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Cardiology Flashcards

1
Q

Clinical signs severe AS. Echo findings severe AS.

A

Clinical signs:
o Slow rising low volume pulse
o Narrowed pulse pressure
o Muted or absent second heart sounds
o The pitch of murmur
o If radiates to carotids
o Presence of LV heave
o ?4th heart sound if significant LVH
Echo signs:
o Peak velocity >4m/sec
o Mean pressure gradient >40mmHg
o Aortic valve area <1cm^2

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2
Q

Indications for valve replacement in AS?

A

o Severe AS with symptoms
o Asymptomatic but severe AS and LVEF <50%
o Severe AS (+moderate AS) if undergoing other cardiac surgery

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3
Q

Medical management AS?

A

o Medical management: beta blockers mainly
o Need to avoid vasodilators which can increase gradient across valve: sildenafil, ACEi, nitrates

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4
Q

Procedural options for AS advantages/disadvantages?

A

 Mechanical aortic valve – more durable but need lifelong anticoagulation
 Tissue aortic valve – not as durable but don’t need anticoagulation
 TAVI – transaortic valve intervention – if not fit for surgical intervention

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5
Q

Symptoms to illicit of AS?

A

Breathlessness, syncope, angina

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6
Q

Clinical signs of AR?

A

o Collapsing pulse
o Widened pulse pressure
o Holodiastolic murmur throughout diastole
o Thrusting and displaced apex beat
- Thrill in aortic area
(S3, collapsing pulse and pulmonary oedema are signs severity)

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7
Q

What are the main ongoing management steps following metallic valve repalcement?

A
  • Long term anticoagulation
  • Serial echo to evaluate function of valve
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8
Q

What are the 4 pillars of disease modifying drugs in the management of heart failure?

A

ACE inhibitor (ramipril)
Beta blocker (bisoprolol)
Mineralocorticoid receptor antagonist (spironolactone)
SGLT2 inhibitor (dapagliflozin)

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9
Q

What device therapy may be used in the management of chronic HF and when are they indicated?

A

ICD - LVEF </=35%, QRS <130msec and shown most benefit in those of ischaemic aetiology
CRT - LVEF </=35%, QRS >/=130msec

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10
Q

How is a diagnosis of HFpEF made?

A
  • Signs and symptoms of HF
  • LVEF >/=50%
  • Objective evidence cardiac structural and/or functional abnormalities eg. raised LV filling pressures/raised NPs
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11
Q

What is the medical management of HFPEF?

A
  • Treat comorbidities
  • Furosemide for overload
  • SGLT2i
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12
Q

What would be the indications for MV replacement?

A

o Mitral stenosis – but likely to have signs of pulmonary hypertension or be in AF
o Mitral regurgitation
o Infective endocarditis

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13
Q

Causes of tricuspid regurgitation?

A
  • Usually due to pulmonary HTN (primary or secondary)
  • Other causes include:
    o Endocarditis - ?any evidence of IVDU
    o Ebstein’s anomaly – apical displacement of the tricuspid valve so there is always a degree of regurgitation
    o Rheumatic valve disease (but rare as R sided valves not usually involved
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14
Q

Clinical signs of TR?

A

o CV wave in JVP
o Parasternal heave indicates severe TR
o Pansystolic murmur left lower sternal edge loudest on inspiration
o Pulsatile hepatomegaly
o Don’t get signs of LV failure (unless other co-existing pathology)

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15
Q

Management of TR?

A
  • Management:
    o Management of any condition leading to pulm HTN
    o Diuretics
    o If low cardiac output or uncontrolled peripheral oedema becomes a problem then valve replacement
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16
Q

Causes pulmonary stenosis?

A

o Can be valvular (most frequently), supravalvular or subvalvular
o Congenital is most common cause (PS makes up 10% of all congenital heart disease)
 Noonan’s syndrome
 Alagille syndrome – rare AD condition, cardiac, liver, renal, eye and skeletal abnormalities, typical face, broad forehead, deep set eyes and pointy chin
 Congenital rubella
 Williams syndrome
 Leopard syndrome
 In combination with other defects such as Tetralogy of Fallot – overriding aorta, RVH and VSD
o Acquired
 Carcinoid syndrome
 Rheumatic heart disease

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17
Q

Brief investigation and management of pulmonary stenosis?

