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92 Chapter 5 Hypertension
immediate relief in asthma. As a result, -adrenoceptor
antagonists are usually avoided for asthmatics. Not
surprisingly, there has been considerable interest in
developing 1-adrenoceptor selective antagonists. e
following drugs are described as selective for 1- over
2-adrenoceptors (cardioselective): bisoprolol, atenolol,
metoprolol, and nebivolol. Importantly, though, none of
these drugs are devoid of antagonism at 2-receptors, and
therefore should be avoided for asthmatics where
possible.
-Blockers can aect carbohydrate metabolism by
blocking 2-adrenoceptors on hepatocytes which, when
stimulated, mediate glycogenolysis to supplement
circulating glucose levels. ose drugs with signicant
2-adrenoceptor activity are best avoided for diabetics
who have compromised control of blood glucose levels;
the cardioselective drugs should preferentially be
prescribed.
Partial agonists Partial agonists such as oxprenolol and
pindolol occupy -adrenoceptors, weakly stimulating
them. In doing so, they act to antagonize the stronger
stimulation which would result from noradrenaline or
adrenaline occupying those receptors. Such drugs may be
expected, therefore, to smooth out the peaks and troughs
of activity at these receptors.
Combined - and -adrenoceptor antagonists Given
the signicance of 1-adrenoceptors in maintaining
peripheral resistance, a drug with combined antagonist
action at 1- and -adrenoceptors would appear desirable
for use in the treatment of hypertension: carvedilol and
labetalol are two examples.
All these drugs are available for oral administration. Some
are also available for intravenous use; for example,
labetalol can be given as an intravenous infusion in a
hypertensive crisis. e duration of action varies but,
where this is short, modied-release preparations are
usually available to enable once-daily dosing.
Adverse eects of -adrenoceptor antagonists Adverse
eects mainly follow predictably from their mode of
action, and include bradycardia and heart block, heart
failure, and disorders of electrical conductance in the
heart. Fatigue is often reported—the combined result of
decreased cardiac output and vasoconstriction in the
vascular beds of skeletal muscle. Coldness of the
extremities is also commonly experienced, resulting from
reduced vasodilatation. e drugs acting as partial
agonists tend to cause less bradycardia, and less coldness
of the extremities, than other -blockers. Sleep
disturbance is associated with the more lipid-soluble
drugs, such as propranolol, which readily cross the
blood–brain barrier.
5.2.6 Other drugs available to treat
hypertension
e drugs described above provide tools for adequately
controlling blood pressure in the majority of patients
presenting with uncomplicated hypertension. However, a
number of other drugs are available that may be used
where there are unusual hypertensive issues. ese
include patients who present with extremely high blood
pressures (e.g. 220/120 mmHg systolic/diastolic), with
blood pressures resistant to the mainstream strategy, or
with other relevant conditions such as heart failure or
arrhythmias.
Vasodilators
is group of agents includes the widely employed
1-adrenoceptor antagonists mentioned above, and in
addition the following less commonly used drugs.
In Workbook 2 Andreas presents with a blood pressure of
210/135 mmHg, requiring immediate treatment, and the
possibility of using sodium nitroprusside is introduced.
Sodium nitroprusside acts as a nitric oxide (NO) donor—
the NO enters the vascular smooth muscle cells,
stimulating the synthesis of cyclic GMP and causing a
rapid and profound vasodilatation (Box 5.2) of both
arterial and venous smooth muscle. is generally
produces a rapid reduction in blood pressure, after which
sodium nitroprusside is discontinued and a long-term
blood pressure management strategy is pursued. Sodium
nitroprusside has a very short half-life and so must be
given as an intravenous infusion. Its use is associated with
two major disadvantages.
• It brings about very rapid blood pressure reduction,
which is not usually desirable and can have serious
adverse consequences. Use must be carefully
monitored.
• A product of decomposition is cyanide which can
accumulate and cause toxicity; use of sodium
nitroprusside is therefore limited to the short-term.
Patients must be monitored for cyanosis (see Workbook
2) which can manifest as tachycardia, sweating,
hyperventilation, or arrhythmias. is toxicity can be
counteracted with sodium thiosulphate.
5.2 Antihypertensive drugs 93
Vascular endothelial cells
Box 5.2
The vascular nitric oxide system
NO
Vascular smooth
muscle cells
Guanylyl cyclase
Cyclic GMP
Vasodilatation
Figure b Nitric oxide (NO) release from vascular
endothelium and its effect on vascular smooth muscle
cells.
Endothelial cells are shown in grey and smooth muscle cells in
orange.
Nitric oxide (NO) is a major endothelium-derived
relaxing factor (EDRF), and is released from
endothelial cells in response to many vasodilating
inuences (e.g. shear stress and pressure from the
blood passing over the endothelium, as well as
stimulation of receptors for bradykinin or ACh). NO is
a very small molecule—once synthesized it passes
through membranes and drifts out of the cells—and
its rate of release is therefore determined by its rate of
synthesis. NO is unstable once released, so only
NO donor (e.g.
NO
inuences cells locally and does not survive to
circulate in the blood. e NO released from
endothelial cells can also pass into the blood vessel
lumen where it exerts a local antiplatelet eect (see
Chapter 4, Box 4.3, Figure d). Various drugs interact
with the NO system. ese include NO donors such as
sodium nitroprusside and GTN, which enter the
smooth muscle cells, interact with intracellular
protein SH groups, and form NO inside the target cells,
bringing about vasodilatation.
sodium
nitroprusside,
glyceryl trinitrate)
NO
For these reasons the use of sodium nitroprusside in
hypertensive crises is in decline.
Glyceryl trinitrate (GTN) is similarly a NO donor and
very eectively causes widespread vasodilatation,
preferentially of venous capacitance blood vessels. is
reduces venous return, and therefore also end-diastolic
volume, with the result that cardiac output (and hence
blood pressure) is reduced (see Section 5.1.3). Like
sodium nitroprusside, GTN has a short half-life and can
be administered by intravenous infusion for a rapid
response in a hypertensive crisis. GTN is now used for this
indication more widely than sodium nitroprusside, as its
use is not complicated by the danger of cyanosis. e
vasodilatory properties of GTN also provide rapid relief
from the symptoms of angina (see Chapter 6) when it is
most usually administered sublingually, thereby avoiding
94 Chapter 5 Hypertension
extensive rst-pass metabolism. Tolerance to organic
nitrates must be considered when using longer-acting
nitrates in the treatment of angina (see Chapter 6, Section
6.3.5). is does not, however, present an obstacle to the
short-term use described here to control a hypertensive
crisis.
Minoxidil is a potassium channel activator which
favours movement of K+ out of vascular smooth muscle
cells, leading to their hyperpolarization and
concomitant reduction in contractility. It is reserved for
severe drug-resistant hypertension. It must be used
together with a -blocker and diuretic to prevent its
associated increases in cardiac output and uid
retention. Amongst its side eects is hypertrichosis, or
excessive hair growth all over the body, making it
unsuitable for women. is eect, though, is taken
advantage of in its topical use in the treatment of
alopecia. Diazoxide is another K+ channel activator
available (by intravenous injection) in cases of
hypertensive emergency including that associated with
renal disease. Hydralazine is a vasodilator mainly on the
arterial side, acting in a poorly understood manner to
interfere with mechanisms of Ca2+ elevation. Like
minoxidil, it is used as adjunct therapy which controls
unwanted eects.
Centrally acting sympatholytics
A sympatholytic drug is one that reduces the inuence of
the sympathetic nervous system. Centrally acting
sympatholytics act in the brain to reduce the amount of
sympathetic activity, and so decrease noradrenaline
release from nerve terminals in the cardiovascular system
and elsewhere.
Methyldopa is metabolized into -methylnoradrenaline,
which is an agonist at brain 2-adrenoceptors. is
accumulates in the vesicles of noradrenergic terminals and
is released instead of noradrenaline. is agonist provides
a greater stimulation of the presynaptic 2-receptors
compared with the endogenous ligand. Since stimulation
of these receptors in the brain and elsewhere inhibits the
further release of noradrenaline, the eect of methyldopa
is to reduce sympathetic activity. Methyldopa is used for
the management of hypertension during late pregnancy,
as adverse eects on the baby are deemed to be lower than
with alternatives. Side eects typically include sedation.
Clonidine is a direct 2-adrenoceptor agonist that
similarly inhibits noradrenaline release, principally by its
action in the brain, but it is only rarely used. Moxonidine
is an antihypertensive agent, which also reduces
sympathetic outow by a central mechanism.
5.3 Strategies for the drug treatment of hypertension
When deciding about antihypertensive drug treatment
ve questions should be considered.
1) What comorbidities (other known illnesses or
conditions) are present?
2) Have non-drug measures been attempted?
3) What is the threshold for treatment?
4) How urgent is treatment?
5) What are the target blood pressures the treatment is
aiming to achieve?
e coexistence of additional medical conditions will
inuence the threshold for treatment. For example, this may
be lowered, and there may be a greater urgency for drug
treatment in the mid-hypertensive range if there is evidence
of cardiovascular complications, end-organ damage (e.g.
kidney or retina), diabetes, or a 10-year risk of over 20% (e.g.
with concurrent dyslipidaemias; see Chapter 6).
Non-drug measures refer to lifestyle changes, including
stress reduction, smoking cessation, exercise regimes,
etc. ese should be pursued in all patients with
hypertension and may be the only interventions
necessary, particularly for those with mild hypertension
and at low risk.
5.3.1 Thresholds and urgency
When considering thresholds for treating, the following
may act as a guide.
• Sustained (repeated measurements over months)
blood pressures between 140 and 159 mmHg systolic or
90 and 99 mmHg diastolic are treated with lifestyle
guidance and, if this is not sucient, with drugs, with
the target of bringing readings down to below 140/90
mmHg.
• A patient with recorded blood pressures of 160–179
mmHg systolic or 100–109 mmHg diastolic should be
reassessed weekly over 3–4 weeks; if readings are
consistent, despite lifestyle advice, drug therapy should
be initiated.
5.3 Strategies for the drug treatment of hypertension 95
• Patients with pressures of 180–219 mmHg systolic or
110–119 mmHg diastolic maintained over 1–2 weeks
should be prescribed drugs without delay.
• Pressures of 220 mmHg systolic or 120 mmHg diastolic
or above indicate a hypertensive crisis that should be
treated immediately.
5.3.2 Target blood pressures
Treatment of hypertension usually aims to achieve target
blood pressures of <140/90 mmHg. However, if
complications exist, which include diabetes and chronic
kidney disease, targets are likely to be set lower (typically
<130/80 mmHg).
5.3.3 Dangers of overtreating hypertension
and the ‘J curve’
ere are two commonly encountered situations when
concerns may be raised about drug treatments that bring
down hypertension too far or too quickly.
1) e use of intravenous vasodilators to very rapidly
reduce blood pressure in hypertensive crises can be
associated with organ damage, and this approach is now
less popular (this is further explored in Workbook 2).
2) e management of a standard hypertensive patient—
is there a danger in setting the target too low
(sometimes described as the ‘J curve’)? ere is some
evidence that excessive pharmacological reduction of
diastolic blood pressure (e.g. below 80 mmHg) may
reduce coronary blood ow during diastole, increasing
the risk of myocardial infarction (MI) in certain patients
(e.g. those with a history of coronary artery disease).
We have described hypertension as a symptomless
disease, but in Workbook 2 we encounter Andreas, who
suers persistent headaches and an acute attack of
dizziness and confusion. He presents with pressures of
210/135 mmHg and is treated as a case of hypertensive
crisis illustrating that, at the upper end, hypertension
may not be symptom-free. ese very high blood
pressures should be treated with urgency. ey are
associated with end-organ damage (e.g. damage to
kidney or retina) and a much enhanced risk of major
cardiovascular incidents, such as MI or stroke.
Andreas’s case illustrates two other aspects of
hypertension treatment.
• Only one measurement, his diastolic pressure of
140 mmHg, fell within the highest category in the
scheme set out above. e categories are dened by the
highest of either systolic or diastolic pressure; both do
not need to be above the cut-o to meet the denition.
• He has previously been diagnosed as hypertensive and
prescribed drugs, but has not maintained his drug
therapy. Poor compliance is understandably
commonplace, particularly as in the vast majority of
hypertension cases there are no symptoms. Andreas’s
poor compliance contributes to his crisis.
5.3.4 Recommendations for treating
hypertension
Combining the clinical pharmacology, the outcome of
trials, and clinical experience to create a strategy for the
treatment of hypertension across the population is
demanding. It is not surprising that strategies vary between
countries and are subject to change. e same ve classes of
drugs are prescribed universally: thiazide diuretics, ACE
inhibitors, angiotensin receptor blockers (ARBs), calcium
channel blockers, and -blockers. Recommendations
between countries dier in the order in which drugs from
each of the classes are prescribed, and also in the degree of
choice oered to the prescriber. Reaching blood pressure
targets with a single drug should always be the rst objective
of drug treatment. However, for the majority of patients,
regardless of which drug is administered rst, monotherapy
will not be sucient to reach target blood pressure. As
patients receive additional drugs the dierences between
recommendations start to lose their signicance.
It is of note, though, that as far as -adrenoceptor
antagonists are concerned, substantive dierences do
exist. In the UK there has been a downgrading of their role
over a number of years—rstly removing this class of drug
as recommended for rst-line treatment and, more
recently, relegating it to possible use as a fourth-line drug
(Figure 5.10). Elsewhere in Europe, and in the USA, there
has been no such change—rather, other drugs have risen in
prole to compete with -blockers as mainstream therapy.
It should always be remembered that the actual choice of
drug will depend on the individual patient, most notably
if other clinical conditions coexist. For example,
asthmatic patients should not be prescribed
-adrenoceptor antagonists (see Section 5.2.5).
In the UK, the recommended drug choice strategy for
uncomplicated hypertension, typically presenting
repeatedly with pressures in the region of 140–179 mmHg
systolic and 90–109 mmHg diastolic, is dened by the
96 Chapter 5 Hypertension
Person aged under 55
Step 1
Step 2
Step 3
Step 4
Figure 5.10 A scheme in use in the UK for prescribing to newly diagnosed
hypertensive patients.
*Black is defined as of African or African Caribbean origin
A: ACE inhibitor or ARB C: Ca
A + C + D: thiazide diuretic
Add α-blocker orβ-blocker
plan set out in Figure 5.10. In this scheme, initial
treatment is guided by the expected contribution of the
RAAS to the patient’s hypertension according to his/her
age and race. e scheme is divided on this basis; patients
having less RAAS involvement (black people of African or
African Caribbean origin, who are known to have reduced
renin activity) are less likely to respond well to ACE
inhibitors. Note also that ACE inhibitors can be replaced
by ARBs as necessary, for example as discussed above for
those patients who develop an unacceptable cough.
Beyond step 1, though, and as more drugs are added, the
distinction between the two groups disappears.
e scheme is only intended as a guide for newly
diagnosed patients, and does not direct prescribers to
change the treatment for those whose medication is
already established so as to t into this scheme.
In Australia the National Prescribing Service
recommends low-dose thiazides as initial treatment for
Person aged over 55
or black* person of any age
2+
channel blocker
A + C
most patients, ACE inhibitors in patients with diabetes,
and calcium channel blockers or -blockers in patients
with angina.
Understanding the physiological control of blood
pressure enables the prescriber to understand, up to a
point, why certain drug combinations are optimal for use
in hypertension. For example, the eects of ACE
inhibitors on cardiac output and vasculature through
attenuation of the RAAS, complement a dihydropyridine
calcium channel drug, which mainly aects the
vasculature and peripheral resistance. From a
mechanistic point of view it can then be predicted that
adding a diuretic, with its independent eects on blood
volume and cardiac output, has additional eects beyond
those of ACE inhibition and calcium channel blockade.
