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Phase2a > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What are the outcomes of an atherosclerotic plaque?

A
  • Occlusion

- Rupture

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2
Q

Give three conditions that are principally caused by atherosclerosis.

A
  • Heart attack
  • Stroke
  • Gangrene
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3
Q

Give seven risk factors for atherosclerosis.

A
  • Age
  • Tobacco smoking
  • High cholesterol
  • Obesity
  • Diabetes
  • Hypertension
  • Family history
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4
Q

In which arteries are atherosclerotic plaques found?

A

Coronary and peripheral arteries

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5
Q

What is the ultimate initiating factor for atherogenesis?

A

Endothelial cell damage

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6
Q

What is a neointima?

A

Scar tissue in blood vessels which thickens the vessel wall.

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7
Q

Altered gene expression in which four cell types contributes to atherogenesis?

A
  • Endothelial cells
  • Macrophages
  • Smooth muscle
  • Fibroblasts
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8
Q

Give four components of atherosclerotic plaque structure.

A
  • Lipid
  • Necrotic core
  • Connective tissue
  • Fibrous cap
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9
Q

Give seven inflammatory cytokines involved in atherosclerotic plaque formation.

A
  • IL-1
  • IL-6
  • IL-8
  • IFN-y
  • TGF-b
  • MCP-1
  • CRP
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10
Q

How does modified LDL cause inflammation in an arterial wall?

A

It accumulates in the arterial wall and undergoes oxidation and glycation.

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11
Q

What two things cause inflammation in arterial walls, leading to atherogenesis?

A
  • Modified LDL

- Endothelial dysfunction

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12
Q

What 2 factors mediate leukocyte adhesion to the arterial wall in atherogenesis?

A
  • Selectins

- Integrins

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13
Q

Name the four stages of atherogenesis.

A
  1. Fatty streaks
  2. Intermediate lesions
  3. Fibrous plaques / advanced lesions
  4. Plaque rupture
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14
Q

What age do fatty streaks first appear?

A

<10yrs

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15
Q

Describe the histology of fatty streaks.

A

Aggregations of lipid laden macrophages and T lymphocytes.

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16
Q

Describe the components of intermediate atherosclerotic lesions.

A
  • Foam cells (lipid-laden macrophages)
  • Vascular smooth muscle cells
  • T lymphocytes
  • Adhesion of platelets to wall
  • Pools of extracellular lipid
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17
Q

Describe the formation of the fibrous cap of an atherosclerotic plaque.

A

Smooth muscle cells migrate to the surface of the plaque and secrete collagen and elastin.

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18
Q

How is the fibrous cap of an atherosclerotic plaque maintained?

A

Has to be resorbed and redeposited.

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19
Q

How does the fibrous cap weaken, leading to atherosclerotic plaque rupture?

A

Macrophages secrete matrix metalloproteinases.

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20
Q

Apart from plaque rupture, give one other process that can cause thrombus formation related to an atherosclerotic plaque.

A

Plaque erosion.

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21
Q

Give six conditions that the ECG can identify.

A
  • Arrhythmias
  • Myocardial ischaemia/infarction
  • Pericarditis
  • Chamber hypertrophy
  • Electrolyte disturbances
  • Drug toxicity (digoxin)
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22
Q

What is the dominant pacemaker of the heart, and at what rate does it work?

A

SA node

60-100bpm

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23
Q

What are the two back-up pacemakers of the heart and what rate do they work at?

A
  • AV node, 40-60bpm

- Ventricular cells, 20-45bpm

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24
Q

What is the standard paper speed in an ECG?

A

25mm/s

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25
Q

What is the amplitude in an ECG?

A

0.1mV/mm

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26
Q

What are the small and large boxes worth horizontally on an ECG?

A

Small box = 0.04s

Large box = 0.20s

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27
Q

What is one large box worth vertically on an ECG?

A

0.5mV

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28
Q

Why doesn’t atrial repolarisation show up on an ECG?

A

It is masked by ventricular depolarisation (QRS complex).

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29
Q

What are the bipolar ECG leads?

