= 160Isolated systolic hypertension
Adapted from the 1988 Report of the Joint National Committee on
Detection, Evaluation and Treatment of High Blood Pressure.
The classification is based on the average of two or more
readings on at least three or more occasions.
In subjects aged 50 or less the diastolic level always takes
precedence over the systolic level.
Before diagnosis is made the variation between readings should
not exceed 10 mm of mercury for systolic blood pressure or 6 mm of
mercury for diastolic blood pressure.
Table 111.2 Classification of hypertension
Essential (90-95%)
Secondary (approximately 5-10%)
Renal (3-4%) glomerulonephritis reflux nephropathy renal artery
stenosis other renovascular disease
Endocrine primary aldosteronism (Conn's syndrome) Cushing's
syndrome phaeochromocytoma oral contraceptives other endocrine
factors Coarctation of the aortaImmune disease, e.g. polyarteritis
nodosa DrugsPregnancy
Table 111.3 Classification of hypertension by extent of organ
damage (WHO guidelines)
Stage INo objective signs of organic changes
Stage II At least one of the following signs of organ
involvement: left ventricular hypertrophy (X-ray, etc.) generalised
and focal narrowing of the retinal arteries proteinuria and/or
slight elevation of plasma creatinine concentration (1.2-2.0 mg/dL)
ultrasound or radiological evidence of atherosclerotic plaque
Stage III Both symptoms and signs have appeared as a result of
organ damage.These include:
Heart:angina pectoris myocardial infarction heart failure
Brain:TIA, strokehypertensive encephalopathy
General Practice, Chapter 111
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Optic fundi: retinal haemorrhages and exudates papilloedema
Kidney:plasma creatinine concentration > 2.0 mg/dL, renal
failure
Vessels: dissecting aneurysm, symptomatic arterial occlusive
disease
Key facts and checkpoints
In the United States, 15% of 18-24 year olds and 60% of 65-74
years olds have hypertension. 3In the US, studies show that only
54% of all hypertensives are aware of their disease and only 11%
are being treated adequately. Similar figures have been shown in
the UK. 4The risk of cardiovascular disease rises significantly
with increasing blood pressure.If both parents have hypertension
there is a 50% chance of the offspring developing hypertension and
if one parent has HT there is a 25% chance.Headache may occur in
hypertensive patients (most are asymptomatic): it is typically
early morning, occipital and throbbing: it appears to be related to
severity of blood pressure.Any dizziness in hypertensive patients
is usually due to postural hypertension from treatment.An analysis
of the results available from 17 randomised controlled trials
involving 47 653 subjects followed for an average of 5 years showed
that an average fall in blood pressure of 11/5 mmHg conferred a 38%
reduction in stroke, and a 16% fall in the incidence of coronary
heart disease.Target organs (including some specific examples) that
can be damaged by hypertension include the heart (failure, LVH,
ischaemic disease), the kidney (renal insufficiency), the retina
(retinopathy), the blood vessels (peripheral vascular disease,
dissecting aortic aneurysm) and the brain (cerebrovascular
disease).Deaths in hypertensive patients have been shown to be due
to stroke 45%, heart failure 35%, renal failure 3% and others 17%.
4Factors increasing chances of dying in hypertensive patients are:
male patient; young patient; family history; increasing diastolic
pressure. 4
Secondary hypertensionSecondary hypertension may be suggested in
patients below 40 by the history ( Table 111.4 ), physical
examination, severity ofhypertension or the initial laboratory
findings. It is also more likely in patients whose blood pressure
is responding poorly to drug therapy, patients with well-controlled
hypertension whose blood pressure begins to increase, and patients
with accelerated or malignant hypertension. 2Table 111.4 Clinical
features suggesting secondary hypertension 5
Clinical featuresLikely cause
Abdominal systolic bruitRenal artery stenosis
Proteinuria, haematuria, castsGlomerulonephritis
Bilateral renal masses with or without haematuriaPolycystic
disease
History of claudication and delayed femoral pulseCoarctation of
the aorta
Progressive nocturia, weaknessPrimary aldosteronism (check serum
potassium) Paroxysmal hypertension with headache, pallor, sweating,
palpitations Phaeochromocytoma
The most common causes of secondary hypertension are various
renal diseases, such as renovascular disease, chronic
glomerulonephritis, chronic pyelonephritis (often associated with
reflux nephropathy) and analgesic nephropathy. 1 There will often
be no physical findings to suggest the existence of such renal
diseases, but an indication will generally be obtained by the
presence of one or more abnormalities when the urine is examined.
Clinical pointers include proteinuria, an abnormal urine sediment,
general atheroma, smokers and abdominal bruit.
Physical findings that may suggest secondary hypertension
include epigastric bruits (indicating possible renal artery
stenosis) and abdominal aortic aneurysm. Less common findings
include abdominal flank masses (polycystic kidneys), delayed or
absent femoral pulses (coarctation of the aorta), truncal obesity
with pigmented striae (Cushing's syndrome), and tachycardia,
sweating and pallor (phaeochromocytoma).Further investigation will
be required to confirm or reveal secondary hypertension.Conn's
syndrome: clinical features
weakness due to hypokalaemia polyuria and polydypsiaNa , K ,
alkalosisaldosterone (serum and urine) plasma renin
Phaeochromocytoma: clinical featuresParoxysms or spells of
hypertension headache (throbbing) sweatingpalpitations
pallor/skin blanchingrising sensation of tightness in upper chest
and throat (angina can occur)
24 hour urinary free catecholamines (VMA)Detection of
hypertension 1Hypertension can only be detected when blood pressure
is measured. Therefore every reasonable opportunity should be
takento measure blood pressure.Diagnosis should not be made on the
basis of a single visit. Initial raised blood pressure readings
should be confirmed on at least two other visits within the space
of 3 months; average levels of 90 mmHg diastolic or more, or 140
mmHg systolic or more, are needed before hypertension can be
diagnosed. This will avoid the possibility of an incorrect
diagnosis, committing an asymptomatic normotensive individual to
unjustified, lifelong treatment.Measurement 1Blood pressure varies
continuously and can be affected by many outside factors. Care
should therefore be taken to ensure thatreadings accurately
represent the patient's usual pressure. The essential steps in this
process are outlined below.PositionPatients should be seated with
their bare arm supported and positioned at heart level. Any sleeve
should be loose above the sphygmomanometer cuff.Cuff size and
placementA cuff size that will completely occlude the brachial
artery is essential for accurate measurement. Cuffs that are too
short or too narrow may give falsely high readings. The cuff's
rubber bladder should have a width of at least 40% of the
circumference of the patient's arm and a length at least double
that. The commonly used cuffs are often shorter than this
recommendation. Suitable cuffs are made by Trimline (PyMaH) and
Accosan. Several sizes, including cuffs for children and the obese,
should be available. The bladder of the cuff deteriorates over
about two years and should be replaced at intervals. 6A preferable
cuff placement is to have the tubes emerging from the bladder point
proximally ( Fig 111.1 ) thus leaving the cubital fossa free. 6
Fig. 111.1 Correct placement of the cuff
EquipmentIdeally, measurement should be taken with a reliable
and properly maintained sphygmomanometer. Otherwise, a recently
calibrated aneroid manometer or a calibrated electronic
instrument can be used. It is essential that all equipment is
maintained regularly. All tubing connections should be
airtight.PalpationInitially, systolic blood pressure should be
recorded by the palpatory method at the radial or brachial artery
(the brachial artery is felt just medial to the biceps tendon in
the cubital fossa). This will prevent low auscultatory systolic
pressures caused by a 'silent gap'.Note this reading and add 30
mmHg to it as the upper level to which to inflate the cuff, while
accurately measuring the BP with the bell of the stethoscope over
the brachial artery.Taking the readingWhile the BP is being
measured, the cuff should be deflated at a rate no greater than 2mm
of mercury for each beat. One of the commonest errors is to allow
the column of mercury to fall too rapidly.Pressure should be
recorded to the nearest 2 mm of mercury (it should not end in 5).
Parallax errors should be avoided when reading levels ( Fig 111.2
). 6 7 Wait 60 seconds and repeat the BP measurement.
Fig. 111.2 Correct eye level: the observer should be within 1
metre of the manometer, so the scale can be easily read to avoid a
parallax errorthe eye should be on the same horizontal level as the
mercury meniscus
RecordingOn each occasion when BP is taken, two or more readings
should be averaged. Wait at least 30 seconds before repeating the
procedure. If the first two readings differ by more than 6 mmHg
systolic or 4 mmHg diastolic, more readings should be taken. Both
systolic and diastolic levels should be recorded. For the diastolic
reading the disappearance of sound (Phase 5)that is, the pressure
when the last sound is heard and after which all sound
disappearsshould be used. 8 This is more accurate than the muffling
of sounds (Phase 4) ( Fig 111.3 ), which should only be used if the
sound continues to zero.
Fig. 111.3 Illustration of blood pressure measurement in
relation to arterial blood flow, cuff pressure and auscultation
Heart rate and pulseAt the same time the BP is measured, the
heart rate and rhythm should be measured and recorded. A high heart
rate mayindicate undue stress that is causing the associated
elevated BP reading. An irregular heart rhythm may cause difficulty
in obtaining an accurate BP reading.BP modifying
factorsApprehension: Patient should be rested for at least 5
minutes and made as relaxed as possible.Caffeine: Patients should
not take caffeine for 4-6 hours before measurement. Smoking:
Patients should also avoid smoking for 2 hours before measurement.
Eating: Patients should not have eaten for 30 minutes.Strategies
for high initial readingsIf the initial reading is high (DBP >
90, SBP > 140) repeat the measures after 5 minutes of quiet
rest. The 'white coat'influence in the medical practitioner's
office may cause higher readings so measurement in other settings
such as the home or the workplace should be managed whenever
possible.Confirmation and follow-up 1Repeated blood pressure
readings will determine whether initial high levels are confirmed
and need attention, or whether theyreturn to normal and need only
periodic checking. Particular attention should be paid to younger
patients to ensure that they are regularly followed up.Initial
diastolic blood pressure readings of 115 mmHg or more, particularly
for patients with target organ damage, may need immediate drug
therapy.Once an elevated level has been detected, the timing of
subsequent readings should be based on the initial pressure level,
as shown in Table 111.5 .If mild hypertension is found, observation
with repeated measurement over 3-6 months should be followed before
beginning therapy. This is because levels often return to
normal.Table 111.5 Follow-up criteria for initial blood pressure
measurement for adults 18 years and older 1 2
Range (mmHg)Recommended follow-up*
Diastolic< 8585-8990-104
Recheck within 2 years Recheck within 1 year Confirm within 2
months
105-114> 115
Systolic, when diastolic is < 90< 140140-159> 200
Evaluate or refer within 4 weeks Evaluate or refer
immediately
Recheck within 2 years Confirm within 2 monthsEvaluate or refer
within 2 weeks
* If recommendations for follow-up of diastolic and systolic
blood pressure are different the shorter recommended time for
recheck and referral should take precedence. 2
Ambulatory 24 hour monitoringThis is not required for the
diagnosis and followup of most hypertensive patients but in some
patients with fluctuating levels,borderline hypertension or
refractory hypertension (especially where the 'white coat' effect
may be significant) ambulatory monitoring has a place in
management. Studies have shown that this method provides a more
precise estimate of blood pressure variability than casual
recordings. This has implications for the timing of drug therapy in
individual patients.'White coat' hypertensionThis group may
comprise up to 25% of patients presenting with hypertension. These
people have a type of conditionedresponse to the clinic or office
setting and their home BP and ambulatory BP profiles are normal.
They appear to be at low risk of cardiovascular disease but may
progress to sustained hypertension.EvaluationAs well as defining
the blood pressure problem, the clinical evaluation for suspected
hypertension should also determine
whether the patient has potentially reversible secondary
hypertension whether target organ damage is presentwhether there
are other potentially modifiable cardiovascular risk factors
present and what co-morbid factors exist.
