Hypertension - BMH/Tele

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Hypertension - BMH/Tele

  1. 1. Hypertension Telemetry Course
  2. 2. Course Objectives <ul><li>Discuss the incidence & prevalence of hypertension in the US </li></ul><ul><li>Review blood pressure regulation: baroreceptors, endotehlium, R-A-A-S </li></ul><ul><li>Discuss the stages of hypertension and primary versus secondary </li></ul><ul><li>Understand the difference between hypertension and hypertensive crises </li></ul><ul><li>Review pathophysiology, etiologies, risk factors (controllable vs. uncontrollable), epidemiological data, signs and symptoms, and risks of uncontrolled hypertension </li></ul><ul><li>Discuss diagnostic evaluation of hypertension </li></ul><ul><li>Discuss treatment regimen for patients with hypertension with and without contributing factors </li></ul>
  3. 3. Blood Pressure Regulation <ul><li>Systemic arterial pressure is a function of stroke volume, heart rate, and total peripheral resistance </li></ul><ul><li>The major organs involved in regulation of blood pressure are the heart (HR & SV), the SNS (TPR), and the kidneys (ECF volume & secretion of renin). </li></ul><ul><li>(Wynne, Woo, & Olyaei, 2007, p. 1093) </li></ul>
  4. 4. BP Regulation: Baroreceptors <ul><li>A change in blood pressure is sensed by baroreceptors located in the carotid arteries and the arch of the aorta </li></ul><ul><li>They are sensitive to stretch and they inhibitory impulses to the sympathetic vasomotor center in the brainstem with increased B/P </li></ul><ul><li>(Wynne, Woo, & Olyaei, 2007, p. 1094) </li></ul>
  5. 5. BP Regulation: Baroreceptors <ul><li>Long-standing hypertension, the baroreceptors adapt to the elevated B/P levels and “rests” what the body accepts as “normal” B/P. </li></ul><ul><li>Diminished responsiveness to these baroreceptors is one of the most significant cardiovascular effects of aging and a major factor in the lifetime risk of hypertension </li></ul><ul><li>(Wynne, Woo, & Olyaei, 2007, p. 1094) </li></ul>
  6. 6. BP Regulation: Endothelium <ul><li>Nitric oxide is secreted by endothelial cells which results in relaxation of blood vessels </li></ul><ul><li>It also produces local vasodilators, such as prostacylcin and endothelium-derived hyperpolarizing factor </li></ul><ul><li>Endothelin is an extremely potent vasoconstrictor and also stimulates vascular smooth muscle growth </li></ul><ul><li>(Wynne, Woo, & Olyaei, 2007, p. 1094) </li></ul>
  7. 7. BP Regulation: Kidneys <ul><li>RAAS = Renin-Angiotensin-Aldosterone System </li></ul><ul><li>Renin is relased by the juxtaglomerular appartus of the kidney – renin converts AT1 to AT2 – resulting in vasoconstriction </li></ul><ul><li>AT2 triggers the adrenal gland to release aldosterone which causes retention of water and sodium </li></ul><ul><li>(Wynne, Woo, & Olyaei, 2007) </li></ul>
  8. 8. Angiotensin II <ul><li>“ Recent evidence suggests that angiotensin II also stimulates growth of vascular smooth muscle and may contribute to atherosclerosis and hypertension” </li></ul><ul><li>(Wynne, Woo, & Olyaei, 2007, p. 1094) </li></ul>
  9. 9. BP Regulation: Genetics <ul><li>B/P levels are strongly familial! </li></ul><ul><li>However, exact mechanisms are unknown </li></ul><ul><li>Genetic polymorphisms have been discovered that may harbor genes contributing to primary hypertension </li></ul><ul><li>(Wynne, Woo, & Olyaei, 2007, p. 1095) </li></ul>
  10. 10. What Is Hypertension? <ul><li>Hypertension as a diagnosis is considered when the average of TWO or more consecutive clinical visits documents a DBP of 90 mmHg or greater or a SBP of 140 mmHg or greater. </li></ul><ul><li>Elevated SBP is the main contributor of target organ damage. </li></ul><ul><li>(McCance et al, 2006, p. 1086) </li></ul>
