Professional Documents
Culture Documents
POSITION: patient lying in bed with enough pillows to support him at 45 degrees
GENERAL APPEARANCE
• general state of health? apparently ill?
• rapid and laboured respiration?
• cachectic (severe loss of weight and muscle wasting)? (commonly caused by malignant disease or
severe cardiac failure [cardiac cachexia])
• Marfan's syndrome (tall stature, thoracic kyphosis, high arched palate, pectus excavatum, long
limbs, arachnodactyly (spider fingers))? Marfan's syndrome is associated with aortic regurgitation
• Down's syndrome? associated with congenital heart disease, especially endocardial cushion
defects
• Turner's syndrome? associated with coarctation of the aorta
ARTERIAL PULSE
• following observations should be made for radial pulse:
• rate of pulse
• rhythm
• presence or absence of delay of femoral pulse compared with radial pulse (radiofemoral
delay)
• character and volume are better assessed from palpation of brachial or carotid arteries
• rate of pulse
• bradycardia = pulse < 60 beats/min
• causes of bradycardia:
• regular rhythm
• physiological (athletes, sleep: due to increased vagal tone)
• drugs (e.g. beta blockers, digoxin, amiodarone)
• hypothyroidism (decreased sympathetic activity secondary to lack of
TH)
• hypothermia
• jaundice (in severe cases only, due to deposition of bilirubin in
conducting system)
• raised intracranial pressure (due to effect on central sympathetic
outflow) - a late sign
• third degree AV block or second degree AV block (type 2)
• MI
• paroxysmal (def: sudden onset, usually with recurrent
manifestations) bradycardia:
• vasovagal syncope
• acute hypoxia or hypercapnia
• acute hypertension
• regularly irregular rhythm
• sinus arrhythmia (normal slowing of pulse with expiration)
• second degree AV block (type I)
• irregularly irregular rhythm
• atrial fibrillation, with AV nodal disease or drugs
• frequent extrasystoles
• apparent
• pulse deficit (there is a difference between the heart rate counted
over the praecodrium and that observed at the periphery; in beats
where diastole is too short for adequate filling of the heart, too small
a volume of blood is ejected during systole for a pulse to be
appreciated at the wrist)
• atrial fibrillation
• ventricular bigeminy (paired ventricular beats)
• tachycardia = pulse > 100 beats/min
• causes of tachycardia:
• regular rhythm:
• hyperdynamic circulation due to:
• exercise or emotion
• fever (allow 20 beats/min per degree Celsius above normal)
• pregnancy
• thyrotoxicosis
• anaemia
• arteriovenous fistula
• beri beri (thiamine deficiency)
• congestive cardiac failure
• constrictive pericarditis
• drugs (e.g. salbutamol and other sympathomimetics, atropine)
• normal variant
• denervated heart of diabetes has a resting rate of 106-120 beats/min
• hypovolaemic shock
• supraventricular tachycardia
• atrial flutter with regular 2:1 AV block
• ventricular tachycardia
• irregular rhythm
• atrial fibrillation due to:
• myocardial ischaemia
• mitral valve disease or any cause of left atrial enlargement
• thyrotoxicosis
• hypertensive heart disease
• sick sinus syndrome (chaotic or absent atrial activity, often
with bradycardia alternating with tachycardia, recurring
ectopic beats, including escape beats, and runs of
supraventricular and ventricular arrhythmias)
• pulmonary embolism
• myocarditis
• fever, acute hypoxia, or hypercapnia (paroxysmal)
• other: alcohol, post-thoracotomy, idiopathic
• multifocal atrial tachycardia
• atrial flutter with variable block
• rhythm:
• rhythm can be regular or irregular
• irregular rhythm can be completely irregular with no pattern
• usually due to atrial fibrillation
• coordinated atrial contraction lost and chaotic electrical activity occurs with
bombardment of AV node with impulses at a rate of over 600 per minute -
only some are conducted to ventricles since the rate is too high
• hence ventricles beat irregularly, at a rate of about 150 minute
• the pulse also varies in amplitude from beat to beat because of differing
diastolic filling
• this type of pulse also can occur by frequent irregularly occurring ectopic beats
(supraventricular or ventricular)
• irregular rhythm can be regular:
• sinus arrhythmia:
• in sinus arrhythmia, pulse rate increases with each inspiration and decreases
with each expiration
• is associated with changes in venous return to heart
• Wenckebach phenomenon
• AV nodal conduction time increases progressively until non-conducted atrial
systole occurs
• following this, the AV conduction time shortens and cycle begins again
