The Short cases
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Cardiovascular examination
Vascular system examination
Respiratory system examination
Examination of precordium
GIT examination
Abdominal examination
Scrotal examination
Musculoskeletal examination – spine, knee, shoulder, elbow.
Nervous system examination
o Cranial nerves
o Peripheral nervous system
o Higher mental function
o Mental state examination
Examination of the hands
Examination of neck
Examination of the breast
Procedures
o Control of epistaxis
o Fundoscopy
o Eye examination
o Chest drain – needle and tube
o Breaking bad news
o Airway assessment
o Urgent airway maneuvers – cricothyrotomy or transtracheal jet ventilation
o Lumbar puncture
o RSI
o Defibrillation and cardioversion
o Intraosseous access
o Suprapubic catheter placement
o CPR – single and two person
Cardiovascular System examination
(Includes general/peripheral examination and examination of precordium)
General appearance:
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Notice any obvious clinical findings – ill vs. well looking, dyspnea ±, syndromic appearances – Down’s,
Marfan’s, and Turner’s.
Notice any drips, infusions, drugs, puffers, mobilization aids, monitoring, and oxygen device.
Ask for vitals and temperature now
Clean hands with antiseptic solution provided (or own if carrying).
Place patient in preferred position
Syndrome
Marfan’s
Down’s
(trisomy 21)
Klinefelter’s
(XXY)
Turner’s (XO)
Obesity
syndromes
Acromegaly
Characteristics
Tall stature, thoracic kyphosis, pectus
excavatum, arachnodactyly, long limbs
and high arched palate. Ectopia lentis.
Disorder with fibrillin gene FBN1.
Microgenia (small chin), round face,
macroglossia, epicanthic fold of eye, upslanting palpebral fissures, shorter limbs,
single transverse palmar crease,
hypotonia.
Tall stature males, long extremities,
eunuchoid configuration and
gynecomastia with atropic testes
Females, short-stature, lymphedema of
hands and feet, broad shield chest, low
hairline, low set ears, obesity, shortened
fifth finger, webbed neck
Cushing’s, Pickwickian
Associations
Cystic medial degeneration of valves and great
vessels → mitral/aortic valve prolapse, AR/MR,
dilated aorta → aortic aneurysm/dissection.
↑risk for spontaneous pneumothorax
Endocardial cushion defect → ASD (40%), VSD
(30%)
Tall stature, spade hands, hypertelorism,
↑ears/nose size
Hypertension, cardiac hypertrophy,
cardiomyopathy and conduction defects
ASD/VSD, PDA and some cases tetralogy of Fallot.
Bicuspid aortic valve and coarctation of aorta.
↑ CAD/IHD risk
Initial position of patient: lying in bed semi-reclined at 45˚ angle with bed end raised or pillows
General examination: start peripherally at hands and moving centrally
Hands:
Condition
Cyanosis
Clubbing
Splinter
hemorrhages
Osler’s nodes
Findings
Central – around lips, tip of
nose/ears, tongue (usually with
peripheral) – central CNS/CVS/Resp
cause
Peripheral – fingers and extremities –
inadequate circulation – all cause of
central + peripheral causes
Differential – lower extremity >
upper – PDA/ coarctation
Stages – softening of nail bed, loss of
normal <165˚ angle, ↑convexity of
nail fold, thickening of whole DIP
(drumstick), wrist involvement
Linear h’hages parallel to long axis of
nail
Red raised tender nodules on pulp of
Cardiovascular diseases
Cyanotic heart disease – tetralogy of Fallot,
transposition of great vessels, tricuspid atresia,
pulmonary stresia, critical pulmonary stenosis and
late PDA. Eissenmenger syndrome→ reversal of L-toR shunt in c/o ASD/VSD. CCF/PE/AMI/Shock
Isolated peripheral – vasoconstriction d/t local and
central causes
CVS causes – chronic hypoxia, cyanotic heart disease,
SBE and atrial myxoma.
Differential clubbing – PDA, Eissenmenger,
coarctiation.
