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PACES > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Causes of aortic stenosis

A
  1. Age-related calcification
  2. Congenital bicuspid valve (younger patient)
  3. Connective tissue disease
  4. Accelerated calcification e.g. CKD
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2
Q

Pathophysiology of aortic stenosis

A

Pathological narrowing of the aortic valve, causing left ventricular outflow obstruction.
This leads to LV hypertrophy as a result of chronic increased afterload.

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3
Q

What signs may be seen in aortic stenosis?

A

Inspection: if replaced, may have midline sternotomy scar

Palpation:
- Pulsus parvus et tardus (weak and slow rising pulse)
- May have LV heave due to LVH

Auscultation:
- Ejection systolic murmur radiating to carotids
- May have quiet or absent S2 if severe

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4
Q

DDx in aortic stenosis

A
  • Aortic sclerosis
  • HOCM (ESM at LLSE and apex - louder on valsalva)
  • ASD (ESM at pulm. region)
  • VSD (pan systolic at LLSE)
  • Mitral regurgitation
  • Tricuspid regurgitation
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5
Q

What is the difference between aortic stenosis and aortic sclerosis?

A

Aortic sclerosis: Thickening of the valve without narrowing
- Normal pulse volume
- No radiation of murmur to carotids

Aortic stenosis: Thickening of the valve with narrowing, causing left outflow obstruction

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6
Q

Investigations if suspecting aortic stenosis

A
  • 12-lead ECG: May see LVH
  • Echo with doppler: Assess valvular pressure gradient and valve area
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7
Q

Management of aortic stenosis

A

Symptomatic management with caution:
- Reduction in preload e.g. with AHTs or beta blockers, can increase the pressure gradient across the valve

Symptomatic or severe: Aortic valve procedure
- 1st line: surgical valve replacement (low-intermediate surgical risk)
- 2nd line: Trans-catheter Aortic Valve Implantation (if non-bicuspid and high surgical risk)

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8
Q

How can pacemakers be classified?

A

Number of chambers paced:
- Single chamber (RA or RV)
- Dual chamber (RA + RV)
- Biventricular (RA + RV + LV)

Duration:
- Permanent pacemaker
- Temporary pacemaker
- Temp-perm (insertion of a PPM until arrhythmia resolved or long-term solution achieved)

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9
Q

Indications for permanent pacemaker

A

Symptomatic sinus node disease
- Sinus bradycardia
- Sinus pauses

High-degree AV block
- Mobitz II
- CHB

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10
Q

Complications of pacemakers

A

Insertion-related:
- Pocket haematoma
- Pocket infection
- Pneumothorax
- Lead dislodgement
- Cardiac perforation or tamponade (rare)

Delayed:
- Delayed infection
- Lead fracture
- Thrombosis or stenosis of the veins through which the leads travel
- Inappropriate pacing i.e. incorrectly sensing/pacing electrical activity

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11
Q

How does ICD work?

A

Dual chamber: RA and RV

Senses high-risk ventricular arrhythmias (VT/VF) and delivers a defibrillation shock

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12
Q

ICD indications

A

Prevention of VT/VF arrest

PRIMARY PREVENTION:
- HOCM (sustained VT/cardiac arrest)
- LQTS
- Brugada (most patients)

SECONDARY PREVENTION:
- Previous VT/VF arrest
- Sustained VT

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13
Q

Cardiac resynchronisation therapy - principles and indication

A

CRT is a biventricular pacemaker with 3 leads in the RA, RV and LV

Aims to restore synchronised contractions of the left and right ventricles to improve cardiac output

Generally indicated in:
LVEF <35% and broad QRS and refractory symptoms

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14
Q

Causes of heart failure

A

Vascular causes:
- Ischaemic heart disease
- Chronic hypertension

Structural causes
- Valve pathology e.g. aortic stenosis causing LVOO
- dilated Cardiomyopathy

Infection e.g. IE

Right heart failure
- Most commonly caused by left heart failure
- Right sided valve disease (tricuspid or pulmonary)
- Lung pathology
- Pulmonary vascular disease

Iatrogenic e.g. cardiotoxic medications (chemo)

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15
Q

Signs of severe AS

A

Severe aortic stenosis:

  • Quiet or absent S2
  • Weak and slow rising pulse
  • Evidence of left ventricular failure
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16
Q

Management of heart failure

A

HFpEF: Symptomatic only (diuretics)

HFrEF:
Pharmacological: ABS
- ACE inhibitor
- Beta blocker
- Consider spironolactone
- Dapagliflozin

