3/26/2013

1

David M. Schneider, MDAssociate Clinical Professor of Family & Community Medicine, UCSFFull-Time Faculty Physician, Santa Rosa Family Medicine Residency

Faculty Disclosure� Nothing to disclose.

HTN: Scope of the Problem—Prevalence� Most common reason for office visits in non-pregnant

pts in US.� ~ 30% of adults >18 y.o.� 58-65 million hypertensive adults in US.� Hypertension on the rise:� Obesity epidemic.� Elderly (>1/2 of pts >65 – systolic or systolic + diastolic).

Prevalence – 2� African-Americans >45 y.o.:� 35% of women.� ~40% of men >45 y.o.

� European Americans >45 y.o.:� 15% of women.� 25% of men.

�Worldwide: 1 billion.

3/26/2013

2

Scope of the Problem – Control

•We’re finally making some progress.•More than half of hypertensive pts still uncontrolled.•Another study showed 44% of men & 55% of women w/HTN have adequate control.

NHANES data 1988-91 1991-94 1999-2000 2005-06Aware of HTN 73 68.4 70 78Treated for HTN

55 53.6 59 68

HTN controlled 29 27.4 34 43.5

ArchIntMed 2002;162(4):413-20; JAMA 2003;289(19):2560-71; AmJMed 2006;119(1):42-9; http://www.cdc.gov/nchs/data/databriefs/db03.pdf

Making the Diagnosis of HTN� 2 or more “properly measured” readings at each of 2 or

more visits after an initial screen. � Elevation of either SBP (>139) or DBP (>89) or both. � If SBP and DBP fall into different categories, the higher

value is used.� For adults who are not acutely ill and not on HTN

meds.� Confirm elevated BP in contralateral arm.� No caffeine, exercise, or smoking for ≥ 30 min before

measurement.� Sitting quietly X ≥ 5 min, feet on floor.

AnnIntMed 2007;147:783-6; http://www.uptodate.com/contents/technique-of-blood-pressure-measurement-in-the-diagnosis-of-hypertension?source=search_result&selectedTitle=5~150

Classification of BP in Adults

•Treat pre-HTN only if compelling indication (DM, CAD, CKD, etc).•Goal in pre-HTN w/o compelling indication = reduce BP to normal range, & prevent progressive incr in BP, w/lifestyle modification.

BP Classification SBP DBPNormal < 120 AND < 80Prehypertension 120 – 139 OR 80 – 89Stage 1 HTN 140 – 159 OR 90 – 99Stage 2 HTN ≥ 160 OR ≥ 100

JNC 7—2003

BP Changes & CV Risk� In people aged 40 – 70, and from BP range 115/75 –

185/115:� For every increase of 20 mm Hg in SBP, OR 10 mm Hg in

DBP, there is a doubling (2-fold) of the risk for cardiovascular disease.� Pre-HTN doubles risk vs normal.� Stage 1 doubles risk vs pre-HTN � 4-fold > normal.� Stage 2 doubles risk vs stage 1 � 8-fold > normal.

� Treatment goal for pts w/HTN and no compelling indications: < 140/90.

JNC 7—2003

3/26/2013

3

Target BP Goals� General population: < 140/90.� Diabetes: < 130/80.� Chronic kidney disease: < 130/80.� Elderly: same goals as anybody else.� N.B.—From JNC-7:� “Impressive evidence has accumulated to warrant greater

attention to the importance of SBP as a major risk factor for CVDs.”� “DBP is a more potent cardiovascular risk factor than SBP

until age 50; thereafter SBP is more important.”JNC 7—2003

Why We Work-up HTN� 3 objectives:� Assess lifestyle & identify other cardiovascular risk

factors or coexisting disorders that may affect prognosis & guide treatment.� Reveal identifiable causes of HTN.� Assess presence of target organ damage & cardiovascular

disease.

JNC 7

Target Organ Damage� Heart:� CAD—angina, MI, h/o revascularization.� Heart failure.� LVH.

� Brain:� Stroke, TIA.� Dementia.

� Kidney: chronic kidney disease.� GFR is a better indicator than serum Cr.

� Eye: retinopathy.� Vascular: peripheral arterial disease.

