HYPERTENSION
| IS IT AN EMERGENCY ?—Brad Frazee, MD, Associate Clinical Professor of Medicine, University of California, San
Francisco, School of Medicine, and Attending Physician, Alameda County Medical Center-Highland General Hospital,
Oakland, CA
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| Hypertensive emergency: defined as acute target organ damage, ie, heart, kidneys, brain, retina, aorta, placenta in pregnant
women
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| Hypertensive urgency: concept flawed and out of date; implies immediate treatment and discharge
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| Emergencies accompanied by hypertension: hypertension in emergency department (ED) can be epiphenomenon; start
treatment within minutes
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| Malignant hypertension: hypertension root problem; immediate effects on brain, retina, or kidney, ie, encephalopathy,
severe retinopathy, acute nephropathy
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| Chronic hypertension: patients can be risk-stratified into high risk (severe blood pressure [BP] elevation plus previous
target organ disease) or low risk (mild to severely elevated BP)
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| Malignant hypertension issues: diagnosis main issue; no need to start parenteral agent in ED, can start in intensive care unit
(ICU)
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| Presentation: if patient presents with severe BP elevation or is ill or altered, look for acute target organ damage, ie, standard
work-up, electrocardiography (ECG), chest x-ray, chemistries (including creatinine), head computed tomography
(CT); if acute problem found, patient has hypertensive emergency; admit patient and start therapy in ED; if no acute target
organ damage, no treatment required
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| Complications of hypertension: stroke, dementia, coronary artery disease (CAD), congenital heart failure (CHF), renal failure;
aortic, and carotid and peripheral vascular disease; linear relationship between BP elevation and risk for complications
(risk approximately doubles for every 20 mm Hg systolic/10mm Hg diastolic increase; study (2001)—cross-sectional, conducted
in United States by epidemiologists; of 16,000 patients (“microcosm of American population”), 20% had hypertension;
high BP not controlled in 77% of patients, which broke down to unaware 31%, aware but untreated 17%, treated but
uncontrolled 29% (PCPs commonly do not follow treatment algorithm); only 23% treated and controlled; risk factors for
lack of awareness—old age; isolated systolic hypertension; Hispanic race; note—in patients unaware or not well controlled,
>70% insured and in regular medical care; conclusion—hypertension underdiagnosed and undercontrolled; unfortunate
because benefits of therapy so well established and easy to achieve with 1 or 2 drugs once a day; relative risk after 5 yr
successful therapy—stroke 0.6% (reduction 40%); MI 0.8%; risk for CHF reduced by 50%; decrease in renal failure demonstrated;
mortality 0.9%
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| Study data: in Medical Research Council (MRC) trial that enrolled healthy young patients, very few in placebo group had
stroke; in Swedish Trial in Old Patients with Hypertension (STOP-Hypertension) and Coope trials that enrolled elderly
patients >60 yr (most had diabetes and other cardiovascular comorbidity), many died of stroke; trial data show consistent
relative reduction in stroke of 40%; big difference across trials in absolute number of strokes prevented per 1000 patient
years; in MRC trial, 1 stroke prevented per 1000 patient years; in STOP-Hypertension and Coope trials, 10 to 15 strokes
prevented; demonstrates importance of targeting elderly patients with underlying cardiovascular disease
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| Assessing BP in ED: proper-sized cuff key (bladder should encircle 80% of arm); Velcro must line up; take 2 measurements
30 min apart (never single triage reading); sources of error—small cuff; white-coat hypertension; 2 readings in
one day of diastolic BP >115 mm Hg corresponds to real hypertenison
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| Risk stratification: determine absolute degree of BP elevation; identify major cardiovascular risk factors; if patient hypertensive
and has previous target organ damage (eg, history of stroke, MI, revascularization, CHF), must treat hypertension;
left ventricular hypertrophy (LVH) doubles risk for MI, sudden death, or stroke; ECG criteria for LVH—RaVL
>11 mm; SV1 + R(V5 or V6) >35mm
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| Cerebral small vessel disease: patients do not have acute stroke on exam but cerebral circulation impacted, evidenced by lacunar
infarcts (also called periventricular white matter changes); indicates patient likely to develop dementia; speaker has low
threshold for admitting these patients as hypertensive emergency
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| Risk stratification illustrated: 2 patients with ankle sprain; 1) 40-yr-old black woman, nonsmoker, slightly overweight,
with BP 145/95 mm Hg on 3 readings; possibly white-coat hypertension, probably real hypertension; not worthwhile to
treat on busy ED shift; 2) 61-yr-old man with noninsulin-dependent diabetes and previous stroke; BP 160/90 mm Hg on
multiple readings; ED physician should ensure patient on medical regimen and has PCP
|
| Whether to start treatment in ED: imperative to treat hypertension given nationwide underdiagnosis, benefit of treatment,
and lack of primary care; but problems with initiating treatment in ED include overdiagnosis; physician strategy
