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: o femoral vein (medial) o femoral artery (the landmark) o femoral nerve (lateral)
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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 lims, arachnydactyly (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
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HANDS AND FOREARM

nails
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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

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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 rheymatoid arthritis  polyarteritis nodosa  sepsis  haematological malignancy  profound anaemia

fingers
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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 Janway lesions  def: non-tender erythematous maculopapular lesions containing bacteria which can occur on pulms of pulps of fingers  are a rare manifestation of infective endocarditis forearm
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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: o rate of pulse o rhythm o presence or absence of delay of femoral pulse comparied with radial pulse (radiofemoral delay) • character and volume are better assessed from palpation of brachial or carotid arteries • rate of pulse o 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

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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:  myocardia 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 arrhytmias)  pulmonary embolism  myocarditis  fever, acute hypoxia, or hypercapnia (paroxysmal)  other: alcohol, postthoractotomy, idiopathic  multifocal atrial tachycardia  atrial flutter with variable block

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rhythm: o rhythm can be regular or irregular o 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 occuring ectopic beats (supraventricular or ventricular) o irregular rhythm can be regular:  sinus arryhtmia:  in sinus arrhythmia, pulse rate increases with each inspiration and decreases with each expiration  is associated with changes in venous return to heart  Wenckebach phenomen  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: o 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) o 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 o 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 o use carotid or brachial to determine character and volume o however, do use the radial pulse to test for:
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the collapsing (bouding) pulse of aortic regurgitations pulsus alternans of left ventricular failure

BLOOD PRESSURE systolic blood pressure = peak pressure that occurs in artery following ventricular systole

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as deflation continues.diastolic blood pressure = level to which arterial pressure falls during ventricular diastole • normal blood pressure < 140/90 • brachial artery is found in antecubital fossa. sound becomes muffled (softer blowing sound that disappears) (is the 1st diastolic) 5.only the systolic blood pressure is high enough to overcome the cuff's pressure 2. sound increases in intensity (a blowing or swishing sound) 3. iif the reduction in blood pressure is exaggerated over the normal. althogh it is a slight underestimate o however. hence left heart filling is reduced. pressure at which sound is first heard over artery is systolic blood pressure (a sharp thud) . systolic and diastolic pressure normally increased becuase intrathoracic pressure is reduced. there is an auscultatory gap (the sounds disappear just below the systolic pressure anbd reappear before diastolic pressure) in healthy people o the systolic pressure may normally var by up to 10 mmHg. as deflation continues. one third of the way over from the medial epicondyle • first get an approximate estimation of systolic blood pressure o cuff is inflated and then deflated slowly until radial pulse returns • then get more accurate estimation of blood pressure: o cuff is inflated and then deflated slowly whilst listening to brachial artery with stethescope's diaphragm o 5 diferent sounds will be heard as the cuff is slowly released: (Korotkoff sounds) 1. sound decreases in intensity (a softer thud than phase 1) 4. sound disappears (is 2nd diastolic) because flow is now constant since even the diastolic pressure is enough to overcome the cuff's pressure o the 2nd diastolic (5th soudn [K5]) is the best measure for diastolic blood pressure. the 1st diastolic (K4) is a better indication of diastolic pressure o occasionally. and blood pools in the pulmonary vessels. the pressure is higher in the legs o pulsus paradoxus: •  1 during inspiration. the term pulsus paradoxus is applied (pulsus paradoxus is a fall in arterial pulse pressure on inspiration of more than 10 mg) 1 causes:  constrictive pericarditis  pericardial effusion  severe asthma postural blood pressure o postural blood pressure should routinely be taken with patient lying and standing 6 . in severe aortic regurgitation.

usually in old men) o FACE • eyes o o o o 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 . diabetes mellitus.a fall of more than 15 in systolic or 10 in diastolic is abnormal and called postural hypotension o causes include 1 hypovolaemia (e.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 7 . bleeding) 1 drugs (e.see Figure 3. vasodilators) 1 Addison's disease (low cortisol and aldosterone) 1 hypopituirism 1 autonomic neuropathy (e. including aortic regurgitation secondary to aortic root dilatation. dehydration.central cyanosis?  inspect mucosa for petechiae . which is associated with congeintal heart disease.g. amyloidosis) 1 idiopathic orthostatic hypotension (rare progressive degeneration of ANS.do they look diseased? they can be a source of organisms responsible for infective endocarditis  tongue and lips .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.g.g. and also mitral regurgitation due to mitral valve prolapse  teeth .

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 o therefore. use internal jugular vein o pulsations which occur there reflect movements of teh top of a column of blood which extends into the right atrium o 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 o note that the jugular venous pulsation can be distinguished from the arterial pulse because: • 11 it is visible but not palpable 8 . notched wave on upstroke causes: aortic stenosis plateau pulse o slow upstroke o causes: aortic stenosis bisferiens pulse o anacrotic and collapsing o causes: aortic stenosis and regurgitation collapsing pulse o causes:  aortic regurgitation  hyperdynamic circulation  patent ductus arteriosus  peripheral arteriovenous fistula  arteriosclerotic aorta (elderly patients in particular) small volume pulse o causes  aortic stenosis  pericardial effusion pulsus alternans o alternating strong and weak beats o causes: left ventricular failure jerky o causes: hypertrophic cardiomyopathy o o JUGULAR VENOUS PRESSURE (JVP) internal jugular venous pressure gives information about right atrial and right ventricle • position: o patient must be lying at 45 degrees o internal jugular vein is medial to sternomastoid muscle.• • • • • • small volume. slow uptake. external jugular vein is lateral to sternomastoid muscle o the external jugular vein is more readily visible.

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. usually seen to flicker twice with each cardiac cycle 1 1 moves on respiration. the tricuspid valve opens and rapid ventricular filling occurs  any condition in which right ventricular filling is limited. and S1. can cause elevation of the venous pressure.e. the right heart filling pressure is raised. causes include:  right ventricular failure  tricuspid stenosis or regurgitation  pericardial effusion or constrive pericarditis  superior vena caval obstruction  fluid overload  hyperdynamic circulation character of the jugular venous pressure: see Figure 3. and coincides with right atrial systole. this is the called Kussmaul's sign.o it has a complex wave form. normally decreases on inspiration 1 1 it is at first obliterated and then filled from above when light pressure is applied at the base of the neck height: 11 o elevated: when the JVP is raised more than 3cm above zero point. 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.11  there are 2 positive waves in normal jugular venous pressure  a wave:  timing: this is the first wave. i. which is more marked on inspiration when venous return to the heart increases. a cannon a wave is just a much more severe dominant a wave  9 .

constrictive pericarditis y descent  sharp: severe tricuspid regurgitation.atrial fibrillation  exaggerated . lying just below manubriosternal anglle  located at: 5th intercostal space. note that a chest wall deformity or pleural or pulmonary disease can also displace the apex beat o character of apex beat: abnormal beats include: 11 pressure loaded (hyperdynamic or systolic overloaded) apex beat:  def: is a forceful and sustained impulse  causes: aortic stenosis or hypertension 10 . constrictive pericarditis  slow: tricuspid stenosis.see Talley Figure 3. 1cm medial to midclavicular line) .acute cardiac tamponade.   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 . 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. first palpable interspace is the 2nd. 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: o apex beat may be seen (normal position is in 5th intercostal space. or both.12 o pulmonary artery pulsations may be visible in severe pulmonary hypertension • • Palpation • palpate apex beat o position of apex beat:  count down number of interspaces.

may sometimes be palpable  feel for thrills with flat hand. just left of sternum) may reveal palpable tap of pulmonary valve closure thrills  turbulent blood flow. emphysema.• 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. with fingers lifted slightly off chest  in right ventricular enlargement. anterior MI) 11 double impulse apex beat  def: 2 distinct impulses are felt with each systole  causes: hypertrophic cardiomyopathy 11 tapping apex beat  def: first heart sound is actually palpable (normal heart sounds  causes: mitral stenosis. the heel of hand is lifted off the chest wall with each systole in pulmonary hypertension:  palpation over pulmonary area (2nd intercostal space. over: apex. left sternal edge. in this the apex beat will be palpable to right of sternum) other praecordial impulses: o may occur in various heart diseases o right ventricular enlargement: 11 o o parasternal impulse may be felt when heel of hand is rested just to left of sternum. pericardial effusion.g. and rarely dextrocardia (inversion of heart and great vessels. shock (or death). or severe left atrial enlargement (where the right ventricle is pushed anteriorly). which causes cardiac murmurs on auscultation. all it does it define the cardiac outline 11 . 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. or rarely tricuspid stenosis 1 1 non-palpable apex beat: note that this can be normal  causes: thick chest wall (normal).

