EXAMINATION OF CARDIOVASCULAR SYSTEM

SOME DEFINITIONS AND REVISION

• 1st degree AV block: prolongation of AV conduction time
• 2nd degree AV block: some, but not all atrial impulses fail to reach the ventricles
• 3rd degree (complete) AV block: all atrial impulses fail to reach ventricles
• anatomy in femoral triangle:
• femoral vein (medial)
• femoral artery (the landmark)
• femoral nerve (lateral)

POSITION: patient lying in bed with enough pillows to support him at 45 degrees

GENERAL APPEARANCE
• general state of health? apparently ill?
• rapid and laboured respiration?
• cachectic (severe loss of weight and muscle wasting)? (commonly caused by malignant disease or
severe cardiac failure [cardiac cachexia])
• Marfan's syndrome (tall stature, thoracic kyphosis, high arched palate, pectus excavatum, long
limbs, arachnodactyly (spider fingers))? Marfan's syndrome is associated with aortic regurgitation
• Down's syndrome? associated with congenital heart disease, especially endocardial cushion
defects
• Turner's syndrome? associated with coarctation of the aorta

HANDS AND FOREARM

• nails
• clubbing - see Figure 3.3
• def: increase in soft tissue of distal part of fingers or toes
• for patient with clubbing examine finger nails - and determine if there is loss of
angle between nail bed and finger
• causes of clubbing:
• common
• cardiovascular
• cyanotic congenital heart disease
• infective endocarditis
• respiratory
• lung carcinoma (usually not small cell carcinoma)
• chronic pulmonary suppuration:
• bronchiectasis
• lung abscess
• empyema
• idiopathic pulmonary fibrosis
• uncommon
• respiratory
• cystic fibrosis
• asbestosis
• pleural mesothelioma (benign fibrous type) or pleural
fibroma
• gastrointestinal
• cirrhosis (especially biliary cirrhosis)
• inflammatory bowel disease
 • coeliac disease
• thyrotoxicosis
• familial or idiopathic
• rare
neurogenic diaphragmatic tumours
•
• pregnancy
• unilateral clubbing - bronchial arteriovenous aneurysm or axillary
artery aneurysm
• splinter haemorrhages - see Figure 3.4
• def: linear haemorrhages lying parallel to long axis of nail
• causes:
• trauma
• infective endocarditis
• rare:
• vasculitis as in rheumatoid arthritis
• polyarteritis nodosa
• sepsis
• haematological malignancy
• profound anaemia
• fingers
• Osler nodes
• def: red, raised tender nodules on pulps of fingers (or toes) or thenar or hypothenar
eminences
• are a rare manifestation of infective endocarditis
• palms
• Janeway lesions
• def: non-tender erythematous maculopapular lesions containing bacteria which can
occur on plums of pulps of fingers
• are a rare manifestation of infective endocarditis
• forearm
• xanthomata - see Figure 3.5 and Figure 3.6
• def: (yellow or orange) deposits of lipid in tendons
• can occur in hyperlipidaemia