A

I, II, III

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30
Q

What is the J point on an ECG?

A

The point where the S wave becomes the ST segment.

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31
Q

What do unipolar leads compare on an ECG?

A

One point on the body and a virtual reference point with zero electrical potential, located in the centre of the heart.

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32
Q

What axis does aVL measure?

A

-30

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33
Q

What axis does lead I measure?

A

0

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34
Q

What axis does lead II measure?

A

+60

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35
Q

What axis does aVF measure?

A

+90

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36
Q

What axis does lead III measure?

A

+120

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37
Q

What axis does aVR measure?

A

-150

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38
Q

Which ECG leads give a lateral view of the left ventricle?I?

A
  • I
  • aVL
  • V5
  • V6
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39
Q

Which ECG leads give an inferior view of the left ventricle?

A
  • II
  • III
  • aVF
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40
Q

Which ECG leads give a septal view of the left ventricle?

A
  • V1

- V2

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41
Q

Which ECG leads give an anterior view of the left ventricle?

A
  • V3

- V4

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42
Q

How long should the PR interval be?

A

0.12-0.20s (3-5 little squares)

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43
Q

How long should the QRS complex be?

A

Shouldn’t exceed 0.12s (3 little squares)

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44
Q

In which leads should the QRS complex be dominantly upright?

A

I and II

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45
Q

How does the direction of the T wave compare to the QRS complex in limb leads.

A

Should be same general direction.

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46
Q

In which ECG lead are all the waves negative?

A

.aVR

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47
Q

How does the R wave change in the chest leads of an ECG?

A

Grows from V1 to at least V4.

V5>V6

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48
Q

How does the S wave change in the chest leads of an ECG?

A

Grows from V1 to at least V3.

Disappears in V6.

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49
Q

How should the ST segment appear on an ECG?

And which leads are the exceptions?

A

Start isoelectric.

Except in V1 and V2

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50
Q

In which leads should P waves be upright?

A

I, II, V2-V6

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51
Q

Which leads should feature no Q waves (or Q waves <0.04s)?

A

I, II, V2-V6

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52
Q

In which ECG leads should the T wave be upright?

A

I, II, V2-V6

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53
Q

What should the amplitude of the P wave be?

A

<2.5 small squares

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54
Q

In which ECG lead is the P wave commonly biphasic?

A

V1

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55
Q

Which lead is the P wave best seen in?

A

II

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56
Q

How are the P waves altered in right atrial enlargement?

What is the ‘official’ name for this?

A

Tall, pointed P waves.

P Pulmonale

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57
Q

How do the P waves differ in left atrial enlargement?

What is the ‘official’ name for this?

A

‘M’ shaped P waves.

P Mitrale

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58
Q

What does the Q wave represent?

A

Left to right bundle branch depolarisation

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59
Q

What does the R wave represent?

A

Septal depolarisation

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60
Q

What does the S wave represent?

A

Purkinje depolarisation

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61
Q

Describe the appearance of a normal T wave.

A

First half has a more graduated slope than the second.

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62
Q

How long should the QT interval be?

A

0.35-0.45s

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63
Q

What do U waves represent on an ECG?

A

Related to after depolarisations which follow repolarisation.

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64
Q

How can you determine the regular heart rate using an ECG?

A

300/number of big boxes between QRS complexes

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65
Q

How can you determine the irregular heart rate on an ECG?

A

Number of QRS complexes on the rhythm strip x 6

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66
Q

What is the normal heart axis?

A

-30 to +90

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67
Q

What is a left axis deviation?

A

-90 to -30

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68
Q

What is a right axis deviation?

A

+90 to +180

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69
Q

If the QRS complex is positive in lead aVF and Lead I, what is the heart axis?

A

Normal

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70
Q

If the QRS complex is negative in aVF and positive in Lead I what is the heart axis?

A

Left axis deviation

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71
Q

If the QRS complex if positive in aVF and negative in lead I what is the heart axis?

A

Right axis deviation

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72
Q

If the QRS complex is negative in both aVF and lead I what is the heart axis?

