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MBBS - Year 2 > Cardiology - Valvular Disease > Flashcards

Cardiology - Valvular Disease Flashcards

1
Q

Where are most valve disease found

A

L side

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2
Q

What can go wrong with valves

A

Stenosis - doesn’t fully open

Regurgitation - doesn’t close properly

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3
Q

What is valve disease caused by

A

Disease of valve leaflets OR

Stretching of the structure that the valve is attached to

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4
Q

Congenital causes of valve disease

A

Bicuspid aortic valve

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5
Q

Acquired causes of common valve disease

A

Degenerative
Rheumatic
Endocarditis

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6
Q

Secondary/ functional regurgitation

A

Stretching of structure the valve is attached to causing leakage

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7
Q

How do valves work in a normal ventricle

A

Valve cusps meet –> valve closes

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8
Q

How do valves work in a dilated ventricle

A

In a stretched valve ring, cusps don’t meet –> valve doesn’t close (leaking valve)

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9
Q

Causes of 2’ regurgitation

A

Dilated LV

Dilated aortic root

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10
Q

Causes of dilated L ventricle

A

IHD
Dilated cardiomyopathy
HTN

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11
Q

What type of regurgitation can be caused by dilated LV

A

MR

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12
Q

What can cause dilated aortic root

A

Cystic medial necrosis
Bicuspid AV
Aortic dissection

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13
Q

Cystic medial necrosis

A

Medial layer undergoes necrosis of connective tissue –> weakening

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14
Q

When does cystic medial necrosis happen

A

Aging
CTD e.g Marfan’s, EDS

Accelerated by hTN

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15
Q

What type of regurgitation can be caused by dilated aortic root

A

AR

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16
Q

What can high LA pressure cause

A

Pulmonary oedema

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17
Q

What can high RA pressure cause

A

Increased JVP
Ascites
Peripheral oedema

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18
Q

What is rheumatic fever

A

An infl condn involving heart, skin and connective tissue usually affecting children (occasionally young adults)

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19
Q

When does rheumatic fever develop

A

3 weeks after sore throat from group A strep

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20
Q

What % of rheumatic fever pts have cardiac involvement

A

50%

Usually occurs after recurrent episodes (fibrosis)

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21
Q

How can rheumatic fever cause valve damage

A

Abnormal immune response to Group A Strep

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22
Q

How can rheumatic fever be prevented

A

Penicillin after sore throat

Also treated w/ penicillin

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23
Q

Rheumatic heart disease

A

Long-term consequence of rhematic fever

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24
Q

Primordial prevention of RHD

A

Improved living condn

Access to medical care

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25
Q

Primary prevention of RHD

A

Penicillin for confirmed strep pharyngitis

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26
Q

Secondary prevention of RHD

A

Extended abx (yrs - lifelong)

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27
Q

Epidemiology of rheumatic disease causing valve disease

A

Commonest cause in developing world but rare in developed world

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28
Q

How does valve disease present

A

Incidental finding - hearing murmur or in ECG

Heart failure symptoms - fatigue, breathlessness on exertion, swollen legs

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29
Q

What is mitral valve disease often associated with

A

AF

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30
Q

What can aortic valve disease be associated with

A

Angina
Dizziness
Sudden death

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31
Q

Normal valve function in systole

A

Mitral valve closed

Aortic valve open

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32
Q

Normal valve function in diastole

A

Mitral valve open

Aortic valve closed

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33
Q

What can cause MS

A

Thickening of leaflets that fuse at commisures

Repeated infl also causes valve damage

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34
Q

Where do valve leaflets meet

A

Commisures

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35
Q

What can cause MR

A 
Damage to any part of MV structures 
LV dilatation (2' MR)
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36
Q

Pathophysiology of MR

A

Blood leaks back from LV into low pressure LA during systole

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37
Q

What can be heard during MR

A

Pan-systolic murmur radiating to axilla

Displaced apex beat

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38
Q

Which pts with MR will have surgery

A

Severe symptomatic MR
Asymptomatic with LV impairment

Most pts are asymptomatic

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39
Q

Mitral valve prolapse

A

Displacement of some part of one/both mitral valve leaflets into LA during systole

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40
Q

Commonest cause of c/c MR

A

Mitral valve prolapse

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41
Q

Auscultation of mitral valve prolapse

A

Mid-systolic click with a late systolic murmur

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42
Q

Mitral valve repair

A

Removal of extra tissue
Leaflet edges closed with sutures
Annuloplasty ring tightens valve

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43
Q

Normal mitral valve area

A

4 - 6 cm2

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44
Q

Area of mitral valve when stenosed

A

<2 cm2

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45
Q

Mitral valve stenosis pathophysiology

A

Problem of diastole - blood unable to be pushed from LA to LV
Reduced filling of LV –> reduced SV and CO
High pressure of LA transmitted back to pulmonary circulation –> pulmonary oedema
Increases risk of AF