Medical historyThe following should be included in the medical
history of the patient:History of hypertension
method and date of initial diagnosisknown duration and levels of
elevated blood pressuresymptoms that may indicate the effects of
high blood pressure on target organ damage, such as headache,
dyspnoea, chest pain, claudication, ankle oedema and
haematuriasymptoms suggesting secondary hypertension ( Table 111.4
)the results and side effects of all previous antihypertensive
treatment
Presence of other diseases and risk factors
a history of cardiovascular, cerebrovascular or peripheral
vascular disease, renal disease, diabetes mellitus or recent weight
gainother cardiovascular risk factors, including obesity,
hyperlipidaemia, carbohydrate intolerance, smoking, salt intake,
alcohol consumption, exercise levels and analgesic intakeother
relevant conditions, such as asthma or psychiatric illness
(particularly depressive illness)
Family historyParticular attention should be paid to the family
history of hypertension, cardiovascular or cerebrovascular
disease,hyperlipidaemia, obesity, diabetes mellitus, renal disease,
alcohol abuse and premature sudden death.Medication historyA
history of all medications, including over-the-counter products,
should be obtained because some can raise blood pressureor
interfere with antihypertensive therapy. These include:
oral contraceptiveshormone replacement therapy
steroidsnon-steroidal anti-inflammatory agents (NSAIDs)
nasal decongestants and other cold remedies appetite
suppressantsamphetaminesmonoamine oxidase inhibitors
analgesicsergotamine cyclosporincarbenoxolone and licorice
Caffeine intake 1Caffeine has an acute dose-related pressor
effect. People who have recently ingested significant amounts will
have a blood pressure reading which is elevated above their usual
level. The amount of caffeine in a cup (225 ml) in common dietary
sources is as follows:
Instant coffee90 mg
Brewed coffee125 mg
Decaffeinated coffee4.5mg
Tea60 mg
Chocolate drinks (e.g. hot chocolate) 5 mg Cola drinks25 mg
Alcohol intake 1Alcohol has a direct pressor effect that is
dose-related. An assessment of the average daily number of standard
drinks isimportantmore than two standard drinks (20 g alcohol) a
day is significant.Physical examinationThe approach to the physical
examination is to examine possible target organ damage and possible
causes of secondaryhypertension. The main features to consider in
the physical examination are illustrated in Figure 111.4 .
Fig. 111.4 Physical examination of patient with hypertension:
what to look for
The four grades of hypertensive retinopathy are illustrated in
Figure 111.5 .
Fig. 111.5 The four grades of hypertensive retinopathy
Leg pulses and pressureTo assess the remote possibility of
coarctation of the aorta in the hypertensive patient, perform at
least one observationcomparing:
1. the volume and timing of the radial and femoral pulses2. the
blood pressure in the arm and leg
Blood pressure measurement in the leg
Place the patient prone.Use a wide, long cuff at mid-thigh
level.Position the bladder over the posterior surface and fix it
firmly. Auscultate over the popliteal artery.
InvestigationsThe following are the basic screening tests
recommended for all patients:
Urine testsurinalysis (for protein and glucose) micro-urine
(casts, red and white cells)urine culture (only if urinalysis
abnormal)Biochemical testspotassium and sodium creatinine and urea
glucoseuric acidcholesterol (total, HDL, LDL ratios)ECG
Other investigations, such as echocardiography, renal imaging
studies (especially renal ultrasound), 24 hour urinary
catecholamines, aldosterone and plasma renin, are not routine and
should be done only if specifically indicated. A chest X-ray may
serve as a base-line against which to measure future changes.
However, if a chest X-ray shows the heart is enlarged, it is more
likely to represent chamber dilatation than increased ventricular
wall thickness. 1 Specific renal studies now favoured include
isotope scans, doppler studies of renal arteries and renal
arteriography.
TreatmentA correct diagnosis is the basis of management.
Assuming that the uncommon secondary causes are identified and
treated,treatment will focus on essential hypertension.Management
principles
The overall goal is to improve the long-term survival and
quality of life. Promote an effective physician-patient working
relationship.Aim to reduce the levels to 140/90 mmHg or less
(ideal). Undertake a thorough assessment of all cardiovascular risk
factors.Instruct all patients in the use of non-drug treatment
strategies and their potential benefits.In patients with mild to
moderate hypertension and no target organ damage, consider
ambulatory or home BP monitoring.Drug therapy should be given to
those with:sustained high initial readings, e.g. DBP > 95 mmHg
target organ damagefailed non-drug measures.Make a careful
selection of an antihypertensive drug and an appraisal of the side
effects against the benefits of treatment.Avoid drug-related
problems such as postural hypotension. Avoid excessive lowering of
blood pressure.Aim to counter the problem of patient
non-compliance.Be aware of factors that may contribute to drug
resistance.
Patient educationPatient education should include appropriate
reassurances, clear information and easy-to-follow instructions. It
is important toestablish patients' understanding of the concept of
hypertension and its consequences by quizzing them about their
knowledge and feelings.Correction of patients' misconceptions
1Patients are likely to have several misconceptions about
hypertension which may adversely affect their treatment.For
example, they might believe that:
hypertension can be curedthey do not need to continue treatment
once their BP is controlled they do not have a problem because they
do not have symptomsthey need to take additional pills, or stop
treatment in response to symptoms they believe are caused by high
or low blood pressure levelsthey need not take prescribed pills if
they attend to lifestyle factors such as exercise and diet they can
gauge their blood pressure by how they feel
Tips for optimal compliance
Establish a good caring rapport.Give patients a card of their
history with BP readings. Give advice about pill-taking times.Set
therapeutic goals. Establish a recall system.Provide patient
education material. On review:Ask if any pills were missed by
accident.Attempt to reduce waiting time to a minimum, e.g. direct a
patient to a spare room upon arrival. Review all cardiovascular
risk factors.Enquire about any side effects.
Non-pharmacological treatment modalitiesIf the average diastolic
BP at the initial visit is 90-100 mmHg, and there is no evidence of
end-organ damage, non-pharmacological therapy is indicated for a 3
month period without use of antihypertensive drugs. Remember to
remove, revise or substitute drugs which may be causing
hypertension, e.g. NSAIDs, corticosteroids, oral contraceptives,
hormone replacement
therapy.Behaviour intervention measures include:
Weight reductionThere is considerable evidence that weight loss
and gain are linked to a corresponding fall and rise in BP. Hovell
has estimated that for every 1 kg of weight lost, blood pressure
dropped by 2.5 mmHg systolic and 1.5 mmHg diastolic. 9 The BMI
should be calculated for all patients and where required a weight
loss program organised to reduce the BMI to between 20 and
25.Reduction of alcohol intake 1The direct pressor of alcohol is
reversible. Drinking more than 20 g of alcohol a day raises blood
pressure and makes treatment of established hypertension more
difficult. People with hypertension should limit their alcohol
intake to one or two standard drinks (10 g) per day. Reduction or
withdrawal of regular alcohol intake reduces BP by 5-10 mmHg.
