initial doses should not exceed
12.5 mg, with repeat doses an hour or more later if necessary
Caution:captopril can induce severe renal failure in
patients with bilateral renal artery stenosis
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USE OFLABETALOLIN
HYPERTENSIVE URGENCIES
Use oflabetalol have been shown to be effective to
lower BP in acute settings(Gonzalez ER et al. 1991; Zell-KanterM, Leikin JB 1991; Atkin S et al 1992)
Labetalol can cause profound orthostatic
hypotensionPatients should remain in the supine position and
should be checked for orthostasis before ambulation.
Labetalol should be avoided in patients with
asthma, bradycardia, or advanced heart block.
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HYPERTENSIVE
EMERGENCY
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GOAL OF THERAPY
Immediate reduction of BP is requiredto limit progression of target organ damage
to prevent development of new target organ damage
Initial goal is BP reduction of up to 25% within minutes to
hours
If the patient is then stable, BP can be reduced toward
160/100 mm Hg within the next 2 to 6 hoursPrecipitous drop in BP may lead to end-organ ischemia or infarction
If patients tolerate this reduction well, additional gradual
reductions toward goal BP values can be attempted after 24 to
48 hours
The exception to this goal is for patients with an acute
ischemic strokemaintaining an elevated BP is needed for a much longer period of
time
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APPROACH TO TREATMENT
Antihypertensive drug therapy has been shown
to improve mortality and morbidity in patients
presenting with hypertensive emergencies(Vadera R.
2011)
Optimal pharmacotherapy depends on the
specific organ at risk
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Drugs Dose Onset of
action
Duration Remarks
Sodium
nitroprusside
0.25-10 mcg/kg/min seconds 1-5 min Caution in
renal failure
Labetalol IV bolus 50 mg (over atleast 1 min) may
repeat at 5 min
interval
IVI 2 mg/min
(max 200 mg)
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NEUROLOGIC EMERGENCIES
Hypertensive encephalopathy
Hypertensive encephalopathy was used to describe the
encephalopathic findings associated with the malignant
hypertensive phase
Results from hydrostatic exudation of fluid into the braindue loss of blood-brain barrier integrity
The clinical symptoms are usually reversible with prompt
initiation of therapy
The treatment target is to reduce the MAP 25% over 8
hours(Pancioli AM. 2007)
Labetalol,nicardipine, esmolol are the preferred
medications(Pancioli AM. 2007)
Nitroprusside andhydralazine should be avoided(Pancioli AM.2007)
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NEUROLOGIC EMERGENCIES
Acute ischemic stroke
Brain vascular occlusion results in depletion of
oxygen and ATP to the neurons
UNLESS the patient is receiving IV fibrinolysis,ntihypertensive medications should be withheld
unless the BP is >220/120 mmHg(Castillo J et al. 2004)
An elevated BP (up to 220/120 mmHg) is desirable to aid
cerebral perfusion
If the patient is receiving IV fibrinolysis - then, the goalBP is < 185/110 mmHg to minimize risk for hemorrhage(Adams HP et al. 2007; Khaja AM, Grotta JC. 2007)
Preferred medications arelabetalol and
nicardipine (Adams HP et al. 2007)
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NEUROLOGIC EMERGENCIES
Intracerebral hemorrhage / hemorrhagic
stroke
Bleeding that occurs directly into the brain
parenchyma
The usual mechanism is thought to be leakage
from small intracerebral arteries damaged by
chronic hypertension
The treatment is based on evidence of increased
intracranial pressure (ICP)(Anderson CS et al. 2008)
For the 1st 24 hours after onset: With increased ICP, maintain the MAP < 130 mmHg or
SBP < 180 mmHg
Without increased ICP, maintain the MAP < 110 mmHg orSBP < 160 mmH
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NEUROLOGIC EMERGENCIES
Intracerebral hemorrhage / hemorrhagic
stroke
Preferred medications arelabetalol,nicardipine,
and esmolol (Anderson CS et al. 2008)
Avoidnitroprusside andhydralazine (Anderson CS et al.2008)
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NEUROLOGIC EMERGENCIES
Subarachnoid hemorrhage (SAH)
Extravasation of blood into the subarachnoid
space
~80% of non-traumatic SAH are due to aruptured berry aneurysm related to
hemodynamic stress on the arterial walls
Preferred medications arelabetalol,nicardipine,
and esmolol (Anderson CS et al. 2008)
Avoidnitroprusside andhydralazine (Anderson CS et al.2008)
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CARDIOVASCULAR EMERGENCIES
Aortic Dissection
Separation of the layers within the aortic wall
Occurs when blood pushes into the intima-media
space through a tear in the intimal layerCan be rapidly fatal, even with immediate
medical attention
Treatment goal is to maintain maintain the SBP
at < 110 mm Hg, unless signs of end-organhypoperfusion are present(Cheung AT, Hobson RW. 2008)
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CARDIOVASCULAR EMERGENCIES
Aortic Dissection
Preferred treatment includes a combination of
narcotic analgesic (morphine), B-blockers
(labetalol, esmolol), and vasodilators
(nicardipine,nitroprusside)(Cheung AT, Hobson RW. 2008)
Non-DHP CCB (verapamil,diltiazem) are an
alternative to beta blockers
AVOID B-blockers if there is aortic valvular
