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Presentation Overview
Definition Scope of the problem Systolic & Diastolic blood pressure Aetiology Clinical Manifestation End Organ Damage Blood pressure measurement Guidelines Goals of therapy Algorithm for hypertension management Lifestyle modifications Pharmacological treatment

What is Hypertension?


high arterial blood

The continuous relationship between the level of blood pressure and cardiovascular risk makes any numerical definition and classification of hypertension arbitrary. 1

The scope of the problem

Heart Attack (MI) Heart Failure Stroke Kidney Disease


Systolic & Diastolic Blood Pressure

Systolic Blood Pressure: BP when the heart contracts and expels the blood into the arteries. This is what gives rise to the pulse, known as the maxima Diastolic blood pressure:
While the heart is filling between two contractions, the blood in the main arteries flows towards the smallest arteries: the blood pressure in the main arteries then falls to the minima

Definitions and Classification of Blood Pressure Levels (mmHg)

Category Optimal Systolic <120 and Diastolic <80

High Normal Grade 1 hypertension Grade 2 Hypertension Grade 3 Hypertension Isolated Systolic Hypertension

130-139 140-159 160-179 180 140

and/or and/or and/or and/or and

85-89 90-99 100-109 110 <90

Blood Pressure Thresholds (mmHg) for Definition of Hypertension with Different Types of Measurement

SBP Office or Clinic 24-hour Day Night Home 140 125-130 130-135 120 130-135

DBP 90 80 85 70 85

Primary / Essential Hypertension

Accounts for approximately 95% of the hypertensive population.

Has no single identifiable cause but may be affected by a number of factors.

Primary / Essential Hypertension
1) Age - Young people: arteries are supple and easily absorb the pressure of the blood pumped out by the heart. With age: they lose their elasticity and the systolic blood pressure increases at rest and even more during exertion or when experiencing emotion.

Primary / Essential Hypertension
2) Genetics Up to 40% of hypertension may be genetically determined. Indicated by family and adoption studies. 3) Environment a Excessive sodium intake b Mental & Physical stress can cause transient increases in blood pressure.

Primary / Essential Hypertension
3) Environment c
tends to increase blood pressure.

Alcohol - intake in large amounts ( >6 units/day)

d Weight - Obese patients have higher

blood pressure.

e Physical inactivity Less than 30min

moderate daily activity

Primary / Essential Hypertension
4) Race 5) Intrauterine influences

6) Humoral mechanisms 7) Insulin Resistance

Sympathetic nervous system. Dotted arrows represent inhibitory neural influences and solid arrows represent excitatory neural influences on sympathetic outflow to the heart, peripheral vasculature, and kidneys. EPI = epinephrine; NTS = nucleus tractus solitarius; NE = norepinephrine; Ach = acetylcholine; A II = angiotensin II.

Endothelium-derived relaxing and constricting factors. Various blood- and platelet-derived substances can activate specific receptors (orange circles) on the endothelial membrane to release relaxing factors such as nitric oxide (NO), prostacyclin (PGI2), and an endothelium-derived hyperpolarizing factor (EDHF). Contracting factors also are released, such as endothelin (ET-1), angiotensin (A II), and thromboxane A2 (TXA2), as well as prostaglandin H2 (PGH2). ACE = angiotensin-converting enzyme; 5-HT = serotonin; Bk = bradykinin; ECE = endothelin-converting enzyme; L-Arg = l-arginine; NOS = nitric oxide synthase; O2- = superoxide; TGF1 = transforming growth factor beta-1; Thr = thrombin.

The renin-angiotensin-aldosterone system. A I = angiotensin I; A II = angiotensin II; ACE = angiotensin-converting enzyme; AT1R = angiotensin I receptor.

Schematic representation of the

central role played by angiotensin 1 receptor

(AT1R)mediated signaling in cardiovascular disease progression. A II = angiotensin II; MI = myocardial infarction.

Vascular remodeling of small and large arteries in hypertension. Diagrams represent arteries in cross section showing the tunica adventitia, tunica media, and tunica intima.

