1. HYPERTENSIVE EMERGENCIES Trevor Langhan PGY-2 September 2, 2004

2. CASE 67 y male Known small cell lung CA, prev CVA, DM, COPD, chronic steroids. Admitted to CCU one month ago with ACS Today was at TBCC getting CT scan for malignancy staging Brought directly by wife after acute c/o SOB and mild chest pain

3. CASE BP 190/100, HR 140, RR 33, sats 81% r/a Working hard to breathe, mottled skin, diaphoretic Doesn’t want to lay down for EKG, IV pokes Swollen legs R > L Portable CXR RUL consolidation ?collapse Increased vascular markings bilaterally

4. CASE Further Hx: Received 2 units PRBC 3 days prior Chemotherapy yesterday with large volume load Volume of fluid IV with contrast for CT Known LV dysfunction from prev echo Documented LEVEL II care in chart (NO intub) Clinical exam:  accessory muscle use  elevated JVP  inspiratory/expiratory wheezes bilat  minimal air entry

5. CASE (our management) Unable to get IV access Couple/three NTG SL sprays ABG - 7.09/61/98/30 Move to code room Femoral langhan – i mean line

6. CASE (our management) Started on BIPAP Medications: IV NTG  5 ug/min to maximum 100 ug/min (we went to 200 ug/min and he improved)  Mechanism: venous and mild arteriolar dilator IV Lasix  40 mg x 2  Any better than oral?

7. CASE (our management) We chose venous and arteriolar vasodilatation + lasix labetalol – decrease cardiac contractility COPD Known previous bronchospasm Hydralazine – increase cardiac work, causes alpha blockade

8. Pulmonary edema Pts with CHF usually have increased PVR Acute elevations in their BP may be secondary to hypoxia and subsequent catecholamine release Aggressive treatment of the pulmonary edema will help decrease the BP Nitrates Morphine Lasix Oxygen

9. Hypertension HTN will present to the ED in a variety of ways: 1. Hypertensive crisis/emergency 2. Hypertensive urgency 3. Mild hypertension without EOD 4. Transient hypertension

10. Hypertensive Emergency Severely elevated blood pressure with signs of acute damage to target organs Brain, eyes, heart, kidneys

11. Hypertensive Emergency Conditions defined by Rosen’s as HE: Malignant hypertension  Hypertensive encephalopathy  Microangiopathic hemolytic anemia  Acute renal failure Aortic dissection Eclampsia/preeclampsia Severe HTN in setting of:  MI  Left ventricular failure  Bleeding  Thrombolytic therapy

12. Hypertensive Urgency Situation where blood pressure elevation is an imminent risk for target- organ damage No acute end organ damage but risk is high if BP elevation continues Relative increase in BP more important than specific numbers

13. Brief pathophysiology Mild to moderate increase in BP leads to initial vasoconstriction “autoregulation” Maintains perfusion at relatively stable level Prevents increased pressure from being transmitted downstream to smaller vessels As BP further increases, autoregulation fails Elevated BP disrupts vasc endothelium, causing narrowing

14. Brief pathophysiology Chronic increase in BP causes arteriolar hypertrophy Will decrease the amount of pressure passed on to more distal vessels Chronically hypertense people need diastolic BP’s >130 for symptoms Normotensive people can have hypertensive crisis at DBP > 100

15. Case 2 45 y male c/o 12 hour history of SOBOE, mild chest heaviness Vomiting, drowsy Bi-frontal headache Blurred vision both eyes BP 240/150, HR 102, RR 16, sats 95%

16. Case 2 PMHx: ? HTN, was on a “water pill” many years ago. No DM, no CAD, generally healthy Labs normal, except Creat: 150 DDx? Mgnt?

17. Case 2 Goal of therapy is to reduce MAP by 25% in the first hour Keeping DBP > 110 mmHg Reduction to pt’s relative normal BP by 4-6 hours is more long term goal What agents? Nitroprusside - 0.25-0.5 ug/kg/min, up to 10 ug/kg/min, titratable, easy off, potential toxicity labetalol – infusion 0.5-2 mg/min, or bolus 20 mg then 20-80 mg q 10 minutes (up to 300mg), alpha and beta blocker

18. Hypertensive Encephalopathy Cerebral edema by breakthrough hyper-perfusion from severe and sudden increase BP BP has exceeded the capacity of autoregulation Elevated BP in vessels that can’t accommodate the pressure – leakage and edema Autoregulation must be considered during treatment I.e. Hypertrophied vessels can’t vasodilate, so caution with lowering blood pressure to avoid a relative hypoperfusion and resultant ischemia

19. Hypertensive Encephalopathy HE is a true medical emergency Is an acute presentation, but reversible Progression of untreated cerebral edema leads to coma and death Admission and invasive BP monitoring is the recommended mainstay of therapy

20. Case 3 67 y female known CAD, DM, smoker, atrial fib. Presents with c/o weakness left side BP 160/100, HR 94, RR 14, sats 99% O/E left facial droop, markedly weak left upper/lower extremity EKG a fib, nil acute Chest exam unremarkable

