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Essential Hypertension

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Essential Hypertension By Raheef Alatassi
Definition & classifications
Prevention & detection & importance
Causes
HTN in pregnancy
Management
Goals of treatment
Classes of drugs & side effects
Specific management in e.g. IHD,DM
HTN emergency & urgency with management

Veröffentlicht in: Gesundheit & Medizin
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Essential Hypertension

  1. 1. Essential Hypertension Raheef Alatassi 4th year medical student Internal medicine
  2. 2. Objectives  Definition & classifications  Prevention & detection & importance  Causes  HTN in pregnancy  Management  Goals of treatment  Classes of drugs & side effects  Specific management in e.g. IHD,DM  HTN emergency & urgency with management
  3. 3. Definition & classifications
  4. 4. Definition of essential hypertension Essential, primary, or idiopathic hypertension is defined as high BP in which secondary causes such as Reno vascular disease, renal failure, aldosteronism, or other causes of secondary hypertension or mendelian forms (monogenic) are not present.
  5. 5.  Essential hypertension accounts for 95% of all cases of hypertension.  Essential hypertension is a heterogeneous disorder, with different patients having different causal factors that lead to high BP.  Essential hypertension needs to be separated into various syndromes because the causes of high BP in most patients presently classified as having essential hypertension can be recognized.
  6. 6. Detection Hypertension is diagnosed when  systolic blood pressure is consistently equal to or more than 140 mm Hg,  or diastolic blood pressure is equal to or more than 90 mm Hg; a single elevated blood pressure reading is not sufficient to establish the diagnosis of hypertension.
  7. 7. Detection
  8. 8. Detection  Blood pressure should be measured with a well- calibrated sphygmomanometer.  The bladder length within the cuff should encircle at least 80% of the arm circumference.  Readings should be taken after the patient has been resting comfortably, back supported in the sitting or supine position, for at least 5 minutes and at least 30 minutes after smoking or coffee ingestion.
  9. 9. classification
  10. 10. Importance  Sixty-six million Americans have elevated blood pressure.  The prevalence of hypertension increases with age and is more common in blacks than in whites.  Cardiovascular morbidity and mortality increase as both systolic and diastolic blood pressures rise.
  11. 11. Importance
  12. 12. Prevention -1 Maintaining a healthy diet a. Reduction of dietery sodium (salt) intake. b. Minimizing saturated fat and cholestrol intake c. Including fresh fruits and vegetables in every day meals.
  13. 13. Prevention -2 Maintaing a healthy weight. Being overweight can raise BP and losing weight can lower BP.
  14. 14. Prevention -3 Physical activity. An average of 2 hours and 30 minutes of moderate-intensity exercise weekly is ideal for preventing hypertension.
  15. 15. Prevention -4 Cessation of smoking Smoking decreases the elasticity of the blood vessels and increase blood vessel resistance which causes hypertension.
  16. 16. Prevention -5 Limitation of alcohol intake . Heavy drinkers who cut back to moderate drinking can lower their systolic blood pressure by 2 to 4 (mm Hg) and their diastolic blood pressure (by 1 to 2( mm Hg.
  17. 17. Causes of primary & secondary hypertension
  18. 18. PRIMARY (ESSENTIAL) HYPERTENSION  95% of the cases The cause is unknown  Between the age of (25 – 50)
  19. 19. Precipitating Factors Genetic factors Obesity Alcohol Salt Smoking Low K intake Sympathetic overactivity Insulin resistance NSAIDs Polycythemia
  20. 20. SECONDARY ( IDENTIFIABLE ) HYPERTENSION  5% of the cases  The cause of hypertension can be discovered  Common in ages ( below 20 or after 50 )
  21. 21. Causes of SECONDARY ( IDENTIFIABLE ) HYPERTENSION SECONDARY HTN Endocrine disease Renal disease Drugs
  22. 22. Hypertension and pregnancy
  23. 23. Its classified into 4 categories: 1. Chronic hypertension. 2. Gestational hypertension. 3. Preeclampsia. 4. Preeclampsia superimposed on chronic hypertension.
