RIA BANDIARA dr. Sp.

PD

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

What is the JNC VII?

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

Why Control Hypertension?

Heart disease and stroke are the 1st and 3rd leading causes of death in the U.S.

More than $259 billion in direct and indirect costs

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

physical stress mental stress

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

At what blood pressure is a patient hypertensive?

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

New (2003) WHO-ISH Definitions and Classification of BP Levels

Category Optimal BP Normal BP High-Normal Grade 1 Hypertension (mild) Subgroup: Borderline Grade 2 Hypertension (moderate) Grade 3 Hypertension (severe) Systolic BP (mm Hg) <120 <130 130-139 140-159 140-149 160-179 >180 Diastolic BP (mm Hg) <80 <85 85-89 90-99 90-94 100-109 >110

Isolated Systolic Hypertension Subgroup: Borderline

>140 140-149

<90 <90

Guidelines for Measurement of Blood Pressure

1. Patient conditions
1.1. Posture
Initialy, particularly in patients over age 65, diabetic, or receiving antihypertensive therapy, check for postural changes by taking readings after 5 minutes supine, then immediately and 2 minutes after they stand For routine follow-up, sitting pressures are recommended. The patient should sit quietly with the back supported for 5 minutes and the arm supported at the level of the heart.

Guidelines for Measurement of Blood Pressure (continued)

1.2. Circumstances
No caffeine during the hour preceeding the reading No smoking during the 15 minutes precding the reading No exogenous adrenergic stimulants (e.g. phenylephrine in nasal decongestants or eye drops for pupillary dilation) A quiet, warm setting. Home readings taken under varying circumstances and 24 hours ambulatory recordings may be preferable and more accurate in predicting subsequent cardiovascular disease.

Guidelines for Measurement of Blood Pressure (continued)

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)

Guidelines for Measurement of Blood Pressure (continued)

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.

Guidelines for Measurement of Blood Pressure (continued)

3.2. Performance
Inflate the bladder quickly to a pressure 20 mmHg above the systolic pressure, as recognized by disappearance of the radial pulse. Deflate the bladder 3 mmHg every second Record the Korotkoff phase V (disappearance), except in children, in whom ose of phase IV (muffling) may be preferable. If the Korotkoff sounds are weak, have the patient raise the arm, open and close the hand.

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

Children > 5 years Usually supplied

12 cm

23 cm 35 cm 42 cm

Strongly recommended for routine use

Normal and lean arms Muscular and Obese arms

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.

Control of blood pressure

Blood pressure is controlled by an integrated system Prime contributors to blood pressure are:

Cardiac output

Stroke volume Heart rate

Peripheral vascular resistance

Each of these factors can be manipulated by drug therapy

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

Renal Sodium retention

Descreased filtration surface

Sympathetic nervous overactivity

Reninangiotensin excess

Cell membrane alteration

Hyperinsuli nemia

Excess sodium intake

Genetic alteration

Stress

Genetic alteration

Obesity

Endothelium derived factors

capacitance

preload Cardiac output

veins venules
Peripheral resistance
Sympathetic system

heart Blood volume

arterioles Blood pressure Angiotensin/ aldosterone

Renin release

Sympathetic Nervous System

Sympathetic system activation produces

vasoconstriction reflex tachycardia increased cardiac output

In this way blood pressure is increased The actions of the sympathetic system are rapid and account for second to second blood pressure control

The renin-angiotensin-aldosterone system

The RAAS is pivotal in long-term BP control The RAAS is responsible for:

maintenance of sodium balance control of blood volume control of blood pressure

The RAAS is stimulated by:

fall in BP fall in circulating volume sodium depletion

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

Myocyte and smooth muscle hypertrophy:

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

Macula densa signal Renal arteriolar pressure Renal nerve activity

ANGIOTENSIN III

ANGTIOTENSINASE A

Adrenal cortex

Kidney

Intestine

CNS

Peripheral nervous system Adrenergic facilitation

Vascular smooth muscle

Heart

Aldosterone Sympathetic discharge Distal nephron reabsorption

Contractility

Sodium and water reabsorption

Thirst salt appetite

Vasopressin release

Vasoconstriction

Maintain or increase ECFV

Total peripheral resistance

Cardiac output

Angiotensinogen
Renin

Angiotensin I
ACE vasoconstriction

Angiotensin II
aldosterone (inc. reabsorp of Na)

