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Cardio Flashcards

1
Q

What are the clinical signs of aortic stenosis?

A
  1. Slow rising pulse
  2. Narrow pulse pressure
  3. Right ventricular failure - v waves, loud P2, basal creps
  4. Soft A2
  5. Loud P2
  6. Late peaking of a long systolic murmur
  7. S4 (Tenesee)
    Gallavardin phenomenon - all over pre-cordium but importantly not radiating to axilla
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2
Q

How do you classify AS severity?

A
  1. Character of murmur
  2. Slow rising pulse
  3. Cardiac decompensation
  4. LVH (S1+R6 >35mm (7 large squares), LBBB, AF
  5. Echo - peak gradient >64mmHg, or mean gradient >40mmHg; best measure is ratio of valve velocity vs. LVOT velocity (dimensionless index)
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3
Q

What are the causes of AS?

A

Bicuspid AV
Calcification
Rheumatic valve disease
Congenital
Rare: IE, Paget’s

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4
Q

Treatment of AS?

A

If >75 = TAVI
If <75 = surgical aortic valve replacement unless surgeons dont agree

Main contraindications to TAVI
1. PVD
2. Malignant features of annulus (wont sit correctly)
3. CAD

Main contraindications for surgical aortic valve
1. RT to chest
2. Prev sternotomy
3. CLD
4. PHTN
5. Poor LV

Untreated, severe AS has a 50% 1 year mortality

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5
Q

What is the workup for TAVI?

A

Routine bloods
PFTs if smoker
ECG gated CT
Angiogram if CT doesnt show coronary arteries well enough

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6
Q

Complications of TAVI

A

Arrhythmias
Vascular haematomas
Stroke / MI / annular rupture

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7
Q

Indications for Mitral valve repair/replacement?

A

When indicated and feasible, repair is the preferred treatment

Indications for surgery:
Symptoms + severe MR on echo
Severe MR on echo + AF, LV diastolic or systolic dysfunction (all of these predict worst POST-OP outcomes, and so trigger early surgery in asymptomatic patients)
Acute MR post MI

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8
Q

Causes for MR?

A

Acute:
1. Rupture of chords
2. IE
3. Trauma

Chronic:
1. Structural
MV prolapse
Mitral annular calcification (age related)
LV dilation
Cardiomyopathies

  1. Connective tissue
    Marfan’s
    EDS
    Pseudoxanthoma elasticum
    Osteogenesis imperfecta
  2. Inflammatory
    RA
    Rheumatic fever (typically causes mixed rheumatic valve disease)
  3. Endocarditis
    Sub-acute IE
    SLE
    Malignancy
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9
Q

Ix for MR?

A

ECG (AF, p mitrale)
Urine dip - haematuria
Fundoscopy (Roth spots)
Temp
FBC (anaemia), WCC, CRP, ESR, renal profile
Echo - MV and extent / severity of regurg, any vegetation or prolapse, PHTN, LVEF

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10
Q

What are the features of pulmonary hypertension?

A

TR with giant v waves, Loud P2, creps

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11
Q

S3 -

A

Ken T.UCKY

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12
Q

S4

A

Te.NE SEE

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13
Q

What are the clinical signs of severe MR?

A

Soft S1
S3/S4
Displaced heaving apex
Precordial thrill
Widely split S2 (earlier emptying of LV as some goes out of aorta, some goes into LA)
PHTN
AF

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14
Q

Murmur of MV prolapse?

A

S1 -> mid-systolic ejection click -> S2. Valsalva causes earlier ejection click (reduced pre-load)

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15
Q

What are the causes for MV prolapse?

A

Primary (Inherited) - myxomatous degeneration
Seconday: Marfan’s, Ehler-Danlos, Pseudoxanthoma elasticum, osteogenesis imperfecta, PKD, SLE

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16
Q

What is the prevelance of MV prolapse?

A

5-10% of gen pop, more common in females

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17
Q

Complications of MV prolapse?

A

Can progress to mitral stenosis and them mitral regurgitation
Stroke
Endocarditis
Prolonged QT
Sudden death

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18
Q

What is the inheritance of MV prolapse?