Trauma, infective endocarditis, vasculitis – RA, PAN,
hematologic malignancy
Infective endocarditis
Janeway
lesions
Tendon
xanthomata
fingers, thenar/hypothenar
eminences
Non-tender erythematous
maculopapular lesions on palms,
finger pulp
Yellow orange deposits of lipids of
tendons
Infective endocarditis
Hand and arm – type II hyperlipidemia,
elbows/knees – type III
Pulse:
Radial pulse: rate, rhythm, radio-femoral delay, character and volume, and condition of vessel wall
Characteristic
Disorder
Causes
Rate
Bradycardia
Drugs, CHB, athlete, hypothermia, hypothyroid, arrhythmia
Tachycardia
Drugs, fever, pregnancy, hypethyroid, CCF, SVT, anemia,
hypovolemia, PE
Rhythm
Regularly irregular
AV blocks, dropped beats, VPC, bigeminy
Irregularly irregular
Atrial fibrillation
Radio-femoral
Different strength of
Coarctation of aorta, occlusion
delay
pulse
Character
Use brachial or carotid
Collapsing (bounding)
Aortic regurgitation
Pulsus alternans
Advanced CCF
Pulsus paradoxus
Severe asthma, constrictive cardiac conditions, sever COPD
Blood pressure:
Abnormality
Pulsus
paradoxus
Hypertension
Postural
hypotension
Finding
↓BP >10mmhg with
inspiration
BP >145/90mmhg
>15mmhg sys, >10mmhg
dias on standing
Causes
Constrictive pericarditis, effusion
Classify as mild/moderate/severe
Hypovolemia, anti-HT drugs esp. α adrenergic
blockers/TCA/diuretics, Addison’s, autonomic neuropathy
e.g. DM
Face
Abnormality
Jaundice
Finding
Yellow sclera, MM.
Xanthalesma
Cholesterol deposits around
eyes
Rosy cheeks with bluish tinge
Marfan’s syndrome
Central cyanosis
Malar flush
High arched palate
Tongue/ears/nose
cyanosis
Causes
Severe CCF, prosthetic valve RBC
destruction
Type II or III hyperlipidemia
Pulmonary HT + ↓CO – severe MS
AR, MR, MVP
As above
Neck
Carotid pulse
Character
Anacrotic
Plateau
Bisferiens
Collapsing
Finding
Small volume, slow uptake,
notched wave on upstroke
Slow upstroke with sustained
plateau then fall
Anacrotic and collapsing
Slow upstroke rapid fall
Cause
Aortic stenosis
Aortic stenosis
AS + AR
AR, hyperdynamic circ, PDA, AV
fistula, severe atherosclerosis
Small volume
Alternans
Alternating strong and weak
AS, pericardial effusion
Severe LVF
Jugular venous pulse (JVP)
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Measured in 45˚ supine patient with sternal notch as zero point. Normal value is 3cm above sternal notch
(5cm +3cm = 8cmH2O). Sternal notch to mid right atrium distance 5cm.
Two positive waves –
o ‘a’ wave coincides with right atrial systole and first heart sound and precedes carotid pulsation
o ‘v’ wavedue to atrial filling with tricuspid valve closed during ventricular systole
Two troughs/descents –
o ‘x’ descent – between ‘a’ and ‘v’ waves caused due to atrial relaxation. May be interrupted by ‘c’
point (notch) due to transmitted carotid pulse.
o ‘y’ descent – opening of tricuspid valve and rapid ventricular filling
Abnormality
Raised JVP
Finding
General rise in
volume/height
Dominant ‘a’
wave
Cannon ‘a’
waves
Dominant ‘v’
wave
Causes
RVF, tricuspid stenosis/regurgitation, pericardial effusion,
constrictive pericarditis, SVC obstruction, fluid overload.
