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
-Slow-rising pulse
-HF
-Late systolic peaking of a long murmur
-S4 present
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
Differentials include:
MR
TR
VSD (very loud, throughout precordium)
Although these would generate a PSM
Or:
PS (normal pulse, louder on inspiration)
HOCM (jerky pulse, normal S2, gets quieter if patient crouches)
ASD (fixed split S2)
Also:
Aortic sclerosis (normal pulse and S2 and no radiation)
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
Dimensionless index <0.25 (LVOT velocity/AV velocity)
N.B. Valve area should be normalised to BSA
Management of AS? (ESC)
Managed by cardiology team
-Serial echocardiograms and regular review in clinic to assess symptoms
-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
Intervention recommended in symptomatic patients
Or in asymptomatic patients if severe AS with LVSD or demonstrable symptoms on exercise testing
Decision of AVR versus TAVI made by the Heart Team
AVR versus TAVI (ESC)
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%)
CI to TAVI? (ESC)
Estimated life expectancy <1 year
Improvement of quality of life by TAVI unlikely because of comorbidities
Anatomical: inadequate annulus size (<18 mm, >29 mm) or inadequate vascular access or risk of coronary ostium obstruction
Thrombus in the left ventricle
Active endocarditis
TAVI/AVR work-up? (NHS)
MAY include ECG, CXR, TTE/TOE, CMR, exercise testing, cardiac CT (is the preferred imaging tool to assess anatomy for TAVI) and coronary angiogram
Complications of TAVI? (Paper)
AV block
Paravalvular leak
Bleeding
Stroke
AKI
Cardiac CT for TAVI? (ESC)
CCT to look for:
Extent of calcification
Aortic valve and annular anatomy
Risk of ostial obstruction
Feasibility of vascular access
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)
-Bloods (FBC, U+E, LFTs, CRP, coagulation, +/- BNP)
-CXR (often normal, calcified valve)
-Echo (mean gradient >40 or valve area <1 if severe, to assess LV function)
-Exercise testing (symptoms, fall in BP)
-CCT (calcification severity, annulus size, coronary/peripheral artery patency)
-Coronary 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
N.B. Valve gradient may be falsely low if LV impaired
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:
-Atypical organism
-Echo suggestive
-Embolic (splinters, Janeway) or immunological (GN, Osler’s, Roth’s) phenomena
-Predisposed e.g. prosthetic valve, IVDU, prior IE
-Pyrexia
If 2 major
1 major and 2 minor
OR 5 minor
Complications of IE? (Think about Duke’s)
SIRS
Direct valve destruction
Heart block
Septic emboli
Glomerulonephritis
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)
Managed by cardiology team with input from IE team +/- cardiac surgeons
A to E and consider ITU
Antibiotics according to local guidelines then based on organism grown
IE team input
Indicators for urgent surgery (ESC):
-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)
-Urinalysis (microscopic haematuria) and fundoscopy
-ECG (widening PR suggests aortic root abscess)
-Bloods (inflammatory markers, renal function as GN, liver function)
-Blood cultures x3
-Serology for culture negative
-TTE followed by TOE (if TTE positive to further characterise vegetations; if negative TTE but remains high clinical suspicion)
EDS complications? (BMJ)
EDS characterised by joint hypermobility, skin hyperextensibility, and tissue fragility
Complications include musculoskeletal and skin manifestations, cardiovascular and gastrointestinal features, autonomic dysfunction, features of chronic pain syndrome, and marfanoid habitus
Vascular EDS is associated with blood vessel rupture and visceral perforation
MVP associated