3. 2. auscultate mitral area with the bell and diaphragm o bell is efficient in amplifying low pitched sounds (it must be lightly applied to chest).heart normally produces 2 sounds each cycle.1 cm left of sternum.mitral and tricuspid valve closure o mitral closure occurs ever so slightly before tricuspid. 2nd intercostal space aortic area . 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. related to closure of valves and rapid changes in blood flow first heart sound (S1) o has 2 components . but only one sound is audible o first heart sound indicates beginning of ventricular systole • second heart sound (2) o is made up of aortic and pulmonary valve closure o because of lower pressure in pulmonary circulation compared with aorta. for example  diastolic murmur of mitral stenosis  a third heart sound o diaphragm is good for reproducing higher pitched sounds. Normal heart sounds . on these occasions. 4. 3.midclavicular line. also note that pulmonary valve closure is further delayed with inspiration because of increased venous return to right ventricle o marks the end of systole. mitral area . for example  systolic murmur of mitral regurgitation  a fourth heart sound auscultate tricuspid area ausculate pulmonary area auscultate aortic area 2.15 (page 51) 1. 4th intercostal space tricuspid area . you may notice splitting). palpation of the carotid pulsation will indicate the timing of sytole • it is clearly crucial to define systole and diastole so that timing of murmurrs can be worked out • Abnormal heart sounds • alterations in intensity 12 .see Talley Figure 3. the pulomary valve usually closes slightly after closure of aortic valve (if you listen carefully.1 cm right of sternum. 5th intercostal space pulmonary area .Auscultation Areas of auscultation . 4.1 cm right of sternum. 2nd intercostal space Process of auscultation 1.

but may be noticed in complete right bundle branch block o increased normal splitting of S2 occurs when there is any delay in right ventricular emptying. so that there is no diminution in flow towards the end of diastole. the nomal 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) o soft S1  causes:  prolonged diastolic filling time (occurs in 1st degree heart block)  delayed onset of left ventricular systole (left bundle brunch block)  failsure of leaflets to coapt normally (mitral regurgitation) o 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.• loud S1  physiology: occurs when mitral or tricuspid valve cusps remain widely open at the end of diastole and shut forcefull with the onset of ventricular systole  causes:  reduced filling volume in mitral or tricuspid steonsis because the narrowed valve orifice limits ventricular filling. 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) o fixed splitting (no respiratory variation) o 13 . and closely suddenly at end of systole o loud pulmonary component of second heart sound (loud P2)  causes:  pulomnary hypertension o soft A2  causes:  aortic valve calcification because leaflet movemnet is reduced  aortic regurgitation because leaflets cannot coapt splitting o splitting of S1 is usually not clinically detectable.

coarctation of the aorta)  increased left ventricular volume load (large patent ductus arteriosus) extra heart sounds o 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.• atrial septal defect equalises volume loads between two atria --> atria acting as a common chamber o reverse spltting (P2 occurs first. 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 o 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  advaced age  right ventricular S4  reduced right ventricular compliance  pulmonary hypertension  pulmonary stenosis o summation gallop  if there heart rate is >120m S3 and S4 may be superimposed rsulting in a summation gallop  14 . and splitting occurs on expiration) is caused by:  left bundle branch block (delayed left ventricular depolarisation)  delayed left ventricular emptying (severe aortic stenosis.

occur during ventricular systole  may be 1. late systolic  pansystolic murmur 1 timing: extends through systole. ejection systolic 3. may be followed by systolic murmur  cause: prolapse of one or more redundant mitral valve leaflets during systole. severe ventricular dysfunction is implied additional sounds o 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 follwed by diastolic murmur of mitral stenosis o systolic ejection click  timing: early systolic high pitched sound over aortic or pulmonary or left sternal edge area  cause: congenital aortic or pulmonary stenosis o non-ejection sysolic click  timing: high pitched sound heard during systole. atrial septal defects o tumour plop  cause: during atrial systole. best over mitral area. then going right up to the second 15 . pansystolic 2. when both S3 and S4 are present (quadruple rhythm). beginning with the first heart sound. pedunculated atrial myxoma may be propelled into mitral or tricuspid valve orifice causing a diastolic plopping sound o diastolic pericardial knock  cause: constrictive pericardial disease --> sudden cessation of ventricular filling o prosthetic hearft valve sounds o pacemaker sounds: a click due to contraction of chest wall muscle  Murmurs of the heart • • must consider: o associated features (peripheral signs) o timing o area of greatest intensity o volume and pitch o effect of dynamic manoeuvres including respiration and Valsalva manoeuvre timing o systolic murmurs .• this does not necessarily imply ventricular stress unless one/or both the heart sounds persist when the heart rate slows.

g. as occurs in anaemia)  late systolic murmur: 1 timing: appreicable gap between first heart sound and murmur. and wanes late in systole (i.e. loudest at the beginning because this is when aortic and pulmonary artery pressure are highest 1 causes:  aortic regurgitation  pulmonary regurgitation 16 .occur during ventricular diastole  early diastolic murmur 1 timing: begins immediately with the S2 and has a decreascendo quality. crescendo-decrescendo murmur) 1 pathophysiology: caused by turbulent blood flow through aortic or pulmonary valve orifices or greatly increased flow through a normal sized orifice or outflow tract 1 causes:  aortic stenosis  pulmonary stenosis  hypertrophic cardiomyopathy  pulmonary flow murmur of an atrial septal defect  increased cardiac sympathetic stimulation (e. generally high pitched 1 pathophysiology: due to regurgitation through leaking or aortic or pulmonary valves. which then continues right up to second heart sound 1 pathophysiology: mitral regurgitation begins in mid-systole 1 causes:  mitral valve prolapse  papillary muscle dysfunction (due usually to ischaemia or hypertrophic cardiomyopathy) diastolic murmurs .o heart sound although loudness and pitch vary during systole 1 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 1 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.

extend throughout systole and diastole  pathophysiology: communcation 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 1 arteriovenous fistula (coronary artery. have lower pitch than early diastolic murmurs 1 pathophysiology: impaired flow during ventricular filling 1 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. systemic) 1 aorto-pulmonary connectoin (e. pulmonary.o o mid-diastolic murmur: 1 timing: begin part way through diastole and may be short or extend to S1. 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.g. congenital) 1 venous hum 1 rupture of sinus of Valsalva into right ventricle or atrium 1 mammary souffle (in late pregnancy or early postpartum period) pericardial friction rub .superficial scratching sound  17 . 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 (blubberying apical middiastolic murmur occurring in the acute stage of rheumatic mitral valvulitis and disappearing as the valvulitis subsides)  presystolic murmur: 1 timing: just before S1 1 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 continous murmurs . heart best at the cardiac apex.

as in mitral regurgitation dynamic manoeuvres o all patients with a newly diagnosed murmur should undergo dynamic manoevre testing o respiration 11  inspiration --> decrease intrathoracic pressure --> increase venous return --> blood flow in right heart 1 hence.very loud. low pitched murmurs indicate turbulent flow under low pressure.moderate. for example. thrill easily palpable 1 1 grade 6/6 . there is not thrill 11 grade 4/6 . as in mitral stenosis o in general.beginning the manoeuvre. thrill just palpable 11 grade 5/6 .very soft and only audible to consultants and students who have been told a murmur is present 11 grade 2/6 .ending the maneouvre)  most murmurs softer because reduced cardiac output aortic stenosis mitral regurgitation left ventricular volume is reduced hence:    18 . and hold this --> decreased preload) . but can be detected almost immediately by an experienced auscultators 11 grade 3/6 . hold nose and close mouth and breath out fully so as to pop eardrums. but are graded anyway:  • grade 1/6 .very. phase 3 .soft.loud.  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 pricardial surfaces (pericarditis)  sound comes and goes area of greatest intensity o not a reliable sign loudness and pitch o loudness is unhelpful is deciding severity of lesion. high pitched murmurs indicate high velocity of flow. but requires a great deal of practice to identify its type o in general.straining phase. can be heard without placing the stethoscope on the chest o the loudness is useful because a change in intensity of a murmur may be of significance. phase 2 . after a MI o pitch is useful guide to murmurs. murmurs that arise on right side tend to be louder during inspiration and softer on expiration o valsalva manoeuvre (forceful expiration against a closed glottis.the following refers to phase 2 of the manoeuvre (phase 1 . very loud.

particularly patients who have been in bed) • ABDOMEN . in particulate late.get patient to sit up percuss and auscultate the lungs .lie patient down flat • liver o enlarged liver? may occur when hepatic veins are congested because of right heart failure o tender liver? distension of liver capsule can cause tenderness o pulsatile liver? may occur in tricuspid regurgitation because right ventriuclar 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 • • • palpaate femoral arteries auscultate femoral arteries (a bruit may be heard if narrowed) palpate popliteal (behind knee) 19 .signs of cardiac failure may be detected in lungs.o  systolic murmur of hypertrophic cardiomyopathy is louder  systolic click and murmur of mitral valve prolapse begins earlier (and goes longer) squatting  increases venous return and systomic arterial resistance causing rise in stroke volume and arterial pressure .hence murmurs are louder aortic stenosis louder mitral regurgitation louder left veniricular size is increased which reduces obstruction to outflow therefore:    intensity of systolic murmur of hypertrophic cardiomyopathy is decreased  mid-syolic click and murmur of mitral valve prolapse are delayed (and shorter)  BACK . or pan-inspiratory crackles or a pleural effusion may be present • feel for pitting oedema in sacrum (occurs in severe right heart failure.

