HypertensionHypertension

Resting BP consistently Resting BP consistently

>140 mmHg systolic or >140 mmHg systolic or

>90 mmHg diastolic>90 mmHg diastolic

EpidemiologyEpidemiology

20% of adult population20% of adult population• ~~35,000,000 people35,000,000 people

25% do not know they are hypertensive25% do not know they are hypertensive Twice as frequent in blacks than in Twice as frequent in blacks than in

whiteswhites 25% of whites and 50% of blacks > 65 25% of whites and 50% of blacks > 65

y/oy/o

TypesTypes

Primary (essential) hypertensionPrimary (essential) hypertension Secondary hypertensionSecondary hypertension

Primary HypertensionPrimary Hypertension

85 - 90% of hypertensives85 - 90% of hypertensives IdiopathicIdiopathic More common in blacks or with positive More common in blacks or with positive

family historyfamily history Worsened by increased sodium intake, Worsened by increased sodium intake,

stress, obesity, oral contraceptive use, or stress, obesity, oral contraceptive use, or tobacco usetobacco use

Cannot be curedCannot be cured

Secondary HypertensionSecondary Hypertension

10 - 15% of hypertensives10 - 15% of hypertensives Increased BP secondary to another Increased BP secondary to another

disease processdisease process

Secondary HypertensionSecondary Hypertension

Causes: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

Small number curable with surgerySmall number curable with surgery

Hypertension PathologyHypertension Pathology

Increased BP Increased BP inflammation, sclerosis inflammation, sclerosis of arteriolar walls of arteriolar walls narrowing of vessels narrowing of vessels decreased blood flow to major organs decreased blood flow to major organs

Left ventricular overwork Left ventricular overwork hypertrophy, CHFhypertrophy, CHF

Nephrosclerosis Nephrosclerosis renal insufficiency, renal insufficiency, failurefailure

Hypertension PathologyHypertension Pathology

Coronary atherosclerosis Coronary atherosclerosis AMI AMI Cerebral atherosclerosis Cerebral atherosclerosis CVA CVA Aortic atherosclerosis Aortic atherosclerosis Aortic Aortic

aneurysmaneurysm Retinal hemorrhage Retinal hemorrhage Blindness Blindness

Signs/SymptomsSigns/Symptoms

Primary hypertension is Primary hypertension is asymptomaticasymptomatic until complications developuntil complications develop

Signs/Symptoms are Signs/Symptoms are non-specificnon-specific• Result from target organ involvementResult from target organ involvement

Dizziness, flushed face, headache, fatigue, Dizziness, flushed face, headache, fatigue, epistaxis, nervousness are epistaxis, nervousness are notnot caused by caused by uncomplicated hypertension.uncomplicated hypertension.

HTN Medical ManagementHTN Medical Management

Life style modificationLife style modification• Weight lossWeight loss• Increased aerobic activityIncreased aerobic activity• Reduced sodium intakeReduced sodium intake• Stop smokingStop smoking• Limit alcohol intakeLimit alcohol intake

HTN Medical ManagementHTN Medical Management

MedicationsMedications• DiureticsDiuretics• Beta blockersBeta blockers• Calcium antagonistsCalcium antagonists• Angiotensin converting enzyme Angiotensin converting enzyme

inhibitorsinhibitors• Alpha blockersAlpha blockers

HTN Medical ManagementHTN Medical Management

Medical management prevents or Medical management prevents or forestalls all complicationsforestalls all complications

Patients Patients mustmust remain on drug remain on drug therapy to control BPtherapy to control BP

Categories of HypertensionCategories of Hypertension Hypertensive Emergency (Crisis)Hypertensive Emergency (Crisis)

• acute acute BP with sx/sx of end-organ injury BP with sx/sx of end-organ injury Hypertensive UrgencyHypertensive Urgency

• sustained DBP > 115 mm Hg w/o evidence of sustained DBP > 115 mm Hg w/o evidence of end-organ injuryend-organ injury

Mild HypertensionMild Hypertension• DBP > 90 but < 115 mm Hg w/o symptomsDBP > 90 but < 115 mm Hg w/o symptoms

Transient HypertensionTransient Hypertension• elevated due to an unrelated underlying elevated due to an unrelated underlying

conditioncondition

Hypertensive CrisisHypertensive Crisis

Acute life-threatening increase Acute life-threatening increase in BPin BP

Usually exceeds 200/130 mmHgUsually exceeds 200/130 mmHg

Hypertensive EmergencyHypertensive Emergency

Severe hypertension associated with end Severe hypertension associated with end organ damageorgan damage• Malignant hypertension (htn with retinal Malignant hypertension (htn with retinal

hemorrhages, exudates or papilledema, hemorrhages, exudates or papilledema, also renal involvement)also renal involvement)

• Hypertensive encephalopathyHypertensive encephalopathy• Subarachnoid/Intracerebral hemorrhageSubarachnoid/Intracerebral hemorrhage• Acute pulmonary edemaAcute pulmonary edema• Dissecting aneurysmDissecting aneurysm• AnginaAngina

Hypertensive Urgency Hypertensive Urgency

Diastolic bp equal to or above 130 Diastolic bp equal to or above 130 mm Hg mm Hg

No signs of end organ damageNo signs of end organ damage

When you are called..When you are called..

