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2 History and examination
1
https://t.me/med1917
Always have a chaperone present.
• Positi on pati ent sit ting at edge of bed wit h hands by s ide, ex posed t o waist.
• Inspect with hands on hips, then again with hands on head to accentuate asymmet-
rical changes.
• Inspect for: masses, contour anomalies, asymmetry, scars, ulceration, skin changes
(peau d’orange: ora nge pe el app earanc e resulti ng from oedem a).
• Look for nipple inversion and nipple discharge.
Inspection
While patient has arms raised, inspect axillae for any masses as well as inspecting
under the breasts.
2
• Position pa tient sitting at 45° with hand behind head (ie right hand behind head
when examining right breast,
• Ask about pain and discharge. Examine painful areas last. Ask patient to express
any discharge.
• Examine each breast (asymptomatic side first). Examine each quadrant as well as
axilla ry tail of Spence (
fingers to feel breast tissue against chest wall.
• Define lumps/ lumpy areas. If you discover a lump, to examine for fixity to skin and
Palpat ion of the breast
fig
2.46
).
fig
2.45
), or use a concentric spiral method (fig
2.47
). Use flat
pectoral muscles: ask patient to push against their hip to contract muscle and then
try to move at right angles to the long axis of pectoralis muscle fibres.
Fig 2.
47
Fig 2.
46
Correct patient position for
breast examination.
Reproduced from Thomas J, et al. (eds)
Oxford Handbook of Clinical Examination
and Practical Skills (
2014
), with permission
from Oxford University Press.
Methods for systematic breast
palpation.
Reproduced from Thomas J, et al. (eds)
Oxford Handbook of Clinical Examination and
Practical Skills (
2014
), with permission from
Oxford University Press.
81
Examine both axillae. When examining the right axilla, support the patient’s
right arm on your examining left arm. Similarly, examine the left axilla with your
right hand, supporting the patient’s left arm on your right arm.
Palpate five sets of axillary nodes:
1
Apical: palpate against glenohumeral joint.
2
Anterior: palpate against pectoralis major.
3
Central: palpate against lateral chest wall.
4
Posterior: palpate against latissimus dorsi.
5
Medial: palpate against humerus.
• Other lymphadenopathy.
• Spine for tenderness.
• Abdomen for hepatomegaly (p59).
• Respiratory examination for eusion (p49, p51).
• Neurological examination if symptoms (pp62– 7).
3
Palpat ion of the axilla
4
Furt her exa min ati on
2 History and examination
The peripheral vascular system: examination
(a)(b)
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82
Arterial
The ‘P’s suggest acute ischaemia, which is a surgical emergency (p
Pale Pulseless Painful
Paralysed Paraesthetic ‘Perishingly’ cold
1
Inspection
• Skin Hair loss, pallor, shiny skin, ulceration, gangrene, cyanosis, scars.
• Pressure points Bet ween to es, li ft up h eels t o inspect for ulc eratio n unde rneat h.
2
Palpat ion
• Temperature Check thighs, legs, and feet with dorsum of hand on both legs. Is
there a level above which the skin is warmer?
• Capillary refill Press/ squeeze great toe until blanches, release, and count time
for colour to return (normal <
• Peripheral pulses Assess whether palpable bilaterally. Detect rate and rhythm
(?irregularly irregular raising possibility of emboli from atrial fibrillation).
1
Femoral— mid- inguinal point.
2
Popliteal— flex knees slightly and press into centre of popliteal fossa (fig
3
Posterior tibial— just posterior & inferior to medial malleolus.
4
Dorsalis pedis— between bases of 1st & 2nd metatarsals, lateral to extensor
hallucis longus. For brachial and carotid, determine volume and character (
• Abdominal aorta Midline above umbilicus. A pulsatile, expansile mass is an
aortic aneurysm until proven otherwise (
Fig 2.
48
Palpation of popliteal pulse.
Reproduced from Thomas J, et al. (eds). Oxford
Handbook of Clinical Examination and Practical
Skills (
2014
), with permission from Oxford
2
s).
University Press.
fig
2.49
).
Fig 2.