A

o Echo for diagnosis and monitoring – attention focussed on gradient across the valve and RV systolic pressure
o If there are associated lesions such as supravalvular abnormalities then might do cardiac MRI to show cardiac and pulmonary artery anatomy
o Most cases seen in adulthood are mild, requiring no treatment or will have undergone correct procedure
- Treatment for moderate/severe:
o Can include valvuloplasty or surgical reconstruction of the RVOT, sometimes valve replacement

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18
Q

3 questions to answer if you suspect congenital heart disease?

A
  1. Cyanotic versus acyanotic (blue versus pink)
  2. Any scars indicative of previous surgery – look front and back
  3. Associated conditions? Down’s, Turners or Noonans syndrome?
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19
Q

Clinical signs of pulmonary stenosis?

A

o ES murmur loudest in pulmonary area and louder on inspiration, radiates to L infraclavicular region
o Softening/delay of the pulm component of 2nd HS
o Pulmonary thrill
o Prominent a wave of JVP in severe cases due to RV hypertrophy
o RV heave with significant stenosis
o RV gallop rhythm

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20
Q

Causes of mitral regurgitation?

A
  • Degenerative causes such as age related MR
  • Mitral valve prolapse
  • Rheumatic heart disease
  • Left ventricular dilatation
  • Cardiomyopathy
  • Connective tissues disorders (Ehlers Danlos may have MVP)
  • Marfan syndrome
  • Acute: MI with papillary muscle rupture, infective endocarditis
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21
Q

Clinical features of severe/significant MR?

A
  • Raised JVP
  • Loud P2 or S3 gallop rhythm
  • RV heave
  • Apex may be thrusting and would be displaced
  • Symptoms of dyspnoea, reduced ET and overload
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22
Q

Indications for MV replacement in MR?

A
  • Severe MR with reduced LVEF or AF caused by MR or pulmonary HTN
  • Acute MR following an MI
  • MR secondary to infective endocarditis
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23
Q

Differential diagnosis for pan systolic murmur?

A
  • VSD
  • TR
  • MVP
  • MR
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24
Q

What are the ESC guidelines for when you use bioprostehtic valve versus metallic?

A
  • Bioprosthetic valves should be considered in:
    o Those >65 for MV
    o Those >70 for AV
    o Those at particular risk of haemorrhage
    o Those who are poorly compliant with medication
    o Young women of childbearing age
  • Metallic valves should be considered in all others patients and in the elderly who are already anticoagulated
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25
Q

What is your waffle for why you look at JVP?

A
  • The JVP is a visible reflection of the pressures in the RA
  • Abnormalities in the RH pressures will be seen in JVP
  • Eg. In pulmonary HTN you have an elevated JVP
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26
Q

What investigations would you do is suspected patient had mitral regurgitation?

A
  • ECG ?AF or P mitrale
  • Urine dipstick – haematuria/proteinuria in IE
  • FBC ?anaemia which exacerbates breathlessness
  • Inflammatory markers
  • Biochemistry
  • Echo to specifically look at mitral valve, severity of any regurge, any vegetations, LVEF and any evidence of pulmonary HTN
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27
Q

What are the clinical signs of Marfan’s you might see on examination?

A
  • Arachnodactyly
  • Hypermobile joints
  • Clubbing
  • High arched palate
  • Mild collapsing pulse
  • Evidence of cardiac surgery eg. Median sternotomy scar
  • Evidence of AV replacement due to AR – metallic S2, might have non radiating systolic murmur in aortic area
  • Evidence of previous aortic surgery eg. A massive scar somewhere
  • May have evidence of arthritis relating to Marfan’s
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28
Q

What is the inheritance of Marfan’s syndrome?

A
  • Autosomal dominantly inherited condition affecting fibrillin gene and therefore collagen generation
  • Would consider genetic testing and also family screening
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29
Q

What are the 4 main cardiac features of Marfan’s sydnrome?

