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Hypertensive Crisis Sofiya Lypovetska MD PhD Ternopil state medical university SCOPE of the PROBLEM Hypertension is an increasingly important medical and public health issue. The prevalence of hypertension increases with advancing age to the point where more than half of people aged 60 to 69 years old and approximately three-fourths of those aged 70 years and older are affected Data from observational studies involving more than 1 million individuals have indicated that death from both ischemic heart disease and stroke increases progressively and linearly from BP levels Definitions and classification of blood pressure levels (mmHg) Factors influencing prognosis Factors influencing prognosis High/Very high risk subjects Blood pressure measurement Position statement: Ambulatory and home BP measurement JNC –VII Guidelines Patient characteristics associated with resistant hypertension Secondary causes of resistant hypertension Medication that can interfere with blood pressure control Conditions favouring use of some antihypertensive drugs versus others Compelling and possible contraindications to use of antihypertensive drugs Hypertensive Crisis Definitions- Is This : A Crisis? An Emergency? An Urgency?… Clinical Presentations Treatments Other Terminology Severely elevated BP (JNC VII) Defined as BP > 180/120 “accelerated HPT” – term used to describe individuals with chronic hypertension with associated group 3 KeithWagener-Baker retinopathy “malignant HPT” – describe those individuals with group 4 KWB retinopathy changes + papilledema Definitions Hypertensive Crisis Hypertensive Emergency………1-2 hours – Rapid / progressive end organ damage Hypertensive Urgency………….24-48 hrs – Inc. BP without evidence of end organ damage Uncontrolled Hypertension……..1 week – Do not require acute intervention Shayne PH - Ann Emerg Med - 01-APR-2003; 41(4): 513-29 Hypertensive Emergency BP >180/120 with evidence of target organ dysfunction Hypertensive encephalopathy Intracerebral bleed Acute MI Acute CHF with pulm edema Unstable angina Aortic dissection Eclampsia Tx: parenteral agent Cerebrovascular Hypertensive Emergencies Cerebral Infarct Intracerebral Hemorrhage Hypertensive Encephalopathy Cerebral Edema Cerebral Perfusion Pressure Cerebral blood flow a function of CPP Autoreg. Fails at 25% of MAP ICP CPP – Vulnerable to MAP CBF = blood flow; CPP = cerebral perfusion pressure; ICP = intracranial pressure; MAP = mean arterial pressure; TCA = total circulatory arrest. Hypertensive Encephalopathy Pathophysiology: - Loss of Cerebral Autoregulation of blood flow resulting in hyperperfusion of the brain, loss of integrity of the blood brain barrier, and vascular necrosis. - Loss of Autoregulation occurs at a constant cerebral blood flow of above MAP 150 to 160 mmHg. - Acute Onset - Reversible Hypertensive Encephalopathy Symptoms: Headache, Nausea/Vomiting, Lethargy, Confusion, Lateralizing neurological symptoms that are not often in an anatomical distribution. Signs: Papilledema, Retinal Hemorrhages Decreased level of consciousness, Coma Focal neurological findings Hypertensive encephalopathy Clinical manifestation of cerebral edema and microhemorrhages seen with dysfunction of cerebral autoregulation Defined as an acute organic brain syndrome or delirium in the setting of severe hypertension HPT Encephalopathy Not adequately treated – cerebral heamorrhage, coma and death. BUT with proper treatment – completely reversible Clinical diagnoses (exclusion) Management of Hypertensive Encephalopathy Reduce Mean Arterial Pressure (MAP) by 20 to 25% (T.397) and do not exceed this within first 30 to 60 min. Rosen recommends reduction of 30 to 40% (R.1759) MAP= 1/3(SBP-DBP) + DBP Treatment Reduces vasospasm that occurs at these high pressures Avoid excessive BP reduction to prevent hypoperfusion of the brain and further cerebral ischemia Hypertensive Encephalopathy Cerebral overperfusion – MAP overwhelms autoregulation – Vasodilation and Inc. Perm. – Cerebral Edema Hemorrhage, Coma, Death Tx: Nipride, Fenoldopam, Labatalol, Nicardipine Hemorrhagic CVA causes Hypertensive Vascular Disease Arteriovenous Anomalies (AVM) Arterial Aneurysms Tumors Trauma Hemorrhagic CVA Management Hemorrhagic CVA’s commonly results in a profound reactive rise in blood pressure Management is CONTROVERSIAL. Subarachnoid Hemorrhage: oral nimodipine (nimotop) 60mg po q 4 hours to reverse vasospasm. Nicardipine: 2mg IV boluses followed by an IV infusion of 4 to 15 mg/hr is used by some to treat Subarachnoid Hemorrhage. Ischemic CVA Pathophysiology: Elevated Blood Pressure can be the cause of the central nervous system event, OR, it may be a normal physiologic response (Cushing’s Reflex) Ischemic CVA Management Favors lowering MAP (mean arterial pressure) by 20%. Recommends IV Labetalol in small doses of 5mg