Cardiology Flashcards
AV replacement indications?
AS
AR
IE with failed medical therapy
Clinical signs AS? Symptoms?*
-Loud, high-pitched, crescendo-decrescendo ESM loudest in aortic area during expiration and radiating to carotids
-Low volume, slow-rising pulse
-Narrow pulse pressure
-Systolic thrill in aortic area
-Heaving apex beat
If severe:
-Soft or absent S2
-Reverse split S2
-Late systolic peaking of a long murmur
-S4 present
-Slow-rising pulse
-HF
N.B. Intensity of murmur doesn’t correlate with severity
If complications:
-Signs LV dysfunction (dyspnoea, displaced apex, bibasal crackles)
-Signs of pulmonary HTN and RV failure (this is pre-terminal)
-Conduction problems (acute suggests endocarditis, chronic suggests calcified aortic node)
-IE signs (splinters, Osler’s, Janeway, Roth spots)
Angina
Syncope
Breathlessness
Differential diagnosis ESM?*
AS
Aortic sclerosis (normal pulse and S2 and no radiation)
PS
HOCM
ASD
Aortic flow in high-output clinical states e.g. pregnancy or anaemia
Severe AS on echo?
Mean gradient >40mmHg, peak
velocity >4.0m/s, valve area <1cm
Aortic valve calcium scoring can also be used on CT
N.B. Valve area should be normalised to BSA
Management of AS? (ESC)
-No medical therapies influence the natural history of AS
-Patients not suitable for intervention should be treated as per ESC heart failure guidelines
-Coexisting hypertension
should be treated to avoid additional afterload, although medication
(particularly vasodilators) should be titrated carefully to avoid symptomatic hypotension
Asymptomatic:
Good dental health
Counsel on symptoms
Regular review 6 months to 2 years depending on severity to assess symptoms and echo to assess gradient and LV function
Intervention recommended if severe aortic stenosis and LVSD OR demonstrable symptoms on exercise testing
Symptomatic:
Decision of AVR versus TAVI made by the Heart Team
AVR +/- CABG (preferred if lower surgical risk <75 years and EuroSCORE II <4%)
TAVI if high surgical risk or inoperable (>75 years, EuroSCORE II
>8%)
Tell me about the grading of murmurs?
Grade 1 to 6
3 is moderately loud murmur with no thrill
Most common causes of aortic stenosis?*
Degenerative calcification (most common)
Congenital (e.g. associated with bicuspid AV, subaortic membrane and William’s syndrome)
Rheumatic valve disease (rare now)
What does ESM mean?*
Crescendo-decrescendo murmur after S1, ending before S2, peaking in mid-to-late systole
What is aortic sclerosis?*
Mild thickening or calcification of the AV and can be distinguished from AS by absence of outflow tract obstruction
Complications of AS?*
-LVF
-Sudden death (predominantly in symptomatic individuals)
-Pulmonary HTN
-Arrhythmias
-IE/Embolic events
-IDA (Heyde’s syndrome)
How would you investigate ?AS patient?*
History (dyspnoea, syncope, angina)
-ECG (LVH, conduction defect)
-CXR (often normal, calcified valve)
-Echo (mean gradient >40 or valve area <1 if severe, to assess LV function)
-ETT (symptoms, fall in BP)
-CT (calcification severity, annulus size, coronary/peripheral artery patency)
-Cardiac catheter (transvalvular gradient and angiography)
N.B. Stress echo helpful as can help decide whether impaired LV due to AS (may benefit from surgery) or intrinsic myocardial disease with incidental AS finding
Conditions associated with AS? (Ox mini)
Coarctation (RF delay)
Other valvular disease if RF
Angiodysplasia (Heyde’s)
Cardiac causes clubbing?