Tricuspid stenosis, pulmonary stenosis, pulmonary HT
CHB, nodal tachycardia with retrograde atrial conduction, VT with
AV dissociation
Tricuspid regurgitation
The precordium
Inspection
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Scars – median sternotomy, lateral thoracotomy → CABG, valve replacements
Shape of chest – pectus excavatum, kyphoscoliosis, barrel chest
Pacemaker/defibrillator
Apex beat and abnormal pulsations
Palpation
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Apex beat – only palpable in 50%, in mid-clavicular line in 5th ICS, lateral and inferior displacement
indicates enlargement (chest wall deformity, pleural or pulmonary disease)
Type
Finding
Cause
Pressure loaded
Heaving, hyperdynamic
Systolic overload
Thrusting
Displaced, diffuse, non-sustained
Advanced MR, dilated CMpathy
Dyskinetic
Uncoordinated, diffuse
LV dysfunction
Double
Two distinct impulses
HOCM
Absent
None
Thick chest wall, emphysema, effusion, shock,
dextrocardia
 Parasternal impulse – RV enlargement, severe LA enlargement, palpable P2 in c/o pulmonary HT
 Thrills – palpable murmurs
Percussion – usually not conducted for CVS
Auscultation
Auscultation sites – mitral – 4th ICS medial to mid-clavicular line, tricuspid – 5th ICS L parasternal, pulmonary –
2nd ICS L parasternal, aortic – 2nd ICS R parasternal, axilla and carotids.
Normal heart sounds
 S1 – two components – mitral and tricuspid valve closure indicates beginning of ventricular systole
 S2 – softer, shorter and slightly higher pitch marks the end of systole, composed of sounds arising from
aortic and pulmonary valve closure. Normally split in 70% adults due to low pressure RV closure occurs
later in pulmonary valve best appreciated in pulmonary area.
Abnormalities of heart sounds
Abnormality
Mechanism
Loud first HS
Mitral or tricuspid valve wide open at end
of diastole and forceful shutting at
beginning of systole
Soft first HS
Prolonged diastolic filling time or delayed
onset of systole or failure of cusps to
close fully
Loud A2
Forceful aortic valve closure
Loud P2
Forceful pulmonary valve closure
Soft S2
Failure of aortic valves to close
Splitting S1
Delayed cardiac conduction
Splitting S2
Normal, increased if conduction delay
Reversed
splitting S2
P2 occurs first d/t delayed LV
depolarization, emptying or load
Extra heart sounds
Sound Mechanism
S3
Low-pitched mid-diastolic, triple rhythm
– gallop rhythm – tautening of
mitral/tricuspid muscles at end of rapid
diastolic filling
S4
Late diastolic sound pitched higher than
S3 d/t high pressure atrial wave
reflecting from non-compliant
ventricular wall
Causes
Mitral stenosis, tachycardia or shortened AV
conduction time
1st HB, LBBB or mitral regurgitation
Hypertension, congenital AS
Pulmonary HT
Aortic regurgitation
RBBB
RBBB, pulmonic stenosis(delayed ejection), VSD
(↑RV load), mitral regurgitation (early AV
closure d/t rapid filling)
LBBB, PDA, severe AS, coarctation of aorta
Causes
Physiologic in children/young, pathologic – reduced
ventricular compliance, increased atrial pressure. LV S3 –
left sternal edge, louder in expiration d/t ↑CO, LVF and
dilatation, AR/MR/VSD/PDA
RV S3 – left sternal edge louder in inspiration –
RVF/constrictive pericarditis
LV S4 – AS/acute MR, HT/IHD or advanced age,
sometimes only sing in angina
RV S4 – pulmonary HT or pulmonary stenosis
Additional heart sounds
Sound
Mechanism
Opening snap
High pitched sound at variable distance from S2 d/t sudden
opening of mitral valve followed by diastolic murmur
Ejection systolic Early systolic high-pitched sound heard over aortic or
click
pulmonary and LSB due abnormal valve doming in early
systole
Non-ejection
High-pitched sound during systole due to prolapse of
systolic click
redundant mitral valve leaflet during systole
Cardiac murmurs – MSMD, MRMS, ASMS, ARMD
Timing
Type
Mechanism
Systolic
Pansystolic
Ejection (mid)
systolic
Ventricle leaks to
lower pressure
chamber or vessel
begins at S1 and
continues until
pressure equalizes S2.
S1-murmur peaks midsystole –S2. Turbulent
flow across aortic/
pulmonary valve or
↑flow through normal
Causes
Mitral stenosis
Congenital
aortic/pulmonary stenosis
ASD or Ebstein’s anomaly
Associated
features
MR heard best
over apex radiating
to axilla, louder
with isometric
handgrip.
