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Causes
Recognising
pseudo-resistant
hypertension
Managing
resistant
hypertension
Detailed case
studies
The author
RESISTANT
PROFESSOR DAVID W
JOHNSON,
director of nephrology and
chair of medicine, Princess
Alexandra Hospital, Brisbane;
professor of medicine, University
of Queensland, St Lucia,
Brisbane, Queensland.
hypertension
Background
HYPERTENSION is the most commonly managed condition in Australian general practice and contributes about 5.4% to the overall
burden of disease in this country.
However, the available evidence suggests considerable room for improvement in the recognition, treatment and
subsequent control of hypertension in
the primary care setting.
A recent population-based survey of
11,247 Australian adults found that
the overall prevalence of hypertension
was 29%. However, only 47% of these
people were receiving antihypertensive
medications, and less than 20% had
adequate blood pressure control
1
(defined as a BP <140/90mmHg).
This article primarily focuses on
the approach to managing patients
with BP that is difficult to control.
How often is BP truly difficult to
control?
Resistant hypertension has generally
been defined as an inability to reduce
BP to <140/90mmHg despite treatment with a rational combination of at
least three antihypertensive medications (including a diuretic) for at least
one month.
The prevalence of this condition
ranges from 3% to 5% in primary
health care to 21% in groups of
patients referred to tertiary institutions. Studies of higher-risk populations enrolled in large clinical trials
suggest an even higher incidence in
the general population, ranging from
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2
12% (HOT study ) to as high as
3
74% (LIFE study ).
In the Antihypertensive and LipidLowering Treatment to Prevent Heart
4
Attack Trial (ALLHAT ), 27.3% of
patients required three or more drugs,
but 34% of such patients failed to
achieve the goal BP of <140/90mmHg.
Despite these sobering findings,
most patients with resistant hypertension can achieve their BP targets if
they are carefully evaluated and
appropriate therapy is instituted.
20 April 2007 | Australian Doctor |
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How to treat – resistant hypertension
Causes of resistant hypertension
THE potential causes of resistant hypertension are listed in
table 1. The most common is
volume overload, which often
arises from a combination of
excessive salt intake, inadequate diuretic therapy and
underlying chronic kidney disease (CKD).
Certain antihypertensive
medications such as vasodilators (eg, minoxidil) or dihydropyridine calcium-channel
blockers also tend to promote
avid sodium resorption by the
kidneys.
The second most common
cause of resistant hypertension
is non-adherence with treatment. Only 50-60% of
patients adhere well to prescribed regimens, 5-10%
adhere poorly and 30-40%
exhibit an intermediate degree
of adherence. More than half
of patients with insufficient
reductions in BP display suboptimal medication compliance.
Prescribing insufficient
dosages and numbers of different medications is the next
most common cause, accounting for between 43% and
60% of difficult-to-control
BP.
For example, Berlowitz and
colleagues conducted a survey
of 800 patients with hypertension over a two-year
5
period. About 40% had BP
>160/90mmHg despite an
average of more than six
hypertension-related consults
a year.
Even though significantly
elevated BP was clearly documented by clinicians, increases
in antihypertensive therapy
occurred in less than 7% of
visits, suggesting that most of
the physicians were not sufficiently aggressive with medical therapy.
It should also be emphasised that monotherapy
achieves an optimal BP
response in less than 20% of
patients, so multiple antihypertensive agents are usually
required (table 3).
This is particularly true in
the presence of CKD, when
the median number of medications required for BP control rises from one in patients
with an estimated glomerular
filtration rate (eGFR)
Table 2: Examples
of drug interactions
that interfere with
hypertension control
Table 1: Causes of
resistant hypertension
Volume overload
Excessive salt intake
Inadequate diuretic therapy
Chronic kidney disease
Non-adherence to therapy
Lack of consistent and
continuous primary care
Inconvenient dosing
schedules
Medication side effects
Medication costs
Instructions not understood
Inadequate patient
education
Impaired cognition
Pseudo-resistance
‘White-coat’ hypertension,
or office elevations
Pseudo-hypertension
Use of inappropriately small
sphygmomanometer cuff
for arm size
Drug-related causes
Inadequate dosages
Inappropriate combinations
(eg, ACE inhibitor and beta
blocker)
Rapid inactivation (eg,
hydralazine, clonidine)
Drug interactions
(see table 2)
Coexisting conditions
Smoking
Obesity
Insulin resistance (metabolic
syndrome)
Alcohol
Anxiety disorders
Chronic pain
Secondary causes of
hypertension
Chronic kidney disease
(renoparenchymal and
renovascular)
Primary hyperaldosteronism
Cushing’s syndrome
Phaeochromocytoma
Hyperparathyroidism
Myxoedema
Acromegaly
Obstructive sleep apnoea
Coarctation of the aorta
Polycythaemia rubra vera
Acute intermittent porphyria
Pre-eclampsia
Neurogenic (dysautonomia,
raised intracranial pressure,
lead poisoning, GuillainBarré syndrome)
NSAIDs (conventional and
COX-2 selective) — most
common
■ Sympathomimetics (nasal
decongestants, appetite
suppressants, caffeine,
cocaine, amphetamines)
■ Buproprion
■ Oral contraceptives
■ Corticosteroids
■ Antidepressants
(monoamine oxidase
inhibitors, tricyclic
antidepressants)
■ Hepatic enzyme
inducers (rifampicin,
phenobarbitone)
■ Cholestyramine
■ Cyclosporin, Tacrolimus
■ Erythropoietin,
darbepoietin
■ Licorice
■
2
>90mL/min/1.73m to 3.5 in
patients with an eGFR 402
49mL/min/1.73m .
Another frequent cause of
drug-related resistant hypertension is the concomitant use
of pro-hypertensive drugs. The
most common of these are
conventional and COX-2selective NSAIDs, which promote avid sodium and fluid
retention by the kidneys.
A recent survey of 601 Australian adults taking BP medications demonstrated that
nearly 10% were also taking
NSAIDs. This is not only worrying from the point of view
of undermining the effectiveness of hypertension control,
but most of these patients
were additionally at risk of the
‘triple whammy’ (the combination of an NSAID, diuretic
and either an ACE inhibitor
or angiotensin-II-receptor
antagonist) — the most
common cause of druginduced acute renal failure in
the community.
Secondary hypertension,
when there is a clearly identifiable (often treatable) cause
for BP elevation, is now considered to be more frequent
than the previously widely
quoted figure of 5%.
