michigan hypertension core curriculum - State of Michigan

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side of the vascular tree. Arterial BV is determined by the difference in the BV ejected by the heart/unit of time (cardiac output, C.O.) and the outflow through the arterial resistance vessels into the venous capacitance vessels (peripheral runoff). When C.O. and peripheral runoff are balanced, arterial BV and arterial pressure remain constant. If C.O. increases but peripheral runoff doesn’t rise commensurately, then arterial BV rises and BP also increases. Arterial elasticity is an important determinant of the rise in SBP that occurs for any given increase in BV. Generally speaking, arterial elasticity is inversely related to age; that is, younger persons have greater arterial elasticity and with advancing age arterial elasticity declines. Arterial compliance is determined by elastic properties of the large conduit vessels. Arterial compliance is dV/dP - the change in pressure that occurs with a given change in arterial volume. It should be clear that the greater the arterial elasticity, the smaller the rise in systolic pressure during the systolic ejection phase of the cardiac cycle. Conversely, lesser arterial elasticity causes a greater rise in systolic BP during the systolic ejection phase. This also places an extra burden of work on the myocardium to maintain cardiac output, in part because the systolic ejection phase is prolonged under these circumstances. B. Physiological Factors: Cardiac output (stroke volume [SV] * heart rate [HR]) and peripheral arterial resistance, largely determined at the level of the arterioles, are the major physiological factors involved in the determination of arterial BP. C. Age-Related Changes in the Aortic Conduit Vessel There is an age-related reduction in arterial elasticity. This means that the rise in SBP is going to be greater because, for a given stroke volume, less of the SV is “stored” in the stiffer aorta. Pressure waves travel faster in stiff/less elastic arterial blood vessels leading to increased pressure wave reflection from the peripheral arterial vasculature. Thus, SBP rises to a greater degree than would be seen in a younger person with greater arterial elasticity for any given level of stroke volume. Also, because less of the SV is “stored” in the aorta during the systolic ejection phase, there is a greater run-off of the stroke volume to the periphery. Thus, BP falls to a lower level during diastole. These physiologic changes in the vasculature underlie the higher levels of SBP, lower levels of DBP, and widening of the pulse pressure that have been well documented with advancing age. Accordingly, the stiffening of the vasculature places an increased work burden on the myocardium, in part attributable to lengthening of the systolic ejection phase. The normal aortic distension that occurs when blood is ejected from the heart is mediated by the aortic elastin fibers located in the media of the vessel wall. However, with advancing age and elevated blood pressure, aortic elastin fibers fragment thus transferring the pulsatile aortic stress to collagen fibers. This leads to aortic stiffening, a process that is further accelerated by diabetes mellitus and arterial wall calcification. Plausibly the fragmented elastin fibers with their plethora of calcium binding sites plausibly contribute to arterial wall calcification. Chronic kidney disease, smoking, and diabetes mellitus also contribute to calcium deposition in the media of the arterial wall. Figure 3 displays the hemodynamic consequences of aortic stiffening 26 Hypertension Core Curriculum
Figure 3. Hemodynamic Consequences of Aortic Stiffening 2. Blood Pressure Measurement A variety of techniques are available for the measurement of arterial BP. The primary, though not exclusive, method used in clinical settings is indirect estimation of brachial artery pressure using an appropriately sized sphygmomanometer. The arm should be at the level of the heart with the palm facing upward. The BP cuff is inflated above the level of systolic BP by ~ 20 mm Hg. How do you know how high to inflate the BP cuff to determine the SBP level ~ 20 mm Hg above where the systolic BP likely is? Before you listen for Korotkoff sounds, apply an appropriate size cuff to the arm, inflate it until the radial pulse is no loner palpable. Now you are ready to listen for Korotkoff sounds – inflate the cuff ~ 20 mm Hg above the systolic pressure level where the radial pulse was no longer palpable. This stops all blood flow in the brachial artery. Next the cuff is gradually deflated and as the pressure inside the brachial artery exceeds that in the cuff, tapping (Korotokoff phase 1) sounds become audible. The cuff is continually deflated. However, the flow of blood through the brachial artery remains episodic until the pressure in the brachial artery during diastole exceeds the external pressure supplied exerted by the cuff. When this occurs, blood flow during becomes continuous and the tapping sounds disappear (Phase V Korotokoff sound). In some patients the Korotokoff sounds may muffle before they disappear - the BP level of this muffling is (Phase IV Korotokoff sounds). In adults, the Phase I and V Korotokoff sounds are what are recorded as the SBP and DBP, respectively. Systolic blood pressure may vary by 10 or more mm Hg between the arms in ~ 25% of hypertensives. Blood pressure values over the popliteal artery are either as high or more than 20 mm Hg higher than BP determinations obtained over the brachial artery (arm). 