Congenital cyanotic heart disease
Infective endocarditis
Atrial myxoma
Duke’s critera?*
Major:
-Typical organism in 2 blood cultures
-Echo showing abscess, large vegetation, dehiscence
Minor:
-Pyrexia
-Echo suggestive
-Embolic (splinters, Janeway) or immunological (GN, Osler’s, Roth’s) phenomena
-Predisposed e.g. prosthetic valve
-Atypical organism
If 2 major
1 major and 2 minor
OR 5 minor
Causative organisms for IE? (180)
Most commonly:
1) Staph. Aureus (most common, most virulent)
2) Strep. Viridans
3) Coagulase negative Staph
HACEK
Culture negative (Bartonella, Brucella and Coxiella Brunetii)
Fungal
Of note:
Strep. Gallolyticus associated with colon Ca
Management of IE? (BMJ)
A to E and consider ITU
Antibiotics according to local guidelines then based on organism grown
IE team input
Indicators for urgent surgery:
-HF
-Uncontrolled infection
-High risk of embolism or established embolism
Consider pacing if aortic root abscess
In future:
Advice on prophylactic antibiotics
Investigations for IE? (180)
History (previous endocarditis, cardiac history, dental history, IVDU, immunosuppression)
-Bloods (inflammatory markers, renal function as GN, liver function)
-Blood cultures x3
-Urinalysis (microscopic haematuria)
-Serology for culture negative
-ECG (12 lead ECG suggests aortic root abscess)
-TTE followed by TOE (if TTE positive to further characterise vegetations; if negative TTE but remains high clinical suspicion)
Clinical signs of aortic incompetence?*
-Collapsing pulse reflecting a wide pulse pressure
-Apex beat is thrusting and displaced laterally
-Thrill in aortic area
-A soft, high-pitched EDM loudest at left lower sternal edge with patient sat forward on expiration
Severe if:
-EDM short
-Collapsing pulse and wide pulse pressure
-S3
-HF
-Austin-Flint murmur is when MDM at apex due to regurgitant murmur impeding the mitral opening
Eponymous signs:
Corrigan’s (pulse), Quincke’s (nails), De Musset’s (head)
N.B. Collapsing pulse PP > diastolic pressure
Causes of AR?*
Degenerative (most common)
‘CRAP’
Congenital (bicuspid AV, peri-membranous VSD)
Rheumatic valve disease or syphilis
Ankylosing spondylitis or Marfan’s
(Pressure) Hypertension
Acute causes ‘DIP’:
Aortic dissection
IE
Prosthetic valve failure
Differentials of diastolic murmur?
AR
PR
MS and TS
How would you investigate a patient with AR?*
-ECG (lateral TWI)
-CXR (cardiomegaly, pulmonary oedema, widened mediatstinum)
-CT (size of aortic root, dissection, coronary patency)
-TTE/TOE (LVEF, LV size, aortic root size/dissection, vegetation, jet width)
-Cardiac catheter (coronary patency usually pre-op)
How to manage a patient with AR?* (ESC)
Medical management:
-ACEi may improve symptoms if surgery not feasible
-ACEi, ARBs, beta blockers useful post-surgery if HF or hypertension persist
-Beta blockers remain the mainstay in Marfan’s
-Regular review of symptoms and echo
Surgical management:
-Replace valve when symptomatic (dyspnoea, reduced ETT)
-Or if asymptomatic and echo features of LV enlargement or reduced function
In Marfan’s when root >45mm, operate regardless of AR severity
Acute surgery:
Dissection
Endocarditis
Differential for AR? (Ox mini)
PR
Prognosis in AR?*
Asymptomatic with EF >50%: 1% mortality at 5 years
Symptomatic with all 3 criteria met 65% mortality at 3 years
Severity on echo for AR? (ESC)
-LV dilation
-Regurgitant volumes >60mls
-Regurgitant orifice area >30mm2
Other causes of a collapsing pulse?*
Pregnancy
PDA
Anaemia
Clinical signs of MS?*
-Malar flush
-Tapping apex (palpable first heart sound)
-Left parasternal heave if pulmonary HTN or enlarged LA
-Loud S1, opening snap, mid-diastolic murmur heard best at apex in left lateral position on expiration
-Bruising
Severe if:
-Irregularly irregular pulse
-OS occurs nearer A2 (left atrial pressure higher, opens MV earlier) or is inaudible
-Longer MDM
-Signs of pulmonary hypertension or RV failure
Complications:
-Pulmonary HTN and R heart failure (TR, RV heave, loud P2, sacral and pedal oedema)
-Pulmonary oedema
-Endocarditis
-Embolic complications (stroke risk high if MS and AF)
What are the causes of MS?*
Rheumatic disease (commonest)
Senile degeneration (MAC)
SLE
Rarely carcinoid or congenital
Differential diagnoses for MS?*
Austin-Flint murmur
L atrial myxoma
How to investigate a patient with MS?*
History (exertional dyspnoea, palpitations, rheumatic fever)
-ECG (p-mitrale and AF)
-CXR (enlarged LA (splayed of carina), calcified valve, pulmonary oedema)
-TTE/TOE (valve area and gradient, cusp motility, calcification and LA thrombus, RV failure and pulmonary HTN (>50mmHg is severe))
-Cardiac catheter (pre-surgery)
How would you tell MS is severe from echo?*
Valve area <1cm2, gradient >10mmHg
Management of MS? (ESC)
Medical:
-Manage AF
-Diuretics, beta-blockers, digoxin, non-dihydropyridine calcium channel blockers and ivabradine can improve symptoms
-Serial testing every 1-3 years
Intervention if symptomatic or asymptomatic (but high risk of embolism or haemodynamic decompensation)
-Percutaneous
mitral commissurotomy
-Or mitral valve replacement
Counselling on pregnancy
Prognosis of MS?*
Latent asymptomatic phase 15-20 years
NYHA >II 50% mortality at 5 years
Tell me about rheumatic fever?*
Jones diagnostic criteria
Beta-haemolytic streptococcal infection
Rest, high-dose aspirin and penicillin
Prophylaxis to avoid recurrence
Signs of MR?*
-Pulse: AF small volume
-Apex: displaced and volume-loaded
-Palpation: thrill at apex
-Auscultation: high-pitched PSM loudest at apex radiating into axilla, loudest on expiration
-S3
-Bruising
-Scars (prosthetic valve, IHD)
Severe if:
-AF
-Wide split S2
-Displaced apex beat and signs of LV failure
-Holosystolic
-AF (LA enlargement)
-Pulmonary hypertension
Differentials of PSM?