A

Autosomal dominant inheritance, exhibiting age and sex-dependant penetrance
Elastin, fibrillin, collagen I and II

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19
Q

What causes reverse splitting of S2?

A

LBBB
HOCM
Severe AS
WPW
PDA
MR

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20
Q

What is your differential for an ejection systolic murmur?

A
  1. AS
  2. Aortic sclerosis
  3. HOCM
  4. PS

Pan-systolic
1. MR (AS NEVER radiates to axilla)
2. VSD

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21
Q

What medications must you AVOID in AS?

A

Vasodilators (increase gradient across the valve) - ACEi, nitrates, sildenafil

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22
Q

What is the mainstay of medical management in AS?

A

Beta-blockers

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23
Q

What are the causes for pulmonary stenosis?

A
  1. Congenital
  2. Noonans, Turner’s, Down syndrome
  3. Rubella
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24
Q

What are the causes of a widely split S2?

A

RBBB
Pulmonary stenosis
VSD
ASD

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25
Q

What are the causes of a reverse split S2?

A

LBBB
AS
HOCM
WPW Type B (right sided pathway)

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26
Q

What are the cardiac manifestations of Marfan’s syndrome?

A

Aortic root dilation
Aortic dissection
Aortic regurgitaiton
Mitral valve prolapse

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27
Q

What are the non-cardiac manifestations of Marfan’s syndrome

A

Arachnodactyly
Hypermobile joints
Kertoconus and upward lens dislocation
Blue sclera
Heterochromia of irides
Iridodonesis (asymetric iris) - prev lens dislocation + repair
High arched palate
Pneumothorax
Spontaneous intracranial hypotension
Dural ectasia
Pes planus

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28
Q

What is Steinberg and Walker sign?

A

Steinberg: Marfan syndrome. When patient makes a fist enclosing thumb - thumb sticks out

Walker: 1st and 5th digit of one hand overlap over wrist of the other hand

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29
Q

What is the gene in Marfan?

A

AD fibrillin-1 - extracellular matrix protein

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30
Q

How do you manage aortic regurg in patients with Marfan’s syndrome?

A

Lifelong beta-blockade
Monitoring of aorta with echocardiography
Replace aortic root before diameter >45mm if FHx, 50 otherwise, or if rate of expansion is >3mm/year

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31
Q

What are the signs of a failing aortic valve?

A
  1. Blurred S2
  2. Absence of silence in diastole
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32
Q

What are the causes for clubbing?

A

Thought to be mediated by vasodilation of the clubbed portions due to vasodilators, hypoxia, platelet precursors

Cardiac
1. Cyanotic heart disease
2. Atrial myxoma
3. Infective Endocarditis

Resp
1. Suppurative lung disease
2. Lung fibrosis
3. Lung cancer
4. Asbestos
5. Mesothelioma
6. Lung abscess

GI
1. IBD
2. Liver cirrhosis
3. HCC
4. Coeliac

Endocrine
1. Thyroid acropachy

Congenital

POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, M-protein plasmacytoma, Skin changes

If unilateral
1. Stroke
2. Aneurysm
3. Brachial plexus injury
4. AV fistula

Pseudoclubbing
-Lovibond angle maintained, but nailbed has increased curvature

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33
Q

What are the stages of clubbing?

A
  1. Normal but fluctuant nailbed
  2. Loss of angle of Lovibond
  3. Increased pulp
  4. Increased breadth
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34
Q

What is Noonan syndrome?

A

Autosomal Dominant with multiple implicated genes including SHP2

Short stature
Webbed neck
Cubitus Valgus
Widely spaced nipples
Mild facial changes
Proptosis
Ptosis
Strabismus
Pectus excavatum
Learning difficulties
Impaired coagulation
Congenital heart disease - PS (most common), VSD, ASD, HOCM.

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35
Q

What are the cardiac manifestations of Noonan’s syndrome?

A

PS is most common
Also VSD, ASD, HOCOM

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36
Q

What are the cardiac manifestations of Turner syndrome?

A

Bicuspid aortic valve
Dilation and dissection of aortic root

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37
Q

Williams Syndrome

A
38
Q

What are the causes for PS?

