2007 EMA Advanced Emergency & Acute Care Medicine Conference Atlantic City, NJ September 24, 2007

1. Emergency Department Hypertensive Patient Emergencies: Case Presentations and Panel Discussion

2. 2007 EMA Advanced Emergency & Acute Care Medicine ConferenceAtlantic City, NJSeptember 24, 2007

3. Edward P. Sloan, MD, MPH FACEPProfessorDepartment of Emergency MedicineUniversity of Illinois College of MedicineChicago, IL

4. Attending PhysicianEmergency MedicineUniversity of Illinois HospitalOur Lady of the Resurrection HospitalChicago, IL

5. Disclosures • FERNE Chairman and President • FERNE advisory board for The Medicine Company in May 2007 • FERNE grant by The Medicines Company to support this program • No individual financial disclosures

6. www.ferne.org

7. Learning Objectives • Determine the definition of hypertensive emergencies, and discuss their epidemiology and pathophysiology in ED patients with stroke syndromes. • Identify what therapies are available for the treatment of ED patients with hypertensive emergencies and stroke syndromes.

8. Learning Objectives • Discuss the clinically relevant endpoints for the evaluation and management of ED patients with hypertensive emergencies. • Understand what guidelines and recommendations assist emergency care providers in optimally treating ED patients with hypertensive emergencies and stroke syndromes.

9. Case Presentation • A 64 year old male patient with a history of hypertension and diabetes presents to the Emergency Department with a new onset of ipsilateral right-sided facial droop, arm and leg weakness, aphasia, and gaze to the left. His vital signs are BP 240/135, HR110, RR 16, and Temp 98.4.

10. ED Neuroprotection: Key Concepts Outcome related to infarct volume Need to limit infarct size Aggressively Rx ischemic penumbra

11. ED Neuroprotection: Key Concepts Outcome related to infarct volume

12. Infarct Volume and Outcome Vessel occlusion Infarct core Ischemic penumbra How large is the core in the ED? What is the penumbra conversion? Do ED therapies limit infarct growth?

13. ED Neuroprotection: Key Concepts Outcome related to infarct volume Need to limit infarct size

14. Limiting Infarct Size Enhance perfusion Treat hypoxia, hypotension Limit ischemic cascade effects Prevent complications Compare the results with a conventional training protocol. Most people do at least two exercises per muscle group, perform three sets and perhaps 12 or 15 reps per set. Allowing just five seconds per rep, that makes for at least 36 minutes of exercise per workout. This is usually done three times per week. So in six weeks, a conventional program would involve 648 minutes of exercise. That's 42 times more than the subjects in our study. Are your results in the last six weeks 42 times better than theirs? I doubt it. Remember, these golfers were exercising in a way that did not involve stretching or moving the weight over a full range of motion. So how did this affect a full range of motion activity like a golf drive? Every one of them showed an improvement. The increase in drive distance varied from 5 to 31 yards. Keep in mind that these subjects had been golfing for up to 40 years and had handicaps as low as eleven. So getting any improvement in golfers who already play at this level is impressive. Getting it with 14 minutes of exercise spread over six weeks is truly revolutionary. The fact is every sport -- even a finesse sport like golf -- is improved by an increase in strength. Muscles are responsible for all movement in the body and stronger muscles deliver more power to every aspect of movement, irrespective of its range of motion. Since this study, I've gone on to improve this method of training. Further research showed that static hold times could be reduced to even less than what the golfers used. Workouts can be spaced further apart as a trainee gets stronger. I work with advanced trainees who train once every six weeks, yet they gain strength on every exercise each time they work out. The weights they hoist are enormous. I believe the time is coming when most people will have a better understanding of the role of proper, efficient strength training methods and frequency. For the guy who wants maximum results with minimum time invested, an ultra-brief but ultra-intense workout will be performed about as often as he gets a haircut. Anything more is just lifting weights as a busy work hobby. Train smart!

15. Preventing Complications Compare the results with a conventional training protocol. Most people do at least two exercises per muscle group, perform three sets and perhaps 12 or 15 reps per set. Allowing just five seconds per rep, that makes for at least 36 minutes of exercise per workout. This is usually done three times per week. So in six weeks, a conventional program would involve 648 minutes of exercise. That's 42 times more than the subjects in our study. Are your results in the last six weeks 42 times better than theirs? I doubt it. Remember, these golfers were exercising in a way that did not involve stretching or moving the weight over a full range of motion. So how did this affect a full range of motion activity like a golf drive? Every one of them showed an improvement. The increase in drive distance varied from 5 to 31 yards. Keep in mind that these subjects had been golfing for up to 40 years and had handicaps as low as eleven. So getting any improvement in golfers who already play at this level is impressive. Getting it with 14 minutes of exercise spread over six weeks is truly revolutionary. The fact is every sport -- even a finesse sport like golf -- is improved by an increase in strength. Muscles are responsible for all movement in the body and stronger muscles deliver more power to every aspect of movement, irrespective of its range of motion. Since this study, I've gone on to improve this method of training. Further research showed that static hold times could be reduced to even less than what the golfers used. Workouts can be spaced further apart as a trainee gets stronger. I work with advanced trainees who train once every six weeks, yet they gain strength on every exercise each time they work out. The weights they hoist are enormous. I believe the time is coming when most people will have a better understanding of the role of proper, efficient strength training methods and frequency. For the guy who wants maximum results with minimum time invested, an ultra-brief but ultra-intense workout will be performed about as often as he gets a haircut. Anything more is just lifting weights as a busy work hobby. Train smart!

