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1
Q

Classifying AF

A

Paroxysmal - recurrent episodes lasting longer than 30s but less than 7 days, self terminating
Persistent - lasting longer than 7 days or <7 days but requiring pharmacological/electrical cardioversion
Permanent- fails to terminate using cardioversion or is terminated but relapses within 24 hrs or long standing AF where cardioversion is not indicated or has not been attempted

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2
Q

Pathophysiology of AF

A

Rapidly firing foci cause propagating wavelets which lead to re-entrant circuits in the abnormal atrial myocardium. The AVN receives more electrical impulses than it can conduct whichleads to irregular ventricular rhythm

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3
Q

Investigations for AF

A

Bloods inc. FBC, all electrolytes and TFTS
ECG
echo
CXR

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4
Q

Clinical signs of aortic stenosis

A

Slow rising, low volume pulse
Narrow pulse pressure
Thrill in the aortic area
Crescendo/decrescendo ejection systolic murmur loudest in the aortic area during expiration and radiated to the carotids

Anaemia (chronic disease, angiodysplasia/Heyde syndrome)

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5
Q

Clinical findings of severe aortic stenosis

A

Soft and delayed A2
Delayed ejection systolic murmur
Fourth heart sound
High pitch
Evidence of cardiac failure

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6
Q

Differential diagnosis for systolic murmur

A

Aortic stenosis
Aortic sclerosis (shorter, softer, no radiation)
Mitral regurgitation ( pansystolic)
HOCM (young)
Pulmonary stenosis ( rare, young, >on inspiration)
VSD (post MI, high mortality)

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7
Q

Aetiology of aortic stenosis

A

-Degenerative and calcific (80% 70s and above)
- Bicupsid (presents younger 40s-60s)
- Rheumatic fever

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8
Q

Echo findings of severe aortic stenosis

A
  • Peak gradient across the valve of > 64 or a mean gradient of > 40
  • valve area <1
  • Dimensionless index (ratio of LVOT velocity to aortic valve)
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9
Q

ECG findings of aortic stenosis

A

Left ventricular hypertrophy
LBBB
10% of patients who have a TAVI go on to have a pacemaker so important to know about re-existing conduction abnormalities

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10
Q

When to consider TAVI

A

75 or over unless technically not suitable ( bad PVD, bad coronary artery disease)
Or <75 and not suitable for surgery (chest radiation, previous sternotomy, chronic liver disease, pulmonary hypertension, LVSD)

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11
Q

Work up for valve replacement

A

Routine bloods
Lung function tests
Angiogram
For TAVI: TAVI CT

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12
Q

Complications of TAVI

A

Conduction abnormality requiring PPM
Damage to vasculature
Stroke
MI

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13
Q

Signs of prosthetic valve

A
  1. Midline sternotomy scar without evidence of vein harvesting scar
  2. AF
  3. Infective endocarditis signs
  4. Bruising suggesting warfarin use
  5. Audible and palpable prosthetic click
  6. PPM ( 10% of pts with aortic valve replacement require PPM due to damage to AVN)
  7. Metallic aortic valve will have a soft systolic murmur (AR or loud AS would be abnormal)
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14
Q

Pros and cons of metallic vs. tissue valve

A

Metallic: more durable, life long Warfarin
Tissue: no warfarin, less durable (10-15 yrs)

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15
Q

Complications of valve replacement

A

Thromboembolism
Bleeding on warfarin
Haemolysis
Infective endocarditis
- <2 months post op staph epidermis is from the skin
- late infections are strep viridans by haematogenous spread
AF particularly if MVR

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16
Q

What INR range for metallic valve

A

Does depend on valve type
Mitral ball socket valve requires higher INR: 3-4
Bileaflet mitral: 2.5-3.5
Bileaflet aortic: 2-3

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17
Q

Clinical signs of tricuspid regurgitation

A

Raised JVP with giant CV waves
Thrill left sternal edge
Pansystolic murmur loudest at the lower left sternal edge loudest on inspiration

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18
Q

Causes of tricuspid regurgitation

A

Congenital: Ebstein’s anomaly (tricuspid valve dysplasia with a more apical position to the valve
Acquired: IE, functional due to right ventricular dilatation ( most common), rheumatic fever or carcinoid syndrome (would be associated with nodular hepatomegaly and telangiectasia)

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19
Q

How does tricuspid regurgitation present?

