BASICSLisa M. Schroeder, MD • Sobia Ahmad, MD
BASICS
DESCRIPTION
• Hypertension (HTN) is defined (Joint National Committee [JNC] 8) as ≥2 elevated BPs
– Age 60 years or older: systolic BP (SBP) ≥150 mm Hg and/or diastolic BP (DBP) ≥90 mm Hg at ≥2 visits (1)
– Age <60 years: SBP ≥140 mm Hg and/or DBP ≥90 mm Hg at ≥2 visits (1)
– With diabetes or chronic kidney disease: SBP >140 and/or DBP >90 mm Hg
• HTN is a strong risk factor for cardiovascular disease and strokes.
• Synonym(s): benign, chronic, idiopathic, familial, or genetic HTN; high BP
Geriatric Considerations
• Isolated systolic HTN is common.
• Therapy has been shown to be effective and beneficial at preventing stroke, although target SBP is higher than in younger patients (~150 mm Hg systolic), and adverse reactions to medications are more frequent. The benefit of therapy has been conclusively demonstrated in older patients for SBP ≥160 mm Hg.
• New evidence suggests that an aggressive target for the elderly is both beneficial and safe (2)[A].
Pediatric Considerations
• Measure BP during routine exams for >3 years of age.
• Defined as SBP or DBP ≥95th percentile on repeated measurements (3)
• Pre-HTN: SBP or DBP between 90th and 95th percentile (3)
Pregnancy Considerations
• Elevated BP during pregnancy may be either chronic HTN or pregnancy-induced preeclampsia. ACE inhibitors and angiotensin II receptor blockers (ARBs) are contraindicated.
• Maternal and fetal mortality benefit from treatment of severe HTN. Evidence is not clear for mild HTN (see topic “Preeclampsia”).
• Methyldopa, labetalol, hydralazine, or nifedipine preferred agents
EPIDEMIOLOGY
Incidence
• Lifetime risk for men and women aged 55 to 65 years by age 80 to 85 years is >90%.
• Predominant age: essential (primary, benign, idiopathic) onset usually in the 20s to 30s
• Predominant sex: male > female; males tend to run higher than females and have a significantly higher risk of cardiovascular disease at any given pressure.
Prevalence
In 2009 to 2010, prevalence in adults was 28.6% (2009–2010 National Health and Nutrition Examination Survey [NHANES]).
ETIOLOGY AND PATHOPHYSIOLOGY
• >90% of HTN has no identified cause.
• Secondary causes of HTN (see “Hypertension, Secondary and Resistant”): renal parenchymal: glomerulonephritis, pyelonephritis, polycystic kidneys; endocrine: primary hyperaldosteronism, pheochromocytoma, hyperthyroidism, Cushing syndrome; vascular: coarctation of aorta, renal artery stenosis; chemical: commonly, oral contraceptives, NSAIDs, decongestants, corticosteroids, black licorice, caffeine; sleep apnea
Genetics
BP levels are strongly familial, but no clear genetic pattern exists. Familial risk for cardiovascular diseases should be considered.
RISK FACTORS
Family history, obesity, alcohol use, excess dietary sodium, stress, physical inactivity, tobacco abuse, insulin resistance
DIAGNOSIS
HISTORY
• HTN is asymptomatic except in extreme cases or after related cardiovascular complications develop.
• Headache can be seen with higher BP, often present on awakening and occipital in nature.
PHYSICAL EXAM
• Evaluate signs of end-organ damage.
• Retinopathy: narrowed arteries, arteriovenous (AV) nicking, copper or silver wiring of retinal arterioles
• Increased/louder S2 (aortic component heart sound)
• Synchronous radial and femoral pulse can help to rule out coarctation of the aorta.
DIFFERENTIAL DIAGNOSIS
• Secondary HTN: Because of the low incidence of reversible secondary HTN, special tests should be considered only if the history, physical exam, or basic laboratory evaluation indicate the possibility. (See “Hypertension, Secondary and Resistant.”)
