Cardio Flashcards
Causes of clubbing
Cardiac - congenital heart disease, IE
Resp - ILD/ TB/ CF/ Bronchiectasis
Gastro - IBD
Familial
What is a PDA?
The ductus arteriousus is a connection between the proximal left pulmonary artery and the descending aorta just distal to the left subclavian artery in the foetus which allows the blood to bypass the lungs which are filled with amniotic fluid. After birth this closes to become the ligamentum arteriosus. Failure to close = PDA
Is PDA associated with congenital heart disease?
In adults it is usually an isolated finding but can be associated with congenital heart disease
When are patients with PDA considered for surgery?
If they develop either LV volume overload or RV pressure overload will be considered for closure
PDA murmur
Continuous machine like murmur ‘rolling thunder’ (quieter flow during diastole)
Heard best 2nd IC left sternal edge but also posteriorly (heard when listening to lung bases)
Eisenmengers syndrome features
Clubbing, central cyanosis, loud and widely split 2nd heart sound with associated RV heave (and no murmur = original left to right shunt has now reversed)
What is Eisenmengers syndrome?
Longstanding left to right shunt from congenital heart disease
Typically VSD/ ASD or PDA
causing pulmonary hypertension, reversal of the shunt and then cyanosis
Complications of Eisenmengers
RVF
Paradoxical embolism
IE
Haemoptysis
Hypoxia
Congenital syndromes associated with VSD
Downs
Edwards
Di George
What happens to murmur of VSD in Eisenmengers?
Murmur decreases as pulmonary hypertension ensues and subsequent reversal of shunt
Pulmonary hypertension management (3)
Endothelial antagonists - bosentan
Phosphodiesterase 5 inhibitors - sildenafil
Prostanoid infusions
Differentials for VSD murmur (4)
ASD - wide fixed split 2nd heart sound
MR - Pansystolic murmur loudest on expiration at apex and radiates to axilla
TR - pansystolic murmur heard best on inspiration at lower left sternal edge
PS - ejection systolic murmur loudest on inspiration in pulmonary area
Common causes of constrictive pericarditis
Viral or bacterial
Post surgery eg after CABG
After TB
Radiation
Causes of restrictive cardiomyopathy
Primary: endomyocardial fibrosis (Loeffler’s syndrome - eosinophils infiltrate the endocardium)
Systemic: sarcoidosis, scleroderma, haemochromatosis, malignancy, amyloidosis
Why do we need to differentiate between constrictive and restrictive cardiomyopathy?
Briefly - very diff management plans so constrictive the mainstay is surgery
Restrictive cardiomyopathy signs
Minimal unless RVF
What is restrictive cardiomyopathy?
Rare disease of myocardium
Diastolic dysfunction with restrictive ventricular physiology but systolic function usually preserved
Rhythm control of AF
Flecainide only if no structural heart disease
Or DCCV
Chadvasc
Score >1 = anticoagulation
For AF stroke risk
CCCF
HTN
>/= 75
DM
Stroke/ TIA - 2 (the rest are 1 point each)
Risk of stroke with AF if chadvasc = 0
1.9%
=1 then 2.8%
=2 then 4%
= 3 then 5.9% etc
2nd most frequent indication for valve surgery
MR
Most frequent aetiology of mitral regurgitation
Degenerative i.e. prolapse or flail leaflet
Secondary / functional MR is
Where valve leaflets and chordae are structurally normal and MR results from LV abnormality ie dilated or ischaemic cardiomyopathy
Management of secondary MR
No evidence that valve replacement helps so medical management ie of heart failure
HASBLED
HTN
Renal disease
Liver disease
Stroke
Prior major bleeding or predisposition to
Labile INR
>65
Medications ie anti platelets nsaids
Alcohol excess
Score of greater than 2 = high risk for major bleeding
Indication for anti coagulation in mitral valve disease
Presence of AF or previous emboli
How to diagnose IE?
Dukes criteria
2 major and 5 minor
Both major / 1 major and 3 minor / all 5 minor
Major: positive echo (mobile vegetation), specific bacteria on 2 separate blood cultures
Minor: fever >38, other positive BCs, different echo findings, septic embolism, janeway lesions/ osler nodes
Bacteria in IE
Staph aureus
Strep viridans, strep bovis
HACEK group
How does rheumatic disease most commonly affect the mitral valve?
Mixed valve disease
ECG of mitral valve disease
AF
P mitrale due to left atrial enlargement
LVH
CV waves in JVP
Tricuspid regurgitation
How might murmur change with severe mitral disease?