If refractory to medical treatment and LVEF <35% - consider cardiac resynchronisation therapy

Smoking cessation
Vaccinations

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17
Q

Investigations in suspected heart failure

A

Bedside:
- ECG
- Urine dip if suspecting IE

Blood tests:
- FBC, U+Es, LFTs (hepatic congestion)
- NT-proBNP
- Lipid profile, HbA1c
Imaging
- CXR
- Echocardiogram: assess LVEF

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18
Q

Features of mitral regurgitation

A
  • Pan systolic murmur radiating to axilla, louder on expiration
  • May have displaced, thrusting apex beat

Check for complications:
- AF
- Pulmonary HTN (P2 + raised JVP)

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19
Q

Mitral regurgitation DDx:

A
  • Mitral valve prolapse
  • Tricuspid regurgitation
  • VSD
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20
Q

Complications of mitral regurgitation:

A
  • Atrial fibrillation
  • Left ventricular dilatation
  • Cardiac failure
  • Pulmonary HTN
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21
Q

Investigations for mitral regurgitation:

A

Bedside:
- ECG
- Urine dip (protein/blood)

Bloods:
- FBC
- If suspecting endocarditis: WCC, CRP, 3x blood cultures
- NT-proBNP
- consider troponin

Imaging:
- Echocardiogram (valve function, LV function, vegetations)
- CXR (Cardiomegaly/pulm oedema)

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22
Q

Causes of mitral regurgitation

A

Valvular disease:
- Degenerative
- Infective (endocarditis, rheumatic fever)

Non-structural:
- Functional MR in LV dilatation
- Myocardial infarction - papillary muscle rupture
- Connective tissue disorder

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23
Q

Management of mitral regurgitation

A

1) Patient education: e.g. smoking cessation

2) Pharmacological:
- management of HF
- management of AF

3) Surgical
- Mitral valve repair or replacement
- Transcatheter mitral valve replacement (Mitraclip) if high anaesthetic risk

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24
Q

Indications for surgery in mitral regurgitation

A

Symptomatic

OR

Asymptomatic with
- LVEF < 60%
- LV dilatation

OR

Acute mitral regurgitation e.g. papillary muscle rupture in myocardial infarction

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25
Q

Signs of severe AS

A

Quiet or absent S2
Narrow pulse pressure
Weak and slow rising pulse

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26
Q

A metallic S1 is…

A

mitral valve replacement

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27
Q

A metallic S2 is…

A

aortic valve replacement

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28
Q

A right venticular heave indicates…

A

Pulmonary HTN (loud P2)

or

Pulmonary stenosis (no loud P2)

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29
Q

Pulmonary stenosis DDx

A
  • Pulmonary hypertension (should have loud P2)
  • ASD (ESM at pulm area with split S2)
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30
Q

A lateral thoracotomy scar could be…

A
  • Descending aorta surgery
  • Mitral valvotomy (older patients)
  • Lung surgery
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31
Q

What does inspiration do to venous return/preload?

A

INspiration INcreases venous return

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32
Q

Target INR for metallic mitral valve

A

3-4
(think Mitral is More than aortic)

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33
Q

Target INR for metallic aortic valve

A

2.5 - 3.5

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34
Q

Pulmonary HTN in congenital heart disease - management

A
  • Assess for any shunts which may require treatment
  • Otherwise may develop Eisenmenger’s (shunt reversal) whch can lead to central cyanosis
35
Q

Causes of pulmonary valve disease

A
  • Infection: maternal Rubella
  • Syndrome: Downs, Turner’s, Noonan
36
Q

Features of Tetralogy of Fallot

A

PROVE:

  • Pulmonary stenosis
  • Right ventricular hypertrophy
  • Over-riding aorta
  • Ventricular septal defect
  • Eisenmenger’s syndrome may develop (cyanosis)
37
Q

Causes of tricuspid regurgitation

A
  • Pulmonary hypertension
  • Infection e.g. endocarditis
  • Congenital heart disease e.g. Ebstein’s anomaly
38
Q

Why does endocarditis tend to affect the tricuspid valve in IVDU?

A

The particulate that injectable recreation drugs are ‘cut’ with deposit mostly on the tricuspid valve, as the substances flow through the heart. This predisposes the tricuspid valve to vegetations.

