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
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
-HF
-Displaced apex
-S3
-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?*
Can be split into primary disease of the aortic valve leaflets versus dilation of the aortic root OR acute versus chronic
Chronic:
Degenerative (most common)
‘CRAP’
Congenital (bicuspid AV, peri-membranous VSD)
Rheumatic valve disease or syphilis (i.e. infectious)
Ankylosing spondylitis (and other inflammatory conditions) or Marfan’s (and other CTD such as OI)
(Pressure) Hypertension
Acute causes ‘DIP’:
Aortic dissection
IE
Prosthetic valve failure
Differentials of diastolic murmur?
AR
PR (not maximal at left lower sternal edge)
MS (Austin Flint) and TS
Atrial myxoma
How would you investigate a patient with AR?*
-ECG (lateral TWI)
-Bloods (FBC, U+E, CRP, LFTs, clotting +/- BNP)
-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 >65%)
-Coronary angiogram
If concerns regarding IE, urine dip, fundoscopy and blood cultures x3
How to manage a patient with AR?* (ESC)
Refer to cardiologists
-Regular review of symptoms and echos
-ACEi may improve symptoms if surgery not feasible
-Beta blockers remain the mainstay in Marfan’s
-Control CV risk factors
—
Replace valve when symptomatic (dyspnoea, reduced ETT)
Or if asymptomatic and echo features of LV enlargement or reduced function
In Marfan’s when root >50mm, operate regardless of AR severity
Acute surgery:
Dissection
Endocarditis
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?*
Cardiac: PDA
Non-cardiac: anaemia and pregnancy
Long-term management of patients with mechanical valves? (M)
Serial echos to assess function
Warfarinise and monitor INR
ESC advise prophylactic antibiotics
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, low-pitched 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 (TR, RV heave, loud P2) and R heart failure (sacral and pedal oedema)
-Pulmonary oedema
-Endocarditis
-Embolic complications (stroke risk high if MS and AF)
Indications for warfarin? (NHS)
Mechanical valves
AF in moderate-to-severe MS
LV thrombus
Antiphospholipid syndrome
What are the causes of MS?*
Rheumatic disease (commonest)
Senile degeneration (MAC)
SLE
Rarely carcinoid or congenital
How to investigate a patient with MS?*
History (exertional dyspnoea, palpitations, rheumatic fever)
-ECG (p-mitrale and AF)
-Bloods (FBC U+E CRP LFTs clotting +/- BNP)
-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)
Managed by cardiology team
Medical:
-Serial testing every 1-3 years
-Manage AF
-Diuretics, beta-blockers, digoxin, non-dihydropyridine calcium channel blockers and ivabradine can improve symptoms
Intervention if symptomatic
Or asymptomatic (but high risk of embolism or haemodynamic decompensation)
-Percutaneous
mitral valvotomy
-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 (dilated LV) and thrusting
-Thrill at apex
-High-pitched PSM loudest at apex radiating into axilla, loudest on expiration, soft S1
-S3
-Bruising
-Scars (prosthetic valve, IHD)
Severe if:
-AF
-Wide split S2
-Displaced apex beat
-Signs of LV failure
-Pulmonary hypertension (parasternal heave, P2, evidence of TR)
Differentials of PSM?