regurgitation or cardiac tamponade(Cheung AT, HobsonRW. 2008)
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CARDIOVASCULAR EMERGENCIES
Acute Coronary Syndrome & Heart Failure
Treatment is indicated if the BP rises >160/100
mm Hg(Diercks EB, Ohman EM. 2008)
Reduce the BP by 25% of baseline
For ACS, B-blockers andnitrates are the
preferred drugs(Diercks EB, Ohman EM. 2008)
Thrombolytics are contraindicated if the BP is
>185/100 mm Hg
In LVF with APO,nitroprusside ornicardipine,
plusnitrates and a loop diuretic ( frusemide) are
recommended
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PREECLAMPSIA/ECLAMPSIA
Treatment is indicated when BP >160/110 mm
Hg in the antepartum and intrapartum periods(Barton JR. 2008)
If the platelet count is less than 100,000 cells mm3,
target BP < 150/100 mm HgThe preferred medications arehydralazine,
labetalol, andnifedipine (Barton JR. 2008)
Should also be treated with IVmagnesium
sulfate to avoid seizures Avoidnitroprusside, ACE inhibitors, esmolol (BartonJR. 2008)
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CONCLUSION
Hypertensive urgencies and emergencies both are characterized
by the presence of very elevated BP, typically greater than
180/120 mm Hg
Hypertensive urgencies are ideally managed by adjusting
maintenance therapy, by adding a new antihypertensive, and/or
by increasing the dose of a present medicationHypertensive urgency requires BP reductions with oral
antihypertensive agents to stage 1 values over a period of hours
to days
Hypertensive emergencies are situations that require immediate
BP reduction to limit new or progressing target-organ damageHypertensive emergencies require parenteral therapy, at least
initially, with one of the specific agents listed
In most of the hypertensive emergencies, IVlabetalol are
preferred unless contraindicated
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REFERENCES
Abdul Rashid AR et al. Clinical Practice Guideline: Management of Hypertension. 3rd Ed. MOH.
2008
Adams HP Jr, del Zoppo G, Alberts MJ, et al. Guidelines for the early management of adults with
ischemic stroke: A guideline from the American Heart Association. Stroke 2007;38:1655–1711.
Anderson CS, Huang Y, Wang JG, et al. Intensive blood pressure reduction in acute cerebral
haemorrhage trial (INTERACT): a randomised pilot trial. Lancet Neurol. May 2008;7(5):391-9.
Angeli P et al. Comparison of sublingual captopril and nifedipine in immediate treatment of
hypertensive emergencies. Arch Intern Med 1991;151:678. Atkin S et al. Oral labetalol versus oral clonidine in the emergency treatment of severe
hypertension. Am J Med Sci 1992;303:9.
Barton JR. Hypertension in pregnancy. Ann Emerg Med. Mar 2008;51(3 Suppl):S16-7.
Castillo J, Leira R, García MM, Serena J, Blanco M, Dávalos A. Blood pressure decrease during
the acute phase of ischemic stroke is associated with brain injury and poor stroke outcome.
Stroke. Feb 2004;35(2):520-6.
Cheung AT, Hobson RW 2nd. Hypertension in vascular surgery: aortic dissection and carotid
revascularization. Ann Emerg Med. Mar 2008;51(3 Suppl):S28-33.Diercks DB, Ohman EM. Hypertension with acute coronary syndrome and heart failure. Ann
Emerg Med. Mar 2008;51(3 Suppl):S34-6.
Fami MJ et al. Another report of adverse reactions to immediate-release nifedipine.
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Gemici K et al. Evaluation of the effect of sublingually administered nifedipine and captopril via
transcranial Doppler ultrasonography during hypertensive crisis. Blood Press 2003;12:46.
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REFERENCES
Gonzalez ER et al. Dose response evaluation of oral labetalol in patients presenting to the
emergency department with accelerated hypertension. Ann Emerg Med 1991;20:333.
Grossman E et al. Should a moratorium be placed on sublingual nifedipine capsules given for
hypertensive emergencies and pseudoemergencies? JAMA 1996;276:1328.
Khaja AM, Grotta JC. Established treatments for acute ischemic stroke. Lancet 2007;369:319–
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Komsuoglu B et al. Treatment of hypertensive urgencies with oral nifedipine, nicardipine, and
captopril. Angiology 1991;42:447.
Leavitt AD, Zweifler AJ. Nifedipine, hypotension, and myocardial injury. Ann Intern Med
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Misra A et al. Sublingual captopril in hypertensive urgencies. Postgrad Med J 1993;69:498.
O'Mailia JJ et al. Nifedipine-associated myocardial ischemia or infarction in the treatment of
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Pancioli AM. Hypertension management in neurologic emergencies. Ann Emerg Med. Mar
2008;51(3 Suppl):S24-7.
Psaty BM et al. The risk of myocardial infarction associated with antihypertensive drug therapies.JAMA 1995;274:620.
Schwartz M et al. Oral nifedipine in the treatment of hypertensive urgency: cerebrovascular
accident following a single dose. Arch Intern Med 1990;150:686.
Summers K et al. Hypertensive Crises. Applied Therapeutics. 2009.
Vadera R. Does antihypertensive drug therapy decrease morbidity or mortality in patients with a
hypertensive emergency?. Ann Emerg Med. Jan 2011;57(1):64-5.
Zell-Kanter M, Leikin JB. Oral labetalol in hypertensive urgencies. Am J Emerg Med 1991;9:136.
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THANK YOU!!!