Hypertension - Roger Kunes, PDF
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University of Mount Union
Roger W. Kunes
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This presentation covers various aspects of hypertension, including definition, objectives, causes, diagnosis, and treatment options. It also addresses secondary hypertension, exacerbating factors, and complications. The presentation includes relevant tables and figures.
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Hypertension Roger W. Kunes, MMSc., PA-C Associate Professor University of Mount Union PA Program 1 Objectives Differentiate essential and secondary hypertension Identify causes of secondary hypertension and their management Outline t...
Hypertension Roger W. Kunes, MMSc., PA-C Associate Professor University of Mount Union PA Program 1 Objectives Differentiate essential and secondary hypertension Identify causes of secondary hypertension and their management Outline the stages of hypertension (HTN) Identify exacerbating factors of HTN Describe complications of HTN Prescribe therapeutic lifestyle changes for patients with essential hypertension Describe the proper selection of initial and subsequent antihypertensive agents Identify patients that should be referred to a HTN specialist Diagnose and manage hypertensive urgency & emergency 2 Elevated blood pressure Hypertension: Definition 3 What drug should I choose? 38 yo white female w/ BP 158/95 40 yo black male w/ BP 158/95 58 yo male PMH: angina, DM, w/ BP 165/100 62 yo white pt. w/ HTN, gout 85 yo pt. w/ BP of 148/90, BPH, depression, migraine HAs, CHF, CKD 4 33% adults in US 48% on meds controlled M&M increase w/ increase in systolic or diastolic Epidemiology/ Systolic and pulse pressure better predictors, once > 50 yo Prevalence of HTN Per National Health & Prevalence increases w/ age Nutrition Survey through 2017-20: Blacks > whites (20-30% black, 10-15% whites) Adequate control reduces incidence of: ACS 20-25% Stroke 30-35% HF 50% 5 Diagnosis Sphygmomanometer Bladder width at least 80% of arm circumference Measure after 5 min rest (30 min after coffee or cigarette), sitting or supine r/o “white coat” phenomenon (elevated in office, normal at home) “masked” HTN (opposite) Dx not made on 1 isolated BP reading, unless obvious end-organ damage from HTN 6 Screen for HTN USPSTF: 18 yrs or older w/ office BP measurement (confirm elevation w/ home BP) 7 Measurement & Diagnosis ACC/AHA 2017 Normal BP < 120/80 mmHg Elevated BP 120-129/less than 80 Stage 1 HTN 130-139/80-89 Stage 2 HTN >= 140/90 8 HTN – primary vs secondary Primary (“Essential”) Secondary – Table 13-2 CMDT 95% 5% Complex interaction btwn genetic Endocrine & environmental factors Renal Overactivation of the sympathetic Vascular nervous and RAAS Abnormal CV or kidney Autonomic development Medications Defect in natriuresis Other (OSA, pregnancy) Elevated intracellular Na & calcium levels 9 Renin Angiotensin Aldosterone System (RAAS) 10 Exacerbating factors of HTN Obesity Sleep apnea Increased salt intake ETOH Smoking Polycythemia NSAID use Low potassium intake 11 Metabolic syndrome A constellation of metabolic abnormalities which puts the pt at: 2-fold increased risk of ASCVD, events (MI, stroke, HF) 5-fold increased risk of DM 3 or more to diagnose metabolic syndrome: Central obesity (increased waist circumference) Insulin resistance HTN (elevated BP): > 130 mmHg systolic or 85 diastolic Dyslipidemia low HDL High TG 12 Secondary HTN causes 13 Secondary HTN – Renal disease Renal parenchymal dz is the most common cause of secondary HTN Increased intravascular volume Increased RAAS activity +/- increased sympathetic