depends on risk stratification, practice setting, availability of primary care, and ED resource availability; could also give
patient free BP screening card (in event of 3 high BP readings, card instructs nurse to refer patient for urgent care)
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| Recommended follow-up: Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High
Blood Pressure (JNC) VI—for prehypertension, recheck in 1 yr; for stage I hypertension, recheck in 2 mo (may start
medication or counsel about weight loss and exercise); for systolic BP 160 to 179 mm Hg or diastolic BP 100 to 109 mm
Hg, risk-stratify or refer to source of care within 1 mo; for severe hypertension, risk-stratify or treat immediately, or refer
to source of care immediately or within 1 wk; if starting medications in ED, take time to talk to patient about lifelong management
of condition
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| Paradigm shifts: JNC VII (2003)—changed semantics and redefined normal BP as <120/80 mm Hg; systolic BP more
important predictor of risk than diastolic BP; treatment threshold lowered in diabetic patients with renal disease to BP
130/90 mm Hg; thiazide recommended as first-line treatment; other medication classes grouped together as second-line
treatment; for patients with BP 160/110 mm Hg, begin with 2 medications (traditionally one)
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| Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT): large trial conducted
in United Kingdom; 33,000 patients ≥55 yr of age with CAD risk randomized to 1 of 3 antihypertensives (chlorthalidone,
amlodipine, or lisinopril); 5-yr follow-up; results— no difference in primary outcome, MI, or all-cause mortality
between groups
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| Choosing therapy for chronic hypertension: hydrochlorothiazide plus angiotensin converting enzyme (ACE) inhibitor
potent combination (works well in African-Americans); speaker usually starts with hydrochlorothiazide 25 mg but does
start in patients with history of gout or prone to hyponatremia; keep exercise intolerance in mind when considering β-
blockers; bump in creatinine seen with initiation of ACE inhibitor therapy but drifts down over 2 mo (withhold ACE inhibitor
if creatinine >3 mg/dL)
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| Malignant hypertension: accelerated nephropathy, grade 4 retinopathy, and encephalopathy (all rare diagnoses); very little
evidence about how to diagnose; nephropathy—increase in renin and angiotensin that drives BP higher; presents clinically
with proteinuria, hematuria, azotemia, and retinopathy; clinical definition vague; experts use severe hypertension plus creatinine
>1.2 mg/dL or 25% above baseline; if associated with long-standing hypertension, encephalopathy usually absent;
grade 4 retinopathy—evidenced by papilledema, high-grade arteriovenous (AV) nicking, and exudates;
encephalopathy—BP affects posterior part of brain; vasogenic edema on magnetic resonance imaging (MRI); rule out cocaine
and alcohol intoxication; perform head CT and funduscopy to support diagnosis
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| Treatment: challenge is diagnosis; admission always required to work up secondary causes; speaker believes immediate
parenteral therapy unwarranted; sodium nitroprusside (SNP)—only rapidly reversible agent; drug of choice in most
cases; labetalol—commonly used; 20 to 40 mg every 10 min; problem if overshoot because duration 2 hr;
fenoldopam—dopamine-1 (DA-1) receptor agonist; not too expensive; nicardipine—similar action to IV nifedipine;
very expensive; short-acting nifedipine—practically taken off market; unsafe; oral clonidine—same story as short-
acting nifedipine
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| Severe hypertension in ED: common case example—41-yr-old man complaining of headache and low back pain; history
of hypertension; recently released from prison; uses alcohol and cocaine; BP 220/115 mm Hg on multiple readings;
normal vital signs; severe hypertension—defined as BP >180 to 220 mm Hg systolic and >110 mm Hg to 120 mm Hg diastolic;
constitutes 10% of hypertension population but excess of cardiovascular disease morbidity; 5% of patients in urban
teaching EDs; 98% of patients have history of hypertension; patients often lack PCPs, noncompliant with medications, use
alcohol and recreational drugs; presentation—often straight from dental office; asymptomatic; 10% of patients have
acute intoxication or withdrawal; two thirds have nonspecific symptom or asymptomatic (eg, headache, muscle pain,
epistaxis, blurred vision)
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| ED management: thorough evaluation; acute target organ damage assessment
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 | Acute target organ damage: kidneys—normal urinalysis (no hematuria and ≤1+ proteinuria) excludes acute azotemia;
serum creatinine usually required; cellular urinary sediment and significant creatinine rise indicates organ damage (focus
on 25% above baseline); heart—ischemia or CHF; symptoms include chest pain, history of anginal symptoms,
signs of CHF, edema; speaker performs ECG on all patients, but not chest x-ray, to look for LVH; resting troponin may
be performed based on patient’s age; brain—ask about symptoms of transient ischemic attack (TIA), eg, clumsiness
of hands; look for hemorrhage, lacunar infarcts, or mass on CT; obtain head CT for severe BP elevations and neurologic
symptoms; retina—perform funduscopy
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| PULMONARY HYPERTENSION —Wyong (Nick) Kim, MD, Assistant Clinical Professor of Medicine, University of
California, San Diego, School of Medicine