A
  • Aortic root dilation
  • Aortic valve regurgitation
  • Aortic dilatation along any part
  • Mitral valve prolapse
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30
Q

What are the indications for aortic root replacement in patients with Marfan’s?

A
  • Dilatation >50mm at aortic root
  • Dilatation >45mm in a patient with Fhx of aortic dissection
  • Aortic root expanding >3mm per year
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31
Q

Clinical findings of significant pulmonary stenosis

A

o Large A waves in JVP due to delayed RA emptying
o RV heave due to RVH
o Pansystolic murmur due to functional TR from RH dilatation
o Signs of R sided HF – elevated JVP and peripheral oedema
o A widely split 2nd heart sound with quiet pulmonary component

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32
Q

Symptoms of pulmonary stenosis?

A

o Effort intolerance
o SOBOE
o Pre-syncope and syncope
o Symptoms of RHF
Chest pains
Palpitations

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33
Q

What would be the differential for an ejection systolic murmur?

A

o PS – valvular, supravalvular or subvalvular (due to RVOT obstruction)
o AS or LVOT obstruction
o ASD
o VSD

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34
Q

Echo cardiographic features of severe pulmonary stenosis?

A

o Gradients >64mmHg
o Valve area reduced <1cm squared
o Velocity >4m/sec across the valve

35
Q

Noonans pattern of inheritance?

A

Autosomal dominant, males and females equally affected

36
Q

Features of Noonan’s syndrome?

A
  • Clinical signs of Noonan’s:
    o Describe as ‘phenotypical signs’
    o Cubitus valgus
    o Webbed neck
    o Widely spaced nipples
    o Pectus excavatum
    o Impaired clotting
    o Short stature
    o May have mild intellectual disability and motor developmental delay but unlikely to assess for these in PACES
    o Proptosis
    o Ptosis
    o Strabismus
    o Cardiac defects: PS most common, HOCM, ASDs
37
Q

Duke’s criteria infective endocarditis?

A

Major:
- 2 blood cultures positive with typical organism
- Echo large vegetation, dehiscence or abscess
Minor:
- Echo suggestive
- Embolic phenomena
- Predisposition (eg. prosthetic valve)
- Pyrexia >38
- Blood cultures with atypical organism
- Vasculitis phenomena (eg. raised ESR)

38
Q

Causes of aortic regurgitation?

A

Congenital:
- Bicuspid valve
- Perimembranous VSD
Acute:
- Endocarditis
- Aortic dissection
- Prosthetic valve failure
Chronic:
- Marfans
- Ankylosing spondylitis
- Rheumatic fever
- Syphillis
- Drugs (slimming agents, pergolide)
- Osteogenesis imperfecta

39
Q

Management of aortic regurgitation?

A

Medical:
- ARBs and ACEi (reduce afterload)
- Regular review of Echo and symptoms
Surgery:
- Aortic root abscess
- Dissection
Valve replacement:
- Symptomatic
- Asymptomatic with wide pulse pressure, LV enlargement and reduced EF

40
Q

What are the possible causes of atrial fibrillation?

A

Cardiac causes:
- IHD, HTN, valvular disease, HF
Respiratory causes:
- Infection, malignancy
Systemic causes:
- Excessive alcohol intake, thyrotoxicosis, electrolyte depletion, infection

41
Q

Broad management of AF?

A
  • Urgent cardioversion if haemodynamic instability, ischaemia, LOC or acute HF
    If not:
  • Investigation of underlying cause (+ treatment)
  • Rate or rhythm control
  • Rhythm control may be appropriate if: reversible cause, HF caused or worsened by AF, rate control has failed to control symptoms
  • Anticoagulation depending on CHADSVASC score and ORBIT score
  • Rate control using BB, rate limiting CCB (or digoxin as 2nd line if sedentary)
42
Q

Echocardiographic grading of pulmonary stenosis and likely associated symptoms in mild/mod/severe?

A

o Mild
 Gradient <36mmHg – asymptomatic, rarely progresses or requires Rx and echo only every 5y for monitoring
o Moderate
 Gradient 35-64mmHg – develop dyspnoea and fatigue
o Severe:
 Gradients >64mmHg
 Valve area reduced <1cm squared
 Velocity >4m/sec across the valve
 May develop early RVF and cyanosis

43
Q

What are the clinical findings in mitral valve prolapse and what are the differentials for this?

