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How to handle a Hypertension Crisis

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10:45 11:45 am How to Handle Hypertension Crisis SPEAKER Karol E. Watson, MD, PhD, FACC Presenter Disclosure Information The following relationships exist related to this presentation: Karol E. Watson,
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10:45 11:45 am How to Handle Hypertension Crisis SPEAKER Karol E. Watson, MD, PhD, FACC Presenter Disclosure Information The following relationships exist related to this presentation: Karol E. Watson, MD, PhD, FACC: Advisory Board for AstraZeneca; Daiichi Sankyo; Merck & Co., Inc.; and Quest Diagnostics. Off-Label/Investigational Discussion In accordance with pmicme policy, faculty have been asked to disclose discussion of unlabeled or unapproved use(s) of drugs or devices during the course of their presentations. Learning Objectives How to handle a Hypertension Crisis Define hypertensive crises: Hypertension urgency and hypertension emergency Outline the pathophysiology of hypertensive urgencies and emergencies Karol Watson, MD, PhD Professor of Medicine David Geffen School of Medicine at UCLA Los Angeles, California Identify treatment goals and treatment options for hypertensive crises. Current State of Hypertensive Crisis Management Hypertensive crises are among the most misunderstood and mismanaged of acute medical problems seen in clinical practice Delays in initiating therapy can cause severe complications in target end organs Overzealous therapy resulting in a too-rapid reduction in blood pressure is equally damaging Consideration of the pathophysiologic principles involved in hypertensive crises is of utmost importance Acute Severe Hypertension Epidemiology and Mortality Historical Study 1939: First study of the natural history of hypertensive emergencies published Untreated hypertensive emergencies had a 1- year mortality rate of 79%, with median survival of 10.5 months Varon J, Marik PE. Chest. 2000;118: Epstein M. Clin Cornerstone. 1999;2: Varon J. CHEST 2007; 131: Hypertension Emergencies in context Severe hypertension is relatively common Chronic Hypertension Hypertension Urgencies There are ~100,000 ER visits each year for hypertension ~15,000 of those visits are for severely high BP Hypertension Emergencies Pitts et al. Natl Health Stat Report 2008;7:1-38. Terminology and Definitions (JNC 7) Urgency Emergency Severe The Hypertension diagnosis plus of hypertensive End-organ Damage BP 180/110 mm Hg CHF emergencies depends on the ACS/AMI clinical manifestations rather Renal failure than only on the absolute Stroke and level ICH of the blood pressure. Encephalopathy Aortic dissection Pre-eclampsia Other? Epidemiology You will almost certainly see a hypertensive urgency in your career You will also likely see a hypertensive emergency - Occur in 1-2% of the hypertensive population - But, 50 million hypertensive Americans - 500,000 hypertensive emergencies/year Higher in the elderly and African Americans Incidence is twice as high in men as compared to women Hypertensive Urgencies / Emergencies: Classification / Definition Etiology / Pathophysiology Evaluation Management Follow up Classification of Severe Hypertension (Hypertensive Crises) Urgencies Severe HTN with NO evidence of acute end organ damage Can be treated as an outpatient Emergencies Severe HTN WITH evidence of acute end organ damage Requires hospitalization and parenteral (IV) medication Hypertensive Urgencies / Emergencies: Classification / Definition Etiology / Pathophysiology Evaluation Management Follow up Most Hypertensive Crises are caused by: Sodium excess Extracellular volume expansion Sympathetic overactivation Too Much Salt Too Much Water Too Much Sympathetic Activity Pathophysiology of Hypertensive Emergencies: a Vicious Cycle Hypertensive Emergency Circulating vasoconstrictors End organ ischemia Abrupt Loss of Abrupt Autoregulatory function Endothelial damage SVR BP Vasoconstriction, often with intravascular hypovolemia causes: - Increased circulating catecholamines - Activation of reninangiotensin-aldosterone system - Altered autoregulatory function Hypertensive Urgencies / Emergencies: Common Etiologies Accelerated hypertension in a patient with preexisting hypertension Medication noncompliance Acute antihypertensive drug withdrawal Renovascular hypertension Acute glomerulonephritis Ault NJ, et al. Am J Emerg Med. 1985;3(6 suppl): Wallach R, et al. Am J Cardiol. 