A

Pulsation sensation in the neck
Signs of right heart failure eg. Peripheral oedema and ascites

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20
Q

Investigations for tricuspid regurgitation

A

CXR: prominent right heart border due to enlarged right atrium
ECG: p-pulmonale, RVH
Echo

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21
Q

Treatment of tricuspid regurgitation

A

Diuretics, b blocker, ACEi
Valve repair or annuloplasty

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22
Q

Clinical signs of mitral regurgitation

A

AF, low volume pulse
Displaced apex beat
Thrill at apex
Pansystolic/ mid to late systolic murmur loudest at the apex radiating to the axilla loudest in expiration
May have raised JVP but this is normally related to co-existing TR

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23
Q

Causes of mitral regurgitation

A

Congenital
Dilated left ventricle
Calcification
Fibrosis
BE
Rheumatic
Connective tissue disorder
Post - MI
Amyloidosis

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24
Q

Investigating MR

A

ECG: p- mitrale, AF, prev. infarction
CXR: cardiomegaly, enlargement of the left atrium and pulmonary oedema
Echo

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25
Treatment for MR
If mild to mod- monitor with 2 yearly Echo. Need to intervene early Intervention guided by severity, symptoms, pulmonary hypertension and left ventricular function. Mitral clip Valve repair Valve replacement
26
Signs of mitral valve prolapse
Young, tall patient Associated with connective tissue disease (Marfans) and HOCM Late systolic murmur with early systolic ejection click Murmur accentuated by standing from a squatting position or straining
27
Evidence of severe mitral regurgitation
AF Thrusting displaced apex beat Palpable thrill Pansystolic murmur Echo findings both direct and indirect (LV impairment)
28
Aetiology of Marfans
Caused by mutations in the fibrillin-1 gene: 75% of mutations are autosomal dominant 25% of cases are spontaneous mutations and are associated with older paternal age
29
Pathophysiology of Marfans
Mutation in the FBN1 gene result in the production of abnormal fibrillin protein. This causes mechanical instability and loss of elasticity of connective tissues. This results in aortic dilatation.
30
Investigating Marfans
Echo CT or USS abdo CXR for pneumothoracices Slit lamp eye examination to assess for subluxed/dislocated lens or raised IOP Fibrillin- 1 blood test
31
Management of Marfans
Surveillance of aortic roof size with annual echo Surgical management of aortic root dilatation B blockers and angiotensin receptor blocker to slow aortic root dilatation Genetic counselling
32
Clinical signs of pulmonary stenosis
Raised JVP with giant A waves Right parasternal heave Thrill in the pulmonary area Ejection systolic murmur loudest in the pulmonary area on inspiration Radiates to infraclavicular region Widely split second heart sound Functional tricuspid regurgitation
33
Associated syndromes with pulmonary stenosis
- Tetralogy of Fallot ( PS, VSD, overriding aorta, and RVH) - Noonans - Carcinoid tumour ( the secreted mediators cause right- sided heart valve fibrosis causes tricuspid regurgitation and/or pulmonary stenosis)
34
Signs of noonans disease
Pulmonary stenosis HOCM Septal defects Short stature Learning difficulties Pectus excavatum Proptosis Ptosis Strabismus Characteristic facial features
35
Clinical signs of Marfans
Tall with long extremities Arachnodactyly ( can encircle their wrist with their thumb and little finger) Hyperextendible joints High arched palate Pectus carinatum or excavatum Scoliosis Aortic regurgitation Mitral valve prolapse Coarctation Inguinal hernia
36
Signs of ehlers danlos
Fragile skin Hyperextensible skin Joint hypermobility Mitral valve prolapse Evidence of surgery from aneurysmal rupture or bowel perforation It is autosomal dominant
