michigan hypertension core curriculum - State of Michigan

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Hypertension. Aug 2003;42(2):161-165. 25. Logan AG, Perlikowski SM, Mente A, et al. High prevalence of unrecognized sleep apnoea in drug-resistant hypertension. J Hypertens. Dec 2001;19(12):2271-2277. 26. Becker HF, Jerrentrup A, Ploch T, et al. Effect of nasal continuous positive airway pressure treatment on blood pressure in patients with obstructive sleep apnea. Circulation. Jan 7 2003;107(1):68-73. 27. Fong MW, Filippone JD, Beck GR, Katz MG, Bisognano JD. Improving care in resistant hypertension: medication trends and nonpharmacologic strategies in a specialty clinic. Am J Cardiovasc Drugs. 2007;7(6):449-452. 28. Sica DA. Chlorthalidone: has it always been the best thiazide-type diuretic? Hypertension. Mar 2006;47(3):321-322. 29. Finnerty FA, Jr., Maxwell MH, Lunn J, Moser M. Long-term effects of furosemide and hydrochlorothiazide in patients with essential hypertension a two-year comparison of efficacy and safety. Angiology. Feb 1977;28(2):125-133. 30. Nishizaka MK, Zaman MA, Calhoun DA. Efficacy of low-dose spironolactone in subjects with resistant hypertension. Am J Hypertens. Nov 2003;16(11 Pt 1):925-930. 31. Eide IK, Torjesen PA, Drolsum A, Babovic A, Lilledahl NP. Low-renin status in therapy-resistant hypertension: a clue to efficient treatment. J Hypertens. Nov 2004;22(11):2217-2226. 32. Nishizaka MK, Calhoun DA. The role of aldosterone antagonists in the management of resistant hypertension. Curr Hypertens Rep. Oct 2005;7(5):343-347. 33. Saha C, Eckert GJ, Ambrosius WT, et al. Improvement in blood pressure with inhibition of the epithelial sodium channel in blacks with hypertension. Hypertension. Sep 2005;46(3):481-487. 34. Chapman N, Dobson J, Wilson S, et al. Effect of spironolactone on blood pressure in subjects with resistant hypertension. Hypertension. Apr 2007;49(4):839-845. 35. Hermida RC, Ayala DE, Calvo C, et al. Effects of time of day of treatment on ambulatory blood pressure pattern of patients with resistant hypertension. Hypertension. Oct 2005;46(4):1053- 1059. 36. Nishizaka MK, Calhoun DA. Use of aldosterone antagonists in resistant hypertension. J Clin Hypertens (Greenwich). Aug 2004;6(8):458-460. 37. Saseen JJ, Carter BL, Brown TE, Elliott WJ, Black HR. Comparison of nifedipine alone and with diltiazem or verapamil in hypertension. Hypertension. Jul 1996;28(1):109-114. 234 Hypertension Core Curriculum
HYPERTENSIVE URGENCY AND EMERGENCY Ankur Sandhu, MD and Mark Faber, MD CASE A 49 year old woman is brought to the emergency department by a relative with a one day history of headache, blurred vision and confusion. She has been out of her anti-hypertensive medications for one week. Her past medical history is significant for stage 3 CKD due to hypertensive nephrosclerosis, and abuse of crack cocaine and marijuana. Blood pressure is noted to be 220/130mmHg. Physical examination reveals a confused patient, with papilledema, elevated JVP, and bibasilar crackles. Neurological exam revealed normal power in all 4 limbs, bilateral clonus, and equivocal Babinski signs. Serum values are significant for K + 3.4mEq/L, BUN 30 mg/dL, creatinine 3.5 mg/dl (baseline 1.7 mg/dL), BNP 1400 pg/ ml, and initial cardiac troponin 1.8ng/mL. Urine toxicology analysis is positive for canabinnoids. ECG reveals left ventricular hypertrophy by voltage criteria with T wave inversions in lateral leads. A chest X-ray reveals bilateral pulmonary edema with cardiomegaly. Computed tomography of the head without contrast reveals low attenuation suggestive of ischemia/ ischemic edema in the cortex and subcortical white matter of the parieto-occipital lobes. The patient was admitted to the cardiac intensive care unit treated with intravenous nitroprusside and intravenous furosemide 80mg Q 12 hours. Her BP decreased to 196/100 mm Hg over the first three hours. During the next 12 hours there was progressive improvement in neurological status and resolution of pulmonary edema. She was switched to oral antihypertensive medications and transferred to a general practice unit. EPIDEMIOLOGY AND ETIOLOGY Approximately 1-2% of the 72 million U.S. patients with hypertension can be expected to experience a hypertensive emergency. Despite the widespread availability of effective antihypertensive medications, hypertensive urgency or emergency (defined in the following section) still accounts for up to 25% of emergency room visits. 1 As this case illustrates, > 90% of patients with hypertensive emergencies have been previously diagnosed with essential hypertension and have received prescriptions for antihypertensive medication 2 but inadequate BP control 3 , medication non-adherence4 , and drug abuse 5 are major risk factors. Despite widespread agreement that the vast majority of hypertensive emergencies are caused by severe essential hypertension, it remains standard practice to evaluate patients for causes of secondary hypertension if it has been done previously at some point following control of their BP. DEFINITIONS The management of extreme elevations in BP has been hampered historically by the use of overlapping, and loosely defined terminology. The JNC 7 complete report 6 retains the term “hypertensive crisis” which is further divided into categories of “hypertensive emergency” and “hypertensive urgency.” Hypertensive emergency is defined as “severe elevation in BP that is typically > 180/120 and complicated by evidence of new or progressive target organ dysfunction (TOD),” such as the complications listed in Table 1. Thus, our case study is an example of a hypertensive NKFM & MDCH 235
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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
Page 184 and 185: 3.) Beta-blockers, ACE inhibitors,
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Page 188 and 189: Preparations and Dosage: Oral antih
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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 222 and 223: References: 1. Hiitola P, Enlund H,
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Page 230 and 231: Treatment of Secondary Causes of Hy
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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
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Page 250 and 251: y sodium restriction or the use of
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Page 256 and 257: GISEN Group (Gruppo Italiano di Stu
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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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