ARTERIAL PULSE
• following observations should be made for radial pulse:
• rate of pulse
• rhythm
• presence or absence of delay of femoral pulse compared with radial pulse (radiofemoral
delay)
• character and volume are better assessed from palpation of brachial or carotid arteries
• rate of pulse
• bradycardia = pulse < 60 beats/min
• causes of bradycardia:
• regular rhythm
• physiological (athletes, sleep: due to increased vagal tone)
• drugs (e.g. beta blockers, digoxin, amiodarone)
• hypothyroidism (decreased sympathetic activity secondary to lack of
TH)
• hypothermia
• jaundice (in severe cases only, due to deposition of bilirubin in
conducting system)
• raised intracranial pressure (due to effect on central sympathetic
outflow) - a late sign
• third degree AV block or second degree AV block (type 2)
 • MI
• paroxysmal (def: sudden onset, usually with recurrent
manifestations) bradycardia:
• vasovagal syncope
• acute hypoxia or hypercapnia
• acute hypertension
• regularly irregular rhythm
• sinus arrhythmia (normal slowing of pulse with expiration)
• second degree AV block (type I)
• irregularly irregular rhythm
• atrial fibrillation, with AV nodal disease or drugs
• frequent extrasystoles
• apparent
• pulse deficit (there is a difference between the heart rate counted
over the praecodrium and that observed at the periphery; in beats
where diastole is too short for adequate filling of the heart, too small
a volume of blood is ejected during systole for a pulse to be
appreciated at the wrist)
• atrial fibrillation
• ventricular bigeminy (paired ventricular beats)
• tachycardia = pulse > 100 beats/min
• causes of tachycardia:
• regular rhythm:
• hyperdynamic circulation due to:
• exercise or emotion
• fever (allow 20 beats/min per degree Celsius above normal)
• pregnancy
• thyrotoxicosis
• anaemia
• arteriovenous fistula
• beri beri (thiamine deficiency)
• congestive cardiac failure
• constrictive pericarditis
• drugs (e.g. salbutamol and other sympathomimetics, atropine)
• normal variant
• denervated heart of diabetes has a resting rate of 106-120 beats/min
• hypovolaemic shock
• supraventricular tachycardia
• atrial flutter with regular 2:1 AV block
• ventricular tachycardia
• irregular rhythm
• atrial fibrillation due to:
• myocardial ischaemia
• mitral valve disease or any cause of left atrial enlargement
• thyrotoxicosis
• hypertensive heart disease
• sick sinus syndrome (chaotic or absent atrial activity, often
with bradycardia alternating with tachycardia, recurring
ectopic beats, including escape beats, and runs of
supraventricular and ventricular arrhythmias)
• pulmonary embolism
• myocarditis
• fever, acute hypoxia, or hypercapnia (paroxysmal)
• other: alcohol, post-thoracotomy, idiopathic
• multifocal atrial tachycardia
• atrial flutter with variable block
 • rhythm:
• rhythm can be regular or irregular
• irregular rhythm can be completely irregular with no pattern
• usually due to atrial fibrillation
• coordinated atrial contraction lost and chaotic electrical activity occurs with
bombardment of AV node with impulses at a rate of over 600 per minute -
only some are conducted to ventricles since the rate is too high
• hence ventricles beat irregularly, at a rate of about 150 minute
• the pulse also varies in amplitude from beat to beat because of differing
diastolic filling
• this type of pulse also can occur by frequent irregularly occurring ectopic beats
(supraventricular or ventricular)
• irregular rhythm can be regular:
• sinus arrhythmia:
• in sinus arrhythmia, pulse rate increases with each inspiration and decreases
with each expiration
• is associated with changes in venous return to heart
• Wenckebach phenomenon
• AV nodal conduction time increases progressively until non-conducted atrial
