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Cecil Medicine Section VIII Chapter 66

Cecil Medicine Section VIII Chapter 66. Arterial Hypertension. Prof. Shen-Jiang Hu.

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Cecil Medicine Section VIII Chapter 66

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  1. Cecil Medicine Section VIII Chapter 66 Arterial Hypertension Prof. Shen-Jiang Hu

  2. made by a Cambridge Reverend, Stephen Hales, in 1733. He measured blood pressure by inserting the end of a long glass tube into the carotid artery of a horse and noting that the blood came up the tube to a height of nine feet eight inches, which was the blood pressure of the horse.

  3. It took Riva-Rocci, together with a Prussian general called Korotkoff, to develop the modern sphygmomanometer which was introduced into clinical practice in about 1905. The device that probably many of us still use today to measure blood pressure has changed very little from this early device.

  4. Blood Pressure has a unimodal distribution in the Population

  5. Question: • Is it important if the person’s blood pressure is higher?

  6. “Hypertension may be an important compensatory mechanism which should not be tampered with, even were it certain that we could control it.” White PD, 1931 “The greatest danger to a man with high blood pressure lies in its discovery, because then some fool is certain to try to reduce it.” Hay J, 1931

  7. “Franklin D. Roosevelt’s health was excellent”!?-1944 • Franklin D. Roosevelt (FDR) was referred to Dr.Howard Bruenn, a cardiologist at Bethesda Naval Hospital who, on March 27, 1944 found him cyanotic, breathless, with an enlarged left ventricle and a blood pressure of 186/108. Bruenn diagnosed hypertensive heart disease and wanted to give digitalis, but was prohibited by Dr.Ross McIntire, the president's personal physician and then surgeon-general of the U.S. Navy.

  8. “Franklin D. Roosevelt’s health was excellent”!?-1944 • The next day, FDR developed moist rales at the base of the right lung. By March 30, Bruenn diagnosed congestive heart failure. On the next day, digitalis was begun. • By April 3, FDR was better. His color was better, he could lie flat without dyspnea, and the crackles disappeared from both lungs. His blood pressure, however, was 210/110.

  9. “Franklin D. Roosevelt’s health was excellent”!?-1944 • The nation was stunned when FDR died unexpectedly on April 12, 1945 -- less than six months after being elected to a fourth term in office. The death was unexpected because the president's personal physician, VADM Ross McIntire, whenever asked, had proclaimed that FDR's health was excellent.

  10. Question: • How do we know the hypertension is responsible for the total risk of CV events?

  11. 1970 Hypertension and Stroke Knowledge about risk and treatment of hypertension 2003 JNC VII:HBP to target BP is central for reduction of the total risk of CV events. 1980 JNC II: DBP for diagnosis and treatment of hypertension WHO: HBP should be reduced to target BP. 2006 1961 1992 2005 Framingham Heart Study: Hypertension and CHD JNC V: SBP and DBP is same important for hypertension China guideline for hypertension: HBP should be reduced to target BP 1978 World Health Organization (WHO):Treatment of Hypertension, firstly

  12. The Relationship between DBP and Cardiovascular Events

  13. Complications of Hypertension Heart Failure LV Hypertrophy MI Atrial Fibrillation Hypertensive Encephalopathy Aortic Dissection Hypertension CHD Dementia Intracerebral Hemorrhage Chronic Renal failure Ischemic Cerebral Infarction

  14. Question: • What is hypertension?

  15. Definition of Hypertension • Hypertension is a clinical syndrome, defined as systolic blood pressure ≥ 140 mmHg and/or diastolic blood pressure ≥ 90 mmHg. • Hypertension should be considered a major risk factor for an array of cardiovascular and related disease as well as diseases leading to a marked increase in cardiovascular risk.

  16. 黑龙江 吉林 辽宁 河北 北京 天津 新疆 内蒙古 山东 陕西 宁夏 青海 江苏 甘肃 河南 山西 安徽 上海 西藏 湖北 浙江 四川 江西 湖南 福建 贵州 广东 云南 广西 台湾 海南 Hypertension in China(1991) • ≥15% • ≥10%~14.9% • <10%

  17. Mortality in China City in 1999 Mortality % Circulatory system - Cerebral disease 38.5 - Heart disease 16.8 Cancer 23.9 Respiratory system 13.9 Trauma, toxicosis 6.3 Digestive system 3.0 Others 6.4

  18. Mortality in China Countryside in 1999 Mortality % Circulatory system 30.8 - Cerebral disease 18.4 - Heart disease 12.4 Respiratory system 22.0 Cancer 18.4 Trauma, toxicosis 11.0 Digestive system 4.0 Others 5.1

  19. Trends in Awareness, Treatment, and Control of Hypertension in China Awareness(%) Treatment(%) Control(%) 1991 26.6 12.2 2.9 2002 30.2 24.7 6.1

  20. Question: • What is etiology of hypertension?

  21. Etiology of Hypertension • Genetic factors play an important role. Children with one- or two-hypertensive parents have higher blood pressures. • Environmental factors also are significant. Increased saltintake has long been incriminated as a pathogenic factor in essential hypertension. It alone is probably not sufficient to elevate blood pressure to abnormal levels; a combination of too much salt plus a genetic predisposition is required.

