Hypertensive Emergencies

1. Hypertensive Emergencies Ingrid Berling 29/09/2010

2. Aims • Epidemiology/pathophysiology • Definitions/common types • Clinical evaluation • Goals of treatment • Pharmacotherapy • Specific treatment

3. Epidemiology • Prevalence of hypertension in Australia is 11% • An estimated 30% of hypertensive patients are undiagnosed • 29% of diagnosed patients are inadequately controlled • Hypertensive crisis are uncommon, about 1-2% of the hypertensive population

4. Pathophysiology

5. Pathophysiology • It is hypothesized that the final common pathway is a sudden increase in systemic vascular resistance (SVR)  an increase in BP due to the action of circulating vasoconstrictors • The ↑ BP damages the endothelium, leading to the release of local vasoconstrictors, such as endothelin, which cause further vasoconstriction • Damage to the endothelium impairs auto-regulatory function. • Further release of humoral vasoconstrictors perpetuates the “vicious circle.”

6. Hypertension JNC-VII, 2003; • Normal: <120 over <80 • Pre-hypertension: 120-139 over 80-89 • Stage I: 140-159 over 90-99 • Stage II: >160 over ≥ 100-109 • Stage III: >180 over >110 JOINT NATIONAL COMMITTEE ON PREVENTION, DETECTION, EVALUATION AND TREATMENT OF HIGH BLOOD PRESSURE 1997/ 2003

7. Definitions A Hypertensive Emergency exists when acute elevation of blood pressure is associated with acute and ongoing organ damage to the kidneys, brain, heart, eyes or vascular system • Does not specifically include BP levels, but • Systolic >240mmHg • Diastolic > 120 - 140mmHg REQUIRES IMMEDIATE BLOOD PRESSURE REDUCTION

8. Definitions A Hypertensive Urgency exists when there is acute or chronic blood pressure elevation not associated with any observable acute organ damage This can be hard to distinguish on clinical evaluation alone. BP control over hours to days

9. Most Common Presentations • CVS • Acute MI • Acute LVF • Aortic dissection • CNS • Hypertensive encephalopathy • Stroke: Ischaemic, cerebral bleed, SAH • RENAL • Glomerulonephritis • Collagen vascular disease • PREGNANCY • Pre-eclampsia and Eclampsia • ENDOCRINE • Phaeochromocytoma crisis • thyrotoxicosis • PERIOPERATIVE • Coronary Bypass • Carotid endarterectomy • AAA stenting • Excess catecholamines • Phaeochromocytoma • withdrawal of anti-hypertensives • Toxicological • Interaction: MOAIs • Ingestions: Cocaine, cold medications • Glucocorticoid therapy

11. Clinical Evaluation Hypertensive emergencies, look like EMERGENCIES. Therefore your approach is going to be simultaneous resuscitation and information gathering.

12. History • Cardiovascular • Chest pain/syncope • Back pain • Dyspnoea • Neurological • Seizures/altered MS • Focal weakness • Headache/visual disturbance • Renal • Decreased UO • Bloody or frothy urine • Non-specific abdominal pain • General • Malaise MI, unstable Angina, dissection Dissection Pulmonary Oedema, CHF Encephalopathy CVA/TIA Central nervous system compromise

13. Examination • BP in both arms • Fundoscopy examination • Cardiovascular examination • Neurological examination

14. Retinopathy HTN Retinopathy (Keith-Wagner) • Grade I • Mild arteriolar narrowing and sclerosis • Grade II • Definite focal narrowing and AV nicking • Moderate to marked sclerosis of the arterioles • Grade III • Retinal haemorrhages, exudates and cotton wool spots • Grade IV • Severe grade III and papilledema

15. Investigations • FBC; schistocytes • Electrolytes; Urea/creat • Urinalysis; proteins • B-hCG • CXR • ECG • Head CT • ? Urine drug screen

16. Goals of Treatment Within 1-2 hrs. Lower MAP 20-25% Controlled environment Use IV titratible meds MAP = 1/3 SBP + 2/3 DBP

17. WHY?  Auto-regulation • Maintains blood flow to vital organs, despite variations in systemic BP • Classically maintained between MAP 60-120mmHg • However, in chronically hypertensive patients the curve is shifted to the right • The average lower limit of auto-regulation is about 20-25% below the resting MAP. Lancet, Hypertensive Emergencies, 2000; 356(9227):411-417

18. Treatment • ↓ CO: inhibit contractility or decrease filling pressure • ↓ filling pressure: Act on venous tone or blood volume • ↓ PVR: relax smooth muscle of resistance vessels or interfere with systems that produce constriction (SNS)

19. Pharmacotherapy Vasodilators Adrenergic Inhibitors α+β BLOCKER Labetolol β BLOCKER Esmolol NITRATES • Sodium nitroprusside (SNP) • Nitroglcerin CALCIUM CHANNEL BLOCKERS • Nicardipine ACE INHIBITOR • Enlaprilat ARTERIAL VASODILATOR • Hydralazine DOPAMINERGIC RECEPTOR AGONIST • Fenoldopam

20. Vasodilators

21. Adrenergic Inhibitors

22. Clonidine • α2 agonist-centrally acting • Results in a reduction in sympathetic outflow from the CNS • The decrease in plasma norepinephrine is correlated directly with the hypotensive effect

23. Specific situations….

24. Ischaemic Stroke • Reduction of BP is at the risk of causing hypo-perfusion of the peri-ischaemic area, resulting in an extension of the stroke. • However, high BP can cause haemorrhagic transformation of infarct • A Cochrane review examining 65 RCTs with 11,500 pts. Concluded that insufficient data exists to evaluate BP lowering post-stroke • AHA guidelines: BP be reduced only if SBP>220 or DBP>120mmHg. (unless end-organ damage is due to BP) • Labetalol and nitroprusside are agents of choice. • Thrombolysis  BP<185/110. (increased risk intracranial bleeding)

25. Haemorrhagic Stroke • No strong evidence for blood pressure management in intracerebral haemorrhage. In trials, nil adverse events from BP reduction of less than 20% • Guidelines: decrease when MAP>130 or SBP>220. • Labetalol and esmolol agents of choice. • DO NOT use nitrates as they theoretically increase ICP

26. SAH • Nimodipine decreases vasospasm that occurs due to chemical irritation of arteries by blood. • Not recommended routinely due to high incidence of hypotension. • Guidelines suggest SBP< 160 MAP <110 • Labetalol and esmolol agents of choice.