systole occurs
• following this, the AV conduction time shortens and cycle begins again
• radiofemoral delay:
• while palpating radial pulse, one places fingers of other hand over radial femoral pulse
(below inguinal ligament, one third of way up from pubic tubercle)
• a noticeable delay in arrival of femoral pulse suggests diagnosis of coarctation of aorta
(congenital narrowing in aortic isthmus occurs at level where ductus arteriosus joins
descending aorta) - note that this lesion can also cause upper limb hypertension
• it is also useful to palpate both radial pulses together to detect radial-radial inequality in
timing or volume (e.g. due to large arterial occlusion)
• character and volume
• use carotid or brachial to determine character and volume
• however, do use the radial pulse to test for:
• the collapsing (bounding) pulse of aortic regurgitations
• pulsus alternans of left ventricular failure

BLOOD PRESSURE
• systolic blood pressure = peak pressure that occurs in artery following ventricular systole
• diastolic blood pressure = level to which arterial pressure falls during ventricular diastole
• normal blood pressure < 140/90
• brachial artery is found in antecubital fossa, one third of the way over from the medial epicondyle
• first get an approximate estimation of systolic blood pressure
• cuff is inflated and then deflated slowly until radial pulse returns
• then get more accurate estimation of blood pressure:
• cuff is inflated and then deflated slowly whilst listening to brachial artery with
stethescope's diaphragm
• 5 different sounds will be heard as the cuff is slowly released: (Korotkoff sounds)
1. pressure at which sound is first heard over artery is systolic blood pressure (a sharp
thud) - only the systolic blood pressure is high enough to overcome the cuff's
pressure
2. as deflation continues, sound increases in intensity (a blowing or swishing sound)
3. as deflation continues, sound decreases in intensity (a softer thud than phase 1)
4. sound becomes muffled (softer blowing sound that disappears) (is the 1st diastolic)
5. sound disappears (is 2nd diastolic) because flow is now constant since even the
diastolic pressure is enough to overcome the cuff's pressure
• the 2nd diastolic (5th sound [K5]) is the best measure for diastolic blood pressure, although
 it is a slight underestimate
• however, in severe aortic regurgitation, the 1st diastolic (K4) is a better indication of
diastolic pressure
• occasionally, there is an auscultatory gap (the sounds disappear just below the systolic
pressure and reappear before diastolic pressure) in healthy people
• the systolic pressure may normally vary by up to 10 mmHg; the pressure is higher in the
legs
• pulsus paradoxus:
1. during inspiration, systolic and diastolic pressure normally increased because
intrathoracic pressure is reduced, and blood pools in the pulmonary vessels, hence
left heart filling is reduced; if the reduction in blood pressure is exaggerated over
the normal, the term pulsus paradoxus is applied (pulsus paradoxus is a fall in
arterial pulse pressure on inspiration of more than 10 mg)
2. causes:
• constrictive pericarditis
• pericardial effusion
• severe asthma
• postural blood pressure
• postural blood pressure should routinely be taken with patient lying and standing
• a fall of more than 15 in systolic or 10 in diastolic is abnormal and called postural
hypotension
• causes include
1. hypovolaemia (e.g. dehydration, bleeding)
2. drugs (e.g. vasodilators)
3. Addison's disease (low cortisol and aldosterone)
4. hypopituirism
5. autonomic neuropathy (e.g. diabetes mellitus, amyloidosis)
6. idiopathic orthostatic hypotension (rare progressive degeneration of ANS, usually
in old men)

