EXAMINATION OF CARDIOVASCULAR SYSTEM

SOME DEFINITIONS AND REVISION

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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)

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

GENERAL APPEARANCE
y y y y

y y

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

HANDS AND FOREARM

y

nails
o

clubbing - see Figure 3.3  def: increase in soft tissue of distal part of fingers or toes  for patient with clubbing examine finger nails - and determine if there is loss of angle between nail bed and finger  causes of clubbing:  common

cardiovascular  cyanotic congenital heart disease  infective endocarditis  respiratory  lung carcinoma (usually not small cell carcinoma)  chronic pulmonary suppuration:  bronchiectasis  lung abscess  empyema  idiopathic pulmonary fibrosis  uncommon  respiratory  cystic fibrosis  asbestosis  pleural mesothelioma (benign fibrous type) or pleural fibroma  gastrointestinal  cirrhosis (especially biliary cirrhosis)  inflammatory bowel disease  coeliac disease  thyrotoxicosis  familial or idiopathic  rare  neurogenic diaphragmatic tumours  pregnancy  unilateral clubbing - bronchial arteriovenous aneurysm or axillary artery aneurysm o 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 o 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 o xanthomata - see Figure 3.5 and Figure 3.6  def: (yellow or orange) deposits of lipid in tendons  can occur in hyperlipidaemia
o

ARTERIAL PULSE
y

y y

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 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


  y

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, post-thoractotomy, idiopathic multifocal atrial tachycardia atrial flutter with variable block

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 nonconducted 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 o

use carotid or brachial to determine character and volume however, do use the radial pulse to test for: 1. the collapsing (bouding) pulse of aortic regurgitations 2. pulsus alternans of left ventricular failure

BLOOD PRESSURE
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systolic blood pressure = peak pressure that occurs in artery following ventricular systole diastolic blood pressure = level to which arterial pressure falls during ventricular diastole normal blood pressure < 140/90 brachial artery is found in antecubital fossa, one third of the way over from the medial epicondyle first get an approximate estimation of systolic blood pressure 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. pressure at which sound is first heard over artery is systolic blood pressure (a sharp thud) - only the systolic blood pressure is high enough to overcome the cuff's pressure 2. as deflation continues, sound increases in intensity (a blowing or swishing sound) 3. as deflation continues, sound decreases in intensity (a softer thud than phase 1) 4. sound becomes muffled (softer blowing sound that disappears) (is the 1st diastolic) 5. sound disappears (is 2nd diastolic) because flow is now constant since even the diastolic pressure is enough to overcome the cuff's pressure o the 2nd diastolic (5th soudn [K5]) is the best measure for diastolic blood pressure, althogh it is a slight underestimate o however, in severe aortic regurgitation, the 1st diastolic (K4) is a better indication of diastolic pressure o occasionally, 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; the pressure is higher in the legs o pulsus paradoxus:

during inspiration, systolic and diastolic pressure normally increased becuase intrathoracic pressure is reduced, and blood pools in the pulmonary vessels, hence left heart filling is reduced; iif the reduction in blood pressure is exaggerated over the normal, the term pulsus paradoxus is applied (pulsus paradoxus is a fall in arterial pulse pressure on inspiration of more than 10 mg)  causes:  constrictive pericarditis  pericardial effusion  severe asthma postural blood pressure postural blood pressure should routinely be taken with patient lying and standing a fall of more than 15 in systolic or 10 in diastolic is abnormal and called postural hypotension causes include  hypovolaemia (e.g. dehydration, bleeding)  drugs (e.g. vasodilators)  Addison's disease (low cortisol and aldosterone)  hypopituirism  autonomic neuropathy (e.g. diabetes mellitus, amyloidosis)  idiopathic orthostatic hypotension (rare progressive degeneration of ANS, usually in old men)


FACE
y

eyes
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 - see Figure 3.8  def: intracutaneous yellow cholesterol deposits around eyes  may be normal variant or indicate hyperlipidaemia cheeks  mitral facies (rosy cheeks with a bluish tinge)  due to dilatation of malar capillaries  associated with pulmonary hypertension and low cardiac output such as occurs in severe mitral stenosis mouth  arched palate? occurs in Marfan's syndrome, which is associated with congeintal heart disease, including aortic regurgitation secondary to

  

aortic root dilatation, and also mitral regurgitation due to mitral valve prolapse teeth - do they look diseased? they can be a source of organisms responsible for infective endocarditis tongue and lips - central cyanosis? inspect mucosa for petechiae - may indicate infective endocarditis