• White coat hypertension: elevation of BP in office setting and normal BP outside office
• Masked HTN: elevated BP at home and normal BP in office
DIAGNOSTIC TESTS & INTERPRETATION
MEASURING BP:
• Caffeine, exercise, and smoking avoided >30 minutes before measurement
• Patient seated quietly for 5 minutes with feet on floor
• Patient’s arm supported at heart level
• Correct cuff size
• Average of two or more measurements
Initial Tests (lab, imaging)
• Hemoglobin and hematocrit or CBC
• Complete urinalysis (may reveal proteinuria)
• Potassium, calcium, creatinine, and uric acid
• Lipid panel (total, HDL, LDL, triglyceride [TG])
• Fasting blood glucose, hemoglobin A1c
• ECG to evaluate possible presence of left ventricular hypertrophy (LVH) or rhythm abnormalities affecting therapy
Follow-Up Tests & Special Considerations
• Special tests (only if history, physical, or labs indicates) (See “Hypertension, Secondary and Resistant.”)
• Ambulatory (24-hour) BP monitoring if “white coat” HTN is suspected, episodic HTN, or autonomic dysfunction
• Home BP monitoring is effective, especially if white coat HTN is a consideration; elevated home BPs correlate with adverse outcomes, possibly more so than office BPs, and normal readings are reassuring.
Diagnostic Procedures/Other
• Age 60 years or older: SBP ≥150 mm Hg and/or DBP ≥90 mm Hg at ≥2 visits
• Age <60 years with CKD or diabetes: SBP ≥140 mm Hg and/or DBP ≥90 mm Hg at ≥2 visits
• The JNC 8 recommends emphasis on
– Family or personal history of HTN; cardiovascular, cerebrovascular, renal disease; and diabetes
– Previous elevated BPs
– Previous treatment for HTN
– History of weight gain, exercise activities, sodium and fat intake, and alcohol use
– Symptoms suggesting secondary HTN
– Psychosocial and environmental factors affecting BP and risk for cardiovascular disease
– Other cardiovascular risk factors, such as obesity, smoking, hyperlipidemia, and diabetes, OSA
– Funduscopic exam for arteriolar narrowing, AV compression, hemorrhages, exudates, and papilledema
– Body mass index (BMI)
– Waist circumference
– BP in both arms
– Complete cardiac and peripheral pulse exam: Compare radial and femoral pulse for differences in volume and timing, auscultation for carotid and femoral bruits.
– Abdominal exam for masses and bruits: Listen high in the flanks over the kidneys.
– Neurologic assessment
TREATMENT
GENERAL MEASURES
• The treatment discussed will follow JNC 8 guidelines. Please note that several important recent studies have concluded that more intensive therapy may be warranted for certain high-risk individuals.
• Benefit of pharmacologic treatment of low-risk patients with Class I hypertension (SBP 140 to 150 mm Hg, DBP 90 to 99 mm Hg) remains uncertain (4)[A].
• Treating patients age <60 years or with CKD or diabetes to lower-than-standard BP targets, <140/90 mm Hg, does not further reduce mortality or morbidity. Individualize goal pressures based on risk factors.
• Target SBP at or just below 150 mm Hg in patients >60 years of age is acceptable in the general population (1).
• Although primary focus is SBP goal, treatment should accommodate patient preferences (1). Majority of treatment benefit is attained with initial 2 to 3 medications. Striving for small additional drops in BP to achieve a “target” is less clinically beneficial and more likely to cause side effects.
• Lower DBP targets were not associated with decreased morbidity/mortality.
• Aerobic exercise (30 minutes of aerobics 4 to 5 days per week), weight reduction for obese patients
• Smoking cessation
• Reduce salt intake <2.4 g/day.
– Assess overall risk and individualize decision to treat.
• Choose from one of four classes of medications: (1)[A]: ACE inhibitors, ARBs, calcium channel blockers (CCBs), or diuretics.
• The decision to treat more aggressively should be considered in patients meeting enrollment criteria for SPRINT, as aggressive treatment does show improvement in outcomes, but 61 nondiabetic patients would need to be treated to a goal of SBP <120 to prevent a major cardiovascular outcome and 90 to prevent one death (5).
