Cardiology Short Cases Flashcards

1
Q

Interpret the following physical findings:

Collapsing pulse
Wide pulse pressure
Displaced apex
Early diastolic murmur, high-pitch, blowing quality best heard at tricuspid area
+/- mid-diastolic, low-pitch rumbling murmur
Systolic flow murmur in aortic area
Thursting apex

Dx and ddx?
What maneuver next?

A

Aortic regurgitation

Ddx:

  • Pulmonary regurgitation: no displaced apex, no collapsing pulse, not high-pitch murmur
  • Mitral stenosis: has opening snap in diastole, loud S1, radiated to axilla from apex, tapping and non-displaced apex

Sit up and lean forward for murmur, best heard at tricuspid area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Causes of Aortic regurgitation?

A

Cusp disease:

  • Rheumatic heart disease
  • Infective endocarditis
  • Congenital bicuspid aortic valve
  • Degenerative
  • Aortic dissection/ trauma

Causes of dilated aortic root/ aortic aneurysm:

  • Marfan syndrome,
  • syphilic aortitis,
  • Seronegative arthritis: ankylosing spondylitis, psoriatic arthropathy…etc
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Additional peripheral signs related to Aortic regurgitation?

A

→ Duroziez sign: to-and-fro murmur over femoral arteries heard
when apply pressure with stethoscope
→ Quincke’s pulse: capillary pulsation in finger tips or mucous
membranes
→ Traube’s sign: ‘pistol-shot’ systolic and diastolic sounds over
large arteries
→ De Musset’s sign: head bobbing with each heartbeat
(↑SV → transfer of momentum to head/neck)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Investigations for Aortic Regurgitation?

A

Investigations:
□ Blood: VDRL, blood culture (IE)
□ ECG: initially normal, later LVH + T wave inversion
□ CXR: dilated aortic arch, cardiomegaly
□ Echo: LV size and function, aortic size and Doppler for severity of regurgitant jet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Interpret the following physical findings:

Small volume and slow rising pulse 
Sustained and heaving apex 
Systolic thrill in aortic area 
Deceased/ soft S2 +/- S4
Ejection systolic murmur radiating to both sides of the neck, harsh 

Dx/ ddx?

Why does the murmur sometimes radiate to the apex?

A

Aortic stenosis

D/dx:
- Aortic sclerosis: normal volume pulse,
normal/wide pulse pressure, intact S2 and no LVH
- HOCM: jerky pulse, normal S2, ↑murmur on standing
- MR: pansystolic murmur best heard at apex with radiation to axilla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Causes of aortic stenosis

Why does the murmur sometimes radiate to the apex?

A

Degenerative calcification
Rheumatic heart disease
Congenital bicuspid aortic valve

AS murmur radiating to apex may be more musical (high frequency vibration) and louder, known as Gallarvardin phenomenon.
It is easily confused with MR. However, in MR the S1 should be soft

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Investigations for Aortic Stenosis?

A

□ ECG: LVH with ‘strain’ pattern
→ Strain pattern: downsloping ST depression + T wave
inversion in lateral leads

□ CXR: usually normal except in LV failure stage

□ Echo:
→ Restricted valve opening with concentric LVH
→ Mean valvular pressure gradient: ≥40mmHg = severe
→ Aortic valve area (AVA): ≤1cm = severe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Interpret the following physical findings:

JVP elevated 
Parasternal heave 
Fixed wide splitting of S2 
Loud S2 
Ejection systolic murmur at pulmonic area 
Mid-diastolic murmur at tricuspid area 

Dx/Ddx?

Cause of the murmurs?

A

Atrial septal defect

D/dx:
Pulmonary stenosis: Soft S2 (very rare as isolated disease, usually part of Tetralogy of Fallot)
Pulmonary hypertension: Loud S2 without splitting/ Single S2

ESM at LUSB due to ↑PV flow
MDM at LLSB due to ↑TV flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Causes of ASD?

Syndromes associated?

A

Failure to close foramen secundum → secundum ASD
Failure to close foramen primum → primum ASD

Down syndrome: Secundum ASD
Noonan syndrome
DiGeorge syndrome
Eisenmenger syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Investigation for ASD?

