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Cardiology Flashcards

1
Q

AV replacement indications?

A

AS
AR
IE with failed medical therapy

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2
Q

Clinical signs AS? Symptoms*

A

Loud, high-pitched, crescendo-decrescendo ESM loudest in aortic area during expiration and radiating to carotids
Low volume, slow-rising pulse
Narrow pulse pressure
Heaving apex
Systolic thrill

If severe:
Soft or absent S2
Late systolic peaking of a long murmur
S4 present

If complications:
Signs LV dysfunction (dyspnoea, displaced apex, bibasal crackles)
Signs of pulmonary HTN and RV failure (this is pre-terminal)
Conduction problems (acute suggests endocarditis, chronic suggests calcified aortic node)
IE signs (splinters, Osler’s, Janeway, Roth spots)

Angina
Syncope
Breathlessness

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3
Q

Differential diagnosis ESM?*

A

AS, aortic sclerosis (normal pulse and no radiation), HOCM, supravalvular AS (as in William’s syndrome), VSD, aortic flow in high-output clinical states e.g. pregnancy or anaemia

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4
Q

Management of AS?*

A

Asymptomatic:
Good dental health
Regular review to assess symptoms and echo to assess gradient and LV function
May be referred if LVEF <50% and low risk

Symptomatic:
AVR +/- CABG
3-5% mortality depending on EuroScore
TAVI if high surgical risk or inoperable

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5
Q

Most common causes of aortic stenosis?*

A

Bicuspid AV

Degenerative calcification

Rheumatic valve disease

Congenital

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6
Q

What does ESM mean?*

A

Crescendo-decrescendo murmur after S1, ending before S2, peaking in mid-to-late systole

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7
Q

Severe AS?*

A

Aortic valve orifice <1cm2
Moderate is 1 to 1.5
Mild is over 1.5

Or a mean gradient >50mmHg

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8
Q

What is aortic sclerosis?*

A

Mild thickening or calcification of the AV and can be distinguished from AS by absence of outflow tract obstruction

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9
Q

Complications of AS?*

A

-LVF
-Sudden death (predominantly in symptomatic individuals)
-Pulmonary HTN
-Arrhythmias/heart block
-IE
-IDA (Heyde’s syndrome)

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10
Q

How would you investigate ?AS patient?*

A

ECG (LVH, conduction defect)
CXR (often normal, calcified valve)
Echo (mean gradient >40 or valve area <1 if severe, to assess LV function)
ETT (symptoms, fall in BP)
CT (calcification severity, annulus size, coronary/peripheral artery patency)
Cardiac catheter (transvalvular gradient and angiography)

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11
Q

Cardiac causes clubbing?

A

Congenital cyanotic heart disease
Infective endocarditis
Atrial myxoma

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12
Q

How would you manage an AS patient?*

A

If asymptomatic:
Regular review
May be referred for intervention if LVEF <50% and low surgical risk

Surgical:
AVR +/- CABG
TAVI in high surgical risk or inoperable cases

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13
Q

Duke’s critera?*

A

Major:
Typical organism n 2 blood cultures
Echo showing abscess, large vegetation, dehiscence

Minor:
Pyrexia
Echo suggestive
Predisposed e.g. prosthetic valve
Embolic or vasculitic phenomena
Atypical organism

If 2 major, 1 major and 2 minor or 5 minor

Indicators for urgent surgery:
HF
Heart block
Refractory to antibiotics

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14
Q

Clinical signs of aortic incompetence?*

A

Collapsing pulse reflecting a wide pulse pressure
Apex beat is hyperkinetic and displaced laterally
Thrill in aortic area
A soft, high-pitched EDM loudest at left lower sternal edge with patient sat forward on expiration

Austin-Flint murmur is when MDM at apex due to regurgitant murmur impeding the mitral opening

Severe if:
EDM short
Collapsing pulse
S3
Pulmonary oedema

Eponymous signs:
Corrigan’s, Quincke’s, De Musset’s

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15
Q

Causes of AR?*

A

Congenital: bicuspid AV, peri-membranous VSD

Acquired:
Acute: endocarditis, type A dissection
Chronic: rheumatic fever, syphilis, Marfan’s, hypertension, ankylosing spondylitis, vasculitis

