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SUBDIVISION NEPHROLOGY AND HYPERTENSION DEPT. INTERNAL MEDICINE FACULTY OF MEDICINE UNIVERSITY PADJADJARAN HASAN SADIKIN GENERAL HOSPITAL BANDUNG
Reference
Kaplans Clinical Hypertension, Norman M.K, 8th Edition, 2002 2003 World Health Organization International Society of Hypertension Guidelines for the Management of Hypertension The Sixth Report of The Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure The Seventh Report of The Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure
Lecture Content
Introduction Definition Pathophysiology Pathogenesis Pathophysiology of T.O.D Measurement of blood pressure History, Physical examination Treatment
Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure Uses evidence-based medicine and consensus Updates approaches to hypertension control including diagnosis, evaluation, lifestyle modification, and drug therapy
Objective
The objective of identifying and treating high blood pressure is to reduce the risk of cardiovascular disease and associated morbidity and mortality
JNC VII
Heart disease and stroke are the 1st and 3rd leading causes of death in the U.S.
Epidemiology
2 million new cases of hypertension diagnosed each year in the U.S. 23% of men and 25% of women over the age of 18 in the U.S. have HTN The prevalence of HTN among African Americans is increased 30-50% in each age group compared to persons of European descent
Epidemiology cont.
The prevalence of HTN increases steadily with age; over 70% of women and 50% of men in the U.S. over the age of 70 have HTN Linear relationship between the degree of HTN and the risk for CV and renal disease
Hypertension
Hypertension is not a disease It is an arbitrarily defined disorder to which both environmental and genetic factors contribute Major risk factor for:
cerebrovascular disease myocardial infarction heart failure peripheral vascular disease renal failure
Blood pressure is a continuous variable which fluctuates widely during the day
The definition of hypertension has been arbitrarily set as: That blood pressure above which the benefits of treatment outweigh the risks in term of morbidity and mortality
BHS 140/90 JNC-VII 140/90 Opt <120/<80 WHO-ISH 140/90 The current recommendation in the UK is 140/90 However risk is important and in diabetes 130/80
Definition
Based on recommendation JNC VII, The Classification of BP for adult 18 years :
Normal : systolic lower than 120 diastolic lower than 80 Pre-hypertension : systolic 120 139 diastolic 80 99 Stage-1 : systolic 140 159 or diastolic 90 99 Stage-2 : systolic equal to or more than 160 or diastolic equal to or more than 100
>140 140-149
<90 <90
2. Equipment :
Cuff size : the bladder should encircle and cover two - thirds of the length of the arm; if it does not, place the bladder over the brachial artery. If bladder is too small, high readings may result. Manometer : Aneroid gauges should be calibrated every 6 months against a mercury manometer. For infants, use ultrasound equipment (e.g. the Doppler method)
3. Technique
3.1. Number of readings
On each occasion, take at least two readings, separated by as much time as is practical. If readings vary by more than 5 mmHg, take additional readings until two are close. For diagnosis, obtain three sets of readings at least 1 week apart. Initially, take pressure in both arms; if the pressures differ, use arm with the higher pressure. If the arm pressure is elevated, take pressure in one leg, particularly in patients younger than 30.
4. Recordings
Note the pressure, patient position, the arm, cuff size ; e.g. 140/90, seated, right arm, large adult cuff.
Bladder Length
Centre of bladder must be over artery
12 cm
23 cm 35 cm 42 cm
2. The cuff must be level with the heart. If Arm Circumference exceeds 33 cm, a large cuff must be used. Place stethoscope diaphragm over brachial artery 3. 1. The patient should be relaxed and the arm must be supported. Ensure no tight clothing constricts the arm The column of mercury must be vertical. Inflate to acclude the pulse. Deflate at 2 to 3 mm/sec. Measure systolic (first sound) and diastolic (disappearance) to nearest 2 mmHg.