A

Clinical findings:
- Dynamic systolic click
- Mid to late systolic murmur heard best at apex
Differentials for the above:
- Bicuspid aortic valve
- Mitral regurgitation
- Atrial myxoma
- Hypertrophic obstructive cardiomyopathy

44
Q

MVP can be primary or secondary with what associated conditions?

A
  • Marfan’s syndrome
  • Ehler’s Danlos syndrome – joint hypermobility and skin hyperelasticity
  • Osteogenesis Imperfecta
  • Polycystic kidney disease
45
Q

In addition to MVP what are the other possible CV complications of Ehler’s Danlos syndrome?

A
  • Aortic dissection
  • Aortic aneurysm
  • Dilated aortic root
  • Spontaneous arterial dissections: carotid artery dissection
  • Raynaud’s disease
46
Q

What are the possible complications of MVP?

A
  • Normally benign with an excellent prognosis but sometimes serious complications can occur:
    o Infective endocarditis
    o Thromboembolic events
    o CVAs
    o MV surgery need
    o Sudden death
47
Q

What is the management of MVP?

A

Many don’t require management just need echocardiographic monitoring for signs of decompensation
Surgery:
- Guided by symptoms and echo findings
- Need cardiac catheterisation prior to surgery to assess for concomitant CV disease
- TOE to assess repairability of valve
o Valvular repair is preferred over replacement
o Replacement reserved for those with unfavourable anatomy
- In absence of coronary artery disease patients may be suitable for minimal access surgery using a right thoracotomy scar
- Percutaneous treatment is just mitral clip which can be used in those with favourable anatomy

48
Q

What follow up may be needed in patients with Ehler’s Danlos and MVP?

A
  • Regular echo to ensure no signs of decompensation
  • Regular follow up with ophthalmologist because of risk of Lens dislocation
49
Q

What are the clinical findings in PDA?

A

Clinical findings:
- Might be young patient, no scars (as otherwise would be repaired at birth and not in exam)
- Continuous murmur loudest in systole, loudest in pulmonary area
- Murmur is loudest in expiration
- Murmur radiates to back
- Loudest over left scapula

50
Q

What would be the 3 clinical findings suggestive of severe PDA?

A
  • Collapsing pulse – present in severe PDA
  • RV heave (high R sided pressures)
  • LV failure
51
Q

How would you investigate suspected PDA?

A
  • Full Hx
  • Full set of blood tests – inflammatory markers and 3 sets BCs
  • ECG
  • Echocardiogram as a diagnostic test
  • Following echocardiogram can consider cardiac MR or CT
  • Invasive investigation needed when pulmonary arterial pressure estimated high on echo, cardiac catheterisation allows invasive investigation of R sided pressures and calculation of pulmonary and systemic vascular resistance
52
Q

What features would be concerning on echocardiogram in PDA?

A
  • Evidence of raised pulmonary pressures
  • Dilated pulmonary arteries
  • Evidence RV dilatation and TR
  • Evidence of LV dysfunction
53
Q

What would be the indications for repair of a PDA in adults and how would this be followed up?

A

Indications for closure:
- LV volume overload or pulmonary HTN
Follow up following closure:
- After closure patients with no residual shunt, normal LV function and normal pulmonary arterial pressure don’t need follow up beyond 6/12.
- If LV dysfunction or residual raised pulmonary arterial pressures will require follow up in a specialised centre

54
Q

Why does inspiration make R sided murmurs louder?

A
  • Inspiration leads to increased venous return
  • Means more flow across R sided valves so murmur is louder
55
Q

What is Eisenmenger’s syndrome?

A
  • Long standing L to R cardiac shunt caused by congenital heart disease - VSD, ASD or less commonly PDA
  • Get pulmonary HTN and eventually get reversal shunt R to L
56
Q

How is a VSD managed and what would be the indications for repair (4)?

