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Severe Hypertension: In a Clinical Pearls Format

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Severe Hypertension: In a Clinical Pearls Format Gregory W. Rutecki, M.D., Bradley M. Wright, Pharm. D., BCPS, Molly Adams Pharm. D., BCPS, U.niversity of S.outh A ... – PowerPoint PPT presentation

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Title: Severe Hypertension: In a Clinical Pearls Format


1
Severe Hypertension In a Clinical Pearls Format
  • Gregory W. Rutecki, M.D.,
  • Bradley M. Wright, Pharm. D., BCPS, Molly Adams
    Pharm. D., BCPS, U.niversity of S.outh A.labama
    Auburn University

2
What is a Clinical Pearls Format?
  • At the 2001 American College of Physicians
    Annual Conference, a new teaching format to aid
    physician learning, Clinical Pearls, was
    introduced. Understanding 3 qualities of
    physician learners allowed the design of Clinical
    Pearls to be created. First, physicians learn
    from cases. Second they like practical points
    they can use in their practice. Finally,
    physicians take pleasure in problem solving.
  • Mayo Clin. Proc. 2010851046-1050.

3
The Format
  • A number of short cases dealing with severe
    hypertension (180 or gt mm/hg systolic//110 or gt
    diastolic) will be presented.
  • A multiple choice question will follow each.
  • Clinical Pearls will be furnished. They are
    defined as practical teaching points supported by
    the literature/evidence.
  • This format has become one of the most popular
    sessions at the National ACP.

4
CASE 1.
  • A 43-year-old black man presents to the Emergency
    Department with a blood pressure of 240/162
    mm/hg.
  • Physical Examination did not include a
    funduscopic examination.
  • He is started on a nitroglycerin drip admitted
    as a hypertensive urgency.
  • Previous BUN/Creatinine values were 20/1.3
    mg/dl., now they have increased precipitously to
    132/11.3 mg/dl for unknown reasons.
  • A new normocytic anemia schistocytes acute
    renal failure are present.

5
Question for Case 1
  • Which of the following choices is most correct?
  • a.) Information in the case presentation suggests
    the patient has a hypertensive emergency.
  • b.) nitroglycerin is the correct therapy.
  • c.) a funduscopic will not add much to the acute
    evaluation.
  • d.) In his situation, the distinction between
    urgency and emergency is not critical.

6
Presence or Absence of Target Organ Injury is the
Key
  • The Fundus
  • Cardiovascular System
  • Brain
  • Hematology
  • Kidney
  • Grade 3 4 hypertensive retinopathy.
  • An ischemic syndrome, failure, or dissection of
    the aorta
  • Caveats with ischemic strokes a possible future
    change in hemorrhagic strokes. Do you know about
    PRES or Posterior Reversible Encephalopathy?
  • Remember the BAD old days of scleroderma and
    schistocytes?

7
Where have all the Ophthalmoscopes gone?
  • Confessions of a midnight Ophthalmologist

8
Lets look at the excuses
  • MYTH Mydriatic drops can precipitate acute
    narrow angle glaucoma (Angels and Ministers of
    Grace Defend us!!!)
  • BMJ studies comprised by 6760, 4870, 3654
    persons dilated randomly 0.03, 0, and 0
    developed narrow angle glaucoma.
  • Systematic Review 600,000 patients--risk of
    glaucoma was 1 in 20,000.
  • 13 studies wherein persons WITH NARROW ANGLE
    GLAUCOMA given drops, not one developed narrow
    angle closure

9
Malignant Hypertension//Hypertensive Emergency
10
CP1098816-1
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13
Case 1 Clinical Pearl
  • It is NOT the blood pressure per se that
    determines urgency versus emergency, BUT
    RATHER whether severe hypertension (gt180/gt110
    mm/hg) is associated with target organ
    damage/injury. The most accessible site for the
    clinician to uncover that damage is the fundus.

14
Eight days in the ICU what do you get, (not a
little bit older.debt)
  • Blood Pressure in a 28 y.o. of 200s/130s mm/Hg.
  • Treated as a stubborn urgency in the ICU,
    meaning that it took 8 days of concoctions
    (hydralazine and labetalol) to reach a semblance
    of control.
  • Transferred to floor and a funduscopic is
    performed. Grade 3 hypertensive retinopathy
    (hemorrhages and exudates) is discovered after
    dilatation.
  • He has acute on chronic renal failure
    (BUN/Creatinine 46/4.7 from 30/2.8 mg/dl) and
    schistocytes.