nerve activity Tx: treat renal dz 14 Secondary HTN – primary hyperaldosteronism Hypersecretion of aldosterone 5-10% of HTN patients MCC of resistant HTN Consider if resistant HTN Labs: aldosterone (elevated) and renin (decreased) levels in AM blood sample Lesion: adrenal adenoma or bilateral adrenal hyperplasia Tx: underlying cause, ie removal of adenoma… 15 Secondary HTN – renal vascular dz Renal artery stenosis Atherosclerosis > fibromuscular dysplasia(suspect in younger, female < 50) 1-2% of HTN pts Excessive renin produced due to decreased renal perfusion Suspect when: 1. onset of HTN before 20 2. resistant HTN 3. epigastric or renal artery bruit 4. atherosclerotic dz of aorta or peripheral arteries 5. abrupt increase (>25%) in creatinine after ACEI 6. episodes of pulm edema w/ surges in BP Test: US of renal arteries 16 Secondary HTN – Cushing Syndrome Elevated cortisol levels (glucocorticoid excess) – salt and water retention, increase angiotensin levels, increased vascular tone Tx – underlying cause of Cushing 17 Secondary HTN - pheochromocytoma Tumor of the sympathetic NS arising from the adrenal medulla secreting epinephrine & norepinephrine. Sx/S: palpitations, sweating, HTN, tachyarrythmias Rare, < 0.1% of HTN pts (2 per million) Labs: elevated plasma fractionated free metanephrines, CT abd Tx: Control BP, surgery to remove tumor(s) 18 Secondary HTN – Coarctation of the Aorta Narrowing of the aorta (usually @ the aortic arch) Consider in young patients with HTN Exam: radial – diminished distal pulses, compare UE & LEs, bilaterally 19 Secondary HTN – pregnancy induced PIH Preexisting w/ worsening in pregnancy Preclampsia, eclampsia 20 Secondary HTN – estrogen use Elevated BP due to estrogen (contraceptives) use (all some, 5% of women have more increase (8/6 mmHg increase)) Low doses for postmenopausal estrogen does not typically cause elevation Especially, obese, > 35, more than 5 yrs of estrogen use Tx: stop estrogen, ideally 21 Secondary HTN – other Thyroid disease Hypercalcemia Increased intercranial pressure Acromegaly 22 HTN Management Lifestyle Modifications (“TLC”) – Table 13-3 CMDT Weight loss DASH diet Increased dietary fiber Lower sodium intake Limit ETOH Exercise (aerobic) 90-150 min/wk Mindfulness – meditation and breathing control Medications 23 Who gets Medication? Table 13-4 note especially ACC/AHA guidelines Note relationship w/ CV risk CV risk factors, Table 13-5 CMDT No increased risk: > 140/90 (goal < 130/80) Increased risk: 130/90 (goal < 130/80) > 65: >130/90 (goal < 130) 24 25 Cardiovascular risk - calculator https://tools.acc.org/ascvd-risk-estimator-plus/#!/calculate/estimate/ App: ASCVD Risk Estimator Plus – downloadable @ https://www.acc.org/ASCVDApp 26 Medications for HTN Management Many classes…6 suitable for initial therapy by efficacy & tolerance ACE inhibitors, ARBs, renin inhibitors, CCBs, diuretics, & BBs Big 4(3): ACEI, ARB, CCB, diuretics (namely thiazide diuretics) Consider compelling reasons to choose an agent (Big 4 or otherwise) 27 Antihypertensive Agents renin and ACE inhibitors, angiotensin II receptor blockers – Table 13-6 Calcium channel blockers – Table 13-7 CMDT nondihydropyridine dihydropyridine Diuretics - Table 13-8 thiazide & related loop aldosterone receptor blockers combination diuretics Beta-adrenergic blockers – Table 13-9 28 Antihypertensive Agents – cont’d Table 13-10 CMDT alpha-adrenergic receptor blockers sympatholytics Vasodilators 29 30 HTN: Choosing an agent Table 11-11 CMDT similar A&C&D A interrupt RAS CD do not (CCB, thiazide Diuretic) 1st Line ACEI ARB CCB Legend: Hypertension treatment guidelines from the United Kingdom’s National Institute