A

Indeterminate axis

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73
Q

How can the equiphasic approach be used to determine heart axis?

A

Identify most equiphasic QRS complex.

See if QRS complex is positive or negative in the lead at a right angle.

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74
Q

Describe the waves in V1 and V6 for a left bundle branch block.

A

W in V1

M in V6

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75
Q

Describe the waves in V1 and V6 in right bundle branch block.

A

M in V1

W in V6

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76
Q

What is the major component of an arterial thrombus?

A

Platelets

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77
Q

What ‘colour’ is an arterial thrombus?

A

White

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78
Q

Give four conditions that arise from arterial thrombosis.

A
  • Myocardial infarction
  • Stroke
  • Cerebrovascular event
  • Peripheral vascular disease
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79
Q

What is the major component of a venous thrombus?

A

Fibrin

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80
Q

What ‘colour’ is a venous thrombus and why?

A

Red, because the fibrin mesh traps red blood cells.

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81
Q

Give five genetic causes of venous thrombosis.

A
  • Factor V Leiden
  • PT20210A
  • Antithrombin deficiency
  • Protein C deficiency
  • Protein S deficiency
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82
Q

What are three acquired causes of venous thrombosis?

A
  • Anti-phospholipid syndrome
  • Lupus anticoagulant
  • Hyperhomocysteinaemia
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83
Q

How does heparin work?

A

Binds to antithrombin to increase activity.

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84
Q

What is the normal INR?

A

<1.1

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85
Q

What is the INR target for people on anticoagulants?

A

2-3

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86
Q

How is heparin administered?

A

Continuous infusion

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87
Q

How is low molecular weight heparin administered?

A

Subcutaneous injection

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88
Q

How does aspirin work?

A

Irreversibly inhibits cyclo-oxygenase

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89
Q

How long does aspirin work for?

A

The lifetime of the platelet (7-10days)

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90
Q

How does clopidogrel work?

A

Blocks platelet P2Y12 ADP receptor.

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91
Q

Name three P2Y12 ADP receptor inhibitors.

A
  • Clopidogrel
  • Ticagrelor
  • Prasegrel
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92
Q

Give three oral anticoagulants.

A
  • Aspirin
  • Warfarin
  • DOAC
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93
Q

How does warfarin work?

A

It is a vitamin K antagonist which prevents synthesis of clotting factors II, VII, IX, and X.

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94
Q

Describe the half life of warfarin.

A

Long (36 hours)

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95
Q

Which clotting factors do direct oral anticoagulants (DOAC) act on?

A

II or X

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96
Q

Why can’t DOACs be used in pregnancy?

A

They can cross the placenta.

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97
Q

Why are DOACs better than warfarin?

A

They don’t need monitoring.

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98
Q

Give seven conditions that hypertension is a major risk factor for.

A
  • Stroke
  • Myocardial infarction
  • Heart failure
  • Chronic renal disease
  • Cognitive decline
  • Premature death
  • Atrial fibrillation
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99
Q

What blood pressure measurement leads to suspected hypertension?

A

140/90mmHg

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100
Q

Give three targets for therapy in hypertension.

A
  • Cardiac output / peripheral resistance
  • RAAS/SNS
  • Vasoconstrictor/dilators
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101
Q

How does angiotensin II affect peripheral blood vessels?

A

It is a potent vasoconstrictor.

102
Q

What affect does angiotensin II have on the sympathetic nervous system?

A

It potentiates it.

103
Q

What are the clinical indications for ACE inhibitors?

A
  • Hypertension
  • Heart failure
  • Diabetic nephropathy
104
Q

Give four examples of ACE inhibitors.

A
  • Ramipril
  • Enalapril
  • Perindopril
  • Trandolapril
105
Q

Give some adverse effects of ACEi relating to reduces angiotensin II formation.

A
  • Hypotension
  • Acute renal failure
  • Hyperkalaemia
  • Teratogenic effects in pregnancy
106
Q

Give some adverse effects of ACEi that are related to increased kinin production.

