1. Hypertension Resting BP consistently >140 mmHg systolic or >90 mmHg diastolic

2. Epidemiology n 20% of adult population ~ 35,000,000 people~ 35,000,000 people n 25% do not know they are hypertensive n Twice as frequent in blacks than in whites n 25% of whites and 50% of blacks > 65 y/o

3. Types n Primary (essential) hypertension n Secondary hypertension

4. Primary Hypertension n 85 - 90% of hypertensives n Idiopathic n More common in blacks or with positive family history n Worsened by increased sodium intake, stress, obesity, oral contraceptive use, or tobacco use n Cannot be cured

5. Secondary Hypertension n 10 - 15% of hypertensives n Increased BP secondary to another disease process

6. Secondary Hypertension n Causes: Renal vascular or parenchymal diseaseRenal vascular or parenchymal disease Adrenal gland diseaseAdrenal gland disease Thyroid gland diseaseThyroid gland disease Aortic coarctationAortic coarctation Neurological disordersNeurological disorders n Small number curable with surgery

7. Hypertension Pathology n Increased BP  inflammation, sclerosis of arteriolar walls  narrowing of vessels  decreased blood flow to major organs n Left ventricular overwork  hypertrophy, CHF n Nephrosclerosis  renal insufficiency, failure

8. Hypertension Pathology n Coronary atherosclerosis  AMI n Cerebral atherosclerosis  CVA n Aortic atherosclerosis  Aortic aneurysm n Retinal hemorrhage  Blindness

9. Signs/Symptoms n Primary hypertension is asymptomatic until complications develop n Signs/Symptoms are non-specific Result from target organ involvementResult from target organ involvement n Dizziness, flushed face, headache, fatigue, epistaxis, nervousness are not caused by uncomplicated hypertension.

10. HTN Medical Management n Life style modification Weight lossWeight loss Increased aerobic activityIncreased aerobic activity Reduced sodium intakeReduced sodium intake Stop smokingStop smoking Limit alcohol intakeLimit alcohol intake

11. HTN Medical Management n Medications DiureticsDiuretics Beta blockersBeta blockers Calcium antagonistsCalcium antagonists Angiotensin converting enzyme inhibitorsAngiotensin converting enzyme inhibitors Alpha blockersAlpha blockers

12. HTN Medical Management Medical management prevents or forestalls all complications Patients must remain on drug therapy to control BP

13. Categories of Hypertension n Hypertensive Emergency (Crisis) acute  BP with sx/sx of end-organ injuryacute  BP with sx/sx of end-organ injury n Hypertensive Urgency sustained DBP > 115 mm Hg w/o evidence of end-organ injurysustained DBP > 115 mm Hg w/o evidence of end-organ injury n Mild Hypertension DBP > 90 but 90 but < 115 mm Hg w/o symptoms n Transient Hypertension elevated due to an unrelated underlying conditionelevated due to an unrelated underlying condition

14. Hypertensive Crisis Acute life-threatening increase in BP Usually exceeds 200/130 mmHg

15. Hypertensive Emergency n Severe hypertension associated with end organ damage Malignant hypertension (htn with retinal hemorrhages, exudates or papilledema, also renal involvement)Malignant hypertension (htn with retinal hemorrhages, exudates or papilledema, also renal involvement) Hypertensive encephalopathyHypertensive encephalopathy Subarachnoid/Intracerebral hemorrhageSubarachnoid/Intracerebral hemorrhage Acute pulmonary edemaAcute pulmonary edema Dissecting aneurysmDissecting aneurysm AnginaAngina

16. Hypertensive Urgency n Diastolic bp equal to or above 130 mm Hg n No signs of end organ damage

17. When you are called.. n Ask about mental status changes, chest pain n Obtain all vital signs n Determine the reason for admission n Ask about the patient’s blood pressure over the last 24 hours

18. When you get to the bedside n Measure the bp again in BOTH ARMS n jvd, thyromegaly, fundoscopic exam n New cardiac murmer, S3, S4, tachycardia n Renal or aortic bruits n Edema to the extremities n Brief mental status exam, gross motor exam

19. If you determine this to be a hypertensive urgency… n There is no evidence of end organ damage n There is NO PROVEN BENEFIT to rapid reduction in bp in asymptomatic patients. n Aggressive antihypertensive therapy can induce cerebral or myocardial ischemia

20. If you determine this to be a hypertensive urgency… n Your goal is to get the patient to around 160/110 mmHg over several hours with conventional oral therapy

21. Labs… n Lytes, BUN/CR n Cardiac enzymes if pt has angina/chf n CXR if indicated if pt in angina/chf n EKG if indicated if pt has angina/chf n CT head if signs of encephalopathy

22. Causes n Sudden withdrawal of anti-hypertensives n Increased salt intake n Abnormal renal function n Increase in sympathetic tone StressStress DrugsDrugs n Drug interactions Monoamine oxidase inhibitorsMonoamine oxidase inhibitors n Toxemia of pregnancy n Pheochromocytoma

