Managing Hypertensive Emergencies: Challenges and Strategies

1. Hypertensive Emergencies H. Haghani Nejad, MD cardiologist Fellowship of echocardiography, Afshar cardiovascular medical & research center

2. Why this is a difficult topic • Hypertension is common (up to 25%) but emergencies are rare <1% • 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(accelerated malignant HTN): 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 Prescribed medications OTC medications Review of systems directed at: CNS (HA, hemiparesis) Cardiac (CP, dyspnea) Compliance Past medical history Family history 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. Hypertensive retinopathy • Grade1 :silver wring • Grade 2: nipping of the venuls at arteriovenous (AV ) crossing • Grade 3: flame-shape retinal hemorrhage and soft cotton-wool exudates • Grade 4: swelling of the optic disc( papilledema) and hard exudate

9. Cotton wool spot (soft exudates)

10. Retinal Hemorrhage

11. Hard exudates

12. Disk Edema

13. Diagnostic Studies • CBC-hemolytic anemia • 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([2x diastole] + systole/ 3) • 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) • 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(.25-.5 mg/kg), or infusion of 2-4 mg/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: 3-6 hrs • Metabolism: Hepatic • Adverse Effects: • May exacerbate CHF and induce bronchospasm

22. Pharmacology-Esmolol • Dose: Loading dose of 0.5-1 mg/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: 1-2 mins • Half-life: 10-30 mins • Metabolism: Erythrocytes • Adverse Effects: • May induce bronchospasm • Avoid as sole agent in catecholamine excess

24. Pharmacology-Nitroglycerin • Dose: Infusion rate 5-200mcg/min, titrate up 5mcg 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: 1-2 mins • Metabolism: Hepatic • Adverse Effects: HA, tachycardia, hypotension • Contraindications: • Other cyclic GMP inhibitors (i.e. sildenafil)

26. Pharmacology-Enalaprilat • Dose: 1.25-5mg IV bolus • Actions: Afterload reduction with lowered MAP, PCWP and increased coronary vasodilatation • Indications: Hypertensive emergencies • Onset: Within minutes • Metabolism: None

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

28. Pharmacology-Others • Trimethaphan-ganglionic blocking agent • Fenoldopam-dopaminergic receptor agonist 0.1-0.6 mic/kg/min • Nicardipine-dihydropyridine calcium channel blocker 5-15 mg/h inf • Lasix 20-40mg iv in 1-2 min

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

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

31. Categories • Catecholamine excess • Pheochromocytoma • MAOI + tyramine • Cocaine/amphetamines/OTCs • Rebound htn(Clonidine withdrawal) • renal • Acute GN • Severe HTN after kidny trasplantation

32. categories • SURGICAL postoperative HTN postoperative bliding from suture line severe HTN in pat,s requiring immediate surgery SEVERE BODY BURN SEVERE EPISTAXIS TTP

33. Hypertensive Encephalopathy • Symptoms: • Mental status change – somnolence, confusion, lethargy, stupor, coma, seizure • Headache – alone not sufficient to diagnose a hypertensive encephalopathy • Nausea and vomiting • Signs: • cotton wool exudates,retinal hemorrhage Papilledema, (accelerated malignant HTN)

34. 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

35. 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

36. Autoregulation • In the uninjured, normotensive brain, autoregulation is effective over MAP ranging from about 60 – 120 • In the chronic hypertensive, this range is increased (e.g. 110 – 180)

37. Autoregulation

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

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

40. Therapy • Labetalol • Nitroprusside • nicardipine

41. Stroke Syndromes

42. 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

43. Embolic CVA - Dilemma • Inappropriate lowering of the BP may convert the potentially salvageable ischemic penumbra to true infarction. • However, persistent BP >180/110 is a contraindication to thrombolytic therapy (it significantly increases risk of intra-cranial bleeding)

44. 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!

45. Embolic CVA – When to Rx HTN • According to National Institutes of Neurologic Disorders and Stroke: • SBP <220, no treatment • DBP <120, no treatment

46. Embolic CVA –How to Rx HTN • Goal is to reduce MAP 15% in 1 hour in uncomplicated embolic CVA with markedly elevated pressures • Labetalol • Nitroprusside • nicardipine

47. 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.

48. 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

49. Hemorrhagic CVA – When to Rx • In 1 hour : • SBP< 180 mmHg • MAP< 130 mmHg

50. Hemorrhagic CVA - Rx • Labetalol is agent of choice • Nitroprusside • Nicardipine • Vasodilators such as nitroglycerin is contraindicated because they may raise the ICP