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46
Q

Mitral faces

A

Rosy cheeks - malar rash

Rest of face has bluish tinge due to cyanosis

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47
Q

Listening for MS

A

Left lateral position
Place bell lightly over apex
Low frequency rumbling sound beginning in mid-diastole

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48
Q

Auscultation of MS

A

Loud S1
Opening snap - sudden tensing of chords
Mid-diastolic murmur (+presystolic accentuation)

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49
Q

Treatment of mitral stenosis

A

Balloon valvotomy

Catheter passed into femoral vein into RA then into MV
Balloon rapidly inflated to crack open commissures

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50
Q

Aortic stenosis

A

Thickening of aortic leaflets causes obstruction to outflow

Issue of systole

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51
Q

How many aortic leaflets are there

A

3

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52
Q

Common causes of aortic stenosis

A 
Calcific disease (older pt)
Bicuspid valve (younger pt)
Rheumatic heart disease
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53
Q

Effects of aortic stenosis on heart structure

A

LV is pressure loaded because of obstruction to flow and hypertrophies

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54
Q

Symptoms of aortic stenosis

A

Exertional dyspnoea
Angina-like chest pain
Light-headedness and syncope
Sudden death caused by arrhythmias

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55
Q

What causes exertional dyspnoea

A

Raised LVEDP

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56
Q

Why is there reduced myocardial oxygen supply in aortic stenosis

A

Coronary Perfusion Pressure = aortic diastolic pressure - LVEDP
In severe AS, the stiff, hypertrophied LV has a high LVEDP –> reduced CPP

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57
Q

Survival in aortic stenosis

A

Short lifespan after onset of severe symptoms

Mortality majorly increased by valve replacement surgery

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58
Q

Commonest congenital heart defect

A

Bicuspid aortic valves - screen 1st degree relatives

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59
Q

Main risks with bicuspid aortic valves

A

Aortic stenosis and/or regurgitation
Associated aortopathy
IE

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60
Q

Aortopathy

A

Dilatation of any part or all of the proximal aorta forth aortic root to aortic arch

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61
Q

What condns are bicuspid aortic valves associated with

A 
Coarctation of action (BAV in 50%)
Turner Syndrome (BAV in 30%)
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62
Q

Mx of bicuspid aortic valve

A

All pts must have lifelong surveillance and will require surgery on valve and/or aorta in their lifetime

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63
Q

Is aortic regurgitation a problem of diastole or systole

A

Diastole - leaflets of aortic valve don’t meet properly allowing blood to leak back into LV

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64
Q

What causes aortic regurgitation

A

Disease of leaflets

Dilatation of aortic root

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65
Q

Clinical features of aortic regurgitation

A

Angina-like chest pain (decreased perfusion pressure and compensatory hypertrophy)
Dilated LV –> displaced apex
Collapsing pulse
Wide pulse pressure

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66
Q

Collapsing pulse

A

High systolic pressure

Low diastolic pressure

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67
Q

Corrigan’s sign

A

Prominent carotid pulsation

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68
Q

Why is there reduced myocardial oxygen supply in AR

A

CPP = Aortic Diastolic Pressure - LVEDP

In severe, ar, the aortic diastolic pressure is low –> reduced CPP

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69
Q

Listening for aortic regurgitation

A 
Ask pt to:
Sit up 
Lean forward 
Exhale completely
Hold breath in full expiration

Hold diaphragm firmly at LSE
Early diastolic murmur - decrescendo

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70
Q

Cause of significant tricuspid regurgitation

A

RV enlargement

Usually functional

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71
Q

Signs of tricuspid regurgitation

A

Distended JVP w/ prominent v wave
Enlarged and pulsatile liver
Systolic murmur at LSE

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72
Q

Treatment of tricuspid regurgitation

A

Of the cause of RV enlargement (occasionally surgery is needed)

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73
Q

How common is tricuspid stenosis

A

Rare

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74
Q

Cause of tricuspid stenosis

A

Rheumatic heart disease

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75
Q

How common is pulmonary stenosis

A

Rare

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76
Q

Usual cause of pulmonary stenosis

A

Congenital

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77
Q

Pulmonary regurgitation as a functional issue

A

Due to dilated pulmonary artery caused by pulmonary HTN

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78
Q

Epidemiology of CVD

A

1 in 4 deaths in England

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79
Q

Modifiable risk factors for CHD

A 
HTN 
DM 
High cholesterol 
Smoking 
Obesity 
Diet 
Alcohol 
Stress 
Sedentery lifestyle
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80
Q

Non modifiable risk factors for CHD

A

Fhx
Gender
Ethnicity
Age

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81
Q

Risk calculator for primary prevention of CVD

A

QRISK2/3

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82
Q

2’ prevention of CHD

A 
Antipltelts (Asp, clop, prasugrel, ticagrelor)
Beta-blockers/ ivabridine
Statin
ACEi
Lifestyle modification 
Cardiac rehab
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83
Q

