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HYPERTENSION

HYPERTENSION. Navdeep Singh Marivic Zerrudo. introduction. The heart is a hollow muscular organ that is somewhat pyramid and lies within the pericardium in the mediastinum . Reference: Snell. Surfaces of the heart. Sternocostal surface Diaphragmatic surface Base of the heart

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HYPERTENSION

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  1. HYPERTENSION Navdeep Singh MarivicZerrudo

  2. introduction The heart is a hollow muscular organ that is somewhat pyramid and lies within the pericardium in the mediastinum. Reference: Snell

  3. Surfaces of the heart • Sternocostal surface • Diaphragmatic surface • Base of the heart • Apex of the heart

  4. Borders • Apex – left ventricle, 5th left intercostal space 3.5 in from the midline • Superior – formed by the roots of the great blood vessels, extends from a point on the 2nd left costal cartilage 0.5 in from the edge of the sternum to a point on the 3rd right costal cartilage from the edge of the sternum • Right border – right atrium, extends from a point on the 3rd right costal cartilage 0.5 in from the edge of the sternum downward to a point on the 6th right costal cartilage 0.5 in from the edge of the sternum

  5. Borders • Left border – left ventricle, extends from a point on the 2nd left costal cartilage 0.5 in from the edge of the sternum to the apex beat of the heart • Inferior border – right ventricle and the apical part of the left ventricle, extends from a point on the 6th right costal cartilage 0.5 in from the edge of the sternum to the apex beat

  6. Anatomy of the Heart

  7. Heart anatomy • Chambers • Right atrium • Right ventricle • Left atrium • Left ventricle

  8. Valves • Specialized excitatory and conducting myocytes • Semilunar valves • Aortic valve • Pulmonary valve • Atrioventricular valves • Mitral valve • Tricuspid valve • Sinoatrial (SA) node pacemaker of the heart • Atrioventricular (AV) node • Bundle of His • Right and left bundle branches

  9. Blood supply: (3) Major Epicardial Coronary arteries: a. Left Anterior Descending Artery - Anterior wall - Anterior two thirds of septum - Entire apex of heart, circumferentially b. Left Circumflex Coronary Artery - Posterior, lateral left aspect of heart. c. Right Coronary Artery - Posterior one third of septum, inferior aspect, and posterior wall of heart

  10. Blood Vessels: types Arteries and arterioles – carry blood away from the heart Arterioles – control conduits - Has a strong muscular wall that can close the arteriole completely or can, by relaxing, dilate it several fold, thus, can regulate blood flow and pressure Capillaries – where nutrient and gas exchange occur Veins and venules – carry blood toward the heart. - much less smooth muscle

  11. Hypertension Definitions: • A progressive cardiovascular syndrome arising from complex and interrelated etiologies • Early markers of the syndrome often are present before elevated blood pressure is observed. Therefore, hypertension cannot be classified solely by discrete blood pressure thresholds. • Progression is strongly associated with functional and structural cardiac and vascular abnormalities that damage the heart, kidney, brain vasculature, and other organs and lead to premature morbidity and death. Pharmacy Times (Hypertension: Beyond JNC 7) page 32, March 2006

  12. Epidemiology • prevalence of hypertension • blood pressure levels • rate of age-related blood pressure increase • Hypertension is present in all populations • It accounts for 6 % of deaths worldwide. • Reference: Harrison vary among countries and among subpopulations within a country.

  13. Epidemiology Top ten provinces with the highest hypertension prevalence • Guimaras (80.1%) • Camiguin (60.4%) • Quirino (54.1%) • Sultan Kudarat (51.4%) • Pasay City (50.7%) • Muntinlupa City (50.6%) • Las Pinas (49.1%) • Davao Oriental (44.8%) • Catanduanes (40.9%) • Kalinga (39.3%). Reference: http://www.nscb.gov.ph/ncs/10thNCS/papers/contributed%20papers/cps-10/cps10-02.pdf