23. Signs/Symptoms n Restlessness, confusion, AMS n Vision disturbances n Severe headache n Nausea, vomiting n Seizures n Focal neurologic deficits n Chest pain n Dyspnea n Pulmonary edema

24. Hypertensive Crisis Can Cause n CHF n Pulmonary edema n Angina pectoris n AMI n Aortic dissection

25. Hypertensive Emergencies Stroke Encephalopathy Decompensated Heart Failure Acute Renal Failure Acute Coronary Syndrome Aortic Dissection

26. Hypertensive Crisis Management n Immediate goal: lower BP in controlled fashion No more than 30%  in first 30-60 minsNo more than 30%  in first 30-60 mins Not appropriate in all settingsNot appropriate in all settings n Oxygen n Monitor ECG n Drug Therapy Targeted at simply lowering BP, ORTargeted at simply lowering BP, OR Targeted at underlying causeTargeted at underlying cause

27. Drug Therapy Possibilities n Sodium Nitroprusside Potent arterial and venous vasodilatorPotent arterial and venous vasodilator –Vasodilation begins in 1 to 2 minutes 0.5  g/kg/min by continuous infusion, titrate to effect0.5  g/kg/min by continuous infusion, titrate to effect –increase in increments of 0.5  g/kg/min –50 mg in 250 cc D 5 W –Effects easily reversible by stopping drip –Continuous hemodynamic monitoring required –Cover IV bag/tubing to avoid exposure to light Used primarily when targeting lower BP onlyUsed primarily when targeting lower BP only

28. Drug Therapy Possibilities n Nitroglycerin VasodilatorVasodilator Nitropaste simplest methodNitropaste simplest method –1 to 2 inches of ointment q 8 hrs –easy to control effect but slow onset Sublingual NTG is faster routeSublingual NTG is faster route –0.4 mg SL tab or spray q 5 mins –easy to control but short acting NTG infusion, 10 - 20 mcg/minNTG infusion, 10 - 20 mcg/min –seldom used for hypertensive crisis Commonly used prehospital when targeting BP lowering only especially in AMICommonly used prehospital when targeting BP lowering only especially in AMI

29. Drug Therapy Possibilities n Nifedipine Calcium channel blockerCalcium channel blocker –Peripheral vasodilator 10 mg Sublingual10 mg Sublingual –Split capsule longitudinally and place contents under tongue or puncture capsule with needle and have patient chew Used less frequently today! Frequently in past!Used less frequently today! Frequently in past! –Concern for rapid reduction of BP resulting in organ ischemia

30. Drug Therapy Possibilities n Furosemide Loop DiureticLoop Diuretic –initially acts as peripheral vasodilator –later actions associated with diuresis 40 mg slow IV or 2X daily dose40 mg slow IV or 2X daily dose –most useful in acute episode with CHF or LVF Often used with other agents such as NTGOften used with other agents such as NTG

31. Drug Therapy Possibilities n Hydrazaline Direct smooth muscle relaxantDirect smooth muscle relaxant –relax arterial smooth muscle > venous 10-20 mg slow IV q 4-6 hrs; initial dose 5 mg for pre-eclampsia/eclampsia10-20 mg slow IV q 4-6 hrs; initial dose 5 mg for pre-eclampsia/eclampsia Usually combined with other agents such as beta blockersUsually combined with other agents such as beta blockers –concern for reflex sympathetic tone increase Most useful in pre-eclampsia and eclampsiaMost useful in pre-eclampsia and eclampsia

32. Drug Therapy Possibilities n Metoprolol, or Labetalol decrease in heart rate and contractilitydecrease in heart rate and contractility DoseDose –Metoprolol: 5 mg slow IV q 5 mins to total ~15 mg –Labetalol: 10-20 mg slow IV q 10 mins Metoprolol is selective beta-1Metoprolol is selective beta-1 –minimal concern for use in asthma and obstructive airway disease Labetalol: both alpha & beta blockadeLabetalol: both alpha & beta blockade Most useful in AMI and Unstable anginaMost useful in AMI and Unstable angina

33. Hypertensive Emergency n Enalapril IV prep of ACE InhibitorIV prep of ACE Inhibitor Response is variable (probably b/c these pts have variable plasm renin activity)Response is variable (probably b/c these pts have variable plasm renin activity) Contraindicated in pregnancyContraindicated in pregnancy Start at 1.25 mg iv and up to 5 mg iv q 6 hrsStart at 1.25 mg iv and up to 5 mg iv q 6 hrs Onset of action: 15 minutes, peak effect 4 hrsOnset of action: 15 minutes, peak effect 4 hrs Duration of action: 12-24 hoursDuration of action: 12-24 hours

34. Hypertensive Crisis Management Avoid crashing BP to hypotensive or normotensive levels! Ischemia of vital organs may result!

35. Hypertensive Crisis Management n Must assure underlying cause of  BP is understood HTN may be helpful to the patientHTN may be helpful to the patient Aggressive treatment of HTN may be harmfulAggressive treatment of HTN may be harmful What patients may have HTN as a compensatory mechanism?