constrictive pericarditis  drugs: calcium antagonists  hepatic: cirrhosis causing hypoalbuminaemia  renal: nephrotic syndrome causing hypoalbuminaemia  gastrointestinal tract: malabsorption. dry beri bery is dietary deficiency of thiamin resulting in painful polyneuritis without the oedema of wet)  cyclical oedema o causes of unilateral lower limb pitting oedema  deep venous thrombosis  compression of large vein by tumour of lymph node o 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) o note that in long standing oedema. marked leg pallor. protein losing enteropathy causing hypoalbuminaemia  wet beri beri (dietary deficiency of thiamin (vitamin B1) resulting in heart failure leading to oedema. perform Buerger's test . femoral systolic bruit.palpate posterior tibial (under medial malleolus) palpate dorsalis pedis (forefood) palpate distal shaft of tibia for oedema by compressing area for 15 seconds . is it pitting or non-pitting o causes of pitting lower limb oedema  cardiac: congestive cardiac failure. absence of hair.if oedema.return of normal red colour is slow) are signs of peripheral vascular disease o in these cases. cool skin and reduced capiilary return (compress toe nails .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: o difficult to diagnose o presening symptom: may be calf pain o on examination: (positives to the following are suggestive of DVT) • • • 20 . starvation.22)? (is due to hyperlipidaemia) • cyanosis and clubbing of toes? (may occur without finger clubbing in patent ductus arteriosus) • peripheral vascular disease: o note that reduced or absent pulses. secondary changes in lymphatics may occur that minimise the oedema • Achilles tendon xanthomata (see Figure 3.

contraceptive pill.common changes in blood flow (cardiac failure or prolonged immobilisation) .common 11 changes in constitution of blood (occult neoplasm. leg elevated   21 .usually arise from thrombus in heart. often secondary to:  myocardial ifnarction or dilated cardiomyopathy  atrial fibrillation  infective endocarditis  thrombosis  injury o symptoms: 4 Ps of acute artertial occlusion of major peripheral limb artery  painful limb  pale limb  pulseless limb  'paralysed' limb varicose veins o examination:  position: if patient complains of varicose veins. 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. disseminated intravascular coagulation. medial to femoral vein). pregnancy) . ask patient to cough: a fluid thrill is felt if the saphenofemoral valve is incompetent  trendelenburg test  patient lying down.o swelling of calf and leg? dilated superficial veins? increased warmth? squeeze calf gently to determine if area is tender causes of thrombosis     11 11 • changes in vessel wall (trauma) .uncommon acute arterial occlusion o causes include: embolism . 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. ask him to stand with legs fully exposed  inspect:  inspect front of whole leg for tortuous.

due to intrapelvic neoplasm which has obstructed deep venous return causes of leg ulcers    11 venous stasis ulcer most common site: around malleoli associated pigmentation.examples  Staphylococcus aureus  syphilitic gumma  tuberculosis  atypical Mycobacterium  fungal neuropathic  11 painless penetrating ulcer on sole of foot: peripheral neurophathy. e.g. stasis eczema ischeamic ulcer    11 11 11 11 large artery disease (atherosclerosis. pressure on saphenous opening in growin patient stands if veins stay empty until groin pressure is released . e. incopetent valves are in thigh or calf. 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. leprosy underlying systemic disease     diabetes mellitus: vascular disease.g.examples  basal cell carcinoma (pearly translucent edge)  squamous cell carcinoma (hard everted edge)  melanoma  lymphoma infection . thromboangiitis obliterans): usually lateral side of leg (pulse absent)  small vessel disease malignant ulcer . but when patient stands. diabetes mellitus. and Perthes' test is performed  Perthes' test  repeat Trendelenburg's test. must try to exclude secondary varicose veins.incompetence of saphenofemoral valve  if veins fill despite groin pressure. example: if pubic varices. neuropathy pyoderma gangrenosum rheumatoid arthritis 22 .

  lymphoma haemolytic anaemia (small ulcers over malleoli) 23 .

apneustic  = post-inspiratory pause in breathing  causes: brain (pontine) damage 7.RESPIRATORY EXAMINATION Background information • • abnormal patterns of breathing 1. trauma. paradoxical  = the abdomen sucks with respiration (normally. chronic renal failure) 4. enlarged tonsils.g. Cheyne-Stokes  = periods of apnoea alternating with periods of hyperpnoae  pathophysiology: delay in medullary chemoreceptor response to blood gas changes  causes  left ventricular failure  brain damage (e.g. it pouches uotward due to diaphragmatic descent)  causes: diaphragmatic paralysis cyanosis o refers to blue discoloration of skin and mucous membranes o is due to presence of deoxygenated haemoglobin in superficial blood vessels o cyanosis does NOT occur in anaemic hypoxia because the total haemoglobin content is low 24 . ataxic (Biot)  = irregular in timing and deep  causes: brainstem damage 6. obesity with upper narrowing.g. sleep apnoea  = cessation of airflow for more than 10 seconds more than 10 times a night during sleep  causes: obstructive (e. pharyngeal soft tissue changes in acromegaly or hypothyroidism) 2. diabetes mellitus. cerebral. hyperventilation  complications: alkalosis and tetany  causes: anxiety 5. haemorrhage)  high altitude 3. Kussmaul's (air hunger)  = deep rapid respiration due to stimulation of respiratory centre  causes: metabolic acidosis (e.

g.o central cyanosis = abnromal amout of deoxygenated haemoglobin in arteries and that blue discoloration is present in parts of body with good circulation such as tongue o peripheral cyanosis = occurs when blood supply to a certain part of body is reduced. the accessory muscles cause elevation of shoulders with inspiration and aid respiration by increasing chest expansion o cyanosis  central cyanosis is best detected by inspecting the tongue . pulmonary embolism) o character of cough 25 .g. e. chronic airflow limitation.examination of tongue differentiates central from peripheral cyanosis  note: severe lung disease may result in significant ventilation-perfusion imbalances (e. pneumonia.characteristically. sulphaemoglobinaemia  peripheral cyanosis  all causes of central cyanosis cause peripheral cyanosis  exposure to cold  reduced cardiac output: left ventricular failure or shock  arterial or venous obstruction Position: patient sitting over edge of bed General appearance • look for the following o dyspnoea  normal respiratory rate < 14 each minute  tachypnoea = rapid respiratory rate  are accessory muscles being used (sternomastoids. and the tissue extracts more oxygen from normal from the circulating blood. massive pulmonary embolism  right to left cardiac shunt (cyanotic congenital heart disease)  polycythaemia  haemoglobin abnromalities (rare): methaemoglobinaemia. strap muscles of neck) . but lips are spared o presence of central cyanosis should lead one to careful examination of cardiovascular and respiratory systems o causes of cyanosis  central cyanosis  decreased arterial saturation  decreased concentration of inspired oxygen: high altitude  lung disease: chronic obstructive pulmonary disease with cor pulmoale. platysma. lips in cold weather are often blue.

mucopurulent)  presence or absence of blood? stridor  = croaking noise loudest on inspiration  causes: (obstruction of larynx. weeks)  laryngeal and pharyngeal tumours  crico-arytenoid rheumatoid arthritis  bilateral vocal cord palsy  tracheal carcinoma  paratracheal compression by lymph nodes  post-tracheostomy or intubation granulomata  is a sign that requires urgent attention hoarseness  causes include:  laryngitis  laryngeal nerve palsy associated with carcinoma of lung  laryngeal carcinoma   The hands • clubbing 26 . mucoid. wheezy ineffective cough suggests airflow limitation  very loose productive cough suggests excessive bronchial secretions due to:  chronic bronchitis  pneumonia  bronchiectasis  dry irritating cough may occur with:  chest infection  asthma  carcinoma of bronchus  left ventricular failure  interstitial lung disease  ACE inhibitors sputum  volume  type (purulent.o o o ask patient to cough several times lack of usual explosive beginning may indicate vocal cord paralysis (bovine cough)  muffled. trachea or large broncus)  acute onset (minutes)  inhaled foreign body  acute epiglottitis  anaphylaxis  toxic gas inhalation  gradual onset (days.

