Cardiology Flashcards

1
Q

What are the stages in the NYHA classification of heart failure?

A

Class I: no limitation to normal activity
Class II: Mild limitation of ordinary level activity
Class III: Marked limitation of activity
Class IV: symptoms at rest

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2
Q

What investigations would you do for a patient with suspected CCF and what might you find?

A

ECG: q waves, LBBB, LVH, AF, non specific T wave changes
BNP
CXR: enlarged heart, upper lobe diversion, kerley B lines, pul.oedema
ECHO: systolic/diastolic dysfunction
Coronary angiography: rule out IHD
Exercise testing: for prognosis
Myocardial viability testing (thaliam scanning, cardiac MRI, stress ECHO or PET)

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3
Q

What are the steps in treatment for heart failure with LV systolic dysfunction?

A
1st line: ACE-i and Beta blocker
2nd line: can consider:
- aldosterone antagonist
- ARB
- hydralazine with nitrate (esp people of African origin)
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4
Q

When is cardiac resynchronisation therapy appropriate?

A
  • patients with LVEF <35% and wide QRS
  • Failed optimal medical treatment

Whether they have ICD or CRS with defibrillator or pacemaker depends on duration of QRS, presence of LBBB and NYHA class

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5
Q

Describe the neurohumeral changes that occur in chronic CCF?

A

Reduced CO -> renal hypoperfusion-> renin release -> converts angiotensinogen to angiotensin II-> causes vasocontriction and salt and water retention and also stimulates aldosterone. Vasoconstriction increases after load putting more pressure on heart.

Atrial natruetic peptides try to counteract this but are inadequate

Acutely the reduced CO -> activation of sympathetic nervous system -> high levels adrenaline and noradrenaline resulting in vasoconstriction, increased afterload, tachycardia which increases myocardial oxygen demand

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6
Q

What are the issues with prosthetic heart valves?

A

Heart failure or valve dysfunction
Endocarditis
Bleeding from anti-coagulation
Anaemia and jaundice from intravascular haemolysis

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7
Q

If the click is before the carotid pulse is the valve replacment mitral or aortic?

A

MV replacement- click before pulse

AV replacment- click after pulse

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8
Q

Discuss the advantages and disadvantages of biological and mechanical valves?

A

Biological:

  • Lack of long term anticoagulation (only 3 months)
  • HIgher incidence of degeneration and failure requiring re-operation
  • Offered to people >70yrs or >60yrs with sig co-morbitiy
  • Lifelong annual ECHO
  • aortic valves degenerate much quicker than mitral- ? due to higher pressures

Mechanical:

  • more durable
  • risk of thromboembolism higher in mitral position presumably due to lower flow.
  • anti-coagulation
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9
Q

What criteria are used for diagnosis of endocarditis?

A

Dukes criteria
2 major or 1 major + 3 minor or 5 minor

Major:
Persistantly positive blood cultlures for a typical organism (strep viridans, strep galloyticus, HACEK, staph aureus, enterococcus, staph epidermitis (prosthetic valve))
Positive ECHO for vegetiation or abcess
New regurgitant murmur
Single positive BC for C.Burnetii or serology

Minor:
Fever
IV drug user
Prosthetic heart valve
Vascular phenomonen- emboli, janeway lesions
Immunological phenomona: glomerulonephritis, roth spots, oslers nodes

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10
Q

What criteria are used in rheumatic heart disease

A
Jones criteria
2 major or 1 major + 2 minor
\+ evidence of recent strep infection
Major:
Carditis
Polyarthritis
Erythema marginatum
Syndenhams chorea
Subcutaenous nodules
Minor:
Previous rheumatic fever
CRP/ESR raised
Arthralgia
Fever
Prolonged PR

+ evidence of recent strep infection

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11
Q

What are the signs of endocarditis?

A

Due to infection

  • fever
  • murmur due to progressive valve destruction
  • Heart failure
  • Hepatosplenomegaly

Due to immune complex formation

  • Roth spots
  • Oslers nodes
  • Proteinuria, haematuria due to GN

Due to embolic phenomena

  • Janeway lesions
  • Splinter haemorrhages
  • Conjunctival haemorrhage
  • Mycotic aneurysm
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12
Q

What are the complications of endocarditis?

A

Direct tissue destruction- Valve failure, aortic root abcess causing heart block and occasionally septic pericarditis
Septic emboli phenomena- lung, brain, splenic abcess and formation of mycotic aneurysms
Renal failure due to sepsis or immune complex GN

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13
Q

What are the indications for surgical intervention in IE?

A

Uncontrolled infection
Haemodynamic instability due to valve failure
Increasing heart block due to aortic root abcess

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14
Q

What are the signs of a VSD?

A

Pansystolic murmur best heard at left sternal edge, 4th intercostal space with assoc thrill
If severe signs of RV ovberload with parasternal heave

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15
Q

What is a Maladie de Roger?

A

Very loud PSM heard at the left sternal edge, indicative of a very small VSD not requiring treatment

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16
Q

What antibiotic prophylaxis should be offered to somebody with a VSD?

A

None

Counselled that there is some risk of endocarditis after undergoing medical/dental procedures

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17
Q

How might somebody present who has an ASD?

A

3rd/4th decade with dyspnoea due to pul.htn and AF, palpatations or stroke (paradoxical embolism), RVF (oedema), resp infections

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18
Q

What are the signs of an ASD?

A
Features of a syndrome- Downs, Holt-Oram syndrome
Signs of previous stroke
Pulse- maybe AF
JVP- normal or raised in RVF
Soft ESM loudest in pulmonary area
PSM may be heard if TR secondary to RV overload
S2 fixed and widely split
Signs of RVF
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19
Q

What antibiotics would you use in IE- intial blind therapy?

A

Native valve: amox +/- gent

Prosthetic: Vanc +rifamp + gent

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20
Q

What would indicate a severe ASD?

A

RV overload
Pul.htn
AF as result of LA enlargement

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21
Q

What are the types of ASD?

A

Primum (atrioventricular septal defect)- often assoc with VSD

Secundum (most common)- enlarged foramen ovale, inadequate growth of septum secundum or excessive adsorption of septum primum

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22
Q

What investigations would you perform if you suspected ASD and what would results be?

A

ECG: AF, 1st degree AV block, LAD in primum defects, RAD in secundum defects
CXR: cardiomegaly, atrial enlargement, pul.arteries
TTE: may need to use bubble contrast
TOE: defines anatomy in more detail
Right and left heart catheterisation- rarely required, toassess pul. pressures and shunt ratio
Cardiac MRI- detailed anatomy

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23
Q

What is the management of ASD?

A

Most require no intervention
Close surgically or with percutaneous closure devices if:
- paradoxical embolism
- symptomatic
- evidence of significant shunt
- significant pul.htn- only offer closure if shown to be reversible

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24
Q

What is Lutembacher syndrome?

A

The coexistence of secundum ASD with rheumatic MS
Acquire the syndrome if develop an ASD as a complication of transseptal puncture required to get the valvuloplasty balloon into LA via RA

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25
Q

What is a PDA?

A

An abnormal connection between aorta and pul.artery

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26
Q

What are the signs of a PDA?

A

Differential cyanosis and clubbing- toes are cyanosed and clubbed, fingers are normal
Pulse: collapsing with wide pulse pressure
Apex: displaced and thrusting if large PDA
Left parasternal heave due to pul.htn
Palpable P2 (pul.htn)
Loud systolic crescendo murmur that peaks just prior to S2 and is heard best at left chest, more lateral to pul.area.

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27
Q

What are the causes of a PDA?

A
Congenital 
Neonatal rubella syndrome
 Prematurity
Born at high altitude
Prostaglandin E1 infusion
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28
Q

What would you find on investigation of a PDA?

A

ECG: biventricular hypertrophy, p.mitrale, AF. When shunt reverses- p.pulmonale

CXR: enlargement of left side of heart, may be able to visualise duct itself if calcified

ECHO: identify ductus and shunt fraction

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29
Q

What is the management of a PDA?

A

Tiny ducts that are not detected clinically can be managed conservatively.

Any duct which has been infected (endarteritis) should be closed once infection has resolved unless irreversible severe pul.htn
All other ducts should be closed unless evidence of irreversibly severe pul.htn

Achieved with percutaneous deployed duct closure device

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30
Q

What are the symptoms of co-arctation of aorta?

A
Fatigue particularly in legs
Intermittent claudication of legs
Symptoms of heart failure
Uncontrolled hypertension
Endarteritis
Chest pain due to atherosclerosis which develops at an accelerated rate
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31
Q

What are the signs of coarctation?