• Multiple drugs at submaximal dose may achieve target BP with fewer side effects. In patients on >1 medication, divide between morning and nighttime for better 24-hour antihypertensive effect.
• Sequential monotherapy attempts might be tried with different classes because individual responses vary.
• Many patients will require multiple medications.
• First-line agents for uncomplicated essential HTN include thiazide diuretics, ACE inhibitors, ARBs, and long-acting CCBs (amlodipine, felodipine) (1,5)[A].
• If concomitant conditions, choose first-line agent based on comorbidity.
• Combination first-line agents: Benazepril combined with amlodipine may be superior to combination with HCTZ in high-risk patients. Some suggest that ACE/ARB + dihydropyridine CCB is the first choice after monotherapy.
• β-Blockers had been strongly recommended until recent meta-analyses. Atenolol may be particularly ineffective in reducing adverse outcomes of HTN (except in patients with left ventricle hypertrophy undergoing dialysis).
• β-Blockers might benefit patients with ischemic heart disease, CHF, or migraine post–ST-segment elevation myocardial infarction (STEMI). ACE inhibitors should be used in patients with diabetes, proteinuria, atrial fibrillation, or heart failure with reduced ejection fraction (HFrEF) but not in pregnancy.
• α-Adrenergic blockers are not the first choice for monotherapy but remain as second line after combination therapy of first-line agents; might benefit males with benign prostatic hypertrophy (BPH)
• CCB could be considered in patients with isolated systolic HTN, atherosclerosis, angina, migraine, or asthma; well documented to reduce risk of stroke
• Thiazide diuretics or CCB preferred as first line in the general black population.
First Line
• Thiazide diuretics (4)[A]
– Chlorthalidone: 12.5 to 25 mg/day (more potent than hydrochlorothiazide but causes more hyponatremia and hypokalemia)
– Hydrochlorothiazide: 12.5 to 50 mg/day
– Indapamide: 1.25 to 2.5 mg/day
• ACE inhibitors
– Lisinopril: 10 to 40 mg/day
– Enalapril: 5 to 40 mg/day
– Ramipril: 2.5 to 20 mg/day
– Benazepril: 10 to 40 mg/day
• CCB
– Diltiazem CD: 180 to 360 mg/day
– Nifedipine (sustained release): 30 to 90 mg/day
– Verapamil (sustained release): 120 to 480 mg/day
– Amlodipine: 2.5 to 10 mg/day
• ARBs
– Losartan: 25 to 100 mg in 1 or 2 doses; has unique but modest uricosuric effect
– Valsartan: 80 to 320 mg daily
– Irbesartan: 75 to 300 mg daily
– Candesartan: 4 to 32 mg daily
– Renin inhibitor: aliskiren 150 to 300 mg daily
• Contraindications
– Diuretics may worsen gout.
– β-Blockers (relative) in reactive airway disease, heart block, diabetes, and peripheral vascular disease; probably should be avoided in patients with metabolic syndrome or insulin-requiring diabetes
– Diltiazem or verapamil: Do not use with systolic dysfunction or heart block.
– ACE inhibitors can worsen bilateral renovascular disease and are pregnancy Category D.
– Amlodipine may cause peripheral edema.
Second Line
• Many may be combined. Choose additional medications with complementary effects (i.e., ACE inhibitors/ARBs with diuretic or a vasodilator with a diuretic or β-blocker).
• Medication-refractory HTN or suspected aldosteronism: spironolactone: 25 to 100 mg/day (6)[A]
• Centrally acting α-2 agonists: clonidine 0.1 to 1.2 mg BID or weekly patch 0.1 to 0.3 mg/day, guanfacine, 1 to 3 mg daily, or methyldopa 250 to 2,000 mg BID
• α-Adrenergic antagonists: prazosin 1 to 10 mg BID, terazosin 1 to 20 mg/day, or doxazosin 1 to 16 mg/day
• Vasodilators
– Hydralazine: 10 to 25 mg QID; risk of tachycardia, so generally combined with β-blocker; also drug-induced systemic lupus erythematosus (SLE)
– Minoxidil: rarely used due to adverse effects; may be more effective than other medications in renal failure and refractory HTN
• Loop diuretics (for volume overload): furosemide 20 to 320 mg/day or bumetanide 0.5 to 2 mg/day
• K+-sparing diuretics in patients with hypokalemia while taking thiazides: amiloride 5 to 10 mg/day or triamterene 50 to 150 mg/day
COMPLEMENTARY & ALTERNATIVE MEDICINE
• Biofeedback and relaxation exercise
• Dietary supplements such as garlic have been suggested for lowering BP, but evidence is lacking.