NECK Carotid arteries

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location: medial to sternomastoid muscle carotid pulse gives information about left ventricle and aorta never palpate both carotid arteries at once! anacrotic pulse o small volume, slow uptake, notched wave on upstroke o 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

JUGULAR VENOUS PRESSURE (JVP)

y y

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; external jugular vein is lateral to sternomastoid muscle o the external jugular vein is more readily visible, but is compressed as it enters chest because of its tortuous course and therefore should not be relied upon to assess the position or waveform of the JVP 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: 1. it is visible but not palpable 2. it has a complex wave form, usually seen to flicker twice with each cardiac cycle 3. moves on respiration, normally decreases on inspiration 4. it is at first obliterated and then filled from above when light pressure is applied at the base of the neck height:  elevated: when the JVP is raised more than 3cm above zero point, the right heart filling pressure is raised; causes include:  right ventricular failure  tricuspid stenosis or regurgitation  pericardial effusion or constrive pericarditis  superior vena caval obstruction  fluid overload  hyperdynamic circulation character of the jugular venous pressure: see Figure 3.11  there are 2 positive waves in normal jugular venous pressure  a wave:  timing: this is the first wave, and coincides with right atrial systole, and S1; it precedes the carotid pulsation  due to: right atrial systole  v wave:

   

 

 

timing: this is the second wave and occurs in the period when the tricuspid valve remains closed during ventricular systole  due to: atrial filling x descent: between the a wave and the v wave there is a trough caused by atrial relaxation c point: the x descent is interrupted at a point which is due to the carotid pulse y descent: following the v wave, the tricuspid valve opens and rapid ventricular filling occurs any condition in which right ventricular filling is limited, can cause elevation of the venous pressure, which is more marked on inspiration when venous return to the heart increases; this is the called Kussmaul's sign, and is the opposite of what normally happens note that pressure exerted over the liver for 15 seconds will also increase the venous return the right atrium causes of a dominant a wave: occur when right atrial pressures are raised  tricuspid stenosis (also causing a slow y descent)  pulmonary stenosis  pulmonary hypertension causes of a cannon a wave: occur when the right atrium contracts against the closed tricuspid valve; i.e. a cannon a wave is just a much more severe dominant a wave  complete heart block  paroxysmal nodal tachycardia with retrograde atrial conduction  ventricular tachycardia with retrograde atrial conduction or atrioventricular dissociation cause of a dominant v wave  tricuspid regurgitation x descent  absent - atrial fibrillation  exaggerated - acute cardiac tamponade; constrictive pericarditis y descent  sharp: severe tricuspid regurgitation, constrictive pericarditis  slow: tricuspid stenosis, right atrial myxoma


PRAECORDIUM Inspection
y

scars? pace-maker box?

y y

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, 1cm medial to midclavicular line) - see Talley Figure 3.12 o pulmonary artery pulsations may be visible in severe pulmonary hypertension

Palpation
y

palpate apex beat o position of apex beat:  count down number of interspaces; first palpable interspace is the 2nd, lying just below manubriosternal anglle  located at: 5th intercostal space, 1cm medial to midclavicular line  normal apex beat is is felt over an area size of 20 cm piece  an enlarged heart gives a displaced apex beat laterally or inferiorly, or both; note that a chest wall deformity or pleural or pulmonary disease can also displace the apex beat o character of apex beat: abnormal beats include: 1. pressure loaded (hyperdynamic or systolic overloaded) apex beat:  def: is a forceful and sustained impulse  causes: aortic stenosis or hypertension 2. volume loaded (hyperkinetic or diastolic overloaded) apex beat:  def: is an uncoordinated impulse felt over a larger than normal area  causes: left ventricular dysfunction (e.g. anterior MI) 3. double impulse apex beat  def: 2 distinct impulses are felt with each systole  causes: hypertrophic cardiomyopathy 4. tapping apex beat  def: first heart sound is actually palpable (normal heart sounds  causes: mitral stenosis, or rarely tricuspid stenosis 5. non-palpable apex beat: note that this can be normal  causes: thick chest wall (normal), emphysema, pericardial effusion, shock (or death), and rarely dextrocardia (inversion of heart and great vessels; in this the apex beat will be palpable to right of sternum) other praecordial impulses: may occur in various heart diseases right ventricular enlargement:  parasternal impulse may be felt when heel of hand is rested just to left of sternum, with fingers lifted slightly off chest

in right ventricular enlargement, or severe left atrial enlargement (where the right ventricle is pushed anteriorly), the heel of hand is lifted off the chest wall with each systole in pulmonary hypertension:  palpation over pulmonary area (2nd intercostal space, just left of sternum) may reveal palpable tap of pulmonary valve closure thrills  turbulent blood flow, which causes cardiac murmurs on auscultation, may sometimes be palpable  feel for thrills with flat hand, over: apex, left sternal edge, base of heart  apical thrills (mitral): may be felt more easily with patient rolled over left side (left lateral position) which brings apex closer to chest wall  thrills over base of heart (pulmonary and aortic): are best felt with patient sitting up leaning forward in full expiration (base of heart is moved closer to chest wall)  systolic thrill = a thrill that coincides with apex beat  diastolic thrill = a thrill that does not coincide with apex beat


Percussion: don't bother doing this; all it does it define the cardiac outline Auscultation Areas of auscultation - see Talley Figure 3.15 (page 51) 1. 2. 3. 4. mitral area - midclavicular line, 4th intercostal space tricuspid area - 1 cm right of sternum, 5th intercostal space pulmonary area - 1 cm right of sternum, 2nd intercostal space aortic area - 1 cm left of sternum, 2nd intercostal space

Process of auscultation 1. auscultate mitral area with the bell and diaphragm o bell is efficient in amplifying low pitched sounds (it must be lightly applied to chest), for example  diastolic murmur of mitral stenosis  a third heart sound o diaphragm is good for reproducing higher pitched sounds, for example  systolic murmur of mitral regurgitation  a fourth heart sound 2. auscultate tricuspid area 3. ausculate pulmonary area 4. auscultate aortic area

Normal heart sounds - heart normally produces 2 sounds each cycle, related to closure of valves and rapid changes in blood flow
y

y y y

first heart sound (S1) o has 2 components - mitral and tricuspid valve closure o mitral closure occurs ever so slightly before tricuspid, 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, the pulomary valve usually closes slightly after closure of aortic valve (if you listen carefully, you may notice splitting); also note that pulmonary valve closure is further delayed with inspiration because of increased venous return to right ventricle o marks the end of systole, and the beginning of diastole note that diastole is usually longer than systole sometimes it can be difficult to tell which heart sound is which; on these occasions, palpation of the carotid pulsation will indicate the timing of sytole it is clearly crucial to define systole and diastole so that timing of murmurrs can be worked out

Abnormal heart sounds

y

alterations in intensity o 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, 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, 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, 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, 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)  atrial septal defect equalises volume loads between two atria --> atria acting as a common chamber o reverse spltting (P2 occurs first, and splitting occurs on expiration) is caused by:  left bundle branch block (delayed left ventricular depolarisation)  delayed left ventricular emptying (severe aortic stenosis, coarctation of the aorta)  increased left ventricular volume load (large patent ductus arteriosus) extra heart sounds 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, 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  this does not necessarily imply ventricular stress unless one/or both the heart sounds persist when the heart rate slows; when both S3 and S4 are present (quadruple rhythm), severe ventricular dysfunction is implied additional sounds 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, best over mitral area; may be followed by systolic murmur


o o

cause: prolapse of one or more redundant mitral valve leaflets during systole; atrial septal defects tumour plop  cause: during atrial systole, pedunculated atrial myxoma may be propelled into mitral or tricuspid valve orifice causing a diastolic plopping sound diastolic pericardial knock  cause: constrictive pericardial disease --> sudden cessation of ventricular filling prosthetic hearft valve sounds pacemaker sounds: a click due to contraction of chest wall muscle


Murmurs of the heart

y

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 - occur during ventricular systole  may be 1. pansystolic 2. ejection systolic 3. late systolic  pansystolic murmur  timing: extends through systole, beginning with the first heart sound, then going right up to the second heart sound although loudness and pitch vary during systole  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  causes:  mitral regurgitation  tricuspid regurgitation  ventricular septal defect  aortopulmonary shunts ejection (mid) systolic murmur  timing: does not begin right at 1st heart sound; its intensity is greatest in midsystole, and wanes late in systole (i.e. crescendodecrescendo murmur)