Secondary polycystic Hypertension kidneys, renal artery stenosis Renal Pyelonephritis, renin secreting tumour Disease contraceptives Drug Induced Oral Carbenoxolone and liquorice derivatives
Pregnancy Hormonal Other
Corticosteroids Pre-eclampsia Cushings syndrome Phaeochromocytoma Hyper- Hypo-thyroidism Acromegally Coarctation of the aorta

Identifiable Causes of Hypertension

Sleep apnea

Drug-induced or related causes Chronic kidney disease Primary aldosteronism Renovascular disease Chronic steroid therapy and Cushings syndrome Pheochromocytoma Coarctation of the aorta Thyroid or parathyroid disease

Renal parenchymal hypertension

Estimated GFR <60 mL/min/1.73 m2 Urine albumin-to-creatinine ratio 30 mg/g Renal ultrasonography

Computed tomographic angiogram with three-dimensional reconstruction. A, The classic string of beads lesion of fibromuscular dysplasia (bilateral in this patient). B, A severe proximal atherosclerotic stenosis of the right renal artery and mild stenosis of the left renal artery.

Renovascular disease
New elevation in serum creatinine, marked elevation in serum creatinine with initiation of ACEI or ARB, refractory hypertension, flash pulmonary edema, abdominal bruit Magnetic resonance or CT angiography, invasive angiography

Algorithm for evaluating patients in whom renal artery stenosis is suspected. Clinical follow-up includes periodic reassessment with duplex ultrasonography, magnetic resonance angiography, and nuclear imaging to estimate fractional blood flow to each kidney. The treatment of risk factors includes smoking cessation and the use of aspirin, lipid-lowering agents, and antihypertensive therapy.

Coarctation of the aorta

Arm pulses > leg pulses, arm BP > leg BP, chest bruits, rib notching on chest radiography Magnetic resonance imaging, aortography

Primary aldosteronism
Hypokalemia, refractory hypertension Plasma renin and aldosterone, 24-hour urine potassium, 24-hour urine aldosterone and potassium after salt loading, adrenal CT, adrenal vein sampling


Cushing's syndrome
Truncal obesity, wide and blanching purple striae, muscle weakness Plasma cortisol, urine cortisol after dexamethasone, adrenal CT

Headaches, paroxysmal hypertension, palpitations, perspiration, and pallor; diabetes Plasma metanephrine and normetanephrine, 24-hour urine catechols, adrenal CT

Obstructive sleep apnea

Loud snoring, daytime somnolence, obesity, large neck Sleep study

Clinical Manifestation
Asymptomatic in the majority of patients. Can remain undetected for many years
Headache may occur when SBP rises above 200mmHg or when blood pressure is rapidly elevated.

Measuring Blood Pressure

Patient seated quietly for at least 5minutes in a chair, with feet on the floor and arm supported at heart level
An appropriate-sized cuff (cuff encircling at least 80% of the arm) At least 2 measurements bladder

Measuring Blood Pressure

Systolic Blood Pressure is the point at which the first of 2 or more sounds is heard
Diastolic Blood Pressure is the point before the disappearance of the sounds

Measuring Blood Pressure

Ambulatory BP Monitoring - information about BP during daily activities and sleep. Correlates better than office measurements with target-organ injury.

Office BP Measurement
Use auscultatory method with a properly calibrated and validated instrument. Patient should be seated quietly for 5 minutes in a chair (not on an exam table), feet on the floor, and arm supported at heart level. Appropriate-sized cuff should be used to ensure accuracy.

At least two measurements should be made.

Clinicians should provide to patients, verbally and in writing, specific BP numbers and BP goals.

Ambulatory BP Monitoring
ABPM is warranted for evaluation of white-coat HTN in the absence of target organ injury. Ambulatory BP values are usually lower than clinic readings. Awake, individuals with hypertension have an average BP of >135/85 mmHg and during sleep >120/75 mmHg. BP drops by 10 to 20% during the night; if not, signals possible increased risk for cardiovascular events.

