Talley Sum Up

8/4/2019 Talley Sum Up

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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)

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

HANDS AND FOREARM

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

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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

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

o 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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o 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)o 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 withbradycardia 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, post-

thoractotomy, 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 nodewith 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 volumeo use carotid or brachial to determine character and volume

o however, do use the radial pulse to test for:

11 the collapsing (bouding) pulse of aortic regurgitations

11 pulsus alternans of left ventricular failure

BLOOD PRESSURE

systolic blood pressure = peak pressure that occurs in artery following

ventricular systole

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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 pressureo 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 (ablowing 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 underestimateo 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:

1 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)

1 causes:


pericardial effusion

severe asthma

postural blood pressure

o postural blood pressure should routinely be taken with patientlying and standing

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o a fall of more than 15 in systolic or 10 in diastolic is abnormal

and called postural hypotension

o causes include

1 hypovolaemia (e.g. dehydration, bleeding)

1 drugs (e.g. vasodilators)

1 Addison's disease (low cortisol and aldosterone)1 hypopituirism

1 autonomic neuropathy (e.g. diabetes mellitus,

amyloidosis)

1 idiopathic orthostatic hypotension (rare progressive

degeneration of ANS, usually in old men)

FACE

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

o xanthelasma - see Figure 3.8

def: intracutaneous yellow cholesterol deposits around

eyes

may be normal variant or indicate hyperlipidaemia

o 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

o 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

location: medial to sternomastoid muscle

carotid pulse gives information about left ventricle and aorta

never palpate both carotid arteries at once!

anacrotic pulse

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o small volume, slow uptake, notched wave on upstroke

o causes: aortic stenosis

plateau pulse

o slow upstroke

o causes: aortic stenosis

bisferiens pulseo 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)

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 veino 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

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11 it has a complex wave form, usually seen to flicker

twice with each cardiac cycle

11 moves on respiration, normally decreases on inspiration

11 it is at first obliterated and then filled from above when

light pressure is applied at the base of the neck

o 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

o 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, andcoincides with right atrial systole, and S1; it

precedes the carotid pulsation

due to: right atrial systole

v wave:

timing: this is the second wave andoccurs 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 heartincreases; 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 cannona wave is just a much more severe dominant a wave

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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;


y descent

sharp: severe tricuspid regurgitation, constrictive

pericarditis

slow: tricuspid stenosis, right atrial myxoma

PRAECORDIUM

Inspection

scars? pace-maker box?

skeletal abnormalities? pectus excavatum (funnel chest)?

kyphoscoliosis? note that skeletal abnormalities can cause distortion of

position of heart and great vessels

visible pulsations:

o

apex beat may be seen (normal position is in 5th intercostalspace, 1cm medial to midclavicular line) - see Talley Figure 3.12

o pulmonary artery pulsations may be visible in severe


Palpation

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 tomidclavicular 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:

11 pressure loaded (hyperdynamic or systolic overloaded)

apex beat:

def: is a forceful and sustained impulse causes: aortic stenosis or hypertension

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11 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)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, or rarely tricuspid

stenosis

11 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:

o may occur in various heart diseases

o 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

o in pulmonary hypertension:

palpation over pulmonary area (2nd intercostal space,

just left of sternum) may reveal palpable tap of pulmonary

valve closure

o thrills

turbulent blood flow, which causes cardiac murmurs on

auscultation, may sometimes be palpable

feel for thrills with flat hand, over: apex, left sternaledge, 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

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Auscultation

Areas of auscultation - see Talley Figure 3.15 (page 51)

1. mitral area - midclavicular line, 4th intercostal space

2. tricuspid area - 1 cm right of sternum, 5th intercostal space3. pulmonary area - 1 cm right of sternum, 2nd intercostal space

4. aortic area - 1 cm left of sternum, 2nd intercostal space

Process of auscultation

1. auscultate mitral area with the bell and diaphragm

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

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 inspirationbecause 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

alterations in intensity

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o loud S1

physiology: occurs when mitral or tricuspid valve cuspsremain widely open at the end of diastole and shut forcefull

with the onset of ventricular systole

causes:

reduced filling volume in mitral or tricuspidsteonsis 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 ofsystole

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 benoticed 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)

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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 tricuspidpapillary 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


o fourth heart sound (S4)

timing: late diastolic sound

pathophysiology: high pressure atrial wave reflectedback 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 stenosis

o summation gallop

if there heart rate is >120m S3 and S4 may be

superimposed rsulting in a summation gallop

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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 afterS2