FACE
• eyes
• inspect sclerae for jaundice
• can occur with hepatic congestion in severe congestive cardiac failure
• can occur with prosthetic heart valves, which may induce haemolysis due to
excessive turbulence
• xanthelasma - see Figure 3.8
• def: intracutaneous yellow cholesterol deposits around eyes
• may be normal variant or indicate hyperlipidaemia
• cheeks
• mitral facies (rosy cheeks with a bluish tinge)
• due to dilatation of malar capillaries
• associated with pulmonary hypertension and low cardiac output such as
occurs in severe mitral stenosis
• mouth
• arched palate? occurs in Marfan's syndrome, which is associated with congenital
heart disease, including aortic regurgitation secondary to aortic root dilatation, and
also mitral regurgitation due to mitral valve prolapse
• teeth - do they look diseased? they can be a source of organisms responsible for
infective endocarditis
• tongue and lips - central cyanosis?
• inspect mucosa for petechiae - may indicate infective endocarditis

NECK
Carotid arteries
• location: medial to sternomastoid muscle
• carotid pulse gives information about left ventricle and aorta
• never palpate both carotid arteries at once!
• anacrotic pulse
• small volume, slow uptake, notched wave on upstroke
• causes: aortic stenosis
• plateau pulse
• slow upstroke
• causes: aortic stenosis
• bisferiens pulse
• anacrotic and collapsing
• causes: aortic stenosis and regurgitation
• collapsing pulse
• causes:
• aortic regurgitation
• hyperdynamic circulation
• patent ductus arteriosus
• peripheral arteriovenous fistula
• arteriosclerotic aorta (elderly patients in particular)
• small volume pulse
• causes
• aortic stenosis
• pericardial effusion
• pulsus alternans
• alternating strong and weak beats
• causes: left ventricular failure
• jerky
• causes: hypertrophic cardiomyopathy

JUGULAR VENOUS PRESSURE (JVP)

• internal jugular venous pressure gives information about right atrial and right ventricle
• position:
• patient must be lying at 45 degrees
• internal jugular vein is medial to sternomastoid muscle; external jugular vein is lateral to
sternomastoid muscle
• the external jugular vein is more readily visible, but is compressed as it enters chest
because of its tortuous course and therefore should not be relied upon to assess the position
or waveform of the JVP
• therefore, use internal jugular vein
• pulsations which occur there reflect movements of the top of a column of blood which
extends into the right atrium
• see Talley Figure 3.10
• sternal angle is taken as the zero point
• maximum height of internal jugular vein above the sternal angle can be measured
• assess height and character
• note that the jugular venous pulsation can be distinguished from the arterial pulse because:
• it is visible but not palpable
• it has a complex wave form, usually seen to flicker twice with each cardiac cycle
• moves on respiration, normally decreases on inspiration
• it is at first obliterated and then filled from above when light pressure is applied at
the base of the neck
• height:
• elevated: when the JVP is raised more than 3cm above zero point, the right heart
filling pressure is raised; causes include:
• right ventricular failure
 • tricuspid stenosis or regurgitation
• pericardial effusion or constrictive pericarditis
• superior vena caval obstruction
• fluid overload
• hyperdynamic circulation
• character of the jugular venous pressure: see Figure 3.11
• there are 2 positive waves in normal jugular venous pressure
• a wave:
• timing: this is the first wave, and coincides with right atrial systole,
and S1; it precedes the carotid pulsation
• due to: right atrial systole
• v wave:
• timing: this is the second wave and occurs in the period when the
tricuspid valve remains closed during ventricular systole
• due to: atrial filling
• x descent: between the a wave and the v wave there is a trough caused by atrial
relaxation
• c point: the x descent is interrupted at a point which is due to the carotid pulse
• y descent: following the v wave, the tricuspid valve opens and rapid ventricular
filling occurs
• any condition in which right ventricular filling is limited, can cause elevation of the
venous pressure, which is more marked on inspiration when venous return to the
heart increases; this is the called Kussmaul's sign, and is the opposite of what
normally happens
• note that pressure exerted over the liver for 15 seconds will also increase the venous
return the right atrium
• causes of a dominant a wave: occur when right atrial pressures are raised
• tricuspid stenosis (also causing a slow y descent)
• pulmonary stenosis
• pulmonary hypertension
• causes of a cannon a wave: occur when the right atrium contracts against the
closed tricuspid valve; i.e. a cannon a wave is just a much more severe dominant a
wave
• complete heart block
• paroxysmal nodal tachycardia with retrograde atrial conduction
• ventricular tachycardia with retrograde atrial conduction or atrioventricular
dissociation
• cause of a dominant v wave
• tricuspid regurgitation
• x descent
• absent - atrial fibrillation
• exaggerated - acute cardiac tamponade; constrictive pericarditis
• y descent
• sharp: severe tricuspid regurgitation, constrictive pericarditis
• slow: tricuspid stenosis, right atrial myxoma

