management of hypertensive emergencies dr. abdulkareem alsuwiada, frcpc, msc
TRANSCRIPT
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Management of Hypertensive Emergencies
Dr. Abdulkareem Alsuwiada, FRCPC, MSc
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Learning Objectives
To identify and triage severe hypertensive states accurately
To effectively manage hypertensive crises with drug therapy
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Hypertensive Urgency
“Severe elevation of blood pressure” Generally DBP >115-130 No progressive end organ damage
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Hypertensive Emergency
Hypertensive Emergency: Severe elevation in blood pressure in the Severe elevation in blood pressure in the presence of acute or ongoing end-organ presence of acute or ongoing end-organ damage.damage.
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“Recognition of hypertensive emergency depends on the clinical state of the patient, not on the absolute level of blood pressure”
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Target Organs
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Hypertensive Emergency Key Points
Cardiac Emergencies• Acute CHF• Acute coronary insufficiency• Aortic dissection
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Hypertensive Emergency Key Points
CNS Emergencies Hypertensive encephalopathy Intracerebral or
subarachnoidal hemorrhage Thrombotic brain infarction
with severe HTN
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Hypertensive Emergency Key Points
Renal EmergenciesRenal Emergencies Rapidly progressive renal Rapidly progressive renal
failure failure
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Fundoscopy/ Neuro
• Hemorrhages• Exudates• Papillodema
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Urgency vs. Emergency
Distinguishing between hypertensive emergency and urgency is a crucial step in appropriate management
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Urgency vs. Emergency
Urgency No need to acutely lower blood pressure May be harmful to rapidly lower blood
pressure Death not imminent
Emergency Immediate control of BP essentialImmediate control of BP essential Irreversible end organ damage or death Irreversible end organ damage or death
within hourswithin hours
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Approach to PatientsApproach to Patients
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Approach to patients
Recheck blood pressure! Appropriate size cuff Cuff not over clothing Check in all limbs
History Prior crises Renal disease Medications
Compliance Recreational drugs
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Approach to patients
Physical Exam Signs of end organ damage?
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Neuro
Hypertensive encephalopathy Severe Headache Nausea/Vomiting Papilledema Visual Changes Seizures
Focal Neurological Deficits Ischemic vs hemorrhagic CVA
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Fundoscopy/ Neuro
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Cardiac
Cardiac ischemia Chest pain EKG for ischemic changes
Acute left ventricular failure Pulmonary edema Hypoxia EKG for left ventricular strain pattern CXR
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Renal
Electrolytes BUN/Cr
Chronic failure/insufficiency vs acute failure
Cause vs effect UA with micro
Protein Blood Casts
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Major Causes of Hypertensive Emergencies and Urgencies
Untreated essential hypertension Withdrawal / non-adherence to
antihypertensive drug therapy Development of secondary
hypertension
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Major Causes of Hypertensive Emergencies and Urgencies
Renal Disease Renal artery stenosis Pregnancy Endorine
Pheochromocytoma Primary aldosteronism Glucocorticoid excess Renin-secreting tumors
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Pathogenesis for Hypertension Arterial and arteriolar vasoconstriction
Prevents the increase in pressure from being transmitted to the smaller, more distal vessels
With increasingly severe hypertension Autoregulation failure Vascular endothelial injury Plasma constituents (including fibrinoid material)
to enter the vascular wall narrowing or obliterating the vascular lumen.
Tissue edema and activation of endothelial vasoactive system
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Goals of TreatmentGoals of Treatment
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Goals of Treatment
Prevent end organ damage NOT normalize BP
Exceptions??
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HTN Urgencies: Goals of Therapy
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
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HTN Urgencies: Therapy 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).
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Hypertensive Emergency
ICU with close monitoring IV and Short acting medications
Avoid sublingual or IM Arterial line
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Goals of Treatment
Within 1-2 hrs Lower MAP 20-25%
CONTROLLED IV titratable meds
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Complications for rapid BP Reduction in Severe Hypertension
Widening Neurologic Deficits Retinal ischemia and Blindness Acute MI Deteriorating renal function
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Goals of Treatment
WHY ?WHY ?