A

Left lateral thoracotomy scar due to surgical repair
Lower body may be relatively undeveloped compared to upper body. If it is preductal (proximal to left subclavian) then left arm may be smaller than right
Stigmata of endocarditis/endarteritis
Radio-femoral delay
Systolic thrills in the suprasternal notch
Signs of Turners syndrome
Systolic murmur usually louder over thoracic spine
ESM if bicuspid aortic valve
Continous systolic and diastolic murmurs audible though the precordium and back from collateral

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32
Q

What disease are assoc with coarctation?

A
Biscuspid aortic valve (85%)
VSD
MV prolapse
PDA
Aortic dissection
Turners syndrome
Neurofibromatosis type 1
Marfans syndrome
SAH
Shones syndrome
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33
Q

What might you find on investigation of coarctation of aorta?

A

ECG: LVH strain
CXR: rib notching due to formation of intercostal collaterals, 3 shaped descending aorta
TTE- identifys
TOE and cardiac MRI can give more information

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34
Q

What is the management of coarctation of aorta?

A

Primary percutaneous endovascular stenting
Surgical repair: resection of coarctation and end-end anastomosis if short segment or graft
Medical therapy- treat htn, modify risk factros

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35
Q

What are the indications for intervention/surgery in coarctation of aorta?

A

All symptomatic patients with a gradient >30mmHg across co-arctation should be offered tx
Asymptomatic patients with htn or signs of LVH
Any patient requiring cardiothoracic surgery for bicuspid aortic valve or aneurysm

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36
Q

What advice should patients with coarcation be given about exercise?

A

Avoid extreme isometric exercise (strength training) eg weight lifting due to risk of dissection.
Both treated and untreated
Encourage other type of exercise

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37
Q

What are the symptoms of hypertrophic cardiomyopathy?

A
Heart failure 
Syncope
AF
Chest pain 
Sudden death
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38
Q

What are the signs of hypertrophic obstructive cardiomyopathy?

A

Infraclavicular scar with underlying device- permanent dual chamber pacemaker to decrease LVOT gradient or ICD if at risk of sudden death

Pulse: jerky, bifid, may get AF
JVP: normal or A wave reflecting increased RA pressures
Apex: heaving in character, may be a double impulse reflecting a palpable atrial contraction
PSM due to MR
ESM at left sternal edge- made longer and louder on standing and shorter on squatting

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39
Q

What is the inheritance of hypertrophic obstructive cardiomyopathy?

A

AD
Mutations have been found in >11 sarcometic protein genes
Assoc with WPW

40
Q

What would you find on an echo in HOCM?

A

Echo - mnemonic - MR SAM ASH
•mitral regurgitation (MR)
•systolic anterior motion (SAM) of the anterior mitral valve leaflet
•asymmetric hypertrophy (ASH)

Assess severity of LVOT obstruction and pattern of hyperteophy

41
Q

What would you find on ECG in HOCM?

A
>95% abnormal
p-mitrale
LVH
Marked lateral T wave inversion 
Deep septal Q waves
AF
Occasionally WPW
42
Q

How would you manage somebody with HOCM?

A

Assess for RF of sudden death (any RF should be considered for ICD):

  • Previous arrythmogenic cardiac arrest
  • Sustained VT >30sec
  • FH of sudden cardiac death in 1st defree relative
  • Unexplained syncope (esp during exertion)
  • Abnormal BP response to exercise (hypotension, failure to rise)
  • Massive LVH >30mm thick
  • LV apical aneurysm
  • Dilated end stage heart failure

Medical treatments

  • beta blockers
  • Verapamil
  • Disopyramide- used for negative inotropic properties, always use with beta blocker
  • Diuretics

Treatment of LVOT obstruction
- NYHA III.IV due to LVOT obstruction (gradient >50mmHg) refractory to medical therapy- offered percutaneous alcohol ablation- causes a controlled MI of hypertrophied septum
- Surgical myomectomy
(no longer use dual ventricular pacing as shown not be effective)

43
Q

What is the defect in marfans syndrome and how is it inherited?

A

AD condition
Defect in fibrillin-1 gene on chromosome 15
Fibrillin is found in association with elastin and is required for proper formation of elastic fibres

44
Q

How would you diagnose Marfans syndrome?