• radiofemoral delay:
• while palpating radial pulse, one places fingers of other hand over radial femoral pulse
(below inguinal ligament, one third of way up from pubic tubercle)
• a noticeable delay in arrival of femoral pulse suggests diagnosis of coarctation of aorta
(congenital narrowing in aortic isthmus occurs at level where ductus arteriosus joins
descending aorta) - note that this lesion can also cause upper limb hypertension
• it is also useful to palpate both radial pulses together to detect radial-radial inequality in
timing or volume (e.g. due to large arterial occlusion)
• character and volume
• use carotid or brachial to determine character and volume
• however, do use the radial pulse to test for:
• the collapsing (bounding) pulse of aortic regurgitations
• pulsus alternans of left ventricular failure
BLOOD PRESSURE
• systolic blood pressure = peak pressure that occurs in artery following ventricular systole
• diastolic blood pressure = level to which arterial pressure falls during ventricular diastole
• normal blood pressure < 140/90
• brachial artery is found in antecubital fossa, one third of the way over from the medial epicondyle
• first get an approximate estimation of systolic blood pressure
• cuff is inflated and then deflated slowly until radial pulse returns
• then get more accurate estimation of blood pressure:
• cuff is inflated and then deflated slowly whilst listening to brachial artery with
stethescope's diaphragm
• 5 different sounds will be heard as the cuff is slowly released: (Korotkoff sounds)
1. pressure at which sound is first heard over artery is systolic blood pressure (a sharp
thud) - only the systolic blood pressure is high enough to overcome the cuff's
pressure
2. as deflation continues, sound increases in intensity (a blowing or swishing sound)
3. as deflation continues, sound decreases in intensity (a softer thud than phase 1)
4. sound becomes muffled (softer blowing sound that disappears) (is the 1st diastolic)
5. sound disappears (is 2nd diastolic) because flow is now constant since even the
diastolic pressure is enough to overcome the cuff's pressure
• the 2nd diastolic (5th sound [K5]) is the best measure for diastolic blood pressure, although
it is a slight underestimate
• however, in severe aortic regurgitation, the 1st diastolic (K4) is a better indication of
diastolic pressure
• occasionally, there is an auscultatory gap (the sounds disappear just below the systolic
pressure and reappear before diastolic pressure) in healthy people
• the systolic pressure may normally vary by up to 10 mmHg; the pressure is higher in the
legs
• pulsus paradoxus:
1. during inspiration, systolic and diastolic pressure normally increased because
intrathoracic pressure is reduced, and blood pools in the pulmonary vessels, hence
left heart filling is reduced; if the reduction in blood pressure is exaggerated over
the normal, the term pulsus paradoxus is applied (pulsus paradoxus is a fall in
arterial pulse pressure on inspiration of more than 10 mg)
2. causes:
• constrictive pericarditis
• pericardial effusion
• severe asthma
• postural blood pressure
• postural blood pressure should routinely be taken with patient lying and standing
• a fall of more than 15 in systolic or 10 in diastolic is abnormal and called postural
hypotension
• causes include
1. hypovolaemia (e.g. dehydration, bleeding)
2. drugs (e.g. vasodilators)
3. Addison's disease (low cortisol and aldosterone)
4. hypopituirism
5. autonomic neuropathy (e.g. diabetes mellitus, amyloidosis)
6. idiopathic orthostatic hypotension (rare progressive degeneration of ANS, usually
in old men)
FACE
• eyes
• inspect sclerae for jaundice
• can occur with hepatic congestion in severe congestive cardiac failure
• can occur with prosthetic heart valves, which may induce haemolysis due to
excessive turbulence
• xanthelasma - see Figure 3.8
• def: intracutaneous yellow cholesterol deposits around eyes
• may be normal variant or indicate hyperlipidaemia
• cheeks
• mitral facies (rosy cheeks with a bluish tinge)
• due to dilatation of malar capillaries
• associated with pulmonary hypertension and low cardiac output such as
occurs in severe mitral stenosis
• mouth
• arched palate? occurs in Marfan's syndrome, which is associated with congenital
heart disease, including aortic regurgitation secondary to aortic root dilatation, and
also mitral regurgitation due to mitral valve prolapse
• teeth - do they look diseased? they can be a source of organisms responsible for
infective endocarditis
• tongue and lips - central cyanosis?