pathophysiology: caused by turbulent blood flow through aortic or pulmonary valve orifices or greatly increased flow through a normal sized orifice or outflow tract  causes:  aortic stenosis  pulmonary stenosis  hypertrophic cardiomyopathy  pulmonary flow murmur of an atrial septal defect  increased cardiac sympathetic stimulation (e.g. as occurs in anaemia) late systolic murmur:  timing: appreicable gap between first heart sound and murmur, which then continues right up to second heart sound  pathophysiology: mitral regurgitation begins in mid-systole  causes:  mitral valve prolapse  papillary muscle dysfunction (due usually to ischaemia or hypertrophic cardiomyopathy) diastolic murmurs - occur during ventricular diastole early diastolic murmur  timing: begins immediately with the S2 and has a decreascendo quality; generally high pitched  pathophysiology: due to regurgitation through leaking or aortic or pulmonary valves; loudest at the beginning because this is when aortic and pulmonary artery pressure are highest  causes:  aortic regurgitation  pulmonary regurgitation mid-diastolic murmur:  timing: begin part way through diastole and may be short or extend to S1; have lower pitch than early diastolic murmurs  pathophysiology: impaired flow during ventricular filling  causes:  mitral stenosis  tricuspid stenosis  atrial myxoma (tumour mass can obstruct the valve orifice)  Austin Flint murmur of aortic regurgitation (a diastolic murmur similar to that of mitral stenosis, heart best at the cardiac apex; it is thought to be caused by turbulent regurgitation stream from the aorta mixing into the stream simultaneously entering from the left atrium through the mitral valve, causing posterior movement of the anterior


leaflet of the mitral valve with transient acceleration of blood flow through the mitral valve) Carey-Coomb's murmur of acute rheumatic fever (blubberying apical mid-diastolic murmur occurring in the acute stage of rheumatic mitral valvulitis and disappearing as the valvulitis subsides)

presystolic murmur:  timing: just before S1  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 - 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:  patent ductus arteriosus  arteriovenous fistula (coronary artery, pulmonary, systemic)  aorto-pulmonary connectoin (e.g. congenital)  venous hum  rupture of sinus of Valsalva into right ventricle or atrium  mammary souffle (in late pregnancy or early postpartum period) pericardial friction rub - superficial scratching sound not confined to systole or diastole and can vary with respiration and posture (often louder when patient is sitting up and breathing out) caused by movement of inflamed pricardial surfaces (pericarditis) sound comes and goes area of greatest intensity not a reliable sign loudness and pitch loudness is unhelpful is deciding severity of lesion, but are graded anyway: 0. grade 1/6 - very soft and only audible to consultants and students who have been told a murmur is present 1. grade 2/6 - soft, but can be detected almost immediately by an experienced auscultators 2. grade 3/6 - moderate; there is not thrill 3. grade 4/6 - loud; thrill just palpable 4. grade 5/6 - very loud; thrill easily palpable 5. grade 6/6 - very, very loud; can be heard without placing the stethoscope on the chest the loudness is useful because a change in intensity of a murmur may be of significance, for example, after a MI

pitch is useful guide to murmurs, but requires a great deal of practice to identify its type in general, low pitched murmurs indicate turbulent flow under low pressure, as in mitral stenosis in general, high pitched murmurs indicate high velocity of flow, as in mitral regurgitation dynamic manoeuvres all patients with a newly diagnosed murmur should undergo dynamic manoevre testing respiration  inspiration --> decrease intrathoracic pressure --> increase venous return --> blood flow in right heart  hence, murmurs that arise on right side tend to be louder during inspiration and softer on expiration valsalva manoeuvre (forceful expiration against a closed glottis; hold nose and close mouth and breath out fully so as to pop eardrums, and hold this --> decreased preload) - the following refers to phase 2 of the manoeuvre (phase 1 - beginning the manoeuvre, phase 2 straining phase, phase 3 - ending the maneouvre)  most murmurs softer because reduced cardiac output  aortic stenosis  mitral regurgitation  left ventricular volume is reduced hence:  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 - get patient to sit up

y

percuss and auscultate the lungs - signs of cardiac failure may be detected in lungs, in particulate late, or pan-inspiratory crackles or a pleural effusion may be present

feel for pitting oedema in sacrum (occurs in severe right heart failure, particularly patients who have been in bed)