MR
MV prolapse
TR
VSD
If murmur at apex could be Gallavardin phenomenon (AS)
Causes of MR?*
Primary (degenerative disease of one or more components of the mitral valve) or secondary (annular dilatation) causes and either acute or chronic
C. DIF = CRAP
Chronic causes:
-Calcification/degenerative (most common)
-Ischaemic
-Functional e.g. dilated LV or LA enlargement in AF
-CTD e.g. Marfan’s
-Rheumatic
and
-Prolapse
Acute causes:
-Endocarditis
-Rupture of papillae
Investigation of MR?*
History (symptoms of HF, palpitations, fevers, history of MI)
-ECG/24 hour tape: AF, Q waves if previous infarction
-Bloods (FBC, U+E, CRP, LFTs, coagulation +/- BNP)
-CXR: cardiomegaly, LA enlargement, pulmonary oedema
-TTE/TOE: assess MR jet, LV/LA dilatation, reduced EF AND cause (prolapse, vegetations, torn chordae or ruptured papillae, fibrosis, infarction, LV size)
-Coronary angiography (CAD pre-surgery or ischaemic cause for MR)
If concerned about IE, do bloods, blood cultures x3, urine dip and fundoscopy
CMR may be useful in addition to assess severity and exercise testing
Echo signs of severe MR? (ESC)
Regurgitant jet >60 mL
Dilated left heart
Primary or secondary MR? (AAC)
Primary mitral regurgitation (MR) is a disease of the mitral leaflets or chords, whereas secondary MR is caused by disease of the left ventricle (LV) or left atrium (LA)
Management of MR?*
Managed by cardiology team
Medical:
-Serial echocardiograms and regular review in clinic to assess symptoms
-AF management
-CV risk factors
-If in heart failure, treat as per ESC guidelines
-In acute MR, nitrates and diuretics are used to reduce filling pressures and sodium nitroprusside reduces afterload
-Treat IE if this is the cause
Intervention considered if symptomatic
Or when asymptomatic with LV dysfunction
Decision surrounding surgery versus percutaneous intervention is made by Heart Team
Urgent surgery is indicated in patients with acute severe mitral regurgitation
Transcatheter edge to edge repair
MR surgery versus percutaneous?
Surgical:
Valve repair (preferable) or valve replacement
Percutaneous:
TEER (if high surgical risk) e.g. Mitraclip
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
6) Pericardial constriction (Kussmaul’s sign, rise in JVP on inspiration)
N.B. JVP is elevated if the vertical distance between the sternal angle and the highest point of the pulse is greater than 4cm
Differentials for peripheral oedema? (180)
-CCF
-CLD
-Renal impairment
-Hypoalbuminaemia (e.g. liver disease, GI losses, renal losses)
-Nephrotic syndrome
-Chronic venous insufficiency
-Lymphoedema (primary or secondary)
-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 on chromosme 15
Tall (arm span > height)
Arachynodactyly
High-arched palate
Scoliosis
Lens subluxation and/or cataract/glaucoma/retinal detachment
Pneumothorax
Pectus excavatum or carinatum
Dural ectasia
Hyper-extensible joints: Steinberg (thumb sticking out) and Walker’s sign (fingers round wrist)
Dilated aortic root/AR/dissection
MV prolapse progressing to severe MR
N.B. UPward lens dislocation
Management of Marfan’s? (BMJ)
Management:
-Family screening
-Beta blockers
-Should have a yearly echo and be under cardiology team (operate pre-emptively when root >50mm or if rapidly growing)
-May require ophthalmology or orthopaedic input and PT/OT
-Avoid intense isometric exercises, burst exertion, and collision sports
-Pregnancy counselling
Differential for Marfan’s? (BMJ)
-Homocystinuria (intellectual disability, DOWNward lens dislocation, pro-thrombotic)
-EDS
-Erdheim’s deformity
-Loeys-Dietz
Target INR for mechanical valves? (ESC)
Target INR should be based upon prosthesis thrombogenicity and
patient-related risk factors (e.g. AF, LV EF <35%, previous VTE, MVR)
Usually:
Aortic: 2 - 3
Mitral: 2.5 - 3.5
Antibiotics prophylaxis?
ESC advise AP for patients who are undergoing high risk dental procedures who have 1) prosthetic valves 2) previous IE 3) cyanotic congenital heart disease or who have undergone palliative intervention
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
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?*
DR L CC
Dilated RV and annulus due to left heart disease (most common)
Rheumatic fever and IE (especially in IVDU)
Lead implantation for implantable electronic devices
Carcinoid
Congenital e.g. Ebstein’s anomaly (atrialisation of the RV and TR)
How to investigate TR?*
History (fevers, IVDU, dental procedures, flushing, diarrhoea, history of rheumatic heart disease)
-ECG: p-pulmonale, AF, right-heart strain (large R wave V1, TWI V1-3)
-Bloods (FBC U+E CRP LFTS +/- BNP)
-CXR: double right heart border
-TTE: TR jet, RV dilatation
-Cardiac MRI (preferred technique for evaluation of RV size and function)
If concerns for IE, needs urine dip, fundoscopy and blood cultures x3
Management of TR?*
Managed by cardiology team
Medical: diuretics, rate control and anticoagulation AF, ACEi
Percutaneous: transcatheter TV repair
Surgical: valve repair
(Valve replacement usually only done if repair can’t be done)
Findings in PR? (180)
-Brief EDM loudest in left upper sternal edge on inspiration
If severe:
-Shorter duration of murmur (provided not cause by PH)
-N.B. Graham Steell is PR murmur in the context of severe PH, for duration of diastole
-Right heart failure
May also have associated TR
Investigations for PR? (180)
History (history of CHD and intervention, fevers, dental procedures, flushing diarrhoea, rheumatic fever)
-ECG (RVH)
-CXR (PA enlargement)
-Echo (severity, RV dysfunction, aetiology by looking at leaflets, annulus, PA)
-Cardiac MRI
If concerns for IE, needs bloods, fundoscopy, urine dip and 3x blood cultures
Management of PR? (180)
Managed by cardiology team
Diuretics
Surgery if progressive RV dilatation irrespective of symptoms and following ventricular arrhythmias and syncope
Can either be surgical or transcatheter
Causes of PR? (180)
Congenital:
Bicuspid valve
Acquired:
-Carcinoid
-Rheumatic fever
-IE
-After intervention for tetralogy or PS
-Pulmonary hypertension
-Pulmonary trunk dilatation due to Marfan’s
Clinical findings in PH? (180)
Loud P2
RV heave (RV hypertrophy)
Paradoxical splitting of S2
Graham Steel murmur (PR) or TR murmur
JVP distension (RV failure)
Turner’s cardiac complications? (BMJ)
Aortic coarctation and bicuspid aortic valves
Turner’s syndrome? (BMJ)
Disorder of female patients that is typically associated with the absence of one sex chromosome (45,X)
Short stature, delayed/absent pubertal development,
primary amenorrhoea,
congenital heart defects
Causes of PS? (180)
Congenital:
Tetralogy
Noonan’s (male version of Turner’s), Watson’s, William’s
Congenital rubella
Acquired:
Carcinoid
Rheumatic fever
N.B. Functional TR and VSD also associated with PS
Clinical signs of PS?*
-Raised JVP with giant A waves
-Left parasternal heave
-Thrill in pulmonary area
-Auscultation: high-pitched ESM loudest in pulmonary area on inspiration, widely split S2
-Signs of RV failure (ascites, peripheral oedema)
Severe if: inaudible P2, longer murmur duration
Symptoms of PS?
Dyspnoea
Reduced ET
Fatigue
Syncope
Differential for PS murmur?
AS
PDA
Investigations for PS?*
-ECG: p-pulmonale, RVH, RBBB
-Bloods: secondary erythrocytosis
-CXR: oligemic lung fields, large RA
-TTE: pressure gradient >10mmHg, severity, valve area, RV function and associated cardiac lesions
-Cardiac catheterisation: to guide intervention
How to manage PS?*
Managed by cardiology team
-Diuretics
-Percutaneous balloon pulmonary valvuloplasty
-Surgical valvuloplasty
Noonan’s syndrome? (BMJ)
Rare AD syndrome:
-Congenital heart defects including PS, ASD, HOCM
-Short stature
-Pectus excavatum
-Dysmorphic facial features
-Learning disabilities
-Impaired blood clotting
Carcinoid syndrome?*
Gut primary with liver mets secreting 5-HT into bloodstream
Diarrhoea, wheeze and flushing
Right heart valve fibrosis causing TIPS
Treatment with somatostatin analogue and cytoreduction
Tetralogy of Fallot?