Reduction of sodium intakeSome individuals seem to be more
sensitive to salt restriction. Advise patients to put away the salt
shaker and use only a little salt with their food. Reduction of
sodium intake to less than 100 mmol sodium per day is
advised.Increased exerciseRegular aerobic or isotonic exercise
helps to reduce BP. 10 Hypertensive patients beginning an exercise
program should do so gradually. Walking is an appropriate exercise.
Weights and other forms of isometric exercises should be avoided
because they will significantly elevate blood pressure in the
hypertensive subject.Reduction of particular stressIf avoiding
stress or overwork is difficult, recommend relaxation and/or
meditation therapy.Other dietary factorsThere is evidence that
lactovegetarian diets and magnesium supplementation can reduce BP.
11 12 A diet high in calcium, and low in fat and caffeine, may also
be beneficial. Avoid licorice and licorice-containing substances.
SmokingSmoking causes acute rises in blood pressure but does not
appear to cause sustained hypertension. However, the elimination of
smoking is important as it is a strong risk factor for
cardiovascular disease and continuing to smoke may negate any
benefits of antihypertensive therapy. 1Management of sleep
apnoea
Pharmacological therapyThe benefits of drug therapy appear to
outweigh any known risks to individuals with a persistently raised
diastolic pressure > 95mmHg. Although the ideal antihypertensive
drug has yet to be discovered there are many effective
antihypertensive drugs available. 13 Deciding which one to use
first involves an assessment of the patient's general health, the
medication's known side effects, the simplicity of its
administration and its cost. A useful plan is outlined in Figure
111.6 .Various disorders such as diabetes, asthma, chronic
obstructive airways disease, Raynaud's phenomenon, heart failure,
and elevated serum urate and/or lipid levels may restrict the use
of some classes of drugs.Common combinations of the therapeautic
drug classes used for first-line therapy ofhypertension
Adjacent drug classes are useful combinations in that effects on
blood pressure are additive and adverse effects are no more likely
than with either drug used alone.Verapamil (V) generally should not
be used with -antagonists.Drug groups that are diametrically
located on the diagram may be used together, but may not have fully
additive effects. Drugs on the left side should be combined in
patients with hypertension and heart failure, and those on the
right side are useful in patients with hypertension and coexisting
coronary disease.Drug groups on the lower panel lack metabolic
effects and may be preferred combinations in the presence of
diabetes or lipid abnormalities as well as hypertension.Prazosin
and other a-antagonists are also often used as monotherapy and may
be combined with any of the above drug groups.Small doses of
centrally acting anti-adrenergic drugs (e.g. methyldopa, clonidine)
can probably also be used with any of the other agents although
data on their use in combination are scarce with the newer drug
groups.
Fig. 111.6 Common combinations of the therapeutic drug classes
used for first-line therapy of hypertensionADAPTED FROM MANAGEMENT
OF HYPERTENSION: A CONSENSUS STATEMENT, MED J AUST, 1994, 160:
SUPPLEMENT 21 MARCH. COPYRIGHT 1994. THE MEDICAL JOURNAL OF
AUSTRALIA. REPRODUCED WITH PERMISSION
When to treat
failed genuine non-pharmacological trial all SBP > 180 or DBP
> 100
Guidelines
Start with a single drug.A period of 4-6 weeks is needed for the
effect to become fully apparent.If ineffective, consider increasing
the drug to its maximum recommended dose, or add an agent from
another compatible class, or substitute with a drug from another
class.Use only one drug from any one class at the same time.A
summary of first-line therapy options and the uses of the various
pharmacological agents is shown in Table 111.6 . Measure the BP at
the same time each day.A good strategy is to get patients to
self-measure.
Table 111.6 First-line pharmacological options for the
management of hypertension 7
Drug class
DiureticBeta-blocker
Calcium channelantagonistACE inhibitor
Central-acting agentAlpha-blocker
Typical examples and starting dose (oral therapy)
chlorothiazideatenololverapamil
SRcaptoprilmethyldopaprazosin
250 mg daily25-50 mg daily160 mg daily6.25 mg bd125 mg bd0.5 mg
nocte
hydrochlorothiazidemetoprololfelodipine
SRenalaprilclonidineterazosin
12.5 mg daily50 mg daily2.5 mg daily5 mg daily50 g, bd0.5 mg
nocte
pindolol5 mg dailyamlodipine2.5 mg dailylisinopril5 mg daily
indapamidepropranololnifedipineramiprilNote: labetalol (100 mg
bd)
2.5 mg daily40 mg daily10 mg bd2.5 mg dailyis a combined a
and
diltiazem 180 mg daily
perindopril 2 mg daily
Angiotensin II receptor antagonist
losarten50 mg daily
blocker
Recommended in
Heart failure (mild) Older patients
Contraindications
Maturity onset diabetics Hyperuricaemia
Precautions
Anxious patient Young patients Angina Postmyocardial infarction
Migraine
Asthma COADHistory of wheeze Heart failureHeart block (2,3)
PVDBrittle IDDM
Asthma Angina PVDRaynaud's phenomenon
Heart block 2nd & 3rd degree (verapamil, diltiazem)
irbesartan 150 mg daily
Heart failure PVDDiabetes Raynaud's
Bilateral renal artery stenosis
Asthma Pregnancy
Liver disease (methyldopa)
Asthma PVDHeart failure LUTS (prostatism)
Heart failure (mechanical obstruction)
Hypokalaemia Thiazides + ACE inhibitors Renal failure
Important side effects
Avoid abrupt cessation with anginaUse with verapamil Use with
NSAIDsUse in smokers
With -blockers and digoxin CCF
Chronic renal diseaseAvoid K sparing diuretics and NSAIDs
DepressionElderly patients
RashesSexual dysfunction WeaknessBlood dyscrasias Muscular
cramps Hypokalaemia Hyponatraemia Hyperuricaemia
HyperglycaemiaLipid metabolism effect
Fatigue Insomnia Vivid dreamsBronchospasm Cold extremities
Sexual dysfunction Lipid metabolism effect
Headache Flushing Ankle oedema Palpitations Dizziness Nausea
Constipation (verapamil) Nocturia, urinary frequency
Cough Weakness RashDysgeusia (taste)
Hyperkalaemia First dose hypotension Angioedoma
Sedation Dry mouth Bowel disturbances Fatigue Orthostatic
hypotension Sexual dysfunction Haemolytic anaemia(methyldopa)
