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Hypertensive Emergencies

Hypertensive Emergencies. Alyssa Morris, R2 March 5, 2009. Objectives. Definitions Pathophysiology Secondary causes of HTN Cases Treatment options and goals. Definitions. Hypertensive Emergency Acute, life threatening, usually a BP> 180/120 Target organ damage Reduce BP in 1-3 hours

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Hypertensive Emergencies

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  1. Hypertensive Emergencies Alyssa Morris, R2 March 5, 2009

  2. Objectives • Definitions • Pathophysiology • Secondary causes of HTN • Cases • Treatment options and goals

  3. Definitions • Hypertensive Emergency • Acute, life threatening, usually a BP> 180/120 • Target organ damage • Reduce BP in 1-3 hours • Hypertensive Urgency • Asymptomatic, severe HTN, usually >180/120 • NO target organ damage • Usually no need to reduce BP in ED • Both of these are spectrums and the BP at which they occur is variable

  4. Hypertensive Emergencies • Neurological • Hypertensive Encephalopathy • CVA • SAH • ICH • Cardiovascular • MI/ischemia • Acute LV dysfxn • Ao dissection • Pulmonary • Acute edema • Other • Acute renal failure/insufficiency • Retinopathy • Eclampsia • MAHA

  5. Hypertensive Emergencies • Occurs in 1% pts with HTN • Single organ involvement found in 83% • Two organ involvement in 14% • Three or more organs involved in 3% • Most common presentations: • Cerebral infarction 24.5% • Pulmonary edema 22.5% • Hypertensive encephalopathy 16.3% • CHF 12%

  6. Pathophysiology Physiologic Mechanisms Involved • Cardiac output • Peripheral/systemic vascular resistance • Renin-Angiotensin-Aldosterone System • Autonomic Nervous System • Other: bradykinin, endothelin, etc…

  7. Components of BP BP= CO x SVR CO= HR x SV Think of the components as: • CO= heart • BP= arteries • SVR= arterioles

  8. RAAS

  9. ANS BP= CO x SVR CO= HR x SV • Adrenal medulla • Releases catecholamines which act on the adrenergic receptors • Kidney • Releases renin in response to increased sympathetic tone • Alpha 1 receptors result in renal artery constriction • Blood vessels • Alpha receptors result in constriction • Heart • B1/2 receptors result in increased CO, chronotropy (HR) and inotropy (SV)

  10. Case 1 • 70M brought in by EMS. Wife called because he had been complaining of a severe h/a, vomitted and then later became altered. • PMHx: HTN, Afib, cataracts, NIDDM • Meds: HCTZ, Metoprolol, Metformin • O/E: T= 37.6, P=80, BP= 210/124, 02=94%, altered level of consciousness, no focal deficits, fundi difficult to see • Is this a hypertensive urgency or emergency? • Which major clinical syndrome does this case represent?

  11. Hypertensive Encephalopathy • Uncommon syndrome • Acute and reversible • Results from an abrupt, sustained rise of BP that exceeds the limits of cerebral autoregulation of the small resistance arteries in the brain • Arises from “breakthrough” hyperperfusion and leakage of fluid thru BBB

  12. CPP=MAP-ICP

  13. Clinical Presentation • Severe h/a • Drowsiness • ALOC • Vomitting • Seizures • Focal neuro deficits • Blindness

  14. Tx • How fast would you try to reduce the BP? • Why do you not want to reduce it too quickly? • What would you consider using to reduce the BP?

  15. Drug Options • VASODILATORS • Nitroprusside • Nitroglycerin • Fenoldopam • Hydralazine • BETA BLOCKERS • Labetalol • Esmolol • CALCIUM CHANNEL BLOCKERS • Enalaprilat • ALPHA BLOCKERS • Phentolamine • Clonidine

  16. Nitroprusside • Potent smooth muscle relaxing agent • Acts on both resistance and capacitance vessels • Reduces both preload and afterload • Rate of onset rapid • Duration of action very short • Also a cerebral vasodilator • Can increase ICP secondary to increased cerebral blood flow • What is an intermediate metabolite?

  17. Nitroprusside • Complications: • Hypotension :. Reflex tachycardia and inc SV • Prolonged use can produce hypothyroidism • Cerebral edema • Local necrosis if extravasates from line • Unstable in UV light, therefore wrapped in tinfoil • Infusion at 0.25-0.5ug/kg/min -then increase by 0.5mcg/kg/min • Max of 10 mcg/kg/min • Is there a group you would not use this in?