37
Conditions associated with a VSD
Edwards Patau Down’s Turner Holt Oram Fetal alcohol syndrome Tetralogy of Fallot ( right ventricular hypertrophy, overriding aorta, VSD, pulmonary stenosis)
38
Pathophysiology of VSD
Left to right shunt Elevated right heart pressures and consequent pulmonary hypertension
39
Clinical presentation of VSD
Failure to thrive/ poor feeding Poor exercise tolerance Ejection systolic or Pansystolic murmur localised to left sternal edge Hyper dynamic apex beat Parasternal heave
40
Investigating a VSD
ECG - left ventricular hypertrophy - biventricular hypertrophy - pulmonary hypertension CXR - cardiomegaly - enlarged pulmonary artery ECHO
41
Management of VSD
High calorie diet Digoxin Failure treated with diuretics and ACEi Surgery
42
When is surgery indicated for VSD
Significant left to right shunt Other defects requiring cardiac surgery Pulmonary hypertension Endocarditis Acute VSD post MI
43
Pathophysiology of Eisenmenger
Severe irreversible pulmonary hypertension leads to reversal of the left- to- right shunt Resulting in cyanosis
44
Signs of Eisenmenger syndrome
Clubbing Central cyanosis Decreased murmur intensity Loud S2 Palpable P2 Widely split second heart sound Right ventricular heave Graham steel murmur ( due to pulmonary regurgitation)
45
Causes of Eisenmenger
VSD ASD PDA
46
Complications of Eisenmenger
Right ventricular failure Massive haemoptysis Cerebral embolism IE
47
Causes of VSD
Congenital Acquired - traumatic, post- operative or post- MI
48
What is a Blalock- Tausig shunt?
It partially corrects the Fallot’s abnormality by anastomosing the subclavian artery to the pulmonary artery There will be an absent/weak radial pulse and a left thoracotomy scar
49
Associations with TOF
DiGeorge syndrome Down’s syndrome Fetal alcohol syndrome Maternal diabetes Maternal phenylketonuria
50
Presentation of TOF
Ultrasound detection Cyanosis Feeding difficulties Failure to thrive Exertions dyspnoea Clubbing
51
Clinical signs tetralogy of Fallot
Loud second heart sound Crescendo- decresendo murmur Aortic ejection click Systolic thrill at the left sternal border
52
Management of tetralogy of Fallot
Timing of surgery depends on degree of cyanosis and symptoms at birth. Prostaglandin infusion to keep ductus arteriorsus patent. Primary surgical repair within the first year of life.
53
Complications of TOF (following surgery)
Pulmonary regurgitation requiring valve replacement Endocarditis Coagulopathy Polycythaemia Paradoxical embolism Arrhythmias
54
Complications of mitral valve prolapse
Thromboembolic events IE CVA
55
Causes of mitral valve prolapse
Myxomatous Marfans, ehlers danlos, osteogenesis imperfecta, PKD
56
Causes of restrictive cardiomyopathy
Myocardial - idiopathic - scleroderma - amyloid - Haemachromatosis - glycogen storage disorders - Gauchers Endomyocardial - endomyocardial fibrosis - hyper- eosinophilic syndromes ( inc. lofflers) - carcinoid - malignancy or radiotherapy - toxin related
57
Pathophysiology of restrictive cardiomyopathy
Increased stiffness of the myocardium causes ventricular pressures to rise precipitously with small increases in volume. The atria dilate in response and may develop AF. Infiltration of the conducting tissues leads to conduction abnormalities.
58
Investigating restrictive cardiomyopathy
Bloods ECG Cardiac catheterisation (increased right heart pressures) Echo- small ventricular chamber size, thickened left ventricular wall, restricted diastole Cardiac MRI Cardiac biopsy
59
Managing restrictive cardiomyopathy
Management of heart failure and AF Management of underlying cause Transplantation
60
Clinical signs of mitral stenosis
Malar flush AF Tapping apex (palpable first heart sound) Left parasternal heave if pulmonary hypertension present Opening snap of S1, then mid diastolic murmur Tricuspid regurgitation, right ventricular heave and loud p2 if pulmonary hypertension Embolic complications