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, bestover mitral area; may be followed by systolic murmur

cause:prolapse of one or more redundant mitral valve

leaflets during systole; atrial septal defects

o tumour plop

cause: during atrial systole, pedunculated atrialmyxoma 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 fillingo 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 pitcho 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

1 timing: extends through systole, beginning withthe first heart sound, then going right up to the second

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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) untilpressure 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, and wanes late in

systole (i.e. crescendo-decrescendo murmur)

1 pathophysiology: caused by turbulent bloodflow 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.g. as occurs in anaemia)

late systolic murmur:

1 timing: appreicable gap between first heart

sound and murmur, 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 hypertrophiccardiomyopathy)

o diastolic murmurs - occur during ventricular diastole

early diastolic murmur

1 timing: begins immediately with the S2 and hasa decreascendo quality; generally high pitched

1 pathophysiology: due to regurgitation throughleaking or aortic or pulmonary valves; loudest at the

beginning because this is when aortic and pulmonary

artery pressure are highest

1 causes:

aortic regurgitation pulmonary regurgitation

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mid-diastolic murmur:

1 timing: begin part way through diastole and maybe short or extend to S1; have lower pitch than early

diastolic murmurs

1 pathophysiology: impaired flow during

ventricular filling1 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 leftatrium 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:

1 timing: just before S1

1 pathophysiology: atrial systole increases bloodflow across the valve jet just before S1; are an extension

of middiastolic murmurs of mitral stenosis or tricuspid

stenosis

o continous murmurs - extend throughout systole and diastole

pathophysiology: communcation exists between twoparts 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,

pulmonary, systemic)

1 aorto-pulmonary connectoin (e.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)

o pericardial friction rub - superficial scratching sound

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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, but are

graded anyway:

11 grade 1/6 - very soft and only audible to consultants and

students who have been told a murmur is present

11 grade 2/6 - soft, but can be detected almost immediately

by an experienced auscultators

11 grade 3/6 - moderate; there is not thrill11 grade 4/6 - loud; thrill just palpable

11 grade 5/6 - very loud; thrill easily palpable

11 grade 6/6 - very, very loud; 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, for example, after a MI

o pitch is useful guide to murmurs, but requires a great deal of

practice to identify its type

o in general, low pitched murmurs indicate turbulent flow under

low pressure, as in mitral stenosis

o in general, high pitched murmurs indicate high velocity of

flow, as in mitral regurgitation

dynamic manoeuvres

o all patients with a newly diagnosed murmur should undergo

dynamic manoevre testing

o respiration

inspiration --> decrease intrathoracic pressure --> increase

venous return --> blood flow in right heart

1hence, 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; 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:

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systolic murmur of hypertrophic

cardiomyopathy is louder

systolic click and murmur of mitral valve

prolapse begins earlier (and goes longer)

o 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

percuss and auscultate the lungs - signs of cardiac failure may be

detected in lungs, in particulate late, or pan-inspiratory crackles or a pleural

effusion may be present

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

ABDOMEN - lie patient down flat

liver

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)

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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, constrictivepericarditis

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 oedemao 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, 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 ofDVT)

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swelling of calf and leg?

dilated superficial veins?

increased warmth?

squeeze calf gently to determine if area is tender

o causes of thrombosis

11 changes in vessel wall (trauma) - common

11 changes in blood flow (cardiac failure or prolonged

immobilisation) - common

11 changes in constitution of blood (occult neoplasm,

disseminated intravascular coagulation, contraceptive pill,

pregnancy) - uncommon

acute arterial occlusion

o causes include:

embolism - 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, 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 orpigmented (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

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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 intrapelvicneoplasm which has obstructed deep venous return

causes of leg ulcers

11 venous stasis ulcer

most common

site: around malleoli

associated pigmentation, stasis eczema

11 ischeamic ulcer

large artery disease (atherosclerosis, thromboangiitis

obliterans): usually lateral side of leg (pulse absent)

small vessel disease

11 malignant ulcer - examples

basal cell carcinoma (pearly translucent edge)

squamous cell carcinoma (hard everted edge)

melanoma

lymphoma

11 infection - examples

Staphylococcus aureus

syphilitic gumma tuberculosis

atypical Mycobacterium

fungal

11 neuropathic

painless penetrating ulcer on sole of foot: peripheral

neurophathy, e.g. diabetes mellitus, leprosy

11 underlying systemic disease

diabetes mellitus: vascular disease, neuropathy

pyoderma gangrenosum rheumatoid arthritis

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lymphoma

haemolytic anaemia (small ulcers over malleoli)

