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Cardio paces Flashcards

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
Q

Treatment for MR

A

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

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26
Q

Signs of mitral valve prolapse

A

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

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27
Q

Evidence of severe mitral regurgitation

A

AF
Thrusting displaced apex beat
Palpable thrill
Pansystolic murmur
Echo findings both direct and indirect (LV impairment)

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28
Q

Aetiology of Marfans

A

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

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29
Q

Pathophysiology of Marfans

A

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.

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30
Q

Investigating Marfans

A

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

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31
Q

Management of Marfans

A

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

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32
Q

Clinical signs of pulmonary stenosis

A

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

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33
Q

Associated syndromes with pulmonary stenosis

A
  • 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)
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34
Q

Signs of noonans disease

A

Pulmonary stenosis
HOCM
Septal defects
Short stature
Learning difficulties
Pectus excavatum
Proptosis
Ptosis
Strabismus
Characteristic facial features

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35
Q

Clinical signs of Marfans

A

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

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36
Q

Signs of ehlers danlos

A

Fragile skin
Hyperextensible skin
Joint hypermobility
Mitral valve prolapse
Evidence of surgery from aneurysmal rupture or bowel perforation

It is autosomal dominant

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37
Q

Conditions associated with a VSD

A

Edwards
Patau
Down’s
Turner
Holt Oram
Fetal alcohol syndrome
Tetralogy of Fallot ( right ventricular hypertrophy, overriding aorta, VSD, pulmonary stenosis)

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38
Q

Pathophysiology of VSD

A

Left to right shunt
Elevated right heart pressures and consequent pulmonary hypertension

39
Q

Clinical presentation of VSD

A

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
Q

Investigating a VSD

A

ECG
- left ventricular hypertrophy
- biventricular hypertrophy
- pulmonary hypertension
CXR
- cardiomegaly
- enlarged pulmonary artery
ECHO

41
Q

Management of VSD

A

High calorie diet
Digoxin
Failure treated with diuretics and ACEi
Surgery

42
Q

When is surgery indicated for VSD

A

Significant left to right shunt
Other defects requiring cardiac surgery
Pulmonary hypertension
Endocarditis
Acute VSD post MI

43
Q

Pathophysiology of Eisenmenger

A

Severe irreversible pulmonary hypertension leads to reversal of the left- to- right shunt
Resulting in cyanosis

44
Q

Signs of Eisenmenger syndrome

A

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
Q

Causes of Eisenmenger

A

VSD
ASD
PDA

46
Q

Complications of Eisenmenger

A

Right ventricular failure
Massive haemoptysis
Cerebral embolism
IE

47
Q

Causes of VSD

A

Congenital
Acquired
- traumatic, post- operative or post- MI

48
Q

What is a Blalock- Tausig shunt?

A

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
Q

Associations with TOF

A

DiGeorge syndrome
Down’s syndrome
Fetal alcohol syndrome
Maternal diabetes
Maternal phenylketonuria

50
Q

Presentation of TOF

A

Ultrasound detection
Cyanosis
Feeding difficulties
Failure to thrive
Exertions dyspnoea
Clubbing

51
Q

Clinical signs tetralogy of Fallot

A

Loud second heart sound
Crescendo- decresendo murmur
Aortic ejection click
Systolic thrill at the left sternal border

52
Q

Management of tetralogy of Fallot

A

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
Q

Complications of TOF (following surgery)

A

Pulmonary regurgitation requiring valve replacement
Endocarditis
Coagulopathy
Polycythaemia
Paradoxical embolism
Arrhythmias

54
Q

Complications of mitral valve prolapse

A

Thromboembolic events
IE
CVA

55
Q

Causes of mitral valve prolapse

A

Myxomatous
Marfans, ehlers danlos, osteogenesis imperfecta, PKD

56
Q

Causes of restrictive cardiomyopathy

A

Myocardial
- idiopathic
- scleroderma
- amyloid
- Haemachromatosis
- glycogen storage disorders
- Gauchers

Endomyocardial
- endomyocardial fibrosis
- hyper- eosinophilic syndromes ( inc. lofflers)
- carcinoid
- malignancy or radiotherapy
- toxin related