  11. 11. Stages of Hypertension <ul><li>7 th Report of the Joint National Commission of Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC-VII) </li></ul><ul><li>Stages of Hypertension: </li></ul><ul><li>Normal SBP < 120 mmHg or DBP < 80 mmHg </li></ul><ul><li>Pre-Hypertension SBP 121 – 139 mmHg or DBP 81 – 89 mmHg </li></ul><ul><li>Stage 1 SBP 140 – 159 mmHg or DBP 90 – 99 mmHg </li></ul><ul><li>Stage 2 SBP > 160 mmHg or DBP > 100 mmHg </li></ul>
  12. 12. Hypertensive Crises <ul><li>2 Types: </li></ul><ul><li>Hypertensive Emergency </li></ul><ul><li>and </li></ul><ul><li>Hypertension Urgency </li></ul>
  13. 13. Hypertensive Emergency <ul><li>It is extremely elevated B/P and must be lowered immediately in order to prevent target organ damage </li></ul><ul><li>SBP > 180 or DBP > 110 </li></ul><ul><li>Assessment will reveal actual or developing clinical dysfunction of the target organ </li></ul><ul><li>(Smeltzer et al, 2008, p. 1033) </li></ul>
  14. 14. Hypertensive Emergency <ul><li>Treatment: </li></ul><ul><li>Gradually decrease blood pressure usually with fast-acting intravenous medications </li></ul><ul><li>Reduction Goals: </li></ul><ul><li>Reduction of B/P by up to 25% within the 1 st hour </li></ul><ul><li>160/100 within 6 hours </li></ul><ul><li>Then gradual reduction over a period of days </li></ul>
  15. 15. Hypertensive Urgency <ul><li>Extremely elevated B/P but without evidence of impending or progressive target organ damage </li></ul><ul><li>SBP > 180 and/or DBP > 110 </li></ul><ul><li>S/S: Severe HA’s, nosebleeds, anxiety </li></ul><ul><li>(Smeltzer et al, 2008, p. 1033) </li></ul>
  16. 16. Hypertensive Urgency <ul><li>Treatment: </li></ul><ul><li>Gradually decrease blood pressure usually with fast-acting oral medications </li></ul><ul><li>Fast-Acting PO Agents: </li></ul><ul><li>Beta-blockers: labetolol </li></ul><ul><li>ACEI’s: captopril, enalapril </li></ul><ul><li>Alpha 2 -agonists: clonidine </li></ul>
  17. 17. Pathophysiology <ul><li>2 Types of Hypertension </li></ul><ul><li>* Primary (Essential) Hypertension* </li></ul><ul><li>Primary cause is unknown </li></ul><ul><li>*Secondary Hypertension* </li></ul><ul><li>Caused by another disease process </li></ul>
  18. 18. Primary Hypertension <ul><li>Etiological Theories </li></ul><ul><li>Inability of kidneys to excrete sodium </li></ul><ul><li>Overactive renin/angiotensin system </li></ul><ul><li>Overactive sympathetic nervous system </li></ul><ul><li>Decreased vasodilatory reaction </li></ul><ul><li>Resistance to insulin action </li></ul><ul><li>Genetic Inheritance (polygenic) </li></ul>
  19. 19. Prevalence & Incidence <ul><li>The estimated global prevalence of hypertension for the year 200 was 26.4% or 972 million adults worldwide </li></ul><ul><li>The national prevalence for the Unites States is similar at 28.7% of adults (approximately 65 million persons. </li></ul><ul><li>The JNC-VII estimates that about 1 in 5 persons in the United States (1 in 3 adults) has hypertension. </li></ul><ul><li>(Moser & Riegel, 2008, p. 431) </li></ul>
  20. 20. Prevalence & Incidence <ul><li>The JNC-VII estimates that about 1 in 5 persons in the United States (1 in 3 adults) has hypertension. (Moser & Riegel, 2008, p. 431) </li></ul><ul><li>“ Approximately 73.6 million people in the United States aged 20 years and older are affected by hypertension.” (Smithburger et al, 2010, p. 24) </li></ul>
  21. 21. Prevalence & Incidence <ul><li>28% to 31% of U.S. adults have hypertension </li></ul><ul><li>Of these people… </li></ul><ul><li>90% - 95% of people diagnosed with hypertension have primary hypertension! </li></ul><ul><li>(Smeltzer et al, 2008, p. 1021) </li></ul>