MR
TR
VSD
If murmur at apex could be Gallavardin phenomenon (AS)
Causes of MR?*
C. DIF = CRAP
Chronic causes:
-Calcification/degenerative (most common)
-Dilated LV
-Infiltration
-Fibrosis e.g. post-MI
-CTD
-Rheumatic
and
-Prolapse
Acute causes:
-Endocarditis
-Rupture of papillae
Investigation of MR?*
History (symptoms of HF, palpitations, fevers, history of MI)
-ECG: p-mitrale, AF, Q waves if previous infarction
-CXR: cardiomegaly, LA enlargement, pulmonary oedema
-TTE/TOE: assess MR jet, LV dilatation, reduced EF AND cause (prolapse, vegetations, torn chordae or ruptured papillae, fibrosis, infarction, LV size)
-Cardiac MR: volume of MR, LV dimension and infarct
-Cardiac catheter: CAD pre-surgery or ischaemic cause for MR
N.B. If concerned about IE, do bloods, urine dip and fundoscopy
Echo signs of severe MR? (ESC)
Regurgitant jet >60 mL
Dilated left heart
Management of MR?*
Medical:
-Serial testing
-AF management
-If in heart failure, treat as per ESC guidelines
-In acute MR (MEDICAL EMERGENCY), nitrates and diuretics are used to reduce filling pressures and sodium nitroprusside reduces afterload
-Treat IE if this is the cause
Surgery if symptomatic or asymptomatic with LV dysfunction
Percutaneous:
TEER (if high surgical risk) e.g. Mitraclip
Surgical:
Valve repair (preferable) or valve replacement
Urgent surgery is indicated in patients with acute severe mitral regurgitation
Differentials for midline sternotomy without vein harvesting scar?
CABG and LIMA
Valve repair/replacement
Cardiac surgery for structural heart defects
Causes of a raised JVP? (180)
1) CCF or isolated right-heart failure (e.g. RV infarction or PE)
N.B. Former requires diuresis, latter requires fluids
2) PH
3) TR (giant V waves)
4) SVC obstruction
5) Cardiac tamponade and pericardial constriction (Kussmaul’s sign, rise in JVP on inspiration)
Differentials for peripheral oedema? (180)
CCF
Hypoalbuminaemia (e.g. liver disease, GI losses, renal losses)
Renal impairment
Nephrotic syndrome
Chronic venous insufficiency
Pelvic mass with impaired lymphatic drainage
What is an S3? What is an S4?
Tell me about Marfan’s syndrome and the cardiac complications?
AD condition defects in fibrillin-1 gene
Tall
High-arched palate
Arachynodactyly
Upwards lens dislocation
Arm span > height
Pectus excavatum
Dilated aortic root
Family screening
Beta blockers
Should have a yearly echo
Prognosis of MR?*
25% mortality at 5 years if symptomatic
MV prolapse?*
Young lean tall women
Caused by myxomatous degeneration
Associated with CTD e.g. Marfan’s (90%), EDS, osteogenesis imperfecta, PCKD and HOCM
Often asymptomatic and benign but may present with CP, syncope, palpitations
May rarely present with severe MR, AF, emboli
On auscultation:
-Mid-systolic ejection click
-Pan-systolic murmur that gets louder up to A2
-Accentuated by standing from squatted position
EDS?
Signs of TR?*
-Raised JVP with giant CV waves
-Left sternal thrill
-Auscultation: high-pitched PSM loudest in tricuspid area on inspiration, radiating to right sternal border, reverse split S2, S3
-May be signs of RV failure: pulsatile liver, ascites, peripheral oedema
-Pulmonary hypertension: RV heave and loud P2
N.B. Comment on whether any signs of IVDU
Causes of TR?*
Dilated RV and annulus due to left heart disease (most common)
Rheumatic fever and IE (especially in IVDU)
Carcinoid
Cardiac implantable electronic device-lead
implantation
Congenital e.g. Ebstein’s anomaly (atrialisation of the RV and TR)
