Management of Hypertensive Emergencies Dr. Abdulkareem Alsuwiada, FRCPC, MSc

Learning Objectives To identify and triage severe hypertensive states accurately To effectively manage hypertensive crises with drug therapy

Hypertensive Urgency “Severe elevation of blood pressure” Generally DBP >115-130 No progressive end organ damage RISK OF IMMINENT TARGET ORGAN DAMAGE ALTHOUGH INJURY HAS NOT YET OCCURRED NO EVIDENCE BASED DATA EXISTS TO GUIDE PRACTITIONER IN MANY CASES CLINICIANS MAY BE FORCED TO INITIATE ANTI-HTN TREATMENT WITHOUT BEING CERTAIN OF DIAGNOSTIC CLASSIFICATION

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 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 COTTON WOOL EXUDATES PAPILLEDEMA Hemorrhages Exudates Papillodema

Urgency vs. Emergency Distinguishing between hypertensive emergency and urgency is a crucial step in appropriate management

Urgency vs. Emergency Urgency Emergency No need to acutely lower blood pressure May be harmful to rapidly lower blood pressure Death not imminent Emergency Immediate control of BP essential Irreversible end organ damage or death within hours MAIN CAUSE IS OF HYPERTENSIVE URGENCY IS MEDICATION NON-COMPLIANCE SO GENERALLY FIND OUT WHY NOT TAKING AND RESTART OR CHOOSE NEW AGENTS.

Approach to Patients

Approach to patients Recheck blood pressure! History Appropriate size cuff Cuff not over clothing Check in all limbs History Prior crises Renal disease Medications Compliance Recreational drugs Generic approach…

Approach to patients Physical Exam Signs of end organ damage? Is the patient in a resuscitation room or are they smiling and eating cheetos? In distress? OVERT signs of end organ damage? Will cover each organ system in order...

Neuro Hypertensive encephalopathy Focal Neurological Deficits Severe Headache Nausea/Vomiting Papilledema Visual Changes Seizures Focal Neurological Deficits Ischemic vs hemorrhagic CVA Encephalopathy 2/2 brain edema Obviously CT of any patient with neuro findings.

Fundoscopy/ Neuro COTTON WOOL EXUDATES PAPILLEDEMA

Cardiac Cardiac ischemia Acute left ventricular failure Chest pain EKG for ischemic changes Acute left ventricular failure Pulmonary edema Hypoxia EKG for left ventricular strain pattern CXR

Renal Electrolytes BUN/Cr UA with micro Chronic failure/insufficiency vs acute failure Cause vs effect UA with micro Protein Blood Casts Most cases of hypertensive emergencies arise in patients with some underlying renal insufficiency or failure

Major Causes of Hypertensive Emergencies and Urgencies Untreated essential hypertension Withdrawal / non-adherence to antihypertensive drug therapy Development of secondary hypertension

Major Causes of Hypertensive Emergencies and Urgencies Renal Disease Renal artery stenosis Pregnancy Endorine Pheochromocytoma Primary aldosteronism Glucocorticoid excess Renin-secreting tumors

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

Goals of Treatment

Goals of Treatment Prevent end organ damage NOT normalize BP Exceptions?? PAUSE: ??? Acute Aortic Dissecton: Need to actually lower BP to less than normal Hemorrhagic CVA SBP 150-160

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

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).

Hypertensive Emergency ICU with close monitoring IV and Short acting medications Avoid sublingual or IM Arterial line

Goals of Treatment Within 1-2 hrs Lower MAP 20-25% CONTROLLED IV titratable meds As an aside…always do what your surroundings will allow. Nursing availability, med. availability. Till with NTG in flash pulmonary edema.