JNC 7

Mnemonic: Target Organ Damage“Heart, BrainExtremity PainKidneys FailVision wanes”� (Extremity pain � PAD)

� Any musical genre

3/26/2013

4

Mnemonic: CV Risk Factors� Per JNC-7:� Age—65 F (or premature menopause), 55 M� BP (HTN)� Cigarettes (smoking)� DM� Exercise lack (physical inactivity)� FH—65 F, 55 M� Good cholesterol too low (HDL-C <40)� High LDL-C� Kidney dz (microalbuminuria, GFR < 60)� Obesity (BMI > 30)

Diagnostic Workup of HTN� Assess risk factors and comorbidities.� Reveal identifiable causes of hypertension.� Assess presence of target organ damage.

� Conduct history and physical examination.� Remember BP in both arms.

JNC 7

Diagnostic Workup of HTN – 2� Laboratory tests:� UA� Hematocrit� Lipid panel� Blood chemistry tests:� Blood glucose� Serum potassium, creatinine, and calcium� Optional (unless DM or CKD): urinary

albumin/creatinine ratio. � Obtain electrocardiogram

JNC 7

Why Should We Treat HTN?� DASH diet has been shown to reduce CAD & stroke.� Pharmacologic treatment of HTN has been shown to

reduce cardiovascular events (NNT to prevent 1 death = 11; NNT = 9 if CAD or target organ damage).� In unselected population, outcomes are improved

regardless of drug regimen.� More intensive BP lowering leads to more favorable

outcomes (↓ stroke & major CV events) – regardless of regimen (for the most part—ACEI + CCB may be more beneficial per one study).

Lancet 2003;362(9395):1527-35; ArchIntMed 2008; 168:713-720; ArchIntMed 1993;153:578-81; JACC 1996;27:1214-18; Lancet 2010;375:1173-81

3/26/2013

5

The Whole EnchiladaAlgorithm for Tx of HTN—1

Algorithm—2a Algorithm—2b

3/26/2013

6

Algorithm—3

JNC 7

3 Simple Steps to HTN Tx1. Lifestyle—everybody!2. Compelling indication?

a. Yes � use appropriate med.b. No:

i. Stage 1� 1 drugii. Stage 2� 2 drugs

3. Increase or add.

Non-Pharmacologic Therapy for HTNModification Recommendation ~ SBP Reduction

Weight reduction Maintain Nl body wt (BMI 18.5 – 24.9)

5 – 20 mm/10kg wt loss

DASH diet Fruits, veges, lowfat dairy, low saturated & total fat

8 – 14 mm

Dietary Na restriction Max 2.4 g Na = 6 g NaCl 2 – 8 mm

Physical activity Regular aerobic activity, ≥30 min/day, most days

4 – 9 mm

Moderate ETOH (vs higher intake)

Max 2/day in men, 1/day in women or lighter persons

2 – 4 mm

JNC 7

Pharmacologic Therapy of HTN� Monotherapy will control 30-50% of pts.� Majority of pts require ≥ 2 meds for control.� The average hypertensive pt is on 2-3 meds (depending

on study).� Vast majority of hypertensives w/diabetes will require 2

or more meds.� Key points to consider:� How high is the BP?� Other conditions or risk factors?� Target organ damage?

http://www.uptodate.com/contents/choice-of-therapy-in-essential-hypertension-recommendations?source=related_link

3/26/2013

7

Choosing a Medication� ABCD’s:� ACE inhibitors & ARB’s.� Beta blockers.� Calcium channel blockers.� Diuretics.

� Other “forgotten” meds:� Aldosterone receptor antagonists.� Central sympatholytics.� Alpha blockers.� Direct vasodilators.� Loop diuretics (better for CKD).

Diuretics (Thiazides)� Usually the first choice antihypertensive agent.� If pt is on a med from a different class, thiazides are

usually the top choice for the 2nd med to add.� Reduce morbidity & mortality from CAD.� “Virtually unsurpassed in preventing the

cardiovascular complications of HTN.” – JNC 7� Inexpensive.� “Despite the various benefits of diuretics, they remain

underutilized.” – JNC 7

Diuretics in CKD� In pts with chronic kidney disease (CKD), use loop

diuretic if estimated GFR is below ~ 30 (thiazides less effective). � Exception is metolazone (Zaroxolyn). � In these pts, consider loop diuretic (furosemide,

bumetanide, torsemide, etc)

Diuretic Adverse Effects� Increased electrolyte excretion:� Hypokalemia (average ↓ of 0.3-0.4 mmol/L; dietary Na

restriction can minimize thiazide-induced K loss).� Hypomagnesemia.� Hyponatremia.

� Sexual dysfunction in men.