  24. 24. 1)Chronic hypertension Blood pressure is defined as BP exceeding 140/90 mm Hg before pregnancy or before 20 week’s gestation.  When hypertension is first identified during pregnancy and she is at less than 20 weeks gestation, blood pressure evaluation usually represent chronic hypertension.
  25. 25. 2)Gestational hypertension:  Refers to hypertension onset in the latter part of pregnancy >20 weeks without any other features of preeclampsia and normalization of the BP postpartum .  Pathophysiology is still unknown.  Maternal and fetal outcome are usually normal.
  26. 26. Gestational hypertension can develop either of on of these four : Preeclampsia (gestation hypertension + protein urea) Acute fatty liver of pregnancy. HELLP syndrome (hemolysis + elevated liver enzymes + low platelets ) eclampsia (gestation hypertension + protein urea + tonic-colonic seizure )
  27. 27. 3) preeclampsia  Preeclampsia is a disorder of widespread vascular endothelial malfunction and vasospasm that occurs after 20 weeks' gestation and can present as late as 4-6 weeks’ postpartum. It is clinically defined by hypertension and proteinuria, with or without pathologic edema
  28. 28. Risk factors  Maternal RF 1. Women first pregnancy (primigravida) 2. Age younger than 18 or above 35 3. History of preeclampsia 4. Family history 5. Obesity  Maternal medical RF 1. Chronic hypertension especially when its 2ndary (hyperaldostronisim , hypercortisolism) 2. Preexisting diabetes (I or II) 3. History of migraine 4. Use of SSRI beyond 1st trimester.
  29. 29. Symptoms of preeclampsia 1. Visual disturbance. 2. Headache (women describe it as throbbing) 3. Epigastric pain or RUQ (due to hepatic swelling ). 4. Retinal vasospasm (if severe) 5. Hyperactive reflexes (severe stage) 6. On auscultation the presence of S4 suggests LV Hypertrophy or diastolic dysfunction. New seizures in pregnancy suggest preeclampsia- eclampsia .
  30. 30. Management
  31. 31. Management  Current control rates (SBP <140 mmHg and DBP <90 mmHg).  In the majority of patients, reducing SBP has been considerably more difficult than lowering DBP.  the majority will require two or more antihypertensive drugs
  32. 32. Goals of treatment  reduce cardiovascular and renal morbidity and mortality.  Treating SBP and DBP to targets that are <140/90 mmHg is associated with a decrease in CVD complications.  In patients with hypertension and diabetes or renal disease, the BP goal is <130/80 mmHg
  33. 33. Management of HTN  Adoption of healthy lifestyles by all persons is critical for the prevention of high BP.  Two types of management: 1) Lifestyle modification. 2) Pharmacologic Treatment.
  34. 34. Lifestyle modification NO Modification Approximate SBP Reduction (Range) 1 Weight reduction 5–20 mmHg 2 Adopt DASH eating plan 8–14 mmHg 3 Dietary sodium reduction 2–8 mmHg 4 Physical activity 4–9 mmHg
  35. 35. Classes of drugs & side effects
  36. 36. Classes of drugs & side effects  More than 2/3 of hypertensive individuals cannot be controlled on one drug and will require two or more antihypertensive agents selected from different drug classes.  Mild Hypertension can be often controlled with a single drug.
  37. 37. Classes of drugs & side effects Cardiac output & peripheral resistance controlled by two mechanism: 1) Baroreflexes. 2) Renin-angiotensin-aldosterone system.
  38. 38. Anti HTN Diuretics ACE I ARBS Ca Channel Blockers Beta blockers Alpha blockers
  39. 39. Diuretics  tx: mild to moderate HTN  First drug of treatment  Also tx. heart failure or kidney disease  Used with other antihypertensives to enhance effectiveness  Reduce edema assos. with CHF
  40. 40. Diuretics Actions
  41. 41. Diuretics Action  Reduce blood volume through urinary excretion of water and electrolytes  Electrolyte imbalances can occur (mainly hypokalemia)  Also, Hyperglycemia, Hyperuricemia,HyperCa
  42. 42. Side effects  Orthostatic hypotension  Dry mouth,irritation  Disorientation  Dehydration HyperK: with K sparing Gynecomastia
  43. 43. Angiotensin-Converting Enzyme Inhibitors  “ACE” inhibitors  Mainstay of oral vasodilator therapy  More effective when used with diuretics  First line of therapy if the Diuretics or betaB are contraindicated.