49
Pulses: abdominal aorta.
(a) Expansile (aneurysm?).
(b) Transmitted.
Reproduced from Thomas J, et al. (eds). Oxford
Handbook of Clinical Examination and Practical
Skills (
2014
), with permission from Oxford
579
, p
649
):
2.48
p40).
University Press.
).
• Bruits Aortic, iliac, and femoral. (Carotid and renal either now, or at the end.)
• Buerger’s test Lift both legs to 45° above horizontal. Allow a minute for legs to
pale. Then ask patient to sit up, with lower legs o the edge of the bed. Observe
for colour change: usually white to pink. Flushed red (reactive hyperaemia) may
indicate more severe disease.
• Buerger’s angle Angle above horizontal that leads to pallor (<20° = severe
ischaemia).
• Examination of per ipheral vas cular system out side the leg:
• Other pulses: radi al, bra chial , carot id.
• Other bruits: caro tid, re nal.
• Doppler probe to detect pulses and measure ankle– brachial pressure index (p
• Neurological examination of lower limbs (pp64– 5).
3
Auscultation
4
Special tests
5
Furt her exa min ati on
648
).
2 History and examination
Ven ous
SFJ
SPJ
SFJ.
SFJ
SPJ.
https://t.me/med1917
See also p
650
.
1
Inspection
• Varicosities Inspect with patient standing. Decide whether varicosities are:
• Long saphenous vein— medial.
• Short saphenous vein— posterior lateral, below the knee.
• Calf perforators— usually few varicosities but commonly show skin changes.
• Ulcers Around the medial malleolus are more suggestive of venous disease,
whereas those at the pressure points suggest arterial pathology (
• Other skin changes
• Haemosiderin deposition: brow n skin depos its du e to ven ous hypertens ion.
• Atrophy and loss of elasticity.
• Lipodermatosclerosis: induration, hyperpigmentation, erythema, swelling,
p82).
inverted champagne bottle appearance. Pathology is panniculitis (inflammation of subcutaneous fat) caused by a chronic innate immune response in
soft tissues secondary to venous hypertension.
2
Palpation
• Characterize Firm and tender may suggest thrombosis, warm and tender may
suggest infection.
• Cough impulse Ask patient to cough while you palpate for a transmitted im-
pulse (incompetence) at the saphenofemoral junction (
junction (
• Tap test Percuss lower limit of varicosity and feel for impulse at
mitted percussion impulse demonstrates incompetence of superficial valves.
• Arterial pulses If u lceratio n is prese nt, pa lpate to rul e out a rteri al dis ease ( p82).
).
3
Auscultation
) and saphenopopliteal
A trans-
Listen for bruits over any varicosities (occur if arteriovenous malformation).
4
Special tests
• Doppler Test to determine the level of incompetence. On squeezing the leg distal
to the probe you should only hear one ‘whoosh’ if the valves are competent at the
level of probe. Place probe over
at
• Brodie– Trendelenburg test Used if Doppler is not available. Elevate leg and
, squeeze calf, and listen. Repeat with probe
massage veins to empty varicosities. Apply tourniquet to upper thigh. Ask patient to stand. If not controlled, repeat, placing tourniquet below knee.
• Perthes ’ test Used to distinguish between superficial and deep venous pathology.
Apply a tourniquet at mid- thigh level whilst the patient is standing (varicosities
filled/ partially filled). Ask the patient to walk, or alternate between tip- toes and
flat feet, for
is able to pump blood from superficial to the deep venous system normally. If
5
minutes. If the varicosities become less distended, the calf muscle
the varicosities remain distended (or become more distended) it suggests deep
venous pathology, eg thrombus. Contemporary imaging of the deep leg veins
using Doppler ultrasound means this test is largely historical.
83
• Examination of the abdomen (p58), pelvis, rectum (p59), and genitals for masses.
