HYPERTENSIVE EMERGENCIES Pat Melanson, MD McGill University Hypertensive Emergencies : Objectives Distinguish which hypertensive presentations require immediate therapy Describe appropriate therapies for each presentation Describe the risks of treatment
Discuss the advantages and disadvantages of currently available antihypertensive drugs Cases
Asymptomatic 65 year-old, BP 200/115 (143) Embolic CVA, BP 215/105 (142) Hemorrhagic CVA, BP 200/100 (133) SAH, BP 180/100 (127) Aortic dissection, BP 175/105 (128) Pregnant female, BP 150/100 Encephalopathy, BP 260/160 (194) Acute pulmonary edema, BP 220/120 (153) History of Hypertension
It is a mistake, and one made not infrequently, to begin treating the high blood pressure as if it were a disease. MacKenzie,1908 HTN as an associated symptom rather than as a cause of disease Essential hypertension (i.e., FDR) Chronic Hypertension Increases risk of atherosclerosis ( CAD, MI)
cerebrovascular disease (CVA) renal disease These are long-term risks Elevation of BP is often a physiologic response to an acute condition Aggressive treatment of acute HTN may increase morbidity and mortality Hypertensive Emergencies : Definition A rapid decompensation of vital organ
function secondary to an inapropriately elevated BP Require lowering of BP within 1 hour to decrease morbidity Not determined by a BP level, but rather the imminent compromise of vital organ function Hypertensive Emergencies CNS - Hypertensive encephalopathy CVS
Shift to right Chronic hypertensives ICH, SAH, Ischemic infarct Trauma Cerebral edema Age, atherosclerosis Some hypertensives suffer decrease CBF at MAP higher than 120 Cerebral Autoregulation CPP below lower limit
hypoperfusion with ischemia CPP above upper limit breakthrough vasodilation Segmental pseudospasm (sausage-string) fluid extravasation Pathophysiology of Hypertensive Emergencies Rate of change of BP determines likelihood Chronic HTN lowers probability
adaptive vascular changes protect endorgans from acute changes in BP Previous normotensives (eclampsia, acute GN) develop signs and symptoms at lower BPs Pathophysiology of Hypertensive Emergencies Endothelial Role in BP Homeostasis Secretion of vasodilators (NO, Prostacyclin)
Sudden increased vasoreactivity norepinephrine, angiotensin II activation of renin-angiotensinaldosterone Pathophysiology of Hypertensive Emergencies ? ATII direct cytotoxicity to vessel wall ? mechanical stretching Inflammatory vasculopathy cytokines, endothelial adhesion molecules Loss of endothelial function permeability
inhibition of local fibrinolysis activation of coagulation cascade Therapeutic considerations in hypertensive emergencies Need for rapid reduction of BP Potential complications of therapy Prevalence of cerebrovascular disease and coronary artery disease (Stenotic lesions) Altered cerebral autoregulation Impaired baroreflexes Blood viscosity
Ability to increase oxygen extraction How far can BP be safely lowered? Lower limit usually 25% below MAP 50% of chronic hypertensives reached lower autoregulation limit with 11 to 20% reduction in MAP 50% had lower limit above usual mean Kanaeko et al; J Cereb Blood Flow Metab 3:S51,1983
Most ischemic complications develop with reductions greater than 20 - 30 % (over 24 to 48 hours) Blindness, paralysis, coma, death, MI Initial Lowering of BP : Therapeutic Guidelines Do not lower BP more than 20% over the first 1 to 2 hours unless necessary to protect other organs Decreasing to DBP of 110 or patients normal levels may not be safe
Further reductions should be very gradual ( days) Follow neuro status closely Concept of Hypertensive Urgencies Potentially dangerous BP elevation without acute, life-threatening end-organ damage Examples (controversial!) Retinal changes without encephalopathy or acute visual symptoms High BP with nonspecific Sx (headache,
dizziness, weakness) Very high BP without symptoms Hypertensive Urgencies Severe elevation of BP ( DBP > 115) No progressive end-organ disease Joint National Committee on Detection, Evaluation, and Treatment of HBP 1984 - lower BP within 24 hours 1988 - urgent therapy rarely required 1993 - Gradual lowering of BP Risks of rapid reduction (cerebral and myocardial
ischemia) Pharmacologic Therapy Nitroprusside Arteriolar and venous dilation Predictably effective in lowering BP Usual dosage 0.5 - 8 g/kg/min 50 mg/250 ml D5W; start @ approx. 10 drops/min (10 ml/hr) in 70 kg patient = 0.5 g/kg/min
Potential cyanide or thiocyanate toxicity with prolonged infusion Nitroglycerin Predominant venodilation at low infusion rates; significant arteriolar dilation at higher dosages Effective in management of hypertension complicated by CHF or cardiac ischemia Usual dosage 10-250 g/min 50 mg/250 ml D5W; start at approx..