In this way it is possible to understand the
pharmacological basis of strategies for drug treatment of
hypertension.
Key references and suggested reading
Chaplin S, McInnes G. ARBs: concise guide to properties and
recommended use. Prescriber 2009; 20(7); 40–1.
Law MR, Morris JK, Wald NJ. Use of blood pressure lowering
drugs in the prevention of cardiovascular disease: metaanalysis of 147 randomised trials in the context of
expectations from prospective epidemiological studies. BMJ
2009; 338: b1665.
Moser M, Setaro JF. Resistant or dicult-to-control
hypertension. New Engl J Med 2006; 355: 385–92.
NICE. Hypertension: management of hypertension in adults in
primary care. http://www.nice.org.uk/CG34
Ooi S-Y, Ball S. ACE inhibitors: their properties and current role
in hypertension. Prescriber 2009; 20(14): 15–28.
SUMMARY OF DRUGS USED FOR HYPERTENSION
5.3 Strategies for the drug treatment of hypertension 97
Therapeutic class Drugs Mechanism of action Common clinical
uses
ACE inhibitors ’pril drugs e.g.
Angiotensin II
receptor
blockers (ARBs,
A2RAs)
Renin inhibitors Aliskiren Direct inhibitor of renin leads to
Thiazide diuretics Bendroflumethiazide
Loop diuretics Furosemide
Captopril
Enalapril
Fosinopril
Lisinopril
Ramipril
Sartans e.g.
Candesartan
Losartan
Olmesartan
Telmisartan
Valsartan
Thiazide-related:
Chlortalidone
Indapamide
Bumetanide
Inhibit conversion of angiotensin I
to angiotensin II by ACE. Leads to:
a) reduced peripheral resistance
b) reduced aldosterone secretion
c) bradykinin accumulation
Antagonist at AT1 receptor for
angiotensin II
Leads to:
a) reduced peripheral resistance
b) reduced aldosterone secretion
reduced conversion of
angiotensinogen to angiotensin I
Inhibit reabsorption of Na+ in the
distal tubule of the kidney to
promote loss of Na+ and water in
urine leading to decreased plasma
volume
Additional sustained vasodilatory
action (mechanism poorly
understood)
Block reabsorption of Na+, K+, and
Cl– (and therefore water) in thick
ascending limb of loop of Henle
Powerful diuretic effect
Additional vasodilatory effect
(mechanism not understood)
Hypertension
Ischaemic heart disease
Heart failure
Diabetic nephropathy
Hypertension
Ischaemic heart disease
Heart failure
Diabetic nephropathy
Hypertension Metabolized by hepatic P450
Heart failure
Hypertension
Oedema
Resistant hypertension
(combined with thiazide
diuretic)
Heart failure
Pulmonary oedema
Other oedematous states
Comments Common adverse drug reactions
Pharmacokinetics vary widely
Captopril has shortest half-life
(about 2 h), others have longer
e.g. enalapril, 11 h
Bradykinin accumulation likely
to underlie dry cough and
angioedema
Because of higher cost,
usually reserved for secondline use in patients who
cannot tolerate ACE inhibitors
(e.g. due to persistent cough)
enzymes (CYP3A4) leading to
interactions
Long half-life of about 24 h
Relatively new class/drug
Act within 1–2 h of oral
administration
Duration of action about 12 h
Can exacerbate gout and
diabetes
Quick onset of effect (within 1
h of oral administration) and
duration of about 6 h
Hypotension (particularly after first dose)
Renal impairment (risk may be increased by
concomitant use of NSAIDs and diuretics)
Dry cough
Upper respiratory tract infections
Persistent angioedema
Rash and anaphylactic reactions
Hyperkalaemia
Hypotension (particularly after first dose)
Renal impairment (risk may be increased by
concomitant use of NSAIDs and diuretics)
Hyperkalaemia
Diarrhoea
Dizziness
Hyperkalaemia
Rash
Increased urinary frequency
Mild GI disturbance
Hypokalaemia
Hyperglycaemia (risk of diabetes)
Hyperuricaemia (risk of gout)
Hypercalcaemia
Erectile dysfunction
Headache
Dizziness
Increased urinary frequency
Mild GI disturbance
Pancreatitis
Postural hypotension
Hypokalaemia
Hyperglycaemia
Headache
Dizziness
98 Chapter 5 Hypertension
Therapeutic class Drugs Mechanism of action Common clinical
uses
Calcium channel
blockers
Selective
1-adrenoceptor
antagonists
Dihydropyridines,
-dipines e.g.
