JNCVII Classification


Systolic (mmHg)

Diastolic (mmHg)







Stage 1 HTN



Stage 2 HTN


* 100

(jama 2003:289:2560)

(jama 2003:289:2560)

Epidemiology (jama 2003:290:199)

• Prevalence 30% in U.S. adults 60 million affected (29% in whites. 33.5% in blacks)

• 60% of those w/ HTN are on Rx. only half of whom arc adequately controlled


• Essential (95%): onset 25-55 y; © FHx. Unclear mechanism but ? additive microvasc renal injury over time w/ contribution of hyperactive sympathetics (hejm 2002:346:913)

• Secondary: Consider if Pt <20 or >50 y or if sudden onset, severe, refractory or T HTN

Secondary Causes of Hypertensior


Suggestive Findings

Initial Workup

Renovascular (1-2X) Athero (90%) FMD (10%. young women) PAN. scleroderma

h/o DM. polycystic kidney disease, glomerulonephritis ARF induced byACEI/ARB Recurrent flash pulm edema Renal bruit; hypokalemia (nejm 2001:344431)


See "Renal Failure" MRA (-90% Se & Sp) Duplex U/S;Angio Plasma aldo:renin ^10:1


Hyperaldo or Cushing's (1-5%)

Hypokalemia Metabolic alkalosis

See "Adrenal Disorders"


Pheochromocytoma (<1%)

Paroxysmal HTN. H/A. palp.


Myxedema (<i%)

See "Thyroid Disorders"



Hypercalcemia (<1X) Polyuria, dehydration. A MS ICa Obstructive sleep apnea: morning H/A. PHT; abnl polysomnography

Medications: OCP. steroids, licorice; NSAIDs (espec. COX-2); Epo; cydosporine

Coarctation of aorta: i LE pulses, systolic murmur, radiofemoral delay, abnl TTE

Polycythemia vera: t Hct

Standard workup

• Goals: (1) identify CV risk factors or other diseases that would modify prognosis or Rx

(2) reveal 2° causes of hypertension

(3) assess for target-organ damage

• History: CAD. CHF.TIA/CVA. PAD. DM. renal insufficiency, sleep apnea; • FHx for HTN

diet. Na intake, smoking, alcohol, prescription and OTC medications. OCP

• Physical exam: -2 BP measurements separated by >2 mins; verify in contralateral arm funduscopic. cardiac (LVH. murmurs), vascular, abdominal (masses or bruits), neurologic

• Laboratory tests: electrolytes. BUN. Cr. glc. Hct, U/A, lipids.TSH. ECG (for LVH). CXR Complications of HTN

• Each Î 20 mmHg SRP or 10 mmHg DBF — 2x Î CV complications (Lancet 2002:360:1903)

• Neurologic: TIA/CVA. ruptured aneurysms

• Retinopathy: I arteriolar narrowing. II copper-wiring. AV nicking. Ill hemorrhages and exudates. IV papilledema

• Vascular: aortic dissection, aortic aneurysm

• Renal: proteinuria, renal failure

Treatment (Nîjm 2003:348:610)

• Goal: < 140/90 mmHg; if DM or renal disease goal is < 130/80 mmHg. consider 120/80

• Treatment results in 50% I CHF. 40% I stroke, 20-25% I Ml (Lancet 2000:356:1955)

Lifestyle modifications (each I SBP - 5 mmHg) weight loss: achieve BMI 18.5-24.9; exercise: -30 min exercise/d. -5d/wk diet: rich in fruits & vegetables, low in saturated & total fat (DASH. NEj/H 2001;344:3) sodium restriction: ¿2.6 g/d or lower limit alcohol consumption: -2 drinks/d in men; ¿1 drink/d in women & lighter-wt Pts Pharmacologic options (if HTN or pre-HTN • diabetes or renal disease) Pre-HTN; ARB prevents onset of HTN. no i in clinical events (nejm 2006:354:1685) Stage I HTN: thiazide better than ACEI or CCB in preventing CVD (allhat. ;ama