61
Causes of mitral stenosis
1. Congenital 2. Acquired - Rheumatic - Senile degeneration - endocarditis
62
Investigating mitral stenosis
ECG: p- mitrale and AF CXR: enlarged left atrium, calcified valve, pulmonary oedema TTE: valve area <2cm2 for diagnosis, <1cm2 is severe
63
Management of mitral stenosis
1. Medical - if AF rate control and anti coagulation - diuretics 2. Surgery - indicated if symptomatic + severe lesion, if asymptomatic surgery considered if raised pulmonary pressure (>50) - valvotomy or replacement
64
How is rheumatic fever diagnosed?
1. Evidence of recent group A strep infection - positive throat swab, positive antigen test, raised antibody titre, recent episode of scarlet fever 2. Plus either 2 major criteria or 1 major and 2 minor 3. Major criteria - chorea - erythema marginatum - subcutaneous nodules - polyarthritis - carditis 4. Minor criteria - raised ESR/WCC, arthralgia, previous rheumatic fever, pyrexia, prolonged PR
65
How does rhuematic fever affect valves?
Causes endocarditis. Most common affects the mitral valve and more commonly causes regurgitation rather than stenosis.
66
How is rheumatic fever treated?
High dose aspirin Penicillin And then prophylactic PenV
67
How does IE present?
Malaise, tiredness, infective symptoms Fever Arthropathy Heart failure Splinter haemorrhages Oslers nodes (painful), Janeway’s lesions (painless) Clubbing Roth’s spots on fundoscopy Signs of arterial embolisation Vasculitic rash
68
What are Duke’s criteria
2 major or 1 major + 3 minor or 5 minor Major criteria: - 2 x blood cultures positive for typical organism - Positive echo finding Minor criteria: - predisposing heart condition or IVDU - fever - vascular phenomena (arterial emboli, pulmonary infarcts, ICH, janeway haemorrhages) - immunological phenomena (glomerulonephritis, oslers nodes, roths spots, rheumatoid factor) - micro evidence but not sufficient to be major criteria
69
Clinical signs of aortic regurgitation
Collapsing pulse secondary to wide pulse pressure Corrigans sign (visible neck pulsations) Quincke’s sign (nail bed capillary pulsation) De Mussets (head nodding) Hyper dynamic apex and displaced laterally Aortic thrill Early diastolic murmur loudest sat forward in expiration at lower left sternal edge May also be Austin- Flint murmur (mid-diastolic) due to regurgitant flow impeding mitral opening
70
Causes of aortic regurgitation
Congenital - biscuspid valve or perimembranous VSD Acquired - endocarditis, rhuematic fever, aortic dissection, Marfans, hypertension, ankylosing spondylitis
71
Investigations for aortic regurgitation
ECG: lateral T wave inversion CXR: cardiomegaly, widened mediastinum, pulmonary oedema Echo Cardiac catheterisation
72
Management of aortic regurgitation
ACEi or ARB to reduce after load Regular review Valve replacement if symptomatic and/or wife pulse pressure, ECG changes on ETT, or significant LV enlargement or reduced ejection fraction
73
Indications for aortic valve replacement (stenosis)
Symptomatic patient with PPD >50mmHg Moderate to severe AS undergoing CABG VT Valve area <0.6cm2
74
Clinical features of Marfans
Tall Increased arm span to height ratio Arachnodactyly Collapsing pulse Long narrow face Blue scera High arched palate, crowded teeth Pectus excavatum/carinatum Aortic regurgitation or mitral valve prolapse
75
Differentials for Marfans
Homocysteinuria Men 2b (Marfanoid body habitus, mucosal neuromas, medullary thyroid cancer, phaeochromocytoma Ehlers danlos
76
Clinical signs of HOCM
Jerky pulse Double apical impulse (atrial and ventricular contraction) Thrill at the lower left sternal edge ESM at lower left sternal edge radiating through the precordium accentuated by straining (Valsalva) or standing from squatting May be associated with Friedreich’s ataxia or myotonic dystrophy
