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

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

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

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

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

6. Pathophysiology Physiologic Mechanisms Involved 1) Cardiac output 2) Peripheral/systemic vascular resistance 3) Renin-Angiotensin-Aldosterone System 4) Autonomic Nervous System 5) Other: bradykinin, endothelin, etc…

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

8. RAAS

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

12. 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. 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 PMHx: HTN, Afib, cataracts, NIDDM Meds: HCTZ, Metoprolol, Metformin 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 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? Is this a hypertensive urgency or emergency? Which major clinical syndrome does this case represent? Which major clinical syndrome does this case represent?

13. Hypertensive Encephalopathy Uncommon syndrome Uncommon syndrome Acute and reversible 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 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 Arises from “breakthrough” hyperperfusion and leakage of fluid thru BBB

14. CPP=MAP-ICP

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

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

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

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

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

21. Nitroglycerine 1) Activates guanylate cyclase 2) Accumulation of cGMP 3) Sequestration of Ca into SR 4) 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?

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

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

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

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

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

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

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

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

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

32. HTN Mx in Ischemic Stroke HTN common in 1st hours after stroke HTN common in 1st hours after stroke SBP>160 found in 60% pts with acute ischemic 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% 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: Increased BP may be due to: CV event and increased ICP CV event and increased ICP Full bladder Full bladder Nausea Nausea Pain Pain Pre-existing BP Pre-existing BP Hypoxia Hypoxia

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

34. CPP=MAP-ICP

35. HTN Mx in Ischemic Stroke A lot of studies showing harm with reduction of BP 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 Most pts have a decrease in BP a few hours post- stroke w/o intervention Oliveira-Filho et al. Neurology. 2003;61:1047-1051 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 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 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

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

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

39. Case 3 Same story as before but has this CT Same story as before but has this CT

40. HTN Bleeds Where do you get HTN bleeds in the brain? 1) Cerebellum 2) Pons 3) Basal ganglia 4) Thalamus

41. Stroke, 2007;38:2001-2023

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

43. HTN Mx in Hemorrhagic Stroke Summary of studies Isolated SBP<210 is not clearly related to hemorrhagic expansion or neurologic worsening Isolated SBP<210 is not clearly related to hemorrhagic expansion or neurologic worsening Decrease in MAP by 15% does not result in decreased CBF Decrease in MAP by 15% does not result in decreased CBF Baseline BP was not associated with growth of ICH in largest prospective study 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 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 Evidence supports maintaining CPP >60mmHg

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

47. 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 Phase 1 pilot study, RCT, open-label, safety-efficacy study Determine whether lowering BP after ICH will decrease death or long-term disability Determine whether lowering BP after ICH will decrease death or long-term disability N= 404 N= 404 Target BP of 140 vs 180 Target BP of 140 vs 180 Primary outcome of ICH growth Primary outcome of ICH growth Hematoma growth of 13.7% vs 36.3% (p=0.06) Hematoma growth of 13.7% vs 36.3% (p=0.06) No difference in secondary outcomes No difference in secondary outcomes Phase 2 ongoing Phase 2 ongoing

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

49. 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 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 Want to avoid shear stress and wide pulse pressures Reduce the LV ejection force Reduce the LV ejection force Goal is to get SBP 90-110 but just do what you can Goal is to get SBP 90-110 but just do what you can Use labetalol or esmolol Use labetalol or esmolol Can use nipride after have sufficiently BB b/c will blunt the reflex tachycardia and increased SV Can use nipride after have sufficiently BB b/c will blunt the reflex tachycardia and increased SV

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

51. Case 5 24F 4 days post-partum from induced twin vaginal delivery at 36w due to development of PIH called EMS for increased SOB EMS report 24F 4 days post-partum from induced twin vaginal delivery at 36w due to development of PIH called EMS for increased SOB EMS report T= 37.9 P= 115 BP= 200/ 115 RR= 29 O2= 84% BS= 5.6 T= 37.9 P= 115 BP= 200/ 115 RR= 29 O2= 84% BS= 5.6 En route to hospital patient became increasingly distressed En route to hospital patient became increasingly distressed On arrival, patient in extremis On arrival, patient in extremis T= 37.9 P= 140 BP= 190/ 120 RR= 38 O2= 90%NRB T= 37.9 P= 140 BP= 190/ 120 RR= 38 O2= 90%NRB Speaking one word sentences, diaphoretic, looking exhausted. Heart sounds not auscultated, JVP at angle of jaw, crackles to apices, 2+ edema to shins, abdo soft and not tender, normal reflexes, no clonus Speaking one word sentences, diaphoretic, looking exhausted. Heart sounds not auscultated, JVP at angle of jaw, crackles to apices, 2+ edema to shins, abdo soft and not tender, normal reflexes, no clonus