A

Valvular
Congenital
Rheumatic
Noonan’s

Supra-valvular
Wiliams Syndrome

Subvalvular
Fallot’s

39
Q

What do you know about Turner syndrome?

A

45XO

Phenotype
Short stature
Webbed neck
Wide spaced nipples
Primary amenorrhoea
Cardiac defects including bicuspid aortic valve, aortic root dilation, and dissection
Multiple pigmented naevi
Short 4th metacarpal
Horseshoe kidney

40
Q

What are causes of VSD’s?

A

Congenital
Maternal alcohol
Aneuploidy syndromes (Down, Edward, Patau)

Acquired
Ischaemic, iatrogenic (septal puncture)

41
Q

What is the most common type of VSD?

A

Peri-membranous

42
Q

What are the complications of a VSD?

A

IE
PHTN
Aortic regurg if peri-membranous
Arrythmias
Shunt reversal

43
Q

What is Holt-Oram syndrome?

A

AD
ASD + tri-phalangeal thumbs

44
Q

What are the clinical signs of an ASD?

A

Fixed split S2
Ejection systolic murmur (increased flow across pulmonic valve)
PHTN

45
Q

What are the causes for ASD’s?

A

Ostium secondum (PFO, Holt-Oram)
Ostium primum (present earlier and involve mitral and tricuspids)
Sinus venosus (SVC junction) associated with anomalous pulmonary venous drainage

46
Q

What are the complications of an ASD?

A
  1. Arrythmias
  2. PHTN
  3. Eisenmenger’s
  4. Paradoxical embolism
  5. IE
  6. Recurrent pneumonias
47
Q

What are the clinical signs of adult co-arctation of the aorta?

A

Harsh ejection systolic heard in subclavian area (posterior thoracic spine)
Typically distal to left subclavian
If one radial pulse is weak this may be due to subclavian harvest to repair the coarctation
AS/AR (bicuspid valve)
Radio-femoral delay
Forceful heaving apex beat due to internal thoracic artery collaterals

48
Q

What conditions are associated with CoA?

A

PDA
VSD
Bicuspid aortic valve
Berry aneurysms
Turner Syndrome

49
Q

What are the clinical signs of a PDA?

A

Severe - collapsing pulse
Can lead to cyanotic heart disease
Precordial thrill under left clavicle
Continuous machine like murmur with systolic accentuation
To differentiate it from PS, listen at the back - the murmur will be present here - PS will not

50
Q

What are the causes for a persistent PDA?

A

Prematurity
Low birth weight
Maternal use of NSAID’s (prostaglandins keep the PDA open; NSAIDs are prostaglandin antagonists)
Rubella
High altitude
Fetal alcohol syndrome
Maternal amphetamine

51
Q

How do you treat MV prolapse

A

If mod-sev, need to consider surgery. This would be mitral valve repair instead of replacement. Might be suitable for minimally invasive surgery.

52
Q

Clinical signs of mitral stenosis?

A
  1. Malar Flush
  2. AF
  3. Tapping apex (palpable S1)
    Left parasternal heave if PHTN
  4. Opening snap in diastole folllowed by mid-diastolic murmur heard best at apex. The more severe the stenosis, the closer the opening snap is to S2, and the longer the murmur
53
Q

What are the causes of mitral stenosis?

A
  1. Congenital (rare)
  2. Rheumatic heart disease
  3. Valvular endocarditis
  4. Senile degeneration
54
Q

What is the treatment for mitral stenosis?

A
  1. If AF, anticoagulate and rate control
  2. Mitral valvuloplasty
  3. Surgery - valvotomy
55
Q

What do you know about Ehler Danlos?

A

AD mutation affeting collagen III
Hypermobility and elasticity
Fragile skin
Joint hypermobility
Easy bruising
AR, aortic dissection, MV prolapse
Subarachnoid haemorrhage
Angioid retinal streaks

56
Q

In a case of PHTN and suspected Eisenmenger’s, what shunts do you know of, and how would you identify them?

A

PDA - reverse splitting
VSD - Single S2
ASD - fixed split S2

57
Q

What are the indications for closure of a VSD?