15
Clinical Case 2, question
  • If the hypertensive emergency was discovered
    earlier which agent below would have been the
    most appropriate therapy?
  • A.) hydralazine parenterally
  • B.) clonidine loading
  • C.) fenoldopam
  • D.) nitroprusside
  • E.) nitroglycerin

16
The Righteous Brothers were right Time does go
by slowly
  • We have come a long way from diazoxide,
    nitroprusside, clonidine, nitroglycerin,
    hydralazine.
  • Our vocabulary must include nicardipine,
    labetalol, clevidipine, fenoldopam.
  • Lets look at some subtractions some additions
    to the severe hypertension armamentarium

17
Lets look at Fenoldopam
  • How does it work?
  • It is a peripheral dopamine type-1 receptor
    agonist dilating coronary, renal, mesenteric,
    peripheral arteries. An gt in renal blood flow
    GFR can be seen with fenoldopam. Studies
    comparing fenoldopam to nitroprusside in the
    setting of hypertensive emergencies have
    demonstrated NO DIFFERENCE in time to goal blood
    pressure or attainment of mean arterial pressure.
    Studies post-cardiac surgery have reported
    improved outcomes with fenoldopam over both
    nifedipine and nitroprusside after CABG. AVOID
    with neurological injury glaucoma.

18
Lets look at Hydralazine/nitroglycerin -- /--
  • How do they work?
  • Hydralazine direct arterial vasodilator. Onset
    of action 5-15 minutes, BUT its pharmacological
    effect can last up to gt12 hours! In coronary
    disease/dissection, it can worsen the
    cardiovascular situation! It can RAISE
    intracranial pressure. To our OB colleagues
    meta-analysishydralazine increases maternal
    hypotension c-sections, placental abruptions,
    is associated with lower Apgar scores.
  • Nitroglycerin for hypertensive emergency when
    the TOD/I is heart (ischemia, failure), but
    exacerbates volume depletion hypotension and
    gtICP.

19
Lets look at clevidipine labetalol,
  • Clevidipine, How does it work?
  • Short acting Ca Channel Blocker with utility in
    multiple settings except aortic stenosis, heart
    failure, egg and soybean allergy.
  • Labetalol alpha-1 beta antagonist. Across the
    board and no fetal distress.
  • Know about phentolamine, nicardipine, esmolol

20
Clinical Pearl 2 Tailor made medications
  • Haas AR. Marik PE. Current Diagnosis and
    management of Hypertensive Emergency. Seminars In
    Dialysis 2006 19502-12.
  • 1.) Myocardial ischemia/encephalopathy
  • LABETALOL
  • 2.) Acute/chronic renal failure
  • FENOLDOPAM
  • 3.) Pregnancy
  • LABETALOL
  • 4.) Aortic dissection
  • ESMOLOL
  • 5.) Sympathetic crisis
  • NICARDIPINE (phentolamine)

21
Cognizance of Systems Safety
  • Improving quality and safety of hospital care a
    reappraisal an agenda for clinically relevant
    reform. Internal Medicine Journal 2008 3844-55.
  • Prevention of Medication errors Actively involve
    clinical pharmacists in the medication use
    process through attendance on ward rounds

22
Case 3 an ambulatory person with resistant
hypertension
  • Definitions, work up, and therapy

23
Case 3 Resistant, ambulatory hypertension
  • A 54 y.o. Latino man with DM2 and OSA sees you in
    the office for a blood pressure of 210/140 mm/hg.
  • His BP management is enalapril 20 mg/day.
  • He has no target organ damage/injury on
    examination.
  • He brings screening laboratory work Na 141, K
    1.8, Cl- 99, HCO3 51 meQ/L respectively.
  • ABGs pH 7.59, paO2 50 mm/Hg, pCO2 51 mm/Hg
  • Urine lytes (SPOT) Na 46, K48, Cl- 84 meQ/L
    respectively.

