michigan hypertension core curriculum - State of Michigan

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Preparations and Dosages: The Oral Beta Blockers Atenolol (Tenormin) 25–100 mg PO QD Betaxolol (Kerlone) 5–20 mg PO QD Bisoprolol (Zebeta) 2.5–10 mg PO QD Metoprolol (Lopressor) 50–100 mg PO QD/BID Metoprolol extended release (Toprol XL) 50–100 mg PO QD Nadolol (Corgard) 40–120 mg PO QD Nebivolol (Bystolic) QD Propranolol (Inderal) 40–160 mg PO BID Propranolol long-acting (Inderal LA) 60–180 mg PO QD Timolol (Blocadren) 20–40 mg PO BID Beta Blockers with Intrinsic Sympathomimetic Activity Acebutolol (Sectral) 200–800 mg PO BID Penbutolol (Levatol) 10–40 mg PO QD Pindolol (generic) 10–40 mg PO BID Calcium Antagonists Calcium channel blockers (CCBs) were first developed in the 1960s and brought into routine clinical practice in the 1980s. They are widely used for the treatment of hypertension, angina, and cardiac arrhythmias. Numerous studies conducted since the 1980s, including the VA Cooperative Study 6 , the Treatment Of Mild Hypertension Study (TOMHS) 7 , and the German HANE 8 study have demonstrated the CCBs to be equivalent or superior in controlling BP than other agents, including diuretics, ACE inhibitors and beta blockers . Furthermore, a recent meta-analysis of more than 150,000 patients in 29 trials comparing different categories of antihypertensive drugs found that CCB-based therapy was superior to placebo in preventing stroke and coronary heart disease, though inferior to diuretic, blocker therapy and ACE inhibitor therapy in preventing heart failure. 9 Such findings are consistent with the findings of the ALLHAT trial that found amlodipine to be as effective as the compared diuretic (chlorthalidone) in preventing all CVD outcomes except for heart failure. 10 The CCBs are effective and generally well tolerated, and their long duration of action and favorable adverse effect profile make them widely prescribed antihypertensive agents. They seem to be effective as initial therapy or monotherapy for BP treatment and combine very effectively with RAS blockers for lowering BP and reducing CVD. Calcium antagonists are therefore very important antihypertensive drugs in the treatment of hypertension. Calcium antagonists, unlike many other antihypertensive agents, maintain their BP lowering efficacy in high or ad-lib dietary sodium environments and also experience minimal 190 Hypertension Core Curriculum
attenuation of their BP lowering effectiveness when used with non-steroidal anti-inflammatory drugs. Pharmacology/Mechanism of Action: The calcium channel blockers are varied in structural morphology but all function by blocking the transmembrane flow of calcium ions through voltage-derived channels (L-type channels) in vascular and non-vascular smooth muscle. Blockade of these channels prevents calcium influx which is required for smooth muscle contraction and cardiac myocyte contraction. This results in smooth muscle relaxation decreased peripheral vascular resistance, dilation of coronary arteries, and a decrease in myocardial contractility. The agents are further sub classified into the dihydropyridine and non-dihydropyridine classes based on their chemical structure. The dihydropyridine class (members identified with the suffix "-dipine") are relatively more selective for vascular smooth muscle and are probably a bit more potent BP lowering agents than non-DHP calcium antagonists. The non- dihydropyridine CCBs are, in contrast, more selective for the myocardium and cardiac conduction system and less active in vasculature smooth muscle. They are comprised of the phenylalkylamine subclass, including verapamil, and the benzothiazepine subclass, which includes diltiazem. Of the two medications, verapamil is more selective for the myocardium and is effective in the treatment of arrhythmias and for angina by reducing myocardial oxygen demand. Diltiazem is intermediate in its myocardial/vascular smooth muscle specificity and causes a hypotensive effect without provoking as much reflex cardiac stimulation as the dihydropyridines. Toxicity/Adverse Effects: The DHP calcium channel blockers can cause flushing, headache, lower extremity edema and reflex tachycardia with dependent edema being the most common dose-related side effect. The reflex sympathetic response is less common with the longer acting dihydropyridines (e.g. amlodipine). The non-dihydropyridines can cause bradycardia, impaired electrical conduction (e.g., atrioventricular nodal block), and depressed contractility, so patients with conduction defects or systolic dysfunction should not be given these medications. The more cardioselective CCBs can interact dangerously with beta blockers since both classes of drugs have overlapping effects of decreasing cardiac contractility and impeding cardiac conduction. Concomitant administration of these drugs can cause advanced heart block and greatly impaired inotropic function of the heart. Thus, non-DHP CCB’s should not be used with beta blockers; however, DHP CCB’s can be safely used with beta blockers. All CCB’s can depress sino-atrial node firing in patients with sick sinus syndrome so no CCB should be used in NKFM & MDCH 191
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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
Page 140 and 141: 78. Tami LF, McElderry MW, al-Adli
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Page 144 and 145: monitored hypertension screening an
Page 146 and 147: Policy Development: Public health p
Page 148 and 149: Med Clin North Am. Jan 2004;88(1):2
Page 150 and 151: mind they will have no problem iden
Page 152 and 153: Role of Race in the Selection of An
Page 154 and 155: individuals of any race or ethnicit
Page 156 and 157: Older Patients Need Elevated Systol
Page 158 and 159: sister, mother and father. A family
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Page 162 and 163: pulses (lower in the left arm). 4 C
Page 164 and 165: Vital signs suggestive of OSAHS. 20
Page 166 and 167: may shed light on underlying medica
Page 168 and 169: References: patients. 8 However, th
Page 170 and 171: Objectives: 170 Hypertension Core C
Page 172 and 173: and evidence that anti-hypertensive
Page 174 and 175: When subjects are given instruction
Page 176 and 177: interestingly found only a 6.0/4.6
Page 178 and 179: pressure: a meta-analysis of random
Page 180 and 181: isolated systolic hypertension have
Page 182 and 183: Compelling Indications for Specific
Page 184 and 185: 3.) Beta-blockers, ACE inhibitors,
Page 186 and 187: treatment levels - albeit though at
Page 188 and 189: Preparations and Dosage: Oral antih
Page 192 and 193: patients with tachy-brady syndrome
Page 194 and 195: significant proteinuria. Pharmacolo
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Page 204 and 205: Learning Objectives 204 Hypertensio
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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
Page 232 and 233: 4-Direct vasodilators (e.g.minoxidi
Page 234 and 235: Hypertension. Aug 2003;42(2):161-16
Page 236 and 237: emergency by virtue of the associat
Page 238 and 239: PATHOPHYSIOLOGY The underlying mech
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trials included a placebo arm. Seve
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an indication for careful and modes
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ACUTE KIDNEY INJURY (AKI) In additi
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Blood Pressure Research Council, an
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[ACE inhibitors (ACEIs), angiotensi
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y sodium restriction or the use of
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44 months 24 , and were also seen i
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• Hypertension in dialysis patien
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GISEN Group (Gruppo Italiano di Stu
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258 Hypertension Core Curriculum
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DEFINITION AND CLASSIFICATION Hyper
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etween adult socioeconomic position
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women treated with atenolol in earl
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Obstet Gynecol. Dec 12 2008. 5. Vol
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able to dissipate the pressure rise
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Use of Dihydropyridine Calcium Anta
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272 Hypertension Core Curriculum Ca
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Case 4 Hypertensive patient with CK
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Case 6 276 Hypertension Core Curric
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year. Sodium restriction and weight
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What may be causing these new sympt
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