A
  • Main concern is risk of endocarditis and they need to have prophylactic abx if undergoing intervention or surgery on infected tissue if the surgery is likely to liberate a bacteraemia
  • If develop signs of heart failure can manage with diuretics along standard lines
    Indications for closure of VSD if Eisenmengers has not developed
  • Significant shunting (pulmonary: systemic blood flow ratio >2)
  • LV dysfunction
  • History of endocarditis
  • Acute septal rupture following MI
57
Q

What are the possible causes of clubbing?

A
  • Cardiovascular system:
    o Subacute endocarditis
    o Cyanotic congenital heart disease
  • Respriatroy:
    o Lung malignancy
    o TB
    o CF
    o Bronchiectasis
    o ILD
  • GI:
    o IBD
  • Familial is also possible
58
Q

What would the physical signs of pulmonary banding be and what is the purpose?

A
  • May see scar on posterior L thorax
  • Procedure performed in childhood, used to be for palliation of large VSDs which has the primary objective of reducing excessive pulmonary blood flow to protect the pulmonary vasculature from hypertrophy and irreversible fixed pulmonary HTN
  • This has now been replaced by early definitive intracardiac repair
59
Q

What is Heyde syndrome?

A

Triad of aortic stenosis, GI angiodysplasia (from GI bleeding), acquired von willebrand disease

60
Q

Abnormalities of TOF?

A
  1. Large non restrictive VSD
  2. Overriding aorta
  3. RVOT obstruction (may be valvular, subvalvular, supravalvular, or any combo)
  4. RV hypertrophy
61
Q

What is a Blalock Tausig shunt and what would be the signs?

A

Historical surgical technique - connection between subclavian and pulmonary artery used in cyanotic congenital heart disease
Have a lateral thoracotomy scar and weaker radial pulse on ipsilateral side

62
Q

How is TOF repaired?

A

o Repair of VSD with a patch
o Resecting obstructive muscle tissue in RV and enlarging outflow tract with a patch

63
Q

What are the complications of TOF repair?

A
  1. PR – because of how RVOT is repaired, might need PV replacement (likely tissue so midline sternotomy, loud P2 and soft ES murmur over pulmonary valve)
  2. Can get functional TR to do with repair too (pansystolic murmur)
  3. AR and/or aortic root dilatation – due to VSD repair or other reason – might need replacement
  4. Rhythm disturbances (because of all repairs) – sometimes need an ICD
  5. Residual VSD – closed if shunt ratio (pulmonary: systemic flow) exceeds 1.5
64
Q

What are examples of cyanotic congenital heart disease?

A
  • Tetralogy of fallot
  • Pulmonary atresia
  • Tricuspid atresia
  • Transposition of the great arteries
  • Ebstein’s anomaly (as it is often associated with an ASD and get R>L shunt)
  • Eisenmengers
65
Q

What are examples of acyanotic congenital heart disease?

A
  • Atrial septal defect
  • Ventricular septal defect
  • Patent ductus arteriosus
  • Aortic stenosis
  • Pulmonary stenosis
  • Co-arctation of the aorta
66
Q

What would be the possible differentials for a lateral thoracotomy scar?

A
  • Lobectomy
  • Pneumonectomy
  • Surgery for aortic co-arctation
  • Blalok Tausig shunt
67
Q

What genetic association can be found in TOF?

A

15% have 22q11 deletion (if also have DiGeorge) – can be identified by FISH

68
Q

Causes of restrictive cardiomyopathy?

A
  • Primary
    o Endomyocardial fibrosis
    o Loefflers endocarditis (eosinophilic mediated restrictive cardiomyopathy occurring as part of a spectrum of hypereosinophilic syndromes)
  • Secondary and infiltrative
    o Cardiac amyloidosis
    o Cardiac sarcoidosis
    o Iron overload – primary or secondary haemachromatosis
    o Scleroderma
    o Radiation induced (can get several years after radiotherapy but can also co-exist with constrictive pericarditis)
  • Drug induced rare but has been reported with hydroxychloroquine
69
Q

Management of restrictive cardiomyopathy?

A
  • Restrictive cardiomyopathy – address underlying cause and treat and then address any symptoms
    o Low cardiac output might consider options for heart transplantation
    o Without this the prognosis is poor
70
Q

Presentation and echo findings in restrictive cardiomyopathy?