A

Ix: can be normal in small ASD

□ CXR: cardiomegaly, RA/RV dilation, enlarged pA, pulm plethora

□ ECG: R axis deviation, RA/V dilation
→ Incomplete RBBB (in V1) due to RV dilation
→ L axis deviation + 1st degree HB in primum defect

□ Transesophageal Echo: diagnostic, evaluate size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Interpret the following physical findings:

Stunted growth 
Central cyanosis 
Digital clubbing 
Large A wave in JVP 
Left parasternal heave 
Loud S2 
Early diastolic murmur in pulmonary area 
Pansystolic murmur in lower left sternal border 

Causes?

A

Eisenmneger Syndrome

Triad of (1) congenital L-to-R shunt (2) pulmonary arterial disease (3) cyanosis

Causes of Eisenmenger syndrome and their signs:
VSD: single/closely split S2 (equalization of pressure)

ASD: fixed widely split S2

PDA: normally split S2, differential cyanosis and clubbing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Interpret the following physical findings:

Irregularly irregular pulse 
Lack of a wave in JVP 
S1 variable loudness 
ECG: 
□ No distinct P wave ± irregular baseline
(fibrillation waves83)
□ Narrow but irregular QRS complexes

Dx/Ddx?

A

Atrial fibrillation

Ddx:
Atrial flutter with variable block
Atrial tachycardia with variable block
Frequent multifocal ectopic beats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Causes of A-fib?

A

Mitral valve disease**

Ischemic heart disease
Thyroid heart disease
Alcohol
Hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Interpret:

  • Displaced Apex
  • Systolic thrill
  • Left parasternal heave
  • Soft/ absent first heart sound + Pansystolic murmur at apex, radiation to axilla + Obscured S2
    +/- ankle or sacral edema
  • Sinus rhythm, regular pulse

D/dx?
Causes?

A

Mitral regurgitation

D/dx: 
- VSD: murmur best heard at
parasternal border and radiate
to Rt sternum
- TR: giant V wave in JVP,
systolic murmur at Lt sternal
border and pulsatile liver,
accentuated by inspiration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Causes of Mitral regurgitation?

A

Causes:
Valvular leaflet diseases
→ Rheumatic: commonest, 50% a/w MS
→ Mitral valve prolapse due to myxomatous
degeneration of valvular leaflet
→ Infective endocarditis
→ HOCM with systolic anterior movement of mitral leaflet

□ Annulus dilatation due to LV dilatation (CAD, DCMP)

□ Ruptured chordae tendineae:
→ Degenerative or collagen disease
→ Infective, eg. IE
→ Acute rheumatic heart disease

□ Papillary muscle dysfunction: ischaemia or MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Interpret:

Sacral or ankle edema 
Parasternal heave 
Tapping apex, not displaced 
Loud S1, +/- opening snap
Mid-diastolic, rumbling/ low-pitch murmur at apex
Redness of cheeks

Next maneuver for murmur?

D/dx?

A

Mitral Stenosis

Left lateral position to accentuate murmur

D/dx:
- Austin-Flint murmur of AR:
S1 soft, no Opening Snap, AR murmur
- Lt atrial myxoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Causes of Mitral Stenosis?

Early vs late clinical outcomes?

A

Rheumatic heart disease (95%): less common nowadays

Others: congenital (infants), mitral annular calcification (elderly), radiation-associated (classically in
Hodgkin disease survivors), carcinoid valve disease, SLE/RA, mucopolysaccharidoses

Early: insidious onset of SOB
Late:
→ SOB at rest + orthopnoea + PND
→ Right heart failure with systemic oedema
→ Gross LAE: compression of RLN (hoarseness) and oesophagus
(dysphagia, also known as Ortner syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Interpret:

Mid to late systolic click + murmur
Best heard at apex

Next maneuvers to accentuate murmur?

D/dx?

A

Mitral valve prolapse

Sudden standing = earlier MVP click in systole

Sudden squatting = delayed MVP click in systole

D/dx:

  • Other causes of MR, eg. DCMP
  • TR
  • AS
  • HOCM: ESM at LLSB, non-displaced apex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Cause of MVP?