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RESPIRATORY EXAMINATION

Background information

abnormal patterns of breathing

1. sleep apnoea

= cessation of airflow for more than 10 seconds more

than 10 times a night during sleep

causes: obstructive (e.g. obesity with upper narrowing,

enlarged tonsils, pharyngeal soft tissue changes in acromegaly

or hypothyroidism)

2. Cheyne-Stokes

= periods of apnoea alternating with periods of

hyperpnoae pathophysiology: delay in medullary chemoreceptorresponse to blood gas changes

causes


brain damage (e.g. trauma, cerebral,

haemorrhage)

high altitude

3. Kussmaul's (air hunger)

= deep rapid respiration due to stimulation of

respiratory centre

causes: metabolic acidosis (e.g. diabetes mellitus,chronic renal failure)

4. hyperventilation

complications: alkalosis and tetany

causes: anxiety

5. ataxic (Biot)

= irregular in timing and deep

causes: brainstem damage6. apneustic

= post-inspiratory pause in breathing

causes: brain (pontine) damage7. paradoxical

= the abdomen sucks with respiration (normally, 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

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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, and the tissue extracts more oxygen from

normal from the circulating blood, e.g. lips in cold weather are oftenblue, 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, massive

pulmonary embolism right to left cardiac shunt (cyanotic

congenital heart disease)

polycythaemia

haemoglobin abnromalities (rare):

methaemoglobinaemia, 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,

platysma, strap muscles of neck) - characteristically, 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 - examination of tongue differentiates central from

peripheral cyanosis

note: severe lung disease may result in significant

ventilation-perfusion imbalances (e.g. pneumonia, chronic

airflow limitation, pulmonary embolism)o character of cough

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ask patient to cough several times

lack of usual explosive beginning may indicate vocal

cord paralysis (bovine cough)

muffled, wheezy ineffective cough suggests airflow

limitation

very loose productive cough suggests excessivebronchial secretions due to:

chronic bronchitis

pneumonia

bronchiectasis

dry irritating cough may occur with:

chest infection

asthma

carcinoma of bronchus


interstitial lung disease

ACE inhibitorso sputum

volume

type (purulent, mucoid, mucopurulent)

presence or absence of blood?

o stridor

= croaking noise loudest on inspiration

causes: (obstruction of larynx, trachea or large broncus)

acute onset (minutes)

inhaled foreign body

acute epiglottitis

anaphylaxis

toxic gas inhalation

gradual onset (days, 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

o hoarseness

causes include:

laryngitis

laryngeal nerve palsy associated with carcinoma

of lung

laryngeal carcinoma

The hands

clubbing

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o commonly cause by respiratory disease (but NOT emphysema

or chronic bronchitis)

o occasionally, clubbing is associated with hypertrophic

pulmonary osteoarthropathy (HPO)

= arthropathy in association with lung disease

characterised by periosteal inflammation at distal endsof long bones, wrists, ankles, 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 - sign of cigarette smoking (caused by tar,

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, and pulsus paradoxus are important signs of sever

asthma

flapping tremor (asterixis) - unreliable sign

o ask patient to dorsiflex wrists and spread out fingers, with arms

outstretched

o flapping tremor may occur with severe carbon dioxide retention

(severe chronic airflow limitation)

The face

eyes:

o Horner's syndrome? (constricted pupil, 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 - 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.g. due to tumour)

some patients with obstructive sleep apnoea will be obese with a

receding chin, a small pharynx and a short thick neck

The trachea

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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, 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, 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 4.3); 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

ricketso 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 - previous thoracic operations or chest drains for aprevious pneumothorax or pleural effusion