A

Significant right to left shunt
Significant PHTN
Significant LV dilation

58
Q

What are the possible indications for a posterolateral thoracotomy incision?

A
  1. Pneumonectomy/lobectomy
  2. Aortic surgery (Coarctation/dissection)
  3. Blalock Tausig shunt (connects subclavian to pulmonary arteries and is associated with a weak ipsilateral radial pulse)
59
Q

What are causes of cyanotic heart disease?

A

ToF
Transposition of great vessels
Pulmonary atresia/stenosis
Tricuspid atrexia
Ebstein’s (atrialisation of the right ventricle due to low inserting TV leaflets)
Eisenmengers (reversal of left to right shunt)

60
Q

What are causes of acyanotic heart disease?

A

AS
Coarctation
ASD
VSD
PDA

61
Q

Complications of ToF surgery?

A

PR in adolescence following surgery of ToF - needs valve replacement

62
Q

What is ToF?

A

1.VSD
2. Over-riding aorta
3. RVOT obstruction
4. RVH

63
Q

What is restrictive cardiomyopathy?

A

Stiff and non-compliant myocardium that is of relatively normal size
Fails to stretch with blood = diastolic failure = bi-atrial enlargement

64
Q

What are causes of restrictive cardiomyopathy?

A

Primary:
Loflers
Endomyocardial fibrosis

Secondary (infiltrative):
Amyloidosis
Sarcoidosis
Haemachromatosis
Radiation

65
Q

What is constrictive pericarditis?

A

Chronic pericarditis leads to calcification of the pericardium leading to diastolic failure

66
Q

What are common causes of constrictive pericarditis?

A

Any cause of acute pericarditis.

  1. Viral infection (eg. Cocksackie)
  2. Uraemia
  3. Autoimmune
  4. Hypothyroid
  5. SLE
  6. TB (common cause)
  7. Post-MI
67
Q

How do you manage AF?

A

Emergency: DC

Elective

Rate control (preferred)
Bisoprolol
CCB’s
Digoxin (if in heart failure)

Medical rhythm Control
Amiodarone (esp in heart failure)
Flecainide

DC
If <48 hours = heparinise and DC
If >48 hours = anticoagulate for 4 weeks +/- amiodarone if high risk of failure

68
Q

When is rhythm control preferred over rate control in AF?

A

If onset is <48 hours
If cause is reversible
If there is cardiac failure primarily due to AF
Atrial flutter amenable to ablation

69
Q

What is the CHA2DS2VASC score?

A

Risk of stroke in AF

Congestive heart failure
Hypertension
Age (2)
Diabetes
Sex
Stroke
Vascular Disease

If Chadsvasc comes out negative (0 in M, 1 in F) = need an echo to rule out valvular disease which is an absolute indication for anticoagulation in the presence of AF

70
Q

What is the ORBIT score?

A

Assess bleeding risk (CRAB!)

Clopidogrel or Aspirin (antiplatelet)
Renal impairment
Age >74
Bleeding history, Hb <130

71
Q

What are the principle management of chronic heart failure?

A
  1. ACEi and BB
  2. Aldosterone antagonist
  3. SGLT-2 inhibitor
  4. AF?: Digoxin; EF <35% despite optimising ACEi/ARB?: Sabucatril/valsrtan; African American?: Hydralazine; broad QRS? CRT
  5. One off pneumococcal and annual influenza vaccines
72
Q

How does sacubatril valsartan work?

A

Valsartan is an AR II blocker
Sabucatril is a neprillysin antagonist that normally breaks down natriuritic peptides. By blocking this breakdown, it promotes natriuresis

73
Q

What are the medical treatments available for angina?

A

Aspirin, Statin, GTN
Rate control:
1. BB or CCB (rate limiting non-dihydropiridine eg verapamil or diltiazem)
2. BB + CCB (longer acting dihydropiridine eg amlodipine nifedipine)
3. Add third drug only if referred for PCI/CABG. These include nitrates (vasodilator and reduces pre-load), nicorandil (vasodilator), ivabradine (blocks funny channel at SAN), ranolazine (relaxes tension in muscle walls reducing oxygen demand)

74
Q

What are the indications for cardiac pacing?