If pulmonary hypertension becomes pronounced then can develop tricuspid regurgitation
Differential for diastolic murmur
Austin flint murmur
Low pitched diastolic rumbling
Severe aortic regurgitation where the regurgitant jet hits the mitral valve
Best heard at apex so can be mistaken for mitral stenosis
What’s usually the predominant lesion in mixed aortic valve disease?
Usually aortic stenosis with a mild degree of regurgitation- ie when the valve stiffens there’s some leaking
Aortic regurgitation caused by (simple pathophys)
Either valvular pathology ie stenosis or pathology of the aortic root
Acute AR caused by
IE
trauma
Aortic dissection
Why does collapsing pulse happen?
Wide pulse pressure from regurgitant volume in AR
Signs attributed to wide pulse pressure in AR
De maussets- head bobbing
Quinkes- capillary pulsation in fingertips and lips
Mullers - uvular pulsation
Exacerbate AR murmur
Sit up hold breath in expiration
Why do you roll the patient to left in CV exam?
To elicit MS murmur
Mid diastolic murmur, difficult to hear
Use of bell useful for low frequency murmurs
Why do we sit patients forwards during the CV exam?
Bring heart forwards to help to listen for AR best heard in expiration at lower left sternal edge
HOCM murmur
Ejection systolic caused by LVOTO
Or
Pan systolic murmur caused by systolic anterior of mitral valve resulting in MR
Causes of cardiac hypertrophy
Pressure overload is HTN, Aortic stenosis
HOCM
Fabreys
Amyloidosis
HOCM treatment
Symptoms - beta blocker
Myosin inhibitors
Assess risk of cardiac death ? Need for ICD
Genetics - familial evaluation
Severe disease - septal reduction therapy (myomectomy or alcohol)
Congenital heart disease causes
TOF
Pulmonary atresia
Tricuspid atresia
Pulmonary stenosis
Eisenmengers syndrome
Ebstein anomaly
TGA
TOF surgery
Balloon valvuloplasty typically done to relieve pulmonary stenosis
Surgery to improve blood flow to the lungs (plumbing the left subclavian into the pulmonary artery distal to the stenosis) right lateral thoracotomy scar
Repair VSD - midline sternotomy scar
TOF features
4
VSD
pulmonary stenosis
Over riding aorta
RVH
How does apex differ between AR and AS?
Pressure overload conditions cause heaving apex ie AS, HTN, LVH
AR is a volume overload problem so this causes a thrusting apex beat
Severe AS signs
Slow rising low volume pulse
Narrow pulse pressure
Absent 2nd heart sound
Longer murmur
Radiation to carotids
Evidence of LVH ie heaving apex beat and 4th heart sound
What is AS gradient mean?
The gradient is the pressure difference across the aortic valve so severe AS = >40 mm Hg gradient
Criteria for severe AS
Peak velocity >4 m/ sec
Gradient >40 mm Hg
Size <1 cm2
Features of TR
Raised JVP with giant V waves
Thrill left sternal edge
Pan systolic murmur Loudest on inspiration
Pulsatile liver, ascites, peripheral oedema
If PHTN then loud P2 and RV heave
Causes of TR
Congenital; ebsteins anomaly
Acute; IE, trauma
Chronic; PHTN, IE, rheumatic fever, carcinoid
Severe AS features
Soft A2
Delayed ESM
LV heave
Carotid radiation
4th HS w significant LVH
ESM ddx
AS
sclerosis
HOCM
PS
PS features
ESM loudest in inspiration in pulmonary region
Soft delayed P2
Palpable thrill
RV heave and prominent a wave of JVP if severe
PS causes
Commonest is rubella
TOF, turners, noonans
Rarely carcinoid
Acyanotic heart disease
ASD
small VSD
Coarctation
PDA
MV prolapse murmur
Ejection click
Pan systolic murmur
Loudest at apex in left lateral position
Drugs to avoid in severe AS
Vasodilators i.e. nitrates sildenafil ace inhibitors
Marfans genetics
Autosomal dominant secondary to defects on fibrillin gene
MR features
Af
Small volume pulse
Displaced Apex
Thrill at Apex
Pansystolic murmur at Apex radiating to the axilla
Signs of LVF
VSD why does murmur get louder on expiration?
In left to right shunt - in expiration the venous return to the left side of the heart increases so the character of the murmur increases
Pinch osler
Slap Jane
Osler nodes - painful on finger tips
Janeway lesions - painless palm rash