ABDOMEN - lie patient down flat

y

liver 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
o

y y y

LOWER LIMBS
y y y y y y

palpaate femoral arteries auscultate femoral arteries (a bruit may be heard if narrowed) palpate popliteal (behind knee) palpate posterior tibial (under medial malleolus) palpate dorsalis pedis (forefood) palpate distal shaft of tibia for oedema by compressing area for 15 seconds - if oedema, is it pitting or non-pitting o causes of pitting lower limb oedema  cardiac: congestive cardiac failure, constrictive pericarditis  drugs: calcium antagonists  hepatic: cirrhosis causing hypoalbuminaemia  renal: nephrotic syndrome causing hypoalbuminaemia  gastrointestinal tract: malabsorption, starvation, protein losing enteropathy causing hypoalbuminaemia  wet beri beri (dietary deficiency of thiamin (vitamin B1) resulting in heart failure leading to oedema; dry beri 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

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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, secondary changes in lymphatics may occur that minimise the oedema Achilles tendon xanthomata (see Figure 3.22)? (is due to hyperlipidaemia) cyanosis and clubbing of toes? (may occur without finger clubbing in patent ductus arteriosus) peripheral vascular disease: o note that reduced or absent pulses, femoral systolic bruit, marked leg pallor, absence of hair, cool skin and reduced capiilary return (compress toe nails return of normal red colour is slow) are signs of peripheral vascular disease o in these cases, perform Buerger's test - elevate leg to 45 degrees (pallor is rapid if there is a poor arterial supply) and then place them dependent at 90 degrees over edge of bed (cyanosis occurs if the arterial supply is impaired) deep venous thrombosis: o difficult to diagnose o presening symptom: may be calf pain o on examination: (positives to the following are suggestive of DVT)  swelling of calf and leg?  dilated superficial veins?  increased warmth?  squeeze calf gently to determine if area is tender o causes of thrombosis 1. changes in vessel wall (trauma) - common 2. changes in blood flow (cardiac failure or prolonged immobilisation) common 3. changes in constitution of blood (occult neoplasm, disseminated intravascular coagulation, contraceptive pill, pregnancy) - uncommon acute arterial occlusion causes include:  embolism - usually arise from thrombus in heart, often secondary to:  myocardial ifnarction or dilated cardiomyopathy  atrial fibrillation  infective endocarditis  thrombosis  injury symptoms: 4 Ps of acute artertial occlusion of major peripheral limb artery  painful limb


pale limb  pulseless limb  'paralysed' limb varicose veins examination:  position: if patient complains of varicose veins, ask him to stand with legs fully exposed  inspect:  inspect front of whole leg for tortuous, dilated branches of long saphenous vein (medial leg)  inspect back of calf for varicosities of short saphenous vein lateral and posterior leg)  inspect to see if leg is inflamed, swollen or pigmented (signs of venous stasis)  ulcers (chronic venous stasis is a cause of ulceration of lower leg)  palpate veins:  hard veins suggests thrombosis and tenderness suggests thrombophlebitis  perform cough impulse test (put finger over long saphenous vein opening in groin, medial to femoral vein); ask patient to cough: a fluid thrill is felt if the saphenofemoral valve is incompetent  trendelenburg test  patient lying down, leg elevated  pressure on saphenous opening in growin  patient stands  if veins stay empty until groin pressure is released incompetence of saphenofemoral valve  if veins fill despite groin pressure, incopetent valves are in thigh or calf, and Perthes' test is performed  Perthes' test  repeat Trendelenburg's test, but when patient stands, allow some blood to be released and get him to stand up and down on the toes a few times  veins will become less tense if the perforating calf veins are patent and have competent valves (the muscle pump is functioning)  note unusual pattern, example: if pubic varices, must try to exclude secondary varicose veins, e.g. due to intrapelvic neoplasm which has obstructed deep venous return causes of leg ulcers 0. venous stasis ulcer  most common  site: around malleoli


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associated pigmentation, stasis eczema ischeamic ulcer  large artery disease (atherosclerosis, thromboangiitis obliterans): usually lateral side of leg (pulse absent)  small vessel disease malignant ulcer - examples 0. basal cell carcinoma (pearly translucent edge) 1. squamous cell carcinoma (hard everted edge) 2. melanoma 3. lymphoma infection - examples 0. Staphylococcus aureus 1. syphilitic gumma 2. tuberculosis 3. atypical Mycobacterium 4. fungal neuropathic  painless penetrating ulcer on sole of foot: peripheral neurophathy, e.g. diabetes mellitus, leprosy underlying systemic disease  diabetes mellitus: vascular disease, neuropathy  pyoderma gangrenosum  rheumatoid arthritis  lymphoma  haemolytic anaemia (small ulcers over malleoli)