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16
Q

How would you investigate a patient with AR?*

A

ECG (lateral TWI)
CXR (cardiomegaly, pulmonary oedema, widened mediatstinum)
CT (size of aortic root, dissection, coronary patency)
TTE/TOE (LVEF size, aortic root size/dissection, vegetation, jet width)
Cardiac catheter (coronary patency usually pre-op)

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17
Q

How to manage a patient with AR?*

A

Medical management:
ACEi and ARBs to reduce afterload
Regular review of symptoms and echo

Surgical management:
Replace valve when symptomatic (dyspnoea, reduced ETT)

and/or

Criteria are met 1) wide pulse pressure >100mmHg
2) ECG changes on ETT
3) Echo features of LV enlargement or reduced function

Ideally valve should be replaced prior to significant LV dilatation and dysfunction

Acute surgery:
Dissection
Endocarditis

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18
Q

Prognosis in AR?*

A

Asymptomatic with EF >50%: 1% mortality at 5 years

Symptomatic with all 3 criteria met 65% mortality at 3 years

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19
Q

Severity on echo for AR?*

A

-LVEF <50%
-LV size ESD >50mm and/or EDD >65mm
-Degree of AR >65% LVOT width

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20
Q

Other causes of a collapsing pulse?*

A

Pregnancy
PDA
Anaemia

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21
Q

Clinical signs of MS?*

A

-Malar flush
-Irregular pulse
-Tapping apex (palpable first heart sound)
-Left parasternal heave if pulmonary HTN or enlarged LA
-Loud S1, opening snap, mid-diastolic murmur heard best at apex in left lateral position on expiration

Severe if:
-OS occurs nearer A2 (left atrial pressure higher, opens MV earlier) or is inaudible
-Longer MDM

Complications:
-Pulmonary HTN and R heart failure (TR, RV heave, loud P2, sacral and pedal oedema)
-Pulmonary oedema
-Endocarditis
-Embolic complications (stroke risk high if MS and AF)

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22
Q

What are the causes of MS?*

A

Acquired:
-Rheumatic disease (commonest)
-Senile degenration
-L mitral leaflet vegetation from endocarditis

Congenital
-Rare

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23
Q

Differential diagnoses for MS?*

A

Austin-Flint murmur
L atrial myxoma

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24
Q

How to investigate a patient with MS?*

A

-ECG (p-mitrale and AF)
-CXR (enlarged LA (splayed of carina), calcified valve, pulmonary oedema)
-TTE/TOE (valve area, cusp motility, calcification and LA thrombus, RV failure and pulmonary HTN (>50mmHG is severe))
-Cardiac catheter (coronary anatomy, right heart pressures)

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25
Q

How would you tell MS is severe from echo?*

A

Valve area <1cm2, gradient >10mmHg

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26
Q

Management of MS?*

A

Medical:
Manage AF
Diuretics

Mitral valvuloplasty:
If pliable, non-calcified with minimal regurgitation and no LA thrombus

Surgery:
Closed or open mitral valvotomy
OR
Valve replacement

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27
Q

Prognosis of MS?*

A

Latent asymptomatic phase 15-20 years
NYHA >II 50% mortality at 5 years

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28
Q

Tell me about rheumatic fever?*

A

Jones diagnostic criteria
Beta-haemolytic streptococcal infection

Rest, high-dose aspirin and penicillin
Prophylaxis to avoid recurrence

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29
Q

Signs of MR?*

A

-Pulse: AF small volume
-Apex: displaced and volume-loaded
-Palpation: thrill at apex
-Auscultation: high-pitched PSM loudest at apex radiating into axilla, , loudest on expiration, wide split S2, S3

Severe if:
Holosystolic
AF (LA enlargement)
Pulmonary oedema (increased LA pressure and LV failure)
Pulmonary hypertension
Endocarditis