  18. Nitroglycerine • Activates guanylate cyclase • Accumulation of cGMP • Sequestration of Ca into SR • Relaxation of Vascular smooth muscle • Dose dependent • Low dose: venodilator (preload) • High dose: veno and arteriodilator (afterload) • Therefore, usually reduce BP by reducing preload and CO • Start with 10-20ug/min infusion • Titrate up 5-10ug/minQ3-5min Who would you want to be careful using this drug in?

  19. Fenoldopam • Trade name is Corlopam • Peripheral dopamine-1 receptor agonist • Dop-1 R located postsynaptically in systemic and renal vasculature • Mediate systemic, renal and mesenteric vasodilation and natriuresis • Improves renal fxn acutely in malignant htn • Does not cross BBB • Rapid onset and elimination ½ life of 9 min • Hypotension less common side effect • 0.1ug/kg/min, then up by 0.1ug/kg/min every 15 min • Max dose is 1.6ug/kg/min

  20. Hydralazine • Direct arteriolar vasodilator • Used to be used as first line in pregnancy htv emergencies • Starting dose is 5mg IV • Repeat doses of 5-10mg IV every 20 mins to maintain desired BP • Complications: • Marked hypotension • Reflex tachycardia (can give angina) • Flushing and nausea • H/a

  21. Labetalol • Selective α-1 blocker and nonselective β-blocker • α:β blockade ratio between 1:3 and 1:7 • Not a significant drop in CO like other βB • Does not affect cerebral blood flow or renal fxn • BP starts to fall in 5-10 mins • Max effect at 30 mins

  22. Labetalol • Start with 10-20mg IV over 2mins • Repeat dose of 20,40 or 80 mg every 10 mins to max of 300mg • Or after loading dose can start infusion at 1-2mg/min and titrate up • Contraindicated in patients with CHF, heart block, asthma, pheo, cocaine • Give oral when have reached max IV dose

  23. Esmolol • Selective β-1 blocker • Very short acting • Elimination ½ life of 9 minutes • No intrinsic sympathomimetic activity • Loading dose of 500 ug/kg over 1 minute • Follow with infusion of 50-100 υg/kg/min (can rpt Q5min) • Max dose of 300 ug/kg/min • Contraindications same as labetalol

  24. Phentolamine • α-blocking agent • Used for the Mx of catecholamine-induced HTV crisis • What are some examples of this? • Immediate effect • Effect lasts up to 15 mins • 1-5mg IV boluses

  25. Nicardipine • Parenteral dihydropyridine CCB • More titratable, less negatively inotropic, and induces less tachycardia than nifedipine • Acts predominantly as a vasodilator • Onset of action is 5-15 mins • Duration of action is 4-6 hours • Infusions starting at 5 mg/hr • Increase infusion every 15 mins • Max dose of 15mg.hr

  26. Case 2 • 71F brought in by EMS. Last seen normal 1 hour ago and found aphasic and hemiparetic. • PMHx: HTN • Meds: HCTZ • O/E: T= 37.6, P= 78, BP= 200/110, 02= 95%, R Hemiparesis, GCS 12 • How do you want to Mx this pt?

  27. HTN Mx in Ischemic Stroke Stroke. 2007;38:1655-1711.

  28. HTN Mx in Ischemic Stroke • HTN common in 1st hours after stroke • SBP>160 found in 60% pts with acute ischemic stroke • For every 10mmHg raise >180, risk of neurologic deterioration increases by 40% and risk of poor outcome by 23% • Increased BP may be due to: • CV event and increased ICP • Full bladder • Nausea • Pain • Pre-existing BP • Hypoxia

  29. HTN Mx in Ischemic Stroke • Theoretical reasons for lowering BP in stroke • Decrease formation of brain edema • Lessening risk of hemorrhagic transformation of infarction • Preventing further vascular damage • Forestalling early recurrent stroke • BUT remember aggressive tx of BP may lead to neurologic worsening by decreasing perfusion pressure to ischemic areas of brain