First dose syncope Orthostatic hypotension WeaknessPalpitations
Sedation Headache
Starting regimensThe traditional method has been to use stepwise
therapy until ideal control has been reached, commencing with:
1. thiazide or thiazide-like diuretic or -blocker
(cardioselective)2. combination of diuretic and -blocker3. add a
vasodilator
However, the newer classes of drugs can be used as first-line
agents. The following are useful combinations: 1 5
Initial agentAdditional drugs
diuretic-blocker ACE inhibitorora-blocker
-blockerDiureticCalcium antagonist(except verapamil and
diltiazem)
a-b ckerDiuretic -blocker
ACE inhibitorDiureticCalcium antagonist
Calcium antagonist -blockerACE inhibitor
DiureticCentral acting agent ACE inhibitor
Author's preference
DiureticACE inhibitor or-blocker
Relatively ineffective combinations 1Diuretic and calcium
antagonist Beta-blockers and ACE inhibitors Undesirable
combinations 1More than one drug from a particular pharmacological
group: beta-blockers and verapamil (heart block, heart
failure);potassium-sparing diuretics and ACE inhibitors
(hyperkalaemia).Diuretics 1 5
Thiazides are good first-line therapy for
hypertension.Hypokalaemia can be corrected with potassium-sparing
diuretics or changing to another first-line drug.Loop diuretics are
less potent as antihypertensive agents but are indicated where
there is concomitant cardiac or renal failure and in resistant
hypertension.Thiazides are less effective where there is renal
impairment. Thiazides may precipitate acute gout.NSAIDs may
antagonise the antihypertensive and natriuretic effectiveness of
diuretics.A diet high in potassium and magnesium should accompany
diuretic therapy, e.g. lentils, nuts, high fibre. Avoid use if
significant dyslipidaemia.Indapamide has different properties to
the thiazide and loop diuretics and has less effect on serum
lipids.
Beta-blockers
NSAIDs may interfere with the hypotensive effect of
beta-blockers.If blood pressure is not reduced by one beta-blocker
it is unlikely to be reduced by changing to another. Verapamil plus
a beta-blocker may unmask conduction abnormalities causing heart
block.In patients with ischaemic heart disease, or susceptibility
to it, treatment must not be stopped suddenlythis can
precipitate angina at rest.
Calcium antagonists
These drugs reduce blood pressure by vasodilatation.The
properties of individual drugs vary, especially their effects on
cardiac function.The dihydropyridine compounds (nifedipine and
felodipine) tend to produce more vasodilatation and thus related
side effects.Unlike verapamil or diltiazem (which slow the heart),
dihydropyridine drugs can be used safely with a beta-blocker.
Verapamil is contraindicated in second and third degree heart
block.Verapamil and diltiazem should be used with caution in
patients with heart failure.These drugs are efficacious with ACE
inhibitors, beta-blockers, prazosin and methyldopa.
ACE inhibitorsAngiotensin-converting enzyme is responsible for
converting angiotensin I to angiotensin II (a potent
vasoconstrictor andstimulator of aldosterone secretion) and for the
breakdown of bradykinin (a vasodilator). ACE inhibitors are
effective in the elderly; improve survival and performance status
in cardiac failure; are protective of renal function in diabetes;
and cardioprotective in postmyocardial infarction. For patients
with normal renal function, the dose should not exceed 150 mg daily
for captopril, 40 mg daily for enalapril or lisinopril, 10 mg daily
for ramipril, and 8 mg daily for perindopril.Disturbance in taste
is usually transitory and may resolve with continued treatment.
Cough, which occurs in about 15% of patients, may disappear with
time or a reduction in dose but it often persists and requires a
change in drug in some patients. Angioedema, a potentially
lifethreatening condition, may occur in 0.1-0.2% of subjects. Like
cough, it is a class effect and will mitigate against use of any
ACE inhibitor.Angiotensin II receptor antagonistsIrbesartan and
losarten are not ACE inhibitors but are angiotensin II receptor
blocking drugs used for mild to moderate hypertension alone or with
other antihypertensive agents. Cough does not appear to be a
significant adverse effect; otherwise, the adverse effects are
similar to ACE inhibitors.PrazosinA specific problem is the 'first
dose phenomenon'; this involves acute syncope about 90 minutes
after the first dose, hencetreatment is best initiated at bedtime.
Prazosin potentiates beta-blockers and works best if used with
them. It is a useful first- line therapy in patients who are
unsuitable for diuretic or beta-blocker therapy, e.g. those with
diabetes, asthma or hyperlipidaemia.Vascular smooth muscle
relaxants(other than calcium channel antagonists)These include
hydralazine, minoxidil and diazoxide, which are not used for
first-line therapy but for refractory hypertensive states and
hypertensive emergencies.Mild hypertension 1Mild hypertension in
adults is defined as a diastolic pressure (Phase 5) persistently
between 90 and 104 mmHg, without targetorgan damage. 14 This group
includes those with 'white coat' hypertension.Mildly hypertensive
people have almost twice the risk of vascular disease compared with
normotensive people, and evidence shows that morbidity and
mortality rise with an increase in blood pressure. 1 The long-term
risk in patients with 'white coat' hypertension has yet to be
defined.Patients treated appropriately have fewer strokes and
pressure-related cardiovascular complications than those not
treated. Drug treatment has potential side effects which cannot be
ignored; sometimes the risks from this form of treatment could
exceed those if the patient remains untreated. 14 Therefore, the
initial approach to the management of mild hypertension should be
based on non-drug measures and should focus on behaviour change. In
this way, overt side effects are avoided and risk prevention
measures enhanced.Often the success of this approach is improved by
using people with particular skills, such as dietitians. If after 6
months or more these methods have not succeeded, then drug therapy
may be necessary. 14Practical guidelines for patients with
persistent diastolic blood pressure between 90 and 104 mmHg are
shown in Figure 111.7 .