JAMA 2003;289(19):2560-71; JAMA 2002;288(23):2981-97

3/26/2013

8

Diuretic Adverse Effects – 2� Hyperglycemia – but not contraindicated in DM.� Minimal increase in glc w/low dose thiazides (3-5 mg/dl). � Proven beneficial outcomes in DM.

� Hyperlipidemia� Little effect at 12.5 mg HCTZ.� May be temporary (< 1 yr).� Proven beneficial outcomes – ↓ risk of CV events.

� Hyperuricemia – ↑ gout risk, though frank gout is less common.� Hypercalcemia.

Commonly Used Thiazide Diuretics� HCTZ 12.5 – 25 mg.� Chlorthalidone 12.5 mg.� 1.5 – 2 times as strong as HCTZ (i.e., 12.5 mg

chlorthalidone ≈ 25 mg HCTZ).� May have longer duration of action & may be more

effective.� Many outcomes studies done w/this drug.

Thiazide Contraindications� Drug allergy.� RARE crossover w/sulfa

� Anything else (gout, hypoK, h/o arrhythmia, etc) is a caution, not absolute contraindication.

� Negative effect on erectile function.� Reduce excretion of lithium� risk of toxicity.

Angiotensin Converting Enzyme Inhibitors� Preferred med in:� CHF� DM 1 & 2� CAD� High risk for CAD� Nephropathy

3/26/2013

9

ACEI Adverse Effects� Dry cough (5 – 20%).� Reduced GFR (consider D/C med & w/u for RAS if

>30% reduction).� More common in renovascular HTN, CHF, polycystic

kidney disease, or CKD.� Hyperkalemia (3.3 – 11%).� More common in: renal failure, DM, use of other K-

sparing drug (K-sparing diuretic, NSAID), elderly.� Hypotension, dizziness, syncope.� More likely in CHF, volume depletion (diuretics).

AnnIntMed 1992;117(3):234-42; ArchIM 1998;158(1):26-32; http://www.uptodate.com/contents/major-side-effects-of-angiotensin-converting-enzyme-inhibitors-and-angiotensin-ii-receptor-blockers?source=search_result&selectedTitle=1~150

Oddball ACEI Side Effects� Angioedema (rare).� Swelling of lips, tongue, mouth, face.� May be more common in African-Americans (2-4-

fold more common), possibly in elderly.� Skin rash (a possibility with just about any med).� Dysgeusia (taste disturbance) – esp captopril.� Neutropenia (rarer).� Bonus effect: may reduce glc & HbA1C in DM!

AmJHTN 1993;6(5 Pt 1):337-43; AnnIntMed 1992;117(3):234-42

Angiotensin Receptor Blockers� “ACE inhibitors without the cough.”� Similar efficacy to ACEI’s (both are slightly less potent

antihypertensives than other agents like thiazides, CCB’s).� Similar side effect profile to ACEI’s.� Lower incidence of cough (rare, but it happens).� Most pts w/ACEI-induced cough tolerate ARB’s.� ~ 1/3 the (already rare) incidence of angioedema.� More hypotension than ACEI’s (~2X).

NEJM 2008;358:1547-59; AnnPharmacother 2003;37:1024-7; http://www.uptodate.com/contents/major-side-effects-of-angiotensin-converting-enzyme-inhibitors-and-angiotensin-ii-receptor-blockers?source=search_result&selectedTitle=2~150

What if Creatinine Rises?� Renal dysfunction associated with antihypertensive

treatment is independent of the agent used (but more common w/ACEI & ARB).� <30% ↑ in creatinine, which then stabilizes, represents a

hemodynamic change, and not a structural change.� Slight rise in Cr �IG pressure has been reduced.� ACE-I/ARB also dilate efferent arteriole, exaggerating decline

in IG pressure.� If Cr ↑ > 30%, agent should be discontinued and other

causes of renal dysfunction should be evaluated (esp RAS).

NEJM 2002;347(16):1256-61

3/26/2013

10

Beta Blockers� Not usually a 1st choice any more unless a compelling

or other indication:� Post-MI (non-intrinsic sympathomimetic)� CHF� CAD—control of angina� Rate control in A fib

EurHeartJ 2007;28:1462-536; Circulation 2008;117:2706-15; Circulation 2008;117:2691-705; http://www.uptodate.com/contents/choice-of-therapy-in-essential-hypertension-

recommendations?source=search_result&selectedTitle=1~150

Beta Blockers – 2� Still useful:� Resting tachycardia.� LVH.� Migraine.� Essential tremor (non-cardioselective).

