michigan hypertension core curriculum - State of Michigan

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trials included a placebo arm. Seven drug classes were identified: nitrates (9 trials), ACE inhibitors (7 trials), Calcium channel blockers (6 trials), alpha-1- adrenergic antagonists (4 trials), diuretics (3 trials), direct vasodilators (2 trials) and dopamine agonists (1 trial). Table 3 lists the drugs primarily used for the management of hypertensive emergencies. Hypertensive emergencies are treated initially with intravenous medications while hypertensive urgencies are almost always treated with oral medications. Table 3—Dosage of Commonly Used Parenteral Antihypertensive Medications Clevidipine 2 mg/hour, titrate as needed by doubling every 3 minutes to maximum dose 32 mg/hour 13a Enalaprilat 1.25 mg over 5 min every 4 to 6 h, titrate by 1.25-mg increments at 12- to 24-h intervals to maximum of 5 mg q6h Esmolol 500 μg/kg loading dose over 1 min, infusion at 25 to 50 μg/ kg/min, increased by 25 μg/kg/min every 10 to 20 min to maximum of 300 μ/kg/min Fenoldopam 0.1 μg/kg/min initial dose, 0.05 to 0.1 μg/kg/min increments to maximum of 1.6 μg/kg/min Labetalol 20-mg initial bolus, 20- to 80-mg repeat boluses or start infusion at 2 mg/min with maximum 24-h dose of 300 mg Nicardipine 5 mg/h, increase at 2.5 mg/h increments every 5 min to maximum of 15 mg/h Nitroglycerin 5 μg/min, titrated by 5 μg/min every 5 to 10 min to maximum of 60μg/min Nitroprusside 0.5 μg/kg/min, increase to maximum of 2 μg/kg/min to avoid toxicity Phentolamine 1- to 5-mg boluses, maximum 15-mg dose General treatment principles in this setting have been established – immediate lowering of BP to levels that halt additional hypertensive TOD without inducing new TOD due to ischemia. JNC- 7 6 suggests that BP be lowered no more than 25% within the first hour, and then to 160/100-110 within 2-6 hours. An alternative and more cautious set of BP goals would be to lower BP ~ 10% in the first few hours and then by no more than 25% during the first 24 hours. As detailed below, other recommendations exist for particular situations. The need for immediate but controlled decreases in BP usually indicates the need for monitoring in a critical care setting with an arterial BP monitor, and continuously infused intravenous medications. 240 Hypertension Core Curriculum
NEUROLOGICAL EMERGENCIES Acute Ischemic Stroke Patients presenting with an acute stroke frequently demonstrate severe elevations of BP due to multiple underlying mechanisms including preexisting hypertension, Cushing’s reflex, and activation of multiple pathways including the RAA axis, cortisol, and catecholamines. While extreme elevation of BP is a risk factor for poor outcome due to cerebral edema and intracranial hemorrhage, there is also concern that acute lowering of BP will result in extension of infarction size because of loss of cerebral autoregulation in the watershed area around the infarct (ischemic penumbra) and pressure-dependent cerebral blood flow in this area during the acute phase. Recommendations for therapy must be considered expert opinion (level C evidence) based due to the poor quality and conflicting nature of published evidence. The Cochrane Collaboration analyzed the studies available as of July 2007 that assessed the effect of deliberately altering BP within one week following an acute stroke, and the effect of different vasoactive drugs in that setting. 13 Their review included 12 trials with a total of 1153 patients receiving medications that included angiotensin converting enzyme inhibitors, angiotension II receptor blockers, beta blockers, and calcium channel blockers among others. There was no demonstrable overall morbidity or mortality effect. No distinction was made between ischemic and hemorrhagic stroke. In most instances, acute BP lowering with intravenous antihypertensive mediations need not be considered unless BP exceeds 220 mm Hg systolic and/or 120 mm Hg diastolic. However, emergent IV antihypertensive medication(s) will be warranted even at BP levels below the aforementioned BP thresholds in the presence of concomitant new or worsening target-organ injury (e.g., pulmonary edema, heart failure). The least controversy exists in patients considered eligible for thrombolytic therapy. According to recent American Heart Association/ American Stroke Association Stroke Council guidelines 14 , BP should be reduced to 200 mm Hg or mean arterial blood pressure (MAP) > 150 mm Hg is considered an indication for aggressive BP lowering using continuous intravenous infusion therapy, preferably with an arterial line BP monitoring. SBP > 180 mm Hg (MAP >130 mm Hg) is considered NKFM & MDCH 241
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MICHIGAN HYPERTENSION CORE CURRICUL
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April 2010 Dear Colleague: In 2005,
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Kevin L. Piggott, MD, MPH, FAAFP Pr
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Blood Pressure Measurement........
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10 Hypertension Core Curriculum Blo
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of the wrist. Additionally, there i
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asis. National guidelines recommend
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Post-Test Questions: 1. High BP is
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18 Hypertension Core Curriculum Ess
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Masked Hypertension is when the off
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TABLE 1. Prevalence of Awareness, T
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Blood Pressure, Circulatory Physiol
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side of the vascular tree. Arterial
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upon the other co-morbidities prese
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Table 3. Clinically Available Clues
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In the setting of chronic hypertens
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34 Hypertension Core Curriculum Tab
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cause greater disruption of CBF aut
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References/Suggested Reading Agabit
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40 Hypertension Core Curriculum Chr
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development of essential HTN can se
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Figures: Figure 1. Pie-chart with m
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Table 2 Table 3 Screening Test for
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References: 1. U.S. Renal Data Syst
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50 Hypertension Core Curriculum Spe
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side effects particularly well. A h
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14. Gaede P, Vedel P, Larsen N, Jen
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Learning Objectives: 56 Hypertensio
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glycemic risk factdors such as hype
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. Weight loss c. Weight gain d. A a
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References: 1. Association AD. All
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64 Hypertension Core Curriculum Spe
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foods and turn out of necessity to
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Figure 1: Table 1. Metabolic Syndro
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9. Singh GK, Kogan MD, Van Dyck PC,
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Incidence and Prevalence The overal
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access to healthy foods than their
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As a part of the approach to managi
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B Hypertensive Adults (rate, percen
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References: 1. Lewington S, Clarke
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82 Hypertension Core Curriculum
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appear to be related to access to c
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CDC MMWR Feb 24, 2006/55(07); 177-1
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Figure 1; Clinical presentation and
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90 Hypertension Core Curriculum Phe
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ANY patient, who develops paroxysma
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Figure 1: 94 Hypertension Core Curr
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Objectives: 96 Hypertension Core Cu
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Definition Prevalence Clinical Feat
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intake. 4 Figure 1; Ion transport i
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loading with 200 mmoles (4.6 grams)
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Figure 3; Endocrine Society See tex
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INTRODUCTION 106 Hypertension Core
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Renal manifestations. Renal ischemi
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to assess renal dimensions and dupl
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stenosis severity. Patients with no
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ARAS, ischemic nephropathy, and imp
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the goals of minimizing injury to t
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hemodynamically impaired renal arte
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e classified as having “renovascu
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disease of the abdominal aorta and
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Table 1. Contemporary evaluation of
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2. Screening tests for RAS RDU, MRA
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Manifestations of vital organ injur
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Table 6. Clinical evaluation of ren
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Table 9. Assessment of worsening re
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Table 11. New terminology for renal
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References: 1. Murphy TP, Soares G,
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2001;12(6):1235-1241. 40. Subramani
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78. Tami LF, McElderry MW, al-Adli
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142 Hypertension Core Curriculum Pr
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monitored hypertension screening an
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Policy Development: Public health p
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Med Clin North Am. Jan 2004;88(1):2
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mind they will have no problem iden
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Role of Race in the Selection of An
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individuals of any race or ethnicit
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Older Patients Need Elevated Systol
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sister, mother and father. A family
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ecause pressure-related retinopathy
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pulses (lower in the left arm). 4 C
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Vital signs suggestive of OSAHS. 20
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may shed light on underlying medica
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References: patients. 8 However, th
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Objectives: 170 Hypertension Core C
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and evidence that anti-hypertensive
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When subjects are given instruction
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interestingly found only a 6.0/4.6
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pressure: a meta-analysis of random
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isolated systolic hypertension have
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Compelling Indications for Specific
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3.) Beta-blockers, ACE inhibitors,
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treatment levels - albeit though at
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Preparations and Dosage: Oral antih
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Page 192 and 193: patients with tachy-brady syndrome
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Page 208 and 209: Table 2: (JNC VII, 2004) 208 Hypert
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Page 212 and 213: ecently published RCT investigated
Page 214 and 215: Post-test question: 35y/o male w/ h
Page 216 and 217: Orthostatic Hypotension Pretest que
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Page 220 and 221: 1- Fludrocortisone : a mineralocort
Page 222 and 223: References: 1. Hiitola P, Enlund H,
Page 224 and 225: www.neuroanatomy.wisc.edu/.../Image
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Page 230 and 231: Treatment of Secondary Causes of Hy
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Page 234 and 235: Hypertension. Aug 2003;42(2):161-16
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Page 238 and 239: PATHOPHYSIOLOGY The underlying mech
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Page 244 and 245: ACUTE KIDNEY INJURY (AKI) In additi
Page 246 and 247: Blood Pressure Research Council, an
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Page 250 and 251: y sodium restriction or the use of
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Page 260 and 261: DEFINITION AND CLASSIFICATION Hyper
Page 262 and 263: etween adult socioeconomic position
Page 264 and 265: women treated with atenolol in earl
Page 266 and 267: Obstet Gynecol. Dec 12 2008. 5. Vol
Page 268 and 269: able to dissipate the pressure rise
Page 270 and 271: Use of Dihydropyridine Calcium Anta
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Page 274 and 275: Case 4 Hypertensive patient with CK
Page 276 and 277: Case 6 276 Hypertension Core Curric
Page 278 and 279: year. Sodium restriction and weight
Page 280: What may be causing these new sympt
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