michigan hypertension core curriculum - State of Michigan

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DEFINITION AND CLASSIFICATION Hypertension in pregnancy is defined as a SBP of 140 mm Hg and/or a DBP of 90 mm Hg or higher on at least two separate occasions at least six hours apart, after 20th week of gestation. In the outpatient setting, BP should be measured in the seated position, after a period of rest in a quiet environment. For hospitalized patients, the lateral recumbent position eliminates the effect of compression of the inferior vena cava by the enlarged uterus that impairs venous return and causes a decline in BP. Other important aspects of obtaining a reproducible and accurate BP are the use of an appropriate-sized cuff (1.5 times the upper arm circumference) and avoidance of tobacco or caffeine for at least 30 minutes preceding the reading. (Of course, the use of tobacco during pregnancy should be strongly discouraged altogether). White-coat hypertension occurs in up to 29% of women with no history of preexisting hypertension. A noninvasive 24-hour BP monitor can distinguish white-coat hypertension from true hypertension in the pregnant patient. Classification of the Hypertensive Disorders of Pregnancy The most important consideration in the classification of diseases in which BP rises abnormally is differentiation of hypertensive disorders that antedate pregnancy from potentially more serious disease arising from pregnancy itself. Four major categories (or classification designations) of the hypertensive disorders in pregnancy have been designated both by the National High Blood Pressure Education Program and American College of Obstetricians and Gynecologists guideline committees 1,3 : (1) chronic hypertension, (2) preeclampsia, defined as pregnancy-induced hypertension associated with proteinuria, (3) preeclampsia superimposed on chronic hypertension, and (4) gestational hypertension. Any of these may lead to maternal and perinatal complications Chronic Hypertension Chronic hypertension is defined as BP of 140/90 mm Hg or higher that either predates pregnancy or develops before 20 weeks gestation and persists > 6 weeks post-delivery. If hypertension was documented before conception, the diagnosis of chronic hypertension in pregnancy is straightforward. This condition complicates approximately 3% of pregnancies. Higher rates may be seen in any pregnancy; however, it preferentially occurs in older, obese, and African-American women. Chronic hypertension in pregnancy is classified as either mild or severe, with severe defined by diastolic readings of 110 mm Hg or higher. Gestational Hypertension Gestational hypertension is the most frequent cause of hypertension during pregnancy and is seen in 6% of pregnancies. It is defined as de novo hypertension after mid-pregnancy in the absence of systemic features of proteinuria. If preeclampsia is not present at the time of delivery, and BP returns to normal by 12 weeks postpartum, a diagnosis of “transient hypertension of pregnancy” can be made. Occasionally, women with apparent gestational hypertension remain hypertensive after delivery. These women most likely have pre-existing chronic hypertension, which was masked in early pregnancy by physiological vasodilation. In general, BP >140/90 mm Hg that persists beyond 6 – 12 weeks postpartum is indicative of chronic hypertension. Preeclampsia Preeclampsia is a pregnancy-specific syndrome that develops after 20 weeks gestation and is characterized by increased BP (≥ 140/90 mm Hg), proteinuria (> 300 mg/d), and edema in a woman who was normotensive before 20 weeks. This syndrome, which occurs in 2% to 3% of pregnancies, accounts for more than 50% of all the hypertensive disorders of pregnancy and is a major cause of fetal 260 Hypertension Core Curriculum
and maternal morbidity and mortality. A severe and dangerous variant of preeclampsia is the HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome, which occurs in 1 of 1,000 pregnancies. Preeclampsia Superimposed on Chronic Hypertension The incidence of preeclampsia in women with chronic hypertension is about 15% to 25%, compared with 5% of pregnancies in women without preexisting hypertension. A diagnosis of superimposed preeclampsia is made when de novo proteinuria develops in the latter half of pregnancy or when the hypertension accelerates greatly in the last trimester. The rise in BP is SBP > 30 mm Hg or DBP > 15 mm Hg plus proteinuria and/or edema. The recurrence rate in subsequent pregnancies is high. Risk Factors Risk factors for preeclampsia have been studied extensively as preeclampsia is the hypertensive disorder of pregnancy most commonly associated with severe complications. Risk Factors Nullipara First baby before the age of 20 or after 35 Hypertension before pregnancy Having multiple births African descent Family History of pregnancy induced hypertension Chronic kidney disease, diabetes mellitus Obesity (BMI > 30) 1. Race or ethnicity: The risk associated with race or ethnicity is uncertain. Black women have higher rates of preeclampsia complicating their pregnancies compared to other racial groups, mainly because they have a greater prevalence of underlying chronic hypertension and greater obesity. A recent prospective study 4 , identified a significantly increased risk of preeclampsia and decreased risk of gestational hypertension among Hispanic women relative to non-Hispanic Caucasians. 2. Primigravid pregnancy and history of preeclampsia during previous pregnancies: Although the underlying causative factors are not completely delineated, hypertension in preeclampsia is clearly a consequence of a generalized arterial vasoconstriction. Primigravidas have increased risk for preeclampsia. However, women with a history of preeclampsia have an increased risk during subsequent pregnancies. Other risk factors include extremes of reproductive age, obesity, family history of preeclampsia, chronic hypertension, diabetes mellitus, the presence of trophoblastic disease, multiple gestations, mother’s own low birth weight, prematurity, and young age, connective tissue disease, and kideny disease. 3. Stress and socioeconomic status: Although traditionally considered risk factors, a recent prospective community-based cohort study 5 did not show any association of work stress, anxiety, depression or pregnancy-related anxiety early in pregnancy to the development of gestational hypertension or pre-eclampsia later in pregnancy. A recent study suggested that SSRI exposure during late pregnancy may identify women who are at an increased risk for gestational hypertension and preeclampsia. 6 A few studies that examined the association NKFM & MDCH 261
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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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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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Page 212 and 213: ecently published RCT investigated
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Page 216 and 217: Orthostatic Hypotension Pretest que
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Page 224 and 225: www.neuroanatomy.wisc.edu/.../Image
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Page 236 and 237: emergency by virtue of the associat
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 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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