A
  1. Symptomatic sinus node disease
  2. Mobitz II (asymptomatic)
  3. Mobitz I (symptomatic)
  4. Complete heart block
  5. Persistent AV block post-MI
75
Q

This is a DDDR pacemaker. What does that mean?

A
  1. What is paced? V, A, Dual
  2. What is sensed? V, A, Dual
  3. What is the response to sensing? [I]nhibit, [T]rigger, [D]ual - can T+I
  4. Rate response (enables HR increase with excercise)

Most are DDDR unless
Permanent AF - these patients need the atria blocked - so have VVIR

76
Q

What is CRT, and what are the indications?

A

Goal is to re-coordinate biventricular contraction (Leads in LV, RV, and sometimes RA). Can be connected to an AICD and pacemaker.

77
Q

What are the indications for an ICD?

A

Post MI:
LVEF <30% + broad QRS
LVEF + NSVT + EP positive
Familial:
LQTS, Brugada, HCM
Cardiac arrest due to VT/VF

78
Q

What are the benefits of CRT?

A
  1. Improves LVEF + haemodynamics
  2. Improved ET
  3. Improved QoL
79
Q

What are the indications for CRT?

A
  1. Heart failure with ventricular dysynchrony
80
Q

What are the diagnostic criteria for IE?

A

Duke’s.
x2maj, x1maj+3min, 5min

Maj
1. Echo
2. Pathognomic bac x2

Min
1. RF
2. Temp
3. BC’s x1
4. Echo
5. Vasc immune complex

81
Q

What are the risk factors for IE?

A

IVDU/Haemodialysis
Prosthesis
Structural heart/valvular disease
Rheumatic heart disease
Diabetes/CKD

82
Q

What are the signs of SUBACUTE IE?

A

Fingers, feet, eyes, kidneys

Clubbing
Petechia and splinter haemorrhages
Janeway lesions (palmar/plantar)
Osler nodes (distal finger painful)
Roth spots
Glomerulonephritis

83
Q

What are the causes of aortic regurgitaiton?

A

Acute
-Dissection
-Infective endocarditis

Chronic valve problem
-Bicuspid aortic valve
-Rheumatic heart disease
-Calcified valves
-CTD’s
-Paget’s

Chronic root problem
-Bicuspid aortic valve
-HTN
-Marfan
-EDL
-Ank Spond

84
Q

What are the renal complications of infective endocarditis?

A

Glomerulonephritis
Haematuria
Acute interstitial nephritis
Eosinophiluria

85
Q

What are the criteria for valve replacement in aortic regurgitation

A

Symptomatic dyspnoea and reduced excercise tolerance AND/OR
-Wide pulse pressure
-ECG changes (on ETT)
-LV enlargement >5.5cm in systole or EF <50%

86
Q

What is the prognosis in AR?

A

Asymptomatic with EF>50% - 1% mortality at 5 years
Symptomatic and (wide pulse pressure+ECG exertional changes+LV enlargement) = 65% mortality at 3 years

87
Q

What is an Austin Flint murmur?

A

Mid-late diastolic murmur caused by aortic regurgitant jet hitting mitral valve leaflet.

88
Q

What eponymous signs of Aortic Regurgitation do you know?

A

Corrigans (Neck)
De Musset (Head)
Mullers (Uvula)
Quincke’s (nailbed)
Traube’s (femoral)

89
Q

How do you manage AR?

A

Medically
Rate control
Diuresis
ACEi

Symptomatic
Intervention:
-TAVI
-Valve replacement

90
Q

What are the clinical signs of constrictive pericarditis?

A
  1. Rapid a and y descents due to collapsing RA against stiff pericardium
  2. Kussmaul’s sign - increase in JVP on inspiration
  3. Pulsus paradoxus
  4. Pericardial knock
  5. Signs of RHF
91
Q

What are the causes of constrictive pericarditis?

A

TB
Trauma
Tumour
Radiotherapy
Connective tissue disease

92
Q

What are the clinical features of HOCM?

A

PACES (6 decks)

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