VSD
Overriding aorta
RVH
Pulmonary stenosis
Management:
ACHD centre
Prostaglandin infusion at birth to keep ductus arteriosus open
Blalock-Taussig shunt to partially correct abnormality in infancy by anastomosing the subclavian artery to the pulmonary artery (causes absent radial pulse and thoracic scars)
Surgical correction: closure of VSD, resection of RV obstructive muscle tissue, enlarging outflow path
Complications: PR and right-heart failure, TR, arrhythmias
So later: PV replacement, arrhythmia management, manage aortopathy
Pregnancy counselling on need for specialist input
Investigation of TOF? (180)
ECG: RVH, indication for ICD
Holter: arrhythmia burden
Exercise testing: ventricular arrhythmias and exertional desaturation
Echo: PR, RV function
Cardiac MR: gold standard for RV size and function
Causes of absent radial pulse?*
Acute: embolism, aortic dissection, trauma e.g. previous radial artery sheath
Chronic: coarctation, Takayasu’s arteritis, some LVADs
Signs of AVR?*
If metallic:
-Midline sternotomy
-Metal prosthetic CC at S2 (heard after, not with the pulse)
-May be an OC and high-pitched ES flow murmur
Bioprosthetic:
-Midline sternotomy
-Often normal HS
Abnormal findings:
-AR
-Decreased intensity of the closing click (clot or vegetation)
Also:
May be bruising and anaemia
Signs of MVR?*
-Metal prosthetic CC at S1
-May be an OC in early diastole followed by low-pitched diastolic rumble
Abnormal findings:
-MR
-Decreased intensity of CC
Also:
May be bruising and anaemia
Metal versus porcine VR?*
Metal more durable but have to be on warfarin so more suitable for younger or already on warfarin e.g. for AF
Porcine therefore better for elderly or those at risk of haemorrhage
N.B. With the advent of ViV TAVIs for degenerative bioprosthetic valves, fewer metallic valves being implanted
How investigate a patient with valve replacement? (180)
-FBC (anaemia)
-Haemolysis screen
-Clotting studies for anticoagulation
-Renal and liver function
-CRP and blood cultures if any suspicion of IE
-ECG and CXR
-Echo to review valve function
Complications of valve replacement?*
-Thromboembolism 2%/annum despite warfarin
-Bleeding
-Bioprosthetic dysfunction and LVF (usually within 10 years)
-Haemolysis
-IE (early <2/12 Staphylococcus epidermidis, late Strep. viridans)
-AF (particularly in MVR)
Causes of TS?
Rheumatic fever
Carcinoid or congenital
How to investigate someone with a cardiac device? (180)
-ECG (CRT only indicated if broad QRS)
-CXR (number and type of leads, placement and integrity)
-Echo (indications for CRT and ICD)
-Device interrogation (arrhythmia, delivery of ICD therapies, device parameters e.g. battery life)
Complications of implantable devices?*
Local infection
Lead fracture or displacement
Pericardial effusion
Pneumothorax
Battery depletion
More chronic complications:
TR
IE
Primary prevention ICD?* (NICE)
Familial condition with high risk SCD (LQTS, ARVD, Brugada, HCM, complex congenital heart disease)
Post-MI in some cases if low EF and at risk of SCD, but need to wait at least 40 days
Secondary prevention ICD?*
VT or VF arrest
Haemodynamically compromising sustained VT
Sustained VT with LVEF <35%
Indications for pacing? (ESC)
Indications INCLUDE:
Symptomatic sinus node dysfunction
3rd or 2nd degree type 2 AVB, irrespective of symptoms
Reflex syncope with asystolic pauses
Coding for PM? (M)
First letter: chamber paced (A = atria, V = ventricle, D = dual)
Second letter: chamber sensed
Third letter: response to sensed event (inhibited/dual)
Fourth letter: rate response (adapts to changes in physical activity)
Differentials of device? (180)
Single or dual chamber PM (single is one in RA or RV; dual is one in each)
CRT-P
CRT-D
ICD
CRT indications? (ESC)
Recommended by ESC if:
-LVEF <35%
-Sinus rhythm and QRS >150ms and LBBB
-On optimal medical therapy
