Transcript Hypertensive_Crises_..

Management of Hypertensive
Emergencies
Dr. Abdulkareem Alsuwiada,
FRCPC, MSc
Learning Objectives
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To identify and triage severe
hypertensive states accurately
To effectively manage hypertensive
crises with drug therapy
Hypertensive Urgency
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“Severe elevation of blood pressure”
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Generally DBP >115-130
No progressive end organ damage
Hypertensive Emergency
 Hypertensive Emergency:
Severe elevation in blood pressure in the
presence of acute or ongoing end-organ
damage.
“Recognition of hypertensive
emergency depends on the clinical state
of the patient, not on the absolute level
of blood pressure”
Target Organs
Hypertensive Emergency Key Points
 Cardiac Emergencies
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Acute CHF
Acute coronary insufficiency
Aortic dissection
Hypertensive Emergency Key Points
 CNS Emergencies
 Hypertensive encephalopathy
 Intracerebral or
subarachnoidal hemorrhage
 Thrombotic brain infarction
with severe HTN
Hypertensive Emergency Key Points
 Renal Emergencies
 Rapidly progressive renal
failure
Fundoscopy/ Neuro
• Hemorrhages
• Exudates
• Papillodema
Urgency vs. Emergency
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Distinguishing between hypertensive
emergency and urgency is a crucial step
in appropriate management
Urgency vs. Emergency
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Urgency
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No need to acutely lower blood pressure
May be harmful to rapidly lower blood
pressure
Death not imminent
Emergency
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Immediate control of BP essential
Irreversible end organ damage or death
within hours
Approach to Patients
Approach to patients
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Recheck blood pressure!
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Appropriate size cuff
Cuff not over clothing
Check in all limbs
History
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Prior crises
Renal disease
Medications
 Compliance
 Recreational drugs
Approach to patients
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Physical Exam
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Signs of end organ damage?
Neuro
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Hypertensive encephalopathy
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Severe Headache
Nausea/Vomiting
Papilledema
Visual Changes
Seizures
Focal Neurological Deficits
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Ischemic vs hemorrhagic CVA
Fundoscopy/ Neuro
Cardiac
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Cardiac ischemia
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Chest pain
EKG for ischemic changes
Acute left ventricular failure
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Pulmonary edema
Hypoxia
EKG for left ventricular strain pattern
CXR
Renal
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Electrolytes
BUN/Cr
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Chronic failure/insufficiency vs acute failure
Cause vs effect
UA with micro
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Protein
Blood
Casts
Major Causes of Hypertensive
Emergencies and Urgencies
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Untreated essential hypertension
Withdrawal / non-adherence to
antihypertensive drug therapy
Development of secondary hypertension
Major Causes of Hypertensive
Emergencies and Urgencies
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Renal Disease
Renal artery stenosis
Pregnancy
Endorine
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Pheochromocytoma
Primary aldosteronism
Glucocorticoid excess
Renin-secreting tumors
Pathogenesis for Hypertension
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Arterial and arteriolar vasoconstriction
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Prevents the increase in pressure from being
transmitted to the smaller, more distal vessels
With increasingly severe hypertension
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Autoregulation failure
Vascular endothelial injury
Plasma constituents (including fibrinoid material) to enter
the vascular wall
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narrowing or obliterating the vascular lumen.
Tissue edema and activation of endothelial vasoactive
system
Goals of Treatment
Goals of Treatment
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Prevent end organ damage
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NOT normalize BP
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Exceptions??
HTN Urgencies: Goals of Therapy
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No proven benefit of rapid BP reduction in
asymptomatic patients
Goal BP <160/110 mm Hg over several
hours, oral therapy
Initial BP fall less than 25% in first six hours
can be managed using oral antihypertensive
agents in an outpatient or same-day
observational setting
Ensure follow-up: Long-term management
HTN Urgencies: Therapy
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Captopril , 25-mg oral dose initially, followed by
incremental doses of 50 to 100 mg 90 to 120 min
later
The calcium channel blocker nicardipine, 30 mg, q 8
hours until the target BP
Labetolol, the starting dose is 200 mg orally, which
can be repeated every 3 to 4 hours
Clonidine is a central sympatholytic a 0.1 to 0.2 mg
loading dose followed by 0.05 to 0.1 mg every hour
until target BP is achieved (Max 0.7 mg).
Hypertensive Emergency
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ICU with close monitoring
IV and Short acting medications
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Avoid sublingual or IM
Arterial line
Goals of Treatment
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Within 1-2 hrs
Lower MAP 20-25%
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CONTROLLED
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IV titratable meds
Complications for rapid BP
Reduction in Severe Hypertension
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Widening Neurologic Deficits
Retinal ischemia and Blindness
Acute MI
Deteriorating renal function
Goals of Treatment
WHY ?
