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PACES revision > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Midline sternotomy

A

CABG
Valve replacement
Congenital heart surgery
Aortic root repair

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2
Q

Midline sternotomy with leg scar

A

CABG with venous grafting

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3
Q

Tetralogy of fallot

A

Overiding aorta
VSD
Pulmonary stenosis
Right ventricular hypertrophy

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4
Q

Complications of tetralogy of fallot

A

Pulmonary regurgitation requiring valve replacement
Endocarditis
Coagulopathy
Polycythaemia
Paradoxical embolism
Arrhythmia

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5
Q

Midline sterntomy and left thoractomy scar

A

Tetralogy of fallot repair with shunting
or multiple surgeries eg CABG and separate lung surgery

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6
Q

What are different congenital heart diseases

A

Cyanotic:
Tetralogy of fallot
Transposition of the great vessels
Tricuspid atresia
Truncus arteriosus

Non cyanotic (Although can progress to Eisenmengers with shunt reversal)
VSD
ASD
PDA
Coarctation of the aorta

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7
Q

Differentials for systolic murmur

A

Aortic stenosis
Aortic sclerosis
Mitral regurg
Pulmonary stenosis
ASD, VSD
HOCM

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8
Q

Causes of Aortic stenosis

A

Senile calcification
Biscuspid valve
Rheumatic fever

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9
Q

Signs of severe AS
On Exam
On echo
In History

A

Quiet murmur
Narrow pulse pressure

Valve area <1cm or <0.6 depending on guidelines
Gradient across valve >50

Evidence of heart failure
Symptomatic eg syncope,
Abnormal BP response to exercise

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10
Q

Tx options for severe or symptomatic AS

A

Optimise cardiovascular risks
Ix for co-existent coronary artery disease with angiogram
Valve replacement - bioprosthetic or mechanical
Biosposethetic valves have shorter lifespan but do not require anticoagulation
Mechanical last long but need lifelong anticoagulation
Risk vs benefits. Taking into account patients age, lifestyle etc.
TAVI - older patient, or those not suitable for surgery however cannot have if bad PVD or bad coronary artery disease

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11
Q

Complications of TAVI

A

COMPLICATIONS of TAVI
Pacemaker 10%
Vascular access complication eg stent
Stroke, MR, annular rupture, perforation of apex

Mortality higher on waiting list for TAVI than procedure itself

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12
Q

ECG findings with AS

A

Left ventricular hypertrophy
LBBB
10% of patients who have a TAVI go on to have a pacemaker so important to know about re-existing conduction abnormalities

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13
Q

Complications of valve replacement

A

Immediate- risk of bleeding, infection, damage to local structure (inc conduction issues)
Valve failure
Infective endocarditis
Haemolysis
SE of anticoagulation

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14
Q

Mitral regurgitation - causes

A

MI causing papillary muscle rupture
Infective endocarditis/ Rheumatic fever
Connective tissue diseases - Marfans, RA
PCKD
Inflammatory - Dilated left ventricle / Amyloidosis
Degeneration - Calcification / Fibrosis

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15
Q

Tx for MR

A

If mild to mod- monitor with 2 yearly Echo.
Need to intervene early
Intervention guided by severity, symptoms, pulmonary hypertension and left ventricular function.

Mitral clip
Valve repair
Valve replacement

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16
Q

Marfans - underlying pathophysiology

A

Mutation in the FBN1 gene result in the production of abnormal fibrillin protein.
This causes mechanical instability and loss of elasticity of connective tissues.
This results in aortic dilatation.

17
Q

Managing Marfans

A

Surveillance of aortic roof size with annual echo
Surgical management of aortic root dilatation (if over 50mm, if FH of dissection and >45mm, if rapidly progressing)
B blockers and angiotensin receptor blocker to slow aortic root dilatation
Valve replacements as required
Genetic counselling
PT/OT

18
Q

Signs on exam of marfans

A

Tall with long extremities
Arachnodactyly ( can encircle their wrist with their thumb and little finger)
Hyperextendible joints
High arched palate
Pectus carinatum or excavatum
Scoliosis
Aortic regurgitation
Mitral valve prolapse
Coarctation
Inguinal hernia

19
Q

Differentials for Marfans

A

Homocysteinuria (Similar phenotype, but inherited autosomal recessively, not associated with aortic root disease, but is associated with learning difficulties and recurrent aortic and venous thromembolic events. In addition, lens dislocation tends to be upwards in Marfans but downwards in homocysteinuria.)

Men 2b (Marfanoid body habitus, mucosal neuromas, medullary thyroid cancer, phaeochromocytoma
Ehlers danlos

20
Q

Associated with pulmonary stenosis

A

o The causes of pulmonary stenosis are primarily congenital causes, which can simply be pulmonary stenosis on its own, or be associated with other congenital conditions:
o Tetralogy of Fallot
o Williams or Noonan syndrome (phenotypical appearance - short stature, webbed neck, widely spread nipples, proptosis, strabismus)

o There are also infective causes:
o Infective endocarditis
o Rheumatic fever
o Carcinoid syndrome ( the secreted mediators cause right- sided heart valve fibrosis causes tricuspid regurgitation and/or pulmonary stenosis)

21
Q

SIgns on exam of PS

A

Raised JVP with giant A waves
Right parasternal heave
Thrill in the pulmonary area
Ejection systolic murmur loudest in the pulmonary area on inspiration
Radiates to infraclavicular region
Widely split second heart sound
Functional tricuspid regurgitation

22
Q

Ehlers Danlos signs on exam

A

Fragile skin
Hyperextensible skin
Joint hypermobility
Mitral valve prolapse
Evidence of surgery from aneurysmal rupture or bowel perforation

It is autosomal dominant

23
Q
A
24
Q

CAUSES OF MITRAL VALVE PROLAPSE

A

Marfan syndrome
Ehlers–Danlos syndrome
osteogenesis imperfecta
polycystic kidney disease

25
Q

Causes of restrictive cardiomyopathy

A

Myocardial
- idiopathic
- scleroderma
- amyloid
- Haemachromatosis
- glycogen storage disorders
- Gauchers

Endomyocardial
- endomyocardial fibrosis
- hyper- eosinophilic syndromes ( inc. lofflers)
- carcinoid
- malignancy or radiotherapy
- toxin related

26
Q

Signs of mitral stenosis on exam

A

Malar flush
Diastolic murmir loudest in mitral area
Radiates to axilla
Palpable first heart sound
Left parasternal heave if pulmonary hypertension present
Opening snap of S1, then mid diastolic murmur
Tricuspid regurgitation, right ventricular heave and loud p2 if pulmonary hypertension
Embolic complications

27
Q

Causes of mitral stenosis

A

Degeneration
Rheumatic fever / IE
Congenital

28
Q

Diagnosing rheumatic fever

A

Evidence of recent group A strep infection
- positive throat swab, positive antigen test, raised antibody titre, recent episode of scarlet fever
Plus either 2 major criteria or 1 major and 2 minor
Major criteria
- chorea
- erythema marginatum
- subcutaneous nodules
- polyarthritis
- carditis
Minor criteria
- raised ESR/WCC, arthralgia, previous rheumatic fever, pyrexia, prolonged PR

29
Q

Criteria for diagnosing infective endocarditis

A

Duke’s criteria
Major and minor
2 major
1 major and 3 minor
5 minor

BC with organisms of IE and echo findings consistent

Minor - fever, immunological phenomena, vascular phenomena, risks eg IVDU, BC positive for other organisms

30
Q

Most common organisms in infective endocarditis

A

Staph aureus
Staph epidermis
Strep viridans
Strep bovis

Less commonly - HACEK organisms of fungal organisms

31
Q

Aortic regurgitation

A

Quinckes signs
Collapsing pulse
Corrigans sign
De mussetts
Aortic thrill
Diastolic murmur
Heard loudest in tricuspid
Sat forward in expiration

32
Q

Causes of AR

A

Degenerative: Bicuspid valves, age and factors like hypertension.
Infective: Infective endocarditis, rheumatic fever, tertiary syphilis.
Rheumatological: HLA B27 associated arthopathies like ankylosing spondylitis.
Connective tissue disorders: Marfans, ehlers danlos, psuedoxanthoma elasticum, osteogenesis imperfecta.

33
Q

HOCM - management

A

Avoid strenuous exercise, dehydration and vasodilators

If symptomatic and LVOT gradient > 30mmHg:
- b blocker
- Pacemaker
- alcohol septal ablation
- surgical myomectomy

If rhythm disturbance or high risk SCD:
- ICD

Refractory:
Transplant

Genetic counselling (autosomal dominant)

34
Q

Absent radial pulse

A

Iatrogenic - art line, arterial harvesting. Proximal arterial issues
Atherosclerosis - smoking, high BMI, high cholesterol, diabetes
Vasculitis - takayasu’s, giant cell arteritis
Subclavian steal syndrome
(stenosis or occlusion of subclavian artery proximal to origin of vertebral artery so that bloods diverts up caroitds and back down the vertebral artery to reach remaining vasculature in arm. This diverts blood away from the brain causing neurological symptoms on affect arm – sensory, visual , auditory, olfactory or total collapse. May also be arm claudication on use)

35
Q

HOCM- Mx

A

Conservative: genetic counselling, lifestyle advice inc avoiding strenuous exercise, referral to support and information networks
Medical: beta blockers (to reduce outflow tract gradient), amiodarone (suppress arrythmias)
Surgical – alcohol septal ablation, septal myomectomy

36
Q

Poor prognostication in HOCM

A

Poor prognostic markers:
Syncope, FH of sudden cardiac death, poor blood presuure response to exercise, outflow tract gradient >30mmhg at rest, septal wall thickness, certain genetic mutations
Inheritance – autosomal dominant or de novo
Screening – regular ECG and echo

37
Q

Ix for HOCM

A

CXR (heart failure), echo (concentric or septal hypertrophy, septal wall thickness, outflow tract gradient, diastolic dysfunction until late stages where systolic too, associated MVP), cardiac MRI (detailed structural information)
Special: cardiac catheterisation (gradient), genetic tests (eg beta myosin heavy chains, myosin binding protein C, troponin), endomyocardial biopsy (rule out other causes eg amyloid)

PACES revision (2 decks)

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