Acute coronary disease Flashcards

1
Q

What is acute coronary syndrome

A

Any acute presentation of coronary artery disease

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2
Q

What are the characteristics of acute coronary syndrome (4)

A

dynamic stenosis
Supply-led ischaemia
Unpredictable
Dangerous

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3
Q

What is the pathogenesis of acute coronary syndrome (3)

A

plaque ruptures
Clot forms
Vessel is either partially or totally occluded

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4
Q

What factors can affect plaque rupture (6)

A

lipid content
Thickness of fibrous cap
Intraluminal pressure changes
Bending/twisting of artery
Shape
Mechanical injury

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5
Q

What can total vessel occlusion lead to

A

ST elevation MI

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6
Q

What can subtotal vessel occlusion lead to

A

Non-ST elevation MI

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7
Q

What are the three steps of the platelet cascade

A

Adhesion
Activation
Aggregation

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8
Q

How are platelets activated (4)

A

when platelets are exposed to a vascular injury, they release ADP and switch on cycloxygenase
Cycloxygenase generates thromboxane A2
ADP and thromboxane A2 bind to receptors on the surface of platelets
This activates the platelets

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9
Q

Other than platelets, what can be incorporated into a clot (3)

A

Fibrin
White blood cells
Red blood cells

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10
Q

What is the pain caused by STEMI like (5)

A

severe
Radiating
Crushing
Prolonged
Not relieved by GTN

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11
Q

What symptoms other than pain are associated with STEMI (3)

A

sweating
Nausea
Vomiting

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12
Q

What must be observed on an ECG for diagnosis as a STEMI (2)

A

an elevation of more than 1mm in two adjacent limb leads
Or
An elevation of more than 2mm in two contiguous precocial leads

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13
Q

What other abnormal features can be observed on an ECG due to a STEMI (3)

A

New onset bundle branch block
T wave inversion
Q waves

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14
Q

What mechanisms can be used to manage STEMIs (2)

A

preventing platelet activation
Fibrinolysis

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15
Q

What drugs can be used to prevent platelet activation in STEMI (2)

A

P2Y12 receptor antagonists (clopidogrel blocks ADP receptors on platelets)
Aspirin (inhibits cycloxygenase system)

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16
Q

What are the risks of using thrombolytic drugs to manage STEMIs (3)

A

Failure to re-perfuse
Haemorrhage
Hypersensitivity

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17
Q

What does reperfusion therapy include (2)

A

thrombolytic drugs
Percutaneous coronary intervention

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18
Q

What are the indications for reperfusion therapy (2)

A

Chest pain that suggests acute myocardial infarction
ECG changes

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19
Q

What are the contraindications of reperfusion therapy (6)

A

bleeding disorder
stroke
CNS damage/neoplasm
Internal bleeding
Aortic dissection
Trauma/surgery

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20
Q

What increases long-term mortality (in relation to management of STEMIs)

A

failed thrombolysis

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21
Q

When is thrombolysis used to treat STEMIs

A

If angioplasty is not available within 120 minutes

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22
Q

What complications can arise from acute myocardial infarction (4)

A

death
Arrhythmic complications
Structural complications
Functional complications

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23
Q

What are examples of structural complications arising from acute myocardia infarction (3)

A

Cardiac rupture
Ventricular septal defect
Mitral valve regurgitation

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24
Q

What observations are taken for an acute myocardial infarction (7)

A

pulse
Bp
Patient feeling
Heart sounds
Murmurs
Pulmonary crepitations
Fluid balance

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25
Q

What can be used to diagnose an NSTEMI

A

bio markers - troponin complex

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26
Q

Describe the troponin complex (3)

A

Globular protein complex
Found in thin myofilaments
Regulates muscle contraction

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27
Q

How are NSTEMIs managed (2)

A

stent
Dual-anti-platelet therapy

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28
Q

Which drug is preferred as the first agent in treatment of NSTEMIs

A

Clopidogrel

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29
Q

Describe characteristics of unstable angina (3)

A

symptoms suggestive of MI
No troponin I release
Usually no ECG changes

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30
Q

What is type one myocardial infarction

A

ischaemia due to a primary coronary event

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31
Q

What are the characteristics of type one MI (3)

A

major ECG changes
Higher troponin
Severe coronary artery disease

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32
Q

What is type two MI

A

secondary
Ischaemia due to imbalance of oxygen supply and demand

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33
Q

What can cause type two MI (2)

A

coronary embolism
Hypertension

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34
Q

What can cause type one MI

A

plaque rupture

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35
Q

What are the characteristics of type 2 MI (5)

A

less severe chest pain
Minor ECG changes
Mild-moderate coronary disease
Tachycardia
Low blood pressure

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36
Q

What is type three MI

A

sudden cardiac death with symptoms suggestive of ischaemia

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37
Q

What is controlled in secondary prevention of acute coronary syndrome (3)

A

blood pressure
Cholesterol
Diabetes

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38
Q

What are the four phase of cardiac rehabilitation

A

in-patient care
Early post-discharge period
Structured exercise program
Long term maintenance of physical activity and lifestyle changes

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39
Q

What are the target cholesterol levels in cardiac rehabilitation (2)

A

total < 4.0 mmol/l
HDL . 1.0 mmol/l

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40
Q

What are the types of atrial tachycardia (6)

A

Sinus tachycardia
Atrial fibrillation
Atrial flutter
AVNRT
AVRT
EAT

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41
Q

What are the types of ventricular arrhythmia (4)

A

ventricular fibrillation
Ventricular tachycardia
Premature ventricular complexes
Asystole

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42
Q

What are the types of bradycardia (3)

A

sinus bradycardia
Sinus pauses
Heart block

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43
Q

What does the level of threat to life posed by tachycardia depend on

A

how the arrhythmia affects cardiac output and blood pressure

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44
Q

What can be caused by haemodynamically unstable tachycardia (2)

A

syncope
Cardiac arrest

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45
Q

What can be caused by haemodynamically stable tachycardia (4)

A

hypotension
Reduced coronary circulation
angina
Heart failure

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46
Q

In what way can sinus tachycardia be non-pathological

A

Due to reflex changes in vagal tone during respiratory cycle

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47
Q

What is the management for sinus tachycardia (2)

A

treating underlying cause
Βeta blockers

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48
Q

What is idiopathic atria fibrillation (2)

A

Atrial fibrillation that occurs in the absence of any heart disease with no evidence of ventricular dysfunction
A diagnosis of exclusion

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49
Q

What increases incidence of atrial fibrillation

A

increasing age

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50
Q

When would a pacemaker be used to treat atrial fibrillation (2)

A

if atrial fibrillation with a slow ventricular rate coexists with periods of fast ventricular rate - to allow for pharmacological control of fast ventricular rate
If pharmacological fails/is not tolerated

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51
Q

What risks does atrial fibrillation pose (2)

A

thromboembolic stroke
Congestive heart failure

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52
Q

What are the possible causes of atrial fibrillation (8)

A

congenital
Genetic
Infection
Inflammation
Vascular
Metabolic
Structural
Lifestyle

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53
Q

What are the symptoms of atrial fibrillation (7)

A

palpitations
Presyncope
Syncope
Chest pain
Dyspnoea
Sweatiness
Fatigue

54
Q

What are the patterns of atrial fibrillation (3)

A

paroxysmal
Persistent
Permanent

55
Q

Describe paroxysmal atrial fibrillation (3)

A

<48 hrs
Limited period of time
Often recurrent

56
Q

Describe persistent atrial fibrillation (3)

A

> 48hrs
Can be cardioverted to normal sinus rhythm
Unlikely to spontaneously revert to Norma sