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Cardiology
This document is based on the handout from the “Medicine for Finals” course. The notes
provided here summarise key aspects, focusing on areas that are popular in clinical
examinations. They will complement more detailed descriptions and are not intended to be
comprehensive.
Topics covered in these notes
• Examination
• Atrial fibrillation
• Mitral valve disease
• Aortic valve disease
• Coronary heart disease
• Left ventricular failure
These are the core topics of cardiology. Additional topics include:
a) arrhythmias
b) cardiomyopathy
c) hypertensive heart disease
d) the ECG
There is a separate document introducing the ECG, with test-yourself examples.
There are three types of cardiomyopathy- dilated (the commonest), obstructive (HOCM;
causing subvalvular left ventricular outflow obstruction-differential from aortic stenosis) and
restrictive (rare). Dilated cardiomyopathy would be suspected in a patient presenting with
heart failure who did not have a previous history of angina or myocardial infarction. When
angiograms are performed, at least 60% of such patients are found to have “silent” coronary
disease (ie previously undetected) and the remainder, with normal coronary arteries, have
cardiomyopathy. This may be primary or secondary (for example alcohol-related).
Examination
• It doesn’t matter if you miss a physical sign, so long as your technique is good
• You need to look as though you have a routine, even if it is different from the
examiner’s; “acceptable variation”
• You need to look caring and competent
• Everyone misses diastolic murmurs
It is well recognised that diastolic murmurs are hard to detect, particularly with the added
stress of a clinical examination. Cardiologists regularly miss diastolic murmurs too- or else
arrange an echo before examining the patient so they know what they are looking for! The
important point is to give yourself the best opportunity to hear them. This means lying the
patient on the left hand side and listening with the bell for the low-pitched murmur of mitral
stenosis. This murmur is probably the most localised of any heart sound, so “inching your
way around the apex” is appropriate. Remember that to pick up low-pitched sounds the bell
needs to be very lightly applied- too tight and it will convert the patient’s skin into a
diaphragm. Finally, you need to sit the patient forward and listen at the end of expiration with
the diaphragm applied to the left sternal edge for the high pitched early diastolic murmur of
aortic regurgitation.
 Dr R Clarke
www.askdoctorclarke.com
1
Question stop
What causes the first and second heart sounds?
What are the signs of endocarditis?
(Hint: try to mention the ones without people’s names attached first!)
What are the signs of clubbing?
Heart sounds: lub dub
lub
dub
ventricular systole
 Dr R Clarke
www.askdoctorclarke.com
diastole
2
The first and second heart sounds are caused by valve closure. The first sound is caused by
closure of the mitral and tricuspid valves and the second sound by the closure of aortic and
pulmonary. If heart sounds were single, they would sound “le- de…le de”. The fact that each
sound is composed of two valves closing, with a slight separation between them, results in
“lub dub…lub dub”).
General examination
• Anaemia, cyanosis, breathlessness
• Hands for clubbing and splinters (the hand signs of endocarditis)
• Signs of endocarditis:
- 2 in the hands (clubbing and splinters)
- 1 in the heart (changing murmurs)
- 2 in the abdomen (splenomegaly, microscopic haematuria)
- plus a few rarities (Osler, Roth, Janeway etc)
Pay particular attention to the instructions. There is a no win instruction- “examine the heart”.
If you start checking the hand and pulse, the examiner could say “No I said the heart”. On the
other hand, if you go straight for the praecordium (anterior chest wall for apex etc), the
examiner might say “Oh, don’t you bother with the pulse when you examine the heart?”
If you are asked to examine the heart, you might check by saying “Normally I start with the
hands and the pulse, is that what you intend me to do now?” This should make the examiner
apologetic with either:
“Yes, examine the cardiovascular system” or
“No confine your attention to the praecordium”
Stages of clubbing
• Increased fluctuancy (of nail bed)
• Loss of angle
• Increased curvature
• Drum stick appearance (expansion of terminal phalanx)
Stages of Clubbing
Stage 1: normal appearance and angle
but increased fluctuancy of nail bed
Stage 2: loss of angle between nail
and nail bed
Stage 3: increase curvature of nail
Stage 4: expansion of terminal phalanx
Drum stick appearance
 Dr R Clarke
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3
Examination
• Anaemia, cyanosis, breathlessness
• Hands for clubbing and splinters
• Pulse- rate, rhythm, character, volume
• Collapsing pulse test
• Ask for or measure blood pressure
• Neck for collapsing pulse; then JVP
Testing for a
Collapsing Pulse
JVP
• Everyone finds it confusing!
