Hypertensive Emergencies

1. Hypertensive Emergencies Dr. Herb Russell Prepared by Anthony G. Hillier, D.O. September 2005

2. Why this is a difficult topic • Hypertension is common (up to 25%) but emergencies are rare • Failing to treat an emergency AND treating a non-emergency can have serious consequences for the patient • Blood pressure alone is a poor indicator of an emergency

3. Why this is a difficult topic • The physical exam is often not helpful • Different emergencies have vastly different goals in BP reduction • The first line agent for one emergency may be contraindicated for another emergency • Lack of consensus regarding definitions, therapeutic goals, and 1st line medications

4. Definitions • Hypertensive Emergency: A relatively high blood pressure with evidence of target organ damage. • Hypertensive Urgency: Elevated BP with imminent risk of target organ damage

5. Acute Hypertensive Episode: SBP >180 or DBP >110 and no target organ damage Transient Hypertension: Hypertension that occurs in association with Pain Withdrawal syndromes Some toxic substances Anxiety Cessation of medications Definitions

6. History History of HTN Blood pressure trends Prescribed medications OTC medications Review of systems directed at: CNS (HA, hemiparesis) Cardiac (CP, dyspnea) Compliance Past medical history Family history Illicit drug use Renal (hematuria) ED Evaluation

7. ED Evaluation • Physical Exam • Appropriate sized cuff • Measure arms and legs • Brachial difference <20mm Hg • Focus on areas of potential target-organ damage -CNS -Heart -Retina -Pulmonary -Pulses -Renal

8. Cotton wool spot (soft exudates)

9. Cotton wool spots

10. Hard exudates

11. Retinal Hemorrhage

12. Disk Edema

13. Diagnostic Studies • CBC-hemolytic anemia • Glucose-hypoglycemia • Electrolytes-hyperkalemia • BUN/Cr-azotemia, ARF • Urine-proteinuria, RBC cast • CXR-Pulmonary edema, aortic dissection • ECG-ischemia, infarction pattern • Head CT-hemorrhage, infarction

14. Schistocytes

15. What precipitates an emergency? • Non-compliance with medications in a chronic hypertensive patient • Those with secondary hypertension (e.g. pheochromocytoma, reno-vascular hypertension, Cushing’s) • Hypertension during pregnancy is a major risk factor for women

16. General Management Goals • Reduce BP so autoregulation can be re-established • Typically, this is a ~25% reduction in MAP • Or, reduce MAP to 110-115 • Avoid • Lowering the BP too much or too fast. • Treating non-emergent hypertension

17. General Management Goals • Exceptions: aortic dissection and eclampsia • In aortic dissection and eclampsia, BP should be lowered to normal levels • Search for secondary causes

18. Pharmacology-Nitroprusside • Dose: 0.3-10 mcg/kg/min • Actions: Equally rapid decrease of both preload and afterload • Indications: All hypertensive emergencies including post-partum eclamplsia • Half-life: 3-4 minutes • Metabolism: Liver

19. Pharmacology-Nitroprusside • Excretion: Kidney • Adverse Effects: • Cyanide toxicity with prolonged use (rare) • Inhibits hypoxia induced pulmonary vasoconstriction • Coronary steal syndrome • Increased ICP • Contraindications: • Other cyclic GMP inhibitors (i.e. sildenafil)

20. Pharmacology-Labetalol • Dose: Bolus of 20mg IV, double bolus up to 80 mg, or infusion of 2mg/min to maximum total of 300mg • Actions: Selective α1 and nonselective β–blocker 4-8 times that of α-blockade. • Indications: Hypertensive emergencies, including those from catecholamine stimulation and PIH. Does not decrease cerebral or coronary blood flow.

21. Pharmacology-Labetalol • Onset: 5-10 min • Half-life: 5.5 hrs • Metabolism: Hepatic • Adverse Effects: • May exacerbate CHF and induce bronchospasm • In low doses, may have a paradoxical increase in BP when used in catecholamine excess

22. Pharmacology-Esmolol • Dose: Loading dose of 500mcg/kg over 1 min, the infusion of 50-300mcg/kg/min • Actions: Ultra-short acting β1-selective adrenergic blocker • Indications: Used in conjunction with nitroprusside or phentolamine for hypertensive emergencies

23. Pharmacology-Esmolol • Onset: Less than 5 mins • Half-life: 9mins • Metabolism: Erythrocytes • Adverse Effects: • May induce bronchospasm • Avoid as sole agent in catecholamine excess

24. Pharmacology-Nitroglycerin • Dose: Infusion rate 5-10mcg/min, titrate up 10mcg every 5 mins • Actions: Greater preload reduction than afterload, until high rates, then equal • Indications: Agent of choice for moderate hypertension complicating unstable angina, MI or pulmonary edema

25. Pharmacology-Nitroglycerin • Onset: Immediate • Half-life: 4 mins • Metabolism: Hepatic • Adverse Effects: HA, tachycardia, hypotension • Contraindications: • Other cyclic GMP inhibitors (i.e. sildenafil)

26. Pharmacology-Hydralazine • Dose: 10-20 mg, repeated in 30 mins • Actions: Direct arteriolar dilator • Indications: PIH, pre-eclampsia • Onset: 10 mins • Half-life: 2-4 hrs • Metabolism: Liver acetylation • Excreted: Urine

27. Pharmacology-Hydralazine • Adverse Effects: • Decrease dose in renal insufficiency • High incidence of hypotension in “slow acetylators” • Reflex tachycardia • Should not be used in aortic dissection and Coronary artery disease • Lethargy

28. Pharmacology-Enalaprilat • Dose: 0.625-1.25mg IV bolus • Actions: Afterload reduction with lowered MAP, PCWP and increased coronary vasodilatation • Indications: Hypertensive emergencies • Onset: Within minutes • Metabolism: None

29. Pharmacology-Enalaprilat • Excreted: Urine • Adverse Effects: • Angioedema • Cough • Worsening renal function • Hyperkalemia

30. Pharmacology-Others • Trimethaphan-ganglionic blocking agent • Fenoldopam-dopaminergic receptor agonist • Nicardipine-dihydropyridine calcium channel blocker • Urapidil-peripheral a1-receptor blocker and a central 5-HT1A-receptor agonist

31. Categories of Hypertensive Emergencies • Hypertensive encephalopathy • Stroke syndromes • Embolic • Hemorrhagic • Subarachnoid hemorrhage

32. Categories of Hypertensive Emergencies • Cardiovascular • Acute LV failure (“Flash” pulmonary edema) • Acute coronary syndrome • Aortic dissection • Pregnancy related hypertension • Pre-eclampsia • Eclampsia • HELLP syndrome

33. Categories • Catecholamine excess • Pheochromocytoma • MAOI + tyramine • Cocaine/amphetamines/OTCs • Clonidine withdrawal • Other • Renal failure • Epistaxis • Childhood hypertension

34. Hypertensive Encephalopathy • Symptoms: • Mental status change – somnolence, confusion, lethargy, stupor, coma, seizure • Focal neurologic deficit • Headache – alone not sufficient to diagnose a hypertensive encephalopathy • Nausea and vomiting • Signs: • Papilledema, cotton wool exudates

35. Diagnostics • Hypertensive encephalopathy is a diagnosis of exclusion – thus, exclude the other possibilities! • Only definitive criteria is a favorable response to BP reduction. However clinical improvement may lag behind BP improvement by hours to days

36. Pathophysiology • A loss of cerebral autoregulation. • Autoregulation is best studied in the brain but present in heart and kidneys as well • Represents the body’s attempt to maintain constant FLOW of blood to perfuse the cells

37. Autoregulation • In the uninjured, normotensive brain, autoregulation is effective over MAP ranging from about 50 – 150 • In the chronic hypertensive, this range is increased (e.g. 80 – 180)

38. Autoregulation

39. Pathophysiology • Loss of autoregulation leads to: • Cerebral hyper-perfusion • Vascular permeability • Cerebral edema • Vasospasm • Ischemia • Punctuate hemorrhages

40. Therapy • Untreated, hypertensive encephalopathy leads to coma and death • Goal is to reduce MAP by 20-25% in the first hour • This will get MAP back into range where autoregulation is re-instituted

41. Therapy • Nitroprusside • 1st line, 0.3 – 10 mcg/kg/minute • Labetalol • Enalaprilat • Fenoldopam

42. Stroke Syndromes

43. Thrombo-Embolic CVA • Represent 85% of all strokes • BP elevations are generally mild-moderate and represent a physiologic response to maintain cerebral perfusion pressure to the penumbra, which has lost its ability to autoregulate

44. Embolic CVA - Dilemma • Inappropriate lowering of the BP may convert the potentially salvageable ischemic penumbra to true infarction. • However, persistent BP >185/110 is a contraindication to thrombolytic therapy (it significantly increases risk of intra-cranial bleeding)

45. Embolic CVA –When to Rx HTN • For thrombolytic candidates, 1-2 doses of labetalol (5mg) or nitroglycerin paste may be used in attempt to get BP <185/110 • If thrombolytics are given, then the BP MUST be aggressively kept below 185/110!

46. Embolic CVA – When to Rx HTN • According to National Institutes of Neurologic Disorders and Stroke: • SBP <220, no treatment • DBP <120, no treatment • Tintinalli suggests not treating DBP <140 • Others use MAP <130

47. Embolic CVA – When to RX • If complicated by: • Aortic dissection • Hypertensive encephalopathy • AMI • Renal failure

48. Embolic CVA –How to Rx HTN • Goal is to reduce MAP 10-20% in uncomplicated embolic CVA with markedly elevated pressures • Labetalol: 5mg doses • Nitroglycerin paste

49. Why not treat everybody? • Danger of being too aggressive in acute CVA is well documented. • Many studies show a worsening of neurologic outcome when the above guidelines are not followed.

50. Hemorrhagic CVA • Unlike embolic CVA, BP elevations in hemorrhagic CVA are profound • However, this again represents a physiologic response to increased intracranial pressure (and free blood irritating the autonomic nervous system) • Typically is transient