  14. Epidemiology Bottom ten province/area with the lowest hypertension prevalence • San Juan (0%) • Marinduque (2.6%) • TawiTawi (3.0%) • Navotas (4.6%) • Northern Samar (5.2%) • Misamis Occidental (8.3%) • Masbate (8.5%) • Bataan (10.4%) • Siquijor (10.43%) • Sorsogon(11.4%) Reference: http://www.nscb.gov.ph/ncs/10thNCS/papers/contributed%20papers/cps-10/cps10-02.pdf

  15. Mortality Statistics > Hypertensive heart disease (2004) by country Reference: http://www.nationmaster.com/graph/mor_hyp_hea_dis-mortality-hypertensive-heart-desease

  16. Epidemiology Prevalence of Hypertension in the U.S. (HARRISON’S INTERNAL MEDICINE) 33.5 % among Hispanic Blacks 28.9 % among Hispanic Whites 20.7 % among Mexican Americans • Out of the world, incidence of high blood pressure is highest in African Americans • 36.7% of African American men have high blood pressure • One in three blacks have hypertension • 30% of African American male deaths are connected to hypertension/high blood pressure • 27.9% of Latin American male deaths are connected to hypertension/high blood pressure Reference: http://library.thinkquest.org/trio/TTQ03033/hypertension_statistics.htm

  17. Epidemiology • In the United States, average systolic blood pressure is higher for men than for women during early adulthood. • At age 60 and older, systolic blood pressures of women are higher than men. • Diastolic blood pressure increases progressively with age until about 55 years old, after which, it tends to decrease.

  18. Epidemiology • Philippines • 9.6M are hypertensive • 15.4M are predisposed to be hypertensive among adults, 20 years and over • for over 5 years, hypertension ranks as the fifth leading cause of morbidity Reference: http://www.nscb.gov.ph/ncs/10thNCS/papers/contributed%20papers/cps-10/cps10-02.pdf 2005

  19. epidemiology • Hypertension increases with age. • Among aged ≥ 60, prevalence is 65.4 %. • In African Americans, it appears earlier. • Obesity and weight gain are strong and independent risk factors. • Sixty percent of hypertensive patients are > 20 % overweight.

  20. TYPES OF HYPERTENSION • PRIMARY HYPERTENSION • 90 % of all cases, high BP with na apparent cause • Factors – genetics, race, gender, age, diet, weight, lifestyle • SECONDARY HYPERTENSION • 10 % of all cases, high BP by pre-existing physical condition such as kidney or thyroid condition

  21. Mechanisms of Hypertension • intravascular volume • autonomic nervous system • renin-angiotensin-aldosterone system • vascular mechanisms.

  22. Intravascular volume Primary determinant of arterial pressure over the long term Cardiac output • Directly related to stroke volume and heart rate • Directly related to arterial pressure • There is an increase with arterial pressure with increased cardiac output. This occurs with increased blood volume. CO = SV x HR Arterial pressure = CO x TPR

  23. Autonomic Nervous System • Maintains cardiovascular homeostasis via pressure, volume, and chemoreceptor signals. • Adrenergic reflexes modulate blood pressure over the short term. • Adrenergic function with hormonal and volume related factors contributes to the long term regulation of blood pressure.

  24. Renin- Angiotensin-Aldosterone System • It contributes to blood pressure regulation via • the vasoconstrictor properties of angiotensin II • the sodium retaining properties of aldosterone. Renin is an aspartyl protease found in the kidney. Active renin once relased into the circulation cleaves angiotensinogen to form an inactive decopeptide, angiotensin I. A converting enzyme, located primarily but not exclusively in the pulmonary circulation, converts angiotensin I to the active octapeptide, angiotensin II. Angiotensin II further stimulates release of aldosterone.

  25. Renin- Angiotensin-Aldosterone System • Primary Stimuli for Renin Secretion • Decreased NaCl transport in the thick ascending loop of Henle • Decreased pressure or stretch within the renal afferent arteriole • Sympathetic nervous system stimulation of renin-secreting cells via ß1 adrenoreceptors

  26. Renin- Angiotensin-Aldosterone System

  27. Vascular mechanisms • The decrease in lumen size of blood vessels significantly increases resistance. • This contributes to increased peripheral resistance. • This may occur in cases of arteriosclerosis where there is plaque formation in the vessel wall reducing the diameter of a lumen. • The stiffness of a blood vessel also contributes to resistance. • It is found in most hypertensive patients and in the elderly.