A
  • Cough
  • Rash
  • Anaphylactoid reactions
107
Q

Why do ACEi increase kinins?

A

ACE is not specific so also breaks down bradykinin. ACEi prevent this.

108
Q

When are angiotensin II receptor blockers usually used in hypertension?

A

If the patient has an adverse effect to ACEi

109
Q

What are the clinical indications for ARBs?

A
  • Hypertension
  • Diabetic nephropathy
  • Heart failure (when ACEi contraindicated)
110
Q

Give five examples of ARBs.

A
  • Candesartan
  • Losartan
  • Valsartan
  • Irbesartan
  • Telmisartan
111
Q

Give some adverse effects of ARBs.

A
  • Symptomatic hypotension
  • Hyperkalaemia
  • Potential for renal dysfunction
  • Rash
  • Angio-oedema
112
Q

How often do adverse effects of ARBs occur?

A

They are generally well-tolerated.

113
Q

Give a condition in which ARBs are contraindicated.

A

Pregnancy

114
Q

What are the main clinical indications for calcium channel blockers?

A
  • Hypertension
  • IHD (angina)
  • Arrhythmia (tachycardia)
115
Q

Give four examples of calcium channel blockers which are peripheral arterial vasodilators.

A
  • Amlodipine
  • Felodipine
  • Nifedipine
  • Lacidipine
116
Q

Give an example of a calcium channel blocker which has intermediate effects on heart and vessels.

A

Diltiazem

117
Q

Give an example of a calcium channel blocker which has its main effects on the heart.

A

Verapamil

118
Q

Give some adverse effects of CCBs which are due to peripheral vasodilation.

A
  • Flushing
  • Headache
  • Oedema
  • Palpitations
119
Q

Give some adverse effects of CCBs which occur due to negative chronotropic effects.

A
  • Bradycardia

- Atrioventricular block

120
Q

Give an example of an adverse effect of CCBs which is due to negative inotropic effects.

A

Worsening of cardiac failure.

121
Q

Give a side effect of verapamil.

A

Constipation

122
Q

What are the main clinical indications for beta blockers?

A
  • IHD (angina)
  • Heart failure
  • Arrhythmia
  • Hypertension
123
Q

Give two examples of beta blockers which are b1 selective.

A
  • Metoprolol

- Bisoprolol

124
Q

Give an example of a beta blocker which is partially b1 selective.

A

Atenolol

125
Q

Which 3 examples of non-selective beta blockers.

A
  • Propranolol
  • Nadolol
  • Carvedilol
126
Q

Give some adverse effects of beta blockers.

A
  • Fatigue
  • Headache
  • Nightmares
  • Bradycardia
  • Hypotension
  • Cold peripheries
  • Erectile dysfunction
127
Q

Give four conditions which are contraindications for beta blockers.

A
  • Asthma
  • COPD
  • Claudication
  • Raynaud’s
128
Q

What are the main clinical indications for diuretics?

A
  • Hypertension

- Heart failure

129
Q

Give three examples of thiazide diuretics.

A
  • Bendroflumethiazide
  • Hydrochlorothiazide
  • Chlorthalidone
130
Q

Give two examples of loop diuretics.

A
  • Furosemide

- Bumetanide

131
Q

Give two examples of potassium-sparing diuretics which are aldosterone antagonists.

A
  • Spironolactone

- Eplerenone

132
Q

Give an adverse effect of spironolactone.

A

It has oestrogenic effects.

133
Q

Give two examples of potassium-sparing diuretics.

A
  • Amiloride

- Triamterine

134
Q

Which type of diuretic acts the quickest and is strong?

A

Loop diuretics

135
Q

Give some adverse effects of diuretics.

A
  • Hypovolaemia
  • Hypotension
  • Hypokalaemia
  • Hyponatraemia
  • Hypomagnesaemia
  • Hypocalcaemia
  • Raised uric acid (gout)
  • Impaired glucose tolerance
  • Erectile dysfunction
136
Q

Give three examples of classes of other antihypertensives.