BP recommendations for pts at risk of CHD

A

Lower BP to <140/90mmHg

Systolic 120-130 in pts 18 to 69 years old

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84
Q

By how much does medication affect BP

A

Reduces bp by 10/6 mmHg

Doubling dose results in only further 20% drop

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85
Q

Lifestyle modification for HTN

A 
Wt loss 
Mediterranean diet 
Reduced Salt intake (2.4Na/day)
Physical activity (30mins aerobic/ day)
Mod alcohol
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86
Q

When does cholesterol level become worrying

A

> 5.2mmol/l

Contributes to 46% of CHD deaths

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87
Q

Where do HDLs carry cholesterol

A

Away from arteries and back to liver, then excreted from body

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88
Q

What do LDLs do

A

Build up in walls of the arteries to form thick, hard deposits that narrow the arteries and make them less flexible

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89
Q

Main storage form of LDL

A

Triglycerides

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90
Q

Treatment of hypercholesterolaemia

A

Statins first line therapy for all pts with CVD and T2DM

Atorvastatin 80mg OD

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91
Q

Treatment for dysglyceamia

A

Diet, aerobic exercise and resistance training

Improves lipid profile, alters glucose metabolism and tightens glycemic control

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92
Q

1st line therapy for DM

A

Metformin

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93
Q

Issues associated with obesity

A 
Raised BP 
Raised LDL & triglycerides 
Low HDL 
Impaired glucose tolerance 
Increased insulin resistance
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94
Q

What % of pts have depression post-MI

A

15-20%

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95
Q

Cardiac rehab

A

Comprehensive, long-term program involving prescribed exercise, risk-factor modification, education and counselling

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96
Q

What does CVD incl

A

CHD
CVA
PAD

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97
Q

What types of fat should we be eating

A

MUFA/PUFAs

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98
Q

Mediterrenean-style diet

A

More bread, fruit, vegetable and fish

Less meat and replace butter/cheese with products based on plant oils

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99
Q

How does HR affect myocardial demand

A

The higher the HR, the higher the demand

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100
Q

How does force of contraction affect myocardial O2 demand

A

The stronger the force of contraction, the higher the demand

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101
Q

Types of drugs for CAD

A

Reduce cardiac workload

Coronary vasodilators

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102
Q

Drugs that reduce cardiac workload

A

Beta-blockers
Ca channel blockers
Other channel inhibitors - ivabradine, ranolazine

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103
Q

Coronary vasodilators

A

Nitrates

K channel opener - Nicorandil

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104
Q

Block L-type Ca channels present in

A

Arterial smooth muscle
Cardiac muscle
Cardiac pacemaking tissue

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105
Q

What does blocking Ca channels in arterial smooth muscle do

A

Causes vasodilation

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106
Q

What does blocking Ca channels in cardiac muscle do

A

Reduces force of cardiac muscle contraction

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107
Q

What does blocking Ca channels in cardiac pacemaking tissue do

A

Reduce HR

Blocks AVN

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108
Q

Types of Ca channel blockers

A

Non-dihydropyridine (-ve inotropic)

Dihydropyridine (non-inotropic)

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109
Q

Examples of non-dihydropyridine Ca channel blockers

A

Verapamil - mainly cardiac effects

Diltiazem - both cardiac and vascular

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110
Q

Uses of non-dihydropyridine Ca channel blockers

A

Angina
Arrhythmias
(Some effect on BP)

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111
Q

Examples of dihydropyridine Ca channel blockers

A

Amlodipine

Nifedipine (decreases arterial resistance)

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112
Q

Uses of dihydropyridine Ca channel blockers

A

Acts mainly on vascular smooth muscle to reduce BP
Little to no cardiac effect
Widely used for HTN

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113
Q

Known adverse effects of Ca channel blockers - cardiac

A

Slow HR

Reduced contraction - may worsen heart failure

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114
Q

Known adverse effects of Ca channel blockers - vascular

A 
Headache (hypotension)
Peripheral oedema 
Reflex tachycardia (may be harmful to those with CAD)
Rash 
Constipation
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115
Q

How do you choose Ca channel blockers

A

Whether you want arterial or cardiac effects

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116
Q

Types of beta-adrenoceptors

A

Beta-1 in the heart

Beta-2 in the airways

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117
Q

What do beta-adrenoceptors bind to

A

Circulating adrenaline and noradrenaline released by sympathetic system

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118
Q

Example of non-selective beta-blocker

A

Propanolol

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119
Q

Examples of cardio selective beta-blockers

A

Atenolol
Bisoprolol
Metoprolol

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120
Q

Examples of beta-blockers with vasodilator activity

A

Carvedilol

Labetalol

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121
Q

Adverse effects of beta-blockers - cardiac

A 
Bradycardia 
Initially worsens heart failure
Bronchoconstriction
Fatigue 
Cold extremities 
Erectile dysfunction
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122
Q

