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CHAPTER9 Cardiology and vascular disease
Symptoms and signs ofCVD
Chest pain E p. 1064 Breathlessness or dyspnoea E p. 264
Blood pressure E p. 218 Crackles in the chest E p. 269
Peripheral oedema Swelling of the ankles/ legs (or sacrum if bed
bound) occurs when the rate of capillary ltration > rate drainage.
• i capillary ltration occurs due to i venous pressure, hypo-
albuminaemia, or local inammation
• d drainage occurs due to lymphatic obstruction
Consider whether swelling is acute or chronic, symmetrical or asymmetrical, localized or generalized. Ask about associated symptoms, e.g. breathlessness. Treat according to cause. Causes:
Acute
• DVT
• Supercial thrombophlebitis
• Arthritis
Chronic
• Gravitational oedema, e.g. due to immobility— common in the elderly.
Advise elevation of feet above waist level, support stockings (ideally
apply stockings before getting out of bed), avoid standing still. Diuretics
are not a long- term solution
• Heart failure
• Hypoproteinaemia, e.g. nephrotic
syndrome
• Idiopathic oedema
• Reex sympathetic dystrophy
• Post- thrombotic syndrome
Pulmonary oedema Accumulation of uid in the pulmonary tissues
and air spaces. Causes include:
Cardiac/ vascular Other
• Left heart failure
• Mitral stenosis
• MI
• Hypertension
• Pulmonary venous obstruction
• IV uid overload
Lung
• Pneumonia • PE
• Pneumonitis due to inhalation of toxic substances, e.g. gases, radiation
Cyanosis Dusky blue skin.
Central cyanosis Cyanosis of mucus membranes, e.g. mouth. Causes:
• Lung disease resulting in inadequate oxygen transfer (e.g. COPD, PE,
pleural eusion, severe chest infection)
• Cellulitis
• Haematoma
• Baker’s cyst
• Fracture
• Acute arterial ischaemia
• Dermatitis
• Chronic venous insuciency/
venous obstruction
• Lipodermatosclerosis
• Lymphoedema— infection,
tumour, trauma
• Congenital vascular abnormalities
• High altitude
• Kidney failure
• Nephrotic syndrome
• Cirrhosis
• Lymphatic obstruction, e.g. due
to tumour
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SYMPTOMS AND SIGNS OFCVD
• Shunting from pulmonary to systemic circulation (e.g. Fallot’s tetralogy,
PDA, transposition of the great arteries)
• Inadequate oxygen uptake (e.g. met- or sulfhaemoglobinaemia)
Peripheral cyanosis e.g. cyanosis of ngers. Causes:as for central cyanosis plus:
• Physiological (cold, hypovolaemia)
• Local arterial disease (e.g. Raynaud’s syndrome)
0 Feet can be a dusky blue colour due to venous disease. If this occurs
without central cyanosis it does not imply abnormal oxygen saturation.
Mitral facies Dusky bluish red ushing of the cheeks (a form of peripheral
cyanosis) associated with a low cardiac output.
Clubbing Loss of the angle between nail fold and plate, bulbous ngertip,
and the nail fold feels boggy— E p. 577.
• Refer any patient with unexplained nail clubbing for urgent CXRN.
Jugular venous pressure Observe internal jugular vein at 45° with
head turned slightly to the left. Vertical height is measured in relation to the
sternal angle. Raised if >4cm. Causes of i JVP:
• Fluid overload
• Right heart failure and CCF
• SVC obstruction (non- pulsatile)
• Tricuspid or pulmonary valve
disease
Kussmaul’s sign The JVP usually drops on inspiration along with intrathoracic
pressure. The reverse pattern is called Kussmaul’s sign. Caused by raised
intrathoracic pressure or constrictive pericarditis.