5
Furt her exa min ati on
3 Cardiovascular medicine
ACS
ECG
ACHD
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Contents
Cardiovascular health
At the bedside (see 38)
Cardiovascular symptoms
Investigations
ECG
— a methodical approach
ECG
— abnormalities
ECG
— additional points
Cardiac imaging
Echocardiography
Cardiac catheterization
Drugs and the heart
Cardiovascular drugs
Diseases and conditions
Hypertension
Hypertension— management
Angina pectoris
Acute coronary syndromes (
Management of
Complications of MI
Arrhythmias— overview
Continuous
Narrow complex tachycardia
Broad complex tachycardia
Atrial fibrillation (AF) and flutter
Pacemakers
Diseases of heart muscle
Pericardial diseases
Heart failure— basic concepts
Heart failure— management
Mitral valve disease
Aortic valve disease
Right heart valve disease
Cardiac surgery
The heart in various, mostly rare,
systemic diseases
Infective endocarditis (IE)
Rheumatic fever (RF)
Adult congenital heart disease
(
)
148
Driving and the heart
100
102
108
112
ACS
monitoring
128
142
90
116
118
132
138
140
143
106
146
150
85
86
88
92
104
110
)
114
120
121
122
124
126
130
134
136
142
144
Fig 3.
‘One of my daydreams, which I feel to be selfish,
is that of going to school’. Overcoming both a
dicult childhood and initial rejection from
medical school because she was female, she
later became an international authority on heart
disease. Through her work as the assistant curator at the McGill Museum of Medicine, she organized systematized knowledge on congenital
heart disease, laying the foundation for modern
cardiac surgery. Although museum work wasn’t
her first choice of career, she was advised by
her mentor, Sir William Osler, to look past the
‘dreary and unpromising drudgery’ and seize the
‘splendid opportunity’ to do ‘wonderful things’.
2000
In
postage stamp entitled 'The Heart of the Matter’
in her honour.
1
Maude Abbott (
, Canada Post issued a forty- six- cent
1869– 1940
) once wrote
Artwork by Gillian Turner.
We thank Paul Cacciottolo, our Specialist Reader for this chapter.
Cardiovascular health
CKD:
https://t.me/med1917
Fig 3.
2
Top ten global causes of
2019
.
death,
Non-communicable disease.
Communicable disease.
Source: https:// www.who.int/ news-
room/ fact- she ets/ det ail/ the- top- 10-
Cardiovascular disease (
ischaemic heart disease (
IHD
eurysms.
fication is the key to prevention. All adults age
CVD
cohort equation. In discussion with the patient, consider treatment if ≥
developing
and st roke are globall y the lead ing c ause s of d eath (fig 3.2). Risk strati-
assessment using a validated risk model such as
CVD
CVD
) is common in the general population, and includes
IHD
), stroke, peripheral vascular disease, and aortic an-
40– 75
years should undergo routine
QRISK3
(www.qrisk.org) or pooled
within the next 10 years. Adults aged 20– 39 years should also be as-
cau ses- of- death
10
% risk of
sessed periodically as the prevalence of vascular risk factors such as hypertension
and diabetes are increasing at a younger age. Cardiovascular disease starts silently
at a young age, but those with fewer risk factors age more healthily.
Addressing modifiable risk factors
1
• A healthy diet should be c onsumed wit h plenty of fruit and vege tables whil e minim-
izing trans fatty acids, saturated fats, red meat, and refined carbohydrates.
• Regular physical activity of modera te- intensity exercise for ≥
• Obesity, now a global epidemic associated with significant morbidity and mortality,
should be tackled with a structured programme of caloric restriction and physical
activity. Consider a glucagon-like peptide (
for bariatric surgery (
• Smoking cessation saves lives and although sometimes it may seem futile to us, brief
p
618
).
GLP-1
) agonist (eg semaglutide) or referral
advice from doctors has been shown to increase the quit rate.
150
min utes/ week.
2
Refer to behavioural
support resources. Treat hospitalized patients and continue after discharge. First- line
cessation medications are nicotine replacement (gum, patches), varenicline (an oral
selective nicotine receptor partial agonist; start
bupropion (= amfebutamone; avoid if history of seizures). Caution against vaping as
the long- term eects are unknown and may include significant lung morbidity.
• Hypertension (p
the goal should be <
• Lipid- lowering therapy: start a statin for primary prevention if >10%
10
yea rs.