• inspect mucosa for petechiae - may indicate infective endocarditis
NECK
Carotid arteries
• location: medial to sternomastoid muscle
• carotid pulse gives information about left ventricle and aorta
• never palpate both carotid arteries at once!
• anacrotic pulse
• small volume, slow uptake, notched wave on upstroke
• causes: aortic stenosis
• plateau pulse
• slow upstroke
• causes: aortic stenosis
• bisferiens pulse
• anacrotic and collapsing
• causes: aortic stenosis and regurgitation
• collapsing pulse
• causes:
• aortic regurgitation
• hyperdynamic circulation
• patent ductus arteriosus
• peripheral arteriovenous fistula
• arteriosclerotic aorta (elderly patients in particular)
• small volume pulse
• causes
• aortic stenosis
• pericardial effusion
• pulsus alternans
• alternating strong and weak beats
• causes: left ventricular failure
• jerky
• causes: hypertrophic cardiomyopathy
PRAECORDIUM
Inspection
• scars? pace-maker box?
• skeletal abnormalities? pectus excavatum (funnel chest)? kyphoscoliosis? note that skeletal
abnormalities can cause distortion of position of heart and great vessels
• visible pulsations:
• apex beat may be seen (normal position is in 5th intercostal space, 1cm medial to
midclavicular line) - see Talley Figure 3.12
• pulmonary artery pulsations may be visible in severe pulmonary hypertension
Palpation
• palpate apex beat
• position of apex beat:
• count down number of interspaces; first palpable interspace is the 2nd, lying just
below manubriosternal angle
• located at: 5th intercostal space, 1cm medial to midclavicular line
• normal apex beat is is felt over an area size of 20 cm piece
• an enlarged heart gives a displaced apex beat laterally or inferiorly, or both; note
that a chest wall deformity or pleural or pulmonary disease can also displace the
apex beat
• character of apex beat: abnormal beats include:
• pressure loaded (hyperdynamic or systolic overloaded) apex beat:
• def: is a forceful and sustained impulse
• causes: aortic stenosis or hypertension
• volume loaded (hyperkinetic or diastolic overloaded) apex beat:
• def: is an uncoordinated impulse felt over a larger than normal area
• causes: left ventricular dysfunction (e.g. anterior MI)
• double impulse apex beat
• def: 2 distinct impulses are felt with each systole
• causes: hypertrophic cardiomyopathy
• tapping apex beat
• def: first heart sound is actually palpable (normal heart sounds
• causes: mitral stenosis, or rarely tricuspid stenosis
• non-palpable apex beat: note that this can be normal
• causes: thick chest wall (normal), emphysema, pericardial effusion, shock
(or death), and rarely dextrocardia (inversion of heart and great vessels; in
this the apex beat will be palpable to right of sternum)
• other praecordial impulses:
• may occur in various heart diseases
• right ventricular enlargement:
• parasternal impulse may be felt when heel of hand is rested just to left of sternum,
with fingers lifted slightly off chest
• in right ventricular enlargement, or severe left atrial enlargement (where the right
ventricle is pushed anteriorly), the heel of hand is lifted off the chest wall with each
systole
• in pulmonary hypertension:
• palpation over pulmonary area (2nd intercostal space, just left of sternum) may
reveal palpable tap of pulmonary valve closure
• thrills
• turbulent blood flow, which causes cardiac murmurs on auscultation, may
sometimes be palpable
• feel for thrills with flat hand, over: apex, left sternal edge, base of heart
• apical thrills (mitral): may be felt more easily with patient rolled over left side (left
lateral position) which brings apex closer to chest wall
• thrills over base of heart (pulmonary and aortic): are best felt with patient sitting
up leaning forward in full expiration (base of heart is moved closer to chest wall)
• systolic thrill = a thrill that coincides with apex beat
• diastolic thrill = a thrill that does not coincide with apex beat
Percussion: don't bother doing this; all it does it define the cardiac outline
Auscultation
Areas of auscultation - see Talley Figure 3.15 (page 51)
1. mitral area - midclavicular line, 4th intercostal space
2. tricuspid area - 1 cm right of sternum, 5th intercostal space
3. pulmonary area - 1 cm right of sternum, 2nd intercostal space
4. aortic area - 1 cm left of sternum, 2nd intercostal space
Process of auscultation