Cerebral Autoregulation
Strandgaard, et al. BMJ: 1973
Cerebral blood flow
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60
mmHg
120
mmHg
MAP
Adapted from: Chest, 2000; 118:214-227
160
mmHg
Pharmacotherapy
Antihypertensive Drugs for
Hypertensive Crisis
Given by continuous infusion
 Sodium nitroprusside
 Nitroglycerin
 Nicardipine
 Labetalol
 Esmolol
 Fenoldapam
Specific Treatment
Hypertensive Encephalopathy
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Nitroprusside
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Fenoldopam
Nicardipine
Labetolol
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Symptoms of encephalopathy should
improve with treatment
CVA
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Nicardipine
Labetolol
Fenoldopam
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Decrease DBP no more than 20% in 24hrs
Cardiac Ischemia
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Nitroglycerine
Nitroprusside
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Fenoldopam
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Nifedipine
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Reflex tachy
Increases myocardial O2 demand
May aggravate ischemia
Acute LVF
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Nitroprusside
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Afterload reduction
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Nitroglycerine
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If ischemia is suspected
Furosemide
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Fenoldopam
Loop diuretic
Opioids
Acute Aortic Dissection
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Nitroprusside
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Nicardipine, Fenoldopam
Afterload reduction
 Increases ventricular contraction velocity
 Requires B blockade
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Esmolol, metoprolol
Labetolol
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Goal: SBP ~100 mmHg
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Monitor patient closely
Acute Aortic Dissection
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β-block
FIRST!
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Esmolol
Metoprolol
Sympathetic Crisis
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Nicardipine
Nitroprusside
Phentolamine
Acute Renal Failure
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Nicardipine
Nitroprusside
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“Use with caution”
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toxic metabolites...
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Thiocyanate excreted via kidneys
Fenoldopam
Labetolol
Eclampsia
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Hydralazine
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Used historically
Arterial vasodilator
Maintains placental blood flow
Nicardipine
Labetolol
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Magnesium
The Discharged Patient
The discharged patient
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JNC-VII Recommendations
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Stage 2
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Combination tx
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Thiazide + ACEI, ARB, BB, CCB
“Compelling Indications”...
The discharged patient
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JNC-VII Recommendations
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“Compelling Indications”
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URGENCY:
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ALL PATIENTS WITH HTN URGENCY BEING
DISCHARGED HOME SHOULD BE PLACED ON
COMBINATION THERAPY AND HAVE RAPID FOLLOW
UP.
THIAZIDE
ACEI / ARB / BB / CCB
The discharged patient
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Follow up...
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Stage I:
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Stage II:
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140-159 / or 90-99
>160 / or ≥100
Follow-up
2 Months
1 Months
“Higher”:
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≥180 / ≥110
< 1 week
Goals of therapy in JNC7 &
Euro Guidelines
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Maximum reduction in long-term total risk
of cardiovascular morbidity and mortality:
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Smoking
Life style modification
Lipid
Diabetes
Blood pressure
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< 140/90
If DM or renal disease
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<130/80
The following 5 patients in ER
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Patient A is a 65-year-old man with nausea, vomiting,
and confusion.
Patient B is a 73-year-old woman with sudden
shortness of breath, pink sputum, and heavy chest
pain.
Patient C is a 56-year-old man with sharp, tearing
chest and back pain.
Patient D is a 64-year-old woman with a 6-hour
history of right-sided weakness.
Patient E is a 51-year-old woman with a mild
headache, concerned about her history of
hypertension.
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all 5 patients arrive with identical vital
signs: BP of 209/105 mm Hg
Which of the 5 patients require
emergent hypertension treatment?
Patient A is a 65-year-old man with
nausea, vomiting, and confusion.
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Hypertensive encephalopathy
Pure vasodilators like nitroprusside have
risks of intracranial shunting, which
could increase intracranial pressure.
Drug of choice: Intravenous labetalol,
bolus or infusion.
Target: Reduce MAP by 20% to 25%
over 2 to 8 hours.
Patient B: 73-year-old woman with sudden
shortness of breath, pink sputum, and heavy
chest pain.
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Physical examination reveals bilateral crackles in her
lungs, an elevated JVP, and no heart murmurs.
Acute pulmonary edema often presents with extreme
hypertension, which overloads cardiac reserve.
Drug of choice: Nitroglycerin infusion; IV enalaprilat
or sublingual captopril.
Target: Reduce MAP by 20% to 25% and
symptomatic improvement.
Patient C: 56-year-old man with sharp,
tearing chest and back pain.
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Physical examination reveals differential BPs
and evidence of a new aortic insufficiency
murmur.
Aortic dissection is largely a disease of
hypertension.
Drug of choice: Nitroprusside or esmolol
infusion;labetalol boluses or infusion.
Target: Rapidly reduce systolic BP to 110 mm
Hg if there is no evidence of hypoperfusion.
Patient D: 64-year-old woman with a 6hour history of right-sided weakness.
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Marked right-sided hemiplegia is noted.
a higher MAP is essential to maintaining
adequate cerebral blood flow and not
extending the affected stroke territory.
BP should not be lowered in the acute period
except in extreme situations
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BP > 220/120 mm Hg in embolic CVA
> 180/100 in hemorrhagic CVA
Patient D: 64-year-old woman with a 6hour history of right-sided weakness.
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Drug of choice: Labetalol; nicardipine;
hydralazine.
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Target:
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If no thrombolytic is given, reduce BP only if it is
greater than 220/120 mm Hg (embolic) or greater
than 180/100 mm Hg (hemorrhagic)
If a thrombolytic is given, reduce BP to 180/100
mm Hg.
Patient E: 51-year-old woman with a mild
headache, concerned about her history of
hypertension.
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These patients require gradual BP
reduction over time on an outpatient
basis
Summary
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Accurate history and timeline of onset
Evaluate Target organ injury
Set the time frame for intervention
Appropriate “pace” of therapy
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Initial reduction
Stabilization
Follow-up care/ Diagnostic studies
Questions...
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