• Pulmonary hypertension
• Arrhythmia— AF or atrial utter,
complete heart block
• i intrathoracic pressure, e.g.
pneumothorax, PE, emphysema
Signs ofinfectiveendocarditis
• Infective Fever, weight d, clubbing, splenomegaly, anaemia
• Cardiac Murmurs (particularly new murmurs) ± heart failure
• Embolic Neurologic decit due to stroke
• Vasculitic Microscopic haematuria, splinter haemorrhages, conjunctival
haemorrhages, Roth’s spots (retinal vasculitis), Osler’s nodes (painful
lesions on nger pulps), Janeway lesions (palmar macules)
Signs ofhypercholesterolaemia
Corneal arcus Whitish opaque line surrounding the margin of the cornea,
separated from it by an area of clear cornea. Rarely congenital— more
commonly occurs bilaterally in patients >50y (arcus senilis). Sometimes associated with i blood lipids— particularly familial hypercholesterolaemias.
Check lipids. If lipids are normal, no treatment is needed.
Xanthomata Localized collections of lipid- laden cells. Appear as yellowish
coloured lumps. Often caused by i lipids. Commonly seen on the eyelids
(xanthelasma), on the skin, or in tendons (appear as mobile nodules in the
tendon).
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CHAPTER9 Cardiology and vascular disease
Examining theheart
Apex beat Normal position is in the 5th intercostal space, in the
midclavicular line. Moved sideways/ inferiorly if the heart is enlarged (e.g.
CCF) or displaced (e.g. pneumothorax). May not be palpable if the patient
is obese, has hyperexpanded lungs (e.g. COPD) or a pericardial eusion. In
infants/ children apex beat is superior/ more lateral.
Parasternal heave Detect by placing the heel of the hand over the left
parasternal region. If present, the heel of the hand is lifted o the chest wall
with each heartbeat. Causes:Usually right ventricular enlargement— rarely
left atrial enlargement.
Heart sounds Table 9.2. Low/ medium- frequency sounds (e.g. 3rd/ 4th
heart sounds) are more easily heard with the bell applied lightly to the skin.
High- frequency sounds (e.g. 1st/ 2nd heart sounds and opening snaps) are
more easily heard with a diaphragm.
Heart murmurs Due to abnormalities of ow within the heart and
great vessels. Very common. Often incidental ndings. Described by:
• Location Where heard loudest
• Quality e.g. blowing, harsh
• Intensity Graded out of 6 (1— virtually undetectable; 6— heard by an
observer with no stethoscope). Grades 4– 6 are usually palpable (thrills)
• Timing Systolic or diastolic
• Radiation Does the murmur spread elsewhere, e.g. to axilla, carotids
• Red ag symptoms
• Cyanosis
• Breathlessness
Always refer for Echo. Dierential diagnosis— Table 9.1.
Table9.1 Dierential diagnosis ofheart murmurs
Type of murmur Description Causes
Ejection systolic
murmur
Pan-systolic
murmur
Early diastolic
murmur
Mid-diastolic
murmur
• Lethargy/ tiredness
• Collapse
i to reach a peak
midway between the
heart sounds.
Uniform intensity
between the 2 heart
sounds. Merges with
2nd heart sound
Occurs just after the
2nd heart sound. High
pitched. Easily missed.
Midway between 2nd
heart sound of 1 beat
and 1st of the next.
Rumbling/low pitch
• Weight loss (or failure to thrive)
• Flow murmurs, e.g. children, pregnancy,
with fever, during/after exercise
• Aortic stenosis or sclerosis (E p. 251)
• Pulmonary stenosis (E p. 251)
• HOCM (E p. 248)
• Mitral valve regurgitation/prolapse
(E p. 250)
• Tricuspid regurgitation (E p. 251)
• VSD (E p. 252)
• ASD (E p. 252)
• Aortic regurgitation (E p. 251)
• Pulmonary regurgitation (E p. 251)
• Tricuspid stenosis (mitral stenosis coexists)
• Mitral stenosis (E p. 250)
• Aortic regurgitation. (Austin Flint
murmur—E p. 251)
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EXAMINING THEHEART
Table9.2 Heart sounds, abnormalities and their causes
Heart sound Causes
1st heart sound
Heard loudest at
the apex.