CKD, defined as GFR
2
<60mL/min/1.73m , was
Table 3: Summary of the number of medications required to achieve BP targets in
major hypertension clinical trials.
a
Target BP
Average number of
BP medications
MDRD
MAP <92mmHg
3.6
Trial
b
ABCD
DBP <75mmHg
2.7
c
HOT
DBP <85mmHg
3.3
d
UKPDS
DBP <85mmHg
2.8
DBP = diastolic BP; MAP = mean arterial pressure
a
Klahr S, et al. The effects of dietary protein restriction and blood-pressure control on the progression of
chronic renal disease. Modification of Diet in Renal Disease Study Group. New England Journal of
Medicine 1994 330:877-84.
b
Estacio RO, et al. The effect of nisoldipine as compared with enalapril on cardiovascular outcomes in
patients with non-insulin-dependent diabetes and hypertension. New England Journal of Medicine 1998;
338:645-52.
c
Hansson L, et al. Effects of intensive blood-pressure lowering and low-dose aspirin in patients with
hypertension: principal results of the Hypertension Optimal Treatment (HOT) randomised trial. HOT
Study Group. Lancet 1998; 351:1755-62.
d
UK Prospective Diabetes Study Group. Tight blood pressure control and risk of macrovascular and
microvascular complications in type 2 diabetes: UKPDS 38. UK Prospective Diabetes Study Group. BMJ
1998; 317:703-13.
shown in the recent AusDiab
study to be present in about
27% of all Australian adults
6
with hypertension. Most of
this disease is renoparenchymal in nature, although renovascular hypertension occurs
in about 1-2% of cases.
Primary hyperaldosteronism has also been suggested
to occur with reasonable frequency in resistant hypertension, based on the reported
prevalence of abnormal
plasma aldosterone:renin
ratios of up to 40% in
selected groups.
However, this issue is some-
what contentious at present,
as some authors have raised
concerns that extensive use of
the test leads to high false-positive rates and unnecessary,
costly additional testing.
Other rare causes of secondary hypertension are listed
in table 1.
A final category of resistant hypertension is pseudoresistance. The most
common form of this is socalled ‘white-coat’ hypertension, in which clinic BP measurements are elevated, but
home or ambulatory BPs are
normal. Various case series
have reported that up to
40% of patients with resistant hypertension actually
have a component of whitecoat hypertension.
Other causes of pseudoresistance include pseudohypertension in older
patients (due to the presence
of calcific arteriosclerosis
leading to brachial artery
stiffness) and the use of an
inappropriately small sphygmomanometer cuff (the cuff
bladder length should be at
least 80% and the width at
least 40% of the circumference of the mid-upper arm).
Recognising pseudo-resistant hypertension
THE definitive test is confirming
the presence of non-elevated BP by
either 24-hour ambulatory BP
monitoring (daytime average BP
<135/85mmHg, night-time average
BP <120/70mmHg and 24-hour
average <130/80mmHg) or home
BP measurements (BP <140/90
mmHg).
However, performing such investigations may not always be feasible or practical, particularly in
remote practices. Clinical clues to
the possible presence of a whitecoat effect in the setting of apparent resistant hypertension include:
28
| Australian Doctor | 20 April 2007
Mild BP elevations (systolic BP
<180mmHg).
■ Absence of target-organ damage
(eg, retinopathy, proteinuria or
left ventricular hypertrophy).
■ Presence of symptoms compatible with hypoperfusion (eg,
orthostatic light-headedness) in
the absence of excessive reduction of BP.
As a general rule of thumb, if the
patient has evidence of target-organ
damage, one should generally err
on the side of augmenting treatment (unless they have hypoperfusion symptoms).
■
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When to investigate for
secondary causes
Given that the prevalence of CKD is
high (27%) in the general hypertensive population, the Kidney Check
Australia Taskforce recommends
screening all hypertensive patients
with a serum creatinine test, eGFR
and urine dipstick examination for
proteinuria on an annual basis.
A positive urine dipstick examination or an eGFR <60mL/min/
2
1.73m warrants further investigation with at least a renal ultrasound
scan and formal urinary protein
quantification (urine protein:crea-
tinine ratio on a random urine
sample is recommended).
Other forms of secondary hypertension should be investigated in
the settings of:
■ Resistant, malignant or accelerated hypertension.
■ An acute rise in BP over a previously stable value.
■ Age of onset of <30 years, with no
family history of hypertension and
no other risk factors (eg, obesity).
■ Or if any of the clinical or laboratory features listed in table 4
are present.
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How to treat – resistant hypertension
from page 28
Screening for renovascular hypertension is probably best achieved by
either renal artery duplex scan or isotope renography (with or without
captopril), although other tests are
available (eg, magnetic resonance
angiography, helical CT, captopril
renin stimulation test). A positive
screening test warrants proceeding to
a renal angiogram with or without
determination of renal vein renin
level.
The preferred initial screening strategy for primary hyperaldosteronism is
measurement of a plasma aldosterone:renin ratio. This is best done
in the morning and in the upright
position. The typical finding in
Conn’s syndrome is suppressed
plasma renin activity, elevated plasma
aldosterone concentration and hence
an elevated ratio.
This ratio may be modified by
several factors, including the use of
concomitant medications such as
ACE inhibitors and beta blockers,
which stimulate renin release. Most
BP medications affect the ratio,
although verapamil, hydralazine
and prazosin generally do not.
An elevated plasma ratio is therefore not diagnostic of primary
aldosteronism, but warrants further investigation with an aldosterone-suppression test in which
Table 4: Clinical or laboratory features suggestive of secondary hypertension and warranting further
appropriate investigation
Disorder
Suggestive clinical or laboratory features
Generic (any cause of secondary
hypertension)
■
Renoparenchymal disease
Renovascular disease
Primary hyperaldosteronism
Obstructive sleep apnoea
Phaeochromocytoma
Cushing’s syndrome
Coarctation of the aorta
Hypothyroidism
Primary hyperparathyroidism
Polycythaemia rubra vera
Resistant hypertension
■ Malignant hypertension (elevated BP + grade 4 hypertensive retinopathy)
■ Accelerated hypertension (elevated BP + grade 3 hypertensive retinopathy)
■ An acute rise in BP over a previously stable value
■ Age of onset <30, with no family history of hypertension and no other risk factors
(eg, obesity)
2
■ eGFR <60mL/min/1.73m
■ Proteinuria/albuminuria
■ Acute elevation in serum creatinine concentration (or fall in eGFR) by 30% or
more within one month of starting an ACE inhibitor or angiotensin-II-receptor
antagonist
■ Moderate to severe hypertension in a patient with diffuse atherosclerosis or a
unilateral small kidney
■ Repeated episodes of flash pulmonary oedema
■ Unexplained hypokalaemia (Note that more than half of Conn’s syndrome
patients are normokalaemic)
■ Obese patients who describe a history of witnessed apnoeas, loud snoring,
daytime somnolence, early morning headaches, morning confusion or morning sore throat
■ Triad of headache (usually pounding), palpitations and sweating (often episodic)
■ Paroxysmal elevations in BP
■ Cushingoid facies, central obesity, proximal muscle weakness and ecchymoses
■ Hypertension in the arms, with diminished or delayed femoral pulses, and low or
unobtainable BPs in the legs
■ Lethargy, cold insensitivity, weight gain, bradycardia or other features of
hypothyroidism
■ Elevated serum calcium level
■ Elevated haemoglobin concentration
Table 5: Indications for
referral of patients with
hypertension to a specialist
Suspected secondary
hypertension
■ Resistant hypertension plus
2
eGFR < 60mL/min/1.73m
2
■ eGFR <30mL/min/1.73m
■ Proteinuria >1g/day
■ Rapid (>15%) decline in eGFR
within three months (not in context
of starting an ACE inhibitor)
■ Accelerated hypertension
(hypertension with grade 3
retinopathy) (urgent)
■ Malignant hypertension
(hypertension with grade 4
retinopathy) (urgent)
■ Multiple drug intolerances or
complications
■
levels on at least three separate
occasions (phaeochromocytoma).
