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Clinical Flashcards

1
Q

Clubbing

A

Loss of hyponychial angle

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2
Q

Schamroth’s sign

A

Disappearance of the diamond shaped space when nails of two similar fingers are held facing each other

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3
Q

Splinter haemorrhages

A 
Trauma
Infective endocarditis
Vasculitis (e.g. RA, PAN, APLS). 
Haematological malignancy
Profound anaemia
Sepsis
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4
Q

Osler’s nodes

A

Red, raised, tender, palpable nodules

Osler ouch

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5
Q

Janeway lesions

A

Non-tender erythematous maculopapular lesions containing bacteria

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6
Q

Tendon xanthomata

A

Yellow or orange deposits of lipid in the tendons that occur in type II hyperlipidaemia

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7
Q

Palmer and tuboeruptive xanthomata

A

Yellow or orange deposits of lipid are characteristic of type III hyperlipidaemia

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8
Q

Radiofemoral delay

A

Coarctation of the aorta

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9
Q

Radial-radial delay

A

Large arterial occlusion by atherosclerotic plaque or aneurysm
Subclavian artery stenosis
Dissection of the throacic aorta

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10
Q

Pulse of aortic regurgitation

A

Bounding pulse

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11
Q

Pulsus alternans

A

Alternating strong and weak pulse

Advanced LVF

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12
Q

Korotkoff sounds

A

K1: pressure at which the sound is first heard
K2: increase in intensity of sound
K3: sound decreases
K4: sound becomes muffled
K5: sound disappears
? K5 as best measure of diastolic pressure
K4 is more accurate in severe AR

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13
Q

Pulsus paradoxus

A

During inspiration the systolic and diastolic BP normally decrease, if this is exaggerated then is pulsus paradoxus
Abnormal if >10mmHg
Detect: lower cuff pressure slowly until K1 is audible intermittently (expiration), and then at every heart beat. Difference in the two measurements represents the level of the pulsus paradoxus.

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14
Q

Causes of pulsus paradoxus

A

Constrictive pericarditis
Pericardial effusion
Severe asthma

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15
Q

Postural hypotension

A

Fall in BP >15mmHg systolic or 10mmHg diastolic
May or may not be symptomatic
Most common cause is an a-adrenergic antagonist

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16
Q

Xanthelasmata

A

Intracutaneous deposits around the eye
May be a normal variant
May indicate type II or III hyperlipidaemia
Not always associated with hyperlipidaemia

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17
Q

Arcus senilis

A

Half or completegrey circle is seen around the pupil

Probably associated with increased cardiovascular risk

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18
Q

Causes of postural hypotension

A

Hypovolaemia
Addison’s
Neuropathy (DM, amyloidosis, Shy-Drager symdrome)
Drugs (vasodilators, TCAs, antihypertensives, diuretics, antipsychotics)
Idiopathic orthostatic hypotension (rare, progressive degenerative ANS disease seen in elderly men)

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19
Q

Mitral facies

A

Rosy cheeks with a bluish tinge due to dilation of the malar capillaries
Associated with pulmonary hypertension and a low cardiac output

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20
Q

Marfan’s syndrome

A

Congenital heart disease: aortic regurgitation secondary to aortic root dilatation
Mitral regurgitation secondary to mitral prolapse