  22. 22. Prevalence <ul><li>Of the 28% to 31% of people diagnosed with hypertension… </li></ul><ul><li>5% to 10% have secondary hypertension! </li></ul><ul><li>(Smeltzer et al, 2008, p. 1021) </li></ul>
  23. 23. Secondary Hypertension <ul><li>It is caused by another disease process such as: </li></ul><ul><li>Renal Failure </li></ul><ul><li>Diabetes Mellitus </li></ul><ul><li>Cushing’s Syndrome </li></ul><ul><li>Primary Aldosteronism </li></ul><ul><li>Coarctation of the Aorta </li></ul><ul><li>Pheochromocytoma </li></ul><ul><li>Sleep Apnea </li></ul>
  24. 24. Prevalence of Hypertension <ul><li>The prevalence of hypertension increases with advancing age to the point where more than half of people 60 – 69 years of age and approximately three-fourths of those 70 years of age and older are affected. </li></ul><ul><li>(JNC-VII, p. 8) </li></ul>
  25. 25. Risk Factors <ul><li>The American Heart Association has identified several risk factors that lead to the development of hypertension with increased risk of cardiovascular disease. </li></ul><ul><li>They are separated into two categories: </li></ul><ul><li>Uncontrollable Risk Factors </li></ul><ul><li>Controllable Risk Factors </li></ul>
  26. 26. Controllable Risk Factors <ul><li>Smoking </li></ul><ul><li>**Smoking alone does not cause hypertension** </li></ul><ul><li>Cholesterol Level </li></ul><ul><li>Sedentary Lifestyle </li></ul><ul><li>Obesity </li></ul><ul><li>Diabetes Mellitus </li></ul>
  27. 27. Uncontrollable Risk Factors <ul><li>Increasing Age </li></ul><ul><li>Gender (Male) </li></ul><ul><li>Heredity (including Race) </li></ul><ul><li>Highest prevalence among African Americans </li></ul>
  28. 28. Epidemiological Data <ul><li>The prevalence, impact, and control of hypertension differ across racial and ethnic subgroups of the U.S. population </li></ul><ul><li>(JNC-VII, p. 39) </li></ul>
  29. 29. Epidemiological Data <ul><li>“ Hypertension is one of the most common chronic medical conditions, and it occurs almost twice as frequently in African Americans as in whites.” (Smithburger et al, 2010, p,24) </li></ul><ul><li>“ Approximately 60% of American adults have prehypertension or hypertension, and some groups, such as blacks, older persons, those in low socioeconomic groups, and overweight persons, are disproportionately affected.” </li></ul><ul><li>(Moser & Riegel, 2008, p. 442) </li></ul>
  30. 30. Epidemiological Data <ul><li>The pathogenesis of hypertension in different racial subgroups may differ with respect to the contributions of such factors as salt, potassium, stress, cardiovascular reactivity, body weight, nephron number, sodium handling, or hormonal systems, but in all subgroups, the etiology is multifactorial </li></ul><ul><li>(JNC-VII, p. 39) </li></ul>
  31. 31. Epidemiological Data <ul><li>More than 40% of African Americans have high blood pressure </li></ul><ul><li>This includes both females and males </li></ul><ul><li>The 2004 overall death rate from hypertension was 18.1. Death rates were 15.7 for white males, 14.5 for white females, 51.0 for black males and 40.9 for black females. </li></ul><ul><li>American Heart Association, updated 1/14/08 </li></ul>
  32. 32. Epidemiological Data <ul><li>In African Americans, hypertension is more common, more severe, develops at an earlier age and leads to more clinical sequelae that in age-matched non-Hispanic Whites </li></ul><ul><li>African Americans have a greater prevalence of other CV disease risk factors, especially obesity </li></ul><ul><li>(JNC-VII, p. 39) </li></ul>
  33. 33. Epidemiological Data <ul><li>Mexican Americans and Native Americans have lower control rates than non-Hispanic Whites and African Americans </li></ul><ul><li>(JNC-VII, p. 39) </li></ul>