Caused by
closing of the
mitral and
tricuspid valves
2nd heart sound
Caused by
closure of the
aortic (A2) and
pulmonary (P2)
valves
A2 and P2 split
on inspiration so
that P2 is heard
after A2
Clicks and snaps Early
3rd heart sound
Heard in diastole
after the 2nd
heart sound
4th heart sound
Heard in late
diastole
Soft Mitral regurgitation, low BP, rheumatic carditis,
severe heart failure, LBBB
Loud AF, tachycardia, atrial premature beat, mitral stenosis
Variable
Varying duration of diastole, complete AV block
intensity
Split RBBB, paced beat from the left ventricle, left
ventricular ectopics, ASD, Ebstein’s anomaly,
tricuspid stenosis
Soft A2—calcication of the aortic valve, dilatation of
the aortic root
P2—pulmonary stenosis
Loud A2—i BP; thin patients
P2—pulmonary hypertension, ASD
Wide
May be the result of early A2 or delayed P2
splitting
Early A2—mitral regurgitation; VSD
Delayed P2—RBBB, pulmonary stenosis, ASD, right
ventricular failure
Reversed
A2 is delayed. P2 occurs before A2 so the split
splitting
between the sounds d on inspiration
Delayed A2—LBBB, systolic hypertension, HOCM,
severe aortic stenosis, PDA, left heart failure
Single Calcication of the aortic valve, pulmonary stenosis,
Fallot’s tetralogy, Ebstein’s anomaly, pericardial
eusion, large VSD, obesity, emphysema
Caused by opening of the aortic or pulmonary valves
systolic
Aortic—aortic stenosis, bicuspid valve
Pulmonary—pulmonary stenosis, pulmonary
hypertension
Mid/late
Mitral valve prolapse
systolic
Diastolic Caused by opening of the mitral or tricuspid valves.
Silent in the healthy heart
Mitral—mitral stenosis, rapid mitral ow, e.g. PDA,
VSD, severe mitral regurgitation
Tricuspid (rare)—rheumatic stenosis, ASD
Right
Loudest at lower left sternal edge. Never normal.
ventricle
Causes:right heart failure, tricuspid regurgitation,
ASD, constrictive pericarditis
Left
Loudest at the apex when inclined to the left.
ventricle
Can be normal in children and pregnancy. Other
causes:LVF, mitral regurgitation, anterior MI
Maximal at the apex or lower left sternal edge.
Never normal. Causes:ventricular hypertrophy or
brosis and HOCM
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CHAPTER9 Cardiology and vascular disease
Examination ofthe arterialsystem
The main conditions aecting the abdominal and peripheral arteries are:
• Aneurysms (E p. 254)
• Atherosclerosis resulting in ischaemia of the legs and intermittent
claudication, atrophic changes, and/ or rest pain
• Embolization resulting in acute ischaemia of the limbs
Generalscheme
• Look at the limbs— are there any signs of ischaemia? Are the extremities
warm or cold? What colour are they?
• Examine the abdomen looking for a pulsatile mass suggesting abdominal
aortic aneurysm (E p. 254). Auscultation may reveal a bruit
• Check the peripheral pulses
• Tenderness on palpation of an abdominal aortic aneurysm suggests need
for urgent operative repair.
Blood pressure E p. 216
Carotid pulse Ask the patient to lie supine with head/ neck at 45° to the
horizontal. When assessing the carotid pulse, consider:
Rate
• Tachycardia >100bpm— E p. 238
• Bradycardia <60bpm— E p. 242
Rhythm
• Irregularly irregular AF, multiple ectopics
• Regularly irregular 2nd- degree heart block
Character and volume Always assess with a central pulse, e.g. carotid or
femoral.
• Small volume Shock, pericardial tamponade, aortic stenosis (slow- rising)
• Large volume Hyperdynamic circulation (e.g. pregnancy), aortic
incompetence (water- hammer, collapsing pulse), PDA
• Pulsus paradoxus Pulse weakens in inspiration by >10mmHg— asthma,
cardiac tamponade, pericarditis
Carotid bruits May signify stenosis (>30%) often near the origin of
internal carotid. Heard best behind the angle of the jaw. Usual cause is
atheroma.
Peripheralpulses
Location Table 9.3
Examination Check whether each pulse is present. If present check:
• Rate
• Rhythm
• Amplitude
• Compare pulses in the 2 legs/ 2 arms
Check for radiofemoral delay— palpate radial and femoral pulses simultaneously; delay suggests coarctation of the aorta.