■ Thyroid function (hypothyroidism).
■ Urinary free cortisol (Cushing’s
syndrome).
■ Parathyroid hormone levels
(hyperparathyroidism).
■ Polysomnography (obstructive
sleep apnoea).
When to refer
24-hour urinary aldosterone is
measured following salt loading for
at least three days.
Other screening tests that may
be considered for suspected secondary hypertension under appro-
priate circumstances include measurements of:
■ 24-hour urinary catecholamine
The indications for referral of
patients with hypertension to a specialist are listed in table 5.
Management
Is lifestyle modification
important in patients with
resistant hypertension?
Table 6: Anticipated benefits of lifestyle interventions in hypertensive patients
LIFESTYLE modification
plays a crucial role in managing patients with resistant
hypertension, as they can
achieve significant BP reductions on top of those afforded
by drugs.
Particular attention should
be paid to the ‘SNAP’ (smoking, nutrition, alcohol, physical activity) risk factors. Table
6 provides an outline of the
magnitude of BP reductions
that may be expected as a
result of successful lifestyle
modification.
Intervention
Recommendation
Weight reduction
■
■
Dietary salt restriction
DASH (dietary approaches
to stop hypertension) diet
Physical activity
Moderate alcohol
consumption
30
5-7mmHg
8-14mmHg
2.5-4mmHg
2-4mmHg
Table 7: Choice of antihypertensive medications in patients with hypertension and
pre-existing conditions.
Drug class
ACE inhibitor
Angiotensin-II-receptor
antagonist
Diuretic
Calcium-channel blocker
Potentially favourable effect
■ CKD
■ Diabetic nephropathy
■ Heart failure
■ MI
■ Cerebrovascular accident
■ Diabetic nephropathy
■ Heart failure
■ Heart failure
■ Angina
Beta blocker
■
Antihypertensive drug
therapy
Most antihypertensive agents
achieve comparable levels of
BP reduction when prescribed
as monotherapy (of the order
of 12/5mmHg). A metaanalysis of hypertension trials
by the Blood Pressure Lowering Treatment Trialist Collaboration demonstrated no
major differences between
classes of medication with
respect to reducing cardiovascular risk, and greater risk
reductions occurring with
7
larger reductions in BP.
In general terms, the choice
of antihypertensive medications in patients with resistant
hypertension is dictated by the
presence of coexisting conditions (table 7), concomitant
medications and how well
specific antihypertensive medications are tolerated by the
individual patient.
Moreover, simple regimens
that enhance adherence (eg,
once-daily dosing and combination pills) should be tried
BMI 18-24.9
Waist circumference ≤94cm (men) or
≤80cm (women)
■ <90mmol/day (low-salt foods + no adding
salt to food)
■ Fruit, vegetables, low saturated and total
fat
■ Aerobic activity for 30 minutes most days
■ 1-2 standard drinks a day
Approximate systolic
BP reduction
5-20mmHg/10kg lost
Angina
Myocardial infarction
■ Heart failure
■
Alpha blocker
■
Prostatism
Minoxidil
initially. Maximal doses of
each agent should be encouraged, whenever they are possible, except for thiazide
diuretics, when low doses
are often preferred because
of a therapeutic ceiling.
Because CKD and cardiovascular disease are common
in patients with resistant
hypertension, ACE inhibitors, angiotensin-II-receptor
| Australian Doctor | 20 April 2007
antagonists and diuretics
should be among the firstline drugs in the therapeutic
armamentarium.
One study of patients with
resistant
hypertension
attending a tertiary care
clinic demonstrated that
good BP control was ultimately achieved in most
patients and that the most
successful therapeutic strat-
Potentially deleterious effect
Bilateral renal artery stenosis
■
■
Bilateral renal artery stenosis
Gout
Bradycardia
■ Heart block
■ Heart failure
■ Bradycardia
■ Heart block
■ Peripheral vascular disease
■ Asthma
■ Glaucoma
■ Heart failure
■ Angina
■ Heart failure
■
■
egy was either to add (50%
of cases) or modify (24%)
8
diuretic therapy.
Thiazide diuretics are
effective and preferred
because of their longer duration of action in patients
with eGFR >50mL/min/
2
1.73m . For patients with
2
eGFRs <50mL/min/1.73m ,
loop diuretics are more efficacious.
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Combining a diuretic with
an ACE inhibitor or
angiotensin-II-receptor antagonist confers synergistic BP
reduction. Spironolactone has
also been shown to be effective in resistant hypertension,
but patients must be closely
monitored for hyperkalaemia
(especially when it is used in
combination with an ACE
inhibitor and/or angiotensin9
II-receptor antagonist).
Inappropriate drug combinations, such as a beta
blocker with either an ACE
inhibitor or centrally acting
calcium-channel blocker, are
best avoided.
If BP treatment remains
difficult despite the patient
taking three or four different medications, it is often
useful to add one or more
agents requiring twice- or
thrice-daily administration
(eg, hydralazine or methyldopa) to attempt to achieve
better antihypertensive
coverage over a 24-hour
period.
If all else fails, minoxidil
is often effective, although
patients have to be monitored closely for signs of
fluid retention and pericardial effusion. If minoxidil
therapy is instituted, the
diuretic dose usually needs
to be increased and a beta
blocker is also often required
to minimise reflex sympathetic activation.
Achieving BP targets
Reaching BP targets in some
patients is sometimes not
possible, often because of
severe medication intolerances. In the case of therapylimiting symptoms prevent-
ing the attainment of BP
goals, even a partial reduction of BP may achieve significant cardiovascular and
renal benefits. Such patients
often benefit from specialist
referral.