ONGOING CARE
FOLLOW-UP RECOMMENDATIONS
Patient Monitoring
• Reevaluate patients q3–6mo until stable, then q6–12mo. Consider use of home self-BP monitoring; quality-of-life issues including sexual function should be considered.
• Poor medication adherence is a leading cause of apparent medication failure.
• Annual urinalysis, creatinine, and potassium
DIET
• ~20% of patients will respond to reduced-salt diet (<100 mmol/day; <6 g NaCl or <2.4 g Na).
• Consider Dietary Approaches to Stop Hypertension (DASH) diet: http://www.nhlbi.nih.gov/files/docs/public/heart/hbp_low.pdf
• Limit alcohol consumption to <1 oz/day.
• Smoking cessation
PATIENT EDUCATION
• Emphasize the asymptomatic nature of HTN.
• Printed aids for high BP education available: http://www.nhlbi.nih.gov/health/public/heart
COMPLICATIONS
Heart failure, renal failure, LVH, myocardial infarction, retinal hemorrhage, stroke, hypertensive heart disease, drug side effects
REFERENCES
1. James PA, Oparil S, Carter BL, et al. 2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA. 2014;311(5):507–520.
2. Williamson JD, Supiano MA, Applegate WB. Intensive vs standard blood pressure control and cardiovascular disease outcomes in adults aged ≥75 yrs: a randomized clinical trial. JAMA. 2016;315(24):2673–2682.
3. Riley M, Bluhm B. High blood pressure in children and adolescents. Am Fam Physician. 2012;85(7):693–700.
4. Diao D, Wright JM, Cundiff DK, et al. Pharmacotherapy for mild hypertension. Cochrane Database Syst Rev. 2012;(8):CD006742.
5. SPRINT Research Group, Wright JT Jr, Williamson JD, et al. A randomized trial of intensive versus standard blood-pressure control. N Engl J Med. 2015;373(22):2103–2116.
6. Williams B, MacDonald TM, Morant S, et al. Spironolactone versus placebo, bisoprolol, and doxazosin to determine the optimal treatment for drug-resistant hypertension (PATHWAY-2): a randomized, double-blind, crossover trial. Lancet. 2015;386(10008):2059–2068.
ADDITIONAL READING
• Elmer PJ, Obarzanek E, Vollmer WM, et al. Effects of comprehensive lifestyle modification on diet, weight, physical fitness, and blood pressure control: 18-month results of a randomized trial. Ann Intern Med. 2006;144(7):485–495.
• Mancia G, Fagard R, Narkiewicz K, et al. 2013 ESH/ESC guidelines for the management of arterial hypertension: the Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). Eur Heart J. 2013;34(28):2159–2219.
• National Institute for Health and Care Excellence. Hypertension in adults: diagnosis and management. https://www.nice.org.uk/guidance/cg127. Accessed December 22, 2016.
• Xie X, Atkins E, Lv J, et al. Effects of intensive blood pressure lowering on cardiovascular and renal outcomes: updated systemic review and meta-analysis. Lancet. 2016;387(10017):435–443.
SEE ALSO
Hypertension, Secondary and Resistant; Hypertensive Emergencies; Polycystic Kidney Disease
CODES
ICD10
I10 Essential (primary) hypertension
CLINICAL PEARLS
• Treatment of HTN reduces risk of many serious medical conditions with numbers needed to treat to prevent one serious event (e.g., stroke or myocardial infarction) ranging from ~20 patients per year for severe HTN to more than several hundred per year for mild HTN.
• Multiple submaximal doses are likely to have fewer side effects and more effectiveness than fewer maximum-dosed drugs.
• In older patients, measure BP standing to avoid overtreatment and syncope.