3. Central Aortic Blood Pressure Central aortic blood pressure is typically lower than the BP level obtained clinically in the brachial artery. Central aortic blood pressure is likely to be a more important determinant of cardiovascular complications such as stroke and heart failure than peripheral (brachial) blood pressures. This is because aortic SBP is the pressure that the left ventricle ejects blood against and aortic DBP is a major determinant of coronary perfusion pressure. Moreover, central aortic pressure is the pressure that the vasculature in the brain is exposed to. Several non-invasive devices that can be used in clinical settings now allow estimation of central aortic pressure from either radial or carotid pulse waveforms using a validated generalized transfer function. Antihypertensive drugs have been shown to differentially affect central aortic blood pressure. B. Elevated or Hypertensive BP Levels Blood pressure elevations are considered hypertension at different levels of elevation dependent NKFM & MDCH 27
Page 1: MICHIGAN HYPERTENSION CORE CURRICUL
Page 4 and 5: April 2010 Dear Colleague: In 2005,
Page 6 and 7: Kevin L. Piggott, MD, MPH, FAAFP Pr
Page 8 and 9: Blood Pressure Measurement........
Page 10 and 11: 10 Hypertension Core Curriculum Blo
Page 12 and 13: of the wrist. Additionally, there i
Page 14 and 15: asis. National guidelines recommend
Page 16 and 17: Post-Test Questions: 1. High BP is
Page 18 and 19: 18 Hypertension Core Curriculum Ess
Page 20 and 21: Masked Hypertension is when the off
Page 22 and 23: TABLE 1. Prevalence of Awareness, T
Page 24 and 25: Blood Pressure, Circulatory Physiol
Page 28 and 29: upon the other co-morbidities prese
Page 30 and 31: Table 3. Clinically Available Clues
Page 32 and 33: In the setting of chronic hypertens
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Page 36 and 37: cause greater disruption of CBF aut
Page 38 and 39: References/Suggested Reading Agabit
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Page 42 and 43: development of essential HTN can se
Page 44 and 45: Figures: Figure 1. Pie-chart with m
Page 46 and 47: Table 2 Table 3 Screening Test for
Page 48 and 49: References: 1. U.S. Renal Data Syst
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Page 52 and 53: side effects particularly well. A h
Page 54 and 55: 14. Gaede P, Vedel P, Larsen N, Jen
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Page 58 and 59: glycemic risk factdors such as hype
Page 60 and 61: . Weight loss c. Weight gain d. A a
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Page 66 and 67: foods and turn out of necessity to
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Page 72 and 73: Incidence and Prevalence The overal
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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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Preparations and Dosages: The Oral
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patients with tachy-brady syndrome
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significant proteinuria. Pharmacolo
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the effect found by the ACE inhibit
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and nominally statistically signifi
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sensitive K+-channels in vascular s
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clonidine (Catapres†) 0.1-0.8 mg
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Learning Objectives 204 Hypertensio
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general, the response to beta-block
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Table 2: (JNC VII, 2004) 208 Hypert
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Learning objectives: 210 Hypertensi
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ecently published RCT investigated
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Post-test question: 35y/o male w/ h
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Orthostatic Hypotension Pretest que
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BP. It is important to note that la
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1- Fludrocortisone : a mineralocort
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References: 1. Hiitola P, Enlund H,
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www.neuroanatomy.wisc.edu/.../Image
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Learning objectives: 226 Hypertensi
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controlled BP to have been victimiz
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Treatment of Secondary Causes of Hy
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4-Direct vasodilators (e.g.minoxidi
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Hypertension. Aug 2003;42(2):161-16
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emergency by virtue of the associat
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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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