108
) is the leading modifiable risk factor. For most at- risk patients,
130/ 80
mmHg.
3
1
week before target stop date), and
CVD
risk in
• Tigh t glycaemic control in type 1 or 2 diabetic patients. Target HbA1c <48mmol/ mol
if young and not prone to hypoglycaemia.
• Antiplatelet therapy should not be routinely prescribed for primary prevention as
the net harm may outweigh the potential benefits.
•
prevent and treat underlying aetiology (eg diabetes, GN) where possible. Strict
BP
con trol <
120/ 80
mmHg.4 Prote inuri c pati ents are at much h igher risk.
85
3 Cardiovascular medicine
The randomized trial
Cardiovascular medicine has an unrivalled treasure house of randomized trials.
One of the chief pleasures of cardiovascular medicine lies in integrating these
with clinical reasoning in a humane way. After a cardiac event, a protocol may
‘mandate’ statins, aspirin, - blockers,
esterol that makes your patient feel dreadful. What to do? Inform, negotiate,
and compromise. Never reject your patient because of lack of compliance with
your over- exacting regimens. Keep smiling, keep communicating, and keep up to
date: the latest data may show that your patient was right all along.
ACE
- i (p
106
), and a target BP and
LDL
chol-
3 Cardiovascular medicine
Cardiovascular symptoms
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86
Chest pain Cardiac- sounding chest pain may have no serious cause, but always
MI
think ‘Could this be a myocardial infarction (
), dissecting aortic aneurysm, peri-
carditis, or pulmonary embolism?’, particularly if sudden- onset pain.
Character Constricting suggests angina, oesophageal spasm, or anxiety; a sharp
pain may be from the pleura, pericardium, or chest wall. A prolonged (>
dull, central crushing pain or pressure suggests
MI
.
Radiation To shoulder, either or both arms, or neck/ jaw suggests cardiac is-
chaemia. The pain of aortic dissection (
p
646
) is classically instantaneous, tearing,
and interscapular, but may be retrosternal. Epigastric pain may be cardiac.
Precipitants Pain associated with cold, exercise, palpitations, or emotion suggests
cardiac pain or anxiety; if brought on by food, lying flat, hot drinks, or alcohol, consider oesophageal spasm/ disease (but meals can also cause angina).
Relieving factors If pain is relieved within minutes by rest or glyceryl trinitrate
GTN
), suspect angina (
(
help, suspect
GTN
GI
causes. Pericarditic pain improves on leaning forward.
relieves oesophageal spasm more slowly). If antacids
Associations Dyspnoea occurs with cardiac pain, pulmonary emboli, pleurisy, or
MI
anxiety.
onary artery disease— and also by aortic stenosis, hypertrophic cardiomyopathy
(
by anaemia. Chest pain with tenderness suggests self- limiting Tietze’s syndrome.
may cause nausea, vomiting, or sweating. Angina is caused by cor-
HCM
), paroxysmal supraventricular tachycardia (
SVT
)— and can be exacerbated
Odd neurological symptoms and atypical chest pain— think aortic dissection.
Pleuritic pain Pain exacerbated by inspiration. Implies inflammation of the
pleura from pulmonary infection, inflammation, or infarction. It causes us to
‘catch our breath’. : musculoskeletal pain; fractured rib (pain on respiration,
exacerbated by gentle pressure on the sternum); subdiaphragmatic pathology
(eg gallstones).
Chest pain & acutely unwell (See p
(unequal in aortic dissection,
• IV line. • Relieve pain (eg
if hypoxic.
ECG
. •
CXR
lead
p
400
(
Dyspnoea May be from
. • Arterial blood gas (
); ruptured oesophagus; cardiac tamponade (p
LVF, PE
Severity Emergency presentations: p
764
p
646
.) • Admit. • Check pulse, BP in both arms
),
JVP
, heart sounds; examine legs for
2.5–5
mg IV morphine). • Cardiac monitor. • 12-
ABG
). Fa mo us t ra ps Aortic dissection; zoster
132
); opiate addiction.
, any respiratory cause, anaemia, pain, or anxiety.