Ask about mental status changes, Ask about mental status changes, chest painchest pain

Obtain all vital signsObtain all vital signs Determine the reason for admissionDetermine the reason for admission Ask about the patient’s blood Ask about the patient’s blood

pressure over the last 24 hourspressure over the last 24 hours

When you get to the bedsideWhen you get to the bedside

Measure the bp again in BOTH ARMSMeasure the bp again in BOTH ARMS jvd, thyromegaly, fundoscopic examjvd, thyromegaly, fundoscopic exam New cardiac murmer, S3, S4, tachycardiaNew cardiac murmer, S3, S4, tachycardia Renal or aortic bruitsRenal or aortic bruits Edema to the extremitiesEdema to the extremities Brief mental status exam, gross motor exam Brief mental status exam, gross motor exam

If you determine this to be a If you determine this to be a hypertensive urgency…hypertensive urgency…

There is no evidence of end organ There is no evidence of end organ damagedamage

There is NO PROVEN BENEFIT to There is NO PROVEN BENEFIT to rapid reduction in bp in rapid reduction in bp in asymptomatic patients.asymptomatic patients.

Aggressive antihypertensive therapy Aggressive antihypertensive therapy can induce cerebral or myocardial can induce cerebral or myocardial ischemiaischemia

If you determine this to be a If you determine this to be a hypertensive urgency…hypertensive urgency…

Your goal is to get the patient to Your goal is to get the patient to around 160/110 mmHg over several around 160/110 mmHg over several hours with conventional oral therapyhours with conventional oral therapy

Labs…Labs…

Lytes, BUN/CRLytes, BUN/CR Cardiac enzymes if pt has angina/chfCardiac enzymes if pt has angina/chf CXR if indicated if pt in angina/chfCXR if indicated if pt in angina/chf EKG if indicated if pt has angina/chfEKG if indicated if pt has angina/chf CT head if signs of encephalopathyCT head if signs of encephalopathy

CausesCauses Sudden withdrawal of anti-hypertensivesSudden withdrawal of anti-hypertensives Increased salt intakeIncreased salt intake Abnormal renal functionAbnormal renal function Increase in sympathetic toneIncrease in sympathetic tone

• StressStress• DrugsDrugs

Drug interactionsDrug interactions• Monoamine oxidase inhibitorsMonoamine oxidase inhibitors

Toxemia of pregnancyToxemia of pregnancy PheochromocytomaPheochromocytoma

Signs/SymptomsSigns/Symptoms

Restlessness, Restlessness, confusion, AMSconfusion, AMS

Vision disturbancesVision disturbances Severe headacheSevere headache Nausea, vomitingNausea, vomiting

SeizuresSeizures Focal neurologic Focal neurologic

deficitsdeficits Chest painChest pain DyspneaDyspnea Pulmonary edemaPulmonary edema

Hypertensive Crisis Can CauseHypertensive Crisis Can Cause

CHFCHF Pulmonary edemaPulmonary edema Angina pectorisAngina pectoris AMIAMI Aortic dissectionAortic dissection

Hypertensive Emergencies Stroke

Encephalopathy

Decompensated Heart Failure

Acute Renal Failure

Acute Coronary Syndrome

Aortic Dissection

Hypertensive Crisis ManagementHypertensive Crisis Management Immediate goal: lower BP in controlled fashionImmediate goal: lower BP in controlled fashion

• No more than 30% No more than 30% in first 30-60 mins in first 30-60 mins• Not appropriate in all settingsNot appropriate in all settings

OxygenOxygen Monitor ECGMonitor ECG Drug TherapyDrug Therapy

• Targeted at simply lowering BP, Targeted at simply lowering BP, OROR• Targeted at underlying causeTargeted at underlying cause

Drug Therapy PossibilitiesDrug Therapy Possibilities Sodium NitroprussideSodium Nitroprusside

• Potent arterial and venous vasodilatorPotent arterial and venous vasodilator– Vasodilation begins in 1 to 2 minutesVasodilation begins in 1 to 2 minutes

