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Cardiology Flashcards

1
Q

Pathophysiology of heart failure

A

Catecholamines, angiotensin, aldosterone, endothelin, cytokines –> neurohormonal activation –> peripheral vasoconstriction –> fluid retention –> decreased contractility

Neurohormonal activation –> myocyte injury –> decreased contractility

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2
Q

Classes of heart failure

A

NYHA I - no symptoms, even during exercise
NYHA II - reduced physical capacity during medium exercise
NYHA III - severely reduced physical capacity during slight exercise but OK at rest
NYHA IV - symptomatic at rest

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3
Q

TTE for heart failure

A

LV size, shape, global and regional function
Complications - MR, pulmonary HTN, thrombus
Assessment of diastolic function

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4
Q

MRI for heart failure

A

Function
Structure
Viability
Composition

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5
Q

Right heart catherisation transportation

A

R atrium > R ventricle > Main pulmonary artery > PA branch > Pulmonary artery wedge pressure

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6
Q

Definition of HFrEF

A

Symptoms of HF with LVEF < 50%

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7
Q

Definition of HFpEF

A

Symptoms of HF, LVEF > 50% and diastolic dysfunction (evidence of high filling pressure and/or object evidence of relevant structural heart disease)

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8
Q

Role of natriuretic peptides

A

ANP - originated from cardiac atria, released by atrial distension
BNP - originated from ventricular myocardium, released by ventricular overload
CNP - originated from endothelium, released by endothelial stress

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9
Q

BNP physiologically increases with

A

Age
Females
Post menopause

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10
Q

Treatment for HFpEF

A

SGLT inhibitors
Diuretics
Angiotensin receptor blockers
Salt restriction, exercise training
Manage comorbidities (AF, HTN, CAD, OSA)

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11
Q

MOA of SGLT2 inhibitors

A

Blocks reabsorption in PCT –> increases glucose excretion

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12
Q

Outcomes of EMPEROR study

A

Reduced HF hospitalisations (and CV death to lesser degree) in patients who received empagliflozin and dapagliflozin

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13
Q

Goals of treatment in HF

A

Prevent diseases causing LV dysfunction
Prevent progression to symptomatic HF
Reduce symptoms
Reverse remodelling
Improve survival

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14
Q

Management of HFrEF

A

Stage A - high risk, no symptoms
- Risk factor reduction
- Education
- ACE inhibitor
- Treat HTN, DM, hyperlipidaemia

Stage B - structural heart disease, no symptoms
- ACE inhibitor
- B blockers

Stage C - structural disease, previous or current symptoms
- AICD if EF < 35%
- Diuretics
- Aldosterone blockers
- HF rehab
- Ivabradine if HR > 77
- SGLT2 inhibitor
- CRT if LBBB
- Specialised cardiac surgery

Stage D - Refractory symptoms requiring special intervention
- Inotropes
- Transplantation
- Palliation

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15
Q

Four pillars of heart failure

A

ACEI/ARNi/ARB
Beta blockers
Mineralocorticoid receptor antagonists
SGLT2 inhibitors

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16
Q

ARBS vs ACEI for heart failure

A

Far less data for ARBS
Strongest data for candesartan, but can use valsartan
Benefits greatest in ACE-I naive patients

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17
Q

Beta blockers proven benefit in CCF

A

Carvedilol
Bisoprolol
Nebivolol
Long acting metoprolol (succinate)

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18
Q

Evidence for beta blockers in CCF

A

Demonstrated improvement in mortality and morbidity in class II-IV
Must be stabilised and euvolaemic prior to initiation
Reduction in SCD

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19
Q

Spironolactone in CCF

A

Higher doses not shown to have greater benefit but have greater adverse effects
Caution in renal impairment

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20
Q

Indications for ivabradine

A

HR > 70/min (DESPITE adequate beta blocker dose)
If lung disease precludes beta blockers
Beta blockers truly not tolerated - unacceptable symptomatic hypotension, intolerable beta blockers side effects

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21
Q

How does Entresto cause rise in BNP?