Causes
AS murmur
radiates into
carotid arteries.
HOCM murmur
louder with
AS, PS, HOCM, pulmonary
flow of ASD
MR, TR and VSD
sized valves
Late systolic
Diastolic
Early diastolic
Mid-diastolic
Continuous
murmurs
S1 to S2 to S1
Pericardial
friction rub
Superficial
scratching
sound
Mediastinal
crunch
Crunchy sound
with systolic
and diastolic
components
valsalva, squatting
to standing and
softer with
isometric
handgrip.
Appreciable gap b/w
S1 and murmur
Immediately after S2
high-pitched d/t
regurgitant flow
through leaking
aortic/pulm valves
Short or extend up to
S2, lower pitched d/t
impaired during
ventricular filling
Flow throughout
cardiac cycle
MVP, MR
AR, PR
Varies with resp
and posture,
louder when
sitting up and
breathing out
Hamman’s sign
MS, TS, atrial myxoma,
Austin-Flint murmur of AR
and Carey Coombs of
rheumatic fever
PDA, AV fistula, venous
hum, mammary soufflé of
pregnancy
Pericarditis
Post cardiac surgery,
pneumomediastinum or
post-pericardial effusion
drainage
Dynamic maneuvers
 Respiration –
o Inspiration → ↑ venous return → ↑blood flow to right side → right sided murmurs louder; no
effect on left sided murmurs
o Expiration → opposite effects → R murmurs softer; no effect on L murmurs or louder.
 Deep expiration in leaning forward position – AR murmur may become discernible (otherwise absent),
pericardial rub best heard.
 Valsalva maneuver – forceful expiration against closed glottis → ↑HR, ↓BP and ↓stroke volume →
louder HOCM systolic murmur
 Standing to squatting → ↑stroke volume and arterial pressure → ↑ intensity of most murmurs except
HOCM which gets softer.
 Squatting to standing → opposite effect to above
 Isometric handgrip for 20-30s → ↑ arterial resistance, ↑BP and heart size→ AS becomes softer, HOCM
becomes softer and MVP murmur is delayed due to ↑ventricular volume
The neck → carotid bruit and conducted murmur of AS
The lung bases → late or pan-inspiratory crackles – CCF
The back → murmur of coarctation of aorta best heard over upper back, pitting over sacrum.
The abdomen →
 enlarged tender liver in RVF;
 pulsatile liver due to transmission of RV systolic pressure wave to hepatic veins in tricuspid
regurgitation
 hepatojugular reflux – increase in JVP waveforms s/o RVF
 pulsation of abdominal aorta to the left of midline – expansile pulsations in AAA
The lower limbs → peripheral edema, Achilles tendon xanthomata, toe clubbing (isolated or with finger
clubbing)
Peripheral vascular examination
Inspection
 atrophic skin and loss of hair, colour changes of the feet (blue or red)
 muscle wasting or asymmetry
 surgical scars
 ulcers at the lower end of the tibia
Palpation
 temperature
 palpate both femoral arteries for equality, then auscultate them for bruit
 palpate popliteal pulse – supine and if not felt in prone position
 palpate posterior tibial under medial malleolus and dorsalis pedis on forefoot on both sides
 reduced capillary return by compressing toenails
 Buerger’s test – elevate legs to 45˚ (rapid pallor), then place them dependent over the edge of the bed
(cyanosis if arterial blood supply compromised).
Special maneuvers
 Buerger’s test – red coloration of extremity >than normal suggestive of ischemia
 Brodie-Trendelenburg test – empty superficial veins by milking then place tumb over saphenofemoral
junction (2cm below and lateral to pubic tubercle), get patient to stand up with thumb in place → if
superficial veins fill up incompetence below saphenofemoral junction.
Valvular heart disease
Mitral stenosis
Normal area of mitral valve is 4-6 cm2, reduction of area to <50% causes significant obstruction to LV filling and
LA pressures will have to rise for blood to flow to LV.