• The key is to think separately about the internal jugular (a pulsation) and the
external jugular (a visible superficial vein)
Internal jugular vein
 Dr R Clarke
External jugular vein
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4
Jugular venous pulse
• Neck relaxed as internal jugular is behind sterno-mastoid which should be relaxed
• Best to look from in front- you are looking for a pulsation not a visible vein
• JVP usually has a “double pulsation” compared with arterial pulse- may appear to
be “flickering”
• If raised, check for sacral or ankle oedema
The external jugular is best seen from the side, which is why many people look from the side
when assessing the JVP. In fact, it is easier to see the pulsation of the internal jugular from
the front. If in doubt, check both from the front and from the side- then everyone will be
happy!
This is probably all you need to do as a medical student or junior doctor. If you haven’t seen
the JVP, it is usually reasonable to assume the central venous pressure isn’t elevated.
However, some clinicians want to be sure the JVP is not high, even when they haven’t seen
it, and this is where, for many of us, things start to feel confusing.
If JVP not seen, 3 options to prove pressure not high
• Hepato-jugular reflux- painful and many false positives and false negatives
• Move patient slowly, step-by-step, into more horizontal position, noting angle at
which JVP seen (laborious)
• Fill and empty external jugular vein (light pressure just behind sternomastoid)
The first approach involves pressing on the abdomen, which transmits pressure via the
inferior vena cava to the superior vena cava. This may make the JVP become visible in the
neck. Removing the abdominal pressure should then result in a return to the initial situationwith no JVP visible. The problem is that there are both false positive and false negatives with
this manoeuvre and it causes significant discomfort to the patient (“The last doctor punched
me in the guts and looked at my neck- I don’t understand why they do that”).
The second approach is ideal for obsessionals. You move the patient into a progressively
more horizontal position until the JVP becomes visible. If this is less than 45 degrees, the
JVP is not elevated. This procedure involves so much wrestling with the pillow-rest that most
people do not bother with it.
The third approach is quick and easy and where it works can be additional good evidence
that the JVP is not elevated. Light pressure with one finger behind sternomastoid at the base
of the neck, will lead, after a few seconds, to filling of the external jugular vein by blood
draining from the head and neck. Then the examining finger is removed and the vein should
empty again. This confirms that the “manometer pressure” is not high. Compressing the vein
is the equivalent of filling the manometer of a CVP device (by connecting the fluid supply to
the vertical measuring tube). Removing the finger is the equivalent of turning the three-way
tap to connect manometer and patient.
External jugular vein
• Often distended and pulsatile when internal jugular pressure raised
• But false positives- may be distended if vein kinks as it pierces fascia in neck
• And false negatives: not visible if low flow or situated deeply or excess fat
 Dr R Clarke
www.askdoctorclarke.com
5
JVP: the evidence
• Poor validity- correlation with right atrial pressure from cardiac catheter data
• Poor reliability (McGee, S. 1998. American Heart Journal 136:10-18)
• Pulsation 3cm above sternal angle in either external or internal vein is significant
If anyone gives you a hard time about the JVP, it may be worth mentioning that it is one of
the worst physical signs in the whole body- both in terms of reliability and validity. If it is
obviously elevated, this can help, but if it is hard to assess, you may need additional
evidence of heart failure from echocardiography or cardiac catheterisation. This brings us full
circle and is an argument for looking once only with the patient lying relaxed at 45 degrees
and to forget the three manoeuvres to prove the pressure is not high!
Praecordium
• Apex beat (look for scars as well as feel)
• Left parasternal (for right ventricular impulse)
• Aortic and pulmonary areas for thrills
• Auscultation- bell and diaphragm from apex to neck
• Patient on left side with bell for mitral stenosis
• Patient sitting forward, at the end of expiration, with diaphragm (for aortic
regurgitation)
 Dr R Clarke
www.askdoctorclarke.com
6
Case 1: irregularly irregular pulse
•
What are the main two possible explanations and how would you distinguish
them?
• What are the causes of atrial fibrillation?
•
How would you assess whether atrial fibrillation is well controlled?
•
Why is there sometimes a difference between the pulse rate taken at the wrist
and the apex?
•
In a patient with atrial fibrillation taking warfarin, what level of INR would you
aim for?
•
What level would you aim for if the patient had a prosthetic valve?
•
What does INR stand for?
Atrial fibrillation
• Loss of atrial contraction reduces cardiac output- often triggers heart failure
• Relative stagnation within atria gives high risk of thrombo-embolism
• Fast ventricular rate may occur; loss of diastolic filling time worsens heart failure
• Digoxin and verapamil slow rate by increasing delay at a-v node
 Dr R Clarke
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7
Atrial fibrillation is probably the commonest case in clinical exams at undergraduate level.