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| Classification: National Institutes of Health (NIH) and World Health Organization (WHO) currently define pulmonary
hypertension (PH) by mean pulmonary arterial (PA) pressure ≥25 mm Hg at rest or >30 mm Hg with exercise; well-
known that systolic PA pressures do not exceed 20 to 30 mm Hg, even with exercise (very compliant low-pressure system);
heterogenous list of possible causes of PH
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| Main groups: class 1—pulmonary arterial hypertension (PAH); class 2—PH with left heart disease; class 3—PH with
lung disease and/or hypoxemia; class 4—PH due to chronic thrombotic and/or embolic disease; class 5—
miscellaneous or rare disorders
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| Causes of PH: class 2 and 3 most common causes of PH; class 1 and 4 more isolated pulmonary vascular causes of PAH,
elevated peripheral vascular resistance (PVR); class 2 generally elevation in wedge pressure; prognosis and treatment
differ radically depending on PH type; rarer types (eg, class 1) often go unrecognized for several years
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| PH due to chronic thrombotic or pulmonary embolic disease (class 4): more frequent than previously thought
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| PH due to chronic lung disease (class 3): chronic lung disease common (eg, chronic obstructive pulmonary disease
[COPD], interstitial lung disease, sleep apnea, pulmonary fibrosis); pathogenic mechanism underlying hypoxemia or hypoventilation;
treat underlying lung disease and give O2
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| PH with left heart disease (class 2): left heart disease very common (eg, CAD, mitral valve disease); treat underlying
problem rather than using PH-specific therapies
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| Pulmonary arterial hypertension (class 1): recent consensus replaced “primary pulmonary hypertension” with idiopathic
pulmonary arterial hypertension (IPAH) because too often secondary pulmonary hypertension very heterogeneous; “primary”
and “secondary” replaced with either IPAH or PAH related to systemic cause; mostly young women in 30s, often presenting as
otherwise healthy but with isolated severe PAH; ≈6% of IPAH runs in families (≈50% of patients have identified gene defect)
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| PAH associated with systemic disorders: perhaps largest PAH group; predominantly collagen vascular diseases, specifically
scleroderma patients (either limited scleroderma [CREST] or diffuse scleroderma); 12% to 20% lifetime incidence of
PAH; drugs and toxins—Phen-fen (prescription diet pills) can produce identical symptoms to IPAH; now more mepthamphetamine
use; cocaine; important to take careful history; liver disease and HIV—patients present with similar behavior and
pathology of IPAH; congenital shunts—another population treated on regular basis
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| Critical care: do not intubate or give fluids; problem right side failure due to volume overload; diuresis best therapy
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| Presentation: chest pain that mimics angina; shortness of breath; fatigue; severe late findings include syncope, overt right
heart failure, ascites, and severe peripheral edema
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| New York Heart Association (NYHA) functional class: class I—normal; class II—shortness of breath with ordinary
activity; class III—shortness of breath with less than ordinary activity; class IV—shortness of breath with any activity or
passing out; NIH data shows class IV patients have poor survival, ie, <50% survival at 1 yr for otherwise healthy 20- to 30-
yr-olds
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| Treatment: many patients inappropriately treated with calcium channel blockers; current focus on endothelial cells;
prostacyclin—vasodilator that prevents thickening and proliferation of endothelial cells; endothelin—misused; most
potent vasoconstrictor known; level increased in PH patients; led to blocking with endothelin blockade; nitric oxide—
has similar effects to prostacyclin; current therapy—replacing what is depleted and blocking what is made in excess
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| PAH therapies in US: epoprostenol (Flolan)—approved in 1995; bosentan (Tracleer)—only oral therapy; blocks excess
endothelin; approved in 2001; treprostinil (Remodulin)—prostacyclin; IV form approved in 2005; iloprost
(Ventavis)—inhaled iloprost; became available in United States in 2005); sildenafil (Viagra)—positive trial data; soon
to be available under new name Revatio; sitaxsentan and ambrisentan—similar to bosentan; block excess endothelin
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| Treatment algorithm: in past, patients who did not benefit from calcium channel blockers faced central line or lung transplantation;
now, effective therapies mean fewer patients need transplantation; most class 3, moderately ill patients like to
try oral therapy, so important to inform them that benefits seen in 3 to 4 mo; if patient has right heart failure and severely
ill, start with Flolan; future therapy likely involves combination therapy
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Educational Objectives
| The goal of this program is to educate the listener about diagnosis and treatment of emergency hypertension and pulmonary
hypertension (PH). After hearing and assimilating this program, the clinician will be better able to:
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| 1. Identify acute hypertension in the emergency department (ED).