Adverse effects of beta-blockers - sympathetic blockade

A

Bronchostriction (blockade of beta2-adrenoceptors)

Tiredness, feel cold

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123
Q

Nitrates MOA

A

Increases conc of endothelium NO –> vascular smooth muscle relaxation

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124
Q

Effects of nitrates

A

Arterial dilation

Venous dilation that reduces blood return to heart

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125
Q

Effects of arterial dilation - nitrates

A

Improve coronary supply

Reduce afterload by lowering BP

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126
Q

Effects of venous dilation - nitrates

A

Decreased preload and stretching of heart

Decreased pressure in the ventricles (esp diastolic wall pressure)

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127
Q

Commonly used nitrates

A

GTN/ NTG

Isosorbide mononitrate

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128
Q

Administration of GTN/ NTG

A

s/l, spray, buccal

For a/c use

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129
Q

Administration of isosorbide mononitrate

A

po OD

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130
Q

Nitrates and IHD

A

Symptomatic relief of ischaemic pain

NOT shown to have major impact on mortality

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131
Q

Adverse effects of nitrates

A

Hypotension
Reflex tachycardia
Headache
Flushing

132
Q

Who prescribes specialist drugs for angina

A

Experienced drs for 3rd to 4th line treatment

133
Q

Examples of specialist drugs for angina

A

Nicorandil
Ranolazine
Ivabradine

134
Q

Nicorandil

A

Has nitrate action

Opens K channel

135
Q

Ranolazine

A

Late Na current inhibitor

136
Q

Ivabradine

A

Spp sinus node inhibitor
Blocks cardiac conduction
Similar to BB

137
Q

How does cardiac output affect MAP

A

Slower and less vigorous pumps lowers MAP

138
Q

How does vascular resistance affect MAP

A

Wider arteries, lower MAP

139
Q

Types of drugs for HTN

A

Reducing intravascular volume
Reduce sympathetic tone
Relax peripheral arteries
Block neuroendocrine mediators of bp

140
Q

What drugs reduce intravascular volume

A

Diuretics - thiazides

141
Q

Which antihypertensives reduce sympathetic tone

A

Alpha and BB; central acting agents

142
Q

Which antihypertensives relax peripheral arteries

A

Ca-channel blockers

143
Q

Which antihypertensives block neuroendocrine mediators of bp

A

ACEi
ARBs
Renin inhibitors

144
Q

Examples of ACEi

A

Captopril
Enalapril
Ramipril

145
Q

What does aldosterone release cause

A

Salt and water retention

Increasing intravascular volume

146
Q

When to use ACEi

A

1st line HTN except for selected pt (<55 or African descent)

1st line in pervious heart failure or cardiac damage

147
Q

Safety and suitability of ACEi

A 
Drops BP (first dose)
Worsens renal function 
Retains K
148
Q

Mitigating ACEi dropping BP

A

Give small test dose

Check pt not too volume depleted

149
Q

ACEi and renal function

A

Check U&E’s before and one week after

150
Q

ACEi and K retention

A

Stops K supplement or K-sparing diuretic

151
Q

Mechanism of ACEi

A

Inhibits angiotensin converting enzyme

Reducing generation of angiotensin II and thus aldosterone –> Na and water aren’t reabsorbed as much

152
Q

ARBs

A

Angiotensin II receptor blockers

Similar to ACEi

153
Q

What happens when AT1 receptors bind to angiotensin II

A

Vasoconstriction
Increased sympathetic stimulation
Increased ADH secretion

154
Q

Examples of ARBs

A

Losartan

Irbesartan

155
Q

Which pts take ARBs

A

Pts who can’t tolerate ACEi

156
Q

Types of diuretics

A

Loop
Thiazides
Thiazides-like
K sparing

157
Q

What are Loop diuretics v efficient for

A

Heart failure

158
Q

Examples of loop diuretics

A

Furosemide

Bumetanide

159
Q

Na excretion in loop diuretics

A

Up to 25% Na load excreted, can be used in renal impairment

160
Q

How long do loop diuretics take to work

A

30 mins (IV) to 1 hr (rapid action)

161
Q

Administration of loop diuretics

A

po OD in the morning

Can be used orally for long-term control

162
Q

Thiziade diuretiucs

A

Bendroflumethiazide for HTN

163
Q

Thiazide-like diuretics and Na excretion

A

5-10% Na load excreted

Ineffective if eGFR is <30 and should be avoided

164
Q

Example of a thiazide-like diuretic

A

Indapamide

165
Q

K sparing diuretics and Na excretion

A

<5% Na load excreted

Used together with more effective diuretics

166
Q

Example of K sparing diuretics

A

Spironolactone - blocks aldosterone for heart failure and HTN

167
Q

Diuretics safety

A

Hypovalemia, dehydration and hypotension

Electrolyte imbalance

168
Q

Electrolyte imbalance on diuretics

A

Low K, Na
High urea - due to dehydration
Check electrolytes regularly if on high dose

