Cardiology Flashcards
Peripheral signs infective endocarditis
- splinter haemorrhages
- oslers nodes (finger pulp, tender)
- Janeway lesions (palm)
- Roth spots (retina)
- splenomegaly
- haematuria
Aortic stenosis Vs sclerosis
AS - radiation to carotids, may have slow rising pulse
Sclerosis - murmur only
Aortic stenosis causes
- Age/calcification
- Congenital (bicuspid) +/- coarctation
- Rheumatic/streptococcal
Dukes criteria
MAJOR
- BCs with typical org
- Echo evidence - abscess/vegetation/dehiscence
MINOR
- Fever >38
- Suggestive echo
- Predisposition e.g. prosthesis
- Embolic phenomena
- Vasculitic phenomena e.g. ESR
- Atypical org on BC
AS signs besides murmur
- Slow rising pulse
- Narrow pulse pressure
- => “parvus et tardus” carotid = weak/slow
- Delayed A2
AS replacement indications
- Symptoms
- LVEF <50%
Or consider if: - Flow >4m/s
- Gradient >40mmHg
- Valve area <1cm2
AS intervention options
- SAVR (surgical aortic valve replacement) - metallic vs bioprosthetic. Preferred for young, fit. Can be midline or minimally invasive sternotomy.
- TAVI (transcatheter/femoral aortic valve intervention/replacement). Preferred for elderly.
- Discussion with patient! & MDT - anaesthetics, interventional cardio, cardiothoracics, geriatrician.
Balloon valvuloplasty can be used as a stopgap
Aortic Regurg peripheral signs
- Quinkes - nail bed pulsation
- Corrigan - vegorous neck pulsatioi
- De Mussets - head nodding
- “Pistol shot” femoral pulse sounds
- Collapsing/waterhammer pulse
- Wide pulse pressure
AR causes
Acute valve:
- Endocarditis
Chronic valve:
- Rheumatic fever
Acute root:
- Type A dissection
- Trauma
Chronic root:
- Marfan’s -dilation
- HTN - dilation
- Syphilis - aortitis
- Ank spond - aortitis
- Vasculitis
AR valve replacement criteria
- Acute
- pulse pressure>100
- LVEF<50%
- ECG changes
Reason for wide S2 splitting in MR
Aortic valve shuts sooner as it empties rapidly
Causes MR
Primary
- CTDs (ED, Marfan’s, OI)
- Degenerative
- Infective endocarditis
- (Rheumatic heart disease)
Secondary
- Dilated cardiomyopathy
- Ischaemic cardiomyopathy
JVP waves
A wave - atrial systole
C - tricuspid closure
X descent - ventricular systole
V wave - atrial filling
Y descent - Tricuspid opening
https://gramproject.com/wp-content/uploads/2021/01/JVP-waveform.png
AS medical management
If symptoms, replace.
Follow up:
- Echo every 6/12, 1 year, or 3 years dep on severity
Medications:
- Statins
- BP control, avoiding ACE if haemodynamically significant disease. Avoid vasodilators.
- BB good option in heart failure
Clinical features severe AS
Any symptoms.
Or:
- Slow rising, low volume pulse
- Narrow pulse pressure
- Quiet/absent S2
- High pitch, long duration murmur
- LV heave
- S4 in LVH
Mitral stenosis causes
- Rheumatic fever most common
Rarer: - Congenital
- Carcinoid syndrome
- SLE
- Amyloid
HCM inheritance
Usually AD
MYH7 (B myosin) or MYBPC3 (myosin binding protein chain)
Young cardio patient syncope
HCM
Channelopathies (LQT, brugada, WPW)
Other congenital cardiac conditions
Broad categories congenital heart disease
1 - L-R shunts (acyanotic)
2 - R-L shunts (cyanotic)
3 - Obstructive
Eisenmenger’s syndrome
- Any congenital L-R shunt
-> Increase pulmonary vascular resistance
-> Pulmonary hypertension
-> Pulmonary/right heart remodelling
-> R pressure > L
-> Shunt reversal and cyanosis, polycythaemia
Usually around age 20-40
Congenital L-R in order of prevalence
- VSD (outlet, inlet, perimembranous, muscular)
- ASD (sinus venosus, ostium primum, o secundum, unroofed coronary sinus)
- Patent ductus arteriosus (aorta-pulm circ, bypasses pulm circ as maternal blood entering RA -> lower body cyanosis, machinery murmur)
- APVC (anomolous pulmonary venous connection) Rare.