1980;46: Varon J, et al. Chest. 2000;118: Kincaid-Smith P. J Hypertens. 1991;9: Hypertensive Urgencies / Emergencies: LESS Common Etiologies Sympathomimetic drug poisonings Pre-eclampsia How do patients with hypertensive crises present? Pheochromocytoma MAO inhibitor interactions Signs and Symptoms Headache Epistaxis Chest Pain Dyspnea Faintness Agitation Signs and Symptoms Neurologic Deficit Vomiting Arrhythmia HTN Urgency (%) HTN Emergency (%) Zampaglione B, et al. Hypertension 1996;27: Hypertensive Urgencies / Emergencies: Common Clinical Precipitants Myocardial Ischemia Hypercarbia / Hypoxemia Inappropriate vascular clamping (afterload) Malignant Hyperthermia Pain Anxiety Distended Bladder Hypervolemia Signs and Symptoms Headache Epistaxis Chest Pain Dyspnea Faintness Agitation Signs and Symptoms Neurologic Deficit Vomiting Arrhythmia HTN Urgency (%) HTN Emergency (%) Zampaglione B, et al. Hypertension 1996;27: Hypertensive Urgencies / Emergencies: Classification / Definition Etiology / Pathophysiology Evaluation Management Goals of evaluation Outcomes are to determine etiology, and rapidly assess for end organ damage End-Organ Damage Characterizes Hypertensive Emergencies Brain Hypertensive encephalopathy Stroke Cardiovascular System Unstable angina Acute heart failure Acute myocardial infarction Acute aortic dissection Dissecting aortic aneurysm Retina Hemorrhages Exudates Papilledema Kidney Hematuria Proteinuria Decreasing renal function Symptoms Initial Evaluation Medical History - Episodic palpitations and perspiration? Medications - MAO inhibitors - Clonidine Social History - Recreational Drugs Amphetamines Cocaine Phencyclidine Adapted from Varon J, Marik PE. Chest. 2000;118: Physical Exam Blood pressures must be taken in both arms - If the cuff is too small, the BP will be falsely elevated - If the cuff is too low (below the level of the heart), the BP will be falsely elevated Pulses should be checked in upper and lower extremities Neuro exam Cardiac exam Pulmonary exam Ocular exam: only happens in 13% of pts Hypertensive Retinopathy Grade 1 mild narrowing or sclerosis of retinal arteries (arteriolar narrowing) Grade 2 moderate to marked arteriolar narrowing with A-V crossing changes (AV nicking) Grade 3 All the above + hemorrhages or cotton-wool spots Grade 4 All the above + additional swelling of the optic disk (papilledema) Labs / Imaging to consider Hypertensive Encephalopathy Comprehensive Metabolic Panel CBC with peripheral smear (which may suggest microangiopathic hemolytic anemia). Urinalysis EKG Chest X-ray Head CT Echocardiogram PRES: Posterior reversible encephalopathy syndrome Typically symmetrical white matter edema in the posterior cerebral hemispheres Cerebral Autoregulation Is Central to Treatment of Hypertensive Crises Cerebral Blood Flow Normal Regulatory Range (BP ~ 120/70 to 240/150) Autoregulation In the uninjured, normotensive brain, autoregulation is effective over MAP ranging from about (BP ~ 80/40 to 190/130) Increasing risk of hypertensive encephalopathy Increasing risk of ischemia 0 (BP ~ 80/40 to 190/130) Normotensive Chronic hypertensive MAP (mm Hg) In chronic hypertension, this range can be shifted upwards to MAP (BP ~ 120/70 to 240/150) So, in the patients with out of control hypertension, if BP falls too rapidly to below ~120/70 cerebral perfusion can be compromised Adapted from Varon J, Marik PE. Chest. 