39
Q

Causes of atrial fibrillation

A

“SMITHA”

  • Sepsis
  • Mitral valve disease (typically stenosis)
  • IHD
  • Thyrotoxicosis
  • HTN
  • Alcohol
40
Q

Options for rate control in AF

A

BCD

  • Beta blockers
  • Calcium channel blockers
  • Digoxin
41
Q

Importance of valvular pathology and AF

A

This is an absolute indication for anticoagulation

42
Q

Echo criteria for severe AS

A
  • Mean pressure gradient across valve of >40 mmHg
  • Aortic valve area < 1cm2
43
Q

Features of severe mitral regurgitation

A

Displaced apex beat
Pulmonary hypertension - JVP
Left ventricular failure

44
Q

Marfan’s syndrome complications

A

Cardiac - aortic root dilation, aortic dissection, AR, MVP

Resp - spontaneous pneumothorax

Eyes - lens dislocation

MSK - Scoliosis, pectus excavatum, pes planus

45
Q

Pan systolic murmur DDx

A

Mitral regurgitation

Tricuspid regurgitation

VSD (pan-systolic/ejection systolic character at LLSE)

46
Q

Patent ductus arteriosus examination

A

Inspection: Can be young patient
‘Differential cyanosis’: pink fingers and blue toes

Pulse: collapsing pulse may be present

Palpation: may have right ventricular heave, palpaple P2

Auscultation:
- Continuous, machine-like murmur
“rolling thunder” in P area
- radiating to back (loudest over left scapula)
- louder in expiration

47
Q

Complications of PDA

A
  • Pulmonary hypertension
  • Right ventricular dilation → functional tricuspid regurgitation
  • Left ventricular dilatation
  • Endarteritis - infection of the PDA
48
Q

Management of PDA

A

Mild: conservative management

Severe: percutaneous device closure

49
Q

Mitral valve prolapse causes

A

Primary: degenerative

Secondary:
- infection
- connective tissue disorders (Marfans, Ehlers Danlos)
- PKD

50
Q

Mitral valve prolapse complications

A
  • Left heart failure
  • Infective endocarditis
  • Thromboembolic events
  • Atrial fibrillation
51
Q

Mitral valve prolapse examination

A
  • Systolic click
  • Late systolic murmur in (M) area radiating to axilla
  • Check for signs of Marfan’s/EDS
52
Q

Mitral valve prolapse management

A
  • Serial monitoring with echocardiography
  • If decompensated: mitral valve repair
    (valve replacement if anatomy not amenable to repair)
53
Q

Eisenmenger Syndrome complications

A
  • Hypoxaemia → cyanosis
  • Right ventricular failure
  • Thromboembolic events
  • Infective endocarditis
54
Q

Eisenmenger syndrome pathophysiology

A

Left→Right shunt reverses as RV pressure > LV pressure, and becomes Right→Left shunt

Most common causes: VSD, ASD, PDA

55
Q

Eisenmenger Syndrome examination

A

Inspection: Young patient, clubbing, central cyanosis, may have raised JVP

Palpation: RV heave

Auscultation: Fixed split S2 with loud pulmonary component

56
Q

Pulmonary hypertension causes

A

Primary: excess endothelin release

Secondary:
1) Respiratory disease e.g. COPD leading to cor pulmonale

2) Cardio pathology e.g. VSD, ASD, PDA

3) Systemic disease e.g. systemic sclerosis

57
Q

Pulmonary hypertension investigations

A

Echo
- pulmonary arterial pressure >25mmHg
- Look for any shunts
- can get functional TR from RV dilatation

Cardiac catheterisation is diagnostic

58
Q

Pulmonary hypertension management

A

Medications include:
- Calcium channel blockers
- Bosentan
- Iloprost
- Sildenafil

Advise against pregnancy in women (increased mortality)

59
Q

Complications of prosthetic valves

A

During intervention:
- Bleeding
- Infection
- Damage to surrounding structure e.g. PTX
- AVN dysfunction in aortic valve intervention -> conduction delay

Post-intervention:
- Infective endocarditis
- Prosthesis failure (paravalvular leaks, displacement)
- Thromboembolism
- Bleeding related to anticoagulation
- Haemolysis across valve

60
Q

Diastolic murmur DDx

A

Aortic regurgitation

Mitral stenosis

Pulmonary regurgitation (rare)

61
Q

Causes of aortic regurgitation

A

Acute AR = emergency
- Aortic dissection
- Infective endocarditis
- Prosthetic valve failure e.g. displacement