PRAECORDIUM
Inspection
• scars? pace-maker box?
• skeletal abnormalities? pectus excavatum (funnel chest)? kyphoscoliosis? note that skeletal
abnormalities can cause distortion of position of heart and great vessels
• visible pulsations:
• apex beat may be seen (normal position is in 5th intercostal space, 1cm medial to
midclavicular line) - see Talley Figure 3.12
 • pulmonary artery pulsations may be visible in severe pulmonary hypertension
Palpation
• palpate apex beat
• position of apex beat:
• count down number of interspaces; first palpable interspace is the 2nd, lying just
below manubriosternal angle
• located at: 5th intercostal space, 1cm medial to midclavicular line
• normal apex beat is is felt over an area size of 20 cm piece
• an enlarged heart gives a displaced apex beat laterally or inferiorly, or both; note
that a chest wall deformity or pleural or pulmonary disease can also displace the
apex beat
• character of apex beat: abnormal beats include:
• pressure loaded (hyperdynamic or systolic overloaded) apex beat:
• def: is a forceful and sustained impulse
• causes: aortic stenosis or hypertension
• volume loaded (hyperkinetic or diastolic overloaded) apex beat:
• def: is an uncoordinated impulse felt over a larger than normal area
• causes: left ventricular dysfunction (e.g. anterior MI)
• double impulse apex beat
• def: 2 distinct impulses are felt with each systole
• causes: hypertrophic cardiomyopathy
• tapping apex beat
• def: first heart sound is actually palpable (normal heart sounds
• causes: mitral stenosis, or rarely tricuspid stenosis
• non-palpable apex beat: note that this can be normal
• causes: thick chest wall (normal), emphysema, pericardial effusion, shock
(or death), and rarely dextrocardia (inversion of heart and great vessels; in
this the apex beat will be palpable to right of sternum)
• other praecordial impulses:
• may occur in various heart diseases
• right ventricular enlargement:
• parasternal impulse may be felt when heel of hand is rested just to left of sternum,
with fingers lifted slightly off chest
• in right ventricular enlargement, or severe left atrial enlargement (where the right
ventricle is pushed anteriorly), the heel of hand is lifted off the chest wall with each
systole
• in pulmonary hypertension:
• palpation over pulmonary area (2nd intercostal space, just left of sternum) may
reveal palpable tap of pulmonary valve closure
• thrills
• turbulent blood flow, which causes cardiac murmurs on auscultation, may
sometimes be palpable
• feel for thrills with flat hand, over: apex, left sternal edge, base of heart
• apical thrills (mitral): may be felt more easily with patient rolled over left side (left
lateral position) which brings apex closer to chest wall
• thrills over base of heart (pulmonary and aortic): are best felt with patient sitting
up leaning forward in full expiration (base of heart is moved closer to chest wall)
• systolic thrill = a thrill that coincides with apex beat
• diastolic thrill = a thrill that does not coincide with apex beat