A

Revised Ghent criteria 2010

Ectopia lentis + aortic root dilatation or systemic score > 7

Wrist AND thumb sign –3 (Wrist OR thumb sign –1)
▪ Pectus carinatum deformity –2 (pectus excavatum or chest asymmetry –1)
▪ Hindfoot deformity –2 (plain pes planus –1)
▪ Pneumothorax –2
▪ Dural ectasia –2
▪ Protrusio acetabuli –2
▪ Reduced US/LS AND increased arm/height AND no severe scoliosis –1
▪ Scoliosis or thoracolumbar kyphosis –1
▪ Reduced elbow extension –1
▪ Facial features (3/5) –1 (dolichocephaly, enophtalmos, downslanting palpebral fissures, malar hyoplasia, retrognathia)
▪ Skin striae –1
▪ Myopia > 3 diopters –1
▪ Mitral valve prolapse (all types) –1

45
Q

How do you manage a patient with Marfans syndrome?

A

Family screening to detect relatives, involvement in particular systems tends to run in families
Screening for aortic aneurysms
ECHO- aortic dimensions recorded
Beta blockers for anybody with abnormal aortic dimensions

46
Q

What are the indications for aortic root replacement in Marfans?

A

Symptomatic AR
ASymptomatic AR that meets criteria for surgery
Dilation of aortic root with a max diameter >45mm
Aortic growth rate of 1cm or more in a year

47
Q

How may marfans syndrome present acutely?

A

Aortic dissection- mortality of 50%

48
Q

How should people with Marfans be followed up?

A

Yearly ECHO to monitor aortic root. If FH of dissection or aorta starting to dilate then more frequently

49
Q

What is tetralogy of Fallot?

A

Congenital condition

  • Hypertrophy of RV
  • Over-riding aorta
  • VSD- large
  • RVOT obstruction (can be subvalvular, valvular or supravalvular)
50
Q

What signs might you see in somebody with tetralogy of fallot?

A

Sternotomy scar (from total correction)
Lateral thoracotomy scar (from original palliative Blalock Taussig shunt- one arm may be underdeveloped on side of shunt)
Device: Pacemaker or ICD

Assoc syndrome:

  • Long face, low set ears, cleft palate repair: DiGeorge syndrome
  • Unilateral pectoral hypoplasia- Poland syndrome
Pulse: radio-radiodelay due to shunt, may have AF, may be collapsing if AR
Corrigans pulse: suggest AR
JVP: may be elevated, may be CV waves in TR
Left parasternal heave: RV overload
May have a residual VSD- loud PSM
- PSM if MR or TR
- early diastolic murmur in AR
- ESM in pul. area due to PS

Signs of heart failure

51
Q

What would investigations show in tetralogy of fallot?

A

ECG: RAD, RBBB, if QRS >180ms risk of sudden death
CXR: dilated aorta, underdeveloped pul. vasculature, boot shaped heart
Holter: AF/VT
ECHO/cardiac MRI

52
Q

What shunts were used to palliate in tetraology of fallot and when?

A

Blalock Taussig shunt: originally sacrificed the subclavian artery anastomosed to ipsilateral pulmonary artery but now use Gore-Tex.

Waterson shunt: direct anastomosis between ascending aorta and main/right pulmonary artery. Used if subclavian too small for Blalock-Taussig shunt. The increased pul. flow can cause pul. htn

Potts shunt is similar and between descendin aorta and left pul. artery but is assoc with more complications

53
Q

Does a patient with Fallots tetralogy need genetic counselling?

A

Yes
15% have deletion of chromosome 22q11 (detected with FISH) which gives 50% chance of transmission
Otherwise only 2-3%

54
Q

What are the main late problems patients experience following complete repair of tetralogy of fallot?

A

Pul. regurg in those that had a transannular patch placed across the pul. valve annulus to repair RVOT obstruction: need PV replacement
AR and aortic valve diltation: due to distortion of aortic valve during VSD repair: AV/root replacement
Rhythm disturbance due to scarring
Residual VSD

55
Q

What is Kartageners syndrome?

A

Association of dextrocardia, situs inversus, bronchiectasis and male infertility
Rare AR condition
Dysfunction of dynein arm of cilia resulting in dysfunction and dysmotility of cilia.

56
Q

What are the signs of aortic stenosis?

A

LVH: heaving apex beat
ESM radiates to carotids
Slow rising pulse
If severe absent 2nd heart sound

57
Q

What are the causes of AS?

A

Calcific
Degeneration
Congential bicuspid valve
Rheumatic

58
Q

What are the differential diagnosis of AS?

A
Aortic sclerosis
Pulmonary stenosis
VSD
HOCM
Supravalvular obstruction
59
Q

What is the management of AS?