  30. CPP=MAP-ICP

  31. HTN Mx in Ischemic Stroke • A lot of studies showing harm with reduction of BP • Most pts have a decrease in BP a few hours post-stroke w/o intervention • Oliveira-Filho et al. Neurology. 2003;61:1047-1051 • Found >90% pts had a decrease in SBP by 28% in 24hrs post-stroke with no intervention • No data define levels of HTN that mandate emergent tx but many suggest >185/110 b/c greater than this is a contraindication to tPA

  32. Consensus Statement • “ emergency administration of antihypertensive agents should be withheld unless DBP>120 and SBP>220” • “reasonable goal to decrease blood pressure by 15-25% within 24 hours” • This is a case-by-case decision • More research needs to be done

  33. CHIPPS Controlling hypertension and hypotension immediately post-stroke trialLancet Neurol. 2009;:48-56. • Prospective, RCT, pilot study N=179 • Primary outcome of death or dependency • ICH or ischemic strokes with SBP>160 randomized to labetalol, lisinopril or placebo • Reduced BP on average by 20 systolic • Death or 61% vs 59% (p=0.82) for tx vs placebo • No increased serious adverse events or neuro deterioration

  34. Case 3 • Same story as before but has this CT

  35. HTN Bleeds Where do you get HTN bleeds in the brain? • Cerebellum • Pons • Basal ganglia • Thalamus

  36. Stroke, 2007;38:2001-2023

  37. HTN Mx in Hemorrhagic Stroke • Primary rational for reducing BP is to avoid hemorrhagic expansion from potential sites of bleeding • -especially if aneurysm or AVM • BP is correlated with increased ICP and volume of hemorrhage • Difficult to determine whether increased BP is a cause of hemorrhage growth or an effect of increased volumes of ICH and increased ICP • In primary ICH there is little prospective evidence that exists to support a specific BP threshold

  38. HTN Mx in Hemorrhagic Stroke Summary of studies • Isolated SBP<210 is not clearly related to hemorrhagic expansion or neurologic worsening • Decrease in MAP by 15% does not result in decreased CBF • Baseline BP was not associated with growth of ICH in largest prospective study • Hemorrhage enlargement occurs more frequently in pts with increased SBP but it is not clear if this is an effect of increased growth of ICH with associated increase in ICP or a contributing cause to the growth of ICH • Evidence supports maintaining CPP >60mmHg

  39. ATACH Study Antihypertensive treatment of acute cerebral hemorrhage • International, multicenter, open-labeled, RCT • 3-dose-tiered trial of lowering SBP to predetermined levels: 170-200, 140-170, 110-140 • Using IV Nicardipine • Data collection complete • Inclusion criteria • w/I 12h on onset Sxs and ICH on CT • GCS>8 • BP on admission >170 on two separate readings • Not surgical candidates

  40. INTERACT I Intensive blood pressure reduction in acute cerebral hemorrhage. Lancet Neurol. 2008;7:391-9. • Phase 1 pilot study, RCT, open-label, safety-efficacy study • Determine whether lowering BP after ICH will decrease death or long-term disability • N= 404 • Target BP of 140 vs 180 • Primary outcome of ICH growth • Hematoma growth of 13.7% vs 36.3% (p=0.06) • No difference in secondary outcomes • Phase 2 ongoing

  41. Case 4 • 32F with known bicuspid Ao valve with c/o tearing back pain radiating into neck • BP R arm= 220/100 BP L arm= 170/78 • Which BP do you go by? Why? • What do you want to do? • What is the factor you want to reduce to avoid propagation? • What would be your goal BP? What would you use? • What if her pulse is now 55 but her SBP is still 150?

  42. HTN Mx in Ao Dissection • Remember to check BP in legs if you are thinking dissection b/c the flap can give you falsely low BP in arms • Want to avoid shear stress and wide pulse pressures • Reduce the LV ejection force • Goal is to get SBP 90-110 but just do what you can • Use labetalol or esmolol • Can use nipride after have sufficiently BB b/c will blunt the reflex tachycardia and increased SV

  43. HTN Mx in Ao Dissection • Diagnosis and management of aortic dissection. A task force report. Eur Heart J. 2001;22(18):1642 • Use BB first line • Lower SBP <110 • HR <60 • Use nipride only after sufficiently beta blocked • Acute Aortic syndromes. Circulation. 2005;112(24):3802 • Use BB first line • SBP 100-120 • HR <60 • Role of CCBs unknown if don’t tolerate BB

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