Symptoms – dyspnea, orthopnea, PND, hemoptysis, ascites, edema and fatigue
General signs – tachypnea, mitral facies and peripheral cyanosis in severe cases
CV signs
 Reduced pulse volume due to reduced CO
 AF may be present
 JVP normal or reduced in volume, loss of ‘a’ wave if in AF
 Palpation – tapping apex beat, RV heave and palpable P2 if pulmonary HT, diastolic thrill rarely.
 Auscultation – loud S1, loud P2 (if PHT), opening snap, low pitched rumbling diastolic murmur best heard
with bell on mitral area in left lateral position
 Severe mitral stenosis – small pulse pressure, soft S1, early OS, long diastolic murmur, diastolic thrill at
apex with signs of PHT
Causes
 Rheumatic heart disease
 Congenital parachute valve
Mitral regurgitation
A regurgitant mitral valve allows part of the LV stroke volume to return into LA, imposing a load on both LA/LV.
Symptoms – dyspnea, fatigue
General signs – tachypnea
CV signs
 Pulse – normal or sharp upstroke, AF common
 Apex beat displaced, diffuse and hyperdynamic, palpable systolic thrill and parasternal impulse d/t dilated
LA (>than MS)
 Auscultation – soft or absent S1, LV S3 d/t rapid LV filling during diastole. Pansystolic murmur maximal at
apex and radiating to axilla
 Severe mitral regurgitation – small volume pulse, enlarged LV, loud S3, soft S1, early A2, early diastolic
rumble, signs of Pulmonary HT and LVF
Causes
 MVP
 Degenerative changes associated with age
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Rheumatic heart disease
Papillary muscle dysfunction due to LVF or ischemia
Cardiomyopathy – hypertrophic, dilated or restrictive
Connective tissue disease – Marfan’s, RA, Ankylosing spondylitis
Congenital – AV canal defect
Mitral valve prolapse
MVP may cause a systolic murmur or click or both at apex, presence of murmur indicates MR.
CV signs
 Auscultation – systolic clicks at variable times of systole with associate murmur commencing with the click
and extending to rest of systole
 Dynamic maneuvers – increases and comes earlier with valsalva maneuver and becomes softer and
delayed with isometric handgrip.
Causes
 Myxomatous degeneration with age – common
 Associated with ASD, HOCM or Marfan’s syndrome
Aortic stenosis
Normal area of aortic valve is >2cm2. Significant narrowing restricts LV outflow imposing pressure load on LV.
Symptoms: exertional CP (without CAD in 50% of patients), exertional syncope and dyspnea.
General signs – none
CV signs
 Pulse – plateau or anacrotic , ‘pulsus parvus et tardus’ – small volume and late peaking.
 Palpation – hyperdynamic, displaced apex beat, systolic thrill at base of heart.
 Auscultation – narrowly split or reversed S2, harsh midsystolic ejection murmur, maximal over aortic area
extending into carotid arteries. Loudest with patient sitting up and full expiration. Associate AR may be
commonly present. Ejection systolic click sometimes present.
 Severe AS – (valve area <1cm2, pressure gradient >50mmhg) plateau pulse, thrill in aortic area, soft or
absent A2, signs of CCF (late).
Causes
 Degenerative calcific AS (common)
 Calcific change in young patients – usually bicuspid aortic valve.
 Rheumatic heart disease.
 Other – supra-valvular fibrous diaphragm, sub-valvular diaphragm or fibrous ridge, dynamic outflow tract
obstruction in HOCM.
Aortic regurgitation
Incompetent aortic valve allows regurgitation of blood from aorta to LV during diastole during the period that
aortic pressure > LV diastolic pressure
Symptoms – late in disease, exertional dyspnea, fatigue, palpitations and exertional angina.
General signs – Marfan’s syndrome, Ankylosing spondylitis and other CT diseases may be obvious.
CV signs
 Pulse – ‘water hammer pulse’, collapsing, wide pulse pressure. Bisferiens pulse in severe cases.
 Prominent carotid pulsations – ‘Corrigan’s signs’ head-bobbing.
 Palpation – apex beat displaced and hyperkinetic, diastolic thrill at LSB when patient sits up and breathes
out.