A

Asymptomatic 6-12m review
Consider valve replacement if mean gradient >40mmHg + sign of LV dysfunction or EF <45% or VT etc

TAVR (transcatheter) aortic valve replacement recommended in patient high surgical risk

60
Q

What are the complications of AS?

A

Endocarditis
HF
AV block due invasion of calcium from valve ring into HIS-purkinje system
Embolic events

61
Q

How would you differentiate sclerosis of stenosis?

A

Overlaps with mild AS
- normal pulse character
Normal 2nd heart sound
Elderly person

62
Q

What are the signs of aortic regurgitation?

A
Collapsing pulse
Wide pulse pressure
Cardiac dilatation
Early diastolic murmur
Corrigans waterhammer pulse
De mussats sign (head nodding)
Duroziers sign (murmur over femorals)
Quinckes sign
63
Q

What are the causes of aortic regurgitation?

A

Acute

  • IE
  • Aortic dissection
  • Prosthetic heart valve
  • Ruptured sinus of valsalva
  • Acute RF

Chronic

  • Bicuspid aortic valve
  • Marfans syndrome
  • Aorto-annular ectasia
  • Rheumatic HD
  • Endocarditis
  • Seronegative spondyloarthridites
  • Syphillis
  • Osteogenesis imperfecta
64
Q

What is the management of AR?

A

Acute AR: surgery unless very mild

Chronic AR
Symptomatic: surgery
Asymptomatic: HF , EF <50%, Regurg fraction >50% or dilated heart

Medical mx: ACE-I and diuretics

65
Q

Does a longer murmur mean more severe AR?

A

Shorter murmur means more severe flow of block back in LV which finishes sooner

66
Q

What signs would suggest severe AR?

A

Clinically dilated heart
Signs LVF
Very wide pulse pressure
Short murmur

67
Q

What are the signs of mitral stenosis?

A

Malar flush (due to severe pul.htn, low CO, elevated venous pressure)
Inframammary/left thoracotomy scar from previous mitral valvotomy
Bruising (warfarin due to AF)
AF
JVP raised with a wave if SR and pul.htn
Apex: tapping
Left parasternal heave due to RV pressures
Palpable P2 (pul.htn)
Mid diastolic murmur heard best in left lateral psotion at end expiration with bell
MV opening snap
May be a decrescendo early diastolic murmur from PR (Graham Steel murmur)

68
Q

What are the causes of MS?

A

Rheumatic fever (>90%)- around 40% have multivalvular disease with next most common being aortic.
Degenerative- severe calcification
Congenital
Methysergide or ergot derived (eg Cabergoline)
Non-valvular eg myxoma in LA, large vegetation

69
Q

How can you tell mild MS from severe MS?

A

Mild MS: presence of sinus rhythm, no signs of pul.htn, no signs of RVF, short diastolic murmur

Severe MS: AF, pul.htn, short gap between S2 and opening snap, long mid diastolic murmur, signs of RVF/pul.congestion

70
Q

How do you manage MS?

A

Offer percutaneous balloon mital valvuloplasty or MVR
IF moderate or severe disease ( mean gradient >5 mmG or mitral valve area <1.5cm)
PASP >50mmHg
NYHA class 2 or above

71
Q

What determines the suitability of a valve for percutaneous balloon mitral valvulopasty?

A

Leaflet mobility, thickening and subvalvular calcifications are assessed on scale of 1-4 (Wilkins score)
Score >8 is unlikely to be ameanable
Increases severity of MR by one grade

72
Q

How do you manage MS presenting in pregnancy?

A

Severe MS- advise against pregnancy
Asymptomatic pts present in mid trimester with tachycardia
Severe MS with NYHA III/IV treat with PBMV under TOE guidance to minimise radiation exposure

73
Q

What is the normal mitral valve area

A

4-5cm

74
Q

What are the signs of mitral regurgitation?

A
Sternotomy scar or lateral thoracotomy scar: malfunctioning prosthetic valve, previous CABG suggesting ischaemic cause.
Marfans
Bruising (warfarin)
AF
JVP- CV waves pul.htn
Apex: visible and displaced, volume overload
Left parasternal heave
Palpable P2
Soft S1
PSM radiating to axilla
Widely split S2 if severe
Mid systolic click if prolapse
75
Q

What are the causes of MR?

A
Degenerative
Function (LV dilatation)
Ischaemia
Rheumatic
MV prolapse- Marfans, idiopathic, connective tissue disease, hereditary
76
Q

How would you differentiate mild and severe MR?