  28. Identifiable causes of hypertension • Chronic kidney disease • Renal parenchymal disease • Altered excretory function – defects in renal excretion of salt and water • Altered RAAS – ischemic changes resulting from intrarenal scarring may activate the RAAS abd contribute to hypertension in patient with early or advanced renal failure • Coarctation of the aorta

  29. Identifiable causes of hypertension • Cushing’s syndrome • glucocorticoid excess resulting from exogenous glucocorticoid therapy • Hypertension may occur because cortisol has mineralocorticoid-like effects and therefore leads to the retention of sodium and water • Other glucocorticoid excess states – remediable hyperaldosteronism • Chronic steroid therapy

  30. Identifiable causes of hypertension • Drug induced or drug related • Oral contraceptives – hypertension occurs as a result of estrogen-induced increases in angiotensin synthesis in the liver • Obstructive uropathy • Primary aldosteronism and other mineralocorticoid excess states • By inducing sodium and water retention leading to expansion of the ECF volume • Often accompanied by hypokalemia because mineralocorticoids promote renal potassium excretion in the collecting duct of the nephron • Pheochromocytoma • Tumors of the adrenal medulla increases the secretion of the catecholamines leading to hypertension

  31. Identifiable causes of hypertension • Renovascular hypertension • Result from complex interplay between activation of the renin-angiotensin-angiotensin-aldosterone system and the sympathetic nervous sytem • Sleep apnea • Thyroid or parathyroid disease

  32. Genetics of Hypertension • Genetic abnormalities associated with several rare forms of hypertension, includes the following: • mineralocorticoid-remediable aldosteronism • 11beta-hydroxylase and 17alpha-hydroxylase deficiencies • Liddle’s syndrome, the syndrome of apparent mineralocorticoid excess • pseudohypoaldosteronism type • Candidate genes • angiotensinogen • alpha-adducin, beta- and DA-adrenergic receptors • beta-3 subunit of G proteins

  33. Risk Factors: • Non modifiable factors • genetic predisposition to hypertension • disease condition like • diabetes • heart disease • kidney disease • high cholesterol level • stroke • increasing age Modifiable • Unhealthy lifestyle which include • Cigarette smoking • unmanaged stress • salty food consumption • physical inactivity • being overweight Reference: http://www.nscb.gov.ph/ncs/10thNCS/papers/contributed%20papers/cps-10/cps10-02.pdf

  34. Patient Evaluation: Objectives: • to assess lifestyle and identify other cardiovascular risk factors or concomitant disorders that may affect prognosis and guide treatment • to reveal identifiable causes of high BP • to assess the presence or absence of target organ damage and CVD

  35. Patient Evaluation: • Patient evaluation methods • medical history • physical examination • routine laboratory tests • Urinalysis, CBC, electrolytes, renal function test, FBS, total cholesterol, HDL, 12-L ECG • Optional laboratory tests • Creatinine clearance, microalbuminuria, 24-hr urinary protein, blood calcium, uric acid, fasting triglycerides/LDL, HgbA1C, TSH, Echocardiography

  36. Patient Evaluation: • The physical examination includes the following: • an appropriate measurement of BP • with verification in the contralateral arm; an examination of the optic fundi • a calculation of body mass index (BMI) (measurement of waist circumference is also very useful) • an auscultation for carotid, abdominal, and femoral bruits; a palpation of the thyroid gland • a thorough examination of the heart and lungs • an examination of the abdomen for enlarged kidneys, masses, distended urinary bladder, and abnormal aortic pulsation • a palpation of the lower extremities for edema and pulses • Neurological assessment.