Guidelines for Family and Clinical History

1. 2. Duration and previous level of high blood pressure Indications of secondary hypertension: - family history of renal disease (polycystic kidney) - renal disease, urinary tract infection, haematuria, analgesic abuse (parenchymal renal disease) - drug/substance intake: oral contraceptives, liquorice, carbenoxolone, nasal drops, cocaine, amphetamines, steroids, non-steroidal anti-inflammatory drugs, erythropoietin, cyclosporine - episodes of sweating, headache, anxiety, palpitation (phaeochromocytoma) - episodes of muscle weakness and tetany (aldosteronism)

Guidelines for Family and Clinical History

3. Risk factors: - family and personal history of hypertension and cardiovascular disease - family and personal history dyslipidaemia - family and personal history of diabetes mellitus - smoking habits - dietary habits - obesity; amount of physical exercise - snoring; sleep apnoea ( information also from partner) - personality

Target Organ Damage

BRAIN Stroke TIA Vascular dementia
HEART CAD LV hypertrophy LV systolic dysfunction


Hypertensive nephropathy

VASCULAR SYSTEM Hypertensive retinopathy Aortic aneurysm PVD Atherosclerosis

Guidelines for Family and Clinical History

4. Symptoms of organ damage: - brain and eyes: headache, vertigo, impaired vision, transient ischaemic attacks, sensory or motor deficit - heart: palpitation, chest pain, shortness of breath, swollen ankles - kidney: thirst, polyuria, nocturia, haematuria - peripheral arteries: cold extremities, intermittent claudication
Previous antihypertensive therapy: - Drug(s) used, efficacy and adverse effects 6. Personal, family and environmental factors


Physical Examination for Secondary Hypertension, Organ Damage and Visceral Obesity
Signs suggesting secondary hypertension and organ damage Features of Cushing Syndrome Skin stigmata of neurofibromatosis (phaeochromocytoma) Palpation of enlarged kidneys (polycystic kidney) Auscultation of abdominal murmurs (renovascular hypertension) Auscultation of precordial or chest murmurs (aortic coarctation or aortic disease) Diminished and delayed femoral pulses femoral blood pressure (aortic coarctation, aortic disease)

Physical Examination for Secondary Hypertension, Organ Damage and Visceral Obesity
Signs of organ damage

Brain: murmurs over neck arteries, motor or sensory defects

Retina: fundoscopic abnormalities

Heart: location and characteristics of apical impulse, abnormal cardiac rhythms, ventricular gallop, pulmonary rates, peripheral oedema
Peripheral arteries: absence, reduction, or asymmetry of pulses, cold extremities, ischaemic skin lesions Carotid arteries: systolic murmurs

Physical Examination for Secondary Hypertension, Organ Damage and Visceral Obesity
Evidence of visceral obesity Body weight Increased waist circumference (standing position) M: >102 cm, W: >88 cm Increased body mass index [body weight (Kg)/ height (m)] Overweight 25 Kg/m, Obesity 30 Kg/m

Laboratory Investigations
Routine tests Fasting plasma glucose Serum total cholesterol Serum LDL-cholesterol Serum HDL-cholesterol Fasting serum triglycerides Serum potassium Serum uric acid Serum creatinine Estimated creatinine clearance (Cockroft-Gault formula) or glomerular filtration rate (MDRD formula) Haemoglobin and haematocrit Urinalysis (complemented by microalbuminuria dipstick test and microscopic examination) Electrocardiogram

Laboratory Investigations
Recommended tests
Echocardiogram Carotid ultrasound

Quantitative proteinuria (if dipstick test positive)

Ankle-brachial BP index Fundoscopy

Glucose tolerance test (if fasting plasma glucose >5.6 mmol/L (102 mg/dL)
Home and 24h ambulatory BP monitoring

Pulse wave velocity measurement (where available)

Laboratory Investigations
Extended evaluation (domain of the specialist) Further search for cerebral, cardiac, renal and vascular disease, mandatory in complicated hypertension Search for secondary hypertension when suggested by history, physical examination or routine tests: measurement of renin, aldosterone, corticosteroids, catecholamines in plasma and/or urine; arteriographies; renal and adrenal ultrasound; computer-assisted tomography; magnetic resonance imaging

Searching for subclinical organ damage

Due to the importance of subclinical organ damage as an intermediate stage in the continuum of vascular disease and as a determinant of total cardiovascular risk, signs of organ involvement should be sought carefully by appropriate techniques: Heart Electrocardiography should be part of all routine assessment of subjects with high BP in order to defect left ventricular hypertrophy, patterns of strain, ischaemic condition defects and arrhythmias Echocardiography is recommended whenever a more sensitive detection of left ventricular hypertrophy is considered useful. Geometric patterns (concentric and eccentric hypertrophy, concentric remodeling) can be defined echocardiographically, of which concentric hypertrophy carries the worst prognosis Diastolic dysfunction can also be evaluated by Doppler measurement of transmitral blood pressure velocities