 Auscultation – Soft A2, decrescendo high-pitched diastolic murmur immediately after S2, extending
variable time into diastole, loudest at 3rd and 4th ICS; systolic murmur usually present due to associated AS.
Austin Flint murmur – low-pitched rumbling mid-diastolic and presystolic murmur at apex (regurgitant jet
from aortic valve making mitral valve shudder) – differentiate from MS as S1 not loud and no opening
snap.
 Severe AR – collapsing pulse, wide pulse pressure, long decrescendo diastolic murmur, LV S3, soft A2,
Austin Flint murmur, LVF.
Causes
 Chronic – rheumatic, congenital (bicuspid, VSD), Ankylosing spondylitis, aortic root dilatation (Marfan’s, CT
disease, syphilis), dissecting aneurysm
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Acute – valvular – endocarditis, aortic root – Marfan’s, dissecting aneurysm of aortic root.
Tricuspid stenosis
TS is very rare valvular disorder in isolation usually a result of rheumatic heart disease. Murmur similar to MS
except best heard on tricuspid area and louder on inspiration. TR and MS are usually associated d/t RHD.
Abdominal examination may show presystolic liver pulsation.
Tricuspid regurgitation
CV signs
 JVP – large v waves and elevated if RVF present
 Palpation – RV heave
 Auscultation – pansystolic murmur maximal at tricuspid area, increases on inspiration, but diagnosis more
likely on peripheral signs.
 Abdomen – large pulsatile and tender liver usually present. Ascites, edema and pleural effusions may be
present.
 Legs – dilated veins
Causes
 Functional in RVF
 Rheumatic valve disease rarely affects TV alone usually associated MV disease present
 Right sided endocarditis in IVDU
 Tricuspid valve prolapse, RV papillary muscle infarction, blunt steering wheel trauma
 Congenital – Ebstein’s anomaly
Pulmonary stenosis
 General signs – peripheral cyanosis d/t low CO
 Pulse – reduced d/t reduced CO
 JVP – giant a waves d/t RA hypertrophy may be elevated.
 Palpation – RV heave, thrill over pulmonary area.
 Auscultation – ejection click, harsh, loud ejection systolic murmur best heard in pulmonic area, ↑ with
inspiration or only heard then, and not radiating to carotids.
 Abdomen – presystolic pulsation of liver may be present
 Severe PS – signs of RVF and loud murmur with absence of click.
Causes
 Congenital
 Carcinoid rarely
Pulmonary regurgitation
 Rare clinical condition, rarely pathological primarily usually a result of PHT.
Hypertrophic cardiomyopathy
There is abnormal hypertrophy in the LV or RV outflow tract or both. Obstruction occurs towards the end of
systole when the hypertrophied area contracts. Systolic displacement of mitral valve into LV outflow tract also
occurs → MR + further outflow obstruction. Different types may involve the mid-ventricle or apex.
 Symptoms – dyspnea, angina, syncope or sudden death
CV signs
 Pulse – sharp rising and jerky
 JVP – prominent a wave d/t forceful atrial contraction against a non-complaint RV
 Palpation – double or triple apical impulse d/t presystolic expansion of the ventricle caused by atrial
contraction.
 Auscultation – systolic murmur at LSB and apex d/t obstruction of flow and a pansystolic murmur at apex
d/t MR and S4.
 Dynamic maneuvers - ↑with valsalva, standing, and by isotonic exercise; ↓with squatting and isometric
exercise.
 Causes – AD sarcomere or troponin gene mutation, idiopathic and Friedreich’s ataxia
Dilated cardiomyopathy
Cardiac muscle abnormality causing global reduction in cardiac function (CAD excluded by definition). The
signs are those of CCF including MR/TR. Ventricular arrhythmias are common.
Causes
 Idiopathic and familial
 Alcohol and drugs e.g. doxorubicin
 Post-viral
 Myotonic dystrophy
 Hemochromatosis
Restrictive cardiomyopathy
It causes signs similar to constrictive pericarditis with Kussmaul’s sign more common and palpable apex beat.