  44. 44. ACE INHIBITORS
  45. 45. ACE INHIBITORS Angiotensin Converting Enzyme (ends in PRIL) captopril enalapril benzapril (Capoten) (Vasotec) (Lotensin)
  46. 46. ACE INHIBITORS ACTION  peripheral vascular resistanse without Ø cardiac output Ø cardiac rate Ø cardiac contractility
  47. 47. Side effects  Headache  Orthostatic hypotension-infrequent  dry Cough  Hyperkalemia  AKF  Skin rash Are fetotoxic & should not be used in pregnancy.
  48. 48. Drug interactions  Diuretics specially K sparing  Alcohol  Beta-blockers  All the above enhance the effects  It’s standerd in the care of patient following a myocardial infarction
  49. 49. Angiotensin 2 Receptor antagonists  Alternative of ACE I .  Same effect to ACE I .  Produce arteriole and venous dilatation .  Inhibit aldosterone secretion.
  50. 50. ARBS Don’t increase Bradykinin levels. Decrease Nephrotoxixty of Diabetes. Decrease Dry cough Don’t use it in pregnancy
  51. 51. Calcium Channel Blockers  Emerged as major drug to tx. HTN when the preferred first line are contraindicated.  Used for arrythmias also  Alternative to B-blocker (hx. Asthma)  Avoid High dose of SA. CCB because of inc. risk of Myocardial infarction.
  52. 52. Calcium Channel Blockers Examples  Verapamil Very  Procardia (nifedipine)-HTN Nice  Cardizem (diltiazem)-arrythmias Drugs
  53. 53. Calcium Channel Blockers
  54. 54. Calcium Channel Blockers Action blocks ca+ access to muscle cells contractility + conductivity of the ______________________ demand for oxygen PVR (relaxing arterioles)
  55. 55. Calcium Channel Blockers SIDE EFFECTS  BP  Bradycardia  vertigo  Headache  constipation  Peripheral edema  A-V block (due to –ve Inotopic& dromotropic)
  56. 56. Adrenergic Receptors Review of ANS  Sympathetic Nervous System  Alpha 1 = vasoconstriction  Alpha 2 = vasodilation  Beta 1 = increases heart rate  Beta 2 = bronchodilation
  57. 57. Beta Adrenergic Blocking Agents  Known as Beta-blockers  Axn: Inhibit cardiac response to sympathetic nerve stimulation by blocking Beta receptors  Decreases heart rate and C.O.  Decreases blood pressure  First line of therapy in HF
  58. 58. Beta Adrenergic Blocking Agents Examples – “olol” names  Beta 1: Atenolol & Metoprolol  Beta 1 and 2: Propranolol
  59. 59. Implications  Can not be abruptly discontinued  Check baseline b.p.  Check hx. of resp. condition-aggravates bronchoconstriction
  60. 60. Side effects  Bradycardia  Bronchospasm, wheezing  Diabetic: hypoglycemia  Insomnia  Sexual Dysfunction
  61. 61. Alpha-1 adrenergic blockers  Alternative if B-blockers and diuretics do not work  Also used to tx. mild to mod. urinary obstructive dx.  Also used for treat of benign prostate hyperplasia
  62. 62. Alpha-1 Adrenergic Blocking Agents Action  Block postsynaptic alpha-1 adrenergic receptors to produce arteriolar and venous vasodilation  Reduces peripheral-vascular resistance
  63. 63. Examples of Apha-1 blockers  Cardura (doxizosin)  Minipress (prazosin)  Hytrin (terazosin) Examples – “ZOSIN” names
  64. 64. Side effects  Drowsiness  Headache  Weakness,lethargy
  65. 65. Centrally Acting Alpha-2 Agonists  Stimulate Alpha-2 receptors in brainstem  Decreases HR, SBP and DBP  More frequent side effects – drowsiness, dry mouth, dizziness  Never suddenly DC = rebound HTN  Clonidine – Catapres  Methyldopa – (used in Pregnancy)
  66. 66. Direct Acting Vasodilators  Action: direct arteriolar smooth muscle relaxation, decreasing PVR  Uses: HTN, renal dx.,  Ex: Hydralazine, Minoxidel  SE: tachycardia, orthostatic hypotension,dizziness, palpitations, nausea, nasal congestion
  67. 67. Hypertension and ischemic heart disease
  68. 68. Case study 55 year old man known case of IHD and he now diagnosed with HT what is the drug of choose to treat him?  1-BB  2-ACEI  3-CCB
  69. 69. Hypertensive patients are at increased risk for MI or other major coronary events Why? 1-increase in heart o2 demand 2- increase heart work (life ventricle hypertrophy)  If the patient have HT and IHD that even increase the risk more
  70. 70.  Stable angina and silent ischemia  BBs (propranolol) will lower BP; reduce symptoms of angina; improve mortality; and reduce cardiac output heart rate, and AV conduction  Treatment should also include smoking cessation, management of diabetes, lipid lowering, antiplatelet agents, exercise training and weight reduction in obese patients.