• • • • commonly cause by respiratory disease (but NOT emphysema or chronic bronchitis) o occasionally.unreliable sign o ask patient to dorsiflex wrists and spread out fingers. clubbing is associated with hypertrophic pulmonary osteoarthropathy (HPO)  = arthropathy in association with lung disease  characterised by periosteal inflammation at distal ends of long bones. not nicotine) wasting and weakness o compression and infiltration of peripheral lung tumour of lower trunk of brachial plexus results in wasting of small muscles of hand and weakness of finger abduction pulse rate o tachycardia. ankles. with arms outstretched o flapping tremor may occur with severe carbon dioxide retention (severe chronic airflow limitation) o The face • eyes: o Horner's syndrome? (constricted pupil. and pulsus paradoxus are important signs of sever asthma flapping tremor (asterixis) . due to tumour) • some patients with obstructive sleep apnoea will be obese with a receding chin.sign of cigarette smoking (caused by tar. partial ptosis and loss of sweating which can be due to apical lung tumour compressing sympathetic nerves in neck) • nose: o polpys? (associated with asthma) o engorged turbinates? (various allergic conditions) o deviated septum? (nasal obstruction) • mouth and tongue: o look for central cyanosis o evidence of upper respiratory tract infection (a reddened pharynx and tonsillar enlargement with or without a coating of pus) o broken tooth . a small pharynx and a short thick neck The trachea 27 . wrists.g. metacarpals and metatarsals  sweelling and tenderness over wrists and other involved areas  note that rarely HPO occurs without clubbing  causes include: primary lung carcinoma and pleural mesothelioma staining o staining of fingers .may predispose to lung abscess or pneumonia • sinusitis is indicated by tenderness over the sinuses on palpation • facial plethora (an excess of any of the body fluids) or cyanosis may occur if superior vena cava os obstructed (e.

emphysema o pigeon chest (pectus carinatum)  = localised prominence (outward bowing of sternum and costal cartilages)  causes:  manifestation of chronic childhood illness (due to repeated strong contractions of diaphragm while thorax is still pliable)  rickets o funnel chest (pectus excavatum)  = developmental defect involving a localised depression of lower end of sternum (figure 4.causes of tracheal displacement: o toward the side of the lung lesion  upper lobe collapse  upper lobe fibrosis  pneumonectomy o away from the side of teh lung lesion (uncommon)  massive pleural effusion  tension pneumothorax o upper mediastinal masses.previous thoracic operations or chest drains for a previous pneumothorax or pleural effusion 28 .3). in severe cases. lung capacity may be restricted o Harrison's sulcus  = linear depression of lower ribs just above costal margins at site of attachment of diaphragm  causes:  severe asthma in childhood  rickets o kyphosis = exaggerated forward curvature of spine o scoliosis = lateral bowing o kyphoscoliosis: causes:  idiopathic (80%)  secondary to poliomyelitis (inflammation involving grey matter of cord)  associated with Marfan's syndrome  (note: severe thoracic kyphoscoliosis may reduce lung capacity and increase work of breathing) o lesions of chest wall  scars . such as retrosternal goitre • tracheal tug (finger resting on trachea feels it move inferiorly with each inspiration) is a sign of gross overexpansion of the chest because of airflow obstruction • The chest: inspection • shape and symmetry of chest o barrel shaped  = anteroposterior (AP) diameter is increased compared with lateral diameter  causes: hyperinflation due to asthma.

looking down the clavicles during moderate respiration . the thumbs should move symmetrically apart about 5 cm o reduced expansion on one side indicates a lesion on that side o note: lower lobe expansion is tested here. but no longer is because of effective antituberculosis chemotherapy) invovled removal of large number of ribs on one side to achieve permanent collapse of affected lung  erythema and thickening of skin may occur in radiotherapy.diminished movement indicates underlying lung disease  the affected side will showed delayed or decreased movement  causes of reduced chest wall movements on one side are localised:  localised pulmonary fibrosis  consolidation  collapse  pleural effusion  pneumothroax causes of bilateral reduced chest wall movements are diffuse:  chronic airflow limitation  diffuse pulmonary fibrosis  The chest: palpation • • chest expansion o place hands firmly on chest wall with fingers extending around sides of chest (fugyre 4.can be caused by:  pleural effusion 29 .can be caused by:  collapse of lower lobe  localised pulmonary fibrosis  displacement away from site of lesion . there is a sharp demarcation between abnormal and normal skin diffuse swelling of chest wall and neck  pathophysiology: air tracking from the lungs  causes:  pneumothorax  rupture of oesopahagus prominent veins:  cause: superior vena caval obstruction asymmetry of chest wall movements:  assess this by inspecting from behind patient.o o o o thoracoplasty (was once performed to remove TB.5) o as patient takes a big breath in. upper lobe is tested for on inspection (as above) apex beat o (discussed in cardiac section) o for respiratory diseases:  displacement toward site of lesion .

i. it is a sign of hyperinflation usually due to emphysema.this rotates the scapulae anteriorly. pneumothorax) produces a hyperresonsant note • liver dullness: o upper level of liver dullness is determined by percussing down the anterior cehst in mid-clavicular line o normally.• • tension pneumothorax  apex beat is often impalpable in a chest which is hyperexpanded secondary to chronic airflow limitation vocal fremitus o palpate chest wall with palm of hand while patient repeats "99" o front and back of chest are each palpated in 2 comparable positions with palms.e. consolidated lung) produces a dull note • percusion over a fluid filled area (e. asthma • cardiac dullness: o area of cardiac dullness is uaully present on left side of chest o this may decrease in emphysema or asthma • The chest: auscultation • breath sounds 30 .g. pleural effusion) produces an extremely dull (stony dull) note • percussion over the normal lung produces a resonant note • percussion over a hollow structure (e.g. upper level of liver dullness is 6th rib in right midclavicular line o if chest is resonant below this level. the middle finger is pressed firmly against the chest. liver. pad of right middle finger is used to strike firmly the middle phalanx of middle finger of left hand • percussion of symmetrical areas of: o anterior (chest) o posterior (back) (ask patient to move elbows forward across the front of chest . moves it out of the way) o axillary region (side) o supraclavicular fossa • percussion over a solid structure (e. in this way differences in vibration on chest wall can be detected o causes of change in vocal fremitus are the same as those for vocal resonance (see later) ribs o gently compress chest wall anteroposteriorly and laterally o localised pain suggests a rib fracture (may be secondary to trauma or spontaneous as a result of tumour deposition or bone disease)  The chest: percussion with left hand on chest wall and fingers slightly separated and aligned with ribs. bowel.g.

and therefore produce a different quality. comparing each side  remember to listen high up into the axillae  remember to use bell of stethoscope to listen to lung ap[ices from above the clavicles quality of breath sounds  normal breat sounds  are heard with stethoscope over all parts of chest. and there is no gap between the inspiratory and expiratory sounds  bronchial breath sounds  turbulence in large airways is heard without being filtered by the alveoli. adjacent to a pleural effusion) .one should use the diaphragm of stethoscope to leisten to breath sound in each area. they are heard over the trachea normally.o o o o introduction  see figure 4. but not over the lungs  are audible throughout expiration.g.uncommon  (amphoric sound = when breath sounds over a large cavity have an exaggerated bronchial quality) intensity of breath sounds  causes of reduced breath sounds include:  chronic airflow limitation (espescially emphysema)  pleural effusion  pneumothorax  pneumonia  large neoplasm  pulmonary collapse added (adventitious) sounds  two types of added sounds: continuous (wheezes) and interrupted (crackles)  wheezes 31 .7 . produced in airways rather than alveoli although once they had been thought to arise from alveoli (vesicles) and are therefore called vesicular sounds)  normal (vesciular) breath sounds are louder and longer on inspiration than on expiration. and often there is a gap between inspiration and expiration  are heard over areas of consolidation since solid lung conducts the sound of turbulence in main airways to peripheral areas without filtering  causes include:  lung consolidation (lobar pneumonia) common  localised pulmonary fibrosis uncommon  pleural effusion (above the fluid) uncommon  collapsed lung (e.

typically caused by left ventricular failure (due to presence of alveolar fluid)  coarse crackes .airway narrowing wheezes tend to be louder on expiration because airway is normally dilated during inspiration. occur with any disease that leads to retention of secretions.tend to change with coughing. and is determined by velocity of air jet.due to mucosal oedema and excessive secretions  carcinoma causing bronchial obstruction . medium or coarse  fine crackles . wheeze must be timed in relation to respiratory cycle may be heard in expiration or inspiration or both pathophysiology of wheezes .tends to cause a localised wheeze which is monophonic and does not clear with coughing crackles  some terms not to use include rales (low pitched crackles) and creptitations (high pitched crackles)  crackles are due to collapse of peripheral airways on expiration and sudden opening on inspiration  early inspiratory crackles  suggests disease of small airways  characteristic of chronic airflow limitation  are only heard in early inspiration  late or paninspiratory crackles  suggests disease confined to alveoli  may be fine. excessive secretions  chronic airflow diseases . commonly occur in bronchiectasis pleural friction rub      32 . and narrowed during expiration  an inspiratory wheeze implies severe airway narrowing  pitch of wheeze varies.typically caused by pulmonary fibrosis  medium crackles .due to muscle spasm. mucosal oedema. accordingly  high pitched wheezes are produced in smaller bronchi  low pitched wheezes arise from large bronchi  causes of wheezes include:  asthma (often high pitched) .

