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Fig 3.
https://t.me/med1917
17
Two
CXR
On the later image, a pericardial eusion has expanded the cardiac shadow and given it a ‘globular’ shape.
Reproduced from Leeson, Cardiovascular Imaging, 2011, with permission from Oxford University Press.
Fig 3.
stenosis.
S of t he sa me pa tie nt, t he on e on the r igh t was t ake n
18
Cardiac CT demonstrating coronary artery
Reproduced from Camm et al., ESC Textbook of
Cardiovascular Medicine,
2009
, with permission from
Oxford University Press.
6
months after the one on the left.
Fig 3.
19
Cardiac
MRI
asymmetrical left ventricular wall thickening typical of hypertrophic cardiomyopathy.
Cardiovascular Magnetic Resonance,
demonstrating the
Reproduced from Myerson et al.,
with permission from Oxford
2013
University Press.
101
3 Cardiovascular medicine
,
The story of Echo and Narcissus
Echo, in Greek mythology, was a mountain
nymph, or Oread. Ovid’s Metamorphoses,
III
, relates that Echo oended the
Book
goddess Hera by keeping her in conversation, thus preventing her from spying on
her husband Zeus who was with another
lover. To punish Echo, Hera deprived her of
speech, except for the ability to repeat the
last words of another. Echo’s own hopeless
love for the boy Narcissus, who fell in love
with his own image, made her fade away
until all that was left of her was her voice
fig
3.20
).
(
Fig 3.
20
Narcissus and Echo.
Engraving by F. Bartolozzi,
Wellcome Collection. Public Domain Mark.
Source: Wellcome Collection
1791
, after B. Luti.
3 Cardiovascular medicine
Echocardiography
M
TOE
LV
HCM
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102
This non- invasive technique uses the diering ability of various structures within
the heart to reflect ultrasound waves. It not only demonstrates anatomy but also
provides a continuous display of the functioning heart throughout its cycle.
Types of scan
- mode (motion mode) A single- dimension image.
Two- dimensional (real time) A 2D, fan- shaped image of a segment of the heart is
produced on the screen (
are possible, including parasternal long axis and short axis, apical
2D
subcostal.
heart disease,
echocardiography is good for visualizing conditions such as: congenital
LV
aneurysm, mural thrombus, LA myxoma, septal defects.
3D echocardiography Now possible with matrix array probes, and is termed 4D
3D
+ time) if the images are moving.
(
Doppler and colour- flow echocardiography Dierent coloured jets illustrate flow
and gradients across valves and septal defects (
Tissue Doppler imaging This employs Doppler ultrasound to measure the vel-
ocity of myocardial segments over the cardiac cycle. It is particularly useful for
assessing longitudinal motion— and hence long- axis ventricular function, which is
a sensitive marker of systolic and diastolic heart failure.
Contrast studies with Valsalva manoeuvre IV injection of saline after agitation
between two syringes enhances the back- scatter of the ultrasound beam, thus
highlighting venous blood flow. If the ‘bubbles’ generated are visualized in the left
heart chambers, this can indicate either intracardiac or transpulmonary shunting.
Tra ns oe so ph ag ea l ec ho ca rdi og ra ph y (
TTE
cardiography (
aortic dissections; assessing prosthetic valves; finding cardiac source of emboli; and
IE/ SBE
. Contraindicated in oesophageal disease and cervical spine instability.
) as the transducer is nearer to the heart. Indications: diagnosing
Stress echocardiography Used to evaluate ventricular function, ejection fraction,
myocardial thickening, regional wall motion pre- and post- exercise, and to characterize valvular lesions. Dobutamine or dipyridamole may be used if the patient
cannot exercise. Inexpensive and as sensitive/ specific as a thallium scan (
Uses of echocardiography
Quantification of global
ventricular impairment (or both). Echo helps by measuring end- diastolic volume. If
this is large, systolic dysfunction is the likely cause. If small, diastolic. Pure forms of
diastolic dysfunction are rare. Dierentiation is important because vasodilators are
less useful in diastolic dysfunction as a high ventricular filling pressure is required.
Echo is also useful for detecting focal and global hypokinesia,
thrombus, and
LVH
(echo is 5– 10 times more sensitive than
Estimating right heart haemodynamics Doppler studies of pulmonary artery flow
and tricuspid regurgitation allow evaluation of
Val ve dise ase The technique of choice for measuring pressure gradients and valve
orifice areas in stenotic lesions. Detecting valvular regurgitation and estimating its
significance is less accurate. Evaluating function of prosthetic valves is another role.
Congenital heart disease Establishing the presence of lesions, and significance.
Endocarditis Vege tati ons may n ot b e se en if <2mm in size.
best for aortic regurgitation (
leaflet perforation, or looking for an aortic root abscess.
Pericardial eusion Best diagnosed by echo. Fluid may first accumulate be-
tween the posterior pericardium and the left ventricle, then anterior to both
ventricles and anterior and lateral to the right atrium. There may be paradoxical
septal motion.
(p
130
) Echo features include asymmetrical septal hypertrophy, small LV cavity,
,
dilated left atrium
and systolic anterior motion of the mitral valve.
fig
3.21
); the moving image may be ‘frozen’. Several views
p
148
) (Doppler eect, p
) More sensitive than transthoracic echo-
function Heart failure may be due to systolic or diastolic
RV
function and pressures.
AR
).
TOE
is useful for visualizing mitral valve vegetations,
4
- chamber, and
LV
aneurysm, mural
ECG
in detecting this).
TTE
with colour Doppler is
720
).
p
725
).
103
(a)
Interatrial septum
t
Anterior leafle
https://t.me/med1917
(b)
Septum
Inferolateral
wall
MV
Posterior leaflet
(c)
(d)
Ventricular septum
TV
Lateral leaflet
Sepal leaflet
RV
Ascending
LV
t
RV
RA
aorta
LA
Descending
aorta
LV
LA
AV
Right coronary cusp
Non coronary cusp
Lateral wall
(papillary muscle
usually not seen)
MV
Posterior leafle
Anterior leaflet
3 Cardiovascular medicine
Fig 3.
21
Echo images. (a) A normal heart seen with the parasternal long- axis view. (b) Diagram of
can be seen in (c).
Reproduced from Leeson et al., Echocardiography,
Right upper pulmonary vein
2012
, with permission from Oxford University Press.
3 Cardiovascular medicine
Cardiac catheterization
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104
This involves the insertion of a catheter into the heart via the femoral or radial
artery or venous system, and manipulating it within the heart and great vessels to:
• Inject radiopaque contrast medium to image cardiac anatomy and blood flow, see
fig
3.22a
.
• Perform angioplasty (ballooning and stenting), valvuloplasty (eg transcatheter
aortic valve implantation (
septal defect closure.
• Perform electrophysiology studies and radiofrequency ablations.
• Sample blood to assess oxygen saturation and measure pressures.
• Perform intravascular ultrasound or echocardiography.
• During the procedure,
Indications
• Coronary artery disease: diagnostic (assessment of coronary vessels and graft pa-
tency); therapeutic (angioplasty, stent insertion), see
• Valvular disease: diagnostic (pressures indicate severity); therapeutic valvuloplasty
(if the patient is too ill or declines valve surgery).
• Congenital heart disease: diagnostic (assessment of severity of lesions by meas-
uring pressures and saturations); therapeutic (balloon dilatation or septostomy).
• Other: cardiomyopathy; pericardial disease (constriction indicated by equalization
of all intracardiac diastolic pressure); endomyocardial biopsy.
• Right heart catheterization: to confirm pulmonary hypertension in select cases,
assess contribution of left heart disease, vasoreactive testing before therapy.
Pre- procedure checks
• Brief history/ examination; NB: peripheral pulses, bruits, aneurysms.
• Investigations:
• Consent for procedure, including possible extra procedures, eg consent for angio-
FBC, U&E, LFT
plasty if planning to do angiography as you may find a lesion that needs stenting.
Explain reason for procedure and possible complications.
• Patient should be nil by mouth (
• Patients should take all their morning drugs (and pre- medication if needed)— but
withhold oral hypoglycaemics.
Post- procedure checks
• Pulse, BP, arterial puncture site (for bruising or swelling), foot pulses.
• Investigations:
FBC
and clotting (if suspected blood loss),
Complications
• Haemorrhage: apply firm pressure over puncture site. If you suspect a false an-
eurysm, ultrasound the swelling and consider surgical repair. Haematomas are
high risk for infections.
• Contrast reaction: this is usually mild with modern contrast agents.
• Loss of peripheral pulse: may be due to dissection, thrombosis, or arterial spasm.
Occurs in <
• Angina: may occur during or after cardiac catheterization. Usually responds to
sublingual
• Arrhythmias: usually transient. Manage along standard lines.
• Pericardial eusion: suspect if unexplained continued chest pain. Arrange for ur-
gent echo. May need drain depending on severity and haemodynamic status.
• Pericardial tamponade: rare, but should be suspected if the patient becomes hypo-
tensive and anuric.
• Stroke: complicates 0.4% of cases. Can be ischaemic or haemorrhagic.
1
% of radial catheterizations. Rare with femoral catheterization.
GTN
; if not, give analgesia and IV nitrates. MI in <0.1% of cases.
• Infection: post- catheter pyrexia is usually due to a contrast reaction. If it persists
24
h, take blood cultures before giving antibiotics.
for >
Mortality <1 in
1000
Intracardiac electrophysiology This catheter technique can determine types and
origins of arrhythmias, and locate and ablate problem areas, eg aberrant pathways
WPW
or arrhythmogenic foci. Arrhythmias may be induced, and the eectiveness
in
of control by drugs assessed.
TAVI
, fig
3.50
, p
141
)), cardiac biopsies, transcatheter
ECG
and arterial pressures are monitored continuously.
fig
3.22b
.
, clotting screen,
NBM
CXR, ECG. IV
access, ideally in left hand.
) from 6h before the procedure.
ECG
.
Urgent pericardial drain.
patients, in most centres.
Anterior view
(a)
(b)
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(pulmonary
trunk removed)
Left coronary
artery (left
main stem)
105
Right
coronary
artery
(c)
Fig 3.
22
(a) Coronary artery anatomy. (b) and (c) Images from angiography. Panel (b) shows stenosis of the left anterior descending artery (
allowing contrast to flow freely through to the distal vessel. The stenting is a type of angioplasty
(a procedure to widen the lumen of a blood vessel); in the context of coronary arteries, it is called
PCI
(percutaneous coronary intervention).
with acute coronary syndrome (
Images (b) and (c) reproduced from Ramrakha et al., Oxford Handbook of Cardiology,
ACS
LAD
). In (c), the same patient has had their
PPCI
(primary
), see p
116
PCI
.
Circumflex
branch
Left anterior
descending
artery
LAD
stented,
) is
PCI
performed acutely for a patient
2012
permission from Oxford University Press.
, with
3 Cardiovascular medicine
Urine my heart
In
1929
, fresh out of medical school, Werner Forssmann, a 25- year- old surgical
trainee, performed the first cardiac catheterization on himself using a
urethral catheter inserted via his left cubital vein. He then walked to the
65
cm- long
X
- ray
department, where a photograph was taken of the catheter lying in his right auricle. After rejection from a career in academic cardiology because of this style of
self- experimentation, he ended up becoming a urologist. His seminal work on cardiac catheterization was later recognized when he was jointly awarded the Nobel
Prize in Physiology or Medicine in
1956
.
3 Cardiovascular medicine
Cardiovascular drugs
CI
ACE
ACE- I
ARA
ARNI
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106
Antiplatelet drugs Aspirin irreversibly acetylates cyclo- oxygenase, preventing
production of thromboxane
75
dose (eg
mg/ 24h PO) for secondary prevention following MI,
tients with angina or peripheral vascular disease. Indicated for primary prevention
in only select group as harms (bleeding risk) may outweigh benefits.
antagonists (eg clopidogrel, prasugrel, ticagrelor) also block platelet aggregation, but
may cause less gastric irritation. They have a role if truly intolerant of aspirin; with
aspirin after
clopidogrel.
PCI
; and in acute coronary syndrome. Ticagrelor may be preferable to
9
Gl yco prot ein IIb/
for high- risk patients with ongoing ischaemia or large thrombus burden
Anticoagulants See p
inhibitors (eg apixaban) and direct thrombin inhibitors (dabigatran), are increasingly
replacing warfarin for treatment of
2.5
mg BD) may also have a role in secondary
10
Warfarin (antagonizes vitamin K- dependent clotting factor synthesis) remains
tients.
the anticoagulant of choice for mechanical valves. Anticoagulants used in
LMWH
, fondaparinux (Xa inhibitor), & bivalirudin (thrombin inhibitor).
- blockers Block - adrenoceptors. Blocking 1- receptors is negatively inotropic
and chronotropic; blocking
bronchoconstriction. Drugs vary in their
selective, and bisoprolol relatively
clinical ecacy.
Uses Angina, hypertension, anti- dysrhythmic, post- MI (mortality),
heart failure (with caution).
erectile dysfunction, joie de vivre, nightmares, headache.
inhibitors (
hypertension, heart failure, and postor raising
ACE-
i dose, a creatinine rise of >20% is concerning and associated with
worse cardiorenal outcomes and mortality
closely. If renal function deteriorates markedly, consider investigating for renal artery
stenosis. Hold in
vomiting, diarrhoea, etc.
AKI
an d hype rkal aemi a. Teac h pat ient s 'si ck da y rul es'— avoid if fever,
Angiotensin receptor– neprilysin inhibitor (
in chronic symptomatic heart failure with
mortality. Ensure adequate
Diuretics
• Loop diuretics (eg furosemide) are used in heart failure, and inhibit the Na/ 2Cl/ K
co- transporter.
• Thiazides and thiazide- like diuretics are used in hypertension (eg chlortalidone)
and heart failure (eg metolazone).
tence. (
• Potassium- sparing diuretics: aldosterone antagonists (eg spironolactone,
SE
: volume depletion, Na+ , K+ , Ca
NB:
small doses, eg chlortalidone 25mg/ 24h rarely cause significant SE.)
eplerenone) directly block aldosterone receptors; amiloride blocks the epithelial
sodium channel in the distal convoluted tubule.
Vas odi lato rs Used in heart failure,
tially dilate veins and large arteries, filling pressure (pre- load), while hydralazine
(often used with nitrates) primarily dilates the resistance vessels, thus
Hydralazine + nitrates are better at morta lity t han
Calcium channel antagonists These cell entry of Ca
nels in smooth muscle, thereby promoting coronary and peripheral vasodilation and
reducing myocardial oxygen consumption. All current drugs block
nels. However, their eects dier because of dierential binding properties.
• The dihydropyridines, eg nifedipine, amlodipine, are mainly peripheral vasodilators
(also dilate coronary arteries) and cause a reflex tachycardia, so are often used
with a - blocker. They are used mainly in hypertension and angina.
• The non- dihydropyridines— verapamil and diltiazem— also slow conduction at the
AV
and SA nodes and may be used to treat hypertension, angina, and dysrhythmias.
Don’t give non- dihydropyridines with - blockers (risk of severe bradycardia ±
A
, thereby inhibiting platelet aggregation. Used in low
2
III
a antagonists (eg tirofiban) may have a role during
346
. Direct oral anticoagulants (
AF
and clots, see p
CVD
preve ntion i n high- risk polyvascular pa-
- receptors induces peripheral vasoconstriction and
2
Severe asthma/
/ 2 selectivity (eg propranolol is non-
1
selective), but this does not seem to alter their
1
COPD
)/ angiotensin receptor antagonists (
MI
. Monitor
U&E
11
— these patients should be monitored
SE
Inc lude dry cough (sw itch to
BP
and
EF
GFR
SE:
. May further reduce morbidity and
>30 before starting.
Na+ , K+ , Ca
IHD
, and hypertension. Nitrates (p
ACE-
TIA
DOAC
S, previously
346
. Low- dose rivaroxaban (eg
, heart block. SE Lethargy,
when starting (after 1– 2 weeks)
ARA
) and urticaria.
) A replacement for
12
2
+
, ototoxic.
2
+
2
+
, Mg
, urate (±gout), impo-
i for black patients.
2
+
via voltage- sensitive chan-
/ stroke, and for pa-
7,8
ADP
receptor
PCI
.
NOAC
S), eg
ACS
include
s) These are used in
ACE-
i/
ARA
112
) preferen-
BP
(afterload).
2
+
L
- type Ca
chan-
LVF
X
a
).
SE
CI
CI
https://t.me/med1917
Flushes, headache, ankle oedema (diuretic unresponsive), LV function, gingival
hypertrophy.
Digoxin Blo cks t he N a+ / K+ pu mp. I t is u sed to sl ow th e pul se i n fas t AF (p
Heart block, heart failure.
126
). As a weak
+ ve inotrope, it has been shown to improve symptoms, quality of life, and hospitalizations
in heart failure but not mortality; its routine use is not recommended due to its narrow
therapeutic window.
plasma levels >
12
h, then
PO OD. IV
dose: 0.25– 0.5mg in
0.9
% NaCl over 2h. To x i c i t y r i s k i f : K+ ,
2
+
, or Ca
Mg
13
Elderly people are at risk of toxicity: use lower doses. Measure
6
h post- dose (p
125
mcg (if elderly) to
2
+
. SE Any arrhythmia,
740
). Typ i ca l d os e
250
mcg/ d
100
ml of
500
mcg stat PO, repeated after
nausea, appetite, yellow vision, confusion, gynaecomastia. If toxicity is suspected, do an
and check K
+
ECG
, Mg
(fig
2
+
, and Ca
3.23
), digoxin levels,
2
+
. If toxicity is
confirmed, stop digoxin, correct electrolyte imbalances, treat arrhythmias, and
consider antidote with antibody (Fab)
fragments, eg
WPW
IV
syn drome ( p
DigiFab® (p
129
).
826
Fig 3.
digoxin use: downsloping
). CI
HCM
;
stroke back to isoelectric line.
23
Classic ‘reverse tick’ associated with
ST
wave with rapid up-
Sodium channel blockers Class I anti- arrhythmics. Procainamide (1a) and lido-
1
b) can be used to terminate VT. NB: QT interval may be prolonged. Flecainide
caine (
1
c) is useful for AF cardioversion if no CI, and for prophylaxis in patients with
(
or troublesome paroxysmal
Amiodarone A class
AF.
CI Heart failure,
III
anti- arrhythmic. Amiodarone prolongs the cardiac ac-
IHD
, valve disease, and heart block.
tion potential, reducing the potential for tachyarrhythmias. Used in both supraventricular and ventricular tachycardias, including during cardiac arrest. Broad
range of side eects, eg thyroid disease, liver disease, pulmonary fibrosis and peripheral neuropathy. Monitor
TFT
S and
LFT
S every
6
months.
Ivabradine Selective sinus node inhibitor, slowing pulse rate without significantly
dropping blood pressure. Used in angina, heart failure, and (o licence) in autonomic
tachycardia syndromes. No role in atrial tachycardia.
QT
syndrome, shock. Many drug interactions, including with calcium antagonists.
Statins Statins (eg simvastatin, p
682
) inhibit the enzyme
causes de novo synthesis of cholesterol in the liver. This increases
expression by hepatocytes leading to circulating
if given at night, but optimum dose and target plasma cholesterol are unknown.
SE
Muscle aches, abdominal discomfort, transaminases (eg
rarely rhabdomyolysis (more common if used with fibrates). Statins are generally
well tolerated. See also hyperlipidaemia,
PCSK9 Inhibitors Reduce
LDL
cholesterol when combined with statin, eg alirocumab SC injection 2- weekly.
Anti- anginal drugs See p
p
138
. Inotropes See p
See
LDL
receptor degradation. Expensive, but very eective.
112
. Antihypertensives See p
787
.
pp
682– 3
Acute MI, bradycardia, long
HMG- CoA
reductase, which
LDL
cholesterol. More eective
ALT
), CK, myositis,
, fig
14.12
.
110
. SGLT2 inhibitors
LDL
receptor
WPW
107
3 Cardiovascular medicine
Drugs that slow conduction through the atrioventricular node
Drugs that slow conduction through the atrioventricular node (
goxin, verapamil, and adenosine. Uses include cardioverting atrioventricular
nodal re- entry tachycardia (
Drugs that slow
pathways (eg
tive pathways.
eg those with long
AVN
conduction should be avoided in patients with aberrant
WPW
) as blocking the
AVN
blockers are contraindicated in patients with or at risk of VT,
QT
syndrome.
AVNRT
) and diagnosing atrial tachycardias.
AVN
can increase conduction via the alterna-
AVN
) include di-
3 Cardiovascular medicine
Hypertension
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108
Hypertension is the most important risk factor for premature death and
50
causing ~
% of all vascular deaths (8 million per year). Usually asymptomatic, so
regular screening (eg yearly) is a
without universal screening.
Defining hypertension BP has a skewed normal distribution (p
population, and risk is continuously related to
tension’ and guidelines dier in terms of thresholds.
in clinical practice now to treat if ≥
present. Don’t rely on a single reading— assess over a period of time. Confirm with
24
h ambulatory BP monitoring (
Whom to treat All with clinic BP ≥
130/ 80
mmHg if <65 years or CV risk factors present (eg diabetes,
≥
fig
3.24
and see
treating the overcuss with individual patients about their
BP
to <
.15 The
80
130/ 80
mmHg.17 Consider downstream benefits— likely dementia.
White- coat hypertension Refers to an elevated clinic pressure, but normal
(day average <
tality.
130/ 80
18
Lifestyle modifications should be instituted and home BP readings strongly
encouraged to monitor for the development of sustained hypertension.
‘Malignant’ or accelerated phase hypertension (p
BP
leading to vascular damage (pathological hallmark is fibrinoid necrosis). Usually
there is severe hypertension (eg systolic >
eral retinal haemorrhages and exudates; papilloedema may or may not be present. Symptoms are common, eg headache
treatment, and may also precipitate acute kidney injury, heart failure, or encephalopathy, which are hypertensive emergencies. Untreated,
70
% survive 5yrs. It is more common in younger and in black subjects. Look hard
for any underlying cause.
Primary or ‘essential’ hypertension Cause unknown, ~95% of cases.
Secondary hypertension ~5% of cases. Consider if severe/ resistant, abrupt rise,
30
yrs if no risk factors, presents with hypertensive emergency, or associated with
<
electrolyte abnormalities (eg K
• Kidney disease: the most common secondary cause. 75% are from intrinsic kidney
disease: glomerulonephritis, polyarteritis nodosa (
pyelonephritis, or polycystic kidneys.
frequently atheromatous (elderly cigarette smokers, eg with peripheral vascular disease) or rarely fibromuscular dysplasia (young ).
• Endocrine disease: Cushing’s (p
hyperplasia, phaeochromocytoma (
• Others: coarctation (p
oral contraceptive pill, cocaine, amphetamines.
Signs and symptoms Usually asymptomatic (except malignant hypertension, see
earlier in topic). Headache is no more common than in the general population. Always
examine the
cause (phaeochromocytoma,
CVS
fully and check for retinopathy. Are there features of an underlying
weak femoral pulses (coarctation), renal bruits, palpable kidneys, or Cushing’s syndrome? Look for end- organ damage:
verity and duration of hypertension and associated with a poorer prognosis.
Tests To confirm diagnosis
Fasting glucose, cholesterol, e
risk
LV
hypertrophy? past MI?); urinalysis (protein, blood). To ‘exclude’ secondary
(any
U&E
causes
(eg K+ in hyperaldosteronism); Ca
metnoradrenaline/adrenaline (
(renal artery stenosis),
suppression test;
MR
aorta (coarctation).
CVD;
vital task— most preventable deaths are in areas
735
BP
, so it is impossible to define ‘hyper-
14
140/ 90
mmHg, particularly if other CV risk factors
ABPM
); or a week of home readings.
140/ 90
HYVET
study showed that there is even substantial benefit in
There has been a general shift
mmHg (≥
135/ 85
mmHg on 24h
) within the
CKD
, proteinuria)
ABPM
) or
s.16 Guidelines are concordant in their recommendation to dis-
CV
risk and the benefits of further lowering
mmHg). Associated with risk of
200
±
visual disturbance. It requires urgent
CVD
778
; fig
3.25
, diastolic >
90
+
, metabolic alkalosis). Causes include:
PAN
25
% are due to renovascular disease, most
218
) and Conn’s syndromes (p
p
222
148
), pregnancy (
p
222
ABPM
24
hr urinary free cortisol (p
), acromegaly, hyperparathyroidism.
OHCS
, etc.), signs of renal disease, radiofemoral delay, or
LVH
, retinopathy and proteinuria— indicates se-
or home BP monitoring. To help quantify overall
GFR
. To look for end- organ damage
p
222
); renin & aldosterone. Special tests
), systemic sclerosis, chronic
p35), liquorice, drugs: steroids,
2
+
( in hyperparathyroidism); plasma
219
) or overnight dexamethasone
and all- cause mor-
, p
111
120
mmHg) + bilat-
% die in 1yr; treated,
222
), bilateral adrenal
ABPM
) A rapid rise in
MAOI
ECG
or echo
CTA
or
MRA
,
Grading hypertensive retinopathy
II
III
IV
https://t.me/med1917
I To r t u o u s a r t e r ie s w i t h t h i c k s h i n y w a l l s ( s i l v e r o r co p p e r wi r i n g , p
AV nipping (narrowing where arteries cross veins, p
Flame haemorrhages and cotton- wool spots.
Papilloedema, p
558
, fig
12.21
.
558
, fig
12.20
558
).
, fig
Measuring BP with a sphygmomanometer
• Use the correct size cu. The cu width should be >40% of the arm circumference.
The bladd er sh ould be ce ntred over the b rachial artery, and the c u applied snugly.
Support the arm in a horizontal position at mid- sternal level.
• Inflate the cu while palpating the brachial artery, until the pulse disappears. This
provides an estimate of systolic pressure.
• Inflate the cu until 30mmHg above systolic pressure, then place stethoscope over
the brachial artery. Deflate the cu at
• Systolic pressure: ap pearance of sust ained repeti tive t appin g soun ds (Kor otko I).
• Diastolic pressure: usually the disappearance of sounds (Korotko V). However, in
some individuals (eg pregnant women) sounds are present until the zero point. In
this case, the muing of sounds, Korotko
a given reading. For children, see
• For advice on using automated sphygmomanometers and a list of validated devices,
http:// www.bhs oc.org/ lat est- gui deli nes/ how- to- meas ure- blood- press ure/
see
OHCS
2
mmHg/ s.
IV
, should be used. State which is used for
p
267
.
Managing suspected hypertension
12.19
109
).
3 Cardiovascular medicine
Fig 3.
24
Managing suspected hypertension based on the
Source: data from NICE CG
2019
NICE guidelines.
127
, https://www.nice.org.uk/guidance/cg127/resources/
hypertension-in-adultsdiagnosis-and-management-35109454941637
19
.
3 Cardiovascular medicine
ACE
ARB
ALGrawany
https://t.me/med1917
Hypertension— management
110
Look for and treat underlying causes (eg kidney disease, alcohol: see fig
p
112
). Drug therapy reduces the risk of
would benefit from antihypertensives, whatever their starting
tension is not ‘curable’ and long- term treatment is needed. Emphasize the importance of compliance and regular home
Tre at me nt g oa l <
BP
Reduce
See p
stroke.
140/ 90
mmHg (possibly <
slowly; rapid reduction can be fatal, especially in the context of an acute
778
for trea tment of ma ligna nt hype rtension/ emergencies.