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thoracoplasty (was once performed to remove TB, 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; there is a sharp demarcation between abnormaland normal skin

o diffuse swelling of chest wall and neck

pathophysiology: air tracking from the lungs

causes:

pneumothorax

rupture of oesopahagus

o prominent veins:

cause: superior vena caval obstruction

o asymmetry of chest wall movements:

assess this by inspecting from behind patient, looking

down the clavicles during moderate respiration - diminishedmovement indicates underlying lung disease

the affected side will showed delayed or decreased

movement

causes of reduced chest wall movements on one sideare localised:

localised pulmonary fibrosis

consolidation

collapse

pleural effusion

pneumothroaxo 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 4.5)

o as patient takes a big breath in, the thumbs should move

symmetrically apart about 5 cmo reduced expansion on one side indicates a lesion on that side

o note: lower lobe expansion is tested here; 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 - can be caused by:

collapse of lower lobe

localised pulmonary fibrosis

displacement away from site of lesion - can be caused

by: pleural effusion

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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 comparablepositions with palms; 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, the middle finger is pressed firmly against the chest; 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 - this rotates the scapulae anteriorly, i.e. moves it out of

the way)o axillary region (side)

o supraclavicular fossa

percussion over a solid structure (e.g. liver, consolidated lung)

produces a dull note

percusion over a fluid filled area (e.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. bowel, pneumothorax)

produces a hyperresonsant note

liver dullness:

o upper level of liver dullness is determined by percussing downthe anterior cehst in mid-clavicular line

o normally, upper level of liver dullness is 6th rib in right mid-

clavicular line

o if chest is resonant below this level, it is a sign of

hyperinflation usually due to emphysema, 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

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o introduction

see figure 4.7 - one should use the diaphragm of

stethoscope to leisten to breath sound in each area, comparing

each side

remember to listen high up into the axillae

remember to use bell of stethoscope to listen to lungap[ices from above the clavicles

o quality of breath sounds

normal breat sounds

are heard with stethoscope over all parts of

chest, 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 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, and therefore produce a

different quality; they are heard over the trachea

normally, but not over the lungs

are audible throughout 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.g. adjacent to a pleural

effusion) - uncommon

(amphoric sound = when breath sounds over a

large cavity have an exaggerated bronchial quality)

o intensity of breath sounds causes of reduced breath sounds include:

chronic airflow limitation (espescially

emphysema)

pleural effusion

pneumothorax

pneumonia

large neoplasm

pulmonary collapse

o added (adventitious) sounds

two types of added sounds: continuous (wheezes) and

interrupted (crackles) wheezes

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wheeze must be timed in relation to respiratory

cycle

may be heard in expiration or inspiration or both

pathophysiology of wheezes - airway narrowing

wheezes tend to be louder on expiration because

airway is normally dilated during inspiration, andnarrowed during expiration

an inspiratory wheeze implies severe airway

narrowing

pitch of wheeze varies, and is determined by

velocity of air jet, accordingly

high pitched wheezes are produced in

smaller bronchi

low pitched wheezes arise from large

bronchi

causes of wheezes include:

asthma (often high pitched) - due tomuscle spasm, mucosal oedema, excessive

secretions

chronic airflow diseases - due to mucosal

oedema and excessive secretions

carcinoma causing bronchial obstruction

- 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, medium or coarse

fine crackles - typically caused by

pulmonary fibrosis

medium crackles - typically caused by

left ventricular failure (due to presence of

alveolar fluid)

coarse crackes - tend to change with

coughing; occur with any disease that leads to

retention of secretions; commonly occur in

bronchiectasis

pleural friction rub

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when thickened, roughened pleural surfaces rub

together, a continuous or intermittent grating sound may

be heard

suggests pleurisy, which may be secondary to

pulmonary infarction or pnuemonia

rarely may be caused by: malignanyinvolvement of pleura, spontaneous pneumothorax,

pleurodynia (1 - pleuritic pain in chest; 2 - painful

affection of tendinous attachments of throacic muscles,

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);

when a patient with aegophony says "bee" it sounds like "bay"

o listen over each part of chest as patient says "99"; over

consolidated lung, the numbers will become clearly audible; overnormal lung, the sound is muffled

o whispering pectoriloquy - 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; pay close attention to pulmonary component of

P2 (which is best heard at 2nd intercostal space on left) and should not belouder than A2; if it is louder, 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, or right heart failure

Other

Permberton's sign

o ask patient to lift arms over head

o look for development of facial plethora, inspiratory stridor,

non-pulsatile elevation of jugular venous pressure

o occurs in vena caval obstruction

feet

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o inspect for oedema or cyanosis (clues of cor pulmonale)

o 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, at maximal tolerated exertion and supine

o if dyspnoea is not accompanied by tachypnoea when a patientclimbs stairs, 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