Fig. 111.7 Decision tree for managing hypertensionAS RECOMMENDED
BY THE NATIONAL HEART FOUNDATION
Moderate hypertension 1If diastolic pressure is 105-114 mmHg
then a more aggressive approach is necessary, particularly for
patients with target organdamage. Appropriate non-pharmacological
measures should be tried in all subjects, especially where success
is possible, e.g. obesity, high alcohol intake. This will fail in
the majority, who will require drug therapy. If there is poor
response to initial therapy a second drug may be prescribed after a
short time. The interval between the changes in treatment may also
be reduced. Combination therapy may be more effective than maximum
doses of any single agent.Severe hypertension 5The blood pressure
of those with severe hypertension may be life-threatening. Patients
with an average diastolic pressure ofmore than 115 mmHg should be
checked immediately for hypertensive complications, particularly
marked fundoscopic changes, proteinuria or cardiac failure. They
are more likely to have an underlying cause, e.g. renovascular
disease. Hospitalisation may be necessary for these patients.In
such cases the opinion of a specialist is important, because of the
likely risk of serious illness or death. A dihydropyridine calcium
channel blocker (e.g. nifedipine, amlodipine, felodipine) with
early addition of a beta-blocker or ACE inhibitor is suitable for
urgent lowering of blood pressure.Hypertensive emergenciesA
hypertensive emergency occurs when high blood pressure causes the
presenting cardiovascular problem. Typical
presentations of hypertensive emergencies (which are rare)
include hypertensive encephalopathy, acute stroke, heart failure,
dissecting aortic aneurysm and eclampsia.In all such cases referral
to a specialist is essential and the patient should be hospitalised
immediately for monitoring and treatment. Treatment must be
individualised, mindful of the nature of the underlying problem and
associated disorders.Such treatment is the same as for severe
hypertension. Otherwise, sodium nitroprusside IV in an intensive
care setting is the optimal treatment.Isolated systolic
hypertension 1Isolated systolic hypertension is most frequently
seen in elderly people.Definition: systolic BP > 160 mmHg with a
DBP < 90 mmHgPatients with isolated systolic hypertension should
be treated in the same way as those with classic systolic/diastolic
hypertension. Evidence that reducing isolated systolic blood
pressure decreases the mortality and morbidity risk has been
demonstrated by the SHEP (systolic hypertension in the elderly)
study. 16Non-pharmacological therapy should be commenced as is
relevant to the patient. If drugs are used the SBP should be
cautiously lowered to between 140 and 160 mmHg. The drugs of choice
are diuretics, calcium channel-blocking agents and ACE
inhibitors.Refractory hypertensionRefractory hypertension exists
where control has not been achieved despite reasonable treatment
for 3-4 months. A review ofa possible secondary cause is
appropriate.Checklist of possible reasons 1
drug-related causes: doses too low; inappropriate combinations;
effects of other drugs, e.g. antidepressants, adrenal steroids,
NSAIDs, sympathomimetics, nasal decongestants, ergotamine, oral
contraceptives, psychotropicspoor compliance with therapy
renovascular hypertensionnicotine; licorice; caffeine (strong
coffee) obesityexcessive alcohol intake excessive salt intakerenal
insufficiency and other undiagnosed causes of secondary
hypertension illicit substances, e.g. amphetamines, cocaine,
anabolic steroids
When adequate control is not possible and the cause is not
obvious, the patient should be referred to a specialist.
Measurement outside the clinic may help in the assessment of such
people, as may 24 hour ambulatory monitoring.Hypertension in
children and adolescentsThe recording of blood pressure should be
part of the normal examination in children and used in their
continuing care. Bloodpressure should be measured in all children
who are unwell. Blood pressure is less frequently measured in
children for a number of reasons, such as the unavailability of an
appropriately sized cuff or difficulty in measuring BP in the
infant or toddler. The children of parents with hypertension should
be closely watched. Those at risk of secondary hypertension, e.g.
renal or cardiovascular disease, urological abnormalities and
diabetes mellitus, should have routine measurements. Those children
with visual changes, headache or recurrent abdominal pain or
seizures, and those on drugs such as corticosteroids or the pill,
should have their blood pressure checked regularly.Although
secondary causes of hypertension are more common in children than
in adults, young people are still more prone to developing
essential rather than secondary hypertension. Renal parenchymal
disease and renal artery stenosis are the major secondary
causes.The upper limits of normal BP for children in different age
groups are: 1
Age (in years)
Arterial pressure (mmHg)
14-18135/90
10-13125/85
6-9120/80
5 or less110/75
The proper cuff size is very important to avoid inaccurate
readings and a larger rather than a smaller cuff is recommended.
The
width of the bladder should cover 75% of the upper arm. In
infants and toddlers use of an electronic unit may be necessary.
Although cessation of sound (Phase 5) is the better reflection of
true diastolic pressure, there is often no disappearance of sound
in children and so estimation of the point of muffling has to be
recorded.Diagnostic evaluation and drug treatment for children are
similar to those for adults. When a child is obese, reduction in
weight may adequately lower BP. ACE inhibitors or calcium
channel-blocking agents are preferable in the young hypertensive,
with diuretics a second agent. ACE inhibitors should be avoided in
postpubertal girls.Hypertension in the elderlyBlood pressure shows
a gradual increasing linear relationship with age.Guidelines for
treatment
Isolated systolic hypertension is worth treating. 16Older
patients may respond to non-pharmacological treatment. Reducing
dietary sodium is more beneficial than with younger patients.If
drug treatment is necessary, commence with half the normal
recommended adult dosage. 'Start low and go slow.' Patients over 70
and in good health should be treated the same as younger patients.A
gradual reduction in blood pressure is recommended. Drug reactions
are a limiting factor.Drug interactions are also a problem: these
include NSAIDs, antiParkinson drugs and phenothiazines.