for Health and Care Excellence. Guidelines identify ACEI, ARBs, CCBs as first-line medications and suggest a sequence of escalating drug therapy depending on blood pressure response. As noted, the choice of the initial agent is influenced by patient demographics. In step 4, higher doses of thiazide-type diuretics may be used as long as serum potassium levels exceed 4.5 mmol/L. Key: A, ACE inhibitor or ARB; C, calcium-channel blocker; D, diuretic, thiazide- like. (Modified, with permission, from the 2013 hypertension guidelines published by the National Institute for Health and Care Excellence. https://www.nice.org.uk/guidance/cg127/evidence/cg127-hypertension-full-guideline3) 31 Copyright © 2015 McGraw-Hill Education. All rights reserved. 32 Choosing and Agent, cont’d Are their any compelling reasons to use a certain class OR to avoid a certain class? Use: ACE – diabetic, kidney disease, post MI, CHF BB – post MI, CHF, anxiety, migraines, essential tremor Alpha-1 adrenergic blocker - BPH Avoid: thiazide diuretic: gout (uric acid), ~diabetes BB: asthma/COPD (unless cardio-selective), conduction delays (heart block), depression, exercise tolerance 33 From: 2014 Evidence-Based Guideline for the Management of High Blood Pressure in Adults: Report From the Panel Members Appointed to the Eighth Joint National Committee (JNC 8) JAMA. 2014;311(5):507-520. doi:10.1001/jama.2013.284427 Table Title: Strategies to Dose Antihypertensive Drugsa Copyright © 2016 American Medical Date of download: 9/13/2016 34 Association. All rights reserved. How do I dose, when do I add? Add 1 and maximize before adding 2nd,… Add 2nd before maximizing 1st, then titrate both to max before adding 3rd Initiate 2 agents (SBP >160, DBP > 100), then add 3rd and titrate up 35 Know most common side effect(s) Drug Therapy: Current Antihypertensive Agents | Current Medical Diagnosis & Treatment 2024 | AccessMedicine | McGraw Hill Medical (mhmedical.com) 36 Application time 37 38 yo white female w/ BP 158/95 40 yo black male w/ BP 158/95 What drug should I 58 yo male PMH: angina, DM, w/ BP 165/100 choose? 62 yo white pt. w/ HTN, gout 85 yo pt. w/ BP of 148/90, BPH, depression, migraine HAs, CHF, CKD 38 39 Resistant HTN Definition: failure to reach BP control on adherent 3 drug regimen (including a diuretic) Consider causes of resistant HTN Table 13-2 CMDT Aldosterone may be contributing, consider aldosterone receptor blocker Consult HTN specialist 40 Treating other CV risk factors Additional medication therapy in HTN pts: Statin HOPE3 study, says Yes statin for intermediate risk USPSTF says Yes statin for adults 40-75 w/ >= 1 CVD risk (ie HTN…) or 10-yr risk >= 10% ASA Increases risk of GI bleed and hemorrhagic stroke. USPSTF says Yes, for middle-aged adults (40-59) w/ increased CV risk, 10-yr risk >= 10% w/o increased risk of bleeding Shared decision making Get BP to goal first (minimize risk of intracranial hemorrhage) No, for low-risk pts (including, no for >70 health adults) USPSTF says NO for >=60 for primary prevention 41 Uncontrolled HTN Uncontrolled Acute elevation in BP w/o end-organ injury HTN Lower BP w/in hours-days Clonidine, captopril, slow-release nifedipine Emergency vs. Significantly elevated BP (usu > 180/120) w/Sxs/S, findings of end-organ damage Lower BP w/in 1 hour to avoid serious M&M Hypertensive Encephalopathy (HA, irritability, confusion, AMS), nephropathy (hematuria, proteinuria, emergency AKI), stroke, aortic dissection, preclampsia- eclampsia, pulm edema, UA, MI 42 Uncontrolled HTN Uncontrolled Agents: HTN Clonidine, captopril, slow-release nifedipine Emergency vs. Parenteral agents (IV) Lower up to 25% within minutes – 1-2 hours