27. Myocardial Ischaemia • The aim is to reduce myocardial work and promote coronary blood flow, thus reducing ischaemia. • IV GTN agent of choice • (β-Blockers) • Avoid hydralazine, as it increases myocardial oxygen demand.

28. Acute LV Failure • Usually associated with pulmonary oedema and diastolic/systolic dysfunction. • Titrate until BP controlled and signs of heart failure alleviated. • IV nitroprusside and GTN agents of choice.

29. Hypertensive Encephalopathy • Symptoms: • Mental status change – somnolence, confusion, lethargy, stupor, coma, seizure • Headache – • Nausea and vomiting • Hypertensive encephalopathy is a diagnosis of exclusion – thus, exclude the other possibilities! • Only definitive criteria is a favourable response to BP reduction. • However clinical improvement may lag behind BP improvement by hours to days • Agent of choice – SNIP or labetalol

30. Aortic Dissection • Worsening of the dissection dependent on: • Level of elevated BP • Slope of the pulse wave. This increases the “shear force” on the dissection, leading to propagation of the dissection • Goal is to reduce both the BP and the slope of the pulse wave! • BP goal is SBP of 100-120 • If patient presents with normal BP, still need to decrease the shear forces!! • Labetalol • IV SNIP + B-blocker!! • Do not use alone, as vasodilation causes reflex activation of SNS leading to enhanced ventricular contraction and increased aortic shear stress Do not use hydralazine, increased shear stress

31. Catecholamine excess • Labetalol traditional agent of choice, but experimental studies not positive for use. • Nicardipine (or phentolamine in older texts) choice agent • β-blocker - May be added to control tachycardia • Not for use as sole agent – as may result in β-receptor antagonism and unopposed α adrenergic activity - ↑BP • Benzodiazepines - May be helpful in cocaine/amphetamine

32. Hypertensive encephalopathy Embolic CVA Hemorrhagic CVA SAH Nitroprusside, goal ~25 reduction Only if >220/120 or>185/110 for t-PA Labetalol for ~10-20% reduction Nimodipine 60 mg Q4hrs x 21 days Summary – Neurologic emergencies

33. Aortic dissection Acute LV failure Acute coronary syndrome Nitroprusside + Esmolol or Labetalol – SBP ~100 NTG, Lasix, MS04 for symptoms and ~10-15% reduction NTG, MgS04, beta-blocker for symptom improvement Summary – Cardiovascular emergency

34. Eclampsia and HELLP Catecholamine excess Goal DBP ~90; magnesium, hydralazine, labetalol, delivery! labetololfor ~25% reduction over several hours Summary – Other emergencies

35. Scenarios 3 quick questions

36. 1. In which of the following would a SBP of 100-120 be appropriate? • A. Aortic dissection • B. Thrombo-embolic CVA • C. Hemorrhagic CVA • D. Subarachnoid hemorrhage • E. Hypertensive encephalopathy

37. A. Aortic dissection In all the other scenarios, such a precipitous drop in BP is likely to worsen outcome

38. 2. Which emergency – medication is LEAST appropriate? • A. Aortic dissection – esmolol + SNIP • B. Aortic dissection – labetalol • C. Eclampsia – magnesium +/- hydralazine • D. Pheochromocytoma – esmolol • E. Acute LV failure - NTG

39. D. Pheochromocytoma - esmolol Although use of Labetalol is controversial and possibly indicated, a pure beta-blocker like esmolol is grossly inappropriate in emergencies caused by catecholamine excess.

40. 3. All the following regarding CVAs are true EXCEPT: • A. Persistent BP >185/110 is a contraindication to thrombolytics • B. Hemorrhagic CVAs tend to have higher BP than embolic • C. Lowering the BP in the acute setting may worsen outcome • D. If BP needs lowering in hemorrhagic CVA, SNIP is the agent of choice

41. D. If BP needs lowering in hemorrhagic CVA, Nipride is the agent of choice Nipride and other vasodilators are relatively contraindicated in hemorrhagic CVA as they may worsen ICP. Labetalol is the agent of choice IF BP needs to be lowered

42. References • 1. Hoshide, S., et al., Hemodynamic cerebral infarction triggered by excessive blood pressure reduction in hypertensive emergencies. Journal of the American Geriatrics Society, 1998. 46(9): p. 1179-80. • 2. Kitiyakara, C. and N.J. Guzman, Malignant hypertension and hypertensive emergencies. Journal of the American Society of Nephrology, 1998. 9(1): p. 133-42. • 3. Epstein, M., Diagnosis and management of hypertensive emergencies. Clinical Cornerstone, 1999. 2(1): p. 41-54. • 4. Kriegisteiner, S., et al., Hypertensive emergencies. Lancet, 2000. 356(9239): p. 1443. • 5. Mansoor, G.A. and W.H. Frishman, Comprehensive management of hypertensive emergencies and urgencies. Heart Disease, 2002. 4(6): p. 358-71. • 6. Vaughan, C.J. and N. Delanty, Hypertensive emergencies. Lancet, 2000. 356(9227): p. 411-7.