The other cause of an irregularly irregular pulse is the presence of multiple ventricular ectopic
beats. This can be distinguished without an ECG because multiple ectopics should be
abolished by exercise, making the pulse become regular, whereas exercise simply increases
the rate in atrial fibrillation. With an ectopic ventricular focus, beats are transmitted to the
ventricle only occasionally when the refractory period allows. Increasing the sinus node rate
by exercising the patient will make it less likely that the ectopic focus can “drive the ventricle”
Case 2: Mitral stenosis
• Malar flush
• Atrial fibrillation
• JVP not raised
• Apex beat not displaced
• Apex beat tapping in quality
Mitral stenosis: LUB de de
• Loud first heart sound (high left atrial pressure keeps valve open until late in
diastole; systole then slams it shut)
• Opening snap (high pitched sound just after second heart sound- best heard at
lower left sternal edge with diaphragm)
LUB D e De
LU B
De
v e n tr ic u la r s y s to le
De
d ia s to le
Now add a mid-diastolic murmur: LUB de derrr
• LUB de-derrr
• Rumbling low pitched and mid-diastolic if mild stenosis
• If more severe, murmur may extend later into diastole
 Dr R Clarke
www.askdoctorclarke.com
8
L u b D e D e rrrr
LU B
De
D e rrrr
v e n tric u la r s ys to le
d ia s to le
Mitral stenosis: the problem
• If severe, the murmur may become the dominant sound and the
ear plays tricks on you!
• So instead of hearing “LUB de derrr”
• You hear “DurrB de de”
• Particularly likely if atrial fibrillation
• Try to time the murmur with the carotid pulse
E a r p la y s tric k s : D u rrB d e d e
D u rrrrB
De De
v e n tric u la r s ys to le
 Dr R Clarke
D u rrrrB
d ia s to le
www.askdoctorclarke.com
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Mitral Stenosis: x-ray appearance
Aortic knuckle
Pulmonary vessels
Prominent left atrium
Left ventricle
(not enlarged in pure
stenosis)
Case 3: Mitral regurgitation
• More likely to be in sinus rhythm
• Much commoner (eg post myocardial infarction)
• Quiet first heart sound
• Pansystolic murmur
• Radiates LOUDLY to axilla
• Second heart sound not heard separately
M itral regurgitation: “burrr”
no g ap betw e en m urm ur and H S 2
lu b
de
H S 1 q uiet
P ans ysto lic m urm ur
 Dr R Clarke
www.askdoctorclarke.com
diastole
10
Case 4: Aortic regurgitation
• Collapsing pulse (Corrigan’s pulse)
• Collapsing pulse in the neck (Corrigan’s sign)
• JVP not raised
• Apex beat displaced
• Diastolic murmur follows second sound
Aortic regurgitation: lub taaarr
taaar
lub
ventricular systole
diastole
Causes of aortic regurgitation
• Rheumatic heart disease
• Luetic heart disease (tertiary syphilis weakens aortic wall, causing dilatation)
• Endocarditis
• Connective tissue disease (Marfans’ etc)
 Dr R Clarke
www.askdoctorclarke.com
11
Case 5: Aortic stenosis
• Slow rising pulse
• Low volume pulse with low pulse pressure
• JVP not elevated
• Apex beat forceful but not displaced (pressure overload)
• Ejection systolic murmur
Aortic stenosis
audible gap between
mumur and HS2
lub
dub
second sound quiet
with severe stenosis
ventricular systole
diastole
Coronary heart disease
• Draw a diagram showing the main blood supply to the myocardium
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Left main stem
Circumflex
Right coronary artery
Left anterior descending
Myocardial infarction
Left main stem
Left anterior descending
Left circumflex
Right coronary
Large anterior
Anteroseptal
Anterolateral
Inferior
V1-V6
V1-V4
1, aVL, V4-6
2, 3, aVF
Pump problems
Bradyarrhythmias
Case 6: Angina vs MI
• Pain less severe and lasts less than 20 minutes
• Relieved by nitrates
• No sweating, nausea, vomiting
• May get nitrate headache and hypotension
• No fear of impending doom (poor predictive value)
Complications of MI
• Sudden death on PRAED Street
• P- pump failure
• R- rupture of papillary muscle or septum
• A- aneurysm and arrhythmias
• E- embolism
• D- Dressler’s syndrome
 Dr R Clarke
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Investigations
• Temperature chart (often slight fever day 2)
• FBC, U+E (exclude anaemia; avoid low K+- arrhythmogenic)
• Blood glucose; lipids (within 24hours as levels fall thereafter)
• Cardiac enzymes- CPK, AST, LDH (false positives with injury, alcohol, exercise)
• Troponins- myofibrillar proteins which link actin and myosin. More specific than
CPK for myocardial injury. Elevated early after 6 hours, peak 24hours; remain
elevated for 2 weeks; good for diagnosis of missed infarct; not for re-infarction)
• CXR- for cardiac size and evidence left ventricular failure
• Serial ECGs- may be normal initially, ST elevation, then q waves if transmural,
later t wave inversion
Acute Myocardial Infarction
st elevation
q waves
imply a full thickness
transmural infarct;
without them:
subendocardial
Treatment options: "MORE GAS"
M
Morphine or diamorphine with metoclopramide IV
O
Oxygen- high flow unless COPD
R
Reassurance
E
Explanation
G
A
S
GTN
Aspirin
Streptokinase (unless contraindication- local or generalised bleeding risk,
allergic problems etc)
What are the signs of left ventricular failure?