Inc. PVR

Inc. blood volume

Pre hypertension

Established hypertension 30-50 years

10-30 years
CO

Complicated hypertension 40-60 years (T. O. D)

HEREDITY - ENVIRONMENT PRE - HYPERTENSION Normotension EARLY HYPERTENSION ESTABLISHED HYPERTENSION

Age
0 - 30

20 - 40
30 - 50

UNCOMPLICATED

COMPLICATED

Accelerated - CARDIAC malignant Hypertrophy course Failure Infarction

LARGE CEREBRAL VESSEL Ischemia Aneurysm Thrombosis Dissection Hemorrhage

RENAL Nephrosclerosis Failure

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

Aetiology of essential hypertension

The aetiology of hypertension is

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

A sodium homeostatic effect

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

Increased Abdominal Fat

Lipolysis

Release of Free Fatty Acids

TYPE II DIABETES MELLITUS

Peripheral Insulin Resistance

Increased Pancreatic Insulin Secretion Hyperinsulinemia Sodium Retention

Decreased Hepatic Insulin Extraction

Attenuated Vasodilatio n

Increased Sympathetic Nervous Activity

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

Causes for Secondary Hypertension

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

Coarctation of the aorta

Sleep Apnoea

The risks of hypertension

A sustained increase in BP increases the load on the heart and blood vessels This has two effects

Myocardial hypertrophy Smooth muscle hypertrophy in the resistance vessels

Hypertrophy of this type increases the strength of the heart and vasculature However it also reduces compliance

The effects of reduced compliance are:

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

33% in men 21% in women

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

efferent glomerular arteriolar constriction

glomerular hydrostatic pressure

glomerular hyperfiltration

Glomerusclerosis and impairtment of renal function

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

may also see signs of target organ damage

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

Evaluation: History cont.

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

Evaluation: Initial Physical Exam

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

Evaluation: Physical Exam cont.

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

Evaluation: Physical Exam cont.

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

Evaluation: Diagnostic Tests

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

Overall Guide to Workup for Secondary Causes of Hypertension

Diagnosis
Chronic renal disease

Diagnostic Procedure Initial

Urinalysis, serum Creatinine, renal Sonography Plasma renin before and 1 hour after captopril

Additional
Isotopic renogram, renal biopsy

Renovascular disease

Aortagram, isotopic renogram 1 hour after captopril

Coarctation Primary Aldosteronism

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

Which Factors Influence Prognosis? (1)

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

Which Factors Influence Prognosis? (2)

Risk factors of CVD I. Used for risk stratification II. Other factors adversely influencing prognosis Target organ damage (TOD) Associated clinical conditions (ACC)

Which Factors Influence Prognosis? (3)

Risk factors for CVD
I. Used for risk stratification Levels of systolic and diastolic blood pressure (Grades 1-3) Men >55 years Women >65 years Smoking Total cholesterol >6.5 mmol/L (250 mg/dl) Diabetes Family history of premature cardiovascular disease

Which Factors Influence Prognosis? (4)

Risk factors for CVD
II.Other factors adversely influencing prognosis Reduced HDL cholesterol Raised LDL cholesterol Microalbuminuria in diabetes Impared glucose tolerance Obesity Sedentary lifestyle Raised fibrinogen High risk socioeconomic group High risk ethnic group High risk geographic region

Which Factors Influence Prognosis? (5)

Target organ damage (TOD)
Left ventricular hypertrophy (electrocardiogram, echocardiogram, or radiogram)

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

Which Factors Influence Prognosis? (6)

Associated clinical conditions (ACC)
Cerebrovascular disease
Ischaemic stroke Cerebral haemorrhage Transient ischaemic attack (TIA)

Heart disease
Myocardial infarction Angina pectoris Coronary revascularisation Congestive heart failure

Which Factors Influence Prognosis? (7)

Associated clinical conditions (ACC)
Renal disease Diabetic nephropathy Renal failure, plasma creatinine concentration >177 mmol/L (>2.0 mg/dl) Vascular disease Dissecting aneurysm Symptomatic arterial disease Advanced hypertensive retinopathy Haemorrhages or exudates Papilloedema

Which Factors Influence Prognosis? (8)