Causes of VSD
- Congenital (most common CHD)
- Ischaemic
VSD signs
Pansystolic murmur LLSE. Loud 2nd HS if pulm HTN
ASD signs
Systolic murmur at L upper sternal edge
Fixed S2 splitting
Why does ASD cause fixed S2 splitting
ASD equalises pressures in both ventricles, negating physiological variation of splitting with respiration
Explain physiological S2 splitting
- S2 = aortic & pulmonary valves
- At end of systole, aortic pressure > pulmonary artery pressure (V pressure similar)
- Therefore A shuts before P
In inspiration: - Flow of blood into R circulation increased
- Prolonged RV ejection time -> later P2
- Flow of blood out of L circulation decreased
- Therefore shorter ejection rime -> A earlier
Leads to increased split on inspiration
R-L congenital shunts
- Tetralogy of fallot
- Transposition of great arteries (presents in hours of life, emergency surgery)
- Epsteins anomoly (TV misplacement -> RA/LA shunt)
Tetralogy of fallot
- Outlet VSD
- RVOT obstruction/PS
- RV hypertrophy
- Overriding aorta
Congenital
Presents in childhood with cyanosis, dyspnoea, poor growth
Pulmonary stenosis causes
Most commonly congenital
- Noonan’s
- Tetralogy of Fallot (subvalvular)
- Congenital rubella
Acquired:
- Rheumatic heart disease
- Carcinoid syndrom
Pulmonary stenosis management
- Percutaneous valvuloplasty
- Valve replacement
Or if not moderate/severe
- Serial echo/monitoring
MR signs and diff from MV prolapse
- PSM at apex into axilla, loudest expiration
- Wide S2 splitting as LV empties quickly leading to early AV closure
- S3 = rapid LV filling (?Pulm HTN)
- AF common
- ?JVP if pulm HTN
- LV enlargement, hyperdynamic
Prolapse - S1, then click, then murmur as valve prolapses
Prolapse also louder on squatting - this reduces afterload, so reduced pressure to cause prolapse
MR surgery indications
- Acute e.g. ruptured papillary muscles in MI
- Symptomatic
OR
- LVEF <60% or LVESD >40mm
- SPAP >50mmHg (pulmonary hypertension)
Secondary - more complicated!
- Involve MDT
- Often if other intervention (e.g. CABG), valve surgery will be done at same time
MR management
Acute: Afterload reduction:
- Diuretics
- Nitroprusside
- Aortic balloon pump
- Surgery
Chronic:
- Monitoring. No medical therapy shown to improve outcome in preserved LVF
- Medical heart failure treatment (ACE, BB, spiro)
- Surgery
Marfan’s syndrome genetics
Autosomal dominant
Fibrillin-1 gene for collagen generation
Marfan’s findings on examination
Hands:
- Arachnodactyly
- Thumb protrudes from fist, thumb/little finger around wrist
- Touch thumb to wrist
Face:
- High-arched palate
- Retinal detachment
- Myopia, cataracts
Chest:
- AR, MR
- Pectus excavatum/carinatum
- PTx drain scar
- Aortic surgery scars
Marfan’s cardiac complications
- AR
- MR
- Aortic vessel/root dilatation -> dissection
Marfan’s aortic root surgery indications
> 4.5-5cm root diameter, or growing >3mm in a year
Marfan’s management
- Betablockers and ARB/ACEi to reduce aortic root dilatation
Noonan features
Usually presents in infancy with reduced growth/failure to thrive
Short stature
Webbed neck
Facies - down-slanted palpebral fissure, low set ears
Strabismus, ptosis, amblyopia
Wide-spaced nipples
Pulmonary stenosis
Cryptorchidism
Noonan genetics
Autosomal dominant
Noonan cardiac
Pulmonary stenosis most common
ASD, HCM, VSD
Conditions associated with mitral valve prolapse
- Marfan’s
- Ehler’s Danlos
- Osteogenesis imperfecta
- Polycystic kidney disease