  34. 34. Epidemiological Data <ul><li>Variance in hypertension-related sequelae in ethnic or racial groups may be attributable to differences in socioeconomic conditions; access to healthcare services; or attitudes, beliefs, and deficits in accurate health-related information </li></ul><ul><li>(JNC-VII, p. 39) </li></ul>
  35. 35. Signs & Symptoms <ul><li>Hypertension is most often asymptomatic </li></ul><ul><li>Commonly the only sign is the elevation of the blood pressure itself </li></ul><ul><li>The following signs or symptoms may occur with severe hypertension: </li></ul><ul><li>Headaches </li></ul><ul><li>Blurred Vision </li></ul><ul><li>Target Organ Damage </li></ul>
  36. 36. Also Known As… <ul><li>Because hypertension is commonly asymptomatic, it often goes undiagnosed until its advanced stages. For this reason, hypertension is known as… </li></ul><ul><li>The Silent Killer </li></ul><ul><li>31% of people with B/P exceeding 140/90 were asymptomatic and unaware of having hypertension </li></ul><ul><li>(Smeltzer et al, 2008, p. 1022) </li></ul>
  37. 37. Statistics <ul><li>Of All of the People With </li></ul><ul><li>High Blood Pressure: </li></ul><ul><li>71.8% are aware of their condition </li></ul><ul><li>61.4% are under current treatment </li></ul><ul><li>35.1% have it under control </li></ul><ul><li>65.9% do not have it under control </li></ul><ul><li>American Heart Association, updated 1/14/08 </li></ul>
  38. 38. Risks of Uncontrolled Chronic Hypertension <ul><li>The major risks of uncontrolled hypertension are damage to target organs and ultimately death due to secondary processes </li></ul>
  39. 39. Target Organ Damage <ul><li>Caused by damage to the body’s blood vessels which particularly affect the following organs: </li></ul><ul><li>Blood Vessels </li></ul><ul><li>Heart </li></ul><ul><li>Kidneys </li></ul><ul><li>Brain </li></ul><ul><li>Eyes </li></ul>
  40. 40. Target Organ: Blood Vessel Damage <ul><li>Hypertension causes damage to the smooth muscles of the vessel lining resulting in weakening and vasoconstriction leading to decreased blood flow to the periphery and target organs… </li></ul><ul><li>Peripheral Artery Disease </li></ul><ul><li>Target Organ Damage </li></ul>
  41. 41. Target Organ: Kidney Damage <ul><li>Hypertension causes damage to the vessels that supply the kidneys which leads to: </li></ul><ul><li>Acute and/or Chronic Renal Failure </li></ul><ul><li>Manifested by increased BUN/creatinine levels and nocturia </li></ul>
  42. 42. Target Organ: ESRD <ul><li>“ Hypertension is second only to diabetes as the most common cause of ESRD” </li></ul><ul><li>(Wynne, Woo, & Olyaei, 2007, p. 1093). </li></ul>
  43. 43. Hypertension & Renal Disease <ul><li>Approximately 90% of persons with end-stage renal disease have a history of hypertension </li></ul><ul><li>Stage 4 hypertension imparts a 22 times greater risk of developing ESRD </li></ul><ul><li>(Moser & Riegel, 2008, p. 440) </li></ul>
  44. 44. Target Organ: Heart Damage <ul><li>Hypertension causes damage to vessels that supply the heart which leads to: </li></ul><ul><li>Left Ventricular Hypertrophy & Heart Failure </li></ul><ul><li>Due to increased workload of the heart </li></ul><ul><li>Coronary Artery Disease & Angina or MI </li></ul><ul><li>Due to decreased blood flow to the coronary vessels </li></ul>
  45. 45. Target Organ: Heart Damage <ul><li>LVH lowers the threshold for MI by the following mecahnisms: </li></ul><ul><li>Increasing demand for blood flow to the larger muscle mass </li></ul><ul><li>Reducing the ability of the coronary circulation to vasodilate </li></ul><ul><li>Shifting the lower range of coronary flow autoregulation upward </li></ul><ul><li>(Moser & Riegel, 2008, p. 440) </li></ul>