24
Question, Case 3
  • Which of the following statements regarding
    resistant hypertension is most accurate (we will
    revisit case 3, step by step after you answer)
  • a.) The definition of resistant hypertension is
    failure to control after adherence with a 4 drug
    regimen.
  • b.) beta blockers consistently lower blood
    pressure across all demographic groupings.
  • c.) Maxing out monotherapy is superior to
    multiple drugs at lower doses.
  • d.) Aldosterone/renin levels are a valuable
    adjunct in the evaluation of the resistant
    hypertensive.

25
Debunking a Myth beta blockers are good
antihypertensives (defining a good regimen).
  • Brewster L.M., van Montfrans G.A., Kleijnen J.
    Systematic Review Anti-hypertensive Drug Therapy
    in Black Patients. Ann. Intern. Med. 2004 141
    614-627.
  • 1.) B-Blockers did not differ significantly from
    placebo in reducing systolic blood pressure as
    monotherapy in blacks.
  • 2.) Two Other studies (Br Med J/Jamaica Curr.
    Med. Res. Opin./A.A.) found that both selective
    and non-selective b-blockers increased blood
    pressure relative to placebo in up to 38 of
    participants.
  • (n 8,300/BP LVH) composite end points of
    stroke, MI, CVD death was 13 less frequent in
    the losartin group compared to the b-blocker
    group

26
The beta blocker moratorium continued
  • ASCOT-BPLA (n 20,000) atenolol vs. amlodipine,
    stopped early because of a 11 lower all-cause
    mortality in the amlodipine limb.
  • J. Am. Coll. Cardiol. 2009 Hindbrain belief
    that tachycardia beta blocker. NO, unless there
    is heart failure or another Evidence-based
    rationale.
  • 6 trials/ 55,675 pts./ B-blockers conferred a
    31 increased risk of new diabetes vs. placebo
    11 vs. other antihypertensives. The DM persons
    had a gt3x increase in CVD. In GEMINI, this
    specific risk (DM) was mitigated by using
    carvedilol instead of a pure beta-blocker.

27
Conclusions
  • Titration of beta blockers in treating
    hypertension, B-blockade-induced bradycardia
    (80,000 pts. in 9 trials) the lower the heart
    rate, the higher the CV mortality, M.I.s,
    strokes, and incidence of HF!!!!
  • AND ALLHAT (gt10,000 A.A.) A.A. randomized to a
    ACEI mono had a 40 greater risk of stroke, a 32
    greater risk of of HF, and a 19 greater risk of
    CVD than those randomized to a diuretic.

28
Resist the urge to Max out monotherapy!
  • Wald D.S., Law M., Morris J.K., et. al.
    Combination Therapy versus Monotherapy in
    Reducing Blood Pressure Meta-analysis on 11,000
    Participants from 42 Trials. Am J Med. 2009 122
    290-300.
  • N 10,968
  • Doubling the dose of one drug (or monotherapy)
    had approximately one-fifth of the equivalent
    incremental blood pressure lowering effect of
    adding another drug class before trying to
    max-out.
  • CAVEATS 50 mg hctz or combination diuretics!
    (MAXIDER, for example).

29
Love those guys Renin and aldosterone
  • Lane et. al. (J Hypertens 2007 25 891-894.).
    133 patients with resistant hypertension
    spironolactone SBP decline 21.7 mm/Hg DBP
    decline 8.5 mm/Hg.
  • Sens. Spec. PV --PV
  • ARR gt20 78 83 56 93
  • ARR gt50 10 99 86 80
  • ARR gt20
  • 57 88 57
    88
  • PAC gt15

30
Back to Case 3
  • Is he resistant? No, he would have required
    treatment failure on a good 3 drug regimen.
  • Is he a hypertensive emergency?
  • Why does he have hypokalemia, alkalemia, a high
    urine chloride?
  • His aldosterone-renin values were 6 .8.
  • Apparent mineralocorticoid excess His cortisol
    was elevated.
  • His ACTH was sky high adrenals were massive
    so?

31
Clinical Pearl(s)
  • When patients fail on a well thought out 3 drug
    regimen, they need a workup (OSA?).
    Aldosterone-renin profiling is a valuable
    adjunct. Be circumspect when prescribing
    beta-blockers for hypertension.
  • A future pearl All patients with hypertension
    may be renin profiled and treated accordingly.
  • Thank you.
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