57
Q

Pathophysiology of restrictive cardiomyopathy

A

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
Q

Investigating restrictive cardiomyopathy

A

Bloods
ECG
Cardiac catheterisation (increased right heart pressures)
Echo- small ventricular chamber size, thickened left ventricular wall, restricted diastole
Cardiac MRI
Cardiac biopsy

59
Q

Managing restrictive cardiomyopathy

A

Management of heart failure and AF
Management of underlying cause
Transplantation

60
Q

Clinical signs of mitral stenosis

A

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
Q

Causes of mitral stenosis

A
  1. Congenital
  2. Acquired
    - Rheumatic
    - Senile degeneration
    - endocarditis
62
Q

Investigating mitral stenosis

A

ECG: p- mitrale and AF
CXR: enlarged left atrium, calcified valve, pulmonary oedema
TTE: valve area <2cm2 for diagnosis, <1cm2 is severe

63
Q

Management of mitral stenosis

A
  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
Q

How is rheumatic fever diagnosed?

A
  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
Q

How does rhuematic fever affect valves?

A

Causes endocarditis. Most common affects the mitral valve and more commonly causes regurgitation rather than stenosis.

66
Q

How is rheumatic fever treated?

A

High dose aspirin
Penicillin
And then prophylactic PenV

67
Q

How does IE present?

A

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
Q

What are Duke’s criteria

A

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
Q

Clinical signs of aortic regurgitation

A

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
Q

Causes of aortic regurgitation

A

Congenital
- biscuspid valve or perimembranous VSD
Acquired
- endocarditis, rhuematic fever, aortic dissection, Marfans, hypertension, ankylosing spondylitis

71
Q

Investigations for aortic regurgitation

A

ECG: lateral T wave inversion
CXR: cardiomegaly, widened mediastinum, pulmonary oedema
Echo
Cardiac catheterisation

72
Q

Management of aortic regurgitation

A

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
Q

Indications for aortic valve replacement (stenosis)

A

Symptomatic patient with PPD >50mmHg
Moderate to severe AS undergoing CABG
VT
Valve area <0.6cm2

74
Q

Clinical features of Marfans

A

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
Q

Differentials for Marfans

A

Homocysteinuria
Men 2b (Marfanoid body habitus, mucosal neuromas, medullary thyroid cancer, phaeochromocytoma
Ehlers danlos

76
Q

Clinical signs of HOCM

A

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
Q

Investigating HOCM

A

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
Q

Management of HOCM

A

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
Q

Poor prognostic factors for HOCM

A

Young age at diagnosis
Syncope
FHx of sudden death
Septal thickness > 3cm

80
Q

Investigating pulmonary stenosis

A

ECG: p- pulmonale, RVH, RBBB
CXR: oligaemic lung fields and large right atrium
TTE: assess severity, RV function and associated cardiac lesions

81
Q

Management of pulmonary stenosis

A

Pulmonary valvotomy if gradient >70mmHg or RV failure
Percutaneous pulmonary valve implantation
Surgical repair/replacement

82
Q

How does carcinoid syndrome affect the heart?

A

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
Q

What is a third heart sound?

A

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
Q

What is a fourth heart sound?

A

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
Q

What is the pathology in a pda?

A

Connection between the proximal left pulmonary artery and the descending aorta. Should close at birth.

86
Q

Management of PDA

A

Percutaneous device closure

87
Q

Clinical findings of PDA

A

Continuous machinery like murmur
Radiates to left scapula
Loudest in pulmonary area on expiration

88
Q

Indications for PDA closure

A

Left ventricular volume overload
Pulmonary hypertension

89
Q

What are the indications for aortic root surgery in patients with Marfans?

A

Dilation > 50mm at aortic root
Or > 45mm in a patient that has a family history of aortic dissection or if rate >3mm/year

90
Q

Clinical signs of constrictive pericarditis

A

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
Q

Investigations for constrictive pericarditis

A

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
Q

Pathophysiology of constrictive pericarditis

A

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
Q

Causes of constrictive pericarditis

A

TB
Post CABG
Radiotherapy
Connective tissue disease: RA, SLE

94
Q

Management of constrictive pericarditis

A

Diuretics, fluid restriction
Pericardial stripping

Paces (6 decks)

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