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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
What is a PDA?
An abnormal connection between aorta and pul.artery
26
What are the signs of a PDA?
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.
27
What are the causes of a PDA?
``` Congenital Neonatal rubella syndrome Prematurity Born at high altitude Prostaglandin E1 infusion ```
28
What would you find on investigation of a PDA?
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
29
What is the management of a PDA?
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
30
What are the symptoms of co-arctation of aorta?
``` 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 ```
31
What are the signs of coarctation?
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
32
What disease are assoc with coarctation?
``` Biscuspid aortic valve (85%) VSD MV prolapse PDA Aortic dissection Turners syndrome Neurofibromatosis type 1 Marfans syndrome SAH Shones syndrome ```
33
What might you find on investigation of coarctation of aorta?
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
34
What is the management of coarctation of aorta?
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
35
What are the indications for intervention/surgery in coarctation of aorta?
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
36
What advice should patients with coarcation be given about exercise?
Avoid extreme isometric exercise (strength training) eg weight lifting due to risk of dissection. Both treated and untreated Encourage other type of exercise
37
What are the symptoms of hypertrophic cardiomyopathy?
``` Heart failure Syncope AF Chest pain Sudden death ```
38
What are the signs of hypertrophic obstructive cardiomyopathy?
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
39
What is the inheritance of hypertrophic obstructive cardiomyopathy?
AD Mutations have been found in >11 sarcometic protein genes Assoc with WPW
40
What would you find on an echo in HOCM?
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
What would you find on ECG in HOCM?
``` >95% abnormal p-mitrale LVH Marked lateral T wave inversion Deep septal Q waves AF Occasionally WPW ```
42
How would you manage somebody with HOCM?
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
What is the defect in marfans syndrome and how is it inherited?
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
How would you diagnose Marfans syndrome?
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
How do you manage a patient with Marfans syndrome?
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
What are the indications for aortic root replacement in Marfans?
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
How may marfans syndrome present acutely?
Aortic dissection- mortality of 50%
48
How should people with Marfans be followed up?
Yearly ECHO to monitor aortic root. If FH of dissection or aorta starting to dilate then more frequently
49
What is tetralogy of Fallot?
Congenital condition - Hypertrophy of RV - Over-riding aorta - VSD- large - RVOT obstruction (can be subvalvular, valvular or supravalvular)
50
What signs might you see in somebody with tetralogy of fallot?
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
What would investigations show in tetralogy of fallot?
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
What shunts were used to palliate in tetraology of fallot and when?
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
Does a patient with Fallots tetralogy need genetic counselling?
Yes 15% have deletion of chromosome 22q11 (detected with FISH) which gives 50% chance of transmission Otherwise only 2-3%
54
What are the main late problems patients experience following complete repair of tetralogy of fallot?
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
What is Kartageners syndrome?
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
What are the signs of aortic stenosis?
LVH: heaving apex beat ESM radiates to carotids Slow rising pulse If severe absent 2nd heart sound
57
What are the causes of AS?
Calcific Degeneration Congential bicuspid valve Rheumatic
58
What are the differential diagnosis of AS?
``` Aortic sclerosis Pulmonary stenosis VSD HOCM Supravalvular obstruction ```
59
What is the management of AS?
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
What are the complications of AS?
Endocarditis HF AV block due invasion of calcium from valve ring into HIS-purkinje system Embolic events
61
How would you differentiate sclerosis of stenosis?
Overlaps with mild AS - normal pulse character Normal 2nd heart sound Elderly person
62
What are the signs of aortic regurgitation?
``` 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
What are the causes of aortic regurgitation?
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
What is the management of AR?
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
Does a longer murmur mean more severe AR?
Shorter murmur means more severe flow of block back in LV which finishes sooner
66
What signs would suggest severe AR?
Clinically dilated heart Signs LVF Very wide pulse pressure Short murmur
67
What are the signs of mitral stenosis?
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
What are the causes of MS?
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
How can you tell mild MS from severe MS?
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
How do you manage MS?
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
What determines the suitability of a valve for percutaneous balloon mitral valvulopasty?
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
How do you manage MS presenting in pregnancy?
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
What is the normal mitral valve area
4-5cm
74
What are the signs of mitral regurgitation?
``` 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
What are the causes of MR?
``` Degenerative Function (LV dilatation) Ischaemia Rheumatic MV prolapse- Marfans, idiopathic, connective tissue disease, hereditary ```
76
How would you differentiate mild and severe MR?
Mild: Sinus rhythm, no signs of HF | Severe MR: AF, thrusting apex beat, signs of pul.htn-TR, HF
77
What is the management of MR?
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
Why is repair preferable to replacment?
Disconnection of subvalvular apparatus without chordal preservation can result in up to 20% decline in LV function
79
How is ischaemic MR managed differently?
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
What are the causes of tricuspid regurgitation?
Commonest is pulmonary hypertension Acute: endocarditis, trauma Chronic: endocarditis, ebsteins anomaly, rheumatic fever, carcinoid
81
What are the signs of tricuspid regurgitation?
CV wave in JVP Parasternal heave PSM heard best at left sternal edge on inspiration Pulsatile hepatomegaly
82
How do you manage tricuspid regurgitation?
Medical diurectics Treat cause of pul.htn WHen oedema uncontrollable valve replacment is an option but poor outcomes and last resort
83
How do you differentiate TR from MR?
TR is assoc with a CV wave and murmur gets louder on inspiration with no signs of LVF
84
Why is a CV wave so called?
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
Why is tricuspid endocarditis more common in IVDU?
LIkely that particulate matter used to cut illegal drugs damages TV and predisposes to it.
86
What are the causes of tricuspid stenosis?
Carcinoid Rheumatic fever- unusual Congenital- partial tricuspid atresia
87
What are the signs of tricuspid stenosis?
Raised JVP Peripheral oedema Mid diastolic murmur- rarely audible, if suspected ask to examine liver for carcinoid
88
What are the causes of pulmonary stenosis?
Congenital (virtually all)- maternal rubella, fallots tetralogy Ocassionally rheumatic fever and carcinoid
89
What is the management of pulmonary stenosis?
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
How do you differentiate PS from AS?
Murmur is heard louder in inspiration, best heard in pulmonary area, signs of RVF if severe.
91
What are the waves on JVP called and what do they represent?
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
What is familial hypercholesterolaemia?
``` AD, 1/500 Mutation in gene code for LDL receptor Classically tendon xanthoma Cholesterol >7.5 LDL >4.9 Normal triglycerides ``` Treat: statins
93
What is primary hypertriglyceridaemia?
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
What are the different types of mechanical heart valves?
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
What are the INR targets for patients with valve replacments?
Bileaflet aortic- INR=2.5 Bileaflet mitral- INR=3.0 Ball and cage (Starr-Edwards) INR=3.5

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