1. auscultate mitral area with the bell and diaphragm
• bell is efficient in amplifying low pitched sounds (it must be lightly applied to chest), for
example
• diastolic murmur of mitral stenosis
• a third heart sound
• diaphragm is good for reproducing higher pitched sounds, for example
• systolic murmur of mitral regurgitation
• a fourth heart sound
2. auscultate tricuspid area
3. auscultate pulmonary area
4. auscultate aortic area
Normal heart sounds - heart normally produces 2 sounds each cycle, related to closure of valves and rapid
changes in blood flow
• first heart sound (S1)
• has 2 components - mitral and tricuspid valve closure
• mitral closure occurs ever so slightly before tricuspid, but only one sound is audible
• first heart sound indicates beginning of ventricular systole
• second heart sound (2)
• is made up of aortic and pulmonary valve closure
• because of lower pressure in pulmonary circulation compared with aorta, the pulmonary
valve usually closes slightly after closure of aortic valve (if you listen carefully, you may
notice splitting); also note that pulmonary valve closure is further delayed with inspiration
because of increased venous return to right ventricle
• marks the end of systole, and the beginning of diastole
• note that diastole is usually longer than systole
• sometimes it can be difficult to tell which heart sound is which; on these occasions, palpation of
the carotid pulsation will indicate the timing of systole
• it is clearly crucial to define systole and diastole so that timing of murmurs can be worked out
Abnormal heart sounds
• alterations in intensity
• loud S1
• physiology: occurs when mitral or tricuspid valve cusps remain widely open at the
end of diastole and shut forceful with the onset of ventricular systole
• causes:
• reduced filling volume in mitral or tricuspid stenosis because the narrowed
valve orifice limits ventricular filling, so that there is no diminution in flow
towards the end of diastole; the normal mitral cusps drift back towards the
closed position at the end of diastole as ventricular filling slows down
• reduced diastolic filling time (any cause of a short AV conduction time)
• soft S1
• causes:
• prolonged diastolic filling time (occurs in 1st degree heart block)
• delayed onset of left ventricular systole (left bundle brunch block)
• failures of leaflets to coapt normally (mitral regurgitation)
• loud aortic component of second heart sound (loud A2)
• causes:
• systemic hypertension because this results in forceful aortic valve closure
secondary to high pressure
• congenital aortic stenosis because valve is mobile but narrowed, and closely
suddenly at end of systole
• loud pulmonary component of second heart sound (loud P2)
• causes:
• pulmonary hypertension
• soft A2
• causes:
• aortic valve calcification because leaflet movement is reduced
• aortic regurgitation because leaflets cannot coapt
• splitting
• splitting of S1 is usually not clinically detectable, but may be noticed in complete right
bundle branch block
• increased normal splitting of S2 occurs when there is any delay in right ventricular
emptying, and is caused by:
• inspiration
• right bundle branch block (delayed right ventricular depolarisation)
• pulmonary stenosis (delayed right ventricular ejection)
• ventricular septal defect (increased right ventricular volume load)
• mitral regurgitation (because of earlier aortic valve closure due to more rapid left
ventricular emptying)
• fixed splitting (no respiratory variation)
• atrial septal defect equalises volume loads between two atria --> atria acting as a
common chamber
• reverse splitting (P2 occurs first, and splitting occurs on expiration) is caused by:
• left bundle branch block (delayed left ventricular depolarisation)
• delayed left ventricular emptying (severe aortic stenosis, coarctation of the aorta)
• increased left ventricular volume load (large patent ductus arteriosus)
• extra heart sounds
• third heart sound (S3)
• timing: is a low pitched mid-diastolic sound
• pathophysiology: tautening of mitral or tricuspid papillary muscles at end of rapid
diastolic filling
• causes:
• left ventricular S3 (will be louder on expiration, and heard most clearly over
apex)
• physiological left ventricular S3 occurs in people under 40 due to
rapid diastolic filling
• left ventricular failure
• aortic regurgitation