Lifestyle changes Concomitant risk factors: stop smoking; low- fat diet. Alcohol
and salt intake; exercise; weight if obese.
Drugs The
ALLHAT
trial supports the view that adequate BP reduction is more important than the specific drug used.
trial, and meta- analyses suggest they are less eective than other drugs at reducing
major cardiovascular events, particularly stroke. Ethnicity also appears to be important, as chlortalidone was generally better at preventing events than other drugs
in black patients. Many patients will require combination therapy (if >
above their
BP
target) — ideally use a single- pill strategy (caution if frail or elderly).
Monotherapy First- line agents include
ACE
- i or
thiazide diuretics.
ARB
have additional benefits in patients with diabetes or
(chlortalidone/ indapamide) and Ca
black patients. - blockers are not
with coexisting coronary artery disease,
Combination
ACE
- i + thiazide or
dual combinations followed by
diuretics are particularly useful in obese patients. If
equate doses of three drugs, add a
or amiloride
and get help. Check compliance (urinary drug screen, or observed ). Add a statin
if cholesterol raised.
sess ecacy with just one
Drug examples Thiazides eg chlortalidone 25– 50mg/ 24h PO in the morning. SE: K+ ,
Na
: fatigue, gum hyperplasia, ankle oedema;
SE
lisinopril
betes (esp. if microalbuminuria,
angioedema.
10
mg, but monitor
Most drugs take 4– 8wks to gain maximum eect: don’t as-
+
, impotence. CI: gout. Ca
10– 40
mg/ 24h PO (max 40mg/ d).
CI
: bilateral renal artery stenosis; p
BP
measurement.
caution if valve disease or hypertrophic cardiomyopathy; monitor K
tigo, urticaria, pruritus. Useful if
2.5– 5
mg/ 24h PO. SE: bronchospasm, heart failure, cold peripheries, lethargy, impo-
CI
: asthma; caution in heart failure.
tence.
CVD
and death. Almost any adult over 50
BP
monitoring.
130/ 80
in selected cases, eg <40 years).
21
However, - blockers were not included in the
ACE
ARB
, Ca
BP
.20 Essential hyper-
2
+
- channel antagonist, and
may be more eective in younger patients and
CKD
2
+
- channel antagonists are favoured in older or
1
st line for hypertension, but consider in patients
AF
, or stable HF.
2
ACE
ACE
- i + thiazide + Ca
U&E
. Alternatively, - blocker, or selective - blocker
2+
- channel antagonists eg amlodipine 5–10mg
p
310
) or proteinuria.
ACE
+
- i + Ca
- channel antagonist are sensible
4
th— consider: spironolactone 25– 50mg/ 24h
DO NOT
ACE
- i may be 1st choice if coexisting dia-
106
- i induces cough. - blockers eg bisoprolol
. Conversely, thiazides
2
+
- channel antagonist. Thiazide
BP
still uncontrolled on ad-
use short- acting form.
SE:
cough, K+ , renal failure,
.
Candesartan (8– 32mg/ d);
3.24
20/ 10
+
. SE: ver-
, p
109
mmHg
&
OD.
- i eg
Always think about secondary hypertension...
A casual conversation about lifestyle led a 40- year- old woman who had been seen
for
4
years by hypertension specialists to reveal that she was addicted to mighty
imps— liquorice sweets containing glycyrrhizinic acid which inhibits the enzyme
HSD- 11
. This protects the mineralocorticoid receptor from endogenous cortisol...
Sure enough her
A
38
- year- old pregnant normotensive woman complained of palpitations. Plasma
BP
returned to normal on stopping the mighty imps.
metadrenalines were
standing headaches and feeling cold all the time, 'pre- eclampsia' in her pregnancy
10
years ago followed by a cardiac arrest. Sure enough, she had a large phaeochromocytoma. This is one of the rare occasions that patients with hypertension
experience symptoms— unfortunately, rather non- specific ones at that.
10
- fold elevated. On questioning, she complained of long-
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