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EXAMINATION OFTHE ARTERIALSYSTEM
Table9.3 Location ofthe limb pulses
Pulse Location
Brachial 72cm medial to the central point of the antecubital fossa over
Radial 7½–1cm on the radial (lateral) side of the exor carpi radialis
Femoral Below inguinal ligament; ⅓ of the way up from pubic tubercle
Popliteal With knee exed at right angles palpate deep in the midline
Posterior tibial 1cm behind medial malleolus
Dorsalis pedis Variable—on the dorsum of the foot just lateral to the tendons
the elbow skin crease.
tendon at the wrist
to the big toe. 0 Many healthy people have only 1 foot pulse
Check for bruits over the femoral and/ or carotid pulses— these indicate
disturbed blood ow— usually 2° to narrowing due to atherosclerosis.
• Character and waveform of the pulse should only be assessed using the
femoral or carotid pulse.
Signs ofischaemia
Acute ischaemia Acutely pale, cold, and pulseless limb— E p. 1108. Refer
immediately— keep the limb cool in the interim.
Chronic ischaemicchanges
• Atrophic skin changes— pallor, cool to the touch, hairless, shiny
• On lowering, the leg turns a dusky blue- red colour; on elevation, pallor
and venous guttering
• Ulceration— check under the heel and between the toes
• Swelling suggests the patient is sleeping in a chair to avoid rest pain or,
rarely, pain from deep infection
• Absent foot pulses— if pulses are present consider alternative diagnosis
• Ankle– brachial pressure index <0.95
209
Checking theankle– brachial pressure index (ABPI)
• Check BP in one arm (E p. 216). The systolic measurement is the
brachial pressure (B)
• Then inate a BP cu around the lower calf just above the ankle
• Using a Doppler ultrasound probe, record the maximum cu pressure
at which the probe can still record a pulse (ankle pressure— A)
• Calculate the ABPI by dividing the ankle pressure by the brachial
pressure, i.e. ABPI=A ÷ B
Interpretation ofABPIresults
• ABPI <0.8— ischaemia
• ABPI <0.5— critical ischaemia
0 Arterial calcication (e.g. due to DM) can result in falsely elevated
ankle pressure readings.
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CHAPTER9 Cardiology and vascular disease
Cardiacinvestigations
Electrocardiogram (ECG) Graphic recording of electric potentials
generated by the heart. Most surgeries now have ECG machines that interpret themselves and print out their ndings. Analysis is easier but it is still
important to be able to understand the signicance of abnormalities and
check computer analysis in the clinical context.
Interpreting ECGs Many mistakes in ECG interpretation are errors of omission so a systematic approach is best. Check:
• Standardization (calibration) and technical features (including lead
placement and artefacts)
• Heart rate— usual speed (25mm/ sec). Each big square represents
0.2sec; each small square, 0.04sec. Rate=300 ÷ R– R interval in large
squares
• Rhythm— regular/ irregular
• PR interval— normal if <0.2sec
• QRS interval— abnormal if >0.12sec
• QT interval— varies with rate. At 60bpm normal if 0.35– 0.43sec
• P waves— present or absent, shape
• QRS voltages— height of complexes— see Table 9.4, E p. 212
• Mean QRS electrical axis— sum of all ventricular forces during
ventricular depolarization. Normal axis:−30o to +120°
• If more −ve=left axis deviation; if more +ve=right axis deviation
• Rule of thumb 1 If the majority of the QRS complex is above the
baseline (+ve) in leads Iand II the axis is normal
• Rule of thumb 2 The axis lies at 90° to a QRS complex where the
height above the baseline=height below the baseline
• Precordial R- wave progression
• Abnormal Q waves— >25% of the succeeding R- wave and/ or
>0.04sec wide
• ST segments— elevation/ depression, shape
• T waves— height, inversion, shape
• U waves— small, rounded deection (≤1mm), follows T wave and
usually has the same polarity
Brief guide tocommon ECG changes Table 9.4, E p. 212
24h ambulatory ECG ECG monitoring equipment is worn for 24h.
Continuous monitoring may detect intermittent arrhythmia or ischaemia.