Causes
 Idiopathic
 Endomyocaridal fibrosis, infiltrative disease (amyloid), granulomas (sarcoid)
Acyanotic congenital heart disease
Ventricular septal disease (VSD)
CV signs
 Palpation – hyperkinetic displaced apex and thrill at LSB
 Auscultation – harsh systolic murmur maximal and almost confined to lower LSB with S3, S4; louder on
expiration. Murmur may be louder with smaller defects and viv.
Causes
 Congenital
 Acquired – post AMI
Atrial septal defect (ASD)
 Two main types – ostium secundum (90%) not involving the AV valve and ostium primum (10%) involving
the AV valves.
CV signs
 Palpation – normal or RV enlargement
 Auscultation – fixed splitting of S2, no murmurs directly but ↑flow through right side may produce a lowpitched diastolic tricuspid flow murmur and sometimes a pulmonary systolic ejection murmur, both louder
on inspiration.
 Ostium primum defects may be associated with MR/TR or other signs if VSD present.
Patent ductus arteriosus
PDA is a persistent embryonic vessel connecting the aorta to the pulmonary artery. The shunt is usually from
the aorta to the pulmonary artery unless PHT has occurred.
CV signs
 Pulse – collapsing pulse with rapid upstroke and low diastolic pressure d/t ejection of large volume of
blood into empty aorta in systole and rapid decompression of the aorta.
 Palpation – hyperkinetic apex beat
 Auscultation – moderate sized shunt →single S2, significant sized shunt → reversed splitting of S2 d/t
delayed A2 as a result of ↑load on LV. Continuous loud machinery murmur, maximal at 1st LICS and other
flow murmurs may be heard.
Coarctation of aorta
This is a congenital narrowing of the aorta usually just distal to the origin of the left subclavian artery. There is
an association with bicuspid aortic valve and Turner’s syndrome.
CV signs
 Upper body better developed than lower; radiofemoral delay with weak femoral pulses; HT in arms but
not legs
 Midsystolic murmur audible over precordium and back d/t blood flow across the coarct and the collateral
chest vessels
Cyanotic congenital heart disease
Causes
 Eisenmenger’s syndrome – pulmonary HT and right to left shunt
 Tetralogy of Fallot
 Ebstein’s anomaly
 Truncus arteriosus
 Transposition of great vessels
 Tricuspid atresia
 Total anomalous pulmonary venous drainage
Tetralogy of Fallot
Four features due to a single developmental anomaly:
1. Ventricular septal defect
2. RV outflow obstruction d/t pulmonic stenosis or infundibular level
3. Over-riding of aorta due to VSD → cyanosis
4. RV hypertrophy d/t outflow obstruction
CV signs
 Central cyanosis – without pulmonary HT d/t venous mixing at ventricular level, over-riding aorta receives
both RV and LV blood
 Clubbing and polycythemia
 RV enlargement → LSB parasternal impulse; systolic thrill d/t pulmonary valve or RV outflow obstruction
 Pulmonary ejection systolic murmur with normal S2
 Repaired TOF with correction of RV outflow obstruction may leave severe PR leading to exertional
dyspnea. Repair may also lead to arrhythmia due to RV damage from operative scars → palpitations and
syncope.
 Signs of repaired TOF – median sternotomy scar, long diastolic murmur of PR, RV enlargement and later
signs of TR → giant v waves and pulsatile liver.
The Neurological examination
Biographical information
 Name, age, place of birth, handedness, occupation and level of education
General examination
 Level of consciousness
 Examination for neck stiffness
 Assessment of higher centres, speech and abnormal movements
The cranial nerves
 Cranial nerves II to XII
Upper limbs
 Motor system – inspection, tone, power, reflexes, coordination
 Sensory system – pinprick, proprioception, vibration sense and light touch
Lower limbs
 As for upper limbs but including assessment of walking (gait)
Skull and spine for local disease
Carotid arteries for bruits
General signs
 Consciousness – levels of consciousness – alert, verbally arousable, painful stimuli or unarousable
 Neck stiffness – causes →infections of the meninges, cervical spondylosis, cervical fusion, Parkinson’s
disease, raised ICP.
Higher centres and speech
 Handedness – 94% of right-handed and 50% of left-handed people have dominant left hemisphere.
Dominant hemisphere controls language and mathematical function
Orientation