Sometimes, therapy may
also be limited in elderly
patients because of impaired
cerebral or renal autoregulation (leading to cerebral or
renal hypoperfusion with
even modest reductions in
BP) or because of a component of pseudo-hypertension
due to the presence of calcific arteriosclerosis.
The latter may be suspected if antihypertensive
therapy induces symptoms
compatible with hypoperfusion (eg, orthostatic lightheadedness) in the absence
of an excessive reduction in
BP.
Nevertheless, the available
evidence suggests that a
major reason for failure to
reach BP targets is a failure
or reluctance of physicians
to increase antihypertensive
therapy because of their
focus on relieving symptoms,
lack of familiarity or agreement with clinical guidelines,
or discomfort in titrating to
a goal (particularly when the
patient is already taking several BP medications).
One of the most effective
strategies for dealing with
clinical inertia is to institute
decision-support systems
that prompt clinicians to
augment therapy when a
goal has not been achieved.
In the vast majority of
hypertensive patients, it is
appropriate to try to reach
recommended BP targets.
AD_HTT_025_034___APR20_07 13/4/07 8:57 AM Page 31
Summary
Resistant hypertension,
defined as an inability to
reduce BP below
140/90mmHg despite
treatment with a rational
combination of at least
three antihypertensive
medications (including a
diuretic) for at least one
month, occurs in about
5% of patients.
■ The major causes are
volume overload, patient
non-adherence and
reluctance of the clinician
to augment treatment.
■ CKD occurs in about
one-quarter of all patients
with hypertension and
should be screened for by
annual testing of serum
creatinine concentration,
eGFR and urine dipstick
for protein.
■ Other forms of secondary
hypertension should be
investigated in the settings
of:
— Resistant, malignant
or accelerated
hypertension.
— An acute rise in BP over
a previously stable value.
— Age of onset <30, with
no family history of
hypertension and no
other risk factors (eg,
obesity).
— Presence of any of the
clinical or laboratory
features listed in table 4
(page 30).
■ The choice of
antihypertensive
medications is usually
determined by the
presence of coexisting
conditions (table 7),
concomitant medications
and how well specific
antihypertensive
medications are tolerated
by the individual patient.
■ Diuretics are particularly
useful in managing
resistant hypertension.
■ Good BP control is
possible in most patients
with resistant
hypertension.
Author’s case studies
■
Case study 1 — Harry
HARRY, 56, returns to your
clinic for a BP check. He was
last seen by you two weeks
ago for an URTI and was
noted at the time to have a BP
of 175/105mmHg. He now
feels perfectly well. His seated
BP today is 170/105mmHg
(large cuff).
Harry has a past history of
“borderline” hypertension
diagnosed during an insurance
medical 10 years ago, but has
not received antihypertensive
therapy or subsequent BP
checks. His mother and father
were diagnosed with hypertension in their 60s and his
father died at 68 from a heart
attack.
Harry has been overweight
for most of his adult life but
has no symptoms suggestive
of obstructive sleep apnoea.
There is no other past medical history. Harry is on no
regular medications. He
smokes 10 cigarettes a day,
drinks 20-30g of alcohol (2-3
standard drinks) on most
nights and does very little
exercise. He works as an
administrative officer.
Physical examination
reveals obesity (waist circumference 102cm, BMI 30.2).
His pulse is 72bpm and regular. Cardiorespiratory and
abdominal examinations are
normal. There are no audible
carotid or renal bruits. His
peripheral pulses are normal.
Fundoscopic examination
reveals grade 2 hypertensive
retinopathy (figure 1). His
investigations reveal:
■ Urine dipstick 1+ protein,
no blood.
■ FBC normal.
■ Biochemistry:
urea
7.0mmol/L, creatinine
120µmol/L,
eGFR
2
58mL/min/1.73m , urate
0.45mmol/L, fasting blood
glucose 6.2mmol/L.
■ Cholesterol: total 6.3
mmol/L, HDL 0.8mmol/L,
LDL 4.2mmol/L.
■ Triglycerides: 2.2mmol/L.
■ ECG voltage criteria of left
ventricular hypertrophy.
■ Echocardiograph: left ventricular hypertrophy.
■ Urine protein:creatinine
ratio: 40g/mol (normal <15)
Question 1: What would you
do now?
a. Recommend lifestyle modification.
b. See Harry in two weeks
to recheck his BP before considering antihypertensive
medication.
c. Start antihypertensive
medication this visit.
d. Start drug therapy other
than antihypertensive medication.
e. Order 24-hour ambulatory BP monitoring.
f. Order a renal ultrasound
scan.
g. Refer to a nephrologist.
(My answer: a, c, d and f)
Harry has moderate hypertension, with target-organ
damage (retinopathy, CKD,
Figure 1: Grade 2 hypertensive retinopathy (silver wiring and
arteriovenous nipping).
Therapeutic
modifications often
required in resistant
hypertension (after
exclusion of secondary
causes)
Often 4-5 antihypertensive
medications (occasionally
more)
■ Maximal doses (except
thiazide diuretics)
■ Must include a diuretic
■ Use a loop diuretic if
eGFR is
2
<50mL/min/1.73m
■ Consider spironolactone
(beware of the risk of
hyperkalaemia, especially
if the patient is also taking
an ACE inhibitor and/or an
angiotensin-II-receptor
antagonist)
■ Consider adding
medications with twice- or
thrice-daily dosing (eg,
hydralazine, methyldopa)
■ Minoxidil is useful in
severe refractory cases
■ Allow at least 3-4 weeks
after medication change
to assess full impact
■ Follow patients at least
monthly while BP remains
uncontrolled
■
left ventricular hypertrophy).
Under these circumstances the
Hypertension Management
10
Guide for Doctors 2004 recommends instituting lifestyle
modification (table 6) and
drug treatment; 24-hour
ambulatory monitoring is
unlikely to contribute to management.
Based on his many risk factors (hypertension, obesity,
smoking, hypercholesterolaemia, sedentary lifestyle, positive family history of ischaemic
heart disease, impaired fasting
glycaemia, low eGFR, proteinuria) and his high risk (>30%)
of a cardiovascular event in the
next five years, the Guide recommends instituting low-dose
aspirin and a statin, in addition to antihypertensive therapy.
Given that Harry has stage
3 CKD, as evidenced by an
2
eGFR of 58mL/min/1.73m
and mild proteinuria, it would
be reasonable to start therapy
with either an ACE inhibitor
or angiotensin-II-receptor
antagonist. Ultimately he is
likely to require combination
antihypertensive therapy
(including a diuretic) to adequately control his BP.
A renal ultrasound scan is
appropriate in the setting of
stage 3 CKD to assess for evidence of kidney damage (scarring, stones, obstruction or
neoplasms). Despite his moderate hypertension and CKD,
Harry does not meet the
Kidney Check Australia Taskforce guidelines for referral to
a nephrologist.