A

Entresto - Valsartan + neprolysin inhibitor (sacubitril)

Causes rise in BNP (as BNP is neprolysin substrate), however causes fall in NT pro BNP

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22
Q

Current indications for Entresto in HRrEF

A

Add on therapy if NYHA II-IV (symptomatic HF) and LVEF < 40% after 3-6 months of optimal treatment

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23
Q

Practice point if ACEI already commenced and wanting to start Entresto

A

Need to wait 36 hours after cessation of ACE inhibitor before started Entresto

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24
Q

Role of digoxin and diuretics in HF

A

Nil effect on mortality
Reduces symptoms

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25
Q

Chemo agents associated with cardiotoxic effects

A

Anthracyclines - multiple mechanisms, dose related

Platinum-based agents - vascular disease

Antimetabolites (5-FU) - worsening of CAD

Taxanes - arrhythmia

Cyclosphosphamide - idiopathic HF

HER-2 targeted agents - myocardial dysfunction

Tyrosine kinase inhibitors - HTN

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26
Q

Features of hypertrophic cardiomyopathy

A

Autosomal dominant
Most common inherited cardiomyopathy

Very variable and dependent on LVH +/- obstruction

Palpitations and syncope
Sudden death in young (commonest cause)
Endocarditis
Dyspnoea
Angina

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27
Q

Pathophysiology of HCM

A

Abnormal hypertrophy
- asymmetric septal IVS:PW > 1.5
- mid ventricular
- giant negative T waves
Diastolic dysfunction

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28
Q

TTE findings in HCM

A

Wall thickness
- Asymmetrically thickened left ventricular wall, (≥ 15 mm), typically involving the septum
- LV wall thickness ≥ 30 mm is associated with a high risk of sudden death.

Outflow tract abnormalities
- Systolic anterior motion of the mitral valve
- Mitral regurgitation
- ↑ LVOT pressure gradient via Doppler echocardiography

Other findings
- Left atrial enlargement
- Systolic function typically normal
- Diastolic dysfunction

  • Symmetrically thickened interventricular septum
  • Dynamic LVOT obstruction due to contact between the septum and mitral valve during systole
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29
Q

Management of HCM

A

Treatment heart failure
Improve diastolic filling and reduced ischaemia
Reduce outflow obstruction
- avoid things that increase obstruction
- alcohol septal ablation
- surgery: severe LVOT obstruction and symptoms
Prevent sudden death
Screen first degree relatives

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30
Q

Risk factors for SCD in HCM

A

FHx of premature sudden death
Recurrent syndrome (in young)
NSVT
Severe LVH (septum >2.5-3cm)
Severe obstruction
Abnormal exercise BP pressure response
Level of myocardial fibrosis on MRI
Specific genotypes e.g. Arg719Trp mutations

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31
Q

Types of amyloidosis

A

AL amyloid (primary) - plasma cell dyscrasia
AA amyloid (secondary)
ATTR amyloid (wild type or inherited)
Other - dialysis related, age related, organ specific

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32
Q

Presentation of cardiac amyloidosis

A

HFpEF, low voltage ECG, AF
Heart failure
HTN (low output state)
AF common
Hepatomegaly
Periorbital purpura, if present with HF usually AL amyloidosis
ECG - low voltage, AF
High NT pro-BNP
Ventricular hypertrophy

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33
Q

TTE findings for amyloidosis

A

Increase LV wall thickness
Diastolic dysfunction
Dilated atria
Abnormal longitudinal strain (apical sparing)
Small pericardial effusion
Pulmonary HTN
Speckled myocardium

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34
Q

MRI findings for amyloidosis

A

Structural findings similar to TTE
Abnormal deposition of GAD contrast

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35
Q

Suspect restrictive cardiomyopathy if

A

Predominant right heart failure
LV systolic function relatively preserved
Ventricular wall thickness increased
Diastolic dysfunction
Atria dilated
AV regurgitation common

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36
Q

Features of advanced HF

A

Severe symptoms despite optimal medical therapy
Frequent hospitalisations
Secondary organ dysfunction
Ventricular arrhythmias
Progressive cardiac remodelling
Inotrope requirement
High mortality

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37
Q

Use of inotropes in heart failure

A

Critical support until definitive therapy
Support until resolution form other conditions
Acute decompensation form poor tissue perfusion
Bridging to definitive treatment