  46. 46. Target Organ: Heart Damage <ul><li>Hypertension more than doubles the risk of symptomatic coronary artery disease, including AMI and sudden death, and more than triples the risk of HF </li></ul><ul><li>Hypertension is the leading cause of HF </li></ul><ul><li>Persistent increased afterload imposed by HTN leads to LVH in order to compensate </li></ul><ul><li>(Moser & Riegel, 2008, p. 440) </li></ul>
  47. 47. Target Organ: Heart Damage <ul><li>Hypertension reduces the supply and increases the demand and therefore greatly increases the incidence of MI. </li></ul><ul><li>Contributing factors include the following: </li></ul><ul><li>Atherosclerotic narrowing of the coronary arteries </li></ul><ul><li>High resistance of coronary microvasculature </li></ul><ul><li>Impaired endothelium dependent vasodilation </li></ul><ul><li>Limited coronary reserve </li></ul><ul><li>(Moser & Riegel, 2008, p. 440) </li></ul>
  48. 48. Target Organ: Brain Damage <ul><li>Hypertension causes damage to vessels that supply the brain which leads to: </li></ul><ul><li>Headaches </li></ul><ul><li>Increased ICP </li></ul><ul><li>Transient Ischemic Attack </li></ul><ul><li>Cerebral Vascular Accident </li></ul><ul><li>Ischemic or Hemorrhagic </li></ul><ul><li>Dementia </li></ul>
  49. 49. Target Organ: Brain Damage <ul><li>Hypertension is the premier risk factor for stroke (cerebral infarction and hemorrhagic). </li></ul><ul><li>The risk of stroke increases in proportion to increases in BP” </li></ul><ul><li>Smoking significantly increases this risk in hypertensive patients </li></ul><ul><li>In the elderly, the risk of stroke is related more clearly to SBP than to DBP </li></ul><ul><li>Treatment of HTN reduces stroke incidences </li></ul><ul><li>(Moser & Riegel, 2008, p. 440) </li></ul>
  50. 50. Target Organ: Eye Damage <ul><li>Hypertension causes damage to vessels that supply the eyes which leads to: </li></ul><ul><li>Retinopathy </li></ul><ul><li>Manifested as “blurred vision” </li></ul><ul><li>Papilledema (swelling of the optic disc) </li></ul>
  51. 51. <ul><li>Cerebral Vascular Accident </li></ul><ul><li>Myocardial Infarction </li></ul><ul><li>Hypertensive Cardiomyopathy </li></ul><ul><li>Congestive Heart Failure </li></ul><ul><li>Chronic Renal Failure </li></ul><ul><li>Hypertensive Retinopathy </li></ul><ul><li>Hypertensive Neuropathy </li></ul><ul><li>Coronary Artery Disease </li></ul>Complications of Uncontrolled Hypertension
  52. 52. Hypertension & Mortality <ul><li>From 1994 to 2004 the death rate from hypertension increased 26.6%, and the actual number of deaths rose 56.1%. </li></ul><ul><li>54,707 Americans had hypertension listed as a primary cause of death in 2004 </li></ul><ul><li>Of the 2.4 million U.S. deaths, 300,000 had hypertension as a contributing factor </li></ul><ul><li>American Heart Association, updated 1/14/08 </li></ul>
  53. 53. Diagnostic Studies <ul><li>Thorough Health History and Physical </li></ul><ul><li>Retinal Examination </li></ul><ul><li>To assess possible target organ damage of retinal structures </li></ul><ul><li>Routine Labs </li></ul><ul><li>Urinalysis, blood chemistry including a cholesterol panel </li></ul><ul><li>12-Lead EKG </li></ul><ul><li>Echocardiogram </li></ul><ul><li>Determines Presence of Left Ventricular Hypertrophy and/or Heart Failure </li></ul>
  54. 54. Additional Diagnostic Studies <ul><li>Serum BUN/creatinine Level </li></ul><ul><li>Creatinine Clearance </li></ul><ul><li>24-Hour Urine Protein </li></ul><ul><li>To determine target organ kidney damage </li></ul><ul><li>Renin Level </li></ul><ul><li>High levels of renin activate the angiotensin-renin system leading to increased vasoconstriction </li></ul>
  55. 55. Treatment of Hypertension <ul><li>Diet Modification (DASH Diet) </li></ul><ul><li>Exercise Regimen </li></ul><ul><li>Weight Loss </li></ul><ul><li>Control of Secondary Causes </li></ul><ul><li>Antihypertensive Medication Regimen </li></ul><ul><li>Routine Measurement of B/P and Follow-up Appointments </li></ul>