Complications for rapid BP Reduction in Severe Hypertension Widening Neurologic Deficits Retinal ischemia and Blindness Acute MI Deteriorating renal function

WHY ? Goals of Treatment Harington 82/94 treated; 12 not treated--> died Treated with ganglion blocking agent 81/82 had papilledema 17 had neuro findings on presentation; non improved with treatment 7 without neuro findings developed them during treatment 6/7 with hemiparesis or other focal sign indicative of CVA 5 developed seizures 1 facial palsey

Cerebral Autoregulation Strandgaard, et al. BMJ: 1973 Cerebral blood flow EMERGENCY: Far right of RED Increased ICP, increased cerebral edema, or ICH, or ischemia 2/2 edema Cerebral autoregulation in HTNsives has been noted to be 25% less than peak, lower and you loose the autoregulatory effects. Cerebral flow after CVA Curve depresses and flattens--- loss of autoregulatory system 60 mmHg 120 mmHg 160 mmHg MAP Adapted from: Chest, 2000; 118:214-227

Pharmacotherapy

Given by continuous infusion Antihypertensive Drugs for Hypertensive Crisis Given by continuous infusion Sodium nitroprusside Nitroglycerin Nicardipine Labetalol Esmolol Fenoldapam

Specific Treatment

Hypertensive Encephalopathy Nitroprusside Fenoldopam Nicardipine Labetolol Symptoms of encephalopathy should improve with treatment

CVA Nicardipine Labetolol Fenoldopam Decrease DBP no more than 20% in 24hrs Chest 2000 Varon in Houston review does not recommend Nitroprusside 20% is arbitrary Wallace and Levy series of 334 patients in 1981 showed that hypertension after CVA normalizes within 10days of admission General consensus is to treat only for DBP > 120 or SBP > 200 EXCEPTION IS HEMORRHAGIC STROKE WHICH WE TREAT THE HTN MORE AGGRESSIVELY WANT SBP 150-160.

Cardiac Ischemia Nitroglycerine Nitroprusside Nifedipine Fenoldopam Reflex tachy Increases myocardial O2 demand May aggravate ischemia

Acute LVF Nitroprusside Nitroglycerine Furosemide Opioids Afterload reduction Fenoldopam Nitroglycerine If ischemia is suspected Furosemide Loop diuretic Opioids

Acute Aortic Dissection Nitroprusside Nicardipine, Fenoldopam Afterload reduction Increases ventricular contraction velocity Requires B blockade Esmolol, metoprolol Labetolol Goal: SBP ~100 mmHg Monitor patient closely

Acute Aortic Dissection β-block FIRST! Esmolol Metoprolol

Sympathetic Crisis Nicardipine Nitroprusside Phentolamine

Acute Renal Failure Nicardipine Nitroprusside Fenoldopam Labetolol “Use with caution” toxic metabolites... Thiocyanate excreted via kidneys Fenoldopam Labetolol

Eclampsia Hydralazine Nicardipine Labetolol Used historically Arterial vasodilator Maintains placental blood flow Nicardipine Labetolol Magnesium

The Discharged Patient

The discharged patient JNC-VII Recommendations Stage 2 Combination tx Thiazide + ACEI, ARB, BB, CCB “Compelling Indications”... Zeller, et al. UTSW, 1989 Prospective controlled trial Rapid reduction of severe asymptomatic HTN in ED Controls got nothing in ED ALL Discharged with maintenance therapy No difference in reduction in BP at 24 hrs and 1 weekThe discharged patient Follow up... Stage I: 140-159 / or 90-99 Stage II: >160 / or ≥100 “Higher”: ≥180 / ≥110

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 Zeller, et al. UTSW, 1989 Prospective controlled trial Rapid reduction of severe asymptomatic HTN in ED Controls got nothing in ED ALL Discharged with maintenance therapy No difference in reduction in BP at 24 hrs and 1 week

The discharged patient Follow-up Follow up... Stage I: 140-159 / or 90-99 Stage II: >160 / or ≥100 “Higher”: ≥180 / ≥110 2 Months JOINT NATIONAL COMMITTEE ON PREVENTION, DETECTION, EVALUATION AND TREATMENT OF HIGH BLOOD PRESSURE 1 Months < 1 week

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

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.

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. 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. 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. 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 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

Drug of choice: Labetalol; nicardipine; hydralazine. Target: 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.

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

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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