� Labetolol – alpha + beta blocker� Hypertensive emergencies.� Pregnancy – preexisting HTN or pre-eclampsia

(unlabeled).

β-Blocker Adverse Effects� AV block.� Bronchospasm.� Increased PAD symptoms.� CHF exacerbation if given in acute stage.� CNS – overstated, but probably more common in

elderly.� Fatigue – NNH = 57.� Depression – no significant increase.

� Sexual dysfunction – NNH = 199.http://www.uptodate.com/contents/choice-of-therapy-in-essential-hypertension-

recommendations?source=search_result&selectedTitle=1~150; http://www.uptodate.com/contents/major-side-effects-of-beta-blockers?source=search_result&selectedTitle=1~150

β-Blocker Adverse Effects – 2� May increase stroke or overall mortality, esp > age 60.� Impaired glc tolerance; ↑ risk of new onset diabetes.� Vasodilating β-blockers like carvedilol appear OK.� Effect may be temporary.� Still given to post-MI diabetics.

� Adverse lipid effects (labetolol may be least likely).

3/26/2013

11

ß-blocker Contraindications� Active bronchospasm� Severe bradycardia� Heart block > 1° (if no pacemaker)� Pulmonary edema� Hypotension with or without shock� Overt heart failure should be brought under medical

control 1st� Most pts w/MI d/t cocaine should not be treated with

beta blockers (risk of coronary artery spasm)http://www.uptodate.com/contents/major-side-effects-of-beta-

blockers?source=search_result&search=beta+blocker+contraindications&selectedTitle=1~150; http://www.uptodate.com/contents/use-of-beta-blockers-in-heart-failure-due-to-systolic-

dysfunction?source=search_result&search=beta+blocker+contraindications&selectedTitle=2~150

Common/Significant Drug Interactions With ß-BlockersDrug Effects Recommendation Amiodarone Cardiac arrest Extreme cautionAntidiabetic agents HTN, [poss ↓ glc] Monitor Rate-sparing CCB (diltiazem, verapamil)

Brady, CHF, hypotension

Avoid (few clinical issues, however)

Digoxin Worsening bradycardia

Monitor. OK in angina + low EF (? benefit)

Epinephrine, sympathomimetics

HTN crisis Avoid if possible

Lidocaine ↑ lido level ↓ lido dose (NOT listed in ACLS protocol)

Calcium Channel Blockers (CCB)� Dihydropyridines: use long acting meds.� Amlodipine� Felodipine

� Non-dihydropyridines:� Diltiazem� Verapamil

� Avoid short acting dihydropyridines.� Nifedipine (this is often an incorrect answer, esp if

another CCB option).

CCB Candidates� African-Americans.� Elderly.� Angina, incl Prinzmetal’s (amlodipine, felodipine).

� ?↑ CV complications in DM?:� Small studies suggested ? incr MI in DM (2° outcome).� Mult large studies (incl ALLHAT) found no adverse CV

effects.

NEJM 1998;338:645-52; Lancet 1998;351:1755-62; CurrHTNRes 1999;1:225-31; NEJM 1999;340:677-84; JAMA 2002;288:2981-97; AmJMed 2004;116:44-9

3/26/2013

12

CCB Adverse Effects� Edema� More likely w/DHP’s

� Dizziness� HA� BUT: Verapamil may be used in migraine prophylaxis.

� Reflex tachycardia – DHP’s� Non-DHP (verapamil, diltiazem) SE’s:� Bradycardia� AV block� CHF exacerbation

CCB ComparisonDrug Periph

ResisHR Conduction Contractility

DHP’s ↓↓↓ ↑ +/- +/-Diltiazem ↓↓ ↓ ↓ ↓Verapamil ↓ ↓↓ ↓↓ ↓↓

•DHP’s � more peripheral effects.•Non-DHP’s � more cardiac effects.

Alpha-Adrenergic Blockers� Prazosin, terazosin, doxazosin.� Orthostatic hypotension & syncope, esp 1st dose.� Not usually used in initial monotherapy, except

sometimes in men w/BPH, esp if low-mod CV risk.� More CV events & CHF than thiazide—but there was no

control (untreated) group.� May enhance hypotensive effects of PDE-5 drugs for

erectile dysfunction (sildenafil, vardenafil, tadalafil).� Tadalafil (Cialis) not recommended, or 48 h after α1 blocker.� Allow 24h after last sildenafil (Viagra) or vardenafil (Levitra)

dose.