21. Case 3 Management? How do you treat her elevated BP?

22. Stroke syndromes Most patients with this presentation are ischemic strokes (85%) not hemorrhagic Likely don’t have acutely elevated BP ***caution*** with lowering BP as Watershed area sensitive to hypoperfusion Lowering BP may worsen ischemic brain injury

23. Stroke syndromes Rarely may see stoke with grossly elevated DBP > 140 Pts receiving reperfusion therapy may require BP reduction, as BP > 185/110 is contraindication to tPA What do you think about nitroprusside here? Titrate labetalol diligently in 5 mg increments to achieve slow decrease in MAP by a max of 20%

24. Case 4 32 y female awaiting “sweatgland” surgery from plastics for hyperhydrosis, c/o H/A, palpitations BP 170/90, HR 150 sinus, RR 18 Otherwise healthy Treatment: Nitroprusside if emergency Phentolamine – 1-5 mg IV boluses (alpha-block)  Followed by beta-blockade

25. Case 4 Pheochromocytoma Rare tumor – 0.2% of pts with essential HTN Episodic H/A, tachycardia, sweating, HTN Tumor secreting norepinephrine and epinephrine Diagnosis radiographic, measurement of urinary and plasma levels of catecholamines and metabolites

26. Case 5 25 y G2P1, LMP 6 months ago When do you treat HTN in pregnancy? DBP > 110 SBP > 160 Treat to goal of 140-155 and 90-105 What agents? Hydralazine (older agent of choice) Labetalol (preferred modality now)

27. Case 6 33 year male stock broker. Snorted a “couple of rails” of cocaine ½ hour ago. Presents with crushing retrosternal chest pain, diaphoresis and H/A BP 190/100, HR 130, RR 28, sats 96% EKG ST segment elevation V1-V3 Nurse asks “what do you want to give?”

28. Case 6 Give MONA You order IV metoprolol to be hung Before the Beta blocker, any concerns? Beta antagonism will decrease heart rate, but will also block B2 receptors Will have unopposed alpha agonism by cocaine toxicity – dangerous HTN crisis Need alpha blockade first Like pheo can use phentolamine, some sources say hydralazine

29. Case 7 55 year male smoker, HTN, DM, unstable angina getting worse. Shoveling snow and developed left RSCP that radiated to his jaw. HR 120, BP 190/90, RR 19, sats 99% EKG obvious ant/lateral infarct How do you treat his pressure?

30. Case 7 Agents of choice in HTN during ACS Immediate lowering of BP indicated to prevent myocardial damage Also lower BP if pt to undergo reperfusion tx  NTG agent of choice  Beta block  ACE-I (shown improvement in mortality)  CCB (if BB is contraindicated) Anything that’s contraindicated? Hydralazine – reflex tachycardia Nitroprusside – reflex tachycardia

31. Hypertension What is normal BP?  SBP < 140  DBP < 90 What is hypertension?  SBP >160  DBP >100 Anything in between GRAY.

32. Hypertension Possible cardiovascular causes of increased BP: Loss of vessel elasticity with age Coarctation of aorta  Delayed femoral pulses  Hypertensive upper extremities  Bruit in upper back

33. Hypertension Endocrine causes for elevated BP: Pheo Excess steroids  Often iatrogenic  Cushings Look for hypokalemia Volume overload from Na retention

34. Hypertension Other causes include: Withdrawal of sedative drugs  EtOH, benzo Tyramine toxicity in MAO-I patients Aortic dissection Sympathomimmetic drug intoxication Withdrawal of clonidine or beta blocking agents Reno-vascular disease Renin-angiotensin system abnormality

35. drugdoseonsetdurationindicationContra-indication nitroprusside 0.3-10 ug/kg/min 1-2 min Any hypertensive emergency Pregnancy Prolong use Renal failure nitroglycerin 10-100 ug/kg/min 2-5 min 3-5 minAMI, CHF hydralazine 5 mg 5-10mg q20min 10-20 min 3-8 hpregnancyAMI, aortic dissection esmolol 500ug/kg then 50-300 ug/kg/min 1-2 min 10-20 minCAD, aortic dissection CHF, heart block, asthma, catecholamine excess labetalol 20mg then 20-80 q10 min to max 300 OR 1-2 mg/min 2-10 min 2-4 hCAD, aortic dissection, eclampsia, hypertensive crisis CHF, heart block, asthma, catecholamine excess phentolamine 5 mg q 1-2 min 1-2 min 10-30 minCatecholamine excess AMI Drug choices

36. Key concepts Presence of acute target organ damage determines HTN crisis All pts with persistent elevation of BP should be investigated of EOD ER doc should be familiar with indications and contraindications of meds to treat HTN crisis Goal of treat is relative decrease in MAP of 25% in first hour, DBP should not fall <110 mmHg Pts without EOD rarely require urgent management of HTN and should be referred for outpt pharmacotherapy adjustments