increments IF Diastolic Blood Pressure is higher than 140 mmHg. (T. 398) HPT Retinopathy AV crossing changes HPT retinopathy HPT retinopathy Cardiovascular Hypertensive Emergencies Aortic Dissection Congestive Heart Failure Acute MI Congestive Heart Failure Pathophysiology: Increased Afterload with decreased Cardiac Output CHF / Pulmonary Edema Symptoms: Shortness of Breath, Cough, Chest Pain Lower Extremity Swelling Signs: Jugular Venous Distension, Rales, S3 Gallop Hepatomegaly, Pedal Edema CHF / Pulmonary Edema Treatment: – Diuretics – Nitroglycerin – Vasodilators – Digitalis – Beta-adrenoceptor agonists – Other positive inotropic agents Acute Coronary Syndrome Pathophysiology: - Increased afterload, cardiac workload, and myocardial oxygen demand - Decreased coronary artery blood flow Acute Coronary Syndrome / Acute MI Symptoms: Chest Pain, Nausea / Vomiting, Diaphoresis, Shortness of Breath Signs: Congestive Heart Failure Signs, S4 Gallop (due to decreased ventricular compliance) Few physical findings in many patients Clinical History is very Important Acute Coronary Syndrome/ Acute MI - Immediate Blood Pressure reduction is indicated to prevent Myocardial Damage No specific Defined BP target Management: Nitroglycerin IV or Sublingual - Beta Blockers (Esmolol, Lopressor) - Nitroglycerin is Drug of Choice Aortic Dissection Pathophysiology: - Atherosclerotic Vascular Disease, Chronic Hypertension, increased shearing force on the thoracic aorta, leading to intimal tear. - 50% begin in ascending aorta - 30% at aortic arch - 20% in descending aorta Dissection of Thoracic Aorta Symptoms: - Chest pain radiating to the back (classic presentation) Neurological Symptoms (carotid artery dissection) Angina (coronary artery dissection) Shortness of breath (aortic insufficiency, cardiac tamponade) Signs: - Differential Blood Pressure (in UE) - Bruit (interscapular) - Neurological Deficits - Acute Cardiac Tamponade (rare) Dissection of Thoracic Aorta Optimal Blood Pressure in these patients is undefined and must be tailored for each patient, however, SBP of 120-130mmHg may be a intial starting point. (T.408) Acute Renal Failure Pathophysiology: - Hypertensive Glomerulonephropathy, Acute Tubular Necrosis - Worsening renal function in the setting of severe hypertension with elevation of BUN/CR, proteinuria, or the presence of red cells and red cell casts in the urine. Acute Renal Failure Symptoms: - Many times there are few actual symptoms - Facial or Peripheral Edema due to fluid overload or proteinuria may be present, shortness of breath Signs: - Few findings unless edematous Pulmonary Edema Acute Renal Failure Management: Nitroprusside is agent of choice Dialysis (as needed) Lasix to enhance Sodium excretion; Also recommends Nitroprusside or Nifedipine - Nitroglycerin is also a good agent in this setting since it is hepatically metabolized and gastrointestinally excreted. - Preeclampsia / Eclampsia Pathophysiology: - - Systemic arterial vasoconstriction (including placental, leading to decreased uterine blood flow). Defined as SBP = 140/90 mmHg or greater, OR a 20 mmHg rise in SBP or 10 mmHg rise in DBP from baseline and evidence of HELLP Syndrome Preeclampsia / Eclampsia Symptoms: lower extremity swelling, headache, confusion, seizures, coma Signs: edema, hyperreflexia, elevation of blood pressure related to baseline BP prior to pregnancy (elevation may be mild 125/75) Management: IV Magnesium Sulfate, Hydralazine. - May also use nifedipine or labetalol Delivery of Fetus is definitive treatment of pre-eclampsia Treatment of acute severe hypertension in preeclampsia Pheochromocytoma Pathophysiology: - Alpha and Beta stimulation of the cardiovascular system due to adrenergic excess states Symptoms: Episodic Headaches, flushing, tremor, diaphoresis, diarrhea, hyperactivity, and palpitations Signs: Tachycardia, tachypnea, tremor, hyperdynamic state (high output CHF) Pheochromocytoma Management: - - Alpha Blocker FIRST, followed by a Beta Blocker Phentolamine (alpha) + Esmolol (beta) Labetalol IV (combined alpha and beta blockade) Pharmacologic Agents Hypertensive Emergencies Rapid Onset Rapid Maximal effect Rapid offset Ease of Titration Parenteral Agents Parenteral drugs for treatment of hypertensive emergencies Oral Regimens for Treatment of Hypertensive Urgency in the ED Clonidine: 0.1 to 0.2mg PO, repeat 0.1mg q hour to desired BP reduction or max of 0.7mg. - Labetalol: 200 to 400mg PO, repeat every 2 to 3 hours - Captopril: 25mg PO - Losartan: 50mg PO - Key Concepts Acute End-organ damage determines hypertensive emergency Be familiar with the agents of choice in specific emergencies Goal for most is careful reduction of MAP by 2025% over minutes to hours – DBP not less than 100 to 110 – Except: Pregnancy, Dissection, MI, Patients without acute end-organ ischemia rarely require urgent intervention Thank You!