16. ED Neuroprotection: Key Concepts Outcome related to infarct volume Need to limit infarct size Aggressively Rx ischemic penumbra

17. Aggressively Rx Ischemic Penumbra Maximize cerebral perfusion Provide optimal substrates, O2 Avoid cell death Maintain intact blood brain barrier

18. Cerebral Perfusion CPP = MAP - ICP Cerebral perfusion pressure Mean arterial pressure Intracranial pressure

19. Cerebral Perfusion CPP = MAP - ICP If MAP = 110 mmHg, ICP 10 mmHg CPP then equals 100 mmHg Cerebral blood flow auto-regulation CPP maintained over range of MAPs Pathological ICP elevations limited

20. Mean Arterial Pressure 120 / 75 MAP = 90 mmHg 210 / 120 MAP = 150 mmHg 180 / 110 MAP = 132 mmHg How much MAP therapy is OK? What agents provide best Rx? How to avoid watershed infarct?

21. Watershed Infarct wa·ter·shed (wô t r-sh d) n. 1. A ridge of high land dividing two areas that are drained by different river systems. Also called water parting. 2. The region draining into a river, river system, or other body of water. 3. A critical point that marks a division or a change of course; a turning point:

22. ED Neuroprotection: Key Concepts Outcome related to infarct volume Need to limit infarct size Aggressively Rx ischemic penumbra ED MD is the best neuroprotectant

23. MAP Calculation • BP 240/135 • MAP = 1/3 SBP + 2/3 DBP • One third systolic = 80 • Two thirds diastolic = 90 • MAP = 170 mm Hg

24. ED Patient BP Management • BP 240/135 • MAP = 170 mm Hg • 25% reduction?? • MAP = 130 mm Hg • BP 180/105

25. Key Clinical Question • How should this hypertensive emergency be managed in the setting of this stroke syndrome in order to minimize the risk of hemorrhage and to maximize the chance for a good outcome for this patient?

26. Clinical Questions • Are hypertensive urgency and emergencies as well as the need to treat ED patients defined mostly by the severity of end organ illness manifested by the patient as opposed to the actual BP value?

27. Clinical Questions • Is the amount of desired blood pressure reduction based on the initial BP value, the end organ involved, the severity of illness, complication risk, or the apparent response to therapy that the ED patient manifests during the therapy? • What is that amount?

28. Clinical Questions • Is there a consensus in the ED community on an optimum value or range of BP values at which therapy can be terminated because of success in reaching a therapeutic endpoint? • Who determines this consensus?

29. Clinical Questions • What is this optimal endpoint in the treatment of hypertensive blood pressure management, and is it based upon Systolic BP, Diastolic BP, Mean Arterial BP, or some end organ function? • Why?

30. Clinical Questions • Does this optimal therapeutic endpoint need to be modified based on the type of stroke syndrome such as acute ischemic stroke as compared to intracerebral hemorrhage or subarachnoid hemorrhage?

31. Clinical Questions • Does this optimal therapeutic endpoint need to be modified based on specific other end organ involvement, such as acute renal failure or acute myocardial infarction?

32. Clinical Questions • What are the optimal medication therapies available to manage the blood pressure of the patient with a hypertensive emergency? • Is there a “best choice” therapy? • Why?

33. Clinical Questions • What drugs do you most commonly use to treat ED patients with hypertensive emergencies as well as those who have a concomitant stroke syndrome?

34. Clinical Questions • Do you use esmolol? • Do you use labetalol? • Do you use nitrogycerine? • Do you use sodium nitroprusside? • How? Why?

35. Clinical Questions • Do you use nicardipine? • Do you use hydralazine? • Do you use enalaprilat? • Do you use fenoldopam? • Do you use phentolamine? • How? Why?

36. Clinical Questions • Do you use oral agents? • Do you unit dose for IVP agents? • Do you avoid continuous infusion Rx? • Do you mix agents? • How? Why?

37. Clinical Questions • Is there an optimal time course for treatment of elevated blood pressure? • If yes, can this standard be implemented in all comprehensive Emergency Departments, or should it be achieved optimally in the intensive care unit?

38. Clinical Questions • Is there a specific perspective of the treating nurse regarding what we do and how we can improve the process and patient outcomes?

39. Clinical Questions • How are we recording these changing Vitals and Blood Pressures that are automatically generated? • Are they a part of the RN or MD electronic medical record? • Can they be retrieved retrospectively?

40. Clinical Questions • Should patients with hypertensive emergencies be treated in the EMS setting? • How?

41. Clinical Questions • What published guidelines should be studied by all EMS and ED emergency care providers because of their broad scope and proven clinical relevance and applicability to successful hypertension management, enhanced reperfusion and neuroprotection, and correlation to improved clinical outcome?

42. Clinical Questions • What are the medico-legal implications of the ED management of patients with hypertensive emergencies and those with concomitant stroke syndromes?

43. Clinical Questions • Are there any as of yet not discussed or resolved issues? • Is there any other important information to discuss?

44. Conclusions • Medicine is an art, not a science • Vice versa is also true • We conduct clinical trials every day • Therapeutic trials, N = 1 • We observe and converge towards a unified approach without knowing it • This session assists in the process

45. Questions? www.FERNE.org edsloan@uic.edu 312 413 7490 ferne_ema_2007_htn_emergencies_panel_sloan_cases_panel_092407_finalcd 10/1/2014 6:01 AM

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