765
. Ask about shortness of breath at rest,
on exertion, and on lying flat; has their exercise tolerance changed?
Specific symptoms associated with heart failure are orthopnoea (ask about
number of pillows used at night), paroxysmal nocturnal dyspnoea (waking up at
night gasping for breath,
associated with acute onset of dyspnoea and pleuritic chest pain; ask about risk
factors for
Palpitation(s) May be due to ectopics, sinus tachycardia, AF,
cosis, anxiety, and rarely phaeochromocytoma. See
DVT
.
p46), and peripheral oedema. Pulmonary embolism is
p36. History Characterize: do
SVT, VT
they mean their heart was beating fast, hard, or irregularly? Ask about previous
episodes, precipitating/ relieving factors, duration of symptoms, associated chest
pain, dyspnoea, dizziness, or collapse. Did the patient check their pulse?
Syncope May reflect cardiac or
(pulse, pupils dilated). The history from an observer is invaluable in diagnosis.
Prodromal symptoms
Chest pain, palpitations, or dyspnoea point to a cardiac
CNS
events. Vasovagal ‘faints’ are common
cause, eg arrhythmia. Aura, headache, dysarthria, and limb weakness indicate
CNS
causes. During the episode Was there a pulse? Limb jerking, tongue biting,
or urinary incontinence?
Recovery Was this rapid (arrhythmia) or prolonged, with drowsiness
seizures.
NB:
hypoxia from lack of cerebral perfusion may cause
(seizure)?
30
min),
DVT
. • Give O2
Associations
, thyrotoxi-
Chest pain from the patient’s perspective
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On acute wards we are always hearing questions such as ‘Is your pain sharp or
dull?’, followed by an equivocal answer. The doctor goes on: ‘Sharp like a knife—
or dull and crushing?’ The doctor is getting irritated because the patient must
know the answer but is not saying it. A true story paves the way to being less inquisitorial and having a more creative understanding of the nature of symptoms.
OHCM
A patient came to a previous
pain in my chest. Now I’ve woken up, and I’m not sure— have I got chest pain,
author saying ‘Last night I dreamed I had a
doctor? What do you think?’ How odd it is to be asked to examine a patient to
exclude a symptom, not a disease. (It turned out that she did have serious chest
pathology.) Odd, until one realizes that symptoms are often half- formed, and it
is our role to give them a local habitation and a name. Dialogue can transform a
symptom from ‘airy nothingness’ to a fact (
fig
1
3.3
).
Patients often avoid using the word ‘pain’ to describe ischaemia: ‘wind’, ‘tightening’,
‘pressure’, ‘burning’, or ‘a lump in the throat’ (angina means to choke) may be used.
They may say ‘sharp’ to communicate severity, and not character. So be as vague
in your questioning as your patient is in their answers. ‘Tell me some more about
what you are feeling (long pause) . . . as if someone was doing what to you?’ ‘Sitting
on me’ or ‘like a hotness’ might be the response (suggesting cardiac ischaemia).
Do not ask ‘Does it go into your left arm?’ Try ‘Is there anything else about it?’
(pause) . . . ‘Does it go anywhere?’ Note down your patient’s exact words.
A good history, taking account of these features, is the best way to stratify patients likely to have cardiac pain. If the history is non- specific, there are no risk
factors for cardiovascular diseases, and
6– 12
normal
doubt, get help. Features making cardiac pain unlikely:
• Stabbing, shooting pain.
• Pain lasting <30s, however intense.
• Well- localized, left sub- mammary pain (‘In my heart, doctor’).
• Pains of continually varying location.
• Youth.
NB:
h after the onset of pain, discharge will probably be OK. When in
25% of non- cardiac chest pain is musculoskeletal: look for pain on specific
ECG
and plasma troponin T (p
114
) are
postures or activity. Aim to reproduce the pain by movement and, sometimes,
palpation over the structure causing it. Focal injection of local anaesthetic helps
diagnostically and is therapeutic. Tietze’s syndrome: self- limiting costochondritis
± costosternal joint swelling. Causes: idiopathic; microtrauma; infection; psoriatic/ rheumatoid arthritis. :
caused by: fibromyalgia, lymphoma, chondrosarcoma, myeloma, metastases, rib
TB
. Imaging: bone scintigraphy; CT.