Specific treatment1st line choice: indapamide (preferred) or
thiazide diuretic (low dose) 1 ; check electrolytes in 2-4 weeks:
if hypokalaemia develops add a K-sparing diuretic rather than K
supplements. Use a combination thiazide and K-sparing diuretic.
Diuretics may aggravate bladder difficulties, e.g. incontinence.2nd
line choice: beta-blockers (low dose) where diuretic cannot be
prescribed or if angina. Other effective drugs (especially for
isolated systolic hypertension):
ACE inhibitors (especially with heart failure) calcium channel
antagonists
Both these groups are generally well tolerated but constipation
may be a problem with verapamil. Renal function and electrolytes
should be monitored when ACE inhibitors are started.Special
management problemsThese conditions are summarised in Table 111.7
.Table 111.7 Choice of drugs in patients with coexisting
conditions
Diuretic ACE inhibitors Calcium antagonists -blockers
Asthma/COAD
x
x
x
x
Bowel disease/constipationxxxx
Bradycardia/heart blockxxcarex
Cardiac failurex*x*carex
Depressionxxxx
Diabetesxx*xx
Dyslipidaemiaxxxx
Hyperuricaemia/goutxx*x*x
Impotencexxxx
Ischaemic heart diseasexxx*x*
Peripheral vascular diseasexxx*x
Pregnancyxxxx
Raynaud's phenomenon
Renal artery stenosisx
xx
xx*
x*x
x*
Renal failurexcarexx
Tachycardia (resting)xxcarex*
* drug/s of choice. Calcium antagonists need to be selected with
caresome are suitable, others not
Diabetes mellitusFactors contributing to hypertension may be the
same in Type II (NIDDM) diabetes and non-diabetic hypertensive
patients. Inboth Type I and Type II diabetes, nephropathy can be a
significant contributor. The monitoring of patients for early signs
of nephropathy with measurements of microalbumin excretion is
helpful. Microalbuminuria can also be detected in nondiabetic
hypertensives where it appears to be a marker of cardiovascular
disease. Diabetic autonomic neuropathy can cause orthostatic
hypotension. Diabetics with persistent or sustained DBP > 90
mmHg and proteinuria need treatment. The threshold for treatment of
hypertension in the diabetic is lower than in the non-diabetic.
Control of hypertension is an important factor in limiting
progression of diabetic renal disease.Treatment
Use basic non-pharmacological treatments, especially weight
reduction, if applicable.ACE inhibitors and calcium channel
blockers are useful first-line drugs because they do not affect
insulin and diabetes control.Other suitable drugs are prazosin,
hydralazine and methyldopa.Diuretics added to an ACE inhibitor are
effective but caution is required because they can aggravate
glucose intolerance. Proteinuria and renal function need to be
monitored.
PregnancyHypertension in pregnancy can be either pre-eclampsia
(pregnancy-induced hypertension) or essential hypertension.
Bloodpressure levels normally drop during the second trimester and
rise in the third. A DBP > 80 mmHg in late pregnancy is
considered unacceptable. All treatments except for diuretics and
ACE inhibitors can be used. Hypertensive pregnant women should be
supervised in association with a specialist unit.Surgical
patientsPatients whose BP is under control before surgery should
continue the same treatment. If oral medication is affected by
thesurgery, parenteral treatment may be needed to avoid rebound
hypertension. This is a particular problem with clonidine and
possibly methyldopa. Withdrawal of other drugs, such as
betablockers, may have adverse consequences.Renal diseaseRenal
function is not adversely affected by the treatment of severe or
malignant hypertension. Use a loop diuretic, e.g.frusemide,
initially. Betablockers, calcium antagonists, prazosin and
methyldopa can be used, while caution is needed with ACE
inhibitors, particularly if there is underlying renovascular
disease.Heart failureFirst-line treatment for associated
hypertension includes ACE inhibitors and diuretics. Other suitable
drugs are a hydralazine-nitrate combination and methyldopa. Calcium
antagonists should be used with care and verapamil and
beta-blockers should be avoided.Ischaemic heart diseaseRecommended
drugs are beta-blockers and calcium antagonists. 7 The
non-dihydropyridine agents should be used with carewith a
betablocker but the dihydropyridine agents are quite
safe.Obstructive airways diseaseApart from beta-blockers, all other
routine antihypertensives can be used.ImpotenceIt is prudent to
avoid antihypertensives that are possibly associated with
impotence, e.g. thiazide diuretics, methyldopa,resperine and
beta-blockers. Suitable agents to use are ACE inhibitors and
calcium blockers.Can hypertension be overtreated? 17Yes. Excessive
blood pressure reduction, particularly if acute, can seriously
compromise perfusion in vital organs, especially ifblood flow is
already impaired by vascular disease. Careful monitoring of the
patient, including standing BP measurement, is important.One should
avoid excessive blood pressure reduction in the setting of acute
stroke, where there is a tight carotid artery stenosis
(particularly if symptomatic) and in the elderly subject
(especially if there is postural hypotension).It has been suggested
that lowering DBP < 85 mmHg in particular subgroups (e.g. those
with ischaemic heart disease) may raise the cardiovascular risk
above that associated with a lesser reduction in blood pressure. 18
However, the relationship between cardiovascular risk and blood
pressure is a continuous one. Moreover, the SHEP Study did not show
any adverse
effects of lowering DBP in patients with pre-existing coronary
heart disease. The safety of lowering DBP to levels below 85 mmHg
is being more formally addressed in the Hypertension Optimal
Treatment (HOT) Study. 19Step-down treatment of mild hypertension
17This is an important concept that recognises that drug treatment
need not necessarily be lifelong. If blood pressure has beenwell
controlled for several months to years it is often worth reducing
the dosage or the number of drugs.A 'drug holiday' (cessation of
treatment) can be hazardous, however, because satisfactory control
is usually temporary and hypertension will re-emerge. Careful
monitoring under such circumstances is mandatory.When to refer
5
Refractory hypertensionadequate control not possible and cause
not obvious. Suspected 'white coat' hypertensionfor ambulatory
blood pressure monitoring. Severe hypertensiondiastolic BP > 115
mmHg.Hypertensive emergency.If there is evidence of ongoing target
organ impairment.If there is significant renal impairment (serum
creatinine > 0.1 mmol/L). If a treatable cause of secondary
hypertension is found.