• 0.5 0.5 g/kg/min by continuous infusion, titrate to g/kg/min by continuous infusion, titrate to effecteffect

– increase in increments of 0.5 increase in increments of 0.5 g/kg/min g/kg/min

– 50 mg in 250 cc D50 mg in 250 cc D55WW

– Effects easily reversible by stopping dripEffects easily reversible by stopping drip– Continuous hemodynamic monitoring requiredContinuous hemodynamic monitoring required– Cover IV bag/tubing to avoid exposure to lightCover IV bag/tubing to avoid exposure to light

• Used primarily when targeting lower BP onlyUsed primarily when targeting lower BP only

Drug Therapy PossibilitiesDrug Therapy Possibilities NitroglycerinNitroglycerin

• VasodilatorVasodilator• Nitropaste simplest methodNitropaste simplest method

– 1 to 2 inches of ointment q 8 hrs1 to 2 inches of ointment q 8 hrs

– easy to control effect but slow onseteasy to control effect but slow onset

• Sublingual NTG is faster routeSublingual NTG is faster route– 0.4 mg SL tab or spray q 5 mins0.4 mg SL tab or spray q 5 mins

– easy to control but short actingeasy to control but short acting

• NTG infusion, 10 - 20 mcg/minNTG infusion, 10 - 20 mcg/min– seldom used for hypertensive crisisseldom used for hypertensive crisis

• Commonly used prehospital when targeting BP Commonly used prehospital when targeting BP lowering only especially in AMIlowering only especially in AMI

Drug Therapy PossibilitiesDrug Therapy Possibilities NifedipineNifedipine

• Calcium channel blockerCalcium channel blocker– Peripheral vasodilatorPeripheral vasodilator

• 10 mg Sublingual10 mg Sublingual– Split capsule longitudinally and place contents under Split capsule longitudinally and place contents under

tongue or puncture capsule with needle and have patient tongue or puncture capsule with needle and have patient chewchew

• Used less frequently today! Frequently in past!Used less frequently today! Frequently in past!– Concern for rapid reduction of BP resulting in organ Concern for rapid reduction of BP resulting in organ

ischemia ischemia

Drug Therapy PossibilitiesDrug Therapy Possibilities FurosemideFurosemide

• Loop DiureticLoop Diuretic– initially acts as peripheral vasodilatorinitially acts as peripheral vasodilator– later actions associated with diuresislater 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 LVFmost useful in acute episode with CHF or LVF

• Often used with other agents such as NTGOften used with other agents such as NTG

Drug Therapy PossibilitiesDrug Therapy Possibilities HydrazalineHydrazaline

• Direct smooth muscle relaxantDirect smooth muscle relaxant– relax arterial smooth muscle > venousrelax arterial smooth muscle > venous

• 10-20 mg slow IV q 4-6 hrs; initial dose 5 mg 10-20 mg slow IV q 4-6 hrs; initial dose 5 mg for pre-eclampsia/eclampsiafor pre-eclampsia/eclampsia

• Usually combined with other agents such as Usually combined with other agents such as beta blockersbeta blockers

– concern for reflex sympathetic tone increaseconcern for reflex sympathetic tone increase

• Most useful in pre-eclampsia and eclampsia Most useful in pre-eclampsia and eclampsia

Drug Therapy PossibilitiesDrug Therapy Possibilities Metoprolol, orMetoprolol, or

Labetalol Labetalol • decrease in heart rate and contractilitydecrease in heart rate and contractility• DoseDose

– Metoprolol: 5 mg slow IV q 5 mins to total ~15 mgMetoprolol: 5 mg slow IV q 5 mins to total ~15 mg– Labetalol: 10-20 mg slow IV q 10 minsLabetalol: 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 minimal concern for use in asthma and obstructive airway

diseasedisease

• Labetalol: both alpha & beta blockadeLabetalol: both alpha & beta blockade• Most useful in AMI and Unstable angina Most useful in AMI and Unstable angina

Hypertensive EmergencyHypertensive Emergency EnalaprilEnalapril

• IV prep of ACE Inhibitor IV prep of ACE Inhibitor • Response is variable (probably b/c these pts Response is variable (probably b/c these pts

have variable plasm renin activity)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

Hypertensive Crisis ManagementHypertensive Crisis Management

Avoid crashing BP to hypotensive Avoid crashing BP to hypotensive or normotensive levels!or normotensive levels!

Ischemia of vital organs may Ischemia of vital organs may result!result!

Hypertensive Crisis ManagementHypertensive Crisis Management

Must assure underlying cause of Must assure underlying cause of BP is BP is understoodunderstood

•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 What patients may have HTN as a compensatory mechanism?compensatory mechanism?