Amlodipine
Felodipine
Lercanidipine
Nifedipine
Non-dihydropyridines:
(1) Verapamil Blocks L-type calcium channels
(2) Diltiazem Blocks L-type calcium channels in
Doxazosin
Indoramin
Prazosin
Terazosin
Block L-type calcium channels
predominantly on vascular smooth
muscle to cause vasodilatation
predominantly in heart to cause
reduction in heart rate and force of
contraction
Some vasodilatory effects through
inhibition of calcium channels on
vascular smooth muscle
heart and blood vessels
Antagonist at 1 adrenoceptor
Causes arterial and venous
dilatation
Hypertension
Prophylaxis of angina
Hypertension
Angina
Supraventricular
arrhythmias
Hypertension
Angina
Hypertension
BPH
Comments Common adverse drug reactions
Amlodipine has long duration
of action
Others given once daily as
slow-release formulations
Eliminated by liver
Used as add-on therapy in
hypertension
Doxazosin and terazosin have
longer duration of action
First-dose hypotension may
be pronounced
Useful for patients with
hypertension and BPH
Abdominal pain
Hypotension
Nausea
Palpitations
Flushing
Ankle oedema
Headache
Dizziness
Reflex tachycardia (particularly with
short-acting formulations of nifedipine)
Constipation
Nausea
Vomiting
Heart block
Bradycardia
Cardiac failure
Bradycardia
Heart block
Palpitations
Dizziness
Hypotension
Headache
GI disturbance
Ankle oedema
Postural hypotension
Fainting
Drowsiness
Urinary urgency
Dizziness
Headache
5.3 Strategies for the drug treatment of hypertension 99
Non-selective
1- and
2-antagonists
-adrenoceptor
antagonists
(-blockers)
Combined 1 and
adrenoceptor
antagonist
Vasodilators
1. Selective
1-adrenoceptor
antagonists
2. NO donors Sodium nitroprusside
Phenoxybenzamine
Phentolamine
Propranolol
Atenolol
Bisoprolol
Metoprolol
Nebivolol
Oxprenolol
Pindolol
Labetalol
Carvedilol
See above
Glyceryl trinitrate
(GTN)
Block effects of adrenaline and
noradrenaline at 1- and
2-adrenoceptors leading to
vasodilatation
Block action of noradrenaline and
adrenaline at -adrenoceptors to
reduce cardiac output and
secretion of renin
As above with additional
antagonist action at 1-receptors
to reduce peripheral resistance
Nitric oxide donors
Potent vasodilator acting through
increased cGMP levels to
counteract vascular smooth
muscle contraction
Hypertensive crises
caused by
phaechromocytoma
Hypertension
Angina
Arrhythmias
Ischaemic heart disease
Heart failure (not all drugs
used)
Hypertension in
pregnancy (labetalol)
Anxiety
Prophylaxis of migraine
Hypertensive crisis
Controlled hypotension
during surgery to
minimize bleeding
Acute or chronic heart
failure
Phenoxybenzamine binds
irreversibly and has long
duration of action
Phentolamine is shorter acting
Pronounced reflex tachycardia
results from blockade of
presynaptic 2-receptors,
leading to increased
noradrenaline release
Selectivity for receptor
subtypes varies
None is specific for
1-receptors, therefore
avoided in asthmatics
Oxprenolol and pindolol are
partial agonists
Pharmacokinetics vary widely
Sodium nitroprusside
converted to thiocyanate in
body which can accumulate
and cause toxicity
Rarely used because of risk of
cyanosis
Reflex tachycardia
Postural hypotension
Dizziness
Drowsiness
Fatigue
Bronchospasm
Bradycardia
Heart failure
Conductance disorders
Fatigue
Headache
GI disturbance
Dyspnoea
Coldness of extremities
Sleep disturbance
(Partial agonists may have less pronounced
adverse effects)