if it is louder. spontaneous pneumothorax. over consolidated lung.painful affection of tendinous attachments of throacic muscles.• when thickened. the sound is muffled o whispering pectoriloquy . a continuous or intermittent grating sound may be heard  suggests pleurisy. inspiratory stridor. the numbers will become clearly audible.pleuritic pain in chest. over normal lung. non-pulsatile elevation of jugular venous pressure o occurs in vena caval obstruction feet 33 . or right heart failure • Other • • Permberton's sign o ask patient to lift arms over head o look for development of facial plethora. pay close attention to pulmonary component of P2 (which is best heard at 2nd intercostal space on left) and should not be louder than A2. usually of one side only) vocal resonanance o gives information about lungs' ability to transmit sounds o consolidated lung tends to transmit high frequencies so that speech heard through stethoscope takes a bleeting quality (aegophony). 2 . which may be secondary to pulmonary infarction or pnuemonia  rarely may be caused by: malignany involvement of pleura. suspect pulmonary hypertension • cor pulmonale (also called pulmonary hypertensive heart disease) may be due to: o chronic airflow limitation (emphysema) o pulmonary fibrosis o pulmonary thromboembolism o marked obesity o sleep apnoea o severe kyphoscoliosis • • • The abdomen palpate liver for enlargement due to secondary deposits of tumour from lung.vocal resonance is increased to such an extent that whispered speech is distinctly heard  The heart lie patient at 45 degrees measure jugular venous plse for right heart failure examine preacordium. when a patient with aegophony says "bee" it sounds like "bay" o listen over each part of chest as patient says "99". pleurodynia (1 . roughened pleural surfaces rub together.

consult a table o airways obstruction results in reduced and variable PEFR spirometry o spirometer graphically records forced expiration and forced vital capacity o FEV = volume of air expelled from lungs after maximum inspiration using maximum forced effort o FEV1 = volume of air expelled in first second of FEV o FVC = total volume of air expelled from lungs after maximum inspiratory effort follwed by maximum expiration o FEV1/FVC is normally at about 80%.e.600 litres/minute o normal values for young women . at maximal tolerated exertion and supine o if dyspnoea is not accompanied by tachypnoea when a patient climbs stairs. an increased FET indicates airways obstruction o note any audible wheeze or cough peak flow meter o using the device. chronic bronchitis. airways collapse more easily) 34 . FEV/FVC decreases lots  (also elastic recoil is decreased. therefore expiration time is increased)  obstructive diseases include: asthma.400 litres/minute o value depends on age. one should consider malingering o look for paradoxical inward motion of abdomen during inspiration when patient is uspine (indicating diaphragmatic paralysis) • temperature: fever may accompany any acute or chronic chest infection o o Bedside assessment of lung function • • • forced expiratory time o measure the time taken by a patient to exhale forcefully and completely through an open mouth after taking a maximum inspiration o the normal FET is 3 seconds or less. but may decline to as little as 60% in old age o in obstructive airways disease:  airways narrowing occurs  hence: FEV1 decreases lots.inspect for oedema or cyanosis (clues of cor pulmonale) look for evidence of deep vein thrombosisd • respiratory rate on exercise and positioning o patients complaining of dyspnoea should have their respiratory rate measured at rest. FVC decreases a bit. sex and height . ask patient to take a full breath in and to maximally puff suddenly o normal values for young men . emphysema o in restrictive airways disease  elastic recoil is increased (i.

pneumonia. neonatal respiratory distress syndrome • flow volume curve: this measures inspiratory and expiratory flow.hence: FEV1 decreases a bit (only because VC has decreased). reduced over stony dull tracheal only affected area displaced if massive absent absent. sarcoidosis. FEV/FVC increases  restrictive diseases include: pulmonary firosis. and therefore FVC and FEV1 and other figures can be calculated  COMPARISON OF CHEST SIGNS IN COMMON RESPIRATORY DISORDERS Mediastinal Chest wall displacement movement reduced over consolidation none affected area decreased ipsilateral collapse over affected shift area Disorder Percussion Breath note sounds dull dull Added sounds Vocal resonance increased absent bronchial crackles absent or absent reduced pleural effusion heart displaced to opposite side. FVC decreases. but over pleural rub fluid but absent may be may be over found bronchial effusion above at upper effusion border absent or absent reduced absent tracheal deviation to decreased pneumothorax opposite side over affected resonant if under area tension bronchial asthma none interstitial pulmonary fibrosis none normal decreased normal or normal or or wheeze symmetrically decreased reduced reduced fine inspiratory crackles slightly over decreased normal normal affected normal symmetrically lobes unaffected by cough or posture 35 .

3 o porphyria cutanea tarda  = chronic disorder of porphyrin metabolism characterised by fragile vesicles that appear on exposed areas of skin and heal with scarring  urine is dark  is associated with alcoholism. pressure areas and mouth o Peutz-Jeghers syndrome  = discrete brown black lesions around mouth and buccal mucosa. liver disease and hepatitis C  see figure 5.4 o systemic sclerosis 36 . esp in haemochromatosis (haemosiderin stimulates melanocytes to produce melanin)  malabsorption may result in pigemntation of nipples. lymphoma.2 o acanthosis nigricans  = brown/back velvety elevations of epidermis due to confluent papillomas. acromegaly. fingers and toes  associated with harmatomas of small bowel and colon (which can bleed or intussucept)  is an autosomal dominant condition  see figure 5. plamar creases. usually found in axillae and nape of neck  associated with stomach cancer.GI EXAMINATION Positioning patient: patient lying flat General appearance • • • jaundice: yellow discoloration of sclerae and skin weight and wasting o some causes of weght loss and cachexia include:  failure of intestinal absorption  malignancy  alcoholic cirrhosis o folds of loose skin may suggest recent weight loss o obesity can cause fatty infiltration of liver (non-alcoholic steatohepatitis) and lead to liver dysfunction o anabolic steroids can induce increase muscle bulk and various liver tumours (adenomas. diabetes mellitus o hereditary haemorrhagic telangiectasia (Rendu-Olser-Weber syndrome)  = multiple small telangiectasiae often present in lips and tongue  when present in the gastrointestinal tract they can cause chronic blood loss or torrential bleeding  associated with arteriovenous malformation in liver  autosomal dominant condition  see figure 5. hepatocelllular carcinomas) skin o note that gastrointestinal tract and skin have a common origin from embryoblast o a number of diseases can present with both skin and gut involvement o pigmentation  generalised skin pigmentation can result from chronic lever disease.

g.• = systemic disease characterised by formation of hyalinised and thickened collagenous fibrous tissue. dyspnoea (due to pulmonary fibrosis). hypersplenism)  chronic disease Dupuytren's contracture  = visible and palpable thickening and contraction of palmar fascia causing permanent flexion. dysphagia (due to loss of peristalsis and submucosal fibrosis of oesophagus). often leaving only a rim of pink nail bed at the top of the nail  thumb and index nails bilaterally are most often involved clubbing  clubbing may occur in:  cirrhosis  inflammatory bowel disease  coeliac disease  long standing nutritional depletion palmar erythema  = reddening of palms affecting thenar and hypothenar eminences.g. mercaptans. and may affect feet  associated with: 37 • palms o o o . often bilateral. vitamin B12)  haemolysis (e. often soles of feet are affect  may occur in:  normal  chronic liver disease (attributed to raised oestrogen levels)  pregnancy  thyrotoxicosis  rheumatoid arthritis  polycythaemia  chronic febril diseases (only rarely does palmar erythema occur for this)  chronic leukaemia (only rarely does palmar erythema occur for this) anaemia  inspect palmar creases for pallor suggesting anaemia  some gastrointestinal related causes include:  blood loss  malabsorption (folate. with thickening of skin. most often of ring finger. amines)  The hands • nails o o leuconychia  hypoalbuminaemia (e. myocardial fibrosis. chronic liver disease) and Wilson's disease may cause nail beds to become white. renal vascular changes resembling malignant hypertension  associated with gastro-oesophageal reflux and gastrointestinal motility disorders mental state o hepatic encephalopathy:  def: is an organic neurological disturbance that occurs with chronic or acute liver failure  clinical: patients eventually become stuporous and comatose  pathophysiology: hepatocellular damage + portosystemic shunting (disturbed extra and intra hepatic structure) --> failure to remove toxic metabolties (ammonia. short chain fatty acids.

usually bilateral. jaws and eyelids can also be involved.5 cm dimater. secondary to:  obstructive or cholestatic jaundice spider naevi o = central arterioles from which radiate numerous small vessels which look like legs of spiders. occasionally the arms. acute hepatic necrosis) --> diffuse intravascular coagulation muscle wasting: o may be due to alcohol for 2 reasons:  malnutrition  alcohol can cause proximal myopathy scratch marks o may be obvious due scratching because of pruritus (retention of unknown substance normally excreted in bile). X) o some causes of petechiae:  clotting abnormalities  excessive alcohol consumption (bone marrow depression --> thrombocytopenia)  splenomegaly (secondary to portal hypertension) --> excessive platelet destruction  severe liver disease (esp. tongue. usually located in area drained by superior vena cava (arms. neck. including all clotting factors (except factor VIII which is made elsewhere))  obstructive jaundice (shortage of bile acids in intestine --> reduction in absorption of vitamin K (fat soluble) --> lack of production of clotting factors II (prothrombin). neck.interference with inflow of joint position sense information to reticular formation resulting in rhythmical lapses of postural muscle tone o this is not diagnostic of liver failure. flap tends to be absent at rest and is brought on by sustained posture o mechanism . VII.• alcoholism (not liver disease) manual workers familial hepatic flap (asterixis) o ask patient to stretch out arms in front.ecchymoses o petechiae . it can occur in:  liver failure  cardiac failure  respiratory failure  renal failure  hypoglycaemia  hypokalaemia  hypomagnesaemia  barbiturate intoxication    The arms • • • • bruising (discussed in more detail in haematological system) o large bruises . often accompanied by lateral movements of fingers. separate fingers and extend wrists for 15 seconds o flapping of hepatic encephalopathy .pinhead sized bruises o some causes of ecchymoses:  clotting abnormalities  hepatocellular damage (interfere with protein synthesis. chest wall) 38 . jerky. irregular flexionextension movement at wrist and metacarpophalangeal joints. range in size from just visible to . IX.