• Apart from basal crackles?...
 Dr R Clarke
www.askdoctorclarke.com
14
Case 7: Acute LVF: on inspection
• Patient looks acutely unwell- pale and grey
• Cold clammy peripheries ? cyanosis
• Frothy blood stained sputum in sputum pot
• Orthopnoeic using accessory muscles
• May have wheeze (cardiac asthma)
Third heart sound: lub de dub
lub
de dub
diastole
ventricular systole
Acute LVF
• Sinus tachycardia or atrial fibrillation
• Systolic hypotension
• Signs of cardiomegaly (displaced apex, signs of valve disease)
• Third and fourth heart sounds
• Right sided or bilateral pleural effusions
F ourth heart sound: le lub dub
du b
Le lub
ventric ular systo le
 Dr R Clarke
www.askdoctorclarke.com
diastole
15
X-ray changes
• Cardiomegaly
• Upper lobe diversion
• Diffuse mottling of lung fields
• Prominent hilar shadows- bat’s wings
• One bat’s wing= “pseudotumour of heart failure” - usually at right hilum
• Small pleural effusions
• Fluid in fissures
Bat’s wings appearance in pulmonary oedema
Treatment options
• High dose oxygen
• Treat significant arrhythmias
• Intravenous diuretics
• Intravenous diamorphine; if no improvement-
•
•
Repeat diuretics
Vasodilator eg isosorbide infusion
ECG changes of hyperkalaemia
• Low flat p waves
• Broad bizarre qrs
• Slurring into the st segment
• Tall tented t waves
 Dr R Clarke
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16
Low flat P wave
Tall tented T waves
Broad
bizarre
QRS
Slurring
into the
ST segm ent
Treatment of life threatening hyperkalaemia
First arrange ECG monitor and access to resuscitation equipment
Intravenous calcium gluconate (stabilises myocardium)
Glucose and insulin (drives potassium into cells)
Further options include:
Cation exchange resins eg calcium resonium enema (takes several hours to work)
Dialysis
 Dr R Clarke
www.askdoctorclarke.com
17
Examination of the Cardiovascular System: Summary
"Examine the heart"
Clarify whether the examiner wants you to:
• Examine the cardiovascular system or
• Examine the praecodium or
• Auscultate the heart.
Remember
There is acceptable variation in practice.
Check if the examiner wants a running commentary.
Introduce yourself and ask permission.
Check the patient is comfortable, at 45 degrees with neck muscles relaxed.
Routinely checking for radio-femoral delay is probably not justified.
Reasonable to say you would check this later if hypertension or systolic murmur
noted.
General
?anaemic ?cyanosis ?breathless
Hands
For signs of endocarditis: ?clubbing ?splinter haemorrhages
Pulse
Check both radial pulses present (? AV fistula for dialysis)
Then rate, rhythm, character, volume
Collapsing pulse test while
Looking at neck for visible collapsing pulse
BP
Ask for or measure BP
JVP
Look for pulsation behind sternomastoid
Optional extras
If JVP seen, gentle compression eliminates pulsation
If not seen, light pressure at base of neck to fill external jugular;
then release of pressure to demonstrate emptying (proves
pressure not high)
Praecordium
Inspect
Midline scar ?CABG ?valve replacement
Intercostal scar at apex ?closed mitral valvotomy
? apex beat visible
Palpate
Aortic and pulmonary areas, left sternal edge and apex
Auscultation
All areas including neck; bell and diaphragm in each area
Mitral area with bell and patient turned onto left side
Aortic area and left sternal edge, using diaphragm with patient
sitting forward at end of expiration
Extras
If appropriate, look for ankle and sacral oedema
and auscultate lung bases
 Dr R Clarke
www.askdoctorclarke.com
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