NSAID
S or steroid injections. Tenderness is also
87
3 Cardiovascular medicine
Fig 3.
3
The elephant on my chest. Image courtesy Eoin Kelleher.
1
Dialogue- transformed symptoms explain one of the junior doctor’s main vexations: when patients retell
symptoms to a consultant in the light of day, they bear no resemblance to what you originally heard. But do
not be vexed: your dialogue may have helped the patient far more than any ward round.
3 Cardiovascular medicine
ECG
QRS
https://t.me/med1917
88
— a methodical approach
Where to place the chest leads (See fig
v1 Right sternal edge, 4th intercostal space.
v2 Left sternal edge, 4th intercostal space.
v3 Half- way between
v4 5th intercostal space, mid- clavicular line;
all subsequent leads are in the same horizontal plane as
v5 Anterior axillary line.
v6 Mid- axillary line (
Reading an
ECG
First confirm the patient’s name and age, and
ECG
date. Then (see fig
the
• Rate At usual speed (25mm/ s) each ‘big
square’ is
0.2
s and ‘small square’ 0.04s. To calculate the rate, divide
big squares between two consecutive
The normal rate is
• Rhythm If cycles are not clearly regular, use the ‘card method’: lay a card along
ECG
, marking positions of three successive R waves. Slide the card to and fro to
the
check that all intervals are equal. If they are not, note if:
• there is slight but regular lengthening and then shortening (with respiration)—
sinus arrhythmia, common in the young
• there are dierent rates which are multiples of each other— varying block
• it is
Sinus rhythm is characterized by a
discernible
fig
3.40
, p
QRS
regular
following them or absent (
• Axis The overall direction of depolarization across the patient’s anterior chest; this
is the sum of all the ventricular electrical forces during ventricular depolarization.
BOX
See
from a left ventricular focus,
anterolateral
• P wave Normally precedes each
verted in a
P
mitrale: bifid P wave, indicates left atrial hypertrophy. P pulmonale: peaked
P
wave, indicates right atrial hypertrophy. Pseudo- P- pulmonale seen if K+ .
• PR interval Measure from start of P wave to start of
3– 5
small squares). A prolonged PR interval implies delayed AV conduction (1st-
(
60– 100
100
% irregular— atrial fibrillation (
P
waves and
127
) has a ‘sawtooth’ baseline of atrial depolarization (~
complexes. Ventricular rhythm has
. Left axis deviation can result from left anterior hemiblock, inferior MI, VT
MI, WPW
VR
. Absent P wave: AF, P hidden due to junctional or ventricular rhythm.
degree heart block). A short
an accessory pathway, eg
•
complex See fig
conduction defects, eg a bundle branch block (
ventricular origin or a paced rhythm. High- amplitude
tricular hypertrophy (
are often seen in leads
Patholog ical
• QT interval Measure from start of
corrected
interval, ie
longed
• ST segment Usually isoelectric. Planar elevation (>1mm) or depression (>0.5mm)
usually implies infarction (
• T wave Normally inverted in aVR,
lation in lead
fig
(
Q
waves (deep and wide) may o ccur w ithin a few hours of an acute MI.
QT
interval (QTc) is the QT interval divided by the square root of the R– R
QT
c = QT/ √RR. Normal QTc: <0.45s (M) or <0.46s (F). For causes of pro-
QT
interval, see p
III
14.3, p
. Abnormal if inverted in I, II, and
667
) and flattened in hypokalaemia.
3.4
.)
V
and
V
.
2
4
V
.
4
V
: posterior axillary line).
7
2
1
3
4
ECG
leads.
300
III, & aVF
5
/ min) and
RVH, PE
but in-
3.5
):
300
by the number of
R
waves.
Fig 3.
4
bpm.
AF)
P
QRS
fig
wave followed by a
complexes are irregularly irregular. Atrial flutter (p
3.15
, p98).
WPW, LVH
. Right axis deviation can result from
Placement of
or v entri cular fi brill ation (VF).