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21
Q

Anacrotic pulse character

A

Small volume, slow uptake, notched wave on upstroke

Aortic stenosis

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22
Q

Plateau pulse character

A

Slow upstroke

Aortic stenosis

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23
Q

Bisferiens pulse character

A

Aortic stenosis and regurgitation

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24
Q

Collapsing pulse character

A 
Aortic regurgitation
Hyperdynamic circulation
Patent ductus arteriosus
Peripheral arteriovenous fistula
Arteriosclerosis aorta (particularly elderly pts).
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25
Small volume pulse character
Aortic stenosis | Pericardial effusion
26
Alternans pulse character
Alternating strong and weak beats | Left ventricular failure
27
JVP: a wave
Coincides with right atrial systole and S1 Precedes carotid pulsation Due to atrial contraction
28
JVP: v wave
Due to atrial filling | Period when the TV remains closed during ventricular systole
29
Kussmaul's sign
Rise in JVP on inspiration (opposite of what normally happens)
30
Abdominojugular reflex
Pressure exerted over the middle of the abdomen for 10 seconds will increase venous return to RA and thus JVP will transiently rise If RV failure or LA pressures are elevated (LVF) then it may remain elevated for duration of compression
31
Cannon a waves
Occur when right atrium contracts against a closed tricuspid valve Intermittent complete heart block Paroxysmal nodal tachycardia with retrograde atrial conduction
32
Giant a waves
Occur with each beat Occur when right atrial pressures are raised because of elevated pressures in the pulmonary circulation or obstruction to outflow (TS)
33
Causes of an elevated central venous pressure
``` RV failure TS or TR Pericardial effusion or constructive pericarditis SVC obstruction Fluid overload Hyperdynamic circulation ```
34
Causes of dominant a wave, JVP
TS (also causing a slow y descent) Pulmonary stenosis Pulmonary hypertension
35
Causes of a dominant v wave
TR Large v waves of TR should not be missed Reliable sign
36
Causes of an absent x descent
Atrial fibrillation
37
Causes of an exaggerated x descent
Acute tamponade | Constructive pericarditis
38
Causes of a sharp y descent
Severe TR | Constructive pericarditis
39
Causes of a slow y descent
TS | Right atrial myxoma
40
Causes of clubbing
``` Cyanotic congenital heart disease Infective endocarditis Lung cancer (usually not small cell) Chronic pulmonary suppuration (e.g. bronchiectasis, lung abscess, empyema) Idiopathic pulmonary fibrosis ``` Uncommon: cystic fibrosis, as estosis, pleural mesothelioma (benign), pleural fibroma, cirrhosis (esp. biliary cirrhosis), inflammatory bowel disease, coeliac disease, thyrotoxicosis Rare: Neurogenic diaphragmatic tumours, pregnancy, secondary parathryoidism
41
Causes unilateral clubbing
Bronchial AV aneurysm | Axillary artery aneurysm
42
Location of normal apex beat
Fifth left intercostal space | 1cm medial to the midclavicular line
43
Pressure loaded apex beat
Heaving, hyperdynamic or systolic overloaded apex Forceful sustained impulse Aortic stenosis or hypertension
44
Volume loaded apex beat
Thrusting apex beat Displaced, diffuse, non-sustained impulse Occurs in advanced MR or dilated cardimyopathy
45
Dyskinetic apex beat
Uncordinated impulse felt over a larger area than normal in the praecordium and is usually due to LV dysfunction (e.g. In anterior myocardial infarction)
46
Double impluse apex beat
Two distinct impulses felt with each systole | Characteristic of hypertrophic cardiomyopathy
47
Tapping apex beat
Felt when the first heart sound is palpable | Indicates mitral or tricuspid stenosis
48
Parasternal impluse
Felt with heel of hand is resting just to the left of the sternum with the fingers lifted slightly off chest If RV enlargement or severe LA enlargement then the RV is pushed anteriorly and the heel of the hand is pushed off the chest wall
49
Palpable P2
Palpation with fingers over pulmonary area may reveal the palpable tap of pulmonary valve closure in pulmonary hypertension
50
Thrills
Palpable murmurs | Presence of a thrill usually indicates an organic lesion
51
S1
Corresponds to closure of mitral and tricuspid valve closure Mitral valve closes before tricuspid Indicates beginning of systole
52
S2
Softer, shorter, higher pitched Marks end of systole Aortic and pulmonary valve closure The lower pressure in the pulmonary circulation, flow continues into the pulmonary artery after the end of systole and pulmonary valve closes later than aortic valve
53
Loud S1
When the MV or TV cusps remain open at the end of diastole and shut forcefully with the onset of ventricular systole MS: the narrow valve orifice limits ventricular filling so there is no diminution in flow towards then end of diastole Other causes are due to reduced diastolic filling time Tachycardia Short AV conduction time
54
Soft S1
Due to a prolonged diastolic filling time (e.g. first degree AV block) Delayed onset of LV systole (e.g. LBBB) Failure of the leaflets to coapt normally (e.g. MR)
55
Loud A2
Systemic hypertension (forceful valve closure secondary to high aortic pressures). Congenital aortic stenosis
56
Loud P2
``` Pulmonary hypertension (forceful valve closure due) Palpable P2 correlates better with raised pulmonary pressure ```
57
Soft A2
Aortic valve calcification and reduced motion if valve leaflets AR when leaflets do not coast