  71. 71.  If angina and BP are not controlled by BB therapy alone, or if BBs are contraindicated, as in the presence of severe reactive airways disease, severe peripheral arterial disease, high-degree AV block,or the sick sinus syndrome  Use dihydropyridine or nondihydropyridine type CCBs (amlodipine Verapamil)
  72. 72.  If angina or BP is still not controlled on this two-drug regimen, nitrates can be added, but these should be used with caution in patients taking phosphodiesterase-5 inhibitors such as sildenafil. Short-acting dihydropyridine CCBs should not be used because of their potential to increase mortality,particularly in the setting of acute MI.
  73. 73. Diabetes and HT  The combined unadjusted prevalence of total diabetes and impaired fasting glucose in those over age 20 is 14.4 percent and is the leading cause of blindness, ESRD, and nontraumatic amputations  The United Kingdom Prospective Diabetes Study (UKPDS)174 demonstrated that each 10 mmHg decrease in SBP was associated with average reductions in rates of diabetes-related mortality (15 percent), myocardial infarction (11 percent)
  74. 74.  American Diabetes Association recommended that BP in diabetics be controlled to levels of 130/80 mmHg or lower  ACEIs(captopril), BBs(propranolol), ARBs(valsartan), and calcium antagonists(Verapamil) have a demonstrated benefit in the treatment of hypertension in both type 1 and type 2 diabetics
  75. 75.  The question of which class of agent is superior for lowering BP is somewhat moot because the majority of diabetic patients will require two or more drugs to achieve BP control
  76. 76.  The ADA has recommended ACEIs for diabetic patients older than 55 years of age at high risk for CVD, and BBs for those with known CAD  showed a reduction in combined MI, stroke, and CVD death of about 25 percent and a reduction in stroke by about 33  the ADA has recommended both ACEIs and ARBs for use in type 2 diabetic patients with CKD
  77. 77.  BB is indicated in a diabetic with IHD but may be less effective in preventing stroke than an ARB as was found in the LIFE study  CCBs may be useful to diabetics, particularly as part of combination therapy to control BP  The Appropriate Blood Pressure Control in Diabetes (ABCD) Trial in diabetics was stopped prematurely when it was found that the dihydropyridine nitrendipine was inferior to lisinopril in reducing the incidence of ischemic cardiac events.
  78. 78. Hypertensive emergencies  Hypertensive emergencies are characterized by severe elevations in BP (>180/120 mmHg) complicated by evidence of impending or progressive target organ dysfunction  Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of BP and parenteral administration of an appropriate agent
  79. 79.  The initial goal of therapy reduce mean arterial BP by no more than 25 percent (within minutes to 1 hour)  then if stable, to 160/100–110 mmHg within the next 2–6 hours
  80. 80.  Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided. For this reason, short-acting nifedipine is no longer considered acceptable  further gradual reductions toward a normal BP can be implemented in the next 24–48 hours
  81. 81. References

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