A
  • Signs and symptoms HF
  • Echo shows good systolic function but diastolic dysfunction and impaired relaxation of the ventricles and atrial enlargement (due to impaired ventricular filling during diastole)
71
Q

Causes of constrictive pericarditis?

A
  • Viral pericarditis
  • Bacterial pericarditis
  • Post surgery eg. After CABG
  • Post TB
  • Radiation
72
Q

Management of constrictive pericarditis?

A
  • Constrictive pericarditis – managed with surgery and stripping of pericardium
73
Q

What is coarctation of aorta and what are its associations?

A
  • Congenital narrowing of the aortic arch – usually distal to left subclavian artery
  • Normally associated with other cardiac defects such as:
    o Bicuspid AV in 50-80% cases
    o VSD
    o PDA
  • Other associations:
    o Berry aneurysms
    o Turners syndrome
74
Q

How might coarctation of the aorta present?

A
  • Depends on extent of narrowing and formation of collateral arterial supply
  • Infants:
    o Severe HF
  • Adult hood:
    o Unexplained HTN
    o Sometimes HF
  • Symptoms in adults:
    o Due to hypertension
    o SOBOE
    o Leg claudication – reduced blood flow to lower body and extremities
75
Q

What are the possible clinical signs of coarctation of aorta?

A
  • Radial-radial delay
  • Weak femoral pulses
  • R sided radial/brachial – femoral delay
  • Possible murmurs:
    o Pan systolic murmur in setting of VSD
    o Systolic ejection click from a bicuspid aortic valve
    o Continuous bruits over collaterals (over scapula or anterior axillary areas)
    o Coarctation might produce mid systolic murmur loudest posteriorly under left scapula (but also heard in left infraclavicular area)
  • Might see signs of Turner’s in females
  • Left sided lateral thoracotomy scar is what you see if had congenital repair
76
Q

What is the management of coarctation of aorta?

A
  • Balloon angioplasty and stent
  • Surgery with resection and end to end anastomosis is preferred option
77
Q

What would be the necessary investigations for suspected coarctation of aorta?

A
  • ECG – LVH due to HTN
  • CXR - rib notching or figure of 8 shape of aorta
  • Echo
  • CT/MR aortogram to more accurately characterise anatomy
78
Q

What are the possible complications of uncorrected coarctation of aorta?

A
  • Stroke
  • HF
  • Aortic rupture
79
Q

What is your waffle about how you would manage a person in AF?

A
  • Look for underlying cause:
    o Infection
    o Hyperthyroidism
    o OSA
    o Treat any underlying cause
  • Can opt for a rate of rhythm control strategy
  • Rhythm control can be through chemical cardioversion or electrical cardioversion
  • If the onset of AF is known to be within 48h immediate cardioversion may be appropriate
  • If the onset is unknown or outside of 48h can consider rhythm control with appropriate anticoagulation or rate control with a beta blocker/calcium channel blocker or digoxin in patients with concomitant HF
  • Calculate CHADSVASC and ORBIT score to determine the need for anticoagulation as stroke prophylaxis
  • If high suspicion of underlying structural heart disease I would perform an echocardiogram
80
Q

Causes of mitral stenosis?

A
  • Most commonly rheumatic heart disease
  • Calcification
  • Fabrys disease
  • RA
  • SLA
    Carinoid
  • Whipples
81
Q

Management of mitral stenosis?

A
  • Surgery if severe and symptoms or elevated pulmonary pressures
  • If asymptomatic follow up every 6-12 months with echo and symptoms
  • If medical therapy – treat any LVSD and AF
  • Anticoagulation if evidence of AF, thromboembolic disease or LA thrombus
82
Q

Reason you might do a valvuloplasty in AS?

A
  • Temporary procedure whilst awaiting more definitive management
  • Very stenosed valve with cardiogenic shock or unstable angina
83
Q

Investigations in palpitations?

A
  • Full history
  • FBC, electrolytes, TFTs
  • ECG and longer monitoring 24h or 7 day Holter monitor, implanted loop recorder
  • Echo
  • If exercise induced – think about treadmill test
  • Concern about brugada – flecainide challenge

PACES (7 decks)

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