169
Q

Monitoring for diuretics

A

BP, urine output or body wt

170
Q

4th line drugs for resistant HTN

A 
BB 
Alpha-blockers 
Renin inhibitors
Central sympathetic outflow 
K channel opener
171
Q

Renin inhibitors - reistant HTN

A

Aliskiren

172
Q

Central sympathetic outflow - resistant HTN

A

Clonidine

Methyldopa

173
Q

K channel opener - resistant HTN

A

Minoxidil

174
Q

Antihypertensive algorithm

A

Aged <55 yrs - start w/ ACEi/ARB
Aged >55yrs or Afro/carribean - CCB

ACEi/ARB + CCB

ACEi/ARB + CCB + thiazide-like diuretic

4th line drugs

175
Q

What is the early part of P wave due to

A

RA depolarisation

176
Q

What is middle part of p wave due to

A

RA and LA depolarisation

177
Q

What is late part of p wave due to

A

LA depolarisation

178
Q

Normal height of p wave

A

<2.5mm (squares) tall

179
Q

What can cause tall p waves

A

RA abnormality - RA is overloaded, usually associated with enlargement of RA

180
Q

In which leads can you see RA abnormalities in best

A

Tall, peaked P waves, normal duration

Inferior leads - II, III, aVF

181
Q

In which condns do we see tall p waves

A

Pulmonary disease

Congenital heart disease

182
Q

Normal width of p wave

A

<3mm wide

183
Q

What can cause broad p waves

A

LA abnormality

184
Q

In which leads can you see LA abnormality best in

A

Limb leads

185
Q

In what condns do we see broad p waves

A

Valvular heart disease - left side
Hypertensive heart disease
Cardiomyopathies
CAD

186
Q

When might p waves be intermittently absent

A

Sinus arrest

SA exit block

187
Q

Sinus arrest

A

SAN fails to generate impulse

188
Q

SA exit block

A

Impulse fails to leave SAN

189
Q

What can cause a short PR interval

A

Low atrial pacemaker

Accessory pathway

190
Q

Why would a low atrial pacemaker cause a short PR interval

A

Lies closer to AVN so distance is shorter

191
Q

Why would an accessory pathway cause a short PR interval

A

The extra connection may conduct more quickly than AVN e.g. Wolf-Parkinson-White

192
Q

What can cause a long PR interval

A

AV block

Can be 1st, 2nd or 3rd degree

193
Q

1st degree AV block

A

Prolonged PR interval as impulses travel slower from atria

194
Q

2nd degree AV block

A

Leads to intermittent failure off the atrial impulse to conduct to ventricles (some impulses make it through AVN)

195
Q

3rd degree AV block

A

None of the atrial impulses travel to ventricles

196
Q

Possible abnormalities of QRS complex

A

Too wide
Too big (hypertrophy)
Pathological Q waves (after MI)

197
Q

Supraventricular origin of wide QRS complex

A 
Aberrant conduction:
Bundle branch block 
Brugada pattern 
'Toxic' conduction delay 
Preexcitation
198
Q

Ventricular origin of wide QRS complex

A

Ventricular ectopic beat

Ventricular paced beat

199
Q

Wolf-Parkinson-White on an ECG

A

Short PR interval
Wide QRS complex
Delta wave

200
Q

Normal ventricular depolarisation

A

Phase 1 - septum depolarises L –> R

Phase 2 - both ventricles depolarise simultaneously (but LV is electrically predominant)

201
Q

Why is LV electrically predominant

A

LV has more muscle mass so depolarisation move sin that direction (causes -ve deflection in V1 and +ve in V6)
As depolarisation continues, deflections get more pronounced until both ventricles are fully depolarised and everything goes back to baseline

202
Q

Features of bundle branch block on ECG

A

Broad QRS complex
Unique QRS shape - 3mm or more
Repolarisation abnormalities in leads over affected area

203
Q

Repolarisation abnormalities seen on ECG

A

ST depression

T wave inversion

204
Q

Causes of bundle branch block

A 
CAD 
HTN 
Valve disease 
Cardiomyopathy 
Post cardiac surgery
205
Q

Ventricular depolarisation in RBBB

A

Phase 1 - septum depolarises normally

Phase 2 - ventricles depolarise sequentially, RV is delayed

206
Q

RBBB appearance on ECG

A

MaRRoW

M in V1
W in V6

207
Q

Why is RBBB more common than LBBB

A

R bundle is easier to become damaged

208
Q

Ventricular depolarisation in LBBB

A

Phase 1 - septum depolarises abnormally (R –> L)