Percussion: don't bother doing this; all it does it define the cardiac outline
Auscultation
Areas of auscultation - see Talley Figure 3.15 (page 51)
1. mitral area - midclavicular line, 4th intercostal space
2. tricuspid area - 1 cm right of sternum, 5th intercostal space
 3. pulmonary area - 1 cm right of sternum, 2nd intercostal space
4. aortic area - 1 cm left of sternum, 2nd intercostal space
Process of auscultation
1. auscultate mitral area with the bell and diaphragm
• bell is efficient in amplifying low pitched sounds (it must be lightly applied to chest), for
example
• diastolic murmur of mitral stenosis
• a third heart sound
• diaphragm is good for reproducing higher pitched sounds, for example
• systolic murmur of mitral regurgitation
• a fourth heart sound
2. auscultate tricuspid area
3. auscultate pulmonary area
4. auscultate aortic area
Normal heart sounds - heart normally produces 2 sounds each cycle, related to closure of valves and rapid
changes in blood flow
• first heart sound (S1)
• has 2 components - mitral and tricuspid valve closure
• mitral closure occurs ever so slightly before tricuspid, but only one sound is audible
• first heart sound indicates beginning of ventricular systole
• second heart sound (2)
• is made up of aortic and pulmonary valve closure
• because of lower pressure in pulmonary circulation compared with aorta, the pulmonary
valve usually closes slightly after closure of aortic valve (if you listen carefully, you may
notice splitting); also note that pulmonary valve closure is further delayed with inspiration
because of increased venous return to right ventricle
• marks the end of systole, and the beginning of diastole
• note that diastole is usually longer than systole
• sometimes it can be difficult to tell which heart sound is which; on these occasions, palpation of
the carotid pulsation will indicate the timing of systole
• it is clearly crucial to define systole and diastole so that timing of murmurs can be worked out
Abnormal heart sounds
• alterations in intensity
• loud S1
• physiology: occurs when mitral or tricuspid valve cusps remain widely open at the
end of diastole and shut forceful with the onset of ventricular systole
• causes:
• reduced filling volume in mitral or tricuspid stenosis because the narrowed
valve orifice limits ventricular filling, so that there is no diminution in flow
towards the end of diastole; the normal mitral cusps drift back towards the
closed position at the end of diastole as ventricular filling slows down
• reduced diastolic filling time (any cause of a short AV conduction time)
• soft S1
• causes:
• prolonged diastolic filling time (occurs in 1st degree heart block)
• delayed onset of left ventricular systole (left bundle brunch block)
• failures of leaflets to coapt normally (mitral regurgitation)
• loud aortic component of second heart sound (loud A2)
• causes:
• systemic hypertension because this results in forceful aortic valve closure
secondary to high pressure
• congenital aortic stenosis because valve is mobile but narrowed, and closely
suddenly at end of systole
• loud pulmonary component of second heart sound (loud P2)
 • causes:
• pulmonary hypertension
• soft A2
• causes:
• aortic valve calcification because leaflet movement is reduced
• aortic regurgitation because leaflets cannot coapt
• splitting
• splitting of S1 is usually not clinically detectable, but may be noticed in complete right
bundle branch block
• increased normal splitting of S2 occurs when there is any delay in right ventricular
emptying, and is caused by:
• inspiration
• right bundle branch block (delayed right ventricular depolarisation)
• pulmonary stenosis (delayed right ventricular ejection)
• ventricular septal defect (increased right ventricular volume load)
• mitral regurgitation (because of earlier aortic valve closure due to more rapid left
ventricular emptying)
• fixed splitting (no respiratory variation)
• atrial septal defect equalises volume loads between two atria --> atria acting as a
common chamber
• reverse splitting (P2 occurs first, and splitting occurs on expiration) is caused by:
• left bundle branch block (delayed left ventricular depolarisation)
• delayed left ventricular emptying (severe aortic stenosis, coarctation of the aorta)
• increased left ventricular volume load (large patent ductus arteriosus)
• extra heart sounds
• third heart sound (S3)
• timing: is a low pitched mid-diastolic sound
• pathophysiology: tautening of mitral or tricuspid papillary muscles at end of rapid
diastolic filling
• causes:
• left ventricular S3 (will be louder on expiration, and heard most clearly over
apex)
• physiological left ventricular S3 occurs in people under 40 due to
rapid diastolic filling
• left ventricular failure
• aortic regurgitation
• mitral regurgitation
• ventricular septal defect
• patent ductus arteriosus
• right ventricular S3 (will be louder on inspiration and heart most clearly at
left sternal edge):
• right ventricular failure
• constrictive pericarditis
• fourth heart sound (S4)
• timing: late diastolic sound
• pathophysiology: high pressure atrial wave reflected back from a poorly compliant
ventricle
• causes:
• left ventricular S4 (often presents during episode of angina or MI)
• reduced left ventricular compliance
• aortic stenosis
• acute mitral regurgitation
• systemic hypertension
• ischaemic heart diseased
• advanced age
• right ventricular S4
 • reduced right ventricular compliance
• pulmonary hypertension
• pulmonary stenosis
• summation gallop
• if there heart rate is >120m S3 and S4 may be superimposed resulting in a
summation gallop
• this does not necessarily imply ventricular stress unless one/or both the heart
sounds persist when the heart rate slows; when both S3 and S4 are present
(quadruple rhythm), severe ventricular dysfunction is implied
• additional sounds
• opening snap
• timing: high pitched sound at a variable distance after S2
• cause: mitral stenosis or tricuspid stenosis
• pathophysiology: sudden opening of mitral valve is followed by diastolic murmur
of mitral stenosis
• systolic ejection click
• timing: early systolic high pitched sound over aortic or pulmonary or left sternal
edge area
• cause: congenital aortic or pulmonary stenosis
• non-ejection systolic click
• timing: high pitched sound heard during systole, best over mitral area; may be
followed by systolic murmur
• cause: prolapse of one or more redundant mitral valve leaflets during systole; atrial
septal defects
• tumour plop
• cause: during atrial systole, pedunculated atrial myxoma may be propelled into
mitral or tricuspid valve orifice causing a diastolic plopping sound
• diastolic pericardial knock
• cause: constrictive pericardial disease --> sudden cessation of ventricular filling
• prosthetic heart valve sounds
• pacemaker sounds: a click due to contraction of chest wall muscle