3 drops/min [3 ml/hr] = 10 g/mins Nitroglycerin and Nitroprusside Rapid onset and offset; ability to smoothly titrate BP Potential hypotension and end-organ hypoperfusion Require continuous IV infusion, constant patient monitoring Adversely effect cerebral autoregulation May increase ICP
Nifedipine Peripheral and coronary arteriolar v.d. Rapid onset of antihypertensive effect 5-20 minute onset peak effect in 30-60 min duration 4-5 hr Potential hypotension and/or reflex cardiac stimulation Several case reports of cerebral or myocardial ischemia after rapid decrease
Sublingual Nifedipine Should a Moratorium be Placed on Sublingual Nifedipine capsules given for hypertensive emergencies and pseudoemergencies? Grossman, Messerli, Grodzicki, Kowey JAMA, 276 : 1328 - 1331,1996 Sublingual Nifedipine Inappropriate physician habits in prescribing nifedipine capsules in hospitalized patients
Rehman et al; Am J Hypertension 9 ; 1035, 1996 Ordered over phone for asymptomatic Arbitrary use No evidence of bedside evaluation in 98% No follow-up exam documented
Labetalol Combined , adrenergic blockade Usual contraindications to -blockade Rapidly effective when given IV; Onset < 5 min, peak 5-10 min, duration 2-6 hr (sometimes longer) Usual dosage 20 mg IV, then 40-80 mg IV q 10-15
min until achieving desired effect, or total of 300 mg Diazoxide Rapid effect when given as IV bolus Potential hypotension (long-lasting) cerebral and myocardial ischemia Marked reflex increase in HR and CO (myocardial oxygen demand) Rarely a first-line Dose 1-3 mg/kg IV bolus q 10-15 min until desired BP achieved
Hydralazine Unpredictable hypotensive effect Delayed onset compared to other parenteral agents Reflex increase in HR and CO Largely outmoded for acute therapy except in preeclampsia/eclampsia, where it is traditional therapy
Adverse effects on cerebral autoreg Clonidine Central -agonist; sympathetic tone to heart and peripheral vessels Usual regimen: 0.1-0.2 mg po, then 0.1 mg po q hr until desired BP achieved Onset 30-60 min, peak 2-4 hr, duration 6-12 hr Sedation may interfere with neurologic assessment of pt Rarely a first-line agent
ACE inhibitors IV enalaprilat, oral captopril potentially useful for acute BP reduction Little clinical experience in patients with hypertensive emergencies Difficult to titrate (sometimes ineffective, sometimes excessive BP ) Positive effects on cerebral autoregulation New Agents Fenoldopam peripheral Dopamine-1 receptor agonist
direct vasodilation renal artery vasodilation natriuresis Nicardipine dihydropyridine CCB Management of Specific Hypertensive Emergencies Hypertensive Encephalopathy
Abrupt, sustained increased BP exceeds limits of cerebral autoregulation MAP 150 -200 Variable vasospasm, edema, hemorrhages Headaches, nausea, vomiting, confusion Patchy focal neuro deficits Papilledema, retinopathy Signs + symptoms resolve with reduction of BP Hypertensive Encephalopathy: Differential Dx Stroke (Ischemic)
Intracranial (intracerebral or subarachnoid) hemorrhage Intracranial mass Encephalopathy due to drug ingestion, CNS infection, uremia Hypertension with Stroke Syndromes Need for BP therapy controversial rebleed, hemorrhagic transformation increased edema and ICP
Hypertension often transient, physiologic response which resolves spontaneously BP reduction may cause ischemic neurologic deterioration Ischemic penumbra Cerebral autoregulation (right shift) Cautious reduction of very high BP Subarachnoid Hemorrhages 20% rebleed within 2 weeks ( 24 hrs) Increased risk if SBP >160 or MAP > 110