2000;118: Hypertensive Urgencies / Emergencies: Classification / Definition Etiology / Pathophysiology Evaluation Management Outcomes Management of Hypertensive Urgencies (BP 180/110 mm Hg with NO end organ damage) Hypertensive Emergencies Are More Than Blood Pressure Measurement Hypertensive emergencies generally occur with DBP 120 mm Hg, BUT there is no strict cutoff and BP can be much lower Baseline level of hypertension and rate of rise are also very important There is tremendous overlap between groups and categories, i.e., cannot be defined by BP alone Adapted from Kincaid-Smith P. Aust N Z J Med 1981;11(Suppl 1):64-68 Goals of Therapy of Hypertensive Crises Hypertensive urgencies can generally be managed with oral medications as an outpatient. BP should be lowered over hours - Important to prevent too-rapid lowering due to autoregulation of flow by pressure in brain, heart, and kidneys Hypertensive emergencies must be treated as an inpatient, usually in the ICU with parenteral medications. Goal is to reduce MAP by ~ 20% within one hour - Aortic dissection requires even more rapid lowering JNC 7, JAMA 2003; 289: How Low Should You Go? Simple answer % reduction in MAP within 1 st hour Better answer - It really depends on clinical condition Less aggressive with ischemic stroke More aggressive with hemorrhagic stroke, acute HF and aortic dissection Management of Hypertensive Emergencies (BP 180/110 mm Hg WITH end organ damage Marik and Varon. Critical Care 2003, 7: Goals of Therapy of Hypertensive Crises Hypertensive urgencies can generally be managed with oral medications as an outpatient. BP should be lowered over hours - Important to prevent too-rapid lowering due to autoregulation of flow by pressure in brain, heart, and kidneys Hypertensive emergencies must be treated as an inpatient, usually in the ICU with parenteral medications. Goal is to reduce MAP by ~ 20% within one hour - Aortic dissection requires even more rapid lowering JNC 7, JAMA 2003; 289: Hypertensive Emergency: Goals of Therapy Immediate and controlled BP reduction - Reduce BP 20-25% within minutes to 1 hour - If BP is then stable, target toward 160/ mm Hg over the next 2-6 hours - If this level of BP is well tolerated and the patient is clinically stable, further gradual reductions toward normal BP over the next hours More immediate BP reduction in certain cases in - e.g. Aortic dissection Increased caution in acute ischemic stroke patients - Lower cutoffs in certain circumstances JMC 7. US Dept of HHS; NIH publication No ; 2003:54. Adams HP, et al. Stroke. 2005;36: Other Important Points Treatment Typically Parenteral (IV) ***ICU, ICU, ICU*** - Some studies suggest that only 15% of pts are admitted 1 st line to an ICU Once BP is stable, oral medications should be started as parenteral (IV) medications are titrated off Do not use sublingual nifedipine or other therapies that lower BP too quickly Be cautious with nitroprusside (except with aortic dissection) because it can decrease BP too quickly, and may increases intracranial pressure Many patients are volume depleted from pressure naturesis so use caution with diuretics BP may drop too quickly Adrenergic receptor blockers - Esmolol (β 1 ) - Labetalol (α 1 and β) - Phentolamine (α 1 ) - Urapidil (α 1 ) Ca 2+ channel blockers - Nicardipine - Clevidipine ACE inhibitors - Enalaprilat Nitric Oxide (NO) donors Nitroprusside Nitroglycerin Dopamine agonist Fenoldopam Direct vasodilator Hydralazine Agent IV Antihypertensive Agents Onset/ Duration Elimination Half-Life Clevidipine 2-4 mins 5-15 mins Adverse Events Tachycardia, headache, nausea, dizziness, hypotension and vomiting. Cautions/Concerns Contraindicated in patients with allergies to soybeans, soy products, eggs, or egg products. Cautious use in heart failure Conditions requiring special management Enalaprilat Esmolol Fenoldopam mesylate Hydralazine 15 min/ h 1 2 min/ min 5 15 min/ 30 min 4 h min/ 1 4 h 11 h 2 9 min 5 min 1 h Precipitous fall in BP in high-renin states, headache, cough, renal failure, hyperkalemia, angioedema Heart block, hypotension, nausea, bronchospasm, overt heart failure, cardiogenic shock Tachycardia, headache, nausea, dizziness, flushing, hypotension, increased intraocular pressure Marked hypotension, tachycardia, flushing Avoid in acute MI, long