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; an increased FET indicates

airways obstruction

o note any audible wheeze or cough

peak flow meter

o using the device, ask patient to take a full breath in and to

maximally puff suddenly

o normal values for young men - 600 litres/minute

o normal values for young women - 400 litres/minute

o value depends on age, sex and height - 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%, but may decline to as

little as 60% in old age

o in obstructive airways disease: airways narrowing occurs

hence: FEV1 decreases lots, FVC decreases a bit,

FEV/FVC decreases lots

(also elastic recoil is decreased, therefore expiration

time is increased)

obstructive diseases include: asthma, chronic bronchitis,

emphysema

o in restrictive airways disease

elastic recoil is increased (i.e. airways collapse more

easily)

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hence: FEV1 decreases a bit (only because VC has

decreased), FVC decreases, FEV/FVC increases

restrictive diseases include: pulmonary firosis,

sarcoidosis, pneumonia, neonatal respiratory distress syndrome

flow volume curve: this measures inspiratory and expiratory flow, and

therefore FVC and FEV1 and other figures can be calculated

COMPARISON OF CHEST SIGNS IN COMMON RESPIRATORY DISORDERS

DisorderMediastinal

displacement

Chest wall

movement

Percussion

note

Breath

sounds

Added

sounds

Vocal

resonance

consolidation nonereduced over

affected areadull bronchial crackles increased

collapseipsilateral

shift

decreased

over affected

area

dullabsent or

reducedabsent absent

pleural

effusion

heart

displaced to

opposite side;

tracheal only

displaced if

massive

reduced over

affected areastony dull

absent

over

fluid but

may be

bronchial

at upper

border

absent, but

pleural rub

may be

found

above

effusion

absent

over

effusion

pneumothorax

tracheal

deviation to

opposite side

if undertension

decreased

over affected

area

resonantabsent or

reducedabsent absent

bronchial

asthmanone

decreased

symmetrically

normal or

decreased

normal

or

reduced

wheezenormal or

reduced

interstitial

pulmonary

fibrosis

none

slightly

decreased

symmetrically

normal normal

fine

inspiratory

crackles

over

affected

lobes

unaffected

by cough

or posture

normal

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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 dysfunctiono anabolic steroids can induce increase muscle bulk and various liver tumours

(adenomas, 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, esp in

haemochromatosis (haemosiderin stimulates melanocytes to produce melanin)

malabsorption may result in pigemntation of nipples, plamar creases, pressure

areas and mouth

o Peutz-Jeghers syndrome = discrete brown black lesions around mouth and buccal mucosa, fingers and

toes

associated with harmatomas of small bowel and colon (which can bleed or

intussucept)

is an autosomal dominant condition

see figure 5.2

o acanthosis nigricans

= brown/back velvety elevations of epidermis due to confluent papillomas,

usually found in axillae and nape of neck

associated with stomach cancer, lymphoma, acromegaly, 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 5.3

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, liver disease and hepatitis C

see figure 5.4

o systemic sclerosis

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= systemic disease characterised by formation of hyalinised and thickened

collagenous fibrous tissue, with thickening of skin, dysphagia (due to loss of

peristalsis and submucosal fibrosis of oesophagus), dyspnoea (due to pulmonary

fibrosis), myocardial fibrosis, 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 acuteliver 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,

mercaptans, short chain fatty acids, amines)

The hands

nails

o leuconychia

hypoalbuminaemia (e.g. chronic liver disease) and Wilson's disease may cause

nail beds to become white, often leaving only a rim of pink nail bed at the top of the

nail

thumb and index nails bilaterally are most often involved

o clubbing

clubbing may occur in:

cirrhosis

inflammatory bowel disease

coeliac disease

long standing nutritional depletion

palmso palmar erythema

= reddening of palms affecting thenar and hypothenar eminences; 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 forthis)

chronic leukaemia (only rarely does palmar erythema occur for this)

o anaemia

inspect palmar creases for pallor suggesting anaemia

some gastrointestinal related causes include:

blood loss

malabsorption (folate, vitamin B12)

haemolysis (e.g. hypersplenism)

chronic disease

o Dupuytren's contracture

= visible and palpable thickening and contraction of palmar fascia causingpermanent flexion, most often of ring finger; often bilateral, and may affect feet

associated with:

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alcoholism (not liver disease)

manual workers

familial

hepatic flap (asterixis)

o ask patient to stretch out arms in front, separate fingers and extend wrists for 15

seconds

o flapping of hepatic encephalopathy - usually bilateral, jerky, irregular flexion-

extension movement at wrist and metacarpophalangeal joints, often accompanied by lateral

movements of fingers; occasionally the arms, neck, tongue, jaws and eyelids can also be

involved; flap tends to be absent at rest and is brought on by sustained postureo mechanism - 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; 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 - ecchymoses

o petechiae - pinhead sized bruises

o some causes of ecchymoses:

clotting abnormalities

hepatocellular damage (interfere with protein synthesis, 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), VII, IX, 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. 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), secondary to:

obstructive or cholestatic jaundice

spider naevi

o = central arterioles from which radiate numerous small vessels which look like legs of

spiders; range in size from just visible to .5 cm dimater; usually located in area drained by

superior vena cava (arms, neck, chest wall)

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o pressure applied with a pointed object to the central arteriole causes bleeding of the

whole lesion, 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 - related to oestrogen levels probably

o differential diagnosis of spider naevi includes:

Campbell de Morgan spots (flat or slightly elevated red circular lesions whichoccur in the abdomen or front of chest; they do not blanch on pressure and are very

common)

venous stars (2-3 cm lesions which occur on dorsum of feeth, legs, back and

lower chest due to elevated venous pressure; are not obliterated by pressure)

hereditary haemorrhagic telangiectasia

o see figure 5.5

palpate axilla for lymphadenopathy

The face

eyes

o jaundice - see figure 5.6

o anaemia

o Kayser-Fleisher rings

= brownish green rings occurring at peripheray of cornea, 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 - may occur in inflammatory bowel disease

o xanthelasma = yellowish plaques in subcutaneous tissues in periorbital region, 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 - rare; see figure 5.7

parotids

o palpate this by asking patient to clench teeth so masseter is palpable (parotid is just

posterior to masseter, 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 - bilateral painless enlargement of all 3 salivary glands,

probably an early stage of Sjoegren's syndrome

alcohol associated parotitis

malnutrition

severe dehydration - as occurs in renal failure, terminal carcinomatosis and

severe infections

o unilateral causes of parotid enalargement include:

mixed parotid tumour (occasional bilateral)

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tumour infiltration usualyl causing painless unilateral enlargement and may

cause facial nerve palsy

duct blockage, e.g. salivary calculus

mouth

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 - gums become spongy, red, bleedeasily, swollen and irregular)

gingivitis (e.g. from smoking, calculus, plaque, fusobacterial

membranous tonsillitis (Vincent's angina))

leukaemia

pigmentation may be caused by:

heavy metals:

lead, bismuth (blue black line on gingivial margin)

iron (caused by haemochromatosis, shows blue-grey

pigmentation on hard palate)

drugs

oral contraceptives, 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, painless black lesions)

fetor may suggest:

faulty oral hygiene

fetor hepaticus (a sweet smell) - indicates severe liver disease,

probably due to methlymercaptans (substances exhaled which would normally

be demethylatted by a normal liver)

ketosis (diabetic ketoacidosis results in ex cretion of ketones inexhaled air causing sickly sweet smell)

uraemia (fish breath)

alcohol (distinctive)

paraldehyde

putrid (due to anaerobic chest infecitons with large amounts of

sputum)

cigarettes

o tongue

coating

= thickened epithelium with bacterial debrtis and food particles,

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, but can indicate riboflavin (vitamin

B2) deficiency

leucoplakia = white thickening of mucosa of tongue and mouth

causes include:

poor dental hygiene

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smoking

spirits

sepsis

syphilis

idiopathic

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, folate, vitamin B (esp. B12) (tongue is sensitivebecause of rapid turnover of mucosal cells)

alcoholism

carcinoid syndrome - rare; (combination of symptoms and

lesions usually produced by release of serotonin from carcinoid

tumours of GIT that have metastasised to liver; consists of irregular

mottled blushing, flat angiomas of skin, acquired tricuspid and

pulmonary stenosis often with regurgitation (sometimes left heart

valves also affected), diarrhoea, bronchial spasm, mental abberation

and excretion of large quantities of 5-hydroxyindoleacetic acid)

idiopathic - especially in elderly

macroglossia = enlargement of tongue

may occur in:

congenital diseases (e.g. Down's syndrome)

acromegaly (and other endocrine diseases)

tumour infiltration (e.g. haemangioma or lymphangioma)

infiltration of tongue in amyloidosis

o mouth ulcers

causes include:

apthous ulcers - common (are small painfuil vesciles which breakdown

to form shallow ulcer; heal without scarring; usually unknown cause) drugs (e.g. gold, steroids) - common

trauma - common

gastrointestinal diseases: Chron's, ulcerative colitis, 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 - iris,

ciliary body and choroid) or iridocyclitis (inflammation of iris and

ciliary body) with hypopyon (presence of leukocytes in anterior

chamber of eye), often with arthritis)