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30
Q

Causes of MR?*

A

Acquired:
Chronic causes affecting annulus: 1) dilated LV 2) calcification
Chronic causes affecting valve leaflets: 1) prolapse 2) rheumatic 3) CTD 4) fibrosis e.g. pergolide
Chronic causes affecting papillae 1) infiltration 2) post-MI fibrosis

Acute causes: endocarditis, rupture of papillae

Congenital:
Association between cleft MV and primum ASD

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31
Q

Investigation of MR?*

A

ECG: p-mitrale, AF, Q waves if previous infarction
CXR: cardiomegaly, LA enlargement, pulmonary oedema
TTE/TOE: assess MR jet, LV dilatation, reduced EF AND cause (prolapse, vegetations, torn chordae or ruptured papillae, fibrosis, infarction, LV size
Cardiac MR: volume of MR, LV dimension and infarct
Cardiac catheter: right heart pressure

N.B. If concerned about IE, do bloods, urine dip and fundoscopy

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32
Q

Management of MR?*

A

Medical:
AF management
Diuretics, beta blockers, ACEi

Percutaneous:
TEER (if high surgical risk)

Surgical:
Valve repair (preferable) with annuloplasty ring or valve replacement

Aim to operate when symptomatic and prior to severe LV dilatation and dysfunction

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33
Q

Indications for MVR?

A
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34
Q

Differentials for MV murmur?

A

VSD, TR MV prolpase

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35
Q

JVP waveform relevance?

A
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36
Q

What is an S3? What is an S4?

A
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37
Q

Tell me about Marfan’s syndrome and the cardiac complications?

A
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38
Q

Prognosis of MR?*

A

25% mortality at 5 years if symptomatic

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39
Q

MV prolapse?*

A

Young lean tall women

Caused by myxomatous degeneration

Associated with CTD e.g. Marfan’s (90%), EDS, osteogenesis imperfecta, PCKD and HOCM

Often asymptomatic and benign but may present with CP, syncope, palpitations

May rarely present with severe MR, AF, emboli

On auscultation:
-Mid-systolic ejection click
-Pan-systolic murmur that gets louder up to A2
-Accentuated by standing from squatted position

40
Q

EDS?

A
41
Q

Signs of TR?*

A

Raised JVP with giant CV waves
Left sternal thrill
Auscultation: high-pitched PSM loudest in tricuspid area on inspiration, radiating to right sternal border, reverse split S2, S3

May be signs of RV failure: pulsatile liber, ascites, peripheral oedema
Pulmonary hypertension: RV heave and loud P2

42
Q

Causes of TR?*

A

Congenital: Ebstein’s anomaly (atrialisation of the RV and TR)

Acquired: IE (especially in IVDU)

Chronic acquired: dilated RV and annulus due to left heart disease (most common), implantable device leads, carcinoid, rheumatic

43
Q

How to investigate TR?*

A

ECG: p-pulmonale, AF, right-heart strain (large R wave V1, TWI V1-3)

CXR: double right heart border

TTE: TR jet, RV dilatation

44
Q

Management of TR?*

A

Medical: diuretics, beta blockers, ACEi

Percutaneous: TEER

Surgical: valve repair/annuloplasty if medical treatment fails

45
Q

Associations with PS?*

A

Tetralogy
Noonan’s (male version of Turner’s)
TR and VSD

(Carcinoid
Rheumatic fever)

46
Q

Clinical signs of PS?*

A

-Raised JVP with giant A waves
-Left parasternal heave
-Thrill in pulmonary area
-Auscultation: high-pitched ESM loudest in pulmonary area on inspiration, widely split S2
-Signs of RV failure (ascites, peripheral oedema)

Severe if: inaudible P2, longer murmur duration

47
Q

Symptoms of PS?

A

Dyspnoea
Reduced ET
Fatigue
Syncope

48
Q

Differential for PS murmur?