with rapid refilling on release of pressure o a couple of spider naevi on the body isn't considered abnormal o causes include:  cirrhosis  viral hepatitis (occur transiently)  during pregnancy o mechanism .rare. they do not blanch on pressure and are very common)  venous stars (2-3 cm lesions which occur on dorsum of feeth.5 palpate axilla for lymphadenopathy o The face • eyes jaundice . legs.7 parotids o palpate this by asking patient to clench teeth so masseter is palpable (parotid is just posterior to masseter.related to oestrogen levels probably o differential diagnosis of spider naevi includes:  Campbell de Morgan spots (flat or slightly elevated red circular lesions which occur in the abdomen or front of chest. see figure 5.as occurs in renal failure.see figure 5.may occur in inflammatory bowel disease o xanthelasma  = yellowish plaques in subcutaneous tissues in periorbital region. due to excess copper in Descemet's membrane  causes include:  Wilson's disease (copper storage disease that leads to cirrhosis and neurological disturbances) o iritis .• pressure applied with a pointed object to the central arteriole causes bleeding of the whole lesion. terminal carcinomatosis and severe infections o unilateral causes of parotid enalargement include:  mixed parotid tumour (occasional bilateral) o o o • 39 . back and lower chest due to elevated venous pressure.bilateral painless enlargement of all 3 salivary glands. are not obliterated by pressure)  hereditary haemorrhagic telangiectasia o see figure 5.6 anaemia Kayser-Fleisher rings  = brownish green rings occurring at peripheray of cornea. and anterior to ear lobe) o bilateral causes of parotid enlargement include:  mumps (can be unilateral)  parotitis following acute illness or surgery (usually tender)  sarcoidosis or lymphoma  Mikulicz syndrome . caused by lipid deposition  may indicate protracted elevation of serum cholesterol  may occur in:  cholestasis  primary biliary cirrhosis o periorbital purpura following proctosigmoidoscopy (black eye syndrome) is characteristic of amyloidosis . probably an early stage of Sjoegren's syndrome  alcohol associated parotitis  malnutrition  severe dehydration .

fusobacterial membranous tonsillitis (Vincent's angina))  leukaemia  pigmentation may be caused by:  heavy metals:  lead.g. swollen and irregular)  gingivitis (e.tumour infiltration usualyl causing painless unilateral enlargement and may cause facial nerve palsy  duct blockage. plaque. e. antimalarials (brown or black areas of pigmentation)  Addison's disease (low gluco and mineralo corticoids) (brown patches)  Peutz-Jeghers syndrome (lips. buccal mucosa or palate)  malignant melanoma (raised.g. bismuth (blue black line on gingivial margin)  iron (caused by haemochromatosis. occuring particularly in smokers  is NOT a sign of disease  lingua nigra  = black tongue (brown)  due to elongation of papillae over posterior part of tongue which appears dark because of accumulation of keratin  is NOT a sign of disease normally  geographical tongue  = slowly chaning red rings and lines occuring of tongue surface  is not usually a sign of disease.indicates severe liver disease.gums become spongy. painless black lesions)  fetor may suggest:  faulty oral hygiene  fetor hepaticus (a sweet smell) . bleed easily. calculus. but can indicate riboflavin (vitamin B2) deficiency  leucoplakia  = white thickening of mucosa of tongue and mouth  causes include:  poor dental hygiene 40 . from smoking. red. probably due to methlymercaptans (substances exhaled which would normally be demethylatted by a normal liver)  ketosis (diabetic ketoacidosis results in ex cretion of ketones in exhaled air causing sickly sweet smell)  uraemia (fish breath)  alcohol (distinctive)  paraldehyde  putrid (due to anaerobic chest infecitons with large amounts of sputum)  cigarettes tongue  coating  = thickened epithelium with bacterial debrtis and food particles. shows blue-grey pigmentation on hard palate)  drugs  oral contraceptives. salivary calculus  • mouth o o teeth and breath  false teeth can be removed for complete examination of mmouth  gum hypertrophy may be caused by:  phenytoin  pregnancy  scurvey (vitamin C deficiency .

sometimes with diarrhoea)  erythema multiforme  infection:  viral . B12. ulcerative colitis. folate. bronchial spasm.g. steroids) . mental abberation and excretion of large quantities of 5-hydroxyindoleacetic acid)  idiopathic .common (are small painfuil vesciles which breakdown to form shallow ulcer. acquired tricuspid and pulmonary stenosis often with regurgitation (sometimes left heart valves also affected).cracks in corners of mouth. coeliac  rheuamatological diseases:  Behcet's syndrome (syndrome characterised by simultaneously or successively occurring recurrent attacks of genital and oral ulceration (aphthae) and uveitis (inflammation of uveal tract . heal without scarring. often with arthritis)  Reiter's syndrome (association of urethritis. consists of irregular mottled blushing. flat angiomas of skin. mucocutaneous lesions and arthritis. difficult to remove. causes include vitamin B6. haemangioma or lymphangioma)  infiltration of tongue in amyloidosis mouth ulcers  causes include:  apthous ulcers . B12) (tongue is sensitive because of rapid turnover of mucosal cells)  alcoholism  carcinoid syndrome . mucous patches). iridocyclitis.rare.especially in elderly  macroglossia  = enlargement of tongue  may occur in:  congenital diseases (e. gold.common  trauma . herpes simplex  bacterial .iris.syphilis (primary chancre.g. vitamin B (esp. folate and iron deficiency candidiasis  causative agent: Candida albicans (thrush)  clinical features: white patches in mouth. usually unknown cause)  drugs (e. diarrhoea. Down's syndrome)  acromegaly (and other endocrine diseases)  tumour infiltration (e. secondary snail track ulcers. ciliary body and choroid) or iridocyclitis (inflammation of iris and ciliary body) with hypopyon (presence of leukocytes in anterior chamber of eye). (combination of symptoms and lesions usually produced by release of serotonin from carcinoid tumours of GIT that have metastasised to liver. TB  self-inflicted  AIDS is associated with mouth lesions  angular stomatitis .      smoking spirits sepsis syphilis idiopathic o o glossitis  = smooth appearance of tongue which may also be erythematous  causes include:  atrophy a papillae (may result in ulceration) due to nutritional deficiencies of iron. and leave a bleeding surface 41 .herpes zoster.common  gastrointestinal diseases: Chron's.g.

cimetidine) Abdomen • inspection o scars . recent scars pink o generalised distension:  caused by:  fat  fluid (ascites)  foetus  flatus  faeces  filthy big tumour (e. chronically increased intra-abdominal pressure) o prominent veins  if present. older scars white.11  veins surrounding umbilicus. diabetes mellitus  The neck and chest • • • palpate the cervical lymph nodes o left side notes may be involved with advanced gastric cancer.infection may spread to involve oesophagus causing dysphagia or odynophagia  infection is most likely in immunocompromised. congenital abdominal wall defect.g. or lung cancer. or other o presence of large left supraclavicular node in combination iwth carcinoma of stomack is called Troisier's sign spider naevi gynaecomastia (in males) o may be unilateral or bilateral o breasts may be tender o may suggest:  chronic liver disease (changes in oestradiol:testosterone ratio.8. with blood flow away  occurs in severe portal hypertension when portal to systemic flow occurs through the umbilical veins. or spironaloactone treatment (for ascites))  alcoholism without liver disease (damage to Leydig cells of testis from alcohol)  use of some drugs (digoxin. faulty oral hygiene. iron deficienc. flow is occurring towards occluded finger  caput Medusae  see figure 5. ovarian. if these veins become distended and engorged. caput Medusae is present 42 .patient eats too much  umbilicus is shallow (or everted) . broad-spectrum antibiotics. second finger is removed and if vein refills.see figure 5.foetus or large ovarian cyst o local swelling:  may indicate:  enlargement of one of abdominal or pelvic organs  hernia (weakened opening may occur from surgery (incisional hernia). hydatid)  phantom pregnancy (what is this?)  shape of umbilicus may help with cause:  umbilicus buried in fat .ascites  unbilicus pushed upwards . elicit direction of venous flow .finger is used to occlude vein and blood is emptied from vein below occluding finger with second finger.