Murmurs of the heart

• must consider:
• associated features (peripheral signs)
• timing
• area of greatest intensity
• volume and pitch
• effect of dynamic manoeuvres including respiration and Valsalva manoeuvre
• timing
• systolic murmurs - occur during ventricular systole
• may be
1. pansystolic
2. ejection systolic
3. late systolic
• pansystolic murmur
1. timing: extends through systole, beginning with the first heart sound, then
going right up to the second heart sound although loudness and pitch vary
during systole
2. pathophysiology: occur when ventricle leaks to a lower pressure change or
vessel (therefore sound is pansystolic because there is a pressure gradient
from the moment the ventricle begins to contract (S1) until pressure
equalisation at S2
3. causes:
• mitral regurgitation
• tricuspid regurgitation
 • ventricular septal defect
• aortopulmonary shunts
• ejection (mid) systolic murmur
1. timing: does not begin right at 1st heart sound; its intensity is greatest in
midsystole, and wanes late in systole (i.e. crescendo-decrescendo murmur)
2. pathophysiology: caused by turbulent blood flow through aortic or
pulmonary valve orifices or greatly increased flow through a normal sized
orifice or outflow tract
3. causes:
• aortic stenosis
• pulmonary stenosis
• hypertrophic cardiomyopathy
• pulmonary flow murmur of an atrial septal defect
• increased cardiac sympathetic stimulation (e.g. as occurs in anaemia)
• late systolic murmur:
1. timing: appreciable gap between first heart sound and murmur, which then
continues right up to second heart sound
2. pathophysiology: mitral regurgitation begins in mid-systole
3. causes:
• mitral valve prolapse
• papillary muscle dysfunction (due usually to ischaemia or
hypertrophic cardiomyopathy)
• diastolic murmurs - occur during ventricular diastole
• early diastolic murmur
1. timing: begins immediately with the S2 and has a decrescendo quality;
generally high pitched
2. pathophysiology: due to regurgitation through leaking or aortic or
pulmonary valves; loudest at the beginning because this is when aortic and
pulmonary artery pressure are highest
3. causes:
• aortic regurgitation
• pulmonary regurgitation
• mid-diastolic murmur:
1. timing: begin part way through diastole and may be short or extend to S1;
have lower pitch than early diastolic murmurs
2. pathophysiology: impaired flow during ventricular filling
3. causes:
• mitral stenosis
• tricuspid stenosis
• atrial myxoma (tumour mass can obstruct the valve orifice)
• Austin Flint murmur of aortic regurgitation (a diastolic murmur
similar to that of mitral stenosis, heart best at the cardiac apex; it is
thought to be caused by turbulent regurgitation stream from the aorta
mixing into the stream simultaneously entering from the left atrium
through the mitral valve, causing posterior movement of the anterior
leaflet of the mitral valve with transient acceleration of blood flow
through the mitral valve)
• Carey-Coomb's murmur of acute rheumatic fever (blubbering apical
mid-diastolic murmur occurring in the acute stage of rheumatic
mitral valvulitis and disappearing as the valvulitis subsides)
• presystolic murmur:
1. timing: just before S1
2. pathophysiology: atrial systole increases blood flow across the valve jet just
before S1; are an extension of middiastolic murmurs of mitral stenosis or
tricuspid stenosis
• continuous murmurs - extend throughout systole and diastole
 • pathophysiology: communication exists between two parts of the circulation with a
permanent pressure gradient so blood flow occurs continuous
• can be difficult to distinguish between a combined systolic and diastolic murmur
• causes:
1. patent ductus arteriosus
2. arteriovenous fistula (coronary artery, pulmonary, systemic)
3. aorto-pulmonary connection (e.g. congenital)
4. venous hum
5. rupture of sinus of Valsalva into right ventricle or atrium
6. mammary souffle (in late pregnancy or early postpartum period)
• pericardial friction rub - superficial scratching sound
• not confined to systole or diastole and can vary with respiration and posture (often
louder when patient is sitting up and breathing out)
• caused by movement of inflamed pericardial surfaces (pericarditis)
• sound comes and goes
• area of greatest intensity
• not a reliable sign
• loudness and pitch
• loudness is unhelpful is deciding severity of lesion, but are graded anyway:
• grade 1/6 - very soft and only audible to consultants and students who have been
told a murmur is present
• grade 2/6 - soft, but can be detected almost immediately by an experienced
auscultators
• grade 3/6 - moderate; there is not thrill
• grade 4/6 - loud; thrill just palpable
• grade 5/6 - very loud; thrill easily palpable
• grade 6/6 - very, very loud; can be heard without placing the stethoscope on the
chest
• the loudness is useful because a change in intensity of a murmur may be of significance,
for example, after a MI
• pitch is useful guide to murmurs, but requires a great deal of practice to identify its type
• in general, low pitched murmurs indicate turbulent flow under low pressure, as in mitral
stenosis
• in general, high pitched murmurs indicate high velocity of flow, as in mitral regurgitation
• dynamic manoeuvres
• all patients with a newly diagnosed murmur should undergo dynamic manoeuvre testing
• respiration
• inspiration --> decrease intrathoracic pressure --> increase venous return --> blood
flow in right heart
1. hence, murmurs that arise on right side tend to be louder during inspiration
and softer on expiration
• Valsalva manoeuvre (forceful expiration against a closed glottis; hold nose and close mouth
and breath out fully so as to pop eardrums, and hold this --> decreased preload) - the
following refers to phase 2 of the manoeuvre (phase 1 - beginning the manoeuvre, phase 2
- straining phase, phase 3 - ending the manoeuvre)
• most murmurs softer because reduced cardiac output
1. aortic stenosis
2. mitral regurgitation
• left ventricular volume is reduced hence:
1. systolic murmur of hypertrophic cardiomyopathy is louder
2. systolic click and murmur of mitral valve prolapse begins earlier (and goes
longer)
• squatting
• increases venous return and systemic arterial resistance causing rise in stroke
volume and arterial pressure - hence murmurs are louder
1. aortic stenosis louder
 2. mitral regurgitation louder
• left ventricular size is increased which reduces obstruction to outflow therefore:
1. intensity of systolic murmur of hypertrophic cardiomyopathy is decreased
2. mid-systolic click and murmur of mitral valve prolapse are delayed (and
shorter)