N.B. May also be considered in those with shorter QRS 130-149ms and non-LBBB morphology
Causes of constrictive pericarditis?*
4Ts:
TB
Trauma or surgery
Tumour, Therapy (radio)
Connective Tissue disease (SLE, RA)
Signs of constrictive pericarditis?*
Raised JVP
Kussmaul’s sign
Pulsus paradoxus
Pericardial knock
Ascites, hepatomegaly, peripheral oedema
What is Kussmaul’s sign? What is pulsus paradoxus?*
1) Paradoxical increase in JVP on INspiration
2) >10mmHg drop in systolic pressure on inspiration
How to investigate someone with ?constrictive pericarditis?*
-CXR: pericardial calcification, old TB, sternotomy wires
-Echo: high acoustic signal from pericardium, septal bounce, reduced mitral flow velocity on Doppler during inspiration
-Cardiac catheter: dip and plateau of diastolic wave form (square root sign), equalisation of diastolic RV and LV, RA and LA pressures, ventricular interdependence
-CT: thickened pericardium +/- calcification
-Cardiac MR: thickened pericardium, fibrosis, early diastolic flattening of the septum, enlarged atria
Cardiac MRI distinguishes RCM from constrictive pericarditis
Pathophysiology of constrictive pericarditis?*
Thickened, fibrous capsule reduces ventricular filling and ‘insulates’ the heart from thoracic pressure changes during respiration, leading to ventricular interdependence
Treatment of constrictive pericarditis?*
Medical: diuretics
Surgical: pericardiectomy
N.B. Differentiating constrictive pericarditis from restrictive cardiomyopathy is tricky but ventricular interdependence is highly diagnostic for the former
Causes of restrictive CM? (PasTest)
Defined as:
Diastolic failure
Systolic function usually preserved
Primary: Loffler’s
Secondary: amyloid, sarcoid, iron overload, scleroderma, radiation
ASD clinical signs?*
Raised JVP
Pulmonary area thrill
On auscultation: fixed split S2, pulmonary ESM
Signs of deterioration: pulmonary HTN (RV heave and loud P2) with cyanosis and clubbing would suggest Eisenmenger’s; CCF
Types of ASD?*
Primum: associated with AVSD and cleft mitral valve seen in Down’s
Secundum: commonest, defect in fossa ovalis
Investigations for ASD?*
-ECG: RBBB and LAD (primum) or RAD (secundum), AF
-CXR: small aortic knuckle, pulmonary plethora, double-heart border
-TTE/TE: site, size, shunt calculation, ameanability to closure
-Right heart catheter: shunt calculation (not always necessary)
Management of ASD?*
ACHD centre
Indications for closure:
-Symptoms (breathlessness, paradoxical embolus)
-Significant shunt (pulmonary-systemic blood flow ratio ≥1.5)
Contraindication for closure:
-Severe PH and Eisenmenger’s
Percutaneous closure device or surgical patch repair
Prophylactic antibiotics
Signs of VSD?*
-Thrill at left lower sternal edge
-High-pitched PSM at left sternal edge
-No audible A2
-S3 if large shunt
N.B. Loudness doesn’t correlate with size but with pressure gradient
-If Eisenmenger’s develops, murmur disappears
-‘Maladie de Roger’ if haemodynamically insignificant VSD but large pressure gradient
Consider:
-Associated lesions (AR, PDA, Fallot’s, coarctation)
-Pulmonary HTN (RV heave and loud P2) with cyanosis and clubbing would suggest Eisenmenger’s
-Endocarditis
N.B. May see scar on back from PA banding
Causes of VSD?*
-Cardiac lesion as part of an underlying syndrome (Down’s)
-Congenital (alone or with other lesions e.g. Tetralogy)
-Acquired (usually 5 days post-MI)
Investigation of VSD?*
History (previous MI, symptoms of HF, PH and previous surgeries)
-ECG: conduction defect (BBB)
-CXR: pulmonary plethora
-Echocardiography/CMR: site, size, shunt calculation, associated lesions
-Cardiac catheter: shunt size, pulmonary pressures, consideration of closure
Management of VSD?*
Refer to ACHD centre if congenital
Antibiotics prophylaxis
Small peri-membranous VSDs often close spontaneously