Searching for subclinical organ damage

Blood vessels Ultrasound scanning of the extracranial carotid arteries is also recommended whenever detection of vascular hypertrophy (increased thickness of common carotid intima-media) or asymptomatic atherosclerosis (thickening of carotid bifurcation and internal carotid arteries, presence of plagues) is deemed useful Large artery stiffening (an important vascular alteration leading to isolated systolic hypertension in the elderly) can be measured in a relatively simple way by pulse wave velocity. It might be more widely recommended if its availability were greater A low ankle- brachial BP index signals advanced peripheral artery disease

Searching for subclinical organ damage

Kidney The diagnosis of hypertension- related renal damage is based on the finding of a reduced renal function or the detection of an elevated urinary excretion of albumin in hypertensive patients Measurement of serum creatinine as well estimation from serum creatinine values of glomerular filtration rate (MDRD formula also requiring age, gender, race) or creatinine clearance (Cockroft- Gault formula, requiring age, gender body weight) should be part of routine procedures. This allows classification of renal dysfunction and stratification of cardiovascular risk The presence of urinary protein should be sought in all hypertensives by dipstick. In dipstick negative patients low grade albuminuria (microalbuminuria) should also be determined in spot urine and related to creatinine excretion

Searching for subclinical organ damage

Fundoscopy Examination of eye grounds is recommended in hypertensive with severe disease, only. This is because the mildest retinal changes (grade 1: arteriolar narrowing; grade 2: arterio venous nipping) appear to be largely non-specific alterations except in young patients In contrast grade 3 (haemorrhages and exudates) and 4 (papilloedema), only present in severe hypertension, are associated with an increased risk of cardiovascular events More sensitive methods for quantitatively assessing retinal vascular changes are being developed

Grade 1Increased light-striping; mild arteriovenous nicking Grade 2Coppery arteriolar color; moderate arteriovenous nicking veins almost completely invisible below arteriolar crossing

Grade 3Silver arteriolar color; severe arteriovenous nicking

Grade 4Arterioles visible only as fibrous cords without bloodstreams

Hemorrhage and exudatesGrades 14 (based on number of affected quadrants divided by 2)

PapilledemaGrades 14 (based on diopters of elevation)

Searching for subclinical organ damage

Brain Silent brain infarcts, lacunar infarction, microbleeds and white matter lesions are not infrequent among hypertensives and can be detected by MRI or CT (MRI being generally superior to CT) Availability and costs do not allow asymptomatic use of these techniques, however In elderly hypertensive, cognitive tests may also help to detect initial brain deterioration

Availability, Prognostic Value and Cost of some markers of organ damage (scored from 0 to 4 pluses)
Electrocardiography Echocardiography Carotid Intima-Media Thickness Arterial stiffness (Pulse wave velocity) Ankle-Brachial index Coronary calcium content Cardiac/Vascular tissue composition Circulatory collagen markers Endothelial dysfunction Cerebral lacunae/ White matter lesions Est. Glomerular Filtration Rate or Creatinine Clearance

CV predictive value
++ +++ +++

++++ +++ +++

+ ++ ++

++ + ? ? ++ ? +++

++ + + + + ++ ++++

+ ++++ ++ ++ +++ ++++ +




Patient Evaluation
Evaluation of patients with documented HTN has three objectives:

1. Assess lifestyle and identify other CV risk factors or concomitant disorders that affects prognosis and guides treatment.
2. Reveal identifiable causes of high BP. 3. Assess the presence or absence of target organ damage and CVD.

Stratification of CV risk in four categories

Blood pressure (mmHg)
Other risk factors, OD or disease No other risk factors 1-2 risk factors 3 or more risk factors, MS, OD or diabetes Established CV or renal disease Normal High normal SBP 120-129 SBP 130-139 or DBP 80or DBP 85-89 84 Average risk Low added risk Moderate added risk Average risk Low added risk High added risk Grade 1 HT SBP 140-159 or DBP 90-99 Low added risk Moderate added risk High added risk Grade 2 HT SBP 160-179 or DBP 100109 Moderate added risk Moderate added risk High added risk Grade 3 HT SBP 180 or DBP 110 High added risk Very high added risk Very high added risk

Very high added risk

Very high added risk

Very high added risk

Very high added risk

Very high added risk

Causes of Resistant Hypertension

Improper BP measurement

Excess sodium intake Inadequate diuretic therapy Medication Inadequate doses Drug actions and interactions (e.g., nonsteroidal anti-inflammatory drugs (NSAIDs), illicit drugs, sympathomimetics, oral contraceptives) Over-the-counter (OTC) drugs and herbal supplements Excess alcohol intake Identifiable causes of HTN


Goals of Therapy
Reduce CVD and renal morbidity and mortality.