Cardiac MRI/ magnetic resonance angiography Used as the
rst - line investigation to assess patients with chest pain for suspected IHD.
Increasingly used in 2° care to provide detailed structural information about
the heart and rapid angiographic images.
Echocardiogram (Echo) Heart USS. Local referral procedures vary.
• 2- dimensional Produces a fan- shaped, cross- sectional, moving, real-
time image of the heart. May be transthoracic or transoesophageal.
Used to asses valvular abnormalities and prosthetic heart valves; aortic
aneurysm/ dissection; heart failure; pericardial eusion; masses within
the heart; myocardial abnormalities (e.g. aneurysms, hypertrophy); IHD;
congenital heart disease
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CARDIACINVESTIGATIONS
• M- mode Plotted on a scrolling screen. Stationary structures appear as
straight lines across the screen; moving structures appear as undulating
lines. Usually displayed with an ECG trace to enable identication of
phases of the cardiac cycle. Used to investigate movement of individual
structural elements, e.g. valves, chamber walls
• Doppler Enables ow across valves and ASD/ VSDs to be quantied
Cardiac enzymes Biochemical blood assay of molecules released when
the heart is damaged. Used in diagnosis of MI.
• Troponins T and I Preferred markers as more sensitive/ specic than
CK, AST, or lactate dehydrogenase. Together with CK, earliest to i
after MI
• Creatine kinase (CK) i in MI, muscle damage, e.g. prolonged running
or seizures, after IM injection, and with dermatomyositis (e.g. due to
statins). CK- MB assay may help clarify whether a cardiac event has
occurred <48h previously
• AST 2nd to i • Lactate dehydrogenase (LDH) Last to i
Cardiac catheterization Refer via 2° care. Involves passing a catheter,
usually via the femoral or brachial artery, to the heart. Used to:
• Measure pressures within the heart and great vessels
• Assess oxygen saturation via blood samples
• Perform coronary angiography— contrast is injected into the coronary
arteries to assess their anatomy and/ or patency
• Perform intravascular ultrasound
• Perform other procedures, e.g. angioplasty, valvuloplasty, cardiac biopsy
Complications Arrhythmia (0.56%); MI (0.07%); stroke (0.07%); death
(0.14%); haemorrhage at the site of insertion (0.56%); thromboembolism;
trauma to heart and vessels; infection.
Exercise ECG ECG testing while the patient undergoes graded exercise
on a treadmill/ exercise bicycle. Mortality 71 in 10,000. Used for:
• Diagnosis of IHD— although cardiac MRI is now the preferred test. For
patients with IHD, 75% have a +ve exercise test; false +ve rate of 75%
• Assessment of exercise tolerance
• Response to treatment
• As a prognostic indicator
• Assessment of exercise- related arrhythmias
Contraindications Recent MI (<7d), unstable angina, electrolyte disturbance,
aortic stenosis, severe heart failure, known left main coronary artery stenosis, LBBB (may not be possible to interpret the trace).
Radionucleotide imaging 2° care tests. Involves IV administration of
a γ- emitting radionucleotide and gamma camera monitoring.
• Radionucleotide angiography Uses technetium
calculate left ventricular ejection fraction/ assess ventricular action
• Myocardial perfusion scintigraphy Uses thallium
exercise testing to demonstrate areas of poorly perfused myocardium
99m
- labelled RBCs to
201
injected IV during
Patient information
British Heart Foundation F 0300 330 3311 M www.bhf.org.uk
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CHAPTER9 Cardiology and vascular disease
Brief guide tocommon ECGchanges
0 For detailed analysis of ECGs refer to a specialist text (e.g. Hampton
J et al. The ECG Made Easy (9th edition— 2019) Churchill Livingstone,
ISBN:9780702046414).
Table9.4 Common ECG abnormalities and their causes
ECG abnormality Possible causes
Tachycardia R ate >100bpm Physiological, AF, atrial utter, SVT, VT
Bradycardia Rate <60bpm Physiological, drugs (e.g. β-blockers,
Irregular Assess whether any
P–R interval Short P–R interval Nodal rhythm, WPW syndrome
Left bundle
branch block
(LBBB)*
Right bundle
branch block
(RBBB)
Incomplete
bundle branch
block
Q–T interval
abnormalities
Abnormal P
waves
Right ventricular
hypertrophy
(RVH)
*
No comment can be made about ST segment or T wave if LBBB.
pattern or not
Prolonged >0.2sec Heart block—E p. 242; sick sinus
QRS >0.12sec wide.