Chronic AR
- Degenerative valve disease
- Congenital bicuspid valve
- Connective tissue disorder e.g. Marfan’s, ankylosing spondylitis

62
Q

Management of aortic regurgitation

A

Patient education e.g. smoking cessation

Medical management
- Cause: e.g. antibiotics in IE
- Decompensated HF management
- AVOID BETA BLOCKERS

Severe or symptomatic AR:
- Refer for surgical valve replacement ( or TAVI)

Acute AR
- If in cardiogenic shock may need ICU support
- Do not give beta blockers

63
Q

Murmur in HOCM

A

Ejection systolic murmur
Apex and lower left sternal border
No radiation to carotids

Loudest on valsalva
Quieter on hand grip

Valsalva causes decreased venous return
- reduced expansion of the left ventricle
- septal hypertrophy causes more obstruction -> more pronounced murmur

64
Q

HOCM causes

A

Primary: genetic mutations (autosomal dominant)

Secondary:
- Amyloidosis
- Friedrich’s ataxia
- Myotonic dystrophy

65
Q

HOCM examination

A

Inspection:
- Young patient
- Cardiac device?
- Myotonic dystrophy/Friedrich’s ataxia

Palpation:
- Jerky/thrusting apex beat

Auscultation:
- Ejection systolic murmur loudest at apex and left lower sternal edge
- Louder on valsalva
- Quieter on hand grip

66
Q

HOCM investigations

A
  • Full history incl. FH
  • ECG - LVH, LBBB, VT
  • Echo, cMRI
  • Holter to assess for VT

Calculate the HOCM-SCD score
Consider ICD
Genetic testing

67
Q

HOCM management

A
  • Patient education
  • Avoid strenuous exercise and caffeine
  • Inform DVLA for group 2 license only

Medications: BB or CCB
(AVOID ACEi, nitrates)

Surgical:
- Septal ablation
- Septal myectomy

Consider ICD if high risk for life-threatening arrhythmia

68
Q

Complications of HOCM

A
  • Left outflow tract obstruction -> cardiac decompensation
  • Life threatening arrhythmia
  • Sudden death
69
Q

HOCM inheritance

A

Autosomal dominant (if inherited)

Otherwise - de novo mutations

70
Q

VSD causes

A

Primary - congenital

Secondary - rupture in myocardial infarction

Can be associated with Down’s and DiGeorge syndrome

71
Q

VSD - examination

A

May be a young patient

Pansystolic murmur, loudest at LLSE
No radiation

72
Q

Complications of VSD/ASD

A

RVH
Functional TR
Pulm. HTN
Eisenmenger’s syndrome
Endocarditis
YOUNG STROKE

73
Q

VSD/ASD management

A

Small - monitor

Large - surgical closure

74
Q

ASD examination

A

Soft ejection systolic murmur at pulmonary area with fixed widely split S2

75
Q

Septal defects (ASD or VSD) - investigations

A

ECG/Holter
Echo
Bubble echo or cmri may be required
CXR
Bloods incl. infection markers

76
Q

Causes of PDA

A

Primary: congenital

Secondary: Neonatal rubella

77
Q

Mitral stenosis causes

A

Primary: congenital

Secondary:
- Rheumatic fever >90%
- Degenerative calcification
- Infective endocarditis

78
Q

Mitral stenosis examination

A

Inspection: malar flush

Palpation: check for AF
May have palpable P2

Auscultation: mid-diastolic murmur with opening snap
- louder on expiration
- radiates to axilla

79
Q

Mitral stenosis ix

A

ECG
Bloods incl. infection markers
Echo

80
Q

Features of severe Mitral stenosis

A

Symptomatic

Pulmonary HTN
AF

Echo:
Valve gradient >10mmHg
Mitral valve area <1cm2 on echo

81
Q

Mitral stenosis management

A

Asymptomatic: observe, W&W
- Conservative mx of AF and HF

Symptomatic or severe: Percutaneous balloon mitral valvuloplasty or surgical MVR

82
Q

Atrial fibrillation - rate control indications and options

A

Rate control is first line in all patients EXCEPT for:
- New onset AF
- Heart failure
- Reversible cause

Options: BCD
- Beta-blocker
- CCB (avoid in HF)
- Digoxin (sedentary patients)

83
Q

Rhythm control options in AF

A

1) Pharmacological: Amiodarone or fleicanide

2) DCCV (elective, or emergency if unstable)
- Ideally anticoagulate for 4 weeks before

3) Ablation if above unsuccessful
- EP study first to identify correct areas to target

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