Practice tips
Hypertension should not be diagnosed on a single reading.At
least two follow-up measurements with average systolic pressure
> 140 mmHg or diastolic pressures > 90 mmHg are required for
the diagnosis.Beware of using beta-blockers in a patient with a
history of wheezing.Add only one agent at a time and wait about 4
weeks between dosage adjustments. Excessive intake of alcohol can
cause hypertension and hypertension refractory to treatment.If
hypertension fails to respond to therapy, an underlying renal or
adrenal lesion may have been missed.The low-pitched bruits of renal
artery stenosis are best heard by placing the diaphragm of the
stethoscope firmly in the epigastric area.Older patients may
respond better to diuretics, calcium antagonists and ACE
inhibitors. Younger patients may respond better to betablockers or
ACE inhibitors.
References
1. Hypertension Guideline Committee, 1991 report. Hypertension:
diagnosis, treatment and maintenance. Adelaide: Research Unit RACGP
(South Australian Faculty), 1991.2. The 1988 Report of the Joint
National Committee on Detection, Evaluation and Treatment of High
Blood Pressure.National High Blood Pressure Education Program.
Bethesda, Maryland: National Heart, Lung and Blood Institute,
National Institute of Health, May 1988. NIH Publication No.
88-1088.3. Sloane PD, Slatt PD, Baker RM. Essentials of family
medicine. Baltimore: Williams and Wilkins, 1988, 149-153.4. Sandler
G. High blood pressure. In: Common medical problems. London: Adis
Press, 1984, 61-106.5. Stokes G. Essential hypertension. In: MIMS
Disease Index. Sydney: IMS Publishing, 1991-92, 265-271.6. Fraser
A. Measurement of blood pressure. Aust Fam Physician, 1989;
18:355-359.7. ABC of hpertension. London: British Medical
Association. 1989, 1-50.8. Bates B. A guide to physical examination
and history taking (5th edn). Philadelphia: Lippincott, 1991,
284.9. Hovell MF. The experimental evidence for weight loss
treatment of essential hypertension. A critical review. Am J Public
Health, April 1982; 72(4):359-368.10. Blair SN, Goodyear NN,
Gibbons LW, Cooper KH. Physical fitness and incidence of
hypertension in healthy normotensive men and women. JAMA, 1984;
252(4):487-490.11. Rouse IL, Beilin LJ. Vegetarian diet and blood
pressure. Editorial review. J Hypertension, 1984; 2:231-240.12.
Kestlefoot H. Urinary cations and blood pressurepopulation studies.
Ann Clin Research, 1984; 16 Supp (43):72-80.13. Jennings G, Sudhir
K. Initial therapy of primary hypertension. Med J Aust, 1990;
152:198-202.14. Guidelines for the treatment of mild hypertension.
Memorandum from a WHO/ISH meeting. Endorsed by Participants at the
Fourth Mild Hypertension Conference. Bulletin of the World Health
Organisation, 1986; 64(1):31-35.15. Mashford ML (Chairman).
Cardiovascular drug guidelines (2nd edn). Melbourne: Victorian
Medical Postgraduate Foundation, 1995-96, 59-68.16. SHEP
Co-operative research group. Prevention of stroke by
antihypertensive drug treatment in older persons with isolated
systolic hypertension. J Amer Med Assn, 1991; 265:3255-3264.
17. Vandongen R. Drug treatment of hypertension. Aust Fam
Physician, 1989; 18:345-348.18. Cruickshank JM, Thorp JM, Zacharias
FJ. Benefits and potential harm of lowering high blood pressure.
Lancet, 1987; 1:581-584.19. The HOT study group. The Hypertension
Optimal Treatment Study. Blood Pressure, 1993; 2:6.
Chapter 112 - Dyslipidaemia
The landmark Scandinavian Simvastatin Survival Study (4S)
published in 1994, may well be remembered as the study that finally
put to rest many of the apprehensions and misconceptions regarding
lipid-lowering therapy.
Duffy and Meredith 1996 1
Dyslipidaemia is the presence of an abnormal lipid/lipoprotein
profile in the serum and can be classified as:
predominant hyperglyceridaemia predominant
hypercholesterolaemiamixed pattern with elevation of both
cholesterol and triglyceride (TG)
Modern epidemiological studies have established the facts that
elevated plasma cholesterol causes pathological changes in the
arterial wall leading to coronary artery disease (CAD), and that
lipid-lowering therapy results in reduction of coronary and
cerebrovascular events with improved survival.These studies which
can be summarised by their acronyms4S, 2 PLACI, 3 PLACII, 4 ACAPS,
5 KAPS, 6 REGRESS 7 and WOSCOPS 8 all reinforce the benefits of
lipid-lowering therapy for dyslipidaemia and the primary prevention
of coronary heart disease.Established facts 9 10 11
Major risk factors for CAD include:increased LDL cholesterol +
reduced HDL cholesterol ratio LDLC/HDLC > 4Risk increases with
increasing cholesterol levels (90% if > 7.8 mmol/L) Levels TG
> 10 mmol/L increases risk of pancreatitisManagement should be
correlated with risk factors10% reduction of total cholesterol
gives 20% reduction in CAD after 3 years
Investigations 9The following fasting tests are recommended in
all adult patients 18 years and over:
serum triglycerideserum cholesterol and HDLC & LDLC if = 5.5
mmol/L TFTs if overweight elderly female
Confirm an initial high result with a second test at 6-8 weeks.
Patients requiring treatment are summarised in Table 112.1 .
Testing should occur at least every 5 years.Table 112.1 Patients
requiring treatment (adapted from Australian Pharmaceutical
Benefits Guidelines)9
Patient categoryLipid level (mmol/L)
I Patients with existing CHDtotal cholesterol > 5.5
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II Other patients with one or more risk factors: personal
history CHD peripheral vascular disease family history CHD (1
relative < 60 years) diabetes mellitus familial
hypercholesterolaemia hypertension
III Patients with: HDLC < 1 mmol/L
total cholesterol > 6.5 ortotal cholesterol > 5.5 withHDLC
< 1
total cholesterol > 6.5