A

Mild: Sinus rhythm, no signs of HF

Severe MR: AF, thrusting apex beat, signs of pul.htn-TR, HF

77
Q

What is the management of MR?

A

MV repair surgery or replacement with chordal preservation is recommended for:

  • EF 30-60%
  • New AF
  • PASP >50mmHg
  • If EF <30% surgery only recommended if durable repair with chordal preservation is likely.

Percutaneous transcatheter MV clip repair- new for those not fit for surgery with less complications

78
Q

Why is repair preferable to replacment?

A

Disconnection of subvalvular apparatus without chordal preservation can result in up to 20% decline in LV function

79
Q

How is ischaemic MR managed differently?

A

Where leaflets are normal but MR results from restrictions of movement due to ischaemic injury and dysfunction of subvalvular apparatus. Has a worse prognosis and threshold for treatmetn is lower. If undergoing CABG should have a MV replacement at same time.

If severe LVF and not suitable for sugery consider for dyssynchrony and biventricular pacing +/-ICD

80
Q

What are the causes of tricuspid regurgitation?

A

Commonest is pulmonary hypertension

Acute: endocarditis, trauma
Chronic: endocarditis, ebsteins anomaly, rheumatic fever, carcinoid

81
Q

What are the signs of tricuspid regurgitation?

A

CV wave in JVP
Parasternal heave
PSM heard best at left sternal edge on inspiration
Pulsatile hepatomegaly

82
Q

How do you manage tricuspid regurgitation?

A

Medical diurectics
Treat cause of pul.htn
WHen oedema uncontrollable valve replacment is an option but poor outcomes and last resort

83
Q

How do you differentiate TR from MR?

A

TR is assoc with a CV wave and murmur gets louder on inspiration with no signs of LVF

84
Q

Why is a CV wave so called?

A

C wave is point of closing of TV and if TR is present it will start and this point and continue through RV systole- period of R wave

85
Q

Why is tricuspid endocarditis more common in IVDU?

A

LIkely that particulate matter used to cut illegal drugs damages TV and predisposes to it.

86
Q

What are the causes of tricuspid stenosis?

A

Carcinoid
Rheumatic fever- unusual
Congenital- partial tricuspid atresia

87
Q

What are the signs of tricuspid stenosis?

A

Raised JVP
Peripheral oedema
Mid diastolic murmur- rarely audible, if suspected ask to examine liver for carcinoid

88
Q

What are the causes of pulmonary stenosis?

A

Congenital (virtually all)- maternal rubella, fallots tetralogy

Ocassionally rheumatic fever and carcinoid

89
Q

What is the management of pulmonary stenosis?

A

Most cases seen are very mild and require no treatment or will have already undergone corrective procedures
Baloon valvuloplasty of RVOT is frequently used in infant and more recently percutaneous valve replacment has been developed

90
Q

How do you differentiate PS from AS?

A

Murmur is heard louder in inspiration, best heard in pulmonary area, signs of RVF if severe.

91
Q

What are the waves on JVP called and what do they represent?

A

A wave: Atrial contraction

  • Absent in AF
  • Large with increased atrial pressure, tricuspid stenosis, pul.htn

C wave: Cuspid closing

X descent: atrial relaxation (steep in tamponade)

V wave: passiVe filling
- giant in TR

Y descent: triscuspid opens
- slow in TR

92
Q

What is familial hypercholesterolaemia?

A
AD, 1/500
Mutation in gene code for LDL receptor
Classically tendon xanthoma
Cholesterol >7.5
LDL >4.9
Normal triglycerides 

Treat: statins

93
Q

What is primary hypertriglyceridaemia?

A

Usually due to polygenic factors

May also be due to lipoprotein lipase deficiency
Eruptive xanthoma

Management
fibrates are generally used first-line
statins do reduce triglyceride levels and they may be indicated, particularly if there is mixed hyperlipidaemia

94
Q

What are the different types of mechanical heart valves?

A

Have evolved from early Starr- Edwards (ball and cage) valve which is no longer in clinical use
Through single leaflet tilting disc valves to modern bileaflet tilting disc valves which are designed with small leaks or wash jets which together with their less thrombogenic coating allow use of less intense anticoagulation.

95
Q

What are the INR targets for patients with valve replacments?

A

Bileaflet aortic- INR=2.5
Bileaflet mitral- INR=3.0

Ball and cage (Starr-Edwards) INR=3.5