Treat to BP <140/90 mmHg or BP <130/80 mmHg in patients with diabetes or chronic kidney disease. Achieve SBP goal especially in persons >50 years of age.

Algorithm for Treatment of Hypertension

Lifestyle Modifications Not at Goal Blood Pressure (<140/90 mmHg) (<130/80 mmHg for those with diabetes or chronic kidney disease)

Initial Drug Choices

Without Compelling Indications

With Compelling Indications

Stage 1 Hypertension
(SBP 140159 or DBP 9099 mmHg) Thiazide-type diuretics for most. May consider ACEI, ARB, BB, CCB, or combination.

Stage 2 Hypertension
(SBP >160 or DBP >100 mmHg) 2-drug combination for most (usually thiazide-type diuretic and ACEI, or ARB, or BB, or CCB)

Drug(s) for the compelling indications

Other antihypertensive drugs (diuretics, ACEI, ARB, BB, CCB) as needed.

Not at Goal Blood Pressure Optimize dosages or add additional drugs until goal blood pressure is achieved. Consider consultation with hypertension specialist.


Other risk factors, OD or disease Normal SBP 120-129 or DBP 80-84 High normal SBP 130-139 or DBP 85-89 Grade 1 HT SBP 140-159 or DBP 90-99 Lifestyle changes for several months then drug treatment if BP uncontrolled Lifestyle changes for several weeks then drug treatment if BP uncontrolled Grade 2 HT SBP 160-179 or DBP 100-109 Lifestyle changes for several weeks then drug treatment if BP uncontrolled Lifestyle changes for several weeks then drug treatment if BP uncontrolled Grade 3 HT SBP 180 or DBP 110 Lifestyle changes + immediate drug treatment Lifestyle changes + immediate drug treatment

No other risk factors

No BP intervention

No BP intervention

1-2 risk factors

Lifestyle changes

Lifestyle changes

3 or more risk factors, MS, OD or diabetes

Lifestyle changes

Lifestyle changes and consider drug treatment Lifestyle changes + drug treatment
Lifestyle changes + immediate drug treatment


Lifestyle changes

Lifestyle changes + drug treatment

Lifestyle changes + drug treatment

Lifestyle changes + immediate drug treatment

Established CV or renal disease

Lifestyle changes + immediate drug treatment

Lifestyle changes + immediate drug treatment

Lifestyle changes + immediate drug treatment

Lifestyle changes + immediate drug treatment

An algorithm for the decision to manage patients with different average blood pressure (BP) levels, determined by repeated office readings or, preferably, out-of-office readings, with specific attention to those aged 60 to 80 years. The evidence for treatment of those older than 80 is inconclusive. The recommended initial drug choices are indicated. DBP = diastolic blood pressure; LDD = low-dose diuretic; SBP = systolic blood pressure; TOD = target organ damage.

Lifestyle Modification: 1
Weight Reduction
Maintain normal body weight
BMI: 18.5 24.9 BP reduction: 5-20 mmHg/10 kg loss

DASH Eating Plan

Dietary Approaches to Stop Hypertension
Fruits, Vegetables, Low-fat dairy Reduce saturated and total fat 8-14 mmHg BP reduction

Lifestyle Modification: 2
Dietary Sodium Reduction
2.4 grams Sodium or 6 grams Sodium Chloride 2-8 mmHg BP reduction

Physical Activity
Regular aerobic physical activity
4-9 mmHg BP reduction

Lifestyle Modification: 3
Smoking Cessation
Any independent chronic effect of smoking on BP is small Smoking cessation does not decrease BP BUT total cardiovascular risk is increased by smoking.

