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Fig 3.
ECG
I
V
V
II, III
VF
V
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8
Rhythm strips of heart blocks. * P wave.
Location, location, location
When considering rate and rhythm, your findings should be the same in all leads,
albeit clearer in some than others. Other
in terms of what is ‘normal’ and in what a change indicates. For example,
tion in leads
likely
however, suggests instead pericarditis which necessitates entirely dierent management (
and
Table 3.
II, III
PCI
V
but may suggest right ventricular strain or posterior MI if seen in
6
, and aVF suggests an inferior MI requiring immediate treatment,
to the right coronary artery, see table
p
132
). An R wave taller than the S is deep (R dominance) is normal in
1
ECG
territories
leads Heart territory Coronary artery
, aVL,
4– 6
1– 3
, a
7– 9
Lateral Circumflex
Anteroseptal
Inferior
Posterior Circumflex
To detect posterior infarcts, which are often associated with inferior or lateral
MI
, posterior
wall
scapula. Consider if
fig
3.29
See
ECG
leads (
ST
117
.
depression in
, p
The ‘upsi de- down’ changes seen in posterior
changes that appear when ‘looking’ at ischaemic myocardium from the other side of
the heart. These can arise with
important in posterior
See figs
3.12, 3.13, 3.29
MI
for example
ECG
features may vary lead by lead, both
3.1
. ST elevation across
Left anterior descending
Right coronary artery in
Circumflex in
V
–
V
) are applied by moving
7
9
V
or
R/ S
1– 3
MI
s in other locations (fig
MI
20
%: ‘left dominant’
V
–
V
to under the left
4
amplitude ratio in
6
are called ‘reciprocal changes’:
3.12
). They are particularly
as they may be the only cha nges on th e 12- lead
ECG
S. See fig
3.22
for coronary artery anatomy.
91
3 Cardiovascular medicine
ST
eleva-
all
leads,
V
5
V
and
V
.
1
2
80
%
V
or
V
is >1.
1
2
ECG
.
3 Cardiovascular medicine
ECG
LVH
RVH
V
QRS
J
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92
— additional points
2
The r ight- sided ECG for the right diagnosis
(fig
3.9
) If you suspect RV infarction, which com-
40
plicates up to
V
–
V
in a mirror- image position on the right
1
6
side of the chest. Consider if patient is hypoten-
ST
sive,
and ST depression in v2 (highly specific for RV
v
1
infarction), or isoelectric
marked
% of inferior
elevation in lead
ST
depression in v2.
QRS complexes: the long and the short
QRS
complexes represent ventricular depolariza-
tion, and width represents time, so a broader
QRS
complex means depolarization is taking
longer. Normally, a wave of depolarization
reaches the ventricles via the specialist conduction pathways— the bundles of His, which
ensures rapid ecient spread of charge. Hence,
QRS
complex is narrow (<
the
depolarizes first, left to right, giving rise to a small
ultaneous depolarization of both ventricles, from apex to outflow tracts, but voltagewise this is dominated by the larger left ventricle, hence the
depolarization takes longer when depolarization is not initiated in this pattern. For example, if it originates in the ventricles (eg ventricular ectopics,
branches of the bundles of His are blocked— bundle branch blocks— meaning depolarization is initiated in one ventricle but not the other, so it has to travel the long (in time
and space) path from one ventricle to the other.
Ventricular depolarization also takes longer if all conduction is slowed. This may
happen in some electrolyte imbalances, eg hyperkalaemia.
Right bundle branch block (p94, fig
R
in
V
; inverted T waves in
1
variant (isolated
RBBB
Left bundle branch block (p93, fig
V
, inverted T waves in I, aVL,
1
pathic fibrosis.
T
wave. New
or
NB: if there is
LBBB
segment changes in this context, see
Bifascicular block The combination of
as an axis deviation, eg left axis deviation in the case of left anterior hemiblock.
Trifascicular block Bifascicular block plus 1st- degree
trifascicular block are important causes of syncope that may need pacing (
Suspect left ventricular hypertrophy (
S
sum of the
wave in
Suspect right ventricular hypertrophy (
V
–
V
or
version in
Other causes of dominant R wave in
p
129
).
(
V
1
3
4
Causes of low- voltage
chronic obstructive pulmonary disease (
sistivity is related to haematocrit), changes in chest wall impedance (eg in renal
failure & subcutaneous emphysema but not obesity), pulmonary embolism, bundle
branch block, carcinoid heart disease, myocarditis, cardiac amyloid, doxorubicin
cardiotoxicity, and other heart muscle diseases, pericardial eusion, pericarditis.
wave See p
J
A
See
831
. The J point is where the S wave finishes and ST segment starts.
wave is a notch at this point. Seen in hypothermia,
lifeinthefastlane.com for excellent
MI
S, place leads
III
> II,
ST
elevation in
ST
segment in v1 with
Fig 3.
9
120
ms). The septum
3.11
)
V
–
V
1
), pulmonary embolism, cor pulmonale.
V
–
V
5
LBBB
may represent a
V
and the R wave in
1
, deep S wave in
complex (
QRS
or
V
; wide, slurred S wave in
3
4
3.10
)
QRS
>0.12s, ‘M’ pattern in
. Causes:
IHD
6
, no comment can be made on the ST segment
STEMI
BOX
on Sgarbossa criteria.
RBBB
) If the R wave in
V
is >35mm (see fig
6
V
, right axis deviation.
6
RBBB
1
QRS
<5mm in all limb leads.) Hypothyroidism,
COPD)
ECG
tutorials, cases, and examples.
Right- sided chest leads.
Q
wave in
>0.12s, ‘
RSR
, hypertension, cardiomyopathy, idio-
, see p
782
and left bundle hemiblock, manifest
HB.
) If dominant R wave in
, posterior MI, type A
, haematocrit (intracardiac blood re-
SAH
V
. Next there is rapid sim-
6
S
wave in
V
. Ventricular
6
VT
) or if one or more
’ pattern in
V
; dominant
1
V
. Causes: normal
6
V
, dominant S in
5
. Dicult to interpret ST- T
Both bifascicular and
p
128
).
V
, T- wave in-
1
syndrome
.
).
V
is >25mm or the
6
3.25
, p
, and Ca
111
WPW
2
+
93
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WiLLiaM = LBBB.
.
6
V
) and the M pattern in
3
V
3 Cardiovascular medicine
wave— clearer in
S
(slight notching in upstroke of
1
V
with a W pattern in
QRS
Modified Sgarbossa's criteria for MI in left bundle branch block
• ≥1 leads with ≥1mm of concordant ST elevation.
• ≥1 leads of
• ≥1 leads anywhere with ≥1mm ST elevation and proportionally excessive dis-
cordant
S
• Yes to any criteria has an 80% sensitivity and 99% specificity in diagnosis of
acute
V
–
V
with ≥1mm of concordant ST depression.
1
3
ST
elevation, as defined by 25% or greater of the depth of the preceding
wave.
MI
in the context of known
LBBB
Left bundle branch block: wide
10
.
3
Fig
.
5
94
3 Cardiovascular medicine
https://t.me/med1917
. MaRRoW = RBBB.
5
V
wave (with the eye of faith, a ‘W’ shape) in
S
, and sloped
1
V
, M pattern in
QRS
Right bundle branch block— broad
11
.
3
Fig
, indicating lateral involvement. There is a
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6
V
and
5
V
), but also in
VF
, a
III
,
II
elevation in the inferior leads (
ST
; this is often seen with a large inferior myocardial infarction.
VL
and a
I
95
3 Cardiovascular medicine
Acute inferolateral myocardial infarction: marked
12
.
3
Fig
- segment depression in leads
ST
‘reciprocal change’ of
96
3 Cardiovascular medicine
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.
4
–
1
V
deflection is negative) in leads
QRS
- waves (the first
Q
segment elevation and evolving
ST
Acute anterior myocardial infarction—
13
.
3
Fig
97
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3 Cardiovascular medicine
, with permission from Oxford University Press.
2012
) suggesting right ventricular strain.
3
–
1
V
).
PE
suggesting right ventricular hypertrophy.
2
Reproduced from Handler et al., Pulmonary Hypertension,
V
and
1
V
Changes seen in pulmonary hypertension (eg after a
14
.
3
Fig
- waves’) in
R
more negative than positive in lead I).
QRS
complexes (‘dominant
QRS
• Right axis deviation (
• Positive
wave inversion in the right precordial leads (
T-
depression and
ST
•
pulmonale) suggesting right atrial hypertrophy.
P
waves (
P
• Peaked
98
3 Cardiovascular medicine
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Ventricular tachycardia— regular broad complex tachycardiac indicating a likely ventricular origin for the rhythm.
15
.
3
Fig
morph-
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LBBB
complexes are broad with a
QRS
complex.
QRS
wave and each
P
99
3 Cardiovascular medicine
, with permission from Oxford University Press.
2012
Dual- chamber pacemaker. Pacing spikes occur before each
16
.
3
Fig
ology, indicating the presence of a ventricular pacing electrode in the right ventricle. The absence of paced complexes does not always mean
pacemaker failure as it may reflect satisfactory native conduction.
Reproduced from Myerson et al., Emergencies in Cardiology,
3 Cardiovascular medicine
Cardiac imaging
MPS
SPECT
PET
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100
There are many heart conditions associated with structural defects, eg valve
defects, congenital heart diseases, and some muscle disorders (eg hypertrophic
cardiomyopathy (
examination, and
Chest X- ray An enlarged heart (cardiothoracic ratio >0.5) suggests congestive
heart failure; signs of pulmonary oedema suggest decompensated heart failure
fig
(see
HCM
ECG
3.46
, p
135
); a globular heart may indicate pericardial eusion (fig
metal wires and valves will show up, evidencing previous cardiothoracic surgery;
dextrocardia may explain a bizarre
in coarctation of the aorta (
Lung ultrasound This can detect pulmonary oedema with greater sensitivity than
CXR
and can be a useful adjunctive tool for the diagnosis of acute heart failure.
a
Echocardiography This is the workhorse of cardiac imaging. Ultrasound is used
to give real- time images of the moving heart. This can be transthoracic (
transoesophageal (
TOE
logical stressor (eg dobutamine). If the patient is too unwell to be moved, an echo
machine can be brought to them and continuous
guide during surgery. Use of contrast can improve visualization of the endocardium
in patients with poor acoustic windows and allow some estimation of myocardial
perfusion. Contrast studies with Valsalva manoeuvre should be considered to exclude paradoxical embolism through a cardiac shunt from the right heart. In patients with a high clinical suspicion of a cardiac source of embolus, in whom
TOE
normal,
is recommended. See p
Cardiac CT First line if stable anginal symptoms. This can provide detailed infor-
mation about cardiac structure and function.
contrast- enhanced imaging of coronary arteries during a single breath hold with
very low radiation doses. It can diagnose significant (>
artery disease with an accuracy of
predictive value of >
routine transcatheter coronary angiography to rule out coronary artery disease.
Medications are often given to slow the heart down and the imaging may be ‘gated’,
meaning the scanner is programmed to take images at times corresponding to certain points on the patient’s
points in the cardiac cycle. See
Coronary artery calcium screening With multidetector or multislice CT. Many
limitations and generally only used in a select group of intermediate- risk patients.
Cardiac MR Cardiovascular
3D
dimensional (
) analysis of cardiothoracic anatomy, the assessment of global and
regional myocardial function, and viability imaging.
method to look at diseases that directly aect the myocardium (
high diagnostic accuracy for the identification of myocardial ischaemia. Patterns of
late gadolinium enhancement can be helpful to diagnose cardiac amyloid, sarcoid,
or myocarditis. Check pacemaker compatibility. See
Myocardial perfusion scintigraphy with single photon emission computed
tomography (
with
uncertain functional significance or is non- diagnostic. Perfusion is assessed at rest
and with exercise or pharmacologically induced stress. Minimally invasive and not
dependent on overall exercise capacity, this test is particularly useful for assessing
whether myocardium distal to a blockage is viable and so whether stenting or
will be of value. If hypoperfusion is ‘fixed’, ie present at rest and under stress, the
hypoperfused area is probably scar tissue and so non- viable. If hypoperfusion is ‘reversible’ at rest, the myocardium may benefit from improved blood supply. See
Positron emission tomography (
myocardial perfusion than
for diagnosing cardiac sarcoidosis.
)). Whilst clues to these can sometimes be found on history,
, it is imaging that gives the diagnosis.
3.17
ECG
p
; and rib notching may be an important clue
148
).
6
TTE
) or
), at rest, during exercise, or after infusion of a pharmaco-
TOE
imaging may be used as a
3.18
) permits
3.19
) and has
CAD
p
TTE
CABG
725
102
.
CT
angiography (fig
50
89
99
%, which makes it an eective non- invasive alternative to
ECG
%. CT coronary angiography has a negative
. This allows characterization of the heart at dierent
p
724
.
MRI
is the gold standard method for the three-
%) stenosis in coronary
MR
is the first- choice imaging
fig
p
724
.
) Oer if CT coronary angiography has shown
MPS
). Better image quality and quantification of
but very expensive. However, it is the gold standard
);
is
of
.
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