A
49
Q

Investigations for PS?*

A

ECG: p-pulmonale, RVH, RBBB
CXR: oligemic lung fields, large RA
TTE: severity (pressure gradient), valve area <1cm2, RV function and associated cardiac lesions
Cardiac catheterisation: to guide intervention

50
Q

How to manage PS?*

A

-Pulmonary valvotomy if gradient >70mmHg or RV failure
-PPVI
-Surgical replacement or repair

51
Q

Noonan’s syndrome?

A

Rate AD syndrome:

Congenital heart defects including PS, ASD, HOCM
Short stature
Pectus excavatum
Facial features
Learning disabilities
Impaired blood clotting

52
Q

Carcinoid syndrome?*

A

Gut primary with liver mets secreting 5-HT into bloodstream

Diarrhoea, wheeze and flushing

Right heart valve fibrosis causing TIPS

Treatment with somatostatin analogue and cytoreduction

53
Q

Tetralogy of Fallot?

A

VSD
Overriding aorta
RVH
Pulmonary stenosis

Management:
Prostaglandin infusion at birth to keep ductus arteriosus open

Blalock-Taussig shunt to partially correct abnormality in infancy by anastomosing the subclavian artery to the pulmonary artery (causes absent radial pulse and thoracic scars)

Surgical correction: closure of VSD, resection of RV obstructive muscle tissue, enlarging outflow path

Complications: PR, right-heart failure, TR, arrhythmias

54
Q

Causes of absent radial pulse?*

A

Acute: embolism, aortic dissection, trauma e.g. previous radial artery sheath

Chronic: atherosclerosis, coarctation, Takayasu’s arteritis

55
Q

Signs of AVR?*

A

If metallic:
Midline sternotomy
Metal prosthetic CC at S2
May be an OC and high-pitched ES flow murmur

Bioprosthetic:
Midline sternotomy
Often normal HS

Abnormal findings:
AR
Decreased intensity of the closing click (clot or vegetation)

Also:
May be bruising and anaemia

56
Q

Signs of MVR?*

A

Metal prosthetic CC at S1
May be an OC in early diastole followed by low-pitched diastolic rumble

Abnormal findings:
MR
Decreased intensity of CC

Also:
May be bruising and anaemia

57
Q

Metal versus porcine VR?*

A

Metal more durable but have to be on warfarin so more suitable for younger or already on warfarin e.g. for AF

Porcine therefore better for elderly or those at risk of haemorrhage

N.B. With the advent of ViV TAVIs for degenerative bioprosthetic valves, fewer metallic valves being implanted

58
Q

Complications of valve replacement?*

A

-Thromboembolism 2%/annum despite warfarin
-Bleeding
-Bioprosthetic dysfunction and LVF (usually within 10 years)
-Haemolysis
-IE (early <2/12 Staphylococcus epidermidis, late Strep. viridans)
-AF (particularly in MVR)

59
Q

Complications of implantable devices?*

A

Local infection
Pericardial effusion
Pneumothorax

More chronic complications:
TR
IE

60
Q

Primary prevention ICD?*

A

MI >4 weeks ago (and NYHA no worse than class III):
-LVEF <35% and NSVT and positive EP study
-LVEF <30% and QRS >120ms

OR

Familial condition with high risk SCD (LQTS, ARVD, Brugada, HCM)

61
Q

Secondary prevention ICD?*

A

VT or VF arrest

Haemodynamically compromising sustained VT

Sustained VT with LVEF <35%

62
Q

CRT indications?*

A

-LVEF <35%
-NYHA II-IV on optimal medical therapy
-Sinus rhythm and QRS >150ms (if LBBB may be >120ms)

N.B. Extra LV pacemaker lead via coronary sinus improved mortality/symptoms

63
Q

Causes of constrictive pericarditis?*

A

4Ts:
TB
Trauma or surgery
Tumour, Therapy (radio)
Connective Tissue disease

64
Q

Signs of constrictive pericarditis?*

A

Raised JVP
Kussmaul’s sign
Pulsus paradoxus
Pericardial knock
Ascites, hepatomegaly, peripheral oedema

65
Q

What is Kussmaul’s sign? What is pulsus paradoxus?*

A

1) Paradoxical increase in JVP on INspiration
2) >10mmHg drop in systolic pressure on inspiration

66
Q

How to investigate someone with ?constrictive pericarditis?*

A

CXR: pericardial calcification, old TB, sternotomy wires
Echo: high acoustic signal from pericardium, septal bounce, reduced mitral flow velocity on Doppler during inspiration
Cardiac catheter: dip and plateau of diastolic wave form (square root sign), equalisation of diastolic RV and LV, RA and LA pressures, ventricular interdependence
CT: thickened pericardium +/- calcification
Cardiac MR: thickened pericardium, fibrosis, early diastolic flattening of the septum, enlarged atria

67
Q

Pathophysiology of constrictive pericarditis?*

A

Thickened, fibrous capsule reduces ventricular filling and ‘insulates’ the heart from thoracic pressure changes during respiration, leading to ventricular interdependence

68
Q

Treatment of constrictive pericarditis?*

A

Medical: diuretics

Surgical: pericardiectomy

N.B. Differentiating constrictive pericarditis from restrictive cardiomyopathy is tricky but ventricular interdependence is highly diagnostic for the former

69
Q

ASD clinical signs?*

A

Raised JVP
Pulmonary area thrill

On auscultation: fixed split S2, pulmonary ESM and mid-diastolic flow murmur with large LTR shunts

Signs of deterioration: pulmonary HTN (RV heave and loud P2) with cyanosis and clubbing would suggest Eisenmenger’s; CCF

70
Q

Types of ASD?*

A

Primum: associated with AVSD and cleft mitral valve seen in Down’s
Secundum: commonest

71
Q

Complications of ASD?*

A

Paradoxical embolus
Atrial arrhythmias
RV dilatation

72
Q

Investigations for ASD?*

A

ECG: RBBB and LAD (primum) or RAD (secundum), AF
CXR: small aortic knuckle, pulmonary plethora, double-heart border
TTE/TE: site, size, shunt calculation, ameanability to closure
Right heart catheter: shunt calculation (not always necessary)

73
Q

Management of ASD?*

A

Indications for closure:
Symptoms (breathlessness, paradoxical embolus)
Significant shunt

Contraindication for closure:
Severe PH and Eisenmenger’s

Percutaneous closure device or surgical patch repair

74
Q

Signs of VSD?*

A

Thrill at left lower sternal edge
High-pitched PSM at left sternal edge
No audible A2
S3 if large shunt
N.B. Loudness doesn’t correlate with size
If Eisenmenger’s develops, murmur disappears

Consider:
Associated lesions (AR, PDA, Fallot’s, coarctation)
Pulmonary HTN (RV heave and loud P2) with cyanosis and clubbing would suggest Eisenmenger’s
Endocarditis

75
Q

Causes of VSD?*

A

Congenital
Acquired (traumatic, post-operative, post-MI)

76
Q

Investigation of VSD?*

A

ECG: conduction defect (BBB)
CXR: pulmonary plethora
TTE/TOE/CMR: site, size, shunt calculation, associated lesions
Cardiac catheter: shunt size, pulmonary pressures, consideration of closure

77
Q

Management of VSD?*

A

Small peri-membranous VSDs often close spontaneously

Percutaneous: Amplatzer device

Surgical: pericardial patch

Post-infarct VSD: mechanical circulatory support, patch or percutaneous closure, heart transplant

78
Q

Coarctation signs?*

A

-Hypertension in supper limbs
-Prominent upper body pulses, weak femoral pulses, radio-femoral delay
-Heaving apex
-Systolic murmur radiating to back, loud A2

79
Q

Coarctation associations?*

A

Cardiac: VSD, bicuspid AV, PDA
Non-cardiac: Turner’s, intracranial aneurysms

80
Q

Coarctation investigations?*

A

ECG: LVH ad RBBB (if associated VSD)
CXR: rib notching, double aortic knuckle
TTE: increased aortic flow velocity, associated lesions
CT/CMR: anatomy got repair and associated lesions

81
Q

Coarctation management?*

A

-EVAR
-Dacron patch aortoplasty
-Anti-hypertensives
-Surveillance with MRA (late aneurysms and re-coarctation)

82
Q

Signs of PDA?*

A

Collapsing pulse
Thrill left second intercostal space
Thrusting apex
‘Machinery murmur’ loudest below left clavicle

83
Q

Complications of PDA?*

A

Eisenmenger’s
Endocarditis

84
Q

Management of PDA?*

A

Close surgically
Plug percutaneously

85
Q

Signs of HCM?*

A

-Jerky pulse
-Double apical impulse
-Thrill at lower left sternal edge
-ESM at lower left sternal edge radiates throughout precordium, S4, accentuated standing from squatting

May be associated MV prolapse
May be Friedrich’s or myotonic dystrophy

86
Q

Investigations for HCM?*

A

ECG: LVH with strain (TWI across precordial leads)
CXR: often normal
TTE: asymmetrical septal hypertrophy, systolic anterior motion of anterior mitral leaflet, LVOT gradient
CMR: identifies apical HCM better than TTE and detects fibrosis
Cardiac catheterisation
Genetic test: sarcomeric proteins mutation

87
Q

Differentials for LVH?*

A

Athletic heart
Hypertensive heart disease
HOCM
Anderson-Fabry disease
Amyloidosis

88
Q

Management of HOCM?*

A

Avoid strenuous exercise, dehydration, vasodilators
Genetic counselling of first degree relatives

If symptomatic and LVOT >30mmHg:
Beta blockers ad verapamil
Cardiac myosin inhibitors
PM
Alcohol septal ablation or surgical myomectomy

If high risk SCD:
ICD

Refractory:
Heart transplant

89
Q

Prognosis of HCM?*

A

2.5% annual mortality rate

Poor prognostic factors include:
Young age at diagnosis
Syncope
VT or arrest
FH SCD
Septum >30mm
‘Burnt out’ LV i.e. reduced LVEF and fibrosis

90
Q

Causes of HF?*

A

1) CAD
2) HTN
3) Valve disease
4) Arrhythmias
5) Cardiomyopathies (dilated, hypertrophic, restrictive, Takotsubo, ETOH, cocaine, post-partum)
6) Congenital
7) Infective (viral myocarditis, HIV)
8) Drug-induced (anthracyclines)
9) Infiltrative (amyloid)
10) Storage disorders (HH, Fabry’s)
11) Pericardial disease
12) Metabolic (thyroid)
13) Neuromuscular (muscular dystrophy, FA)

91
Q

Investigations for HF?*

A

ECG: ischaemia, LBBB, AF
CXR: increased CTR, interstitial and pulmonary oedema
TTE: LV size and function, associated lesions
Cardiac catheter: coronary patency
CMR: LV size and function, aetiology

92
Q

Treatment of HF?*

A

Treat cause

Medical: fluid restriction, diuretics, beta blocker, ACEi, MRA, SGLT2

Device: ICD/CRT

Surgery: volume reduction surgery, LVAD, heart transplant

93
Q

Indications for heart transplant?*

A

-Severely impaired LVSF, HCM, intractable VT or angina
-NYHA III or IV despite optimal medical management
-CRT/ICD or CRT-D implanted

94
Q

CI to heart transplant?*

A

-Age >65 with other serious health condition
-Sepsis
-Malignancy
-Psychosocial factors
-Irreversible PH

Relative CI:
-High BMI
-Diabetes with EOD
-Severe peripheral or cerebrovascular disease
-Severe lung or kidney disease

95
Q

Predominant AS versus predominant AR?

A

AS predominant:
Low pulse volume
Slow-rising pulse
Apex beat minimally displaced and heaving
Low BP
Narrow PP

AR predominant:
Large pulse volume
Collapsing pulse
Displaced, thrusting apex
High BP
Wide PP

96
Q

Predominant MS versus predominant MR?

A

MS predominant:
Small volume pulse
Undisplaced tapping apex
Loud S1
No S3

MR predominant:
Sharp pulse
Displaced thrusting apex
Soft S1
S3 present

PACES (4 decks)

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