Therefore hypertensives who smoke should be counselled on smoking cessation

Pharmacological Treatment
Diuretics Beta-Blockers ACE-Inhibitors Ca Channel Blockers Angiotensin Receptor Blockers Centrally Acting Drugs Alpha-adrenoreceptor blockers

Possible combinations between some classes of antihypertensive drugs Thiazide diuretics

Angiotensin receptor antagonists

- blockers

Calcium antagonists

ACE inhibitors

Algorithm for therapy of hypertension. ACEI = angiotensin-converting enzyme inhibitor; ARB = angiotensin receptor blocker; CCB = calcium channel blocker. Increasing evidence favors an aldosterone blocker as the fourth choice and perhaps as the third choice in many patients.

Antihypertensive Treatment: Preferred Drugs

General rules: lower SBP and DBP to goal. Use any effective agent at adequate doses, if useful in combination. Use long acting agents to lower BP throughout 24 hours. Avoid or minimize adverse effects. Subclinical organ damage Left ventricular hypertrophy Asymptomatic atherosclerosis Microalbuminuria Renal dysfunction Clinical event Previous stroke Previous MI antagonists Angina pectoris Heart failure Atrial fibrillation Recurrent Continuous Renal failure/proteinuria diuretics Peripheral artery disease Condition Isolated systolic hypertension (elderly) Metabolic syndrome Diabetes mellitus Pregnancy Blacks ACE inhibitors, calcium antagonists, angiotensin receptor antagonists Calcium antagonists, ACE inhibitors ACE inhibitors, angiotensin receptor antagonists ACE inhibitors, angiotensin receptor antagonists Any BP lowering agent -blockers, ACE inhibitors, angiotensin receptor -blockers, calcium antagonists diuretics, -blockers, ACE inhibitors, angiotensin receptor antagonists, antialdosterone agents ACE inhibitors, angiotensin receptor antagonists -blockers, non-dihydropiridine calcium antagonists ACE inhibitors, angiotensin receptor antagonists, loop Calcium antagonists Duretics, calcium antagonists ACE inhibitors, angiotensin receptor antagonists, calcium antagonists ACE inhibitors, angiotensin receptor antagonists calcium antagonists, methyldopa, -blockers diuretics, calcium antagonists

Conditions favoring use of some antihypertensive drugs versus others

Thiaside diuretics Beta-blockers Calcium antagonists (dihydropyridines) Isolated systolic hypertension (elderly) Angina pectoris Calcium antagonists (verapamil/diltiazem) Angina pectoris Isolated systolic hypertension (elderly) Heart failure Angina pectoris

Post-myocardial infarction Heart failure

Carotid atherosclerosis Supraventricular tachycardia

Hypertension in blacks

LV hypertrophy

Tachyarrhythmias Carotid/ Coronary Atherosclerosis Glaucoma Pregnancy Pregnancy Hypertension in blacks

Conditions favoring use of some antihypertensive drugs versus others

ACE Inhibitors Angiotensin receptor antagonists
Heart failure Post-myocardial infarction Diabetic nephropathy Proteinuria/ Microalbuminuria LV hypertrophy Atrial fibrillation Metabolic syndrome ACEI - induced cough

Diuretics (antialdosterone)
Heart failure Post-myocardial infarction

Loop diuretics

Heart failure LV dysfunction Post-myocardial infarction Diabetic nephropathy

End stage renal disease Heart failure

Non-diabetic nephropathy LV hypertrophy

Carotid atherosclerosis Proteinuria/ Microalbuminuria Atrial fibrillation Metabolic syndrome

Compelling and possible contraindications to use of antihypertensive drugs

Compelling Thiazide diuretics

Metabolic syndrome Glucose intolerance Pregnancy Peripheral artery disease Metabolic syndrome Glucose intolerance Athletes and physically active patients Chronic obstructive pulmonary disease Tachyarrhythmias Heart failure


Asthma A-V block (grade 2 or 3)

Calcium antagonists (dihydropiridines)

Calcium antagonists (verapamil, dilitazem) ACE inhibitors
A-V block (grade 2 or 3) Heart failure Pregnancy Angioneurotic oedema Hyperkalaemia Bilateral renal artery stenosis Pregnancy Hyperkalaemia Bilateral renal artery stenosis Renal failure Hyperkalaemia

AT1 blockers

Diuretics (antialdosterone)


Usual dose (mg)















Classification of beta-adrenoreceptor blockers on the basis of cardioselectivity and intrinsic sympathomimetic activity. Drugs not approved for use in the United States for treatment of hypertension are in italics. ISA = intrinsic sympathomimetic activity.