A

Degenerative: myxomatous degeneration

Congenital: primary AD inheritance
(Marfan’s syndrome), secundum ASD, Turner’s
syndrome, PDA …etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Interpret:

Cyanosis and clubbing of toes
Large pulse volume or collapsing pulse
Continuous murmur across S1 S2 S1 +/- increased P2

D/dx?

A

Patent ductus arteriosus

D/dx:
Coarctation of aorta 
Ruptured sinus of Valsalva aneurysm into right heart 
Coronary arteriovenous fistula 
Pulmonary arteriovenous fistula 
VSD and AR 
Venous hum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Causes of PDA?

A

Pulmonary trunk connected to aortic arch, causing LA, LV and PA dilation

Congenital: idiopathic or secondary to maternal rubella
Associated with other congenital heart diseases
Preterm, birth in high altitude

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Interpret:

Visible, elevated JVP, one wave
Parasternal heave
Pansystolic murmur loudest in LLSB
Ankle edema

Next maneuver for murmur?
2 more classical signs?

D/dx?

A

Tricuspid regurgitation

Pansystolic murmur - Louder during inspiration, reduced during expiration

Pulsatile liver
Ascites

MR
VSD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Causes of Tricuspid regurgitation? (10)

A

Functional: right ventricular hypertrophy secondary to left ventricular failure

Rheumatic heart disease

Infective endocarditis

Pulmonary hypertension: cor pulmonale, ASD

Infarct of right ventricular papillary muscles

Tricuspid valve prolapse

Carcinoid heart disease

Trauma

Congenital

Endomyocardial fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Interpret:

Displaced apex 
Parasternal heave 
Raised JVP 
Systolic thrill 
Loud S2 
Pansystolic murmur at LLSB 
Ejection systolic murmur at pulmonary area 
Mid diastolic murmur at apex 

D/dx?

Causes (2)

A

VSD

MR, TR

Congenital: isolated or with other defects
Anterior myocardial infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q
List the cardiovascular diseases associated with:
Turner's 
Marfan 
Down 
Cushing
A

Turner’s = coarctation of aorta

Down = AVSD, VSD

Marfan = MR, AR

Cushing’s = hypertension with LV hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

D/dx splinter hemorrhage

A

→ Most commonly due to trauma
→ Classically due to IE
→ Other causes: vasculitis (and other A/I), sepsis, haematological malignancy, profound anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Differentiate Osler nodes and Janeway lesions

A

Osler’s nodes: red, raised, tender palpable nodules on pulp of fingers (or toes) or on thenar or
hypothenar eminence

Janeway lesions: non-tender erythematous maculopapular lesions on palms or pulps of fingers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

4 types of xanthomas

A
→ Xanthelasma: yellowish collection at or
around eyelids
→ Tendon xanthoma: papules/nodules in
tendons of hands, feet and heel
→ Palmar xanthoma at palms
→ Tuberoeruptive xanthomas: red
papules/nodules appearing inflamed and
tend to coalesce
29
Q

List locations of peripheral pulses (7)

A

Radial pulse: Distal forearm near the base of the thumb

Brachial pulse: Antecubital fossa immediately medial to
the biceps tendon

Carotid pulse: Lateral to the laryngeal prominence
(thyroid cartilage), medial to the SCM Usually use thumb of opposite hands

Femoral pulse: Halfway between the ASIS and pubic
symphysis

Popliteal pulse: In the popliteal fossa at the flexor
(posterior) compartment of the knees

Posterior tibial pulse: Midway between medial malleolus and heel

Dorsalis pedis pulse: On the dorsum of the foot lateral to the extensor hallucis longus tendon

30
Q

Difference between pitting and non-pitting edema causes?

A

→ Pitting oedema: cardiac failure,
hypoalbuminaemia (usually refills more
quickly)

→ Non-pitting oedema: lymphedema (eg.
lymphatic obstruction), myxedema,
lipoedema

31
Q

Causes of regularly irregular and irregularly irregular pulse

A

Regularly irregular

  • Sinus arrhythmia
  • Fixed ectopics
  • 2o heart block (Mobitz type I)

Irregularly irregular

  • AF (most common)
  • AFL or AT with variable block
  • Multifocal AT
  • Frequent variable ectopics
32
Q

Causes of radial- radial delay

A

subclavian artery stenosis/occlusion, thoracic aortic dissection

33
Q

Causes of radial-femoral delay

A

coarctation of aorta, aortic dissection, severe UL/aortoiliac vasculopathy

34
Q

Cause of slow rising pulse?

A

Aortic stenosis

35
Q

Cause of Bisfiriens pulse/ jerky pulse with double peak?

A

AS+AR

HOCM

36
Q

Causes of collapsing pulse

A
AR 
PDA 
Hyperdynamic circulation 
Aortic sinus rupture 
Peripheral AV fistula
37
Q

Cause of Pulsus alternans/ Alternating strong and weak pulses

A

Advanced LV failure

38
Q

Causes of Pulsus paradoxus

A
  • Cardiac tamponade
  • Constrictive pericarditis
  • Hyperinflation of lungs
    (eg. asthma, COPD)
39
Q

Difference between JVP and Carotid pulse

A

JVP:

Non-palpable 
Obliterated by pressure 
Lower and more lateral 
Increase in amplitude with inspiration 
2 peaks 
Decrease when upright 
Increase with hepatojugular reflex
40
Q

Causes of raised JVP and decreased JVP

Normal JVP height

A

Normal: <4.5cm above zero point, below clavicle

Raised JVP:
□ SVC obstruction (loss of normal JVP waveform)
□ Circulatory volume overload (↑central venous
pressure)
□ RV failure and RV volume overload
□ Pericardial effusion or constrictive pericarditis
(look for +ve Kussmaul sign)
□ Severe bradycardia

Decreased JVP indicates ↓RA filling pressure
□ Hypovolemia
□ Dehydration

41
Q

Cause of Cannon A wave

A

Indicates AV dissociation i.e. A and V contracting
together

  • Complete heart block
  • AFL, AT (due to heart block)
  • Non-atrial rhythms
     Nodal tachycardia
     Ventricular ectopics
     VT
     Ventricular pacing
42
Q

Cause of Giant A wave

A

Indicates ↓RA compliance or ↓RA outflow

  • ↓RA compliance:
     PS (∵chronic ↑RAP)
     Pulmonary HTN
  • ↓RA outflow
     TS
     RA mass/thrombus
43
Q

Cause of exaggerated x descent

A

Indicates pericardial compressive pathology

  • Cardiac tamponade
  • Constrictive pericarditis
44
Q

Cause of large V wave./ dominant c-v wave

A

Indicates ↑RA inflow during ventricular systole (i.e. TR)

Tricuspid regurgitation

45
Q

Cause of exaggerated y descent

A

Indicates ↑RA outflow during ventricular filling

  • Severe TR
  • Constrictive pericarditis11
46
Q

Cause of slow y descent

A

Indicates ↓RA outflow during ventricular filling

  • Cardiac tamponade
  • TS
47
Q

Procedures related to midline sternotomy scar

A
CABG, surgery requiring
cardiopulmonary bypass (AV/MV replacement)
48
Q

Procedures related to Lateral sternotomy scar

A

old previous mitral valvotomy (now rare)

49
Q

Procedures related to subclavian scar

A

Pacemaker, ICD, defibrillator box

at Rt infraclavicular region

Defibrillator boxes larger than pacemakers (10×5×1cm)

50
Q

List 4 characters of apex beat, list causes

A

Heaving = Pressure overload = AS, Hypertension

Thrusting = volume overload = AR, MR, Dilated cardiomyopathy

Tapping = MS

Double impulse = palpable A wave in concentric LV hypertrophy = HOCM

51
Q

Cause of parasternal heave?

A

Heaving: RVH or severe LA enlargement (RV pushed anteriorly)
RVH due to RV volume overload → ASD, TR
RVH due to RV pressure overload → TS, pHT

→ LA enlargement → MR

52
Q

What can be auscultated at the neck in cardiovascular exam?

A

AS radiation (bilateral)

Carotid bruit

Thyroid bruit

53
Q

Split S1, Loud S1, Soft S1 causes

A

Split S1 = delayed RV systole → T close after M
- RBBB, right atrial myxoma

Loud S1 = limited atrial outflow, atrial outflow remains strong at onset of ventricular systole

  • ↑HR, hyperkinetic states
  • MS

Soft S1 = ↓atrial outflow or MV pathologies

  • Increase PR interval e.g. first degree HB
  • MR
  • Severe, calcific MS
54
Q

Explain physiological S2

A

closure of aortic (A2) and pulmonic (P2) valves
A2 normally a bit earlier than P2

Mechanism: inspiration → ↓intrathoracic pressure
→ blood attracted towards pulmonary vessels
→ early A2 (less blood in LV) + late P2 (more blood in RV)

55
Q

Wide splitting S2 cause?

A

□ S2 split even during expiration
□ Mechanism: delayed RV systole → delayed P closure

□ D/dx:
→ Early A2: severe MR, WPWS type B
→ Late P2: RBBB, PS

56
Q

Fixed splitting S2 cause?

A

S2 splitting unaffected by breathing
→ RV volume overload → delayed P closure
(obligatory flow volume from RV)
→ ↑VR offset by ↓L-to-R shunt

ASD

57
Q

Reversed splitting S2 cause?

A

S2 splitting occurs during expiration
Mechanism: delayed LV systole → delayed A closure
→ normal inspiration-related P2 delay now abolishes splitting

D/dx:
→ Electrical A2 delay: LBBB, RV pacing
→ Mechanical A2 delay: PDA, severe AS

58
Q

Loud S2 causes?

A

□ Loud both A2 and P2: hyperdynamic state

□ Loud A2:
→ Systemic HTN (↑aortic pressure)
→ Congenital AS (narrowed valve closed suddenly at the end of systole)

□ Loud P2: note that palpable P2 correlates better with pHT
→ Pulmonary HTN (↑pulmonary a. pressure)

59
Q

Soft S2 cause?

A

□ Soft A2:
→ Calcified AS (↓mobility of aortic valve)
→ AR (incomplete closure of aortic valve)

□ Soft P2:
→ PS (↓mobility of pulmonic valve)

60
Q

Single S2 cause?

A

□ Absent A2: severe AS
□ Absent P2: severe PS, ToF, pulmonary atresia
□ Reduced splitting: pulmonary HTN, eg. Eisenmenger syndrome

61
Q

Cause of S3?

A

Mechanism: rapid filling → sudden tensing of ventricles → exaggerated in volume overload

D/dx:
→ Normal in children/young person, pregnancy, thyrotoxicosis
→ LV volume overload (apex, Lt lateral): congestive HF, MR, AR
→ RV volume overload (LLSB): RV failure, TR

62
Q

Cause of S4?

A

atrial systole against a poorly compliant ventricle → vibration of ventricles always absent in A-Fib

D/dx: always pathological
→ ↓LV compliance (apex, Lt lateral): pressure overload (AS, HTN), IHD, ↑age
→ ↓RV compliance (LLSB): pressure overload (PS, pHT)

63
Q

Changes to certain murmurs with sudden squatting?

A

→ Most murmurs become louder (↑preload → ↑CO)

→ HOCM murmur becomes softer (↑LV volume → relieved obstruction to outflow)

→ MVP murmur becomes softer and non-ejection click becomes later
(↑preload → ↑tension of chordae tendineae → prolapse occurs later)

64
Q

How to perform isometric exercise maneuver?

A

sustained handgrip or repeated sit-ups for 20-30s

→ Most murmurs become louder (↑afterload → ↑backflow of blood)

→ AS murmur becomes softer (↑afterload → ↓ejection velocity)

→ HOCM murmur becomes softer (↑afterload → ↓ejection velocity + ↑LV volume)

→ MVP murmur becomes softer and non-ejection click becomes later (↑afterload → ↑LV volume → ↑tension of chordae tendineae → prolapse occurs later)

65
Q

VSD and MR are associated with which myocardial wall infarct

A

VSD - Anterior wall infarct

MR - Inferior wall infarct causing papillary muscle dysfunction

66
Q

Interpret:

Displaced apex
Grade 5/6 S2 at aortic area

Most likely dx, causes?

A

Mechanical aortic valve

Replaced due to aortic regurgitation or stenosis

67
Q

How to differentiate multiple extrasystoles from A-fib

A

On exercise, multiple extrasystole is usually suppressed

A-fib remain irregular

68
Q

4 causes of heart failure

A

Ischemic
Hypertension
Valvular
Idiopathic dilated cardiomyopathy