AnnIntMed 2002;137:313-20; JAMA 2000;283:1967-75

Central Sympatholytic Agents� Clonidine� Dry mouth, constipation, sedation (anticholinergic).� Can cause bradycardia, heart block.� Rebound HTN upon withdrawal (most agents can).

� Methyldopa� Can be used in pregnancy.� Rare lupus-like syndrome.� Rare hemolytic anemia.� Can cause hepatitis, esp in pts with liver dz.

3/26/2013

13

Direct Vasodilators� Mainly for resistant HTN.� Hydralazine� Can be used in pregnancy (unlabeled).� ANA + lupus-like syndrome.� HA, tachycardia (caution in angina/CAD).� May be useful for CHF in African-Americans (unlabeled).� Minoxidil� Hirsutism.� Pericardial effusion.� EKG changes (T wave changes common).

Compelling IndicationsCompelling Indication Diu Beta-

blkrACEI ARB CCB Ald

AntHeart failure X X X X XPost-MI X X XHigh coronary dz risk X X X XDiabetes X X X X XChronic kidney dz X XRecurrent stroke prevention

X X

JNC 7

Reverse-Engineering Compelling Indications� CAD/Angina:� Beta-blocker.� Add if needed: long acting DHP CCB, ACEI, diuretic.� Long acting DHP OK if contraindication to β-blocker.� Caution w/β-blocker + non-DHP CCB (verapamil,

diltiazem) – bradycardia, heart block, CHF.� Post-MI: β-blocker; may add ACEI.� CHF: Diuretic, ACEI or ARB, β-blocker (carvedilol,

metoprolol succinate, bisoprolol), aldosterone antagonist.

JNC 7

Reverse-Engineering Compelling Indications – 2� DM: � Diuretics (yes, they are safe and reduce mortality), ACEI

or ARB, CCB.� β-blocker OK if CAD.

� CKD: ACEI or ARB.� 2° prevention of stroke: thiazide diuretic or diuretic +

ACEI.

Lancet 2001;358:1033-41; JNC 7

3/26/2013

14

Special Populations: Demographic� Elderly & African-Americans respond best to

thiazide diuretics or CCB’s.� Less responsive to ACEI, ARB, & β-blockers—still give if

compelling indication.� ACEI/ARB responsiveness improves if given diuretic.� Still use β-blocker after MI.

� African-Americans may respond better to Na+restriction.� Young pts may respond better to ACEI’s & beta-

blockers.Lancet 1999;353:2008-13; BMJ 2004;328:634-40; NEJM 1993;328:914-21; AmJHTN 2001;14:241-7; JNC 7—2003

Special Populations: Diabetes� HTN is common in diabetics. � Diabetes and HTN � ~ 2X risk of CV disease as

nondiabetics with HTN.� BP ≥ 120/70 is associated with increased CV event rates

and mortality in diabetics.� UKPDS: ↓ BP � ↓ risk of:� Any complication related to diabetes� DM-related death� MI� Microvascular complications

BMJ 2000;321:412-9; BMJ 1998;317:703-13

Special Populations: Diabetes—2� Reduction in CV events and microvascular

complications in diabetics is seen with multiple drug classes, including:� ACEIs� ARBs� Diuretics� β-blockers

JAMA 2002;288:2981-97

Special Populations: Diabetes—3� Calcium channel blockers:� Dihydropyridine CCBs appear inferior to ACEIs and β-

blockers in reducing MI and heart failure.� Non-DCCBs (esp diltiazem) have been shown to reduce

albumin excretion.� No long-term studies of the effect of α1-blockers, loop

diuretics or centrally-acting α2-agonists on long-term complications of diabetes.� α1-blocker arm of the ALLHAT study terminated d/t

increase in new-onset heart failure vs chlorthalidone—but NO placebo.

JAMA 2002;288:2981-97

3/26/2013

15

Special Populations: Erectile Dysfunction� Neutral effect on erectile function: ARBs, ACEI’s,

CCBs.� Negative effect on erectile function: Centrally-

acting α2-agonists, β-blockers, diuretics.� Contraindicated with PDE-5 inhibitors:� Nitrates (severe hypotension / circulatory collapse).� α1-blockers should be used with caution; combination

may trigger hypotension.� Initiate PDE-5 inhibitor at lowest dose.

Combination Therapy� Preferred combinations:� ACEI or ARB + diuretic.� ACEI or ARB + CCB.