Question 2: What should Harry’s
target BP be?
a. 145/95mmHg
b. 140/90mmHg
c. 130/80mmHg
d. 125/75mmHg
(My answer: c)
The Caring for Australians
with Renal Impairment
(CARI) guidelines (see Online
resources, page 32) recommend a target BP of
<130/80mmHg in patients
with hypertension and CKD.
The lower target of
125/75mmHg is only recommended in those with hypertension and diabetes if their
proteinuria exceeds 1g/day
(approximately equivalent to a
urine protein:creatinine ratio
of 120g/mol). The higher
target of 140/90mmHg is recommended for patients with
hypertension without diabetes
or evidence of CKD.
Three weeks later
After giving Harry appropriate lifestyle advice and starting
him on perindopril 5mg in the
morning, aspirin 100mg daily
and atorvastatin 10mg daily,
you ask him to return for a
clinical review.
His BP is 160/100mmHg.
Repeat blood tests demonstrate a serum potassium concentration of 5.3mmol/L and
his serum creatinine concentration has risen to 136µmol/L
2
(eGFR 50mL/min/1.73m ).
His renal ultrasound scan
demonstrated normal-sized
kidneys with a normal
appearance.
Question 3: What would you do
now?
a. Stop the perindopril and
www.australiandoctor.com.au
start an alternative antihypertensive agent.
b. Reduce the dose of perindopril.
c. Refer to a nephrologist.
d. Start a diuretic.
e. Order a renal artery duplex
scan.
(My answer: d)
Current national and international guidelines recommend clinicians tolerate up to
a 30% rise in serum creatinine
concentration and/or a 30%
fall in eGFR within the first
month of starting an ACE
inhibitor or angiotensin-IIreceptor antagonist.
An initial rise in serum creatinine concentration, which
then stabilises and is <30%
above baseline value, is predictive of a renoprotective
benefit, compared with
patients who experience no
alteration in kidney function
at all. It is therefore important
NOT to stop an ACE
inhibitor or angiotensin-IIreceptor antagonist because of
a modest rise in serum creatinine concentration or fall in
eGFR.
If a patient experiences a
progressive rise in serum creatinine concentration or an
absolute rise of >30% above
baseline in the first month of
ACE inhibitor or angiotensinII-receptor antagonist therapy,
the agent should be stopped
and consideration given to
investigating for the possibility
of bilateral renal artery stenosis (eg, with a renal artery
duplex scan).
Elevation of serum potassium concentration to
>6mmol/L, which is not controlled by diuretic therapy,
also warrants cessation of
ACE inhibitor therapy.
Because Harry’s BP is still
poorly controlled, it is reasonable to start a diuretic (which
may be in the form of a combination pill with perindopril).
Six months later
Harry has lost 6kg after
adopting a healthier diet and
regular exercise program. He
has reduced his alcohol consumption but continues to
smoke 10 cigarettes a day. His
current medications include
perindopril/indapamide 4/1.25
mg daily, irbesartan 300mg
daily and ibuprofen for knee
osteoarthritis. His office BP is
140/90mmHg and his serum
creatinine concentration is
160µmol/L (eGFR 41mL/
2
min/1.73m ).
Question 4: What would you do
now?
a. Assess drug compliance.
b. Stop the ibuprofen.
c. Change indapamide to a
loop diuretic.
d. Add another antihypertensive medication.
e. Screen for renal artery
stenosis.
f. Refer to a nephrologist.
(My answer: a, b and c)
Harry has resistant hypertension, given that he has not
reached his BP target despite
treatment with three agents
(including a diuretic). This is
most likely due to progression
of his underlying CKD, which
in turn has been aggravated
by a ‘triple whammy’ (ACE
inhibitor or angiotensin-IIreceptor antagonist, diuretic
and NSAID).
It is therefore critically
important to stop his NSAID.
Harry’s indapamide should
also be changed to a loop
diuretic in view of his low
eGFR. Options d, e and f
would be reasonable if the
above measures did not result
in substantial improvement in
Harry’s BP control.
Follow-up
Harry ’s partner confirmed he
was taking his medications
religiously. After changing his
diuretic from indapamide to
frusemide 40mg in the morning and discontinuing the
ibuprofen, Harry’s BP
improved to 135/80mmHg
and his serum creatinine concentration improved to
140µmol/L.
Doppler examination of the
renal arteries was within
normal limits. Harry was
referred to a nephrologist who
started amlodipine 10mg
daily. Harry’s BP is now well
controlled and he sees his GP
and specialist alternately every
three months.
Case study 2 — Jane
Jane, 42, presents with a oneweek history of constant, generalised headache. She was
diagnosed with white-coat
hypertension at 27 but started
antihypertensive medications
at 35, after elevated BP was
confirmed by 24-hour ambulatory monitoring.
She has numerous medication intolerances, including
enalapril (cough), verapamil
(flushing), hydralazine (palipitations) and prazosin (nausea).
Her current medications
include candesartan 16mg
daily, clonidine 100µg qid and
salbutamol (for asthma).
There is no family history
of hypertension. Her office BP
is 210/110mmHg (confirmed
on repeat testing). Previous
measurements at your clinic
have consistently been in the
range of 120-30/70-80mmHg.
Her physical examination is
unremarkable apart from
grade 2 hypertensive retinopathy and 1+ protein on urine
dipstick. Her serum biochemistry reveals normal renal
function (serum creatinine
concentration 60µmol/L,
2
eGFR >60mL/min/1.73m )
and an ECG demonstrates
voltage criteria of left ventricular hypertrophy.
Question 1: How would you
manage Jane now?
a. See her again in the next
few days to recheck BP before
considering additional antihypertensive therapy.
cont’d next page
20 April 2007 | Australian Doctor |
31
AD_HTT_025_034___APR20_07 13/4/07 8:57 AM Page 32
How to treat – resistant hypertension
from previous page
b. Start a diuretic.
c. Order a renal artery duplex
scan.
d. Order tests for 24-hour urinary catecholamines, plasma
aldosterone:renin ratio, thyroid function and urinary
free cortisol.
e. Refer to a specialist.
(My answer: b, c, d and e)
Jane has developed recentonset, symptomatic grade 3
BP elevation with documented
target-organ damage in the
setting of longstanding adequately controlled hypertension, which developed at a
young age in the absence of a
family history or other risk
factors.
She is at risk of accelerated
or malignant hypertension
and has a high probability of
secondary hypertension. Her
BP requires prompt treatment
to reduce it towards a target
level of <140/90mmHg over
the next few weeks. It is
appropriate to start an additional antihypertensive medication immediately (a diuretic
seems reasonable).