• mitral regurgitation
• ventricular septal defect
• patent ductus arteriosus
• right ventricular S3 (will be louder on inspiration and heart most clearly at
left sternal edge):
• right ventricular failure
• constrictive pericarditis
• fourth heart sound (S4)
• timing: late diastolic sound
• pathophysiology: high pressure atrial wave reflected back from a poorly compliant
ventricle
• causes:
• left ventricular S4 (often presents during episode of angina or MI)
• reduced left ventricular compliance
• aortic stenosis
• acute mitral regurgitation
• systemic hypertension
• ischaemic heart diseased
• advanced age
• right ventricular S4
• reduced right ventricular compliance
• pulmonary hypertension
• pulmonary stenosis
• summation gallop
• if there heart rate is >120m S3 and S4 may be superimposed resulting in a
summation gallop
• this does not necessarily imply ventricular stress unless one/or both the heart
sounds persist when the heart rate slows; when both S3 and S4 are present
(quadruple rhythm), severe ventricular dysfunction is implied
• additional sounds
• opening snap
• timing: high pitched sound at a variable distance after S2
• cause: mitral stenosis or tricuspid stenosis
• pathophysiology: sudden opening of mitral valve is followed by diastolic murmur
of mitral stenosis
• systolic ejection click
• timing: early systolic high pitched sound over aortic or pulmonary or left sternal
edge area
• cause: congenital aortic or pulmonary stenosis
• non-ejection systolic click
• timing: high pitched sound heard during systole, best over mitral area; may be
followed by systolic murmur
• cause: prolapse of one or more redundant mitral valve leaflets during systole; atrial
septal defects
• tumour plop
• cause: during atrial systole, pedunculated atrial myxoma may be propelled into
mitral or tricuspid valve orifice causing a diastolic plopping sound
• diastolic pericardial knock
• cause: constrictive pericardial disease --> sudden cessation of ventricular filling
• prosthetic heart valve sounds
• pacemaker sounds: a click due to contraction of chest wall muscle
LOWER LIMBS
• palpate femoral arteries
• auscultate femoral arteries (a bruit may be heard if narrowed)
• palpate popliteal (behind knee)
• palpate posterior tibial (under medial malleolus)
• palpate dorsalis pedis (forefoot)
• palpate distal shaft of tibia for oedema by compressing area for 15 seconds - if oedema, is it pitting
or non-pitting
• causes of pitting lower limb oedema
• cardiac: congestive cardiac failure, constrictive pericarditis
• drugs: calcium antagonists
• hepatic: cirrhosis causing hypoalbuminaemia
• renal: nephrotic syndrome causing hypoalbuminaemia
• gastrointestinal tract: malabsorption, starvation, protein losing enteropathy causing
hypoalbuminaemia
• wet beri beri (dietary deficiency of thiamin (vitamin B1) resulting in heart failure
leading to oedema; dry beri beri is dietary deficiency of thiamine resulting in
painful polyneuritis without the oedema of wet)
• cyclical oedema
• causes of unilateral lower limb pitting oedema
• deep venous thrombosis
• compression of large vein by tumour of lymph node
• causes of non-pitting lower limb oedema
• hypothyroidism
• lymphoedema
• infection
• malignant (tumour invasion of lymphatics)
• congenital (lymphatic development arrest)
• allergy
• Milroy's disease (unexplained lymphoedema which appears at puberty and
is more common in females)
• note that in long standing oedema, secondary changes in lymphatics may occur that
minimise the oedema
• Achilles tendon xanthomata (see Figure 3.22)? (is due to hyperlipidaemia)
• cyanosis and clubbing of toes? (may occur without finger clubbing in patent ductus arteriosus)
• peripheral vascular disease:
• note that reduced or absent pulses, femoral systolic bruit, marked leg pallor, absence of
hair, cool skin and reduced capillary return (compress toe nails - return of normal red
colour is slow) are signs of peripheral vascular disease
• in these cases, perform Buerger's test - elevate leg to 45 degrees (pallor is rapid if there is a
poor arterial supply) and then place them dependent at 90 degrees over edge of bed
(cyanosis occurs if the arterial supply is impaired)
• deep venous thrombosis:
• difficult to diagnose
• presenting symptom: may be calf pain
• on examination: (positives to the following are suggestive of DVT)
• swelling of calf and leg?