� Acceptable combinations:� Thiazide + most others (β-blocker, CCB, K-sparing

diuretic).� β-blocker + DHP CCB.

� UNnacceptable combinations:� 2 RAA inhibitors (ACEI, ARB, aliskiren)—dangerous.� β-blocker + RAA inhibitor or adrenergic blocker

EurHeartJ 2010;31:2205-2209; http://www.fda.gov/drugs/drugsafety/ucm300889.htm

Resistant HTN� Persistent HTN despite > 3 drugs.� Poor adherence most common cause.� Suboptimal therapy.� Typically inadequate diuresis.� Move to loop diuretic.� Add spironolactone.

�Med interactions.� 2° HTN.

HTN 2008;51(6):1403-19; JNC 7—2003

Identifiable Causes of HTN—1 (i.e., Secondary HTN)� 2 – 10% of hypertensive pts.

� Chronic kidney disease (2.5 – 6%).� Primary aldosteronism and other mineralocorticoid

excess states (1 – 10%).� Renovascular hypertension – renal artery stenosis (0.2

– 4%).� Drug induced or drug related.� Mnemonic: CARD or KARD.

JNC 7; http://emedicine.medscape.com/article/241381-overview#aw2aab6b2b3aa

3/26/2013

16

Identifiable Causes of HTN—2� Sleep apnea.� Thyroid or parathyroid disease.� Obstructive uropathy.� Cushing’s syndrome and other glucocorticoid excess

states, including chronic steroid therapy.� Coarctation of the aorta.� Pheochromocytoma (rare).

“DOG & CAT PARK”� Drugs� Obstructive uropathy� Glucocorticoid excess

� Coarctation of aorta� Aldosterone� Thyroid/parathyroid

� Pheochromocytoma� Apnea (sleep)� Renovascular� Kidney Dz (CKD)

Whom to Screen for 2° HTN� Severe or resistant HTN (uncontrolled on 3 meds of

different classes).� Malignant HTN (severe HTN + signs of end-organ

damage). � An acute rise in blood pressure over a previously stable

value.� Age <30 years in non-obese, non-black patients with a

confirmed negative family history of and no other risk factors (e.g., obesity) for hypertension.� Proven age of onset before puberty.

http://www.uptodate.com/contents/who-should-be-screened-for-renovascular-or-other-causes-of-secondary-hypertension?source=see_link

Additional Clues to 2° HTN� Hypokalemia—aldosteronism.� Don’t just automatically assume it’s due to diuretic.

� ↑ Cr, abnormal UA – renal dz.� Snoring, fatigue, daytime somnolence – sleep apnea.

3/26/2013

17

Clinical Clues to Renovascular HTN� Acute elevation in the plasma creatinine (>30%) after

starting ACEI or ARB.� Systolic-diastolic abdominal bruit that lateralizes to

one side.� And more….

http://www.uptodate.com/contents/who-should-be-screened-for-renovascular-or-other-causes-of-secondary-hypertension?source=see_link; Circulation 2006;113:1474-1547

Clinical Clues to Renovascular HTN—2� Severe HTN w/4 A’s (Age, Atherosclerosis, Atrophic

kidney, Acute pulmonary edema).� Onset of stage II HTN (BP ≥160/100) after age 55.� Moderate to severe HTN in pts w/diffuse

atherosclerosis, esp > age 50. � Moderate to severe HTN in a pt with an unexplained

atrophic kidney or asymmetry in renal sizes of >1.5 cm. � Moderate to severe HTN in patients with recurrent

episodes of acute (flash) pulmonary edema or otherwise unexplained heart failure.

Drug Related Causes of HTN� Nonadherence� Inadequate doses� Inappropriate

combinations� Oral contraceptives� NSAID’s, COX-2 inhibitors� Sympathomimetics

(decongestants, anorectics)

� Cocaine, amphetamines, other illicit drugs� Adrenal steroid hormones� Cyclosporine, tacrolimus� Erythropoietin� Licorice (including some

chewing tobacco)� Some OTC supplements

and medicines (e.g., ma huang, bitter orange, ginseng, St John’s wort)

Screening Tests for 2° HTNDiagnosis TestCKD eGFRCoarctation of aorta CT angioCushing’s, glucocorticoid excess Hx, dexamethasone suppression testDrugs Hx, drug screeningPheochromocytoma (RARE) 24-hr urinary metanephrine and

normetanephrinePrimary aldosteronism and other mineralocorticoid excess states

24-hr urinary aldosterone level or specific measurements of other mineralocorticoids

Renovascular HTN Doppler flow study, MRASleep apnea Sleep study with O2 saturationThyroid/parathyroid disease TSH; PTH

JNC 7

3/26/2013

18

White-Coat HTN� Up to 20-35% of HTN pts.� 37-44% of resistant HTN pts.