A
  • a1 adrenoreceptor blockers
  • Centrally acting antihypertensives
  • Direct renin inhibitor
137
Q

Name an antihypertensive which can be used in pregnancy.

A

Methyldopa

138
Q

Why are people over 55 years and Afro-Caribbean people get a different first line antihypertensive treatment to people under 55?

A

People under 55 tend to have renin-dependent hypertension.

139
Q

What is the first line treatment for hypertension in people under 55 years?

A

ACEi or ARB

140
Q

What is the first line treatment for hypertension for Afro-Caribbean people and people over 55 years?

A

CCB

141
Q

Why don’t treatments for heart failure tend to focus on directly stimulating the left ventricle?

A

This would increase the oxygen demands of the heart and increase damage.

142
Q

Name two systems that are inappropriately activated in heart failure.

A
  • RAAS

- Sympathetic nervous system

143
Q

Why are diuretics used in heart failure?

A

For the symptomatic treatment of congestion.

144
Q

What are the first line treatments for heart failure?

A

ACEi and beta blockers

145
Q

Give five other drugs or classes of drugs that are used to treat heart failure.

A
  • Aldosterone antagonists
  • Angiotensin receptor blocker
  • Hydralazine/nitrate combination
  • Digoxin
  • Ivabradine
146
Q

How does hydralazine work?

A

Vasodilator

147
Q

What effect does digoxin have on the lives of people with heart failure?

A

Reduces hospitalisations but not mortality.

148
Q

How does ivabradine work?

A

Slows sinus node rate.

149
Q

Give two cardiac natriuretic peptides and state where they are released from.

A
  • Atrial natriuretic peptide (from atria)

- b (brain) natriuretic peptide (from ventricles)

150
Q

What is the stimulus for cardiac natriuretic peptide release?

A

Stretching of cardiac muscle.

151
Q

Give five effects of cardiac natriuretic peptides.

A
  • Increase renal sodium/water excretion
  • Relax vascular smooth muscle (except efferent arteriole)
  • Increased vascular permeability
  • Inhibit aldosterone/angiotensin II/endothelin/ADH
  • Counter-regulate renin-angiotensin system
152
Q

How are cardiac natriuretic peptides metabolised?

A

By a neutral endopeptidase (neprilysin).

153
Q

How does sacubitril work to treat heart failure?

A

It is a neprilysin inhibitor which increases levels cardiac natriuretic peptides.

154
Q

Name a drug which sacubitril is often paired with in a combination therapy for heart failure.

A

Valsartan (ARB)

155
Q

Give three effects of nitrates.

A
  • Arterial and venous dilators
  • Reduction of preload and afterload
  • Lower blood pressure
156
Q

What are the indications for nitrates.

A
  • IHD (angina)

- Heart failure

157
Q

Give three examples of nitrates which are used to treat heart failure.

A
  • Isosorbide mononitrate
  • GTN spray
  • GTN infusion
158
Q

Give two adverse effects of nitrates.

A
  • Headaches

- Syncope (GTN spray)

159
Q

Give an example of an anticoagulant which is related to low molecular weight heparin.

A

Fondaparinux

160
Q

Give four classes of drugs used to treat arrhythmia.

A
  • Sodium channel blockers
  • beta adrenoreceptor antagonists
  • Prolong action potentials
  • Calcium channel blockers
161
Q

Give two examples of sodium channel blockers used to treat arrhythmias.

A
  • Lidocaine

- Flecainide

162
Q

Give two medications used to treat arrhythmia which prolong the action potential.

A
  • Amiodarone

- Sotalol

163
Q

How does digoxin work?

A

Inhibits Na/K pump

164
Q

Give four effects of digoxin.

A
  • Bradycardia
  • Slowing of AV conduction
  • Increased ectopic activity (extra beats)
  • Increased force of contraction (increased calcium)
165
Q

Give four adverse effects of digoxin.

A
  • Nausea
  • Vomiting
  • Diarrhoea
  • Confusion
166
Q

Why does digoxin cause side effects?

A

It has a narrow therapeutic range.

167
Q

What are the indications for digoxin?

