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Essential Hypertension
- 1. Essential Hypertension Raheef Alatassi 4th yearmedical student Internal medicine
- 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.
- 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. Essential hypertensionaccounts 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. Detection Hypertension is diagnosedwhen 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.
- 8. Detection Blood pressureshould 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.
- 10. Importance Sixty-six millionAmericans 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.
- 12. Prevention -1 Maintaining ahealthy 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. Prevention -2 Maintaing ahealthy weight. Being overweight can raise BP and losing weight can lower BP.
- 14. Prevention -3 Physical activity. Anaverage of 2 hours and 30 minutes of moderate-intensity exercise weekly is ideal for preventing hypertension.
- 15. Prevention -4 Cessation ofsmoking Smoking decreases the elasticity of the blood vessels and increase blood vessel resistance which causes hypertension.
- 16. Prevention -5 Limitation ofalcohol 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.
- 18. PRIMARY (ESSENTIAL) HYPERTENSION 95% of the cases The cause is unknown Between the age of (25 – 50)
- 19. Precipitating Factors Genetic factors Obesity Alcohol Salt Smoking LowK intake Sympathetic overactivity Insulin resistance NSAIDs Polycythemia
- 20. SECONDARY ( IDENTIFIABLE) HYPERTENSION 5% of the cases The cause of hypertension can be discovered Common in ages ( below 20 or after 50 )
- 21. Causes of SECONDARY (IDENTIFIABLE ) HYPERTENSION SECONDARY HTN Endocrine disease Renal disease Drugs
- 22.
- 23. Its classified into4 categories: 1. Chronic hypertension. 2. Gestational hypertension. 3. Preeclampsia. 4. Preeclampsia superimposed on chronic hypertension.
- 24. 1)Chronic hypertension Blood pressureis 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. 2)Gestational hypertension: Refersto 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. Gestational hypertension can developeither 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. 3) preeclampsia Preeclampsiais 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. Risk factors MaternalRF 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. 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.
- 31. Management Current controlrates (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. 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. 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. Lifestyle modification NO ModificationApproximate 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. Classes of drugs &side effects
- 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. Classes of drugs& side effects Cardiac output & peripheral resistance controlled by two mechanism: 1) Baroreflexes. 2) Renin-angiotensin-aldosterone system.
- 39. Anti HTN Diuretics ACE I ARBS CaChannel Blockers Beta blockers Alpha blockers
- 40. Diuretics tx: mildto 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
- 42.
- 43. Diuretics Action Reduce bloodvolume through urinary excretion of water and electrolytes Electrolyte imbalances can occur (mainly hypokalemia) Also, Hyperglycemia, Hyperuricemia,HyperCa
- 44. Side effects Orthostatichypotension Dry mouth,irritation Disorientation Dehydration HyperK: with K sparing Gynecomastia
- 45. 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.
- 46.
- 47. ACE INHIBITORS Angiotensin Converting Enzyme (endsin PRIL) captopril enalapril benzapril (Capoten) (Vasotec) (Lotensin)
- 48. ACE INHIBITORS ACTION peripheralvascular resistanse without Ø cardiac output Ø cardiac rate Ø cardiac contractility
- 49. Side effects Headache Orthostatic hypotension-infrequent dry Cough Hyperkalemia AKF Skin rash Are fetotoxic & should not be used in pregnancy.
- 50. Drug interactions Diureticsspecially K sparing Alcohol Beta-blockers All the above enhance the effects It’s standerd in the care of patient following a myocardial infarction
- 51. Angiotensin 2 Receptor antagonists Alternative of ACE I . Same effect to ACE I . Produce arteriole and venous dilatation . Inhibit aldosterone secretion.
- 52. ARBS Don’t increase Bradykininlevels. Decrease Nephrotoxixty of Diabetes. Decrease Dry cough Don’t use it in pregnancy
- 53. 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.
- 54. Calcium Channel Blockers Examples Verapamil Very Procardia (nifedipine)-HTN Nice Cardizem (diltiazem)-arrythmias Drugs
- 55.
- 56. Calcium Channel Blockers Action blocksca+ access to muscle cells contractility + conductivity of the ______________________ demand for oxygen PVR (relaxing arterioles)
- 57. Calcium Channel Blockers SIDEEFFECTS BP Bradycardia vertigo Headache constipation Peripheral edema A-V block (due to –ve Inotopic& dromotropic)
- 58. Adrenergic Receptors Review ofANS Sympathetic Nervous System Alpha 1 = vasoconstriction Alpha 2 = vasodilation Beta 1 = increases heart rate Beta 2 = bronchodilation
- 59. 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
- 60. Beta Adrenergic Blocking Agents Examples– “olol” names Beta 1: Atenolol & Metoprolol Beta 1 and 2: Propranolol
- 61. Implications Can notbe abruptly discontinued Check baseline b.p. Check hx. of resp. condition-aggravates bronchoconstriction
- 62. Side effects Bradycardia Bronchospasm, wheezing Diabetic: hypoglycemia Insomnia Sexual Dysfunction
- 63. Alpha-1 adrenergic blockers Alternativeif 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
- 64. Alpha-1 Adrenergic Blocking Agents Action Block postsynaptic alpha-1 adrenergic receptors to produce arteriolar and venous vasodilation Reduces peripheral-vascular resistance
- 65. Examples of Apha-1blockers Cardura (doxizosin) Minipress (prazosin) Hytrin (terazosin) Examples – “ZOSIN” names
- 66. Side effects Drowsiness Headache Weakness,lethargy
- 67. 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)
- 68. 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
- 69.
- 70. Case study 55 yearold 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
- 71. Hypertensive patients areat 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
- 72. Stable anginaand 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.
- 73. If anginaand 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)
- 74. If anginaor 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.
- 75. 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)
- 76. American DiabetesAssociation 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
- 77. The questionof 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
- 78. The ADAhas 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
- 79. BB isindicated 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.
- 80. Hypertensive emergencies Hypertensiveemergencies 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
- 83. The initialgoal 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
- 84. Excessive fallsin 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
- 85.
Editor's Notes
- #19 Unknown before the age of 20
- #22 renal diseases : renovascular disease glomerulonephritis Polycystic kidney disease Endocrine disease : Endocrine disease Pheochromocytoma Cushing syndrome Primary aldosteronism ( conn's syndrome ) Hyperparathyroidism Primary hypothyroidism Thyrotoxicosis Acromegaly …etc Drugs : oral contraceptive containing estrogen NSAIDs Corticosteroids …etc
- #35 Weight reduction : (body mass index 18.5–24.9 kg/m2). Adopt Dietary Approaches to Stop Hypertensioneating plan : Consume a diet rich in fruits, vegetables, and lowfat dairy products with a reduced content of saturated and total fat. Dietary sodium reduction : reduce it to more than 100 mmol per day Physical activity : brisk walking (at least 30 min per day, most days of the week). Smoking and alchol.
- #38 Factors influence HTN
- #54 Myocardial infarction due to excessive vasodiltaion.
- #56 nonDih: heart / Verapamil & Diltizam (used in angina ) Dih: Vessels : vascular smooth muscle to relax.
- #58 Inotopic: contractility Dromotopic: conductivity
- #69 Hydralazine (cause lupus like syndrome) Minoxidel ( treat baldness)