  22. Etiology

  23. Question: • How about the pathogenesis in hypertension is ?

  24. Pathogenesis • The pathogenesis of essential hypertension is multifactorial. • Sympathetic nervous systemhyperactivity. It is most apparent in younger hypertensives, who may exhibit tachycardia and an elevated cardiac output. However, correlations between plasma catecholamines and blood pressure are poor.

  25. Pathogenesis • Renin-angiotensin system (RAS). Renin acts on angiotensinogen to cleave of the ten-amino-acid peptide angiotensin I. This peptide is then acted upon by angiotensin-converting enzyme to create the eight-amino-acid peptide angiotensin II, a potent vasoconstrictor and a major stimulant of aldosterone release from the adrenal glands.

  26. Pathogenesis • Defect of natriuresis. Hypertensive patients exhibit a diminished ability to excrete a sodium load. This defect may result in increased plasma volume and hypertension.

  27. Pathogenesis • Intracellular sodium and calcium. An increase in intracellular Na+ may lead to increased intracellular Ca2 + concentrations as a result of facilitated exchange. This could explain the increase in vascular smooth muscle tone.

  28. Pathogenesis • Exacerbating factors. The best-documented is obesity, which is associated with an increase in intravascular volume and an elevated cardiac output. Some hypertensives respond to high salt intake with substantial blood pressure increases. Excessive use of alcohol also raises blood pressure. Cigarette smoking acutely raises blood pressure.

  29. Question: • Which pathologic changes will be happen in hypertension ?

  30. Pathology • Heart. Left ventricular hypertrophy may cause or facilitate many cardiac complications of hypertension, including congestive heart failure, ventricular arrhythmias, myocardial ischemia, and sudden death.

  31. Pathology • Brain. Hypertension is the major predisposing cause of stroke, especially intracerebral hemorrhage but also ischemic cerebral infarction.

  32. Pathology • Kidney. Chronic hypertension leads to nephrosclerosis, a common cause of renal insufficiency.

  33. Question: • How to know the patient with hypertension?

  34. Clinical Findings Symptoms: • Elevations in pressure are often intermittent early. Even in established case, the blood pressure fluctuates widely in response to emotional stress and physical activity.

  35. Clinical Findings Symptoms: • Mild to moderated essential hypertension is usually associated with normal health and well-being for many years.

  36. Clinical Findings Symptoms: • Suboccipital pulsating headaches, but any type of headache, may occur. Accelerated hypertension is associated with somnolence, confusion, palpitation.

  37. Signs: • High blood pressure. • Physical findings depend upon the duration and severity, and the degree of effect on target organs. • A loud aortic second sound and an early systolic ejection click may occur.

  38. Question: • What should we do if the patient may be with hypertension?

  39. Initial Evaluation for Hypertension • Goal 1: Accurate Assessment of Blood Pressure

  40. How to measure blood pressure

  41. Definition and Classification of Blood Pressure Levels in different Country

  42. Initial Evaluation for Hypertension • Goal 2: Cardiovascular Risk Stratification

  43. Stratification of CV Risk Stratification of CV Risk in four categories. SBP: systolic blood pressure; DBP: diastolic blood pressure; CV: Cardiovascular events; HT: hypertension. Low, moderate, high and very high risk refer to 10 year risk of a CV fatal or non-fatal event. The term “added” indicates that in all categories risk is greater than average. OD: subclinical organ damage; MS: metabolic syndrome. The dashed line indicates how definition of hypertension may be variable, depending on the level of total CV risk.

  44. Estimate total cardiovascular risk • Framingham Study:Risk for cardiovascular events over 10 years • Very high High Moderate Low • >30% 20-30% 15-20% <15% • SCORE charts:the risk of dying from cardiovascular disease over 10 years • Very high High Moderate Low • >8% 5-8% 4-5% <4%

  45. Factors influencing prognosis

  46. Factors influencing prognosis • Risk factors • Systolic and diastolic BP levels • Levels of pulse pressure (in the elderly) • Age (M > 55 years; W > 65 years) • Smoking • Dyslipidaemia • TC > 5.7 mmol/l (220 mg/dl) or: • LDL-C > 3.3 mmol/l (130 mg/dl) or: • HDL-C: < 1.0 mmol/l (40 mg/dl) • Fasting plasma glucose 6.1-6.9 mmol/L • Abnormal glucose tolerance test • Abdominal obesity (Waist circumference > 90 cm (M), > 85 cm (W)) • Family history of premature CV disease (M at age < 55 years; W at age < 65 years)

  47. Factors influencing prognosis Subclinical Organ Damage Electrocardiographic LVH or: Echocardiographic LVH Carotid wall thickening (IMT > 0.9 mm) or plaque Carotid-femoral pulse wave velocity > 12 m/s Ankle/brachial BP index < 0.9 Slight increase in plasma creatinine: M: 115-133 µmol/l (1.3-1.5 mg/dl); W: 107-124 µmol/l (1.2-1.4 mg/dl) Low estimated glomerular filtration rate (<60 ml/min/1.73 m2) Microalbuminuria 30-300 mg/24 h or albumin-creatinine ratio: ≥ 30 mg/g

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