All the listed investigations
Figure 2: Renal angiogram demonstrating the classic ‘beaded’
appearance of the left renal artery, characteristic of
fibromuscular dysplasia.
Her blood tests were normal
apart from:
■ Plasma
renin activity
2.8ng/mL/hour (normal
range <2ng/mL/hour).
■ Aldosterone 810pmol/L
(NR 30-450pmol/L).
■ Aldosterone:renin ratio
289 (NR 80-530).
A renal artery duplex
found elevated flow velocities in the mid-to-distal sections of both renal arteries,
with elevation of renal artery
resistances, suggesting 6099% stenoses.
Question 2: What should be
done now?
are justified and she should be
reviewed within a week. Specialist referral is warranted,
particularly if a secondary
cause is identified.
Follow-up
Jane was started on candesartan/hydrochlorothiazide
16/12.5mg daily. On review
five days later her BP was still
elevated at 180/100mmHg.
a. Arrange for a CT scan of
the abdomen (focusing on
the adrenal glands).
b. Order an isotope renogram.
c. Start an additional antihypertensive medication.
d. Order a renal angiogram.
e. Measure 24-hour urinary
aldosterone after oral salt
loading.
(My answer: c and d)
The investigations suggest
that Jane has bilateral renal
artery stenosis (probably due
Hypertensive emergency and hypertensive urgency
Hypertensive emergency is defined as severe hypertension
with acute impairment of an organ system (eg, the central
nervous, cardiovascular or renal systems). In these conditions,
the BP should be lowered aggressively over minutes to hours.
Typical examples would include:
■ Hypertensive intracranial haemorrhage.
■ Severe hypertension with an aortic dissection.
■ Severe pre-eclampsia.
■ Severe hypertension resulting in acute renal failure.
Hypertensive urgency is defined as a severe elevation of BP
without evidence of progressive target-organ damage. These
patients require BP control over several days to weeks.
In these patients, dropping the blood pressure acutely may
be problematic because of impaired autoregulation (for example, it is possible to precipitate ischaemic strokes or acute renal
failure under such circumstances).
The clinical distinction between hypertensive emergencies and hypertensive urgencies depends on the presence of acutely worsening targetorgan damage and not on the absolute level of the BP.
to fibromuscular dysplasia)
complicated by secondary
hyperaldosteronism (both
renin and aldosterone concentrations elevated). She
should be referred to a
nephrologist or other specialist and have renal angiography. In the meantime, her
BP is still significantly elevated and warrants augmentation of therapy.
Follow-up
Jane was started on methyldopa 500mg tds with good
effect. Her angiogram confirmed the presence of bilateral renal artery stenosis due
to fibromuscular dysplasia
(figure 2). After bilateral
renal angioplasty with stenting, her BP remains well
controlled on candesartan
alone.
GP’s contribution
DR DIANNE CHAMBERS
Leichhardt, NSW
Case study
MJ, 61, had longstanding hypertension over the past 20 years. When she
first came under my care she was
taking a beta blocker and diuretic. She
has a positive family history of cardiovascular disease, with her mother and
father dying of infarct and stroke,
respectively. She also has an uncle and
three brothers who all died of MI in
their 40s.
Marie is overweight at 75kg (BMI
30) and has coexisting gastrooesophageal reflux disease and fatty
liver (persistently mild elevation of liver
enzyme levels). She is not a smoker
but had LDL-cholesterol recorded at
6.8mmol/L in 1993.
Initially, the thrust of treatment was
to encourage weight loss and increase
exercise. With this advice she managed to lose 8kg and her cholesterol
level dropped. However, her BP
slowly climbed and with the advent
of ACE inhibitors I switched her to
Coversyl (BP was 170/100mmHg
before this change).
Marie’s BP was not controlled so I
switched her to Coversyl Plus, but this
needed to be stopped because she
developed ACE inhibitor cough. I
switched her to Atacand Plus
150/12.5mg. Her BP was 150/95
mmHg and I increased the dose to
300/12.5mg.
During 2003 she had an episode of
back pain (osteoarthritis after an old
back injury) and I prescribed pulse
Celebrex and maintenance paracetamol. She developed a severe rash (possibly from the Celebrex) and her BP
32
| Australian Doctor | 20 April 2007
climbed to 210/110mmHg. She was
sent for urgent physician review.
Amlodipine was added and the
COX-2 inhibitor stopped (serum creatinine concentration was 64µmol/L).
BP fell but Marie developed mild pitting oedema secondary to the calciumchannel blocker. Her other medications at this time included tibolone,
aspirin and Xenical.
Full hypertension investigations were
started. Marie had a aldosterone-renin
test, a vasculitic screen, 24-hour catecholamines, a renal ultrasound and
urine examination for proteinuria and
haematuria.
Her renal ultrasound showed kidney
disproportion so she was sent for renal
angiogram, which was normal, as were
other investigations for renal disease.
The aldosterone:renin ratio was elevated, which was said to be consistent
with her prescribed angiotensin-IIreceptor blocker.
Later in 2003, Marie had her first
episode of angina, and an angiogram
confirmed widespread coronary artery
disease. She had a drug-eluting stent
inserted in April 2003 but in 2004 she
had an in-stent thrombosis with a
moderate rise in creatine kinase level,
and required further stenting.
Because of her abnormal LFTs she
had not previously been prescribed a
statin, but Lipitor was cautiously
introduced at this time. A beta blocker
was recommended also, as coronary
protection.
Marie’s recovery was complicated
by recurring pericarditis, which
required prednisone (rheumatology
review did not reveal any autoimmune
cause). While taking steroids her BP
rose to 160/90mmHg. Medication
options were limited because of previous reactions to calcium-channel
blockers, so the dose of her beta
blocker was increased and she was
started on Minipress.
Initially this was 1mg bd but, as a
24-hour BP chart showed significant
hypertension during the day, it was
increased to tds, with some improve-
ment in control. Daytime readings on
the home monitor were up to
160/100mmHg, so the Minipress dose
was increased to 1.5mg at lunch.
Interestingly, recent cessation of vitamin E supplements also resulted in
improvement in BP control.
Current medications are:
■ Avapro 300mg, one tablet in the
morning.
■ Cartia 100mg, one tablet daily.
■ Clopidogrel 75mg, one tablet daily.
■ Endep 25, 25mg, two tablets before
bed.
■ Lasix M 20mg one tablet in the
morning.
■ Lipitor 20mg, one tablet daily.
■ Metoprolol 100mg, one tablet tds.
■ Minipress 1mg, one tablet tds.
Currently Marie is normotensive
and the thrust of her therapy is to
assist with weight loss, as her BMI is
29 despite extensive assistance from
the metabolism and obesity unit.