Blood pressure is controlled by an integrated system Prime contributors to blood pressure are:
Cardiac output
Pathophysiology
BP=TPR X CO (blood pressure is the product of total peripheral resistance and cardiac output)
Autoregulation
BLOOD PRESSURE = CARDIAC OUTPUT X PERIPHERAL RESISTANCE Hypertension = Increased CO and/or Increased PR
Preload
Contractility
Functional Constriction
Structural Hypertrophy
Fluid Volume
Volume Redistribution
Reninangiotensin excess
Hyperinsuli nemia
Genetic alteration
Stress
Genetic alteration
Obesity
capacitance
veins venules
Peripheral resistance
Sympathetic system
Renin release
In this way blood pressure is increased The actions of the sympathetic system are rapid and account for second to second blood pressure control
Any of the above stimulate renin release from the juxtaglomerular apparatus Renin converts angiotensinogen to angiotensin I Angiotensin I is converted to angiotensin II by angiotensin converting enzyme (ACE)
Angiotensin II is a potent
vasoconstrictor anti-natriuretic peptide stimulator of aldosterone release from the adrenal glands
Aldosterone is also a potent antinatriuretic and antidiuretic peptide Angiotensin II is also a potent hypertrophic agent which stimulates myocyte and smooth muscle hypertrophy in the arterioles
are both poor prognostic indicators in patients with hypertension partially explain why hypertension and the risks of hypertension persist in some patients despite treatment
Both the sympathetic and RAAS are key targets in the treatment of hypertension
ANGIOTENSINOGEN
Renin ANGIOTENSIN I Converting enzyme ANGIOTENSIN II
ANGIOTENSIN III
ANGTIOTENSINASE A
Adrenal cortex
Kidney
Intestine
CNS
Heart
Contractility
Vasopressin release
Vasoconstriction
Cardiac output
Angiotensinogen
Renin
Angiotensin I
ACE vasoconstriction
Angiotensin II
aldosterone (inc. reabsorp of Na)
Inc. PVR
Pre hypertension
10-30 years
CO
Age
0 - 30
20 - 40
30 - 50
UNCOMPLICATED
COMPLICATED
Causes of Hypertension
Essential or Primary Underlying pathophysiologic alteration of unknown cause; 95% of cases of HTN
Secondary-Resulting from a specific cause such as renal or endocrine disorders; 5% of cases
Primary Hypertension
Is usually of gradual onset Usually develops between the ages of 30 and 50 Tends to remain asymptomatic for 10 to 20 years Triggers include obesity, psychological stress, high-sodium intake, and alcohol intake over 1 ounce per day
polyfactorial polygenic
Likely causes: Increased reactivity of resistance vessels and resultant increase in peripheral resistance
as a result of an hereditary defect of the smooth muscle lining arterioles In essential hypertension the kidneys are unable to excrete appropriate amounts of sodium for any given BP. As a result sodium and fluid are retained and the BP increases
Other factors
Age Genetics and family history Environment Weight Alcohol intake Race
Age
BP tends to rise with age, possibly as a result of decreased arterial compliance. Hypertension in the elderly should be treated as aggressively as in the young. They have more to lose Studies such as EWPHE, Primary Care Study,MRC Hypertension in the Older Adult, SHEP, SYSTEUR and STOP-1 and 2 have proven that treating both diastolic and systolic hypertension in the elderly significantly reduces stoke and MI.
Genetics
A history of hypertension tends to run in families The closest correlation exists between sibs rather parent and child It is also possible that environmental factors common to members of the family also have a role in the development of hypertension
Environment
Mental and physical stress both increase blood pressure However removing stress does nor necessarily return blood pressure to normal values True stress responders who have very high BP when they attend their doctor but low normal pressures otherwise tend to be highly resistant to treatment
Sodium Intake
The SALT study and more recently the DASH study have confirmed a strong relationship between hypertension, stroke and salt intake Reducing salt intake in hypertensive individuals does lower blood pressure However reducing salt intake in normotensives appears to have no effect Reducing salt intake to 60-80mmol/day does lower BP However there are real difficulties in achieving this level of salt restriction (fast food)
Alcohol
The most common cause oh hypertension in the young Scot Affects 1% of the population Small amounts of alcohol tend to decrease BP Large amounts of alcohol tend to increase BP If alcohol consumption is reduced BP will fall over several days to weeks. Average fall is small 5/3 mmHg
Weight
Obese patients have a higher BP Up to 30% of hypertension is attributable in part or wholly to obesity If a patient loses weight BP will fall In untreated patients a weight loss of 9Kg has been reported to produce a fall in BP of 19/18 mmHg In treated patients a fall in BP of 30/21 mmHg has been reported Weight reduction is the most important non-pharmacological measure available
DYSLIPIDEMIA
Obesity + Androgen
Lipolysis
Attenuated Vasodilatio n
Vascular Hypertrophy
HYPERTENSION
Race