  37. Diagnosis: • Because most individuals with hypertension do not exhibit any symptoms or feelings of malaise, they may assume that their blood pressure is normal. • Occasionally, if blood pressure reaches extreme levels, individuals may experience some symptoms, such as the following: • Dizziness • Diplopia • Headache • Shortness of breath • Chest pain • Abdominal pain

  38. JNC-7 Blood Pressure Classification

  39. Accurate Blood Pressure Measurement in the Office • Persons should be seated quietly for atleast 5 minutes in a chair, with feet on the floor, and arm supported at heart level. • Caffeine, exercise, and smoking should be avoided for at least 30 minutes prior to measurement. • Measurement of BP in the standing position is indicated periodically, especially in those at risk for postural hypotension, prior to necessary drug dose or adding a drug, and in those who report symptoms consistent with reduced BP upon standing. • An appropriately sized cuff (cuff bladder encircling at least 80 percent of the arm) should be used to ensure accuracy.

  40. Accurate Blood Pressure Measurement in the Office • At least two measurements should be made and the average recorded. • For manual determinations, palpated radial pulse obliteration pressure should be used to estimate SBP—the cuff should then be inflated 20–30 mmHg above this level for the auscultatory determinations; the cuff deflation rate for auscultatory readings should be 2 mmHg per second. • SBP is the point at which the first of two or more Korotkoff sounds is heard (onset of phase 1), and the disappearance of Korotkoff sound (onset of phase 5) is used to define DBP. • Clinicians should provide to patients, verbally and in writing, their specific BP numbers and the BP goal of their treatment.

  41. Treatment Although there is no known cure to hypertension, it is treatable using various pharmacologic and nonpharmacologic measures.

  42. Goals of Therapy • The ultimate public health goal of antihypertensive therapy is to reduce cardiovascular and renal morbidity and mortality. • Since most persons with hypertension, especially those >50 years of age, will reach the DBP goal once the SBP goal is achieved, the primary focus should be on attaining the SBP goal. • 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.

  43. treatment • Non-pharmacologic • Lifestyle modification • Pharmacologic • Thiaz • BB • ACEI • ARB • ALDO ANT • CCB

  44. Achieving Blood Pressure Control in Individual Patients: • Therapy begins with lifestyle modification • The maximum protection against combined cardiovascular endpoints is achieved with pressures <135–140 mmHg for systolic blood pressure and <80–85 mmHg for diastolic blood pressure • More aggressive blood pressure targets for blood pressure control (e.g., blood pressure < 130/80 mmHg) may be appropriate for patients with diabetes, CHD, chronic kidney disease, or with additional cardiovascular disease risk factors. • In diabetic patients, effective blood pressure control reduces the risk of cardiovascular events and death as well as the risk for microvascular disease (nephropathy, retinopathy).

  45. Achieving Blood Pressure Control in Individual Patients: • Risk reduction is greater in diabetic than in nondiabetic individuals. • If BP goal is not achieved via lifestyle modification, thiazide-type diuretics should be used as initial therapy for most patients, either alone or in combination with one of the other classes (ACEIs, ARBs, BBs, CCBs) that have also been shown to reduce one or more hypertensive complications in randomized controlled outcome trials. • If the initial drug selected is not tolerated or is contraindicated, then a drug from one of the other classes proven to reduce cardiovascular events should be substituted. • Since most hypertensive patients will require two or more antihypertensive medications to achieve their BP goals, addition of a second drug from a different class should be initiated when use of a single agent in adequate doses fails to achieve the goal.

  46. Achieving Blood Pressure Control in Individual Patients: • When BP is >20 mmHg above systolic goal or 10 mmHg above diastolic goal, consideration should be given to initiate therapy with two drugs, either as separate prescriptions or in fixed-dose combinations. • The initiation of therapy with more than one drug increases the likelihood of achieving BP goal in a more timely fashion. • The use of multidrug combinations often produce greater BP reduction at lower doses of the component agents, resulting in fewer side effects. • The use of fixed-dose combinations may be more convenient and simplify the treatment regimen, and may cost less than the individual components prescribed separately.

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