duration of action Reduces cardiac output, which may impair organ perfusion Caution with glaucoma Avoid in aortic dissection, MI, severe renal disease; prolonged and unpredictable effects; difficult to titrate 1. Ischemic stroke especially if considering thrombolytics 2. Aortic dissection Labetalol Nicardipine 5 min/ 3 6 h 5 15 min/ 15 min 6 h 5.5 h 44.8 min Bradycardia (heart block), overt heart failure, cardiogenic shock, edema, nausea, vomiting Tachycardia, headache, nausea, flushing, thrombophlebitis, hypotension, vomiting Avoid in acute heart failure; severe bradycardia; heart block, asthma Avoid in acute heart failure; caution with coronary ischemia; long duration of action 3. Acute Renal Failure Nitroglycerin 2 5 min/ 5 10 min 1 4 min Flushing, headache, vomiting, hypotension, methemoglobinemia, decreased arterial resistance, reflex tachycardia Reduction in preload and cardiac output undesirable in patients with compromised renal and cerebral perfusion Sodium nitroprusside Immediate/ 2 3 min 2 3 min Nausea, muscle twitching, sweating, thiocyanate and cyanide intoxication, hypotension Increases intracranial pressure; may reduce coronary perfusion pressure (coronary steal ); cyanide toxicity BP Management in Acute Stroke Most acute stroke patients present with hypertension There is a U-shaped relationship between BP and neurologic outcomes Thus, SBP should be maintained ~ mm Hg during acute stroke and not normalized Mortality Rate (%) month 12 months 80 * mm Hg 60 0 220 SBP (mm Hg) Adapted from Vemmos KN, et al. J Intern Med. 2004;255: BP Management in Acute Stroke AHA/ASA 2007 Treatment Guidelines for Arterial Hypertension: Ischemic Stroke Not Eligible for Thrombolytic Therapy BP Level (mm Hg) SBP 220 or DBP 120 SBP 230 or DBP DBP 140 Treatment Emergency administration of antihypertensive agents to be withheld Nicardipine or labetalol to 15% -25% in BP within the first day Nitroprusside to 15% -25% in BP within the first day Adapted from Adams HP, et al. Stroke. 2007;38: BP Management in Acute Stroke Treatment goals differ depending on whether or not the patient is a candidate for thrombolysis Thrombolytic therapy cannot be administered until BP is reduced to safe levels (typically SBP 185 and DBP 110 ) in order to avoid intracerebral hemorrhage Nicardipine or labetalol preferred in acute stroke If patient is a candidate for thrombolysis and BP remains uncontrolled, you may need to add Nitroprusside Adams et al, Stroke 2003; 34: BP Management in Acute Stroke AHA/ASA 2007 Guidelines for BP management if Thrombolytic Therapy Used BP Level (mm Hg) Pretreatment SBP 185 or DBP 110 During/after rt-pa SBP OR DBP SBP 230 OR DBP DBP 140 Treatment Labetalol (may repeat once) or nitropaste or nicardipine; If BP not reduced and maintained, do not administer rtpa Labetalol Nicardipine or labetalol If BP not controlled, consider nitroprusside Nitroprusside Adapted from Adams HP, et al. Stroke. 2005;36: BP Management in Aortic Dissection Treatment of HTN should begin before confirmation of diagnosis, if suspected Goal of therapy is to aortic stress by rapidly lowering BP and controlling pulse rate Target is to reduce MAP by 10-15%, or reduce SBP to 110 mm Hg, in 5-30 minutes Usual drugs are vasodilator + beta blocker, usually Nitroprusside + Esmolol Varon J, Chest 2000;118: BP Management in Acute Renal Failure Goal of therapy is to treat HTN without further decreasing renal perfusion Target is 10-20% in MAP over 1-2h, then 10-15% in next 6-12h; accelerating this process may worsen renal function Fenoldopam appears to be preferred drug - Maintains GFR, Causes natriuresis Nitroprusside should be avoided because of potential toxicity Vaughn, Lancet 2000;356: Caution with Nitroprusside Disadvantages of sodium nitroprusside - Decrease cerebral blood flow and increases intracranial pressure - Can reduce regional blood flow in coronary artery disease - Risk of cyanide toxicity Use when other agents not effective - Monitor thiocyanate levels - Avoid in renal or hepatic dysfunction Sympathetic Crisis Beta-adrenergic antagonists will result in unopposed alpha-adrenergic stimulation In cocaine use, Beta blockers can - Increase blood pressure - Worsen coronary artery vasoconstriction - Decrease survival Avoid beta blockade (including non selective agents such as labetolol) Examples of sympathetic crises Pheochromocytoma Monoamine oxidase inhibitor + tyramine Cocaine/amphetamines/OTC herbals (PPA, ephedra, trytophan) Clonidine withdrawal Sympathetic Crisis Recommended Drugs - Nicardipine - Fenoldopam - Verapamil - Benzodiazepine - If pheo suspected use phentolamine Pheochromocytoma Clonidine withdrawal A catecholamine secreting tumor Most common site is adrenal medulla Increased risk in patients with neurofibromatosis Chronically elevated BP with paroxysms of palpitations, diaphoresis, tachycardia, malaise, apprehension, HA, abdominal pain, and angina Episodes precipitated by physical or emotion stress, eating, position, or micturation Occurs in patients on clonidine who abruptly discontinue therapy Symptoms very similar to pheochromocytoma Occur hours after last dose Treatment is to re-start clonidine MAOI + tyramine Foods containing tyramine Tyramine is found in many foods, is a sympathomimetic like amphetamine, and causes a transient release of norepinephrine (NE) in all people when ingested Patients on MAOIs (Nardil, Parnate, Marplan) experience an exaggerated response to tyramine, resulting in prolonged and severe hypertension Beer Wine Aged cheeses Chocolate Coffee Cream Chicken liver Pickled herring Broad beans (dopamine) Yeast Citrus fruits Snails MAOIs and medications Hypertensive Urgencies / Emergencies: Some pharmaceuticals can also cause severe hypertension when taken with MAOIs Meperidine Ephedrine TCAs Reserpine Dopamine Methyldopa Guanethidine Classification / Definition Etiology / Pathophysiology Evaluation Management Outcomes Follow-up care in hypertensive emergencies Goal: Transition to oral therapy as soon as patient can tolerate therapy Monitor carefully: Abrupt switch may result in BP Most patients may be discharged on oral medication within hours Clinical setting offers an opportunity to improve BP control and medication adherence Acute Severe Hypertension has High Morbidity, Mortality, and Readmission Rates: Results from the STAT Registry CB Granger, J Gore, J Katz, K Kleinschmidt, A Wyman, F Peacock, F Anderson, on behalf of the STAT Investigators. Presented at the European Society of Cardiology Annual Meeting, September 2, Vidt DG. In: Hypertension Primer. In press. Study Population Patients 1,588 Age - median 58 (49-70) Female sex 49% Black race 56% White race 34% Qualifying BP Systolic 200 mm Hg ( ) Diastolic 110 mm Hg (93-123) Length of stay 5 days (range 2-9) Patient Demographics Medical history % Hypertension 89 Tobacco or alcohol use 38 Diabetes 35 Chronic kidney disease 31 End stage renal disease 11 Previous hospitalization for HTN 27 Neurological event 23 Drug abuse 15 Am Heart J Volume 158, Issue 4, October 2009, Pages e1 Am Heart J Volume 158, Issue 4, October 2009, Pages e1 Presenting Characteristics Symptoms % Shortness of breath 29 Chest pain 26 Headache 23 Altered mental status 20 Weak and dizzy 17 Predisposing Factors Contributing to Hypertensive Event (35%) Factors % Medication non-adherence 25 Chronic 16 Current 10 Missed or incomplete dialysis 3 Anxiety/psychosocial reaction 2 Drug abuse 11 Am Heart J Volume 158, Issue 4, October 2009, Pages e1 Am Heart J Volume 158, Issue 4, October 2009, Pages e1 STAT Results Median time to SBP of 160 mmhg: 4 hrs 60% increased to 180 after initial control 4% had iatrogenic hypotension 29% had recurrent, severe HTN necessitating reinstitution of parenteral therapy Multiples antihypertensive agents were necessary to achieve control 65% had no documentation of follow-up appointment being scheduled or attended Am Heart J Volume 158, Issue 4, October 2009, Pages e1 Short-Term (2 to 6 month) Outcomes for various clinical conditions Acute Condition Death Rehospitalization ACS 1,2,3 5-7% 30% CHF 4 8.5% 26% Sev
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