Questions for the author
Primary hyperaldosteronism is listed
as one of the more common causes of
resistant hypertension. You suggested
that abnormal plasma aldosterone:renin ratios may not be a reliwww.australiandoctor.com.au
able investigation. Marie’s ratio was
raised but it was considered that her
medications caused elevation. As both
ACE inhibitors and angiotensin-IIreceptor antagonists make interpretation difficult, can you elaborate on the
investigation of Conn’s syndrome?
Most antihypertensive medications
(except verapamil, hydralazine and
prazosin) can affect the plasma aldosterone:renin ratio (ARR). In this particular patient’s case, the elevated ARR
is not consistent with her prescribed
angiotensin-II-receptor antagonist, as
such agents generally suppress plasma
aldosterone concentrations and
increase plasma renin levels, thereby
decreasing ARR.
Most antihypertensive agents
decrease the ARR, although examples
of medications that increase the ARR
include beta blockers, clonidine,
methyldopa and NSAIDs.
To investigate the possibility of
Conn’s syndrome, the recommended
practice is to convert patients to reninneutral medications, such as verapamil
slow release, hydralazine or prazosin,
alone or in combination.
In cases in which a potentially interfering medication cannot be withdrawn (eg, because of severe hypertension), useful information can still be
obtained by taking into account the
known effects of that medication.
For example, an elevated ARR in
someone who is taking a diuretic, ACE
inhibitor, angiotensin-II-receptor antagonist and/or a dihydropyridine calciumchannel blocker would suggest Conn’s
syndrome (as these medications ordinarily suppress the ARR).
Marie required 24-hour BP monitoring. Although her resting BP was generally satisfactory, she had significant
daytime elevation and needed Minipress tds. Can you comment on the
usefulness of 24-hour BP monitoring
and on tds regimens?
Twenty-four-hour BP monitoring is a
well-validated method of BP measurecont’d page 34
References
Available on request from
julian.mcallan@
reedbusiness.com.au
Further reading
1. Rudd P. Clinicians and
patients with hypertension:
unsettled issues about
compliance. American Heart
Journal 1995; 130:572-79.
2. Yakovlevitch M, Black
HR. Resistant hypertension
in a tertiary care clinic.
Archives of Internal Medicine
1991; 151:1786-92.
Online resources
For GPs
Caring for Australians with
Renal Impairment (CARI):
www.cari.org.au
■ The seventh Joint
National Committee on the
Prevention, Detection,
Evaluation and Treatment
of High Blood Pressure:
www.nhlbi.nih.gov/
guidelines/hypertension/
express.pdf
■ National Heart Foundation
Hypertension Management
Guide for Doctors 2004.
www.heartfoundation.
com.au/downloads/
hypertension_management_
guide_2004.pdf
■ National Heart Foundation
patient information guide
to blood pressure, selfmeasurement and dietary
salt intake:
www.heartfoundation.com.
au/index.cfm?page=141
■
For GPs and patients
■
National High Blood
Pressure Education
Program:
www.nhlbi.nih.gov/
guidelines/hypertension
AD_HTT_025_034___APR20_07 13/4/07 8:57 AM Page 34
How to treat – resistant hypertension
from page 32
ment that correlates closely
with vascular risk and outcomes, and with surrogate
markers of target-organ
damage (eg, left ventricular
hypertrophy and albuminuria).
The main indications for
this investigation include:
■ Possible white-coat hypertension in patients with
newly discovered hypertension and no target-organ
injury.
■ Borderline/labile hypertension.
■ Poor BP control or loss of
BP control despite appropriate therapy and patient
compliance (as in this case).
■ Satisfactory clinic BP but
progressive target-organ
damage.
Adding medications with
twice- or thrice-daily dosing
(eg, hydralazine, methyldopa)
is a useful strategy that should
be considered in patients with
resistant hypertension, to
obtain better 24-hour BP control. Prazosin (Minipress) can
sion. How common is it for a
treatable cause to be found?
Treatable causes have been
reported to occur in up to
40% of cases of therapy-resistant hypertension, although in
my own (albeit skewed) experience, the figure is probably
closer to 5-10%.
certainly be administered tds,
but medication intolerance
(eg, postural lightheadedness
and nasal stuffiness) is often
limiting with this regimen.
Stopping vitamin E resulted in
improved BP control. Can
you comment on herbal and
vitamin contribution to BP?
A recently published randomised, double-blind placebocontrolled trial has demonstrated that vitamin E can raise
both systolic and diastolic BP
by average values of 7 and
11
5mmHg, respectively.
Many herbal products contain considerable amounts of
glycyrrhizic acid, which can
cause aldosterone-like effects,
including hypertension and
hypokalaemia. Examples
include herbal cough mixtures, licorice tea, licorice root,
gancao and Boui-ougi-tou (a
mixture of Chinese drugs
intended to cure obesity).
Glycyrrhiza glabra and
Glycyrrhiza radix have the
same effect and can be found
General questions for the
author
in most Chinese herbal teas.
Ma huang, used to treat
asthma, colds and flus, contains about 1% ephedrine and
has the potential to induce
hypertension. It is also noteworthy that this patient was
receiving tibolone, which is
associated with hypertension
in 2-3% of cases and can raise
the plasma ARR.
Despite extensive investigation, Marie has not been
found to have a cause for
treatment-resistant hyperten-
How to Treat Quiz
2. Which TWO statements about the taking of
BP readings are correct?
❏ a) Using a BP cuff size that is too small for the
patient’s arm can result in a falsely low
reading
❏ b) The cuff bladder length should be at least
80% of the circumference of the upper arm
❏ c) Recent cigarette smoking has no effect on
BP readings
❏ d) Older patients may have a falsely high BP
reading due to a hardened brachial artery
3. Con, 62, presents as a new patient for a
BP check and repeat prescription of his
antihypertensive medication. He has been
taking atenolol 50mg daily for six months
and has been adherent with therapy. His
BP is 165/98mmHg. Which THREE reasons
could explain why Con’s BP is inadequately
controlled?
❏ a) He is one of the 30% of patients who need
more than one antihypertensive medication
❏ b) He has taken some celecoxib daily for the
past few weeks for arthritis
❏ c) He has been eating liquorice recently
❏ d) He eats a diet high in salt
4. You arrange a serum creatinine test, eGFR
and dipstick urinalysis for Con. His eGFR is
2
46mL/min/1.73m and his urine protein
reading is 1+. He takes no other medications
regularly and has no significant past history.
Physical examination reveals no renal bruits
or masses. Which TWO statements about
Con’s further management are correct?
❏ a) He should have a renal ultrasound scan
and a protein:creatinine ratio test
❏ b) He should have a non-dihydropyridine
calcium-channel blocker (such as diltiazem)
added to his treatment regimen
❏ c) The best diuretic choice for Con is a
thiazide diuretic
❏ d) Con has stage 3 chronic kidney disease
and should be prescribed an ACE inhibitor or
angiotensin-II-receptor antagonist
5. In choosing appropriate antihypertensive
medication for patients with resistant hypertension which TWO statements are correct?