BACK - get patient to sit up

• percuss and auscultate the lungs - signs of cardiac failure may be detected in lungs, in particulate
late, or pan-inspiratory crackles or a pleural effusion may be present
• feel for pitting oedema in sacrum (occurs in severe right heart failure, particularly patients who
have been in bed)

ABDOMEN - lie patient down flat

• liver
• enlarged liver? may occur when hepatic veins are congested because of right heart failure
• tender liver? distension of liver capsule can cause tenderness
• pulsatile liver? may occur in tricuspid regurgitation because right ventricular systolic
pressure wave is transmitted to hepatic veins
• ascites? may occur with severe right heart failure
• splenomegaly? can occur in infective endocarditis
• implanted cardioverter-defibrillator box may be palpable below left costal margin

LOWER LIMBS
• palpate femoral arteries
• auscultate femoral arteries (a bruit may be heard if narrowed)
• palpate popliteal (behind knee)
• palpate posterior tibial (under medial malleolus)
• palpate dorsalis pedis (forefoot)
• palpate distal shaft of tibia for oedema by compressing area for 15 seconds - if oedema, is it pitting
or non-pitting
• causes of pitting lower limb oedema
• cardiac: congestive cardiac failure, constrictive pericarditis
• drugs: calcium antagonists
• hepatic: cirrhosis causing hypoalbuminaemia
• renal: nephrotic syndrome causing hypoalbuminaemia
• gastrointestinal tract: malabsorption, starvation, protein losing enteropathy causing
hypoalbuminaemia
• wet beri beri (dietary deficiency of thiamin (vitamin B1) resulting in heart failure
leading to oedema; dry beri beri is dietary deficiency of thiamine resulting in
painful polyneuritis without the oedema of wet)
• cyclical oedema
• causes of unilateral lower limb pitting oedema
• deep venous thrombosis
• compression of large vein by tumour of lymph node
• causes of non-pitting lower limb oedema
• hypothyroidism
• lymphoedema
• infection
• malignant (tumour invasion of lymphatics)
• congenital (lymphatic development arrest)
• allergy
• Milroy's disease (unexplained lymphoedema which appears at puberty and
 is more common in females)
• note that in long standing oedema, secondary changes in lymphatics may occur that
minimise the oedema
• Achilles tendon xanthomata (see Figure 3.22)? (is due to hyperlipidaemia)
• cyanosis and clubbing of toes? (may occur without finger clubbing in patent ductus arteriosus)
• peripheral vascular disease:
• note that reduced or absent pulses, femoral systolic bruit, marked leg pallor, absence of
hair, cool skin and reduced capillary return (compress toe nails - return of normal red
colour is slow) are signs of peripheral vascular disease
• in these cases, perform Buerger's test - elevate leg to 45 degrees (pallor is rapid if there is a
poor arterial supply) and then place them dependent at 90 degrees over edge of bed
(cyanosis occurs if the arterial supply is impaired)
• deep venous thrombosis:
• difficult to diagnose
• presenting symptom: may be calf pain
• on examination: (positives to the following are suggestive of DVT)
• swelling of calf and leg?
• dilated superficial veins?
• increased warmth?
• squeeze calf gently to determine if area is tender
• causes of thrombosis
• changes in vessel wall (trauma) - common
• changes in blood flow (cardiac failure or prolonged immobilisation) - common
• changes in constitution of blood (occult neoplasm, disseminated intravascular
coagulation, contraceptive pill, pregnancy) - uncommon
• acute arterial occlusion
• causes include:
• embolism - usually arise from thrombus in heart, often secondary to:
• myocardial infarction or dilated cardiomyopathy
• atrial fibrillation
• infective endocarditis
• thrombosis
• injury
• symptoms: 4 P's of acute arterial occlusion of major peripheral limb artery
• painful limb
• pale limb
• pulseless limb
• 'paralysed' limb
• varicose veins
• examination:
• position: if patient complains of varicose veins, ask him to stand with legs fully
exposed
• inspect:
• inspect front of whole leg for tortuous, dilated branches of long saphenous
vein (medial leg)
• inspect back of calf for varicosities of short saphenous vein lateral and
posterior leg)
• inspect to see if leg is inflamed, swollen or pigmented (signs of venous
stasis)
• ulcers (chronic venous stasis is a cause of ulceration of lower leg)
• palpate veins:
• hard veins suggests thrombosis and tenderness suggests thrombophlebitis
• perform cough impulse test (put finger over long saphenous vein opening in
groin, medial to femoral vein); ask patient to cough: a fluid thrill is felt if the
saphenofemoral valve is incompetent
• Trendelenburg test
 • patient lying down, leg elevated
• pressure on saphenous opening in groin
• patient stands
• if veins stay empty until groin pressure is released - incompetence of
saphenofemoral valve
• if veins fill despite groin pressure, incompetent valves are in thigh or calf,
and Perthes' test is performed
• Perthes' test
• repeat Trendelenburg's test, but when patient stands, allow some
blood to be released and get him to stand up and down on the toes a
few times
• veins will become less tense if the perforating calf veins are patent
and have competent valves (the muscle pump is functioning)
• note unusual pattern, example: if pubic varices, must try to exclude secondary
varicose veins, e.g. due to intrapelvic neoplasm which has obstructed deep venous
return
• causes of leg ulcers
• venous stasis ulcer
• most common
• site: around malleoli
• associated pigmentation, stasis eczema
• ischeamic ulcer
• large artery disease (atherosclerosis, thromboangitis obliterans): usually lateral side
of leg (pulse absent)
• small vessel disease
• malignant ulcer - examples
• basal cell carcinoma (pearly translucent edge)
• squamous cell carcinoma (hard everted edge)
• melanoma
• lymphoma
• infection - examples
• Staphylococcus aureus
• syphilitic gumma
• tuberculosis
• atypical Mycobacterium
• fungal
• neuropathic
• painless penetrating ulcer on sole of foot: peripheral neurophathy, e.g. diabetes
mellitus, leprosy
• underlying systemic disease
• diabetes mellitus: vascular disease, neuropathy
• pyoderma gangrenosum
• rheumatoid arthritis
• lymphoma
• haemolytic anaemia (small ulcers over malleoli)