A
  • Atrial fibrillation

- Heart failure

168
Q

Why does amiodarone have multiple drug interactions? (Give an example)

A

It is highly protein bound.

It interacts with Warfarin

169
Q

Why does amiodarone cause many side effects?

A

It has a very high volume of distribution so clearance is slow and it builds up in tissues.

170
Q

Explain one major side effect of amiodarone and sotalol.

A

Cause QT prolongation, which can lead to polymorphic ventricular tachycardia and eventually cardiac arrest.

171
Q

Give seven adverse effects of amiodarone.

A
  • Interstitial pneumonitis
  • Abnormal liver function
  • Hyperthyroidism/hypothyroidism
  • Sun sensitivity
  • Slate grey skin discolouration
  • Corneal microdeposits
  • Optic neuropathy
172
Q

Why do multiple blood cultures need to be obtained at different times when testing for infective endocarditis?

A

Bacteria come and go from the blood.

173
Q

In how many cases of infective endocarditis do blood cultures remain negative?

A

2-5%

174
Q

Why is the endocardium particularly susceptible to infection and why are infections there particularly hard to treat?

A

It doesn’t have its own blood supply.

175
Q

Give seven bacteria that are commonly found in blood cultures when testing for infective endocarditis.

A
  • Staphylococcus aureus
  • Streptococcus pneumoniae
  • b-haemolytic streptococci
  • Enterococci
  • Coliforms
  • Pseudomonas
  • Neisseria meningitidis
176
Q

Why are coagulase negative staphylococci present in about 50% of blood cultures when testing for infective endocarditis?

A

The IV line gets contaminated.

177
Q

What marks commonly appear on a patient’s nails with infective endocarditis?

A

Splinter haemorrhages

178
Q

What would be the typical antibiotic treatment for infective endocarditis caused by viridans strep?

A

IV benzylpenicillin (+ gentamicin) for 6 weeks

179
Q

What is the standard antibiotic treatment for infective endocarditis caused by enterococci?

A

High dose IV amoxicillin (+gentamicin) for a few weeks.

180
Q

Why is gentamicin commonly used in combination with other antibiotics to treat infective endocarditis?

A

They have synergistic effects - the beta lactam weakens the cell wall to allow gentamicin into the cell to inhibit protein synthesis.

181
Q

What is the fibrous pericardium made from?

A

Acellular collagen and elastin fibres

182
Q

How much serous fluid is usually present in the pericardial space?

A

50ml

183
Q

Give five major criteria for complications in pericarditis.

A
  • Fever >38 (this suggests bacterial)
  • Subacute onset
  • Large pericardial effusion
  • Cardiac tamponade
  • Lack of response to therapy/recurrence
184
Q

Describe the usual inheritance pattern of inherited cardiomyopathies.

A

Dominant

185
Q

What is an inherited arrhythmia?

A

Channelopathies caused by ion channel protein gene mutations.

186
Q

Give seven examples of inherited arrhythmias.

A
  • Long QT
  • Short QT
  • Brugada
  • CPVT
  • Wolff-Parkinson White
  • Progressive conduction disease
  • Idiopathic ventricular fibrillation
187
Q

What is CPVT?

A

Catecholaminergic polymorphic ventricular tachycardia

Ventricular tachycardia stimulated by adrenaline

188
Q

Give a sign if Brugada found on ECG.

A

ST elevation in the anterior leads.

189
Q

How might channelopathies present?

A

Recurrent syncope

190
Q

Describe the heart in sudden arrhythmic death syndrome (SADS).

A

Structurally normal but may have had arrhythmias.

191
Q

What is familial hypercholesterolaemia?

A

Inherited abnormality of cholesterol metabolism.

192
Q

What are the complications of familial hypercholesterolaemia?

A

Can lead to serious premature coronary and other vascular disease.

193
Q

Give three syndromes that can cause aortic aneurysm/dissection.

A
  • Marfan
  • Loeys-Dietz
  • Ehler Danlos
194
Q

Where does Marfan syndrome usually cause aortic aneurysm and why?

