Cardiology Flashcards
Midline sternotomy
CABG
Valve replacement
Congenital heart surgery
Aortic root repair
Midline sternotomy with leg scar
CABG with venous grafting
Tetralogy of fallot
Overiding aorta
VSD
Pulmonary stenosis
Right ventricular hypertrophy
Complications of tetralogy of fallot
Pulmonary regurgitation requiring valve replacement
Endocarditis
Coagulopathy
Polycythaemia
Paradoxical embolism
Arrhythmia
Midline sterntomy and left thoractomy scar
Tetralogy of fallot repair with shunting
or multiple surgeries eg CABG and separate lung surgery
What are different congenital heart diseases
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
Differentials for systolic murmur
Aortic stenosis
Aortic sclerosis
Mitral regurg
Pulmonary stenosis
ASD, VSD
HOCM
Causes of Aortic stenosis
Senile calcification
Biscuspid valve
Rheumatic fever
Signs of severe AS
On Exam
On echo
In History
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
Tx options for severe or symptomatic AS
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
Complications of TAVI
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
ECG findings with AS
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
Complications of valve replacement
Immediate- risk of bleeding, infection, damage to local structure (inc conduction issues)
Valve failure
Infective endocarditis
Haemolysis
SE of anticoagulation
Mitral regurgitation - causes
MI causing papillary muscle rupture
Infective endocarditis/ Rheumatic fever
Connective tissue diseases - Marfans, RA
PCKD
Inflammatory - Dilated left ventricle / Amyloidosis
Degeneration - Calcification / Fibrosis
Tx for MR
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
Marfans - underlying pathophysiology
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.
Managing Marfans
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
Signs on exam of marfans
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
Differentials for Marfans
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
Associated with pulmonary stenosis
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)
SIgns on exam of PS
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
Ehlers Danlos signs on exam
Fragile skin
Hyperextensible skin
Joint hypermobility
Mitral valve prolapse
Evidence of surgery from aneurysmal rupture or bowel perforation
It is autosomal dominant
CAUSES OF MITRAL VALVE PROLAPSE
Marfan syndrome
Ehlers–Danlos syndrome
osteogenesis imperfecta
polycystic kidney disease
Causes of restrictive cardiomyopathy
Myocardial
- idiopathic
- scleroderma
- amyloid
- Haemachromatosis
- glycogen storage disorders
- Gauchers
Endomyocardial
- endomyocardial fibrosis
- hyper- eosinophilic syndromes ( inc. lofflers)
- carcinoid
- malignancy or radiotherapy
- toxin related
Signs of mitral stenosis on exam
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
Causes of mitral stenosis
Degeneration
Rheumatic fever / IE
Congenital
Diagnosing rheumatic fever
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
Criteria for diagnosing infective endocarditis
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
Most common organisms in infective endocarditis
Staph aureus
Staph epidermis
Strep viridans
Strep bovis
Less commonly - HACEK organisms of fungal organisms
Aortic regurgitation
Quinckes signs
Collapsing pulse
Corrigans sign
De mussetts
Aortic thrill
Diastolic murmur
Heard loudest in tricuspid
Sat forward in expiration
Causes of AR
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.
HOCM - management
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)
Absent radial pulse
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)
HOCM- Mx
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
Poor prognostication in HOCM
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
Ix for HOCM
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)