77
Investigating HOCM
ECG: LVH with strain (t wave inversion across precordial leads) CXR: normal TTE: assymetrical septal hypertrophy, systolic anterior motion of the anterior mitral leaflet across the LVOT due to misalignement of septal papillary muscles Cardiac MRI Genetic testing: sarcomeric protein mutations
78
Management of HOCM
Avoid strenuous exercise, dehydration and vasodilators If symptomatic and LVOT gradient > 30mmHg: - b blocker - Pacemaker - alcohol septal ablation - surgical myomectomy If rhythm disturbance or high risk SCD: - ICD Refractory: Transplant Genetic counselling (autosomal dominant)
79
Poor prognostic factors for HOCM
Young age at diagnosis Syncope FHx of sudden death Septal thickness > 3cm
80
Investigating pulmonary stenosis
ECG: p- pulmonale, RVH, RBBB CXR: oligaemic lung fields and large right atrium TTE: assess severity, RV function and associated cardiac lesions
81
Management of pulmonary stenosis
Pulmonary valvotomy if gradient >70mmHg or RV failure Percutaneous pulmonary valve implantation Surgical repair/replacement
82
How does carcinoid syndrome affect the heart?
Gut primary with liver metastasis secrete 5HT into the blood stream. Secretory mediators cause right sided heart valve fibrosis resulting in TR and PS. Treat with ocreotide and surgical resection
83
What is a third heart sound?
heard in early diastole, during the rapid filling phase of the ventricle after the opening of the atrioventricular valve. It is a dull, low-pitched sound, best heard in the tricuspid area. Normal in the young. Causes include congestive cardiac failure and severe mitral or tricuspid regurgitation
84
What is a fourth heart sound?
occurs in late diastole and coincides with the contraction of the atria. It is generated by the left (or right) atrium contracting against a stiffened ventricle. Due to ventricular hypertrophy or myocardial ischaemia
85
What is the pathology in a pda?
Connection between the proximal left pulmonary artery and the descending aorta. Should close at birth.
86
Management of PDA
Percutaneous device closure
87
Clinical findings of PDA
Continuous machinery like murmur Radiates to left scapula Loudest in pulmonary area on expiration
88
Indications for PDA closure
Left ventricular volume overload Pulmonary hypertension
89
What are the indications for aortic root surgery in patients with Marfans?
Dilation > 50mm at aortic root Or > 45mm in a patient that has a family history of aortic dissection or if rate >3mm/year
90
Clinical signs of constrictive pericarditis
Raised JVP - rapid dominant y-descent due to high RA pressures and an early rise in RV diastolic pressure due to poor pericardial compliance - Kussmaul’s sign - paradoxical increase in JVP on inspiration Pericardial knock - high pitched snap (audible early S3 due to rapid ventricular filling into a stiff pericardial sac) Ascites, hepatomegaly, peripheral oedema Cause: TB, sternotomy scar, radiotherapy tattoos, RA, SLE
91
Investigations for constrictive pericarditis
CXR: pericardial calcification Echo: high acoustic signal from pericardium, septal bounce, reduced mitral flow velocity during insp. Catheterisation: dip and plateau of the diastolic wave form, equalisation of LV and RV diastolic pressures CT: thickened pericardium
92
Pathophysiology of constrictive pericarditis
Thickened, fibrous capsule reduces ventricular filling and ‘insulates’ the heart from intrathoracic pressure changes during respiration leading to ventricular interdependence (ie. Filling of one ventricular reduces the size and filling of the other)
93
Causes of constrictive pericarditis
TB Post CABG Radiotherapy Connective tissue disease: RA, SLE
94
Management of constrictive pericarditis
Diuretics, fluid restriction Pericardial stripping

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