2002:288:2981) (i-blockers no longer first choice (Lone« 2005:366:1545) Stage 2 HTN: concom. disease may lead to compelling indication for specific drug class 4- high-risk CAD: ACEI (hope, nejm 2000:342:145); thiazide (allhat); CCB • ACEI i'd morL by 11% & CV events by 16% c/w PB + diuretic (ASCOT-BPLA Lancet 2005.366:895) 4- angina: p-blockers

4- post-MI: (i-blockers.ACEl (bhat.jama 1982:247:1707;SAVE.nejm 1992:327:669) 4- HF:ACEI/ARB. ^-blockers. diuretics, aldosterone antagonist (see "Heart Failure") 4- CVA prevention: ACEI (PROGRESS. Lancet 2001:358:1033) or ARB (UFE. Lancet 2002:359^95) 4- diabetes mellitus:ACEI (UKPOS 39.8mj 1998:317713) + chronic kidney disease:ACEI/ARB (nejm 1993:329 1456 & 2001:345:851.861) most will require -2 antihypertensive drugs to reach goal; if not at goal — optimize doses or add additional drug (if on 2. one should be thiazide) Secondary causes

Renovasc: control BP w/ diuretic - ACEI/ARB (watch for t Cr w/ bilat. RAS) or CCB Atherosclerosis risk factor modification: quit smoking, i chol. If refractory HTN. recurrent HF. UA. or worse CRI. revasc. indicated (jacc 2006.471) For atherosclerosis: stenting (i'd restenosis rates w/ PTA alone): 20 mmHg i in SBP. no A In Cr. 17% restenosis rate at 9 mos (ASPIRE-2JACC 2005:46:776) For FMD (usually more distal lesions): PTA • bailout stenting Surgery for complex lesions or aortic involvement Renal parenchymal: salt and fluid restriction, t diuretics Endocrine etiologies: see "Adrenal Disorders"

Hypertensive Crisis


• Hypertensive emergency: Î BP— acute target-organ damage neurologic damage: encephalopathy, hemorrhagic or ischemic stroke, papilledema cardiac damage: ACS. HF. aortic dissection renal damage: proteinuria, hematuria, acute renal failure: scleroderma renal crisis microangiopathic hemolytic anemia preedampsia-eclampsia

• Hypertensive urgency: SBP -180 or DBP -120 w/ minimal or no target-organ damage


• Progression of essential HTN * medical noncompliance (espec. clonidine)

• Progression of renovascular disease; acute glomerulonephritis; scleroderma; preeclampsia

• Endocrine: pheochromocytoma. Cushings

• Sympathomimetics: cocaine, amphetamines. MAO inhibitors - foods rich in tyramine

• Cerebral injury (do not treat HTN in acute ischemic stroke unless Pt getting lysed. extreme.

BP. te. 220/120. or Ao dissection, active ischemia, or CHF; Stroke 2003:34 1056)


• Hypertensive emergency: I MAP by 25% in mins to 2 h using IV agents

• Hypertensive urgency, • BP in h using PO agents

Drugs for Hypertensive Crises

Intravenous agents

Oral agents






0.25-10 p.g/kg/min


12.5-50 mg


17-1000 jig/mm


200-1200 mg


20-80 mg bolus q10 min


0.2 mg load -»

or 0.5-2 mg/min

0.1 mg qh


10-20 mgq 20-30 min


10-25 mg


5-15 mg bolus q5-15 min

* Metabolized to cyanide -* A MS, lactic addons, death. Limit use of very high doses (8-10 m/kg/mtn) to < 10 min. Monitor duocyanatc levels. Sodium thiosulfate infusion for cyanide toxicity.

* Metabolized to cyanide -* A MS, lactic addons, death. Limit use of very high doses (8-10 m/kg/mtn) to < 10 min. Monitor duocyanatc levels. Sodium thiosulfate infusion for cyanide toxicity.

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