• dilated superficial veins?
• increased warmth?
• squeeze calf gently to determine if area is tender
• causes of thrombosis
• changes in vessel wall (trauma) - common
• changes in blood flow (cardiac failure or prolonged immobilisation) - common
• changes in constitution of blood (occult neoplasm, disseminated intravascular
coagulation, contraceptive pill, pregnancy) - uncommon
• acute arterial occlusion
• causes include:
• embolism - usually arise from thrombus in heart, often secondary to:
• myocardial infarction or dilated cardiomyopathy
• atrial fibrillation
• infective endocarditis
• thrombosis
• injury
• symptoms: 4 P's of acute arterial occlusion of major peripheral limb artery
• painful limb
• pale limb
• pulseless limb
• 'paralysed' limb
• varicose veins
• examination:
• position: if patient complains of varicose veins, ask him to stand with legs fully
exposed
• inspect:
• inspect front of whole leg for tortuous, dilated branches of long saphenous
vein (medial leg)
• inspect back of calf for varicosities of short saphenous vein lateral and
posterior leg)
• inspect to see if leg is inflamed, swollen or pigmented (signs of venous
stasis)
• ulcers (chronic venous stasis is a cause of ulceration of lower leg)
• palpate veins:
• hard veins suggests thrombosis and tenderness suggests thrombophlebitis
• perform cough impulse test (put finger over long saphenous vein opening in
groin, medial to femoral vein); ask patient to cough: a fluid thrill is felt if the
saphenofemoral valve is incompetent
• Trendelenburg test
• patient lying down, leg elevated
• pressure on saphenous opening in groin
• patient stands
• if veins stay empty until groin pressure is released - incompetence of
saphenofemoral valve
• if veins fill despite groin pressure, incompetent valves are in thigh or calf,
and Perthes' test is performed
• Perthes' test
• repeat Trendelenburg's test, but when patient stands, allow some
blood to be released and get him to stand up and down on the toes a
few times
• veins will become less tense if the perforating calf veins are patent
and have competent valves (the muscle pump is functioning)
• note unusual pattern, example: if pubic varices, must try to exclude secondary
varicose veins, e.g. due to intrapelvic neoplasm which has obstructed deep venous
return
• causes of leg ulcers
• venous stasis ulcer
• most common
• site: around malleoli
• associated pigmentation, stasis eczema
• ischeamic ulcer
• large artery disease (atherosclerosis, thromboangitis obliterans): usually lateral side
of leg (pulse absent)
• small vessel disease
• malignant ulcer - examples
• basal cell carcinoma (pearly translucent edge)
• squamous cell carcinoma (hard everted edge)
• melanoma
• lymphoma
• infection - examples
• Staphylococcus aureus
• syphilitic gumma
• tuberculosis
• atypical Mycobacterium
• fungal
• neuropathic
• painless penetrating ulcer on sole of foot: peripheral neurophathy, e.g. diabetes
mellitus, leprosy
• underlying systemic disease
• diabetes mellitus: vascular disease, neuropathy
• pyoderma gangrenosum
• rheumatoid arthritis
• lymphoma
• haemolytic anaemia (small ulcers over malleoli)