Download Free Medical Hypertensive Emergencies PowerPoint Presentation

Hypertensive Emergencies PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "HYPERTENSIVE EMERGENCIES" by Pat Melanson, MD.

This medical PowerPoint presentation talks about Hypertensive emergencies.

Hypertensive emergencies are situations in which severe elevations in blood pressure occur and can result in acute organ damage or failure. These situations require immediate medical attention in order to prevent serious complications.

Some examples of hypertensive emergencies include Hypertensive encephalopathy, Acute pulmonary edema, Acute myocardial infarction and Acute aortic dissection

Tags : Hypertensive emergencies, blood pressure, Hypertensive encephalopathy, Acute pulmonary edema, Acute myocardial infarction, Acute aortic dissection, cardiology, cardiology PowerPoint presentation

Published on : Mar 19, 2023 | Views : 1547 | Downloads : 1

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

HYPERTENSIVE EMERGENCIES Pat Melanson, MD McGill University
Slide 2-

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
Slide 3-

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)
Slide 4-

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)
Slide 5-

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
Slide 6-

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
Slide 7-

Hypertensive Emergencies CNS - Hypertensive encephalopathy CVS Acute myocardial ischemia Acute cardiogenic pulmonary edema Acute aortic dissection Post-op vascular surgery Renal - Acute renal failure Eclampsia Catechol excess- Pheochrom, Drugs
Slide 8-

Hypertensive Emergencies High BP WITHOUT acute end-organ dysfunction IS NOT a hypertensive emergency “Hypertensive Pseudoemergency”
Slide 9-

Cerebral Blood Flow CBF = CPP / CVR CPP = MAP - ICP MAP = DBP + 1/3 PP Cerebral autoregulation normal between 50 - 150 70/40 to 190/130 Vascular stenosis
Slide 10-

50 150 Cerebral Autoregulation CBF 50 ml/100g/min MAP
Slide 11-

Cerebral Autoregulation Shift to right Chronic hypertensives ICH, SAH, Ischemic infarct Trauma Cerebral edema Age, atherosclerosis Some hypertensives suffer decrease CBF at MAP higher than 120
Slide 12-

Cerebral Autoregulation CPP below lower limit hypoperfusion with ischemia CPP above upper limit “breakthrough” vasodilation Segmental pseudospasm (“sausage-string”) fluid extravasation
Slide 13-

Pathophysiology of Hypertensive Emergencies Rate of change of BP determines likelihood Chronic HTN lowers probability adaptive vascular changes protect end-organs from acute changes in BP Previous normotensives (eclampsia, acute GN) develop signs and symptoms at lower BP’s
Slide 14-

Pathophysiology of Hypertensive Emergencies Endothelial Role in BP Homeostasis Secretion of vasodilators (NO, Prostacyclin) Sudden increased vasoreactivity norepinephrine, angiotensin II activation of renin-angiotensin-aldosterone
Slide 15-

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
Slide 16-

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
Slide 17-

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
Slide 18-

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
Slide 19-

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
Slide 20-

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)
Slide 21-

Pharmacologic Therapy
Slide 22-

Nitroprusside Arteriolar and venous dilation Predictably effective in lowering BP Usual dosage 0.5 - 8 mg/kg/min 50 mg/250 ml D5W; start @ approx.10 mdrops/min (10 ml/hr) in 70 kg patient = 0.5 mg/kg/min Potential cyanide or thiocyanate toxicity with prolonged infusion
Slide 23-

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 mg/min 50 mg/250 ml D5W; start at approx..3 mdrops/min [3 ml/hr] = 10 mg/mins
Slide 24-

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
Slide 25-

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
Slide 26-

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
Slide 27-

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
Slide 28-

Labetalol Combined a, b adrenergic blockade Usual contraindications to b-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 achievingdesired effect, or total of 300 mg
Slide 29-

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
Slide 30-

Hydralazine Unpredictable hypotensive effect Delayed onset compared to other parenteral agents Reflex increase in HR and CO Largely outmoded for acute therapy except in pre-eclampsia/eclampsia,where it is “traditional” therapy Adverse effects on cerebral autoreg
Slide 31-

Clonidine Central a-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
Slide 32-

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
Slide 33-

New Agents Fenoldopam peripheral Dopamine-1 receptor agonist direct vasodilation renal artery vasodilation natriuresis Nicardipine dihydropyridine CCB
Slide 34-

Management of Specific Hypertensive Emergencies
Slide 35-

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
Slide 36-

Hypertensive Encephalopathy: Differential Dx Stroke (Ischemic) Intracranial (intracerebral or subarachnoid) hemorrhage Intracranial mass Encephalopathy due to drug ingestion, CNS infection, uremia
Slide 37-

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
Slide 38-

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)
Slide 39-

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
Slide 40-

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
Slide 41-

Thromboembolic (Ischemic) CVA’s 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
Slide 42-

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
Slide 43-

Acute LV failure / Acute cardiac ischemia HTN® increased 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
Slide 44-

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
Slide 45-

Drug Associated Hypertension "Hypercatecholamine state”
Slide 46-

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)
Slide 47-

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
Slide 48-

CONDITIONS TO BE DIFFERENTIATED FROM A HYPERTENSIVE CRISIS Acute left ventricular failureUremia from any cause, particularly with volume overloadCerebrovascular accident,Subarachnoid hemorrhageBrain tumor,Head injuryEpilepsy (postictal)Collagen diseases(i.e., lupus), with cerebral vasculitisEncephalitisOverdose and withdrawal from narcotics, amphetaminesHypercalcemiaAcute anxiety with hyperventilation syndrome
Slide 49-

ConclusionThe key to the successful management of patients with severely elevated BP is to differentiate hypertensive crises from hypertensive urgencies. Patients with hypertensive urgencies have severe hypertension (diastolic > 110 mm Hg), but without clinical evidence of acute end-organ damage. Rapid antihypertensive therapy is not warranted in these patients. Hypertensive crises constitute a distinct group of clinicopathologic entities associated with acute target organ injury. These patients require immediate BP reduction to prevent progressive end-organ damage. Hypertension associated with cerebral infarction or intracerebral hemorrhage only rarely requires treatment. Patients with hypertensive crises are best treated in an ICU with titratable IV hypotensive agents. Several rapid-acting IV antihypertensive agents are available, including labetalol, esmolol, fenoldopam, nicardipine, and sodium nitroprusside. While nitroprusside is commonly used to treat severe hypertension, it is an extremely toxic drug that should be used only in rare circumstances.