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| 2. Discuss recent developments in hypertension therapies.
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| 3. List standard work-up tests and discuss risk stratification for hypertension in the ED.
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| 4. Name the 5 main categories of PH.
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| 5. Discuss new approaches to treating PH.
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Discussed on This Program
Ambrisentan (investigational)
Bosentan [Tracleer]
Epoprostenol sodium (PGI2 , PGX, prostacyclin) [Cycloprostin, Flolan]
Fenoldopam mesylate [Corlopam]
Hydrochlorothiazide [Esidrix, Ezide, HydroDIURIL, Hydro-Par, Microzide Capsules, Oretic]
Iloprost (Ventavis)
Nicardipine HCl [Cardene, Cardene I.V., Cardene SR]
Sildenafil citrate [Revatio, Viagra]
Sitaxsentan sodium (investigational)
Treprostinol sodium [Remodulin]
Suggested Reading
Abenhaim L et al: Appetite-suppressant drugs and the risk of primary pulmonary hypertension. International Primary
Pulmonary Hypertension Study Group; N Engl J Med 335 (9):609,1996; Burchell C et al: Blood pressure measurement
in a district general paediatric A and E department. Arch Dis Child 90:1097, 2005; Collazos J et al: Acute, reversible pulmonary
hypertension associated with cocaine use. Respir Med 90:171, 1996; Decker WW et al: Clinical policy: critical
issues in the evaluation and management of adult patients with asymptomatic hypertension in the emergency department.
Ann Emerg Med 47:237, 2006; Elliot WJ: Clinical features and management of selected hypertensive emergencies. J Clin
Hypertens (Greenwich) 6:587, 2004; Elliott WJ: Clinical features in the management of selected hypertensive emergencies.
Prog Cardiovasc Dis 48:316, 2006; Escalante CP et al: Hypertension in cancer patients seeking acute care: an opportunity
to intervene. Am J Med Sci 330:120, 2005; Gilhotra Y et al: Blood pressure measurements on children in the
emergency department. Emerg Med Australas 18:148, 2006; Gilmore RM et al: Severe hypertension in the emergency
department patient. Emerg Med Clin North Am 23:1141, 2005; Karras DJ et al: Elevated blood pressure in urban emergency
department patients. Acad Emerg Med 12:835, 2005; Karras DJ et al: Evaluation and treatment of patients with
severely elevated blood pressure in academic emergency departments: a multicenter study. Ann Emerg Med 47:230, 2006;
Epub 2006 Jan 18; Karras DJ et al: Lack of relationship between hypertension-associated symptoms and blood pressure
in hypertensive ED patients. Am J Emerg Med 23:106, 2005; Liu CM et al: Comparison of referral and non-referral hypertensive
disorders during pregnancy: an analysis of 271 consecutive cases at a tertiary hospital. Chang Gung Med J
28:326, 2005; Migneco A et al: Hypertensive crises: diagnosis and management in the emergency room. Eur Rev Med
Pharmacol Sci 8:143, 2004; Rothman RB: The age-adjusted mortality rate from primary pulmonary hypertension, in age
range 20 to 54 years, did not increase during the years of peak "phen/fen" use. Chest 118:1516, 2000; Smith SM: Screening
for hypertension in the emergency department. Emerg Med J 23:325, 2006; Ulger AF et al: Pulmonary hypertension
and acute pulmonary edema in a 23-year-old male with a history of an upper respiratory tract infection. Tuberk Toraks
53:66, 2005; Venkat KK et al: Care of the renal transplant recipient in the emergency department. Ann Emerg Med
44:330, 2004; Vidaeff AC et al: Acute hypertensive emergencies in pregnancy. Crit Care Med 33:S307, 2005; Yakel
DL Jr et al: Pulmonary artery hypertension in chronic intravenous cocaine users. Am Heart J 130:398, 1995.
Faculty Disclosure
In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial
relationship with the manufacturer or provider of any commercial product or service discussed. For this issue, the following
has been disclosed: Dr. Kim is on the Speakers’ Bureau for Actelion Pharmaceuticals.
Dr. Frazee spoke at Topics in Emergency Medicine held in San Francisco, CA, on October 24-27, 2005, and sponsored by
the University of California, San Francisco, School of Medicine. Dr. Kim spoke at Critical Care held in San Diego, CA, on
July 21-23, 2005, and sponsored by the University of California, San Diego, School of Medicine. The Audio-Digest Foundation
thanks the speakers and the sponsors for their cooperation in the production of this program.
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