Phase 2 - ventricles depolarise sequentially, LV is delayed

209
Q

LBBB appearance on ECG

A

WiLLiaM

W in V1
M in V6

210
Q

Brugada pattern

A

RBBB-like in appearance in R precordial leads (V1 - 3) w/ coved ST elevation (shark fin)

211
Q

What is Brugada pattern caused by

A

Abnormal RV depolarisation

212
Q

Epidemiology of Brugada pattern

A

Rare
Inherited
M > F

213
Q

How might pts with Brugada syndrome present

A

With life threatening ventricular arrhythmias —> syncope, seizures & cardiac arrest

214
Q

ECG changes in hyperkaleamia

A

T waves become tall and peaks
PR interval prolongs and P wave becomes smaller (may disappear)
QRS complexes progressively widen –> sinusoidal appearance –> asystole

215
Q

How does hypertrophy affect QRS complex

A

Produces bigger complexes - simply more +ve and more -ve charges

216
Q

Depolarisation in RV hypertrophy

A

Opposite to normal depolarisation

217
Q

Commonest cause of RV hypertrophy

A

Pulmonary HTN
Congenital heart disease e.g. pulmonary stenosis
Chronic lung diseases

218
Q

What is RV hypertrophy associated with

A

R axis deviation and repolarisation abnormalities in leads V1 - V4

219
Q

RV hypertrophy appearance on ECG

A

Large R waves in V1, V2

Deep S waves in V5, V6

220
Q

Depolarisation in LV hypertrophy

A

Exaggeration of normal depolarisation

221
Q

LV hypertrophy appearance on ECG

A

Axis is usually normal but can be L
Abnormally deep S wave in V1
Abnormally tall R wave in V6
May also see depolarisation abnormalities

222
Q

Normal Q wave appearance

A

Short (1mm max) and small (<25% of total QRS height)

223
Q

Pathologic Q waves appearance

A

Wide and/or deep

224
Q

What can cause ST elevation

A 
STEMI - regional ST elevation (V1 - V4)
Pericarditis - widespread ST elevation 
BBB
High take off 
LV aneurysms
225
Q

Causes of ST depression

A

Ischaemia
Posterior MI
Repolarisation abnormalities

226
Q

In which leads would you see an inferior MI

A

II
III
aVF

227
Q

In which leads would you see a lateral MI

A

I
aVL
V5
V6

228
Q

In which leads would you see an anterior MI

A

V1 - V6

229
Q

ECG dx of STEMI

A

ST elevation >1mm in >2 related leads

However, LBBB can hide ST changes in MI and certain areas aren’t seen well by standard ECG

230
Q

ECG appearance in unstable angina/ NSTEMI

A

A/c changes - T wave inversion, ST depression

231
Q

Normal T wave size

A

<50% size of preceding QRS

232
Q

In which leads are T wave normally inverted in

A

aVR

V1

233
Q

Causes of a tall T wave

A

ACS - hyperacute stage of MI

Hyperkalaemia

234
Q

Causes of inverted T wave

A 
May be normal 
Myocardial disease (ischaemia, infarction, cardiomyopathy)
Ventricular hypertrophy 
BBB
CVA
235
Q

Normal range for QT interval

A

0.33 to 0.44 seconds (up to 0.45 in women)

236
Q

What are both long and short QT intervals associated with

A

Increased risk of ventricular arrhythmias —> syncope and sudden death

237
Q

How do people get long or short QT intervals

A

Inherited

Acquired due to drugs (esp antiarrhythmic) or electrolyte disturbance e.g. K, mg, Ca

238
Q

Adjusting QT interval for HR

A

QTc = QT/ square root of RR interval

239
Q

Easy way to check for prolonged QT interval

A

Look at where T wave ends - if its beyond halfway point of RR interval then it is prolonged

240
Q

Systematic ECG checklist

A 
Basics - name, pt identifier, date, speed, calibration
Rate 
Rhythm
Axis 
Waves 
Intervals
241
Q

Determining sinus rhythm from rhythm strip

A

Ask:
Regular or irregular?
P wave before QRS?