� Slightly greater risk for CV events than normotensives, less than hypertensives.� High risk for developing sustained HTN.� Ambulatory BP monitoring:� 24-hr average BP ≥ 138/85.� At equivalent office BP, those w/higher ABP have higher

risk.

HTN 2011;57:898-902; AmJHTN 2005;18:1534-40; HTN 1998;31:712-8; JHTN 2012;6:1211-6; AmJHTN 2005;18:1422-8; BPMonit1999;4:333-41; NEJM 2003;348:2407-15; AmJHTN 2011;24:52-8; JACC 2005;46:508-15; HTN 1998;31:57-63; JHTN 1996;14:327-32

Hypertensive Emergencies� Def: acutely elevated BP with end organ damage (also

called malignant HTN).� Eye: retinal hemorrhages, exudates, or papilledema.� Brain: hypertensive encephalopathy.� Heart: angina, ischemia, CHF, dissecting aortic

aneurysm.� Kidney: hematuria, proteinuria, ARF.

� Goal: reduce BP by 25% within 1st hr, then to 160/100-110 within next 2-6 hrs.

JNC 7; http://www.uptodate.com/contents/hypertensive-emergencies-malignant-hypertension-and-hypertensive-encephalopathy-in-adults?source=search_result&selectedTitle=1~122

Treatment of HTN Emergencies� Na+ nitroprusside.� Rapid action, short duration = titratable drip.� Cyanide toxicity with prolonged use, esp w/renal failure.� Caution w/high intracranial pressure.� Continuous BP monitoring.

� Nicardipine—longer half-life, harder to titrate.� Avoid in acute CHF.� Caution in coronary ischemia.

� Clevidipine – shorter acting, more titratable.

JNC 7; http://www.uptodate.com/contents/drug-treatment-of-hypertensive-emergencies?source=related_link

Treatment of HTN Emergencies� Labetolol—safe in CAD; caution/avoid in asthma,

COPD, CHF (avoid in acute HF), bradycardia, >1° heart block.� Esmolol—ultra-short acting β-blocker. � Aortic dissection.

� [Fenoldopam—dopamine receptor agonist.� Useful in renal failure.� Contraindicated in glaucoma.

� Phentolamine—catecholamine excess (pheochromocytoma).]

3/26/2013

19

Switch Gears: Valvular Heart Dz� Valvular heart disease generalizations:� Most valvular abnormalities give CHF-like sx (DOE).� Regurgitations are often treated with ACEI’s to

vasodilate & improve forward flow (“Regurgitations are relieved by RAA blockers”).� Stenoses are often best treated via surgery or procedures

(“Stenoses are served by surgery”).� Almost all can lead to atrial fibrillation (less w/aortic

regurg) .� Acute regurgitation can lead to cardiogenic shock.

Who Gets SBE Prophylaxis?� Prosthetic heart valves� Prosthetic material used in valve repair� Prior h/o endocarditis� Transplant valvulopathy� Congenital heart dz:� Unrepaired cyanotic dz� Repaired w/prosthetic material—for 6 mo p-procedure� Repaired w/residual defects at or near prosthetic device

http://www.uptodate.com/contents/antimicrobial-prophylaxis-for-bacterial-endocarditis?source=search_result&search=endocarditis+prophylaxis&selectedTitle=1~80

Circumstances for Prophylaxis� Dental procedures involving manipulation of gums or

periapical tissue, or perforation of mucosa.� Incision or bx of respiratory tract mucosa (T & A,

bronch w/bx).� Infected skin or musculoskeletal tissue undergoing

surgery.

NO Prophylaxis� Other valve lesions.� No GI or GU procedures.� Exception: established UTI w/hi risk CV condition

� Vaginal or Cesarean delivery.� Exception: hi risk lesion w/chorioamnionitis or

pyelonephritis.

3/26/2013

20

Meds for Endocarditis Prophylaxis� Single dose 30 – 60 min before procedure — no more 2nd

dose!� Amoxicillin 2 g� NPO: IV/IM amp (2g), cefazolin, ceftriaxone (1g).� PCN allergic:� Po cephalexin 2g, clinda 600 mg, or azithro or clarithro 500 mg.� IM/IV cefazolin, ceftriaxone, or clinda.