QRS
complex. AF has no
QRS
complexes >0.12s with P waves
, and left posterior hemiblock.
QRS
complex, and upright in II,
QRS
. Normal range: 0.12– 0.2s
PR
interval implies unusually fast AV conduction down
WPW
(see fig
3.42
, p
129
3.6
. Normal duration: <0.12s.
). See heart block, p90.
QRS
>0.12s suggests ventricular
p92, p93), metabolic disturbance,
QRS
complexes suggest ven-
p92). Normal Q waves are <0.04s wide and <2mm deep; they
I, aVL, V
, and
V
and reflect normal septal depolarization.
5
6
QRS
to end of T wave. It varies with rate. The
697
. Long QT can lead to VT and sudden death.
p
115
, figs
3.12, 3.13
, pp
95–6
V
, and occasionally
1
) or ischaemia, respectively.
V
. Normal if inverted in iso-
2
V
–
V
. Peaked in hyperkalaemia
4
6
6
126
;
,
Fig 3.
RRR
SSQ S
QQS
HEAD
–
90
°
aVF
+
90
°
FEET
aVR
–
150
°
180
°
+
120
°
III II+
60
°
I
0
°
–
30
°
aVL
RI
GHT
LEF
T
https://t.me/med1917
5
Schematic diagram of a normal
R'
Fig 3.
6
‘
QRS
’ complexes. If the first deflection from the isoelectric line is negative, it is a Q wave.
Any positive deflection is an R wave. Any negative deflection after an R is an S. A second positive
deflection within the same complex is R' (R prime).
ECG
trace.
RR
89
3 Cardiovascular medicine
Determining the
ECG
axis
Each ‘lead’ on the 12- lead
plane (fig
3.7
).
The axis lies at 90° to the
direction of the lead in which
the isoelectric (equally + ve
and −ve)
QRS
complex is
found. For example, if the
QRS
is isoelectric in lead II
(+ 60°), the axis is either:
+ 60° – 90° = –30°, or
+ 60° + 90° = +
If the
150
QRS
is more positive
°.
than negative in lead I (0°)
then the axis must be −30°,
and vice versa.
In practice, the exact axis matters little; what you need to be able to recognize is
whether the axis is normal (−30° to + 90°), left- deviated (<−30°), or right deviated
(>+ 90°). There are many ways of doing this. If the
antly positive (the R wave is taller than the S wave is deep), the axis must be be-
tween −90° and + 90°. If lead II (+ 60°) is mostly positive, the axis must be between
−30° and +
+ 90°— the normal range. When II is negative, the axis is likely to be left- deviated
(<−30°) and when I is negative, the axis is likely to be right- deviated (>+ 90°). One
way of remembering this is:
• Lovers Leaving— Left axis deviation— the
• Lovers Returning— Right axis deviation— the
150
°. So if both I and II are positive, the axis must b e betwe en −30° and
each other.
towards each other (fig
ECG
represents electrical activity along a particular
Fig 3.
7
The planes represented by the limb ‘leads’.
QRS
in lead I (0°) is predomin-
QRS
com plexes in I and II point away from
QRS
3.14
, p97).
complexes in I and
III
± II point
3 Cardiovascular medicine
ECG
AF
https://t.me/med1917
90
— abnormalities
Sinus tachycardia All impulses are initiated in the sinoatrial node (‘sinus
rhythm’) hence all
QRS
Tachycardia means rate >
Sinus bradycardia Sinus rhythm at a rate <60bpm. Causes Physical fitness,
vasovagal syncope, sinus node dysfunction, drugs (- blockers, digoxin, amiodarone,
non- dihydropyridine
p
118
.
See
(
ECG
, p
121
alcohol. See
) Common causes:
p
126
.
Heart block (HB) (See fig
AV
node or His– Purkinje system. 1st- and 2nd- degree HB may be caused by: normal
variant, athletes, sinus node dysfunction,
drugs (digoxin, - blockers).
• 1st- degree HB Delayed AV conduction. The PR interval is prolonged and un-
changing; no missed beats.