242
Q

Clinical evaluation for valve disease pt

A 
Severity of stenosis 
Degree of regurgitation 
Ventricular size and function 
Atrial size 
Estimated pulmonary artery pressure
243
Q

Key ix for valve disease

A

ECG

244
Q

Symptoms of valve disease

A

SOB and HF
Fatigue
Palpitations/AF - spp mitral valve disease

245
Q

Spp symptoms seen in aortic stenosis

A

Angina

Syncope (particularly on exercise)

246
Q

Principles of valve disease mx

A

Limited benefit from meds

Surgery is usually indicated in severe disease

247
Q

Medical therapy for AF

A

Prevent embolism - anticoagulants w/ vit K anatag or DOAC

Rate control - BB and digoxin

248
Q

Do DOACs work in pts with prosthetic valves

A

No

249
Q

Surgical/ interventional options for valve disease

A

Valvotomy
Repair valve surgically
Valve replacement

250
Q

How can a valvotomy be done

A

Surgical

Percutaneous w/ a balloon

251
Q

Different valves used in valve replacement

A

Mechanical valves
Tissue valve - heterograft, homograft
TAVI

252
Q

TAVI

A

Transcatheter aortic valve implantation

253
Q

Using mechanical valves as replacement

A

Durable but anticoags needed

254
Q

Using tissue valves as replacement

A

Last less time (15 yrs approx) and less in the young

No anticoags needed unless AF

255
Q

Repairing valves

A

Best if it can be done - only mitral

Long lasting, no anticoags, better function

256
Q

Factors influencing risk of valve surgery

A

Age
General physical state and comorbidities
Damage already done to heart - particularly LV in c/c cases
Renal function
Cerebral and carotid arteries - risk of CVA

257
Q

What are the best valves to repair

A

Those with leaflet prolapse and chordal rupture

Surgeons can repair chord that support valve and repair valve cusps

258
Q

Use of TAVI

A

Safe
Suitable for elderly pts w/ contraindications to surgery
Durability unknown
Avoid long-term anticoagulant

259
Q

Infective endocarditis

A

Infection of inner lining of heart

Usually affects valves

260
Q

Why is IE difficult to dx

A

Masquerades as many other condns

Rare but 100% fatal w/out abx

261
Q

Examples of organisms causing IE

A

Staph A - very a/c onset
Strep Viridans - slow onset
Strep faecalalis (enterococcus)

262
Q

Sites attacked in IE

A

Prosthetic valves
Previously abnormal valves e.g. MR, AR, AS
High virulence bacteria e.g. staph A attack normal valves

263
Q

Vegetation

A

Collection of organisms and thrombus

Embolisation risk

264
Q

IE clinical px

A

Very variable and diff to dx

Depends of organisms/ underlying cardiac defect

265
Q

Signs and symptoms of IE

A

Fever, night sweats
Roth spots
Osler nodes
Murmur

Janeway lesions
Anaemia
Nail-bed (splinter) haemorrhage
Emboli

266
Q

Symptoms seen in c/c IE

A

Enlarged spleen
Clubbing
Pigmentation
Glomerulonephritis

267
Q

Major complications of IE

A

Systemic embolisation - vegetation breaking off

Heart failure - damage to valve

268
Q

Cerebrovascular complications of IE

A

Embolism
Infected aneurysm - mycotic aneurysm
(May rupture and cause major cerebral damage)

269
Q

Diagnosing endocarditis

A 
Clinical suspicion 
Blood cultures - do before abx
High infl markers 
Low grade anaemia and mildly raised WBC
Echo to image vegetations, valve damage, abcess
270
Q

Types of echocardiogram

A

Transthoracic

Transoesophageal - better views for IE, detects accesses, vegetations and valve damage

271
Q

Mycotic aneurysm

A

Dilation of artery wall due to damage to vessel wall following infection

272
Q

Why is endocarditis so deadly

A

Antibody antigen complexes damage small blood vessels

Direct damage to heart/ valves due top vegetations or abcesses

273
Q

Prosthetic endocarditis

A

V serious complication
May affect any intracardiac device
Makes valves come lose/ detach
Nearly always needs replacement

274
Q

Mx of endocarditis

A

Abx - usually IV for 4-6 wks (50% need surgery as well)

MDT approach - cardiology/ microbiology/ cardiac surgery

275
Q

When should surgery be considered urgently in endocarditis pts

A

Haemodynamic deterioration due to damage caused by infection
Infection not responding to abx
Abcesses seen on echo

276
Q

PND

A

Paroxysmal nocturnal dyspnoea

Waking up gasping for air after 1-2 hrs of sleep

277
Q

Orthopnoea

A

Breathlessness lying down

Seen in heart failure

278
Q

Determining whether murmur is systolic or diastolic

A

Feel radial pulse while listening - pulse syncs with 1st heart sound

279
Q

Examples of systolic murmurs

A

AS
MR
Pulmonary stenosis

280
Q

Examples of diastolic murmurs

A

AR
MS
Tricuspid stenosis
Pulmonary regurgitation

281
Q

Auscultatory areas of heart

A

Aortic - 2nd IC space (R)
Pulmonary - 2nd IC space (L)
Tricuspid - 4th IC space (L)
Mitral - 5th IC space (L)

282
Q

Differentiating between AS and MR murmurs

A

AS radiates to neck and MR radiates to axilla
AS is pan systolic murmur
MR is crescendo-decrescendo