Reiter's syndrome (association of urethritis, iridocyclitis,mucocutaneous lesions and arthritis, sometimes with diarrhoea)

erythema multiforme

infection:

viral - herpes zoster, herpes simplex

bacterial - syphilis (primary chancre, secondary snail track

ulcers, mucous patches), TB

self-inflicted

AIDS is associated with mouth lesions

angular stomatitis - cracks in corners of mouth; causes include vitamin B6,

B12, folate and iron deficiency

o candidiasis causative agent: Candida albicans (thrush)

clinical features: white patches in mouth, difficult to remove, and leave a

bleeding surface

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infection may spread to involve oesophagus causing dysphagia or

odynophagia

infection is most likely in immunocompromised, broad-spectrum antibiotics,

faulty oral hygiene, iron deficienc, diabetes mellitus

The neck and chest

palpate the cervical lymph nodes

o left side notes may be involved with advanced gastric cancer, or lung cancer, or other

o presence of large left supraclavicular node in combination iwth carcinoma of stomackis 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, or

spironaloactone treatment (for ascites))

alcoholism without liver disease (damage to Leydig cells of testis from

alcohol)

use of some drugs (digoxin, cimetidine)

Abdomen

inspection

o scars - see figure 5.8; older scars white, recent scars pink

o generalised distension:

caused by:

fat

fluid (ascites)

foetus flatus

faeces

filthy big tumour (e.g. ovarian, hydatid)

phantom pregnancy (what is this?)

shape of umbilicus may help with cause:

umbilicus buried in fat - patient eats too much

umbilicus is shallow (or everted) - ascites

unbilicus pushed upwards - 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),

congenital abdominal wall defect, chronically increased intra-abdominal

pressure)

o prominent veins

if present, elicit direction of venous flow - finger is used to occlude vein and

blood is emptied from vein below occluding finger with second finger; second finger

is removed and if vein refills, flow is occurring towards occluded finger

caput Medusae

see figure 5.11

veins surrounding umbilicus, with blood flow away

occurs in severe portal hypertension when portal to systemic flow

occurs through the umbilical veins; if these veins become distended and

engorged, caput Medusae is present

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sometimes only one or two veins are apparent

engorgement due to inferior vena caval obstruction

see figure 5.11

may be caused by:

tumour obstruction

thrombosis

tense ascites

mechanism - abdominal veins enlarge to provide collateral blood flow

from legs, avoiding the blocked inferior vena cava

direction of blood flow - away from legs prominent veins may be congenital

o puslations

expanding central pulsation suggests abdominal aortic aneurysm, but may be

normal in thin people

o visible peristalsis

occurs in very thin people occasionally, however, usually suggests intestinal

obstruction

pyloric obstruction (petic ulcer, tumour) shows visible peristalsis as a slow

wave passing across upper abdomen from left to right

distal small bowel obstruction - similar ladder pattern in central abdomen

o skin lesions

herpes zoster - radicular pattern, localised to one side, one nerve root; 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): - 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, purple striae)

o with eyes at level of abdomen, ask patient to take slow deep breath through mouth

and watch for evidence of asymmetrical movement, indicating presence of a mass (esp. large

liver seen to move below right costal margin, or large spleen seen to move below left costalmargin)

palpation

o general:

requires patient to relax abdominal muscles (i.e. reassure patient, use warm

hands)

examine any tender part last

9 descriptive regions of abdomen - see figure 5.12 (right hypochondrium,

epigastrium, left hypochondrium, right lumbar region, umbilical region, left lumbar

region, right iliac fossa, hypogastrium, left iliac fossa)

palpate lightl, noting presence of tenderness or lump

palpate deeply, noting any deep masses descriptive features of intra-abdominal masses

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11 site

11 tenderness

11 size and shape

11 surface (regular or irregular)

11 edge (regular or irregular)

11 consistency (hard or soft)

11 mobility and movement with inspiration

11 whether it is pulsatile

11 whether one can get above the mass

guarding = resistance to palpation due to contraction of abdominal muscles,may result from tenderness or anxiety, 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 - sudden stabbing pain

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Talley Sum Up