ask patient to take slow deep breath through mouth and watch for evidence of asymmetrical movement. noting presence of tenderness or lump  palpate deeply. right iliac fossa. tumour) shows visible peristalsis as a slow wave passing across upper abdomen from left to right  distal small bowel obstruction .see figure 5. left iliac fossa)  palpate lightl. indicating presence of a mass (esp. but may be normal in thin people o visible peristalsis  occurs in very thin people occasionally. purple striae) o with eyes at level of abdomen. may cause severe pain of mysterious origin until rash appears  Sister Joseph nodule = metastatic tumour deposit in umbilicus (anatomical region where peritoneum is closest to skin)  Cullen's sign (umbilical black eye): . one nerve root.away from legs  prominent veins may be congenital o puslations  expanding central pulsation suggests abdominal aortic aneurysm. umbilical region.e.rare  = discoloration of umbilicus with fainly bluish hue  causes include:  extensvie haemoperitoneum  acute pancreatitis  Grey-Turner's sign: skin discoloration in flanks in severe acute pancreatitis  striae  = stretching of abdominal wall severly enough to cause rupture of elastic fibres in skin producing pink linear marks with wrinkled appearance  may be due to:  ascites  pregnancy  recent weight loss  Cushing's syndrome (wide. large liver seen to move below right costal margin. usually suggests intestinal obstruction  pyloric obstruction (petic ulcer. hypogastrium. left hypochondrium. noting any deep masses  descriptive features of intra-abdominal masses   43 . localised to one side. use warm hands)  examine any tender part last  9 descriptive regions of abdomen .12 (right hypochondrium. epigastrium.• sometimes only one or two veins are apparent engorgement due to inferior vena caval obstruction  see figure 5.radicular pattern. left lumbar region.similar ladder pattern in central abdomen o skin lesions  herpes zoster . however. avoiding the blocked inferior vena cava  direction of blood flow .11  may be caused by:  tumour obstruction  thrombosis  tense ascites  mechanism . reassure patient.abdominal veins enlarge to provide collateral blood flow from legs. or large spleen seen to move below left costal margin) palpation o general:  requires patient to relax abdominal muscles (i. right lumbar region.

ask patient to breathe in and out slowly through the mouth  with each expiration the hand is advanced 1 cm closer to the right costal margin  during inspiration.g. and beginning in right iliac fossa. sarcoid). chronic leukaemia. the hand is kept still and the lateral margin of the forefinger waits expedctantly for the liver edge to strike it  if liver edge is identified. amyloid)  mild:  the above causes  hepatitis  biliary obstruction  hydatid disease  HIV infection  method of palpation:  with examining hand aligned parallel to right costal margin.g. amyloid. may result from tenderness or anxiety. lymphoma)  fatty liver (e. granuloma (e. secondary to diabetes mellitus)  infiltration (e.o site tenderness size and shape surface (regular or irregular) edge (regular or irregular) consistency (hard or soft) mobility and movement with inspiration whether it is pulsatile whether one can get above the mass  guarding = resistance to palpation due to contraction of abdominal muscles. feel surface of liver: note that feeling it jsut below the costal margin may be normal  firm and irregular liver suggests:  hepatocellular carcinoma  metastatic disease  cirrhosis  hydatid disease. cysts.sudden stabbing pain liver  causes of hepatomegaly include: 11 11 11 11 11 11 1 1 1 1 1 1 massive:  metastases  alcoholic liver disease with fatty infiltrtaion  myeloproliferative disease  right heart failure  hepatocellular cancer  moderate:  the above causes  haemochromatosis  haematological disease (e. lipoidoses (presence of fat)  tender liver suggests:  hepatitis  44 .g. may be voluntary or involuntary  involuntary guarding suggests peritonitis  rigidity = constant involuntary contraction of abdominal muscles always associated with tenderness and indicates peritoneal irritation  rebound tenderness = tenderness when pressure (which has been slowly placed on abdomen) is quickly released .g.

right heart failure. percussion should become dull  to estimate liver span.on taking deep breath. at this point. and measure from here to palpable liver edge  normal span < 12.14)  method of palpation  left hand is placed posterolaterally over left lower rib  right hand is placed on abdomen parallel to left costal margin  don't start palpation too near costal margin or a large spleen will be missed  as the right hand is advanced closer to left costal margin. irregular swelling)  acute cholecystitis  Murphy's sign occurs in cholecystitis .o o rapid liver enlargement (e.if gallbladder is enlarged and patient is jaundiced. focal rounded mass which moves downwards on inspiration  causes of enlarged gallbladder:  with jaundice  carcinoma of head of pancreas  carcinoma of ampulla of Vater  in situ gallstone formation in common bile duct  mucocele of gallbladder due to stone in Hartmann's pouch and stone in common bild duct (rare)  without jaundice  mucocele or empyema of gallbladder  carcinoma of gallbladder (stone hard. this removes tension from the abdominal wall and enables a slightly enlarged soft 45  . it can be confused with an enlarged gallbladder or right kidney)  note: a small liver is common in advanced cirrhosis and acute hepatic necrosis (due to liver cell death and collapse of reticulin framework) gallbladder  gallbladder is occasionally palpable below right costal margin if it is enlarged  if palpable.6th rib in about midclavicular line.g. patient catches hios breath when inflamed gallbladder presses on the examiner's hand which s lying at the costal margin  Courvoisier's law . Budd-Chiari syndrome (hepatic vein thrombosis))  hepatocellular carcinoma  biliary obstruction/cholangitis  pulsatile liver suggest:  tricuspid regurgitation  hepatocellular carcinoma  vascular abnormalities  if liver edge is palpable the total liver span should be measured  normal upper border . the left hand compresses firmly over the rib cage so as to produce a loose fold of skin.5 cm  causes of normal but palpable liver include  ptsosis (drooping) of liver due to:  emphysema  asthma  subdiaphragmatic collection  Riedel's lobe (tnogue-like projection of liver from right lobe's inferior surface. percuss down along right midclavicular line until liver dullness is encountered. cause is unlikely to be gallstones. if will feel bulbous. rather carcinoma of pancreas or lower biliary tree resulting in obstructive jaundice  note: majority of dilated gallbladders are not palpable spleen  spleen enlarged inferomedially (see figure 5.

a normal left kidney should never be felt  46 . patient must be rolled on to right side towards examiner and palpation repeated causes of splenomegaly  massive  chronic myeloid leukaemia  myelofibrosis  malaria .g. amyloid. lymphoma.g. autosomal recessive)  small  the above causes  other myeloproliferative disroders  polycythaemia rubra vera  essential thrombocythaemia  haemolytic anaemia  megalblastic anaemia (rarely)  infection  viral (e. causes hepatosplenomegaly. leukaemia. regression of neurological maturation. SLE. acute viral hepatitis. EBV. hepatitis)  bacterial (e.g. amyloid. pernicisous anaemia. sarcoid)  connective tissue disease (e. SLE)  acromegaly  thyrotoxicosis o kidneys palpate with bimaniel method:  patient lies flat on hist back  place left handneath back resting heel of hand under right loin  left fingers must remainfree to flex at metacarpophalangeal joints in the area of renal angle  flexing left fingers.g. sickle cell anaemia)  infection (e.  spleen to be felt as it moves down towards the right iliac fossa at end of inspiration  if spleen is not palpable.rare  primary lymphoma .g. Gaucher's disease .g. sarcoid)  note: secondary carcinomatosis is a rare cause of splenomegaly causes of hepatosplenomegaly  chronic liver disease with portal hypertension  haematological disease (e. myeloproliferative disease. malaria)  connective tissue isease (e. RA.g.rare  kala azar (visceral infection with a species of Leishmania (protozoon)) . CMV)  infiltration (e.g.g. polyarteritis nodosa)  infiltrations (e.g. and palpate for kidney with right hand  a normal right kidney may ocasionally be felt.rare  moderate  the above caues  portal hypertension  lymphoma  leukaemia (acute or chronic)  thalassaemia  storage diseases (e. characteristic histiocytes (Gaucher cells) in viscera. infective endocarditis)  protozoal (e. EBV.lysosomal storage disease resulting from glycocerebroside accumulation due to genetic deficiency of glucocerebrosidase.