283
Q

Divisions of left bundle

A

Anterior fascicle

Posterior facsicle

284
Q

In which leads can we see the L anterior fascicle

A

I

aVL

285
Q

In which leads can we see L posterior fascicle

A

II
III
aVF

286
Q

Px of a/c symptomatic MR pts

A

Severe dyspnoea
Pulmonary oedema
Hypotension

287
Q

Contraindications of nitrates

A

Aortic or mitral stenosis
Pericarditis
HCM
Hypotensive condns

288
Q

Contraindications for BB

A

Asthmatics
Hypotension
Unstable cardiac failure

289
Q

Contraindications for CCB

A

A/c anginal attacks
Cardiogenic shock
Significant aortic stenosis
UA within 1/12 of MI

Interacts w/ BB

290
Q

Adverse effects of ACEi

A 
Cough - increase in bradykinin
Hypotension 
Angiodema 
Diarrhoea
Muscle pains, skin reactions
291
Q

Contraindications of ARBs

A

Pregnancy
Severe renal stenosis
Aortic stenosis

292
Q

Adverse effects of ARBs

A 
Cough - not as common 
Hypotension 
Hyperkalemia 
Nausea, vomiting 
Angiodema
293
Q

Contraindications of loop diuretics

A

Severe renal impairment

Treatment with cardiac glycoside

294
Q

Contraindications of thiazides

A

Electrolytic disturbances

Cardiac glycosides

295
Q

Contraindications of K sparing diuretics

A

ACEi

296
Q

How may pts with tricuspid stenosis present

A

Hepatomegaly and distended abdomen due to passive vein congestion

297
Q

Initial ix for heart murmurs

A

Echo
CXR
ECG

298
Q

Qualities of benign murmurs

A 
Soft 
Humming 
Position-dependent 
Usually systolic 
Pt otherwise healthy
299
Q

Janeway lesions

A

Painless spots on palms/soles of feet

300
Q

Oslers nodes

A

Painful nodules in pulp of fingers/ toes

301
Q

What is a low volume pulse usually caused by

A

Low output state (dehydration, heart failure)

Aortic stenosis

302
Q

When is upstroke delayed

A

Aortic stenosis

303
Q

What physiological reasons cause a high volume pulse

A

Advanced age

High output states (exercise, pregnancy)

304
Q

What pathological reasons cause high volume pulse

A

HTN
Aortic regurgitation
High output states (fever, anaemia, thyrotoxicosis)

305
Q

Chest lead placement for ECG

A

V1 - 4th intercostal space at LSE
V2 - 4th intercostal space at RSE
V3 - Midway between V2 & V4
V4 - 5th IC space in mid clavicular line
V5 - same level at V4 but more left (—> axillary)
V6 - Mid axillary line (same level as V4 & V5)

306
Q

Limb lead placement

A

Red - ulnar styloid process of R arm
Yellow - ulnar styloid process of L arm
Green - malleolus of L leg
Black - malleolus of R leg

307
Q

Which murmur is best heard in expiration with th eats rolled onto their left

A

Mitral stenosis

308
Q

Which type of echo is best

A

Transoesphageal

309
Q

Conventional echo

A

Transthroacic

310
Q

Why might pts get pan systolic murmurs post-MI

A

Damage to papillary muscles causes MR

May have ventricular septal defect

311
Q

Myxoma

A

Benign tumour usually found in atria

312
Q

Main ix for AS

A

Cardiac echo

Coronary angio

313
Q

What is usually seen in severe AS

A

LV hypertrophy

314
Q

CXR in AS

A

May still appear normal in severe cases as LV is hypertrophied rather than dilated

315
Q

Causes of increased JVP

A

Congestive or R heart failure
Tricuspid regurg
Iatrogenic volume overload

316
Q

Waveforms of JVP

A

a wave - atrial contraction

v wave - ventricular contraction

317
Q

JVP vs carotid pulse

A

2 peaks vs 1 peak
JVP falls on inspiration
JVP rises with hepatojugular reflux

318
Q

What could high CRT be a sign of

A

Low CO

319
Q

When is the volume of the carotid pulse high

A

Regurgitation

320
Q

When is the volume of the carotid pulse reduce

A

Those with low CO

321
Q

Conditions changing the character of carotid pulse

A

AS - slow to rise

AR - rapid upstroke and downstroke

322
Q

Which murmurs are heard best with the pt lying on their left side

A

Mitral or triscupid murmurs

323
Q

In which positions are aortic murmurs heard best

A

Sitting up

324
Q

Which murmurs are louder in inspiration

A

Right sided - M or P

325
Q

Which murmurs are louder on expiration

A

Left sided murmurs - A or T

326
Q

Describing heart murmurs

A

Timing - sys or diastole
Location
Radiation
Manoeuvres

Pitch
Intensity

327
Q

What is the main trigger for RAAS

A

Decreased blood flow to renal arteries

Can be initiated in a/c haemorrhage

MBBS - Year 2 (20 decks)

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