Caucasians have a lower BP than black populations living in the same environment Black populations living in rural Africa have a lower BP than those living in towns Reasons are not clear Possibly black populations are more susceptible to stress when living in towns Respond in different ways to changes in diet Black populations are genetically selected to be salt retainers and so are more sensitive to an increase in dietary salt intake
Secondary Hypertension
5-10% of all hypertension has an identifiable cause Removal of the cause does not guarantee that the hypertension or risk will return to normal Sustained hypertension produces end-organ damage to blood vessels, heart and kidney This type of damage tends to increase BP further and so a vicious self-propagating cycle is established
Renal disease
20% of resistant hypertensive patients chronic pyelonephritis renal artery stenosis polycystic kidneys
NSAIDs Oral contraceptive Corticosteroids
Drug Induced
Pregnancy
pre-eclampsia
Conns Syndrome Cushings disease Phaeochromocytoma Hypo and hyperthyroidism Acromegaly
Endocrine
Vascular
Sleep Apnoea
A sustained increase in BP increases the load on the heart and blood vessels This has two effects
Hypertrophy of this type increases the strength of the heart and vasculature However it also reduces compliance
A reduction in the ability of the heart to to respond to increased or variable loads a decrease in the ability of the resistance vessels to relax
For the same level of BP and irrespective of age the presence of left ventricular hypertrophy increases 5 year mortality by
Atheromatous disease
Sustained hypertension is associated with accelerated atheromatous disease of the blood vessels Peripheral vascular disease Coronary artery disease Cerebrovascular disease Renal artery disease
MI Heart failure Angina
The Heart
The kidney
Hypertension produces an increase in renal vascular resistance and a reduction in renal blood flow
Renal disease
RBF + afferent glomerular arteriolar resistance
glomerular hyperfiltration
Clinical manifestations
None in the early stages, other than high BP reading, if taken eventually report symptoms, such as persistent headaches, fatigue, dizziness, palpitations, flushing, blurred vision or epitaxis
retinal changes, such as hemorrhages, exudates, arteriolar narrowing, cotton wool spots (small infarctions), and if severe, papilledema (swelling of the optic disc) angina, MI LV Hypertrophy, heart failure BUN & Cr, nocturia stroke & TIA (cerebral infarcts) with such signs as altered vision, speech, hemiplegia,
Evaluation: Objectives
1. To identify known causes of high blood pressure 2. To assess the presence or absence of target organ damage and CV disease, and the response to therapy 3. To identify other CV risk factors or concomitant disorders that may define prognosis and guide treatment
Evaluation: History
Known duration and levels of elevated BP History or symptoms of CHD, heart failure, cerebrovascular disease, PVD, renal disease, DM, dyslipidemia, gout, sexual dysfunction, or other comorbid conditions FH of HTN, premature CHD, stroke, DM, dyslipidemia, or renal disease Symptoms suggesting causes of HTN
History of recent weight changes, physical activity level, tobacco use Dietary assessment including intake of sodium, alcohol, saturated fat, and caffeine History of all prescribed and meds, herbals, and illicit drugs Results and adverse effects of previous antihypertensive therapy Psychosocial and environmental factors
Two or more BP measurements 2 minutes apart with pt either seated or supine and after standing for at least 2 minutes Verification in the contralateral arm Measurement of height, weight, and waist circumference
Funduscopic exam for hypertensive retinopathy (arteriolar narrowing, arteriolar constrictions, AV crossing changes, hemorrhages and exudates, disc edema) Neck exam for bruits, distended veins, or enlarged thyroid Heart exam for rate and rhythm, size, precordial heave, clicks, murmurs, and extra heart sounds
Lung exam for rales and evidence of bronchospasm Abdominal exam for bruits, enlarged kidneys, masses, and aortic pulsation Extremity exam for decreased peripheral pulses and edema Neurological exam
Used to determine the presence of target organ damage and other risk factors
UA: hematuria, proteinuria, and microalbuminuria looking for signs of renal dysfunction evidence of DM or renal disease Lipid panel: as a screen for other risk factors for atherosclerotic disease EKG: assess for LVH and evidence of prior ischemia
Additional
Isotopic renogram, renal biopsy
Renovascular disease
Aortogram potassium, plasma or urinary Plasma potassium, plasma Urinary aldosterone after saline load; adrenal renin and aldosterone (ratio) computed tomography (CT) and scintiscans Blood pressure in legs Urinary cortisol after variable doses of dexamethasone; adrenal CT and scintiscans Urinary catechols; plasma catechols, basal and after 0.3 mg clonidine; Spot urine for metanephrine adrenal CT and scintiscans AM plasma cortisol after 1 mg dexamethasone at bedtime
Cushings syndrome
Pheochromocytoma