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38
Q

Devices for heart failure

A

Implantable defibrillators (AICD)
Biventricular pacing (CRT)
Left ventricular assist device (LVAD)

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39
Q

Indications for HF

A

NYHA II-III HF with LVEF <35% despite optimal medical treatment
Class I HF with IHD if more than 40 days post AMI + EF measured more than 3 months post revascularisation

Primary prevention
Selected patients with an expected survival of > 1 year and any of the following:
- Arrhythmogenic right ventricular cardiomyopathy
- Hypertrophic obstructive cardiomyopathy
- Cardiac channelopathies (e.g., congenital long QT syndrome, Brugada syndrome)
- Severe congestive heart failure
- Neuromuscular disorders (e.g., Duchenne muscular dystrophy, Becker muscular dystrophy)
- Cardiac sarcoidosis

Secondary prevention
All patients with an expected survival of > 1 year, an irreversible cause of ventricular tachyarrhythmias, and any of the following:
- Sudden cardiac arrest (e.g., due to Vfib)
- Unstable VT
- Stable sustained VT
- Inducible VT and/or Vfib on an EP study AND underlying:
- Unexplained syncope and ischemic heart disease
- NSVT due to previous MI or LVEF ≤ 40%

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40
Q

Reason for pacemaker in heart failure

A

LBBB common in heart failure
Leads to LV ‘dysynchrony’
Bi-V pacing aims to resynchronise LV and RV contraction

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41
Q

Effects of LBBB

A

Ventricular systole
- LV activates late
- Relaxed septum pushed into RV
- Aortic valve opens
- Lateral papillary muscle activated late –> MR

Ventricular diastole
- Passive filling late
- Atrial contraction during passive filling

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42
Q

Biventricular pacing indications for CCF

A

Wide QRS >/ 150ms
Low EF < 35%
NYHA II-IV

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43
Q

CRT indications for HF

A

LVEF </35%, NYHA II-IV, optimal medical therapy
Recommended if SR and QRS >/ 150ms
Consider CRT if AF
Consider CRT if QRS 131-140ms
Consider if HFrEF and need for RV pacing

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44
Q

CRT contraindications

A

If QRS < 130ms

45
Q

Surgical management options

A

Mitral valve repair/replacement
Coronary artery bypass
Aortic valve replacement (surgical, TAVI)
Ventricular assist devices) - bridge to more permanent management i.e. transplant, recovery

46
Q

Indications for cardiac transplant

A

Refractory NYHA Class IV HF
VO2 max < 14ml/kg/min + anaerobic metabolism
Severe ischaemia not amenable to intervention
Recurrent refractory ventricular arrhythmias

47
Q

AF epidemiology

A

Prevalence increases with age, gender, comorbidities and heart disease

M > F (30% greater risk)

Associated with 1.5-2 fold increase in all cause mortality

48
Q

Comorbidities associated with AF

A

HTN
Valvular heart disease
Heart failure
Hypertrophic cardiomyopathy
Hyperthyrodiism
Cardiopulmonary disease
Obesity
Diabetes

49
Q

AF pathogenesis

A

Left atrial stretch affecting haemodynamics (via HTN, heart failure, mitral disease)

Genetic

Inflammation

Metabolic syndrome

50
Q

Classification of AF

A

Paroxysmal - terminates spontanously or with intervention within seven days of onset

Persistent - fails to self-terminate within seven days

Long standing persistent - > 12 months

51
Q

Mechanisms of AF

A

1st stage - arrhythmic foci within muscular sleeves extending into pulmonary veins

2nd stage - arrhythmic burden +/- other cardiac factors lead to atrial remodelling

3rd stage - gross electrical and structural atrial remodelling

52
Q

Purpose of beta blocker with flecainide

A

Flecainide organises AF into macro-circuits (often goes from AF to flutter) and simultaneously reduces the refractoriness of the AV node so it can conduct at fast rates  can cause unstable rhythm and cause VF
Thus, AV node blocker needs to be used concurrently with flecainide

53
Q

AF ablation indication

A

Symptomatic AF refractory to medications
Successful in 60-70%
Often requires multiple ablation procedures