A

Usually affects aortic root as this is where the most fibrillin is present and Marfan is an abnormality with fibrillin.

195
Q

Give four molecules that trigger a hypertrophic response from the heart.

A
  • Angiotensin II
  • Endothelin-1
  • Insulin-like growth factor 1
  • Transforming growth factor beta (TGF-b)
196
Q

Give four clinical scenarios/presentation where an ECG would be used.

A
  • Chest pain
  • Palpitation
  • Breathlessness
  • Blackout
197
Q

What does the left bundle branch of the cardiac conducting system split into before purkinje fibres?

A

Anterior and posterior fascicle

198
Q

What is the ECG amplitude related to?

A

The mass of the myocardium.

199
Q

Describe the progression of the QRS complex from leads V1-V6.

A

Predominantly negative S wave in V1, transitioning to positive R wave by V6.

200
Q

Describe and explain the QRS complex in supraventricular tachycardias.

A

Narrow QRS because the ventricles are still being stimulated through the His-Purkinje system.

201
Q

Describe and explain the QRS complex in ventricular tachycardias.

A

Broad QRS complex because the ventricles aren’t being stimulated through the His-Purkinje system.

202
Q

Describe Mobitz type 1 second degree heart block.

A

The PR interval gradually increases until the AV node fails completely and no QRS complex is seen.
The rhythm then starts all over again.

203
Q

Describe Mobitz type 2 second degree heart block.

A

Sudden unpredictable loss of AV conduction and QRS.

Due to a loss of conduction in Bundle of His and Purkinje fibres.

204
Q

What are ectopic heart beats?

A

Non sustained extra beats arising from ectopic regions of atria or ventricles.

205
Q

What can high burden ventricular ectopy cause?

A

Heart failure

206
Q

What can high burden atrial ectopy cause?

A

Atrial fibrillation

207
Q

When do high burden ectopic beats cause risk?

A

When the burden is >20%

208
Q

How are ectopic beats treated?

A

They are generally benign but most patients gain symptomatic relief from reassurance/beta blockers.

209
Q

Describe the ectopic beats arising from ventricular tissue.

A

Broad QRS because the myocardium is not stimulated through the His-Purkinje system.

210
Q

What is the commonest sustained arrhythmia?

A

Atrial fibrillation

211
Q

What is the difference between atrial fibrillation and atrial flutter.

A

They are both many extra depolarisations however in flutter the extra beats are regular whereas in fibrillation the extra beats are irregular.

212
Q

How can atrial fibrillation be treated?

A
  • Treat underlying cause
  • Rate control (beta blockers)
  • Restore sinus rhythm acutely (electrical or pharmacological conversion)
  • Maintain sinus rhythm (amiodarone)
213
Q

How can supraventricular tachycardias be treated?

A
  • Valsalva manoeuvres

- Beta blocker / CCB

214
Q

When should a patient be referred due to supraventricular tachycardia?

A
  • Frequent/sustained episodes
  • Needed adenosine for termination
  • Abnormal ECG
215
Q

What is a delta wave on an ECG?

A

A slurred upstroke in the QRS complex often associated with a short PR interval.

216
Q

What can cause a delta wave on an ECG?

A

Pre-excitation syndrome such as WPW.

217
Q

What is meant by an accessory conduction pathway?

A

Congenital remnant muscle strands between atrium and ventricle.

218
Q

What is meant by an electrical storm in cardiology?

A

3 or more sustained episodes of VT or VF during a 24 hour period.

219
Q

How is an electrical storm treated?

A
  • Correct provoking factors
  • Beta blockers
  • Amidarone
  • Overdrive pacing
  • General anaesthesia
  • Catheter abalation
220
Q

What is Wolff-Parkinson-White syndrome?

A

An extra electrical connection (accessory pathway) in the heart that causes it to beat abnormally fast for periods of time.

221
Q

What are the characteristic ECG findings in Wolff-Parkinson-White syndrome?

A
  • Short PR interval
  • Broad QRS
  • Delta wave (pre-excitation)
222
Q

What is an orthodromic accessory pathway?