Decisions should not be made on BP alone, but also on presence of other risk factors, target organ damage, and concomitant diseases, as well as on other aspects of patients personal, medical, social, economic, ethnic, and cultural characteristics
1999 WHO-ISH HYPERTENSION PRACTICE GUIDELINES FOR PRIMARY CARE PHYSICIANS
26
Proteinuria and/or slight elevation of plasma creatinine concentration 106-177 mmol/L (1.22.0 mg/dl)
Ultrasound or radiological evidence of atherosclerotic plaque (carotid, iliac, and femoral arteries, aorta) Generalised or focal narrowing of the retinal arteries
Heart disease
Myocardial infarction Angina pectoris Coronary revascularisation Congestive heart failure
Low risk Medium risk High risk Very high risk higher
= = = =
Management
The most essential element in reducing the morbidity and mortality associated with hypertension is long term compliance/adherence achieved through life style modification alone or in combination with pharmacologic therapy (stepped care)
Lifestyle modification
weight reduction sodium restriction dietary fat modification exercise alcohol restriction caffeine restriction relaxation techniques potassium supplementation
Recommendation
Maintain normal body weight (BMI, 18.5-24.9)
Consume a diet rich in fruits, vegetables, and 8-14 mm Hg low-fat dairy products with a reduced content of saturated and total fat Reduce dietary sodium intake to no more than 100 mEg/L (2.4 g sodium or 6 g sodium chloride) Engage in regular aerobic physical activity such as brisk walking (at least 30 minutes per day, most days of the week) Limit consumption to no more than 2 drnks per day (1 oz or 30mL ethanol (eg. 24 oz beer, 10 oz wine, or 3 oz 80-proof whiskey) in most men and no more than 1 drink per day in women and lighter-weight persons 2-8 mm Hg
4-9 mm Hg
2-4 mm Hg
Not at Goal BP (<140/90 mm Hg or <130/80 mm Hg for Those With Diabetes Or Chronic Kidney Disease)
Stage 1 Hypertension (systolic BP 140-159 mm Hg Or Diastolic BP 90-99 mm Hg) Thiazide type diuretics for most may consider ACE inhibitor, ARB, -blocker, CCB, or Combination
Stage 2 Hypertension (systolic BP 160 mm Hg Or Diastolic BP 100 mm Hg) 2-Drug combination for most (usually thiazide - type diuretic and ACE inhibitor or ARB or -blocker, CCB)
Drug(s) for the Compelling indication Other antihypertensive drugs (diuretics, ACE inhibitor, ARB, blocker, CCB) as Needed
Not at Goal BP
Optimize Dosages or Add Additional Drugs Until Goal BP is Achieved Consider Consultation With HypertensionSpecialist
Is patient at:
High Risk Medium Risk Low Risk
Stratify Risk
Very High
High
Begin drug treatment Begin drug treatment
Stratify risk
Low
Medium
Monitor BP & other risk factors for 3-6 months
SBP <140 or DBP <90 Continue to monitor SBP >150 or DBP >95 Begin drug treatment SBP <150 or DBP <95 Continue to monitor
Use a low dose of one drug to initiate therapy If good response and tolerability but inadequate control increase the dose of the first drug If little response or poor tolerability change to another drug class
All 6 classes are suitable for the initiation and maintenance of BP lowering therapy, but the choice of drugs will be influenced by cost and by many factors for special groups of patients. In some parts of the world, reserpine and methyldopa are also used frequently.
Indications
Compelling Possible
Diabetes
Diuretics
Contraindications Compelling
Gout
Possible
Dyslipidaemia Sexually active males
Indications
Beta-Blockers
Contraindications
Compelling Asthma and Chronic obstructive Pulmonary disease Heart block (AV 2,3) Possible Dyslipidaemia Athletes and Physically active Patients Peripheral
vascular disease
Indications
Calcium Antagonists
Compelling
Possible
Contraindications Compelling
Heart block (AV 2,3)
* verapimil or diltiazem
Possible
Heart failure*
Indications
ACE Inhibitors
Compelling Heart failure Left ventricular dysfunct After myocardial infarct Diabetic nephropathy
Possible
Contraindications
Compelling Pregnancy Bilateral renal artery stenosis Hyperkalaemia Possible
Alpha-Blockers
Indications
Compelling Prostatic Hypertrophy Possible Glucose intolerance Dyslipidaemia
Contraindications
Compelling Possible Orthostatic
hypotension
Indications
Angiotensin II Antagonists
Contraindications
Compelling Pregnancy Possible
diuretic and beta-blocker diuretic and ACE inhibitor (or Angiotensin II antagonist) calcium antagonist (dihydropyridine) and beta-blocker calcium antagonist and ACE inhibitor alpha-blocker and beta-blocker
Drug-related causes
Doses too low Wrong type of diuretic Inappropriate combinations Rapid inactivation (e.g. hydralazine) Drug actions and interactions
Sympathomimetics - Adrenal steroids Nasal decongestants - Oral contraceptives Appetite suppressants - Cyclosporine, tacrolimus Caffeine - Erythropoietin Licorice (as may be found in chewing tobacco) Cocaine and other illicit drugs Antidepressants Nonsteroidal anti - inflammatory drugs
Associated conditions
Smoking Increasing obesity Sleep apnea Insulin resistance/hyperinsulinemia Ethanol intake of more than 1 oz (30 mL) per day Anxiety-induced hyperventilation or panic attacks Chronic pain Intense vasocondtriction (arteritis) Organic brain syndrome (e.g. memory deficit)