54
Q

Definition of atrial flutter

A

Macro re-entrant circuit in RA (between IVC and tricuspid valve)

55
Q

CHA2DS2-Vasc score simplified

A

Risk stratify with
- Congestive heart failure
- Hypertension
- Age > 75 yrs
- Diabetes
- Ischaemic stroke, TIA< systemic emboli (2 points)

If one positive - ?anticoagulation
If two positive - anticoagulation

56
Q

NOACs contraindications

A

Mechanical heart valves
Rheumatic heart disease

57
Q

Different manifestations of WPW

A

Accessory pathway - Delta wave

Orthodromic tachy - narrow complex

Antidromic tachy - wide complex

58
Q

Differentiating VT from aberrancy

A

Definite VT
- AV dissociation, fusion, capture beats

Probable VT
- No RS pattern, > 100ms from beginning of R-wave to nadir of S-wave

Probable not VT
- Typical RBBB or LBBB pattern

59
Q

Hypertrophic cardiomyopathy features

A

Autosomal dominant
Commonest cause of SCD age < 35 yrs

60
Q

Phenotypes of HOCM

A

Septal hypertrophy with or without outflow obstruction
Concentric hypertrophy
Apical hypertrophy
LV free wall hypertrophy
RV hypertrophy

61
Q

Risk stratification of HOCM for consideration of ICD insertion

A
  • FHx of SCD
  • Unexplained syncope
  • NSVT on Holter
  • IVS > 30mm
  • Abnormal BP response during exercise
62
Q

ARVC diagnostic criteria

A
  • Dysfunction and structural abnormalities of RV (can be revealed by echocardiography, MRI, or RV angiography)
  • Histological characteristics (require myocardial biopsy)
  • Abnormal repolarization (diagnosed with ECG)
  • Depolarization/conduction abnormalities (diagnosed with ECG)
  • Arrhythmias (diagnosed with ECG)
  • Family history (confirmation of ARVC in a relative either by criteria, pathological examination in surgery or autopsy, or by genetic testing)
63
Q

ARVC biopsy results

A

Fibrofatty replacement of myocardial tissue

64
Q

Long QT syndrome genes

A

LQT1 - KCNQ1
LQT2 - KCNH2
LQT3 - SCN5A

Autosomal dominant

65
Q

Long QT syndrome types

A

LQT1 - normal but long (associated with exercise)
LQT2 - biphasic (associated with loud noises, emotions)
LQT3 - late peaking (associated with sleeping)

66
Q

Management of LQTS

A

Avoid QT prolonging drugs
Avoid competitive sports
Beta blockers
ICD if high risk VT or previous VT

67
Q

Brugada features

A

Autosomal dominant
Peak prevalence of SCD in 4th decade
ECG - septal downslopign ST elevation

68
Q

AV blocks

A

1st degree - PR prolongation
Mobitz I - prolonging PR until QRS drop
Mobitz II - no variation in PR interval, non-conducted P waves
3rd degree - no association between P wave and QRS

69
Q

Preferred pacing for heart failure and why

A

Biventricular pacing

RV pacing causes mechanical dysynchrony –> RV depolarises first causing discoordination contraction –> results in increased rate of heart failure and mortality

70
Q

Valves of each heart and amount of cuspids

A

Left heart
- Aorta (3)
- Mitral (2)

Right heart
- Pulmonary (3)
- Triscuspid (3)

71
Q

Bicuspid aortic valve features

A

Most common congenital abnormality

Aortopathy - dilation of aortic sinuses, ascending aorta, arch
Coarctation

72
Q

Aortic stenosis symptoms

A

SOB on exertion/reduced exercise tolerance
Fatigue
Angina
Syncope
LV failure

73
Q

Clinical signs of severe AS

A

Plateau pulse
Aortic thrill
Systolic murmur
S4
Parodoxical splitting of S2
LV failure

74
Q

Grading aortic stenosis factors

A

Peak velocity
Mean gradient
AVA
Indexed AVA
Velocity ratio

75
Q

Definition of low flow low gradient AS

A

AVA < 1
Mean gradient < 40mmHg
LVEF < 50%
SVi < 35ml/m2

76
Q

Investigation to distinguish between true severe AS and pseudo severe AS

A

Dobutamine stress echo

No change in gradient with inotropes –> more likely pseudo severe AS

77
Q

Definition of parodoxical low flow low gradient

A

AVA < 1
Mean gradient < 40
Peak velocity < 4m/s
Normal LVEF

78
Q

SAVR vs TAVI

A

SAVR
- Survival benefit
- Valve durability
- Avoid permanent pacer
- Annular enlargement
- Aortic dilatation
- Concurrent valve disease
Recommended < 65yrs

TAVI
- Survival benefit
- Short hospitalisation
- Transfermoral only
- Less pain
- Good haemodynamics
- Durability less important
Recommended > 65s and high perioperative risk

79
Q

Causes of aortic regurgitation

A

Valve disease
- congenital
- degenerative
- endocarditis
- rheumatic

Aortic root/ascending aorta abnormalities
- aortic root dilatation (Marfans/Loeys-Dietz, AS)
- Aortic dissection

80
Q

Symptoms of AR

A

Usually asymptomatic for prolonged period

Dyspnoea
Orthopnoea/PND
Chest pain - noctural/exertional angina

81
Q

Clinical signs of severe AR

A

Wide pulse pressure
Water-hammer/collapsing pulse
Long decrescendo diastolic murmur
S3
Soft A2
Austin flint murmur (mid diastolic rumble/murmur)

82
Q

Echo features of AR

A

Jet width, regurgitant volume
Holodiastolic flow reversal in proximal abdominal aorta
Features of LV dilatation

83
Q

Surgical management for AR

A

Significant enlargement of ascending aorta
Symptomatic
LVESD > 50mm or LVEF < 50%

84
Q

Recommendations for aortic root aneurysm

A

Valve sparing aortic root replacement recommended in young patients with dilation

Ascending aortic surgery recommended in pts with Marfan syndrome with maximal ascending aortic diameter >/ 50mm

Should be consider in pts with aortic root disease with maximal ascending aortic diameter:
- >/55mm in all pts
- >/45mm in presence of Marfan syndrome and additional risk factors
- >/ 50mm in presence of bicuspid valve with additional risk factors or coarctation

Replacement of aortic root or tubular ascending aorta considered when >/ 45mm

85
Q

Mitral regurgitation causes

A

Primary
- primary valve disease - due to abnormality of leaflets, chordae tendinae, papillary muscles, annulus

Secondary
- primary myocardial disease - functional regurgitation due to abnormalities of left ventricle or left atrium

86
Q

Acute MR cause

A

Occurs with spontaneous chordae tendinae or papillary muscle rupture secondary to MI

87
Q

Management of acute MR

A

Medical
- primary goal is to stabilise the pt in preparation for surgery
- temporary mechanical support device

Surgery
- repair/replacement

88
Q

Signs of severe MR

A

LV dilatation
Soft S1, split S2 S3
Pansystolic murmur radiates to axilla
Pulmonary HTN
Small volume pulse
Signs of LV failure
Early diastolic rumble

89
Q

Management of severe primary MR

A

Symptomatic = surgery

Asymptomatic
- TTE every 6-12 months
- Exercise testing with haemodynamics
- Goal directed medical therapy

90
Q

Indications for surgery with MR

A

Symptomatic
If no symptoms, LVEF </ 60% or LVESD >/ 40mm OR new onset AF OR SPAP > 50mmHg OR high likelihood of durable repair, low surgical risk and LA dilatation

91
Q

Features of rheumatic heart disease

A

Result of valvular damage caused by abnormal immune response to group A strep infection

Mitral valve is most common valve involved

Female predominance 2:1

Echo gold standar

92
Q

Characteristic features of rheumatic heart disease on TTE

A

Mitral valve features
- prolapse of anterior leaflet
- Thickened leaflet tips
- Restricted posterior leaflets
- Chordal thickening
- Leafleft calcification
- Diastolic doming of anterior leaflet

Aortic valve features
- Cusp prolapse
- Cusp thickening
- Rolled cusp edges
- Cusp restriction
- Cusp fibrosis, retraction, calcification
- Dilated aortic root

93
Q

Manifestations of acute rheumatic fever

A

Major
- Carditis
- Polyarthritis or aspetic monoarthritis or polyarthralgia
- Sydenham chorea
- Erythema marginatum
- Subcutaneous nodules

Minor
- Fever
- Monoarthralgia
- ESR > 30 or CRP > 30
- Prolonged PR interval

94
Q

Causes of mitral stenosis

A
  • Rheumatic heart disease
  • Nonrheumatic calcific mitral stenosis
  • Congenital
  • Post radiation
  • Endocarditis
  • Endomyocardial fibroelastosis
95
Q

Clinical signs of mitral stenosis

A

Pulse - AF
Malar flush
Prominent A wave
Apex beat - tapping, palpable S1
Associated valve lesions

Severe MS
- Small pulse pressure, opening snap close to S2
- Rumbling diastolic murmur
- Pulmonary HTN
- Apical diastolic thrill

96
Q

Medical management of rheumatic mitral stenosis

A

Warfarin (NOACs contraindicated)
Percutaneous balloon mitral valvuloplasty

97
Q

Contraindications for percutaneous mitral commisurotomy in rheumatic MS

A
  • MVA > 1.5
  • LA thrombus
  • More than mild MR
  • Severe or bi-commissural calcification
  • Absence of commissural fusion
  • Severe concomitant aortic valve disease or severe combined TS and regurg requriing surgery
  • Concomitant CAD requiring bypass
98
Q

Causes of tricuspid regurgitation

A

Primary
- IE
- RHD
- Carcinoid
- Congenital i.e. Ebstein’s anolamy
- Thoracic trauma
- Iatrogenic valve damage

Secondary
- Due to pressure and/or volume overload
- Mediated RV dilatation or enlarged R atrium and triscupid annulus due to chronic AF

99
Q

Causes of cardiac manifestations in carcinoid disease

A

Caused by paraneoplastic effects of vasoactive substances such as 5-hydroxytrypptamine (5-HT or serotonin), histamine, tachykinins and prostaglandins released by malignant cells

100
Q

Findings on carcinoid heart disease

A

Characteristic pathological findings - endocardial plaques of fibrous tissue involving tricuspid valve, pulmonary valve, cardiac chambers, venae cavae, pulmonary artery and coronary sinus

Results in distortion of valves

101
Q

Ebstein’s anomaly

A

Congenital malformation in which there is apical displacement of insertion of septal and posterior tricuspid valve leaflets

102
Q

Clinical signs of tricuspid regurgitation

A

Pansystolic murmur, left LSE, loud on inspiration
JVP with prominent V wave
Pulsatile liver
Signs of pulmonary HTN - loud and palpable P2, RV heave

103
Q

Management of TR

A

If left sided valve disease –> severe primary or secondary TR or TA dilatation (>40mm) is indicated for TV repair or replacement

If severe primary TR and symptomatic + RV dilatation –> should have TV repair or replacement

If no RV dilatation –> medical therapy

If severe secondary TR + severe RV/LV dysfunction or pulmonary HTN –> medical therapy

If severe secondary TR + RV dilatation with NO severe RV/LV dysfunction or pulmonary HTN –> indicated for TV repair or replacement

104
Q

Pulmonary regurgitation features

A

Sequelae of treatment of congenital disorder involving pulmonary valve and/or RV outflow tract - Tetralogy of Fallot, pulmonary stenosis

105
Q

Severe PS pulmonary artery catherisation findings

A

Peak gradient 64mmHg
Mean gradient > 35mmHg

106
Q

How much do PCKS9 inhibitors reduce LDL in addition to statin therapy?

A

60% further reduction

107
Q

Have PCSK9 inhibitors been proven to reduce risk of AMI and death?

A

ODYSSEY OUTCOMES - 15% reduction in mortality (alirocumab)
FOURIER trial - reduction in myocardial infarction but not death (evolocumab)

108
Q

Inhibition of which proteins lowers LDL cholesterol

A

PCSK9
HMG-CoA reductase
ANGPLT3
ATP Citrate lyase

109
Q
A

BPT Flashcards (32 decks)

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