52. CASE 5 EMS report EMS report T= 37.9 P= 115 BP= 170/ 100 RR= 29 O2= 84% BS= 5.6 T= 37.9 P= 115 BP= 170/ 100 RR= 29 O2= 84% BS= 5.6 En route to hospital patient became increasingly distressed En route to hospital patient became increasingly distressed On arrival, patient in extremis On arrival, patient in extremis T= 37.9 P= 140 BP= 190/ 120 RR= 38 O2= 90%NRB T= 37.9 P= 140 BP= 190/ 120 RR= 38 O2= 90%NRB Speaking one word sentences, diaphoretic, looking exhausted. Heart sounds not auscultated, JVP at angle of jaw, crackles to apices, 2+ edema to shins, abdo soft and not tender, normal reflexes, no clonus Speaking one word sentences, diaphoretic, looking exhausted. Heart sounds not auscultated, JVP at angle of jaw, crackles to apices, 2+ edema to shins, abdo soft and not tender, normal reflexes, no clonus Q: What can cause respiratory failure in the post-partum patient?

53. DDX Respiratory Failure in the post-partum patient Respiratory Failure in the post-partum patient  Pulmonary Embolism  Cardiogenic Pulmonary Edema  Neurogenic Pulmonary Edema  Amniotic Fluid Embolism  Aspiration  Community or hospital acquired pneumonia Q: What are some causes of cardiogenic pulmonary edema in peripartum women?

54. DDX Cardiogenic Pulmonary Edema Cardiogenic Pulmonary Edema  Peripartum cardiomypathy  Pre-eclampsia/Eclampsia  Aortic stenosis  Mitral stenosis  Other cardiomyopathies Cocaine Cocaine Alcoholic Alcoholic Diabetic Diabetic Hypertrophic Hypertrophic Dilated Dilated Restrictive Restrictive Q: What investigations do you want on this patient?

55. How do you want to tx her assuming she has htn induced pulmonary edema?

56. HTN Mx in Pre-Eclampsia Remember they can present weeks after delivery Remember they can present weeks after delivery Nitrates, but in her would need to start high and go up quickly Nitrates, but in her would need to start high and go up quickly Stand by the bed and start at 10ug/min and go up by 10s quickly until effect- she needed 110ug/min Stand by the bed and start at 10ug/min and go up by 10s quickly until effect- she needed 110ug/min Nitroprusside could also be used if post-partum Nitroprusside could also be used if post-partum

57. HTN Mx in Pre-Eclampsia BiPAP/CPAP BiPAP/CPAP FRC Improves V/Q- adrenergic outflow FRC Improves V/Q- adrenergic outflow preload and afterload b/c raised intrathoracic pressure preload and afterload b/c raised intrathoracic pressure Loop Diuretics Loop Diuretics Block Na resorption in Loop of Henle Block Na resorption in Loop of Henle Na/H20 Excretion Na/H20 Excretion Plasma Volume Plasma Volume Preload Preload HR/BP

58. Case 6 69F presents after a home BP of 200/104. No other complaints. 69F presents after a home BP of 200/104. No other complaints. PMHx: Htn, MI 10 years ago PMHx: Htn, MI 10 years ago Meds: HCTZ, metoprolol, lisinopril Meds: HCTZ, metoprolol, lisinopril O/E: BP= 200/112 O/E: BP= 200/112 What do you want to do with this patient? What do you want to do with this patient?

59. Drug Summary Nitroprusside Nitroprusside 0.25-0.5ug/kg/min 0.25-0.5ug/kg/min Inc by 0.5ug/kg/min quickly Inc by 0.5ug/kg/min quickly Nitro Nitro 10-20ug/min 10-20ug/min Inc by 5-10ug/min Q3-10min Inc by 5-10ug/min Q3-10min Labetalol Labetalol 10-20mg IV Q5-10min 10-20mg IV Q5-10min Infusion at 1-2mg/min Infusion at 1-2mg/min