Contraindications to closure are Eisenmenger’s and severe PH
Larger shunts should be closed:
Surgical: pericardial patch
Percutaneous is an option: Amplatzer device
Indication for intervention (PasTest):
-In patients with evidence of LV volume overload and a pulmonary-systemic blood flow ratio ≥1.5 with no PAH
-Consider in history of IE
-Consider in VSD-related AR
-Post-infarct VSD
Complications of a VSD? (BMJ)
AR
IE
Arrhythmias (including post-operatively)
PH which can lead to Eisenmenger’s if untreated
Complications of ASD? (BMJ)
Paradoxical embolism
IE
Arrhythmias
PH which can lead to Eisenmenger’s if untreated
Right atrial and right ventricular enlargement
How does coarctation present? (BMJ)
It typically presents with upper extremity systolic hypertension or murmur
If the narrowing is severe, it may present in the newborn period once the ductus arteriosus closes as low cardiac output and shock (critical coarctation)
Coarctation signs?*
-Hypertension in upper limbs
-Prominent upper body pulses, weak femoral pulses, radio-femoral delay
-Heaving apex
-Systolic murmur left sternal border and radiating to back
Coarctation associations?*
Cardiac: VSD, bicuspid AV, PDA
Non-cardiac: Turner’s, intracranial aneurysms
Coarctation investigations?*
History (headache, nosebleeds, dyspnoea)
-ECG: LVH and RBBB (if associated VSD)
-CXR: rib notching, double aortic knuckle
-TTE: increased aortic flow velocity, associated lesions
-CT/CMR: anatomy for repair and associated lesions
Coarctation management? (BMJ)
-ACHD clinic
-Percutaneous angioplasty (+/- stenting) or surgery
-Anti-hypertensives
-Surveillance with MRA (late aneurysms and re-coarctation)
-Advice to avoid extreme isometric exercise
Signs of PDA?*
-Collapsing pulse
-Thrill left second intercostal space
-Thrusting apex
-‘Machinery murmur’ loudest below left clavicle
May be cyanotic if Eisenmenger’s and murmur will disappear
Complications of PDA?*
Eisenmenger’s
Endocarditis
Management of PDA?*
ACHD centre
Close surgically
Plug percutaneously
Impalpable apex beat?
Dextrocardia
Obesity
Pericardial effusion
Emphysema
Signs of HOCM?*
-Jerky pulse
-Double apical impulse
-Thrill at lower left sternal edge
-ESM at lower left sternal edge radiates throughout precordium, S4, accentuated standing from squatting
-May have an ICD
May be associated MV prolapse
May be Friedrich’s or myotonic dystrophy
Investigations for HOCM?*
History (palpitations, syncope, exertional dyspnoea, chest pain, FH)
-ECG: LVH with strain (TWI across precordial leads)
-CXR: often normal
-TTE: asymmetrical septal hypertrophy, systolic anterior motion of anterior mitral leaflet, LVOT gradient
-CMR: identifies apical HCM better than TTE and detects fibrosis
-Holter monitor and treadmill test
-Screen first degree relatives with ECG and echo
-Genetic test: sarcomeric proteins mutation
Differentials for LVH?*
Athletic heart
Hypertensive heart disease
HOCM
Anderson-Fabry disease
Amyloidosis
Management of HOCM?*
Managed by ICC team
-Avoid strenuous exercise, dehydration, vasodilators
-Genetic counselling of first degree relatives
-DVLA
If symptomatic and LVOT >30mmHg:
-Beta blockers and verapamil
-Cardiac myosin inhibitors
-PM
-Alcohol septal ablation or surgical myomectomy
If high risk SCD e.g. previous arrest, sustained VT, FH SCD:
ICD
Refractory:
Heart transplant
Prognosis of HCM?*
2.5% annual mortality rate
Poor prognostic factors include:
-Young age at diagnosis
-Syncope
-VT or arrest
-FH SCD
-Septum >30mm
-‘Burnt out’ LV i.e. reduced LVEF and fibrosis
Investigations for palpitations? (BMJ)
History (nature, syncope, cardiac history, family history, alcohol)
ECG (bradycardia, WPW, long QT, HOCM, prior ischaemia, Brugada)
FBC, electrolytes, TFTs, plasma (or urine) metanephrines
Ambulatory testing (Holter or loop)
TTE/CMR
Differentials for palpitations? (BMJ)
12!