Typical 10 year risk of stroke or myocardial infarction

Low risk Medium risk High risk Very high risk higher

= = = =

<15 percent 15-20 percent 20-30 percent 30 percent or

Stratifying Risk - Quantifying Prognosis

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

Lifestyle Modification to Manage Hypertension

Modification
Weight reduction Adopt DASH eating Plan Dietary sodium reduction Physical activity

Recommendation
Maintain normal body weight (BMI, 18.5-24.9)

Approximate Systolic BP Reduction, Range 5-20 mm Hg/10-Kg weight loss

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

Moderation of alcohol consumption

2-4 mm Hg

Figure. Algorithm for Treatment of Hypertension

Lifestyle Modification

Not at Goal BP (<140/90 mm Hg or <130/80 mm Hg for Those With Diabetes Or Chronic Kidney Disease)

Initial Drug Choices

Hypertension Without Compelling Indications

Hypertension With Compelling Indications

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

Stratifying Risk - Quantifying Prognosis

Management Strategy (1)

Is patient at:
High Risk Medium Risk Low Risk

Very High Risk

Management Strategy (2)

Stratify Risk

Very High

High
Begin drug treatment Begin drug treatment

Management Strategy (3)

Stratify risk
Low

Medium
Monitor BP & other risk factors for 3-6 months

Monitor BP & other risk factors for 6-12 months

SBP >140 or DBP >90 Begin drug treatment

SBP <140 or DBP <90 Continue to monitor SBP >150 or DBP >95 Begin drug treatment SBP <150 or DBP <95 Continue to monitor

Principles of Drug Treatment (1)

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

Principles of Drug Treatment (2)

It is often preferable to add a small dose of a second drug rather than increase the dose of the first drug Use long-acting drugs providing 24hour efficacy on a once daily basis. Improves adherence to therapy and minimizes BP variability.

Principles of Drug Treatment (3)

More evidence of beneficial CVD effects with older drugs (e.g., diuretics and beta-blockers) Evidence of benefit with newer drugs (e.g., ACE inhibitors and calcium antagonists) is accumulating.

Principles of Drug Treatment (4)

There are six main drug classes used worldwide : diuretics beta-blockers ACE inhibitors calcium antagonists alpha blockers angiotensin II antagonists

Principles of Drug Treatment (5)

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

Heart failure Elderly patients Systolic hypertension

Contraindications Compelling
Gout

Possible
Dyslipidaemia Sexually active males

Indications

Beta-Blockers

Compelling Angina After myocardial infarct Tachyarrhythmias

Possible Heart failure Pregnancy Diabetes

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

Angina Peripheral Elderly patients Vascular disease Systolic hypertension

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

Compelling ACE-I cough

Possible Heart failure

Contraindications
Compelling Pregnancy Possible

Bilateral renal artery stenosis Hyperkalaemia

Combination Therapy (1)

In most patients, appropriate combination therapy produces BP reductions that are twice as great as those obtained with monotherapy, for example, 12-22 mm Hg systolic BP and 7-14 mm Hg diastolic BP for patients with initial BP of >160/95 mm Hg

Combination Therapy (2)

Effective drug combinations to treat hypertension are:

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

Causes of Resistant Hypertension

Improper blood pressure measurement Volume overload and pseudotolerance Excess sodium intake Volume retention from kidney disease Inadequate diuretic therapy Drug-induced or other causes Nonadherence Inadequate doses Inappropriate combinations Nonsteroidal anti-inflammatory drugs; cyclooxygenase 2 inhibitors Cocaine, amphetamines, other illicitdrugs Sympathomimetics (decongestants, anorectics) Oral contraceptives Adrenal steroids Cyclosporine and taerolimus Erythropoictin Licorice (including some chewing tobbaco) Selected over-the-counter dictary supplement and medicines (eg. Ephedra, ma haung, bitter orange) Associated conditions Obesity Excess alcohol intake Identifiable causes of hypertension

Causes of inadequate responsiveness to therapy

Pseudoresistance White-coat hypertension or office elevations Pseudohypertension in older patient Use of regular cuff on very obese arm Nonadherence to therapy Volume overload Excess salt intake Progressive renal damage (nephrosclerosis) Fluid retention from reduction of blood pressure Inadequate diuretic therapy

Causes of inadequate responsiveness to therapy

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

Causes of inadequate responsiveness to therapy

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)

Identifiable causes of hypertension