  56. 56. Diet Modification, Exercise, & Weight Loss <ul><li>Research findings demonstrate that weight loss, reduced alcohol and sodium intake, and regular physical activity are effective lifestyle adaptations to reduce blood pressure </li></ul><ul><li>Studies also show that diets high in fruits, vegetables, and low-fat dairy products can prevent the development of hypertension and can lower elevated blood pressure </li></ul><ul><li>(Smeltzer et al, 2008, p. 1025) </li></ul>
  57. 57. DASH Diet <ul><li>Dietary Approaches to Stop Hypertension </li></ul><ul><li>Recommends four servings of fresh fruits and fresh vegetables per day (Herman, 2010, p. 45) </li></ul>
  58. 58. Exercise Regimen <ul><li>An exercise regimen of at least 30 minutes of a cardiovascular workout 3 – 5 times a week is recommended as a compliment to diet modification and medication regimen </li></ul>
  59. 59. Medication Regimen <ul><li>Diuretics </li></ul><ul><li>Aldosterone Receptor Blockers </li></ul><ul><li>Beta-Adrenergic Blockers </li></ul><ul><li>ACE Inhibitors </li></ul><ul><li>Angiotensin II Receptor Blockers </li></ul><ul><li>Calcium Channel Blockers </li></ul><ul><li>Alpha-1 Blockers </li></ul><ul><li>Vasodilators </li></ul><ul><li>Combination Drugs </li></ul>
  60. 60. Stage 1 Hypertension Without Any other Complications <ul><li>SBP 140 – 159 mmHg or DBP 90 – 99 mmHg </li></ul><ul><li>Common Medication Regimen: </li></ul><ul><li>Thiazide Diuretics </li></ul><ul><li>Considered Drug Therapy: </li></ul><ul><li>ACEI, ARB, BB, CCB, or combination </li></ul><ul><li>(JNC-VII, p. 31) </li></ul>
  61. 61. Stage 2 Hypertension Without Any other Complications <ul><li>SBP > 160 mmHg or DBP > 100 mmHg </li></ul><ul><li>2-Drug Combination: </li></ul><ul><li>Thiazide Diuretic with ACEI, or ARB, or BB, or CCB </li></ul><ul><li>(JNC-VII, p. 31) </li></ul>
  62. 62. Hypertension With Other Complications <ul><li>HEART FAILURE </li></ul><ul><li>Recommended Therapy Options: </li></ul><ul><li>Thiazide Diuretics, BB, ACEI, ARB, Aldosterone Antagonist </li></ul><ul><li>(Clinical Trials and Guideline Basis for Drug Classes, JNC-VII, p. 33) </li></ul><ul><li>Caution: Use of BB may produce many side effects and may exacerbate symptoms of HF. </li></ul><ul><li>(Smeltzer et al, 2008, p. 953) </li></ul>
  63. 63. Hypertension With Other Complications <ul><li>POSTMYOCARDIAL INFARCTION </li></ul><ul><li>Recommended Therapy Options: </li></ul><ul><li>BB, ACEI, Aldosterone Antagonist </li></ul><ul><li>HIGH CORONARY DISEASE RISK </li></ul><ul><li>Recommended Therapy Options: </li></ul><ul><li>Thiazide Diuretic, BB, ACEI, ARB, CCB </li></ul><ul><li>(Clinical Trials and Guideline Basis for Drug Classes, JNC 7, p. 33) </li></ul>
  64. 64. Hypertension With Other Complications <ul><li>DIABETES </li></ul><ul><li>Recommended Therapy Options: </li></ul><ul><li>Clinical trials with diuretics, ACEIs, ARBs, and CCBs have a demonstrated benefit in treatment of hypertension in both type 1 and type 2 diabetics </li></ul><ul><li>(JNC-VII, p. 38) </li></ul>
  65. 65. Hypertension With Other Complications <ul><li>CHRONIC KIDNEY DISEASE </li></ul><ul><li>Recommended Therapy Options: </li></ul><ul><li>ACEI or ARB </li></ul><ul><li>RECURRENT STROKE PREVENTION </li></ul><ul><li>Recommended Therapy Options: </li></ul><ul><li>Thiazide Diuretics or ACEI </li></ul><ul><li>(Clinical Trials and Guideline Basis for Drug Classes, JNC-VII, p. 33) </li></ul>
  66. 66. Treatment of Hypertension in Ethnic or Racial Groups <ul><li>Weight reduction and sodium retention are recommended for all prehypertensive and hypertensive patients but may be particularly effective in minorities </li></ul><ul><li>The salt content of many of minorities’ foods may be very high </li></ul><ul><li>(JNC-VII, p. 39) </li></ul>