 if felt it feels like a swelling with a rounded lower pole and medial dent (hilum) can confuse large left kidney with spleen. amyloid.constipation (faeces). it enlarges appreciably with systole) (AAA grater than 5 cm merits surgical repair)  bowel . hard faeces in sigmoid colon may be palpable  large tumours may be palpable. with an aortic aneurysm. and may represent a normal aorta. the pulsation is expansile (i. mass will not move on respiration  bladder . because of its retroperitoneal position  percussion note is dullt of spleen. or an aortic aneurysm  measure width of pulse gently with two fingers by aligning these parallel to aorta. tumour  large pancreatic pseudocyst following acute pancreatitis may be palpable (usually tense. but usually resonant over kidney because it lies posterior to loops of gas filled bowel  a friction rub may occasionally be heard over spleen.e. and placing them at outmost palpable margins.gastric outlet obstruction  succcussion splash may occur in gastric outlet obstruction  warn patient  grasp one iliac credst with each hand  place stethoscope close to epigastrium  shake patient vigorously from side to side  listen for excessive splashing  (this test is not useful if the patient has had a drink within the last hour or so)  pancreas .g. fixed and does not fall with inspiration)  large tumour may be palpable in thin person  aorta . but kidney is. lymphoma)  acromegaly other abdominal masses  stomach and duodenum .aortic aneurysm or normal  pulsation may be present in thin people.pseudocyst.urinary retention  o 47 . major distinguishing features are:  spleen has no palpable upper border (one cannot feel space between spleen and costal margin)  spleen has a notch which may be palpable  spleen moves inferomedially on inspiration while kidney moves inferiorly  spleen not usually ballottable unless gross ascites is present. but never over kidney  causes of unilateral palpable kidney:  renal cell carcinoma  hydronephrosis or pyonephrosis  polycystic kidneys (with asymmetrical enlargement)  normal right kidney or solitary kidney  acute renal vein thrombosis (unilateral)  acute pyelonephritis  renal abscess  causes of bilateral palpable kidney:  polycystic kidneys  hydronephrisis or pyonephrosis bilaterally  renal cell carcinoma bilaterally  diabetic nephropathy (early)  nephrotic syndrome (many causes of this)  infiltrative disease (e. tumours  in constipation.

nerve entrapment.normal. and then palpate again (Carnett's test)  if tenderness disappears. producing inflammation of overlying muscle (e. cancer  small.   in urinary retention.atrophy (liver disease)  testicular atrophy occurs in chronic liver disease anterior abdominal wall .percuss in midclavicular line down until dullness is encountered  to define lower border . infection.many causes  lump confusion:  try not to confuse lumps in anterior abdominal wall with intraabdominal lumps  to determine whether mass is in abdominal wall. whereas ones within layers of abdominal wall will remain unchanged  causes of lumps in anterior abdominal wall:  lipoma  sebaceous cyst  dermal fibroma  malignant deposits  epigastric hernia  umbilical or para-umbilical hernia  incisional hernia  rectus sheath haematoma  pain confusion:  try not to confuse pain in abdominal wall with intra-abdominal wall pain  to test for abdominal wall pain. myositis)  however. then ask the patient to fold arms across upper chest and sit halfway up. until one is sure bladder is empty inguinal lyph nodes . firm mobile nodes are commonly found in normal subjects  other causes of localised lymph enlargement are:  local infection  metastases from carcinoma  lymphoma (may cause generalised lymphadenopathy as well) testes . muscle strain. this suggests that pain is arising from abdominal wall (e. Carnett test may give positive when visceral disease with involvement of parietal peritoneum. appendicitis)   percussion o percussion used to:  define size and nature of organs and masses  detect fluid in peritoneal cavity  elicit tenderness in patients with peritonitis o liver  percuss to determine liver span  to define upper border .percuss in midclavicular line up to right costal margin until dullness is encountered  (loss of normal liver dullness may occur in massive hepatic necrosis or with free gas in peritoneal gavity) 48 . ask patient to fold arms across upper chest and sit halfway up  an intra-abdominal mass will disappear or decrease in size. the bladder may be palpable above pubic symphysis  cannot feel lower border of bladder  feels rounded  it is unwise to make definite diagnosis concerning swelling coming out of pelvis.g. feel for an area of localised tenderness that reproduces the pain while the patient is in supine. and if this is found.g.

low temperature. dryness and loss of hair.e. as more fluid builds up. muscle weakness)  massive liver metastases  low gradient (<11 gm/L serum albumin)  peritoneal carcinomatosis  tuberculosis  pancreatic ascites 49  o o o . there will not be a resonant area bladder  an area of suprapubic dullness may indicate the upper border of an enlarged bladder or pelvic mass ascites  percussion note over most of abdomen is resonant due to air in intestines  influence of gravity causes fluid to accumulate first in flanks in a supin patient. there will usually be a resonant area because of overlying bowel  in splenic masses. the area of dullness will become detectable closer to the midline  if dullness in flanks is detected.this sign is rare and unreliable (if dull percussion occurs. constrictive pericarditis (cardiac ascites)  Budd-Chiari syndrome (hepatic vein thrombosis) or venoocclusive disease  myxoedema (hypothyroidism characterised by a relatively hard oedema of subcutaneous tissue. splenomegaly is suggestive . thus a dull percussion note is noted in the flank with ascites. with fingers pointing towards groin  examiner flicks side of abdominal wall and pulsation is felt by the hand placed on the other abdominal wall  (also feel fluid thrill in massive ovarian cyst or pregnancy with hydramnios)  causes of ascites:  high gradient (>11 gm/L serum albumin)  cirrhosis  alcoholic hepatitis  fulminant hepatic failure (fulminant = sudden onset. increased fluid in body cavities such as pericardial sac. i. then repalpate) kidneys  percussion over right or left subcostal mass can help distinguish renal from splenic masses:  in renal masses.  stand on right side of bed  percuss left flank until dullness is reached  mark this point  role patient towards examiners  wait 1 minute. the sign of shifting dullness should be sought.o spleen if percussion note over lower left ribs in midaxillary line is dull. a fluid thrill (wave) is detectable (this is not done routinely)  assistant places edge of palm firmly on centre of abdomen. great severity and intensity)  congestive heart failure. with increased content of proteoglycans in fluid. characterised by somnolence. allowing fluid to move  percussion is repeated  the dull area has become resonant if the dullness was due to ascites because the fluid has moved under the influence of gravity  for massive ascites. slow mentation.

rare  indicate inflammation of parietal and visceral peritoneum.bowel sounds often audible without stethoscope = borborygmi o friction rubs .rare  usually occurs because of large volumes of blood flowing in umbilical or para-umbilical veins in falciform ligament (these channel blood from left portal vein to epigastric or internal mammary veins i nabdominal wall) (may occur normally over large veins such as inferior mesenteric vein)  usually heard between xiphisternum and umbilicus in cases of portal hypertension  the presence of venous hum or capud Medusae suggest that the site of portal obstruction is intrahepatic rather than in portal vein itself (why?) o bruit  arerial systolic bruit may be heard over liver (rare) in:  hepatocelar cancer  acute alcoholic hepatitis  auscultate for renal bruit (on either side of midline above umbilicus) if suspect renal artery stenosis  bruit in epigastrium may be heard in patients: with chronic intestinal ischaemia from mesenteric arterial stenosis who are normal bruit may be audible over spleen if there is: 11 11    tumour of body of pancreas splenic arteriovenous fistula  hernias o asking patient to cough may make the hernia appear o inguinal  see figure 5. or gonococcal or chlamydial perihepatitits  splenic causes include splenic infarct o venous hums .bowel sounds high pitched  intestinal rush (e.g. diarrhoea) .no ball sounds  obstruction .17  must decide if swelling in groin is above or below inguinal ligamnet (lies between anterior superior iliac spine and pubic tubercle)  differential diagnosis of solitary groin lump?  above the inguinal line  inguinal hernia . recent liver biospy. in the male it forms the tunica vaginalis testis and normally loses its connection with the 50 . liver infarct. and may be audible over liver or spleen  are heard as rough creaking noise as patient breathes  inflammation of liver capsule causes include tumour within liver.   nephrotic syndrome abdominal masses may be difficult to feel by direct palpation auscultation o bowel sounds  bowel sounds should not be described as increased or decreased. liver abscess. but only as:  present  not present  paralytic ileus .most common  undescended testis  cyst of canal of Nuck (canal of Nuck = processus vaginalis of peritoneum = peritoneal diverticulum in the embryonic lower anterior abdominal wall that traverses the inguinal canal.

flank pain and flexion deformity)  characteristic inguinal hernia is a soft lump which can be palpable if the patient coughs  indirect hernia . and can be mistaken for a lymph node o if a hernia strangulates. disappears when supine)  femoral aneurysm . in males a small indirect hernia may be may be palpated by gently invaginating the scrotum and feeling an impulse when the patient coughs  direct hernia . 2cm medial to femoral pulse  there may not cough impulse  femoral hernia is usually small. the differentiation can only be made at operation between direct and indirect inguinal herniae  remember to count the testes so that you don't mistake a maldescended testis for an inguinal hernia o femoral  occur below pubic tubercle. the overlying skin may become red and tense.passes through internal inguinal ring and descends through the inguinal canal. and the lump is usually tender o herniae are often bilateral Rectal Examination • 51 .pulsatile  psoas abscess (associated with fever.protrudes forwards into the inguinal triangle (but doesn't pass through the internal inguinal ring).rare  below inguinal line  femoral hernia  lymph node  saphena varix (sensation of a jet of water on palpation.peritoneal cavity. direct inguinal hernia appears immediately on standing and disappears on lying down  note that ultimately. a persisent processus vaginalis in the female is known as the canal of Nuck)  encysted hydrocele or lipoma of the cord  iliac node  large femoral hernia .

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