A

A circuit going down the His-Purkinje system then back up between the ventricles and atria.
It shows a narrow QRS complex.

223
Q

What is an antidromic accessory pathway?

A

A circuit going from the atria to the ventricles, then back up the His-Purkinje system.
It shows a broad QRS complex.

224
Q

Describe how ectopic beats can be classified.

A

They can be classified into couplets (2 beats) or triplets (3 beats).

225
Q

What is bigeminy, in relation to ectopic beats?

A

Alternating large and small beats, due to ectopic beats occurring after each sinus beat.

226
Q

Give three causes of a left axis deviation.

A
  • Left anterior fascicular block
  • Left bundle branch block
  • Left ventricular hypertrophy
227
Q

Give two causes of right axis deviation.

A
  • Left posterior fascicular block

- Right heart hypertrophy/strain

228
Q

Give three causes of low P wave amplitude.

A
  • Atrial fibrosis
  • Obesity
  • Hyperkalaemia
229
Q

Give a cause of high P wave amplitude.

A
  • Right atrial enlargement
230
Q

Give a cause of a broad notched ‘bifid’ P wave.

A

Left atrial enlargement

231
Q

Give three causes of a broad QRS complex.

A
  • Ventricular conduction delay/BBB
  • Pre-excitation
  • Ventricular tachycardia
232
Q

Give 3 causes of a small QRS.

A
  • Obese patient
  • Pericardial effusion
  • Infiltrative cardiac disease
233
Q

Give two causes of a tall QRS.

A
  • Left ventricular hypertrophy

- Thin patient

234
Q

Give three causes of ST elevation.

A
  • Early repolarisation
  • Myocardial infarction
  • Pericarditis/myocarditis
235
Q

Give three causes of T wave inversion.

A
  • Ischaemia/infarction
  • Myocardial strain (hypertrophy)
  • Myocardial disease (cardiomyopathy)
236
Q

Give five examples of tachycardias.

A
  • Atrial fibrillation
  • Atrial flutter
  • Supraventricular tachycardia
  • Ventricular tachycardia
  • Ventricular fibrillation
237
Q

At which level in the conducting system does bradycardia occur?

A

It can occur at any level.

238
Q

Give four causes of bradycardias.

A
  • Conduction tissue fibrosis
  • Ischaemia
  • Drugs
  • Inflammation/infiltrative disease
239
Q

Give a medication that can be used to treat bradycardia.

A

Atropine

240
Q

Give a medication that can be used to treat tachycardia.

A

Adenosine

241
Q

Describe the cardiac muscle tone in fibrillation.

A

Muscle is in spasm

242
Q

Why is ventricular tachycardia particularly dangerous?

A

It can lead to ventricular fibrillation (no cardiac output).

243
Q

What causes an atrioventricular reentrant tachycardia?

A

An accessory pathway between the atria and the ventricles.

244
Q

Give an example of an atrioventricular reentrant tachycardia.

A

Wolff-Parkinson-White syndrome

245
Q

In reentrant tachycardias, what does the direction of the circuit depend on?

A

The refractory periods of the two pathways.

246
Q

Describe the conduction pathways and refractory pathways in the AV node.

A
  • Slow pathway with short refractory period

- Fast pathway with long refractory period

247
Q

What is the stimulus for an atrioventricular nodal reentrant tachycardia?

A

An extra premature beat.

248
Q

Give two ECG findings in atrioventricular nodal reentrant tachycardia.

A
  • Narrow QRS

- Tachycardia

249
Q

Describe the pathophysiology in atrioventricular nodal reentrant tachycardias.

A

The premature beat travels down the slow pathway because the fast pathway is still in the refractory period.
By the time the depolarisation has reached the end of the slow pathway, the refractory period of the fast pathway is over.
The depolarisation can travel up the fast pathway to create a loop.

250
Q

Bradycardia is a feature of which type of shock?

A

Neurogenic

251
Q

Where do clots form in atrial fibrillation?

A

Auricular appendage

Phase2a (12 decks)

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