  67. 67. Treatment of Hypertension in Ethnic or Racial Groups <ul><li>The low-sodium DASH eating plan was associated with greater reductions in B/P in African Americans than in other demographic subgroups </li></ul><ul><li>(JNC-VII, p. 39) </li></ul>
  68. 68. Treatment of Hypertension in Ethnic or Racial Groups <ul><li>Clinical trials with more that 15,000 Blacks showed that ACEIs were less effective in lowering B/P than either thiazide-type diuretics or CCBs </li></ul><ul><li>African Americans and Asians have a three- to four-fold higher risk of angioedema and have more cough attributed to ACEIs than Caucasians </li></ul><ul><li>(JNC 7, p. 39) </li></ul>
  69. 69. Treatment of Hypertension in Ethnic or Racial Groups <ul><li>In minority groups the use of combination or multiple antihypertensive drug therapy that usually includes a thiazide-type diuretic will lower B/P and reduce the burden of hypertension-related CV disease and renal disease </li></ul><ul><li>(JNC 7, p. 39) </li></ul>
  70. 70. Nonadherence to Treatment of Hypertension <ul><li>The JNC-VII recognizes the seriousness of poor adherence and suggests the following reasons for nonadherence: </li></ul><ul><li>Misunderstanding of condition or treatment </li></ul><ul><li>Denial of illness because of lack of symptoms or perception of drugs symbols ill health </li></ul><ul><li>Lack of patient involvement in plan of care </li></ul><ul><li>Unexpected adverse effects of medications </li></ul><ul><li>Cost of medications </li></ul><ul><li>Complexity of care (Moser & Riegel, 2008, p. 443) </li></ul>
  71. 71. Nonadherence to Treatment of Hypertension <ul><li>The JNC-VII recognizes the seriousness of poor adherence and suggests the following reasons for nonadherence: </li></ul><ul><li>Misunderstanding of condition or treatment </li></ul><ul><li>Denial of illness because of lack of symptoms or perception of drugs symbols ill health </li></ul><ul><li>Lack of patient involvement in plan of care </li></ul><ul><li>Unexpected adverse effects of medications </li></ul><ul><li>Cost of medications </li></ul><ul><li>Complexity of care (Moser & Riegel, 2008, p. 443) </li></ul>
  72. 72. References <ul><li>Donofrio, J., Haworth, K, Schaeffer, L. & Thompson, G., (Eds.). (2005). Cardiovascular care made incredibly easy. Ambler, PA: Lippincott Williams & Wilkins. </li></ul><ul><li>Herman, A. (2010). Hypertension: The pressure’s on. Nursing Made Incredibly Easy, 8 (4), 40-53. </li></ul><ul><li>McCance, K. L., & Huether, S. E. (2006). Pathophysiology: The biologic basis for disease in adults and children, (5 th ed.). Philadelphia, PA: Elsevier Mosby. </li></ul><ul><li>Moser, D. K., & Riegel, B. (2008). Cardiac nursing: A companion to braunwald’s heart disease. Saunders Elsevier: St. Louis, MO. </li></ul><ul><li>Smeltzer, S. C., Bare, B. G., Hinkle, J. L., & Cheever, K. H. (2008). Brunner and suddarth’s textbook of medical-surgical nursing, (11 th ed.). Philadelphia, PA: Lippincott Williams & Wilkins. </li></ul><ul><li>Smithburger, P. L. et al. (2010) Recent advances in the treatment of hypertensive emergency. Critical Care Nurse, 30 (5), 24-30.Woods, S. L., Froelicher, E. S., Underhill Motzer, S., & Bridges, E. J. (2005). Cardiac nursing, (5 th ed.). Philadelphia, PA: Lippincott Williams & Wilkins. </li></ul><ul><li>Wynne, A. L., Woo, T. M., & Olyaei, A. J. (2007). Pharmacotherapeutics for nurse practitioner prescribers, (2 nd ed.). Philadelphia, PA: F. A. Davis Company. </li></ul><ul><li>The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC-VII) </li></ul><ul><li>American Heart Association Website </li></ul>

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