michigan hypertension core curriculum - State of Michigan

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PATHOPHYSIOLOGY The underlying mechanisms of essential hypertension remain largely speculative. The events that explain the transition from hypertensive urgency to emergency, and the corresponding initiation of acute TOD, are even less well understood. There is general agreement that in a subset of patients the abrupt and/or severe elevation of BP or the neuroendocrine milieu associated with it leads to vasoconstriction and endothelial injury. This in turn activates multiple proinflammatory and procoagulant pathways, which in turn further aggravate the endothelial injury, increased peripheral resistance, hypertension, and adverse neuroendocrine milieu. Ultimately, fibrinoid necrosis of arterioles and tissue ischemia result in the clinical manifestions of TOD. Maladaptive imbalances in the renin-angiotensinaldosterone (RAA) axis, catecholamines, interleukins, vasopressin, endothelin, and nitric oxide are some of the implicated mechanisms. Pressure induced natriuresis and volume depletion is thought to be another common pathogenetic factor. Thus, rather than using diuretics as in chronic hypertension, the treatment of hypertensive emergencies frequently entails the use of intravenous saline except in case of decompensated congestive heart failure and pulmonary edema. TREATMENT Hypertensive Urgency The risks of rapidly lowering the BP in patient with hypertensive urgency, given the absence of acute TOD, are generally agreed to outweigh the benefits. Therefore, following confirmation that TOD is in fact not present and that acute secondary causes have been addressed (Table 2) the goal is to gradually reduce blood pressure to “safer” levels (≤ 160/95) over 24 to 48 hours with usual doses of common oral antihypertensive medications In the emergency room, therapy is often started with relatively short acting and quicker acting drugs such as clonidine, captopril, labetolol, or nicardipine to facilitate discharge after several hours of observation, but the patient should be switched to longer acting drugs more suitable for chronic therapy. Despite the common practice of using intravenous drugs to treat hypertensive urgency, there is rarely a compelling reason to do so. In patients with chronic kidney disease the risks of starting an ACE inhibitor or ARB acutely need to be carefully considered if the patient’s likelihood of obtaining follow-up care appears to be low. Regardless, prior to discharge the ER should ascertain that the patient is asymptomatic, and that provision for short term follow-up has been made. Increasingly, the ER must also work with a social worker or discharge planner to obtain a short term supply of medication for the patient as well, with referral to appropriate resources for medication dispensing as well as medical care. Symptomatic patients, those failing to show any improvement in BP despite initial therapy, those with extreme elevations of blood pressure, and those very unlikely to obtain follow up care should be considered for at least 23 hour admission. Careful discharge instructions, with advice to return if symptoms worsen, are also essential. Multiple adjustments of medications and dosages are likely to be needed over weeks to months. 238 Hypertension Core Curriculum
Table 2. Evaluation of Patient with Hypertensive Urgency and Emergency ETIOLOGIES Medication nonadherence EXAMINATION/ STUDY Hx, pill counts Encephalopathy Pain Hx, PE Cardiac Amphetamine, cocaine, PCP abuse Alcohol withdrawal Drug interaction/ effect (e.g., sympathomimetic ± MAO inhibitor, TCA + MAO inhibitor) Bladder outlet obstruction Volume overload (especially in setting of CKD) Hx, PE, drug screen Hx, PE, ? drug screen COMPLICATIONS EXAMINATION /STUDY Vasculopathy Renal failure, proteinuria Hx, PE Retinopathy Hx, PE, ultrasound if indicated Hx, PE Eclampsia Hx, PE, CT if indicated Hx, PE, EKG; CXR, CT if indicated Hx, PE, CBC, platelets; CXR, CT if indicated Hx, PE, lytes 7, urinalysis Fundoscopy, vision testing Hx, PE, (see section on eclampsia) Hx, PE, U/A, lytes Preeclampsia 7, uric acid Hx = history PE=physical exam U/A= urinalysis U/S=ultrasound CXR=chest X-ray Hypertensive Emergency The specific treatment of hypertensive emergencies remains largely opinion-based. In a metaanalysis examining 15 randomized control trials (869 patients) conducted through August 2007, the Cochrane Collaboration12 concluded that current trials have been unable to prove that in hypertensive emergencies either 1) antihypertensive medications reduce morbidity or mortality in hypertensive emergencies compared to placebo or than 2) any one particular first line antihypertensive medication reduces morbidity or mortality more than any other medication. There has been considerable debate and no real consensus over medication use in patients presenting with hypertensive emergency. Only two NKFM & MDCH 239
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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
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 230 and 231: Treatment of Secondary Causes of Hy
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Page 240 and 241: trials included a placebo arm. Seve
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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 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
Page 272 and 273: 272 Hypertension Core Curriculum Ca
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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