Resulting from over-rapid reduction in blood
pressure:
headache
dizziness
nausea
abdominal pain
Resulting from cyanide toxicity (sodium
nitroprusside):
tachycardia
hyperventilation
arrhythmias
sweating
100 Chapter 5 Hypertension
Therapeutic class Drugs Mechanism of action Common clinical
Comments Common adverse drug reactions
uses
3. K+ channel
activators
4. Other Hydralazine Short-term treatment of
Centrally acting
sympatholytics
ACE, angiotensin converting enzyme; BPH, benign prostatic hyperplasia; GI, gastrointestinal; NO, nitric oxide; NSAID, non-steroidal anti-inflammatory drug
Minoxidil
Diazoxide
Methyldopa
Clonidine
Moxonidine Agonist at central imidazoline-I-1
Activate K+ channels to
hyperpolarize and cause relaxation
of vascular smooth muscle cells
Direct (clonidine) or indirect
(methyldopa) stimulation of
presynaptic 2-receptors leading
to reduced sympathetic outflow
from the brain
and 2 adrenoceptor
Resistant hypertension
Alopecia (minoxidil)
severe hypertension in
pregnancy
Hypertension
Prophylaxis of migraine
(clonidine)
Menopausal flushing
(clonidine)
Hypertension Not to be used in renal
Minoxidil always used in
combination with diuretic and
-blocker to avoid unwanted
cardiac effects and fluid
retention
Used rarely
Adjunct therapy only
Methyldopa can be used in
pregnancy
impairment
Tachycardia
Hypotension
Sodium and water retention
Hypertrichosis (excessive hair growth)
Headache
Tachycardia
Palpitation
Flushing
Hypotension
Fluid retention
Sedation
GI disturbance
Headache
Dizziness
Dry mouth
Weight gain
Tachycardia
WORKBOOK 2
Hypertension
Andreas, a non-compliant patient. A case of hypertensive
The patient: a simplified case history
The day of Monique and Andreas’s wedding has finally arrived. Andreas has arrived at the
RegisterOfce30minutesearly,anxiousfornothingtogowrong.Hesitsandwaitswithhis
father Brian and his brother Eoin, who is also his best man. Eoin is a world-renowned Formula 1
driver who has missed training to attend the wedding.
SuddenlyAndreasfeelsdizzyandwobbly;theheadachehehashadforthelastfewdayshas
got worse. He wonders if this has anything to do with his high blood pressure. His doctor keeps
trying to get him to take the treatment for this seriously. Eoin notices his pallor, but before he
can express his concern, Andreas says he needs to lie down. Eoin rings for an ambulance.
While in the ambulance, Eoin has to do all the talking because Andreas is too confused to be
coherent. Eoin tells the paramedics that although Andreas’s family doctor prescribed tablets for
his blood pressure six months ago, Andreas only took them for a few days, and then threw the
rest away. The paramedics take his blood pressure; it is extremely high, requiring urgent
hospitalization.
And so instead of getting married Monique rushes to the local hospital. She meets Dr Lucy
Knight, a young doctor, and confirms Andreas’s details, which were compiled with Eoin’s help.
A table of clinical clerking abbreviations is given on page xviii.
CLINICAL CLERKING FOR ANDREAS KAISER
Age: 37 years
PMH: Moderate hypertension, poorly controlled
SH: Lives with fiancée and twin daughters. Smokes 20 cigarettes a day. Weight 95 kg (overweight).
1) Smoking, like hypertension, increases the risk of having a stroke or heart attack, although there
is little evidence that long-term smoking leads to increased blood pressure.
2) Being overweight also contributes to high blood pressure.