-Sinus tachy
-Atrial tachy/atrial flutter/fibrillation
-Atrial/ventricular ectopics
-AVNRT/VT (idiopathic or in context of structural heart disease)
-WPW
-Long QT
-Brugada
-HOCM
-Hyperthyroidism
-Alcohol excess or anxiety
-Anaemia
-Phaeochromocytoma
Causes of HF? (ESC)
1) CAD
2) HTN*
3) Valve disease
4) Arrhythmias
5) Cardiomyopathies (hypertrophic* , restrictive* , dilated, Takotsubo, ETOH, cocaine, post-partum)
6) Congenital
7) Infective (viral myocarditis, HIV)
8) Drug-induced (anthracyclines)
9) Infiltrative (amyloid* )
10) Storage disorders (HH* , Fabry’s* )
11) Pericardial disease
12) Metabolic (thyroid)
13) Neuromuscular (muscular dystrophy, FA)
*Causes diastolic heart failure (restrictive, constrictive, HCM, HTN)
N.B. Thyrotoxicosis, pregnancy, nutritional deficiencies, anaemia can cause high output HF
Investigations for HF?*
History (dyspnoea, orthopnoea, PND, oedema, palpitations, angina)
BP
ECG: ischaemia, LBBB, AF
Bloods: anaemia, iron deficiency, raised BNP, U+Es (diuretics and cardiorenal syndrome), thyroid, lipids/HbA1C
CXR: increased CTR, interstitial and pulmonary oedema
TTE: LV size and function, associated lesions
Cardiac catheter: coronary patency
CMR: LV size and function, aetiology e.g. infiltrative
Treatment of HF?*
Under the heart failure team
Treat cause
Medical: fluid restriction, diuretics (bumetanide if gut oedema, metolazone in addition if severe), beta blocker, ACEi, MRA, SGLT2
Consider Entresto or ivabradine
Device: ICD/CRT
Surgery: volume reduction surgery, LVAD, heart transplant
Immunisations
Nutrition
Palliative input at end-stage
Indications for heart transplant? (ESC)
Patients with advanced HF refractory to medical/device therapy and who do not have absolute contraindications should be referred for consideration of heart transplantation
When no other therapeutic option, except for LVAD as BTT
CI to heart transplant?*
-Age >65 with other serious health condition
-Sepsis
-Malignancy
-Psychosocial factors
-Irreversible PH
Relative CI:
-High BMI
-Diabetes with EOD
-Severe peripheral or cerebrovascular disease, severe lung or kidney disease
Predominant AS versus predominant AR?
AS predominant (usually the case):
Low pulse volume
Slow-rising pulse
Apex beat minimally displaced and heaving
Narrow PP
Quiet S2
AR predominant:
Large pulse volume
Collapsing pulse (occasionally bisferiens)
Displaced, thrusting apex
Wide PP
Normal S2
Any cause AS, particularly bicuspid valve
Predominant MS versus predominant MR?
MS predominant:
Small volume pulse
Undisplaced tapping apex
Loud S1
No S3
MR predominant:
Sharp pulse
Displaced thrusting apex
Soft S1
S3 present
RHD
Midline sternotomy differentials? (180)
CABG (will not be a vein harvesting scar if LIMA)
Valve replacement or repair
Cardiac transplant
Congenital heart defect surgery
Lateral thoracotomy differentials (cardiac)? (180)
Mitral valvotomy
Coarctation repair
PDA ligation
BT shunt (subclavian to pulmonary artery to improve blood flow to the lungs)
Thrusting versus heaving apex?
TV
T = volume overloaded
H = pressure overloaded
How to manage AF? (BMJ)
If any adverse features: DCCV with anaesthetic support
If haemodynamically stable:
Rate control with beta blocker or rate-limiting non-dihydropyridine calcium-channel blocker e.g. diltiazem (unless LVSD) or sometimes digoxin monotherapy
Treat underlying cause
Anticoagulation depending on ORBIT or HAS-BLED
If onset <48 hours, consider early rhythm control
If the onset of AF is 48 hours or more, or is uncertain, anti-coagulate for a minimum of 3 weeks then elective electrical or pharmacological cardioversion
Lifestyle advice and manage CV risk factors
Consider AVN ablation (PVI) if refractory
Learn CHADSVASC and HASBLED
How to manage angina? (ESC/NICE)
Lifestyle and risk-factors
First-line (beta-blockers, CCBs) and second-line drugs (long-acting nitrates, nicorandil, ranolazine, ivabradine, trimetazidine)
Antiplatelets
Refer for angiography if:
-Evidence of extensive ischaemia on ECG
-Angina persists despite being on maximum therapeutic doses of two anti-anginal drugs and lifestyle interventions
When might rhythm control be preferred? (BMJ)
CHADSVASC, ORBIT HASBLED
Present prosthetic AV, AS, MR, AR, AV replacement, MS, AF, mitral prolapse, mixed AV disease, VSD.
Ox mini- TR, PS