❏ a) It is better to combine several medications
at low doses than to increase a single agent
to its maximal dose
❏ b) All treatment regimens in patients with
resistant hypertension should ideally include a
diuretic
❏ c) A potential side effect of minoxidil is fluid
retention and heart failure
❏ d) Calcium-channel blockers can potentiate
glaucoma
6. Melinda, 24, presents for contraceptive
advice. She has been previously well, takes
no medication and has not seen a doctor for
several years. Her BP at this visit is
180/100mmHg, checked twice. The remainder of her physical examination is unremark-
Can you explain the advantage of renal imaging with and
without captopril? When
should you definitely use captopril and when should you
definitely not?
Isotope renography without
captopril has a false-negative
rate of 20-25%. Administering oral captopril (25-50mg)
one hour before the isotope is
injected increases the positive
and negative predictive values
of radioisotope scanning by
often augmenting the differential uptake of isotope
between the left and right kidneys in the setting of unilateral renal artery stenosis.
This effect is based upon
the typical ACE-inhibitorinduced decline in GFR in the
stenotic kidney, often accompanied by an equivalent
increase in GFR in the contralateral kidney due to
removal of angiotensin IImediated vasoconstriction.
In the setting of bilateral
renal artery stenosis this test
remains relatively insensitive
(although may be detected by
a delay in the peak uptake of
isotope to more than 10-11
minutes) and the ACE
inhibitor may be potentially
harmful to kidney function.
The 2005 American College of Cardiology and American Heart Association guidelines recommend that the
captopril renogram not be
used as a screening test for
the diagnosis of renal artery
stenosis. I prefer renal artery
duplex or isotope renography
without captopril.
INSTRUCTIONS
Complete this quiz to earn 2 CPD points and/or 1 PDP point by marking the correct answer(s) with an X on this form.
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FAX BACK
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Resistant hypertension
— 20 April 2007
1. Which TWO statements about
hypertension in general practice are correct?
❏ a) 29% of Australian adults have
hypertension
❏ b) Blood pressure is adequately controlled in
about half of people with hypertension
❏ c) Resistant hypertension is defined as an
inability to reduce BP to <140/90mmHg using
three antihypertensive medications
❏ d) In general practice about one-quarter of
patients with hypertension have resistant
hypertension
In cases of white-coat hypertension I have often asked for
a home BP record. How reliable are home BP machines?
Most semi-automated
upper-limb home BP measuring devices are generally quite
reliable, provided an appropriate cuff size is used. However, wrist and finger devices
are not recommended.
Home BP measurements
are often more reproducible
than office pressure measurements and demonstrate
a superior correlation with
cardiovascular risk and
prognosis. Their accuracy
approaches that of 24-hour
BP monitoring (awake average pressure), although there
is a group of patients (especially elderly women) whose
white-coat effect persists
with self measurement.
Home BP machines may
also aid in compliance by
involving patients in their
own management. It is worth
remembering that an office
BP of 140/90mmHg is probably equivalent to a home BP
of about 135/85mmHg.
FREE POST
How to Treat quiz
Reply Paid 60416
Chatswood DC NSW 2067
able. She has no personal or family history of
hypertension. You think Melinda may have
secondary hypertension. Which THREE
conditions could be causing this?
❏ a) Phaeochromocytoma
❏ b) Renal artery stenosis
❏ c) Addison’s disease
❏ d) Conn’s syndrome
ONLINE
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for immediate feedback
❏ b) Alcohol consumption at any level tends to
increase blood pressure
❏ c) Restricting salt to <90mmol/L/day can
result in a 5-7mmHg drop in systolic blood
pressure
❏ d) Roger should aim to achieve a waist
circumference of ≤94cm
7. Melinda returns in a week and her BP is still
at the same level. Which TWO statements
about further investigation of Melinda’s
hypertension are correct?
❏ a) A normal serum potassium result
effectively excludes primary
hyperaldosteronism
❏ b) An elevated plasma aldosterone:renin ratio
is diagnostic of primary hyperaldosteronism
❏ c) Melinda should have a renal artery duplex
or isotope renography to check for
renovascular hypertension
❏ d) Melinda’s blood tests should include
thyroid function tests and serum calcium level
9. After three months Roger returns for review.
He has lost 2kg in weight but had not been
able to significantly change his diet and exercise habits. His BP is 155/95mmHg and you
decide to start him on an ACE inhibitor. After
two weeks on this medication his repeat blood
test shows his creatinine has increased to
110µmol/L, from a baseline level of 95µmol/L.
Which ONE action would you now take?
❏ a) Stop Roger’s ACE inhibitor
❏ b) Arrange a renal angiogram
❏ c) Continue the ACE inhibitor and repeat the
serum creatinine test in a few more weeks
❏ d) Switch from the ACE inhibitor to an
angiotensin-II-receptor antagonist
8. Roger, 48, has recently been diagnosed
with hypertension, with BP readings of about
160/95mmHg. He smokes 15 cigarettes daily,
has a BMI of 29, with total cholesterol
5.4mmol/L and LDL-C 3.0mmol/L. He has no
family history of cardiovascular disease,
takes no medications and has a normal blood
sugar level, electrolytes, serum creatinine and
eGFR. Roger is keen to avoid taking medications and you discuss lifestyle modifications
with him. Which THREE statements about
lifestyle interventions for Roger are correct?
❏ a) If Roger lost 10kg in weight, this could
result in up to a 20mmHg drop in his systolic
blood pressure
10. Which TWO statements about managing
resistant hypertension are correct?
❏ a) Patients with renal impairment need
fewer medications to control their blood
pressure than patients with normal renal
function
❏ b) The combination of an ACE inhibitor,
diuretic and NSAID should be avoided, as it
can result in acute renal failure
❏ c) Patients taking spironolactone should be
monitored for hypokalaemia
❏ d) A secondary cause for hypertension
should be suspected when there is an acute
rise in blood pressure over a previously stable
value
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HOW TO TREAT Editor: Dr Marcela Cox
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Quiz: Dr Marcela Cox
The mark required to obtain points is 80%. Please note that some questions have more than one correct answer. Your CPD activity will be updated on your RACGP records every January, April, July and October.
NEXT WEEK Both macroscopic and microscopic haematuria may be a sign of serious underlying disease. The next How to Treat focuses on microscopic haematuria, which is usually asymptomatic. The
author is Associate Professor Timothy Mathew, nephrologist, department of medicine, Queen Elizabeth Hospital, Adelaide; and national medical director, Kidney Health Australia.
34
| Australian Doctor | 20 April 2007
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