Aortic Stenosis—Key Points� May be asymptomatic even with severe dz.� Once sx appear, course tends to progress fairly rapidly (2-

3 yr avg survival).� Classic triad: Angina, Syncope, HF (once sx appear, it

turns you to ASHes). Esp w/exertion.� Exertional dyspnea is most common presenting sx (↓

exercise tolerance).� Systolic ejection murmur loudest at base, rad to carotids.� Atrial fibrillation, pulmonary hypertension are

preterminal findings.

AS Management� Risk factor reduction.� High prevalence of CAD.� Cautious treatment of HTN is appropriate.

� Exercise limitations:� Mild AS: competitive sports OK w/F/U.� Asymptomatic mod AS: exercise testing to level of

exertion.� Asymptomatic mod AS w/SVT or other complex

tachyarrhythmias: low-intensity.� Severe AS: no sports.

AS Surgical Treatment� Valve replacement.� Symptoms.� Rarely for asymptomatic pts.

� Valve replacement prolongs life and improves sx.� Complications of surgery:� Stroke.� Prolonged ventilation.� Perioperative mortality.

� Valvuloplasty may help congenital AS.

3/26/2013

21

Aortic Regurgitation (Insufficiency)� Etiology:� Congenital bicuspid aortic valve (#1 in US).� Rheumatic (#1 in world).� Aortic root dilation.� Marfan’s.� Syphilis .� Dissection .

� More common with advancing age.

Aortic Insufficiency—Clinical� Chronic:� Long asymptomatic period.� Progressive exertional dyspnea, CHF.� Pounding heart, palpitations (worse when supine or on

L side—heart vs chest wall).� Acute (e.g., ischemia/MI): cardiogenic shock.� Exam findings:� Wide pulse pressure.� Water-hammer pulse (↑ stroke vol � rapid pressure fall

d/t regurg).� Blowing, decrescendo, early diastolic murmur.

Management of AI� Vasodilators (nifedipine, ACEI) slow progression of AI

and reduce risk of CHF.� Use in symptomatic pts.� May help asymptomatic.

� Avoid ß-blockers – ↓rate � long diastole, may worsen regurg.� Activity limitations based on severity of AI + LV

diameter.� Consider surgery (AVR) if symptomatic, increasing LV

dilation, worsening LV function.

Mitral Regurgitation� Trivial (“physiologic”) MR occurs in up to 70% of

adults.� Etiology of pathologic MR:� Mitral valve prolapse (#1 in developed areas)� Endocarditis� Ischemic heart dz – MI can cause acutely� Trauma� Rheumatic (undeveloped nations)� Congenital � Drugs: cabergoline, diet pills, ergotamine

3/26/2013

22

Symptoms & Signs of MR� Chronic:� Asymptomatic until severe w/LV failure or AFib.� DOE, ↓ exercise tolerance, fatigue (↓ CO).� A fib.� Higher risk of endocarditis w/severe dz.

� Acute (e.g., ischemia/MI):� Pulmonary edema, hypotension, cardiogenic shock.

� Murmur:� Holosystolic, loudest @ apex, rad to L axilla +/- back.� Prolapse has midsystolic click, sl later murmur.

Management of MR� Vasodilators (ACEI) – controversial in asymptomatic

pts (often recommended).� Treat ischemia if present.� Treat signs of CHF.� Manage A fib.� Consider surgery if sx.� Repair preferred for most pts (better results).� Ideal to operate before EF deteriorates.� MVR if extensive Ca++ of leaflet or annulus.

Mitral Stenosis� Usually rheumatic.� Sx begin in 30’s.� SOB, DOE.� Pulmonary edema assoc w/exertion, fever, anemia.� Occasional hemoptysis (unique among valvular dz).� PE may occur.

� Endocarditis rare.

MS Exam� Loud S1.� Opening snap.� Diastolic rumbling murmur @ apex.� R sided CHF signs occur later.� Atrial Fib + Diastolic Murmur � consider MS (A fib =

a complication of MS).

3/26/2013

23

MS Management� Treat CHF.� Percutaneous balloon valvuloplasty.� Uncomplicated MS, limited valve Ca++.� Contraindicated in severe MS, LA thrombus.

� Surgical valvotomy—good results.� Valve replacement.� Moderate – severe disease + CHF.� Not candidate for valvotomy.