Last peak is below the
isoelectric line in V1
QRS >0.12sec wide.
Last peak is above the
isoelectric line in V1
QRS <0.12sec with
abnormal shaped QRS
complex
Prolonged Q–T
interval
Shortened Q–T
interval
i P-wave amplitude
(>2.5mm)
Biphasic P wave in V1
± broad (>0.12sec)
often notched P wave
in ≤1 limb lead
Strain pattern—ST
depression and T-wave
inversion in leads
V1–3. Dominant R in
V1 with narrow QRS
digoxin), heart block (see E p. 242),
sick sinus syndrome
AF (no pattern), sick sinus syndrome
(no pattern), ventricular ectopics
(normally no pattern), heart block
(pattern)
(E p. 239)
syndrome, drugs (e.g. β-blockers,
digoxin)
IHD, i BP, cardiomyopathy, aortic valve
disease, SVT. Articial pacemakers may
produce a similar QRS complex
May be normal; congenital heart disease
(e.g. ASD), valvular heart disease, IHD,
pulmonary hypertension, during SVT
As for RBBB or LBBB
d K+, drugs (e.g. TCAs, phenothiazines,
amiodarone), SAH or CVA,
hypothermia, genetic
i Ca2+, digoxin
Right atrial overload—tricuspid stenosis,
pulmonary hypertension, pulmonary
stenosis
Left atrial abnormality—mitral
stenosis, aortic stenosis, conduction
abnormalities
Pulmonary stenosis, mitral stenosis
pulmonary hypertension, ASD (±
RBBB). Similar changes seen with
inferior MI (T-wave upright); WPW
syndrome
(Continued)
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BRIEF GUIDE TOCOMMON ECGCHANGES
Table9.4 (Contd.)
ECG abnormality Possible causes
Left ventricular
hypertrophy
(LVH)
Right axis
deviation
Left axis
deviation
Poor R-wave
progression
Abnormal Q
waves
ST elevation ST segment raised
ST depression ST segment lowered
T-wave inversion Abnormal if inverted
U-waves i amplitude >1mm Drugs (e.g. quinidine, procainamide,
Inversion in precordial leads Subtle sign of ischaemia
Strain pattern—ST d
and T wave d in leads
V4–6. Large voltages
of QRS complex—
sum of S in V1 and
R in V5 or V6 alone
>35mm
E p. 210 RVH/strain (e.g. following PE), cor
E p. 210 LVH /strain (e.g. i BP, aortic stenosis,
Absence of the normal
i in size of the R wave
in the precordial leads
from V1 to V6
>25% of succeeding R
wave and/or >0.04sec
wide
>1mm above baseline
>0.5mm below
baseline
in leads I, II or V4–6
i BP, aortic stenosis, coarctation of the
aorta, HOCM
pulmonale, pulmonary stenosis. Alone
with normal QRS=left posterior
hemiblock
HOCM), VSD, ASD. If occurs alone
with normal QRS=left anterior
hemiblock
Old anterior MI; lead misplacement
(common in obese women); LBBB
or left anterior fascicular block; LVH;
WPW syndrome; dextrocardia; tension
pneumothorax with mediastinal shift;
congenital heart disease
Normal; left pneumothorax;
dextrocardia; MI; myocarditis;
hyperkalaemia; cardiomyopathy;
amyloid; sarcoid; scleroderma; LVH;
RVH; LBBB; WPW syndrome
MI, Prinzmetal angina, pericarditis,
ventricular aneurysm
Angina, ventricular strain, drugs
(digoxin, verapamil), hyperkalaemia,
myocarditis, cardiomyopathy, brosis,
Lyme disease
MI (inverts <24h after MI); ventricular
strain (see above); PE (III); digoxin
(V5–6)
disopyramide) or d K
+
213
0 Always compare with previous ECGs if available.
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