58
Splitting S1
Usually not detectable | Complete RBBB
59
Fixed splitting S2
No respiratory variation | ASD
60
Reversed splitting
P2 occurs first and splitting occurs in expiration LBBB (delayedLV depolarisation) Severe AS, coarctation of the aorta (delayed LV emptying) Large PDA (increased LV volume load n.b. this is a large machinery murmur, so S2 is not usually heard).
61
Pathological S3
Due to reduced ventricular compliance | Strongly associated with increased atrial and ventricular end diastolic pressure
62
Left ventricular S3
Louder at the apex Louder on expiration Can be physiological (due to very rapid diastolic filling) Associated with increased cardiac output (e.g. thyrotoxicosis, pregnancy) Sign of LVF and dilatation Also AR, MR, VSD and PDA
63
Right ventricular S3
Louder at the LSE Louder with inspiration Occurs in RV failure or constructive pericarditis
64
S4
Late diastolic sound Pitched slightly similar to "Tennessee" Due to high pressure atrial wave reflected back from a poorly compliant ventricle n.b. Lost when atrial fibrillation, because sound depends on effective atrial contraction Low pitched. Disappears if the bell of the stethoscope is pressed firmly to the chest.
65
Right ventricular S4
RV compliance is reduced (e.g. pulmonary hypertension, pulmonary stenosis)
66
Left ventricular S4
LV compliance is reduced (e.g. AS, acute MR, systemic hypertension, IHD, advanced age)
67
Summation gallop
S3 and S4 are superimposed Occurs when heart rate is >120 does not imply ventricular stress unless extra sounds persist when the HR slows or is slowed by carotid sinus massage
68
Quadruple rhythm
Occurs when both S3 and S4 are audible | Implies severe ventricular dysfunction
69
Opening snap
High pitched sound that occurs in MS at a variable distance after S2 Due to the sudden opening of the mitral valve and is followed by the diastolic murmur of MS
70
Systolic ejection click
High pitched sound over aortic or pulmonary area and LSE May occur in congenital pulmonary or aortic stenosis Followed by systolic ejection murmur of aortic or pulmonary stenosis
71
Tumour plop
RARE Associated with atrial myxoma during atrial systole a loosely pedunculated tumour may be propelled into the mitral or tricuspid valve orifice causing an early diastolic plopping sound
72
Diastolic pericardial knock
Sudden cessation of ventricular filling because of constrictive pericardial disease
73
Characteristics of a murmur
Timing Area of greatest intensity Loudness and pitch Effect of dynamic manoeuvers (e.g. respiration, Valsalva)
74
Causes of pansystolic murmur
MR, TR, VSD
75
Causes of mid-systolic ejection murmur
Crescendo-decrescendo murmur | AS, PS
76
Causes of a late systolic murmur
Mitral valve prolapse | Papillary muscle dysfunction where MR beings in midsystole
77
Early diastolic murmur
AR or PR | Murmur is loudest at the beginning when aortic and pulmonary pressures are highest
78
Mid-diastolic murmur
MS, TS Due to impaired flow during ventricular filling when valve is narrowed Also atrial myxoma (tumour mass obstructs valve orifice)
79
Continuous murmurs
Extend throughout diastole and systole PDA AV fistula (coronary artery, pulmonary, systemic) Aortopulmonary connection (congenital, Blalock shunt) Venous hum Rupture of the sinus of Valsalva into the right ventricle or atrium (Mammary soufflé: late pregnancy or early postpartum period)
80
Pericardial friction rub
Due to movement of inflamed pericardial surfaces Pericarditis Louder when sitting forward and on inspiration
81
Mediastinal crunch (Hamman's sign)
Crunching sound heard in time with the heart beat, but with systolic and diastolic components Due to presence of air in mediastinum
82
Levine's grading system (murmur)
1/6: very soft and not heard at first 2/6: soft, but detected by experienced auscultator 3/6 Moderate, there is no thrill 4/6: Loud, thrill just palpable 5/6: Very loud with a thrill easily palpable 6/6: very, very loud (heard without using stethoscope)
83
Respiration manoeuvers for murmurs
Murmurs that arise on R side of the heart become louder during inspiration (increased venous return, blood flow to the R side) L sided murmurs are unchanged or become softer Expiration has the opposite effect
84
Deep expiration (murmurs)
AR, pericardial friction rub Have pt. sit up, lean forward and exhale (brings the base of the heart closer to the chest wall)
85
Valsalva manoeuver (murmurs)
LSE: during systole can augment murmur or HCM (becomes louder) Apex: systolic click of mitral prolapse is heard earlier
86
Standing to squatting manoeuver (murmurs)
Pt. squats rapidly, increase in venous return and systemic arterial resistance Augments most murmurs Reduces the intensive to the systolic murmur of HCM and delays the midsystolic click and murmur or mitral prolapse Opposite occurs on standing quickly
87
Isometric exercise (murmurs)
Sustained hand grip or repeated sit-ups (20-30sec) increases systemic arterial resistance, BP and heart size AS murmur becomes softer Most other murmurs are louder HCM murmur is softer Mitral valve prolapse i9s delayed because of an increase in ventricular volume
88
DDx: carotid artery bruit
Carotid artery stenosis AS murmur radiating to the carotids Thyrotoxicosis may result in a systolic bruit due to increased vascularity of the gland If carotid artery stenosis listen in steps back to base of heart, if disappears then carotid stenosis, if continues the AS radiating

RACP Clinical (1 decks)

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