• 2nd- degree HB: Mobitz I (Wenckebach) Intermittent block within the AV node. The
PR
interva l progr essive ly len gthens until a
• 2nd- degree HB: Mobitz II Dysfunction of the His– Purk inje pathway. The PR interval
of the conducted beats is constant until one or more
complex. This is a dangerous rhythm as it may progress to complete
• 3rd- degree HB: complete heart block No impulses are passed from atria to vent-
P
waves and
ricles so
AV
node paces slowly, the patient becomes very bradycardic, and may develop
the
haemodynamic compromise. Urgent treatment is required.
MI
), idiopathic (fibrosis), congenital, infective endocarditis, cardiac surgery/ trauma,
digoxin toxicity, infiltration (abscesses, granulomas, tumours, parasites).
ST
elevation Normal variant, widespread concave pattern in young patients due to
benign early repolarization, acute
carditis (saddle- shaped) (
left ventricular aneurysm.
ST
depression Normal variant (upward sloping), digoxin toxicity (downward sloping),
ischaemic (horizontal): angina,
T
inversion In
block (
arachnoid haemorrhage, lithium. In
branch block
NB: ST-
V
–
V
RBBB), RV
1
strain (eg secondary to PE). In
(LBBB)
. In II,
and T- wave changes are often non- specific, and must be interpreted in the
light of the clinical context.
Myocardial infarction (See p
• Within hours, the T wave may become peaked and ST segments may begin to rise.
• Within 24h, the T wave inverts. ST elevation rarely persists, unless a left ventricular
aneurysm develops.
• Within a few days, pathological Q waves begin to form. Q waves usually persist, but
may resolve in
• The location of these changes indicates the ischaemic area location, see table
10
% of patients.
Pulmonary embolism (See fig
RBBB
(commonest),
R
wave, and T- wave inversion/ ST depression in
occurs: deep
(p92), right ventricular strain pattern
S
waves in I, pathological Q waves in
Metabolic abnormalities Digoxin eect Down- sloping ST depression and in-
T
wave in
V
verted
arrhythmia may occur (ventricular ectopics and nodal bradycardia are common).
Hyperkalaemia Tall, tented T wave, widened
pearance (see
P
peaked
interval, small
–
5
fig
14.3, p
waves. Hypercalcaemia Short QT interval. Hypocalcaemia Long QT
T
waves. See p
ALGrawany
S are preceded by a normal
100
bpm. See p
CCB
s), hypothyroidism, hypothermia, intracranial pressure.
IHD,
thyrotoxicosis, hypertension, obesity, heart failure,
3.8
.) Disrupted passage of electrical impulse through the
3
rd- degree HB is always pathological.
QRS
S appear independently of each other. As tissue distal to
MI (STEMI)
fig
3.45
, p
133
NSTEMI
: normal (black patients and children), right bundle branch
3
T
- wave inversion may or may not persist.
V
(‘reversed tick’, see fig
6
667
, acute posterior
V
–
V
III
4
and aVF: inferior ischaemia.
114
and fig
3.14
, p97.)
). Hypokalaemia Small T waves, prominent U waves,
697
for causes of long QT intervals.
P
123
wave with a normal PR interval.
.
IHD
(esp. inferior MI), acute myocarditis,
QRS
is m issed, the patter n then resets .
P
waves is not followed by a
, Prinzmetal’s angina (p
Causes
HB.
IHD
(esp. inferior
696
), acute peri-
), myocarditis, Takotsubo cardiomyopathy,
MI (ST
depression in
V
–
V
: anterior ischaemia,
2
3.27
; example
5
ECG
S, figs
and aVL: lateral ischaemia,
6
LVH
3.12, 3.13
V
–
V3).
1
HCM
, sub-
, left bundle
, pp95–6.)
3.1
ECG
findings may include: sinus tachycardia
(R-
V
QRS
and
1
axis deviation, dominant
V
,). Rarely, the ‘
2
III
, inverted T waves in
3.23
, p
107
). In digoxin toxicity, any
S1Q3T3
III
.
, absent P waves, ‘sine wave’ ap-
’ pattern
QRS
.
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