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Cerebral Autoregulation
Strandgaard, et al. BMJ: 1973C
ereb
ral b
lood
flo
w
MAP
60mmHg
160mmHg
120mmHg
Adapted from: Chest, 2000; 118:214-227
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PharmacotherapyPharmacotherapy
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Given by continuous infusion Sodium nitroprusside Nitroglycerin Nicardipine Labetalol Esmolol Fenoldapam
Antihypertensive Drugs for Hypertensive Crisis
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Specific TreatmentSpecific Treatment
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Hypertensive Encephalopathy
Nitroprusside• Fenoldopam
Nicardipine Labetolol
Symptoms of encephalopathy should improve with treatment
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CVA
Nicardipine Labetolol Fenoldopam
Decrease DBP no more than 20% in 24hrs
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Cardiac Ischemia
Nitroglycerine Nitroprusside
• Fenoldopam
Nifedipine Reflex tachy Increases myocardial O2 demand May aggravate ischemia
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Acute LVF
Nitroprusside Afterload reduction
Fenoldopam
Nitroglycerine If ischemia is suspected
Furosemide Loop diuretic
Opioids
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Acute Aortic Dissection
Nitroprusside• Nicardipine, Fenoldopam Afterload reduction Increases ventricular contraction velocity Requires blockade Esmolol, metoprolol
Labetolol Goal: SBP ~100 mmHg Monitor patient closely
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Acute Aortic Dissection
ββ-block FIRST!-block FIRST! Esmolol Metoprolol
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Sympathetic Crisis
Nicardipine Nitroprusside Phentolamine
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Acute Renal Failure
Nicardipine Nitroprusside
“Use with caution” toxic metabolites...
Thiocyanate excreted via kidneys
Fenoldopam Labetolol
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Eclampsia
Hydralazine Used historically Arterial vasodilator Maintains placental blood flow
Nicardipine Labetolol
Magnesium
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The Discharged PatientThe Discharged Patient
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The discharged patient
JNC-VII Recommendations Stage 2
Combination tx Thiazide + ACEI, ARB, BB, CCB
“Compelling Indications”...
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The discharged patient
JNC-VII Recommendations “Compelling Indications”
URGENCY: ALL PATIENTS WITH HTN URGENCY BEING
DISCHARGED HOME SHOULD BE PLACED ON COMBINATION THERAPY AND HAVE RAPID FOLLOW UP.
THIAZIDE ACEI / ARB / BB / CCB
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Follow up...
Stage I: 140-159 / or 90-99
Stage II: >160 / or ≥100
“Higher”: ≥180 / ≥110
The discharged patient
Follow-up
2 Months
< 1 week
1 Months
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Goals of therapy in JNC7 & Euro Guidelines
Maximum reduction in long-term total risk of cardiovascular morbidity and mortality: Smoking Life style modification Lipid Diabetes Blood pressure
< 140/90 If DM or renal disease
<130/80
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The following 5 patients in ER
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?
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Patient A is a 65-year-old man with nausea, vomiting, and confusion.
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.
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Patient B: 73-year-old woman with sudden shortness of breath, pink sputum, and heavy chest pain.
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.
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Patient C: 56-year-old man with sharp, tearing chest and back pain.
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.
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Patient D: 64-year-old woman with a 6-hour history of right-sided weakness.
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 BP > 220/120 mm Hg in embolic CVA > 180/100 in hemorrhagic CVA
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Patient D: 64-year-old woman with a 6-hour history of right-sided weakness.
Drug of choice: Labetalol; nicardipine; hydralazine.
Target: 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.
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Patient E: 51-year-old woman with a mild headache, concerned about her history of hypertension.
These patients require gradual BP reduction over time on an outpatient basis
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Summary
Accurate history and timeline of onset
Evaluate Target organ injury Set the time frame for intervention Appropriate “pace” of therapy
Initial reduction Stabilization
Follow-up care/ Diagnostic studies
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Questions...
Comments…