Effects of Different b Blocking Agents

Pharmacological differences Sympathetic activation
b1 receptors Bisoprolol Metoprolol Bucindolol Propranolol Carvedilol Cardiotoxicity b2 receptors 1 receptors

Uptitration of b Blockade in Hypertension

100 mg od 10 mg od 5 mg od 50 mg od Increase dose after 2 weeks if 50 mg is not optimal 2.5 mg od Increments every 2 weeks until optimal dose is reached

20 mg od

200 mg od 100 mg od 50 mg od Weekly increments until optimal dose is reached

50 mg od 25 mg od 12.5 mg od 2 days

Actions of calcium antagonists on smooth muscle and heart

Calcium antagonist
Slow Ca2+ entry
Smooth muscle Heart muscle

Oesophagus Ureter Detrusor vesicae Uterus Intestine Bronchi

Blood vessels Coronary flow Vasospasm Organ protection

Sinus rate AV conduction

Contractility Cardioprotection


Blood pressure

The mechanisms by which chronic diuretic therapy may lead to various complications. The mechanism for hypercholesterolemia remains in question, although it is shown as arising from hypokalemia. Cl = clearance; GFR = glomerular activity. filtration rate; PRA = plasma renin


Simplified schematic view of the adrenergic nerve ending showing that norepinephrine (NE) is released from its storage granules when the nerve is stimulated and enters the synaptic cleft to bind to alpha1 and beta receptors on the effector cell (postsynaptic). In addition, a short feedback loop exists in which NE binds to alpha1 and beta receptors on the neuron (presynaptic) to inhibit or stimulate further release, respectively.


Minority Populations
In general, treatment similar for all demographic groups. Socioeconomic factors and lifestyle important barriers to BP control. Prevalence, severity of HTN increased in African Americans. African Americans demonstrate somewhat reduced BP responses to monotherapy with BBs, ACEIs, or ARBs compared to diuretics or CCBs. These differences usually eliminated by adding adequate doses of a diuretic.

Peripheral Arterial Disease (PAD)

PAD is equivalent in risk to ischemic heart disease.

Any class of drugs can be used in most PAD patients.

Other risk factors should be managed aggressively.

Aspirin should be used.

Hypertension in Older Persons

More than two-thirds of people over 65 have HTN. This population has the lowest rates of BP control. Treatment, including those who with isolated systolic HTN, should follow same principles outlined for general care of HTN. Lower initial drug doses may be indicated to avoid symptoms; standard doses and multiple drugs will be needed to reach BP targets.

Postural Hypotension
Decrease in standing SBP >10 mmHg, when associated with dizziness/fainting, more frequent in older SBP patients with diabetes, taking diuretics, venodilators, and some psychotropic drugs. BP in these individuals should be monitored in the upright position. Avoid volume depletion and excessively rapid dose titration of drugs.

Dementia and cognitive impairment occur more commonly in people with HTN. Reduced progression of cognitive impairment occurs with effective antihypertensive therapy.

Hypertension in Women
Oral contraceptives may increase BP, and BP should be checked regularly. In contrast, HRT does not raise BP. Development of HTNconsider other forms of contraception.

Pregnant women with HTN should be followed carefully. Methyldopa, BBs, and vasodilators, preferred for the safety of the fetus. ACEI and ARBs contraindicated in pregnancy.

Children and Adolescents

HTN defined as BP95th percentile or greater, adjusted for age, height, and gender. Use lifestyle interventions first, then drug therapy for higher levels of BP or if insufficient response to lifestyle modifications. Drug choices similar in children and adults, but effective doses are often smaller.

Uncomplicated HTN not a reason to restrict physical activity.

Hypertensive Urgencies and Emergencies

Patients with marked BP elevations and acute TOD (e.g., encephalopathy, myocardial infarction, unstable angina, pulmonary edema, eclampsia, stroke, head trauma, life-threatening arterial bleeding, or aortic dissection) require hospitalization and parenteral drug therapy. Patients with markedly elevated BP but without acute TOD usually do not require hospitalization, but should receive immediate combination oral antihypertensive therapy.