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PACES > Cardiology > Flashcards

Cardiology Flashcards

1
Q

differentials for ejection systolic murmur

A

1) HOCM
2) aortic sclerosis
3) flow murmur- high output clinic state e.g. pregnancy
4) ASD
5) tetrallogy of fallot

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2
Q

what are the causes of aortic stenosis

A

congenital- bicuspid aortic valve
age- senile degeneration/ calcinosis
infection- rheumatic heart disease

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3
Q

indications for surgery of aortic stenosis

A

symptomatic AS- chest pain, syncope, dyspnoea
asymptomatic
- gradient >40mmHg and
- EF <45%,
- abnormal response to exercise,
- valve area <0.6cm2,
- LVH>15mmh

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4
Q

how do you differentiate aortic stenosis from aortic sclerosis

A

normal pulse character (not slow rising), normal second heart sound

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5
Q

what conditions are associated with aortic stenosis

A

coarctation of the aorta- radio femoral delay
angiodysplasia (Heydes syndrome)
anaemia
William’s syndrome

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6
Q

what are the dukes criteria for IE

A

2 major / 1 major + 3 minor

major
1) typical organisms in bloods culture
2) echo- abscess/ large vegetations/ dihiscence

minor
pyrexia >38
echo suggestive
prosthetic valve
embolic phenomena
vasculitic features (ESR rise)
atypical organism on blood culture

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7
Q

causes of IE

A

Staphylococcus aureus
is the most common cause of infective endocarditis.

Streptococcus viridans- commonly found in the mouth and in particular dental plaque so endocarditis caused by these organisms is linked with poor dental hygiene or following a dental procedure

coagulase-negative Staphylococci such as Staphylococcus epidermidis
commonly colonize indwelling lines and are the most cause of endocarditis in patients following prosthetic valve surgery, usually the result of perioperative contamination.

Streptococcus bovis
associated with colorectal cancer

non-infective
systemic lupus erythematosus (Libman-Sacks)
malignancy: marantic endocarditis

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8
Q

what are the causes of aortic regurgitation

A

acute causes- trauma, aortic dissection, infective endocarditis

chronic- rheumatic fever, dilation of the aortic root- marfans, HTN, ank spond

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9
Q

what are the indications for surgery of AR

A

symptomatic patients with severe AR

asymptomatic patients with severe AR who have LV systolic dysfunction

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10
Q

does a long murmur mean more severe AR

A

a short murmur suggests more severe AR due to more severe flow of bloods back into the LV

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11
Q

what clinical signs suggest more severe AR

A

clinically dilated heart (displaced apex), signs of left sided heart failure, short murmur, wide pulse pressure, collapsing pulse

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12
Q

what are the complications of AR

A

LV heart failure, endocarditis

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13
Q

what is the prognosis of AR

A

asymptomatic and LVF >50 - 1% mortality at 5 years
symptomatic with 3 criteria- wide pulse pressure, ECG changes, echo LV enlargement/ EF <50- 65% mortality at 3 years

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14
Q

Causes of mitral regurtitation

A

acute- bacterial endocarditis/ rupture
chronic- mitral valve prolapse, rheumatic, CTDs- marfans/EDS, functional MR (dilated LV), infiltrative (amyloidosis), fibrosis (post MI/ rupture)

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15
Q

what are the indications for surgery of mitral regurgitation

A

symptomatic patient with severe MR
asymptomatic:
LVEF <60%
LV end systolic dimension >45mm
AF
systolic pulmonary pressure >50mmHg

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16
Q

why is mitral valve repair preferable to replacement

A

disconnection of subvalvular apparatus can cause a 20% decline in LV function

risk of infective endocarditis in valve replacement

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17
Q

how is ischaemic MR managed

A

ischaemic MR has a poor prognosis therefore threshold for surgery is lower.

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18
Q

what features suggest severe or significant MR

A

pulmonary hypertension
displaced thrusting apex beat
AF

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19
Q

what are the causes of mitral stenosis

A

Congenital - rare
rheumatic (commonest)
age related- senile degeneration
endocarditis

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20
Q

what are the indications for anticoagulation

A

any patient with AF should be on anticoagulation, those with rheumatic AF have >3 fold increased risk of thromboembolism

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21
Q

how often should patients with Mitral stenosis be followed up

A

if asymptomic or with mild MS- annual follow ups are required

22
Q

which patients should be offered percutaneous balloon mitral valvuloplasty/ surgery

A

if evidence of PH
new AF
symptomatic with NYHA II heart failure and valve suitable

23
Q

what is the prognosis of MR???

A

latent asymptomatic phase of 15-20 years
NYHA II confers a 50% mortality in 5 years

24
Q

what is rheumatic fever

A

immunological cross reactivity between group A B haemolytic strep infections and valve tissue.

25
Q

what is the diagnostic criteria of rheumatic fever

A

Duckett Jones
proven B haemolytic infection on throat swab/ rapid antigen test/ clinical scarlett fever PLUS
2 major or 1 major+2minor
MAJOR- JONES
J- joints (polyarthralgia)
O- carditis
N- nodules (subcutaneous)
E- erythema marginatum
S- chorea

minor
high ESR, raised WCC, arthralgia, pyrexia, prolonged PR interval

26
Q

treatment of rheumatic fever

A

rest, high dose aspirin, penicillin
Primary prevention: penicillin V for 10 days
Secondary prevention: penicillin V for about 5–10 years

27
Q

discuss the merits of biological valve vs mechanical valves

A

metallic valves are very durable, they are often used in young patients or patients with other conditions requiring anticoagulations such as AF. metallic valves require life-long warfarin which can be cumbersome and also inappropriate for patients with a bleeding/ falls risk

biological valves are generally less durable than metallic but require no warfarinisation therefore can be more appropraite in patients with risk of haemorrhage

28
Q

what are the causes of tricuspid regurgitation

A

acute- endocarditis
chronic- pulmonary hypertension, ebstein’s abnormality, rheumatic valve disease, carcinoidh

29
Q

why is TR endocarditis more common in IVDU

A

substances flow through the heart after being injected and can matter can cause damage to the TV (first valve encountered) and predispose to being seeded from bacteramia

30
Q

what are the 4 features of tetralogy of fallot

A

ventricular septal defect (VSD)
right ventricular hypertrophy/ outflow tract obstruction
pulmonary stenosis
overriding aorta

31
Q

metallic 1st heart sound

A

mitral valve replacement

32
Q

metallic 2nd heart sound

A

aortic valve replacement

33
Q

splitting of the 2nd heart valve

A

mitral regurgitation
tricuspid regurgitation
pulmonary stenosis
ASD (fixed)

34
Q

noonans syndome cardiac features

A

commonly pulmonary stenosis
HOCM
ASD

35
Q

signs from severe pulmonary stenosis

A

R ventricular heave
ejection systolic murmur or pansystolic mumur from function TR
large a waves on JVP
palpable thrill

36
Q

eye signs of noonans syndrome

A

proptosis, ptosis, strabismus

37
Q

signs of pulmonary hypertension

A

RV heave and loud P2, + cyanosis

38
Q

noonans syndrome

A

congenital disorder - autosomal dominant
males and females affected
phenotypical features- short stature, pectus excavatum, facial features, learning difficulties

39
Q

causes of pulmonary stenosis

A

largely congenital- tetrallogy, williams, turners, noonans
congenital pulmonary stenosis
acute- infective endocarditis, rheumatic valve disease, carcinoid syndrome

40
Q

duration of anticoagulation in PE

A

3 months if provoked
6 months if unprovoked, or in case of active malignancy

41
Q

causes of Eisenmengers syndrome

A

reversal of a left to right shunt from pulmonary hypertension
VSD
ASD
PDA

42
Q

complications of eisenmengers syndrome

A

RV failure
IE
haemoptosis
hypoxaemia

43
Q

causes of clubbing

A

respiratory- malignancy, bronchiectasis, ILD
cardiac- subacute endocarditis, cyanotic congenital heart disease
GI- IBD
familial / idiopathic

44
Q

cyanotic vs acyanotic congenital heart disease

A

cyanotic- tetrallogy of fallot, transposition of the great arteries, pulmonary atresia, pulmonary stenosis, eisenmengers, tricuspid. atresia, ebsteins

acyanotic- ASD, uncomplicated VSD, PDA, coarctation, AS

45
Q

causes of constrictive pericarditis

A

viral/ bacterial pericarditis, post surgery, post TB, radiation

46
Q

causes of restrictive pericarditis

A

diastolic dysfunction with restrictive ventricular physiology. systolic function preserved.

endomyocardial fibrosis (lofflers), sarcoidosis, scleroderma, malignancy, amyloidosis, iron overload

47
Q

HOCM clinical signs

A

ejection systolic murmur from LV outflor obstruction
panystolic murmur resulting from MR

48
Q

causes of cardiac hypertrophy

A

Hypertension
aortic stenosis
hypertrophic cardiomyopathy, which is a genetic condition.
Fabry disease
amyloidosis

49
Q

management of HOCM

A

treating patients symptoms with beta blockers. Second line with either disopyramide or a myosin inhibitor, such as mavacamten.
assess a patient for their risk of sudden cardiac death and consider
implanting a defibrillator or ICD.
assess patient’s genetics to aid with familial evaluation
In certain cases of severe disease, patients can be referred for septal reduction
therapy

50
Q

Correction of TOF

A

Surgical correction of these defects in the long term is always necessary. The timing of
correction depends on how symptomatic, cyanosed or hypoxaemic the child is.
Corrective repair of tetralogy of Fallot includes closure of the ventricular septal defect
with a synthetic Dacron patch. Narrowing of the pulmonary valve and the right
ventricular outflow tract obstruction are relieved by a combination of resecting
obstructive muscle tissue in the right ventricle and by enlarging the outflow pathway with
a patch.
Historically, a Blalock-Taussig Shunt, which is done by
plumbing the left subclavian artery into the pulmonary artery

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