No study has shown that treatment of BP reduces risk of rebleeding Acute right shift of curve (ICH,hydrocephalus) Nimodipine for cerebro-protection (vasospasm) Cautious decrease in BP by 20% initially, then below SBP of 160 (if not yet clipped) Intracerebral Hemorrhage HTN associated with increased mortality HTN may be a marker for more advanced chronic arterial compromise Physiologic response to increased ICP from clot
Decrease in BP may raise ICP Ischemic penumbra may exist in ICH No evidence that acute lowering of BP reduces risk of hematoma expansion, rebleed rare after 12 hrs Rate of 24-hour BP decline and mortality after spontaneous ICH Qureshi et al; CCM 1999, 27: 480 - 485 Intracerebral Hemorrhage NSA recomendations SBP > 220 or DBP > 120
NINDS recommendations SBP > 180 , MAP > 130 Lower BP to MAP 100 - 130 Control of BP not been demonstrated to decrease ongoing or recurrent bleeding Thromboembolic (Ischemic) CVAs NSA recommendations SBP > 220, DBP > 120
NINDS recommendations DBP > 140 - NTP SBP >220, DBP > 120, MAP > 130 Labetalol, Enalapril, esmolol, Nitropaste Ischemic penumbra Thrombolytic therapy Aortic Dissection Tear in intima separation or dissection of wall longitudinally 50% mortality in first 48 hours; begin treatment based on suspicion of Dx
Decrease pulse wave contour (dP/dT) Therapeutic regimens: (SBP 100 -120, HR < 80) propranolol plus nitroprusside labetalol trimethaphan Definitive diagnosis (CT, TEE, aortography, MRI) after control of BP,contractility, pain Acute LV failure / Acute cardiac ischemia HTNincreased afterload; may precipitate
LV failure or ischemia Dyspnea, pain, anxiety may cause HTN Specific BP therapy indicated if patient remains hypertensive after conventional measures for CHF or ischemia NTG, NTP, ACEI BB, CCB Pre-eclampsia/ Eclampsia Preeclampsia mild = 140/90 with proteinuria severe = 160/110, 5 gm protein, Sx
"Standard" therapy is hydralazine Other agents: Nifedipine, labetalol, diazoxide (small doses), methyldopa nitroprusside (risk of fetal CN toxicity) Additional measures: MgSO4; Delivery Drug Associated Hypertension "Hypercatecholamine state Cases
Asymptomatic 65 year-old, BP 200/115 (143) Embolic CVA, BP 215/105 (142) Hemorrhagic CVA, BP 200/100 (133) SAH, BP 180/100 (127)
Aortic dissection, BP 175/105 (128) Pregnant female, BP 150/100 Encephalopathy, BP 260/160 (194) Acute pulmonary edema, BP 220/120 (153) CLINICAL CHARACTERISTICS OF HYPERTENSIVE CRISIS BP: Usually >140 mm Hg diastolic Funduscopic findings: Hemorrhage, exudate, papilledema Neurological status:
Headache, confusion, somnolence, stupor, visual loss, focal deficits, seizures, coma Cardiac findings: Prominent apical impulse, cardiac enlargement, congestive failure Renal: Oliguria, azotemia Gastrointestinal: Nausea, vomiting CONDITIONS TO BE DIFFERENTIATED FROM A
HYPERTENSIVE CRISIS Acute left ventricular failure Uremia from any cause, particularly with volume overload Cerebrovascular accident,Subarachnoid hemorrhage Brain tumor,Head injury Epilepsy (postictal) Collagen diseases(i.e., lupus), with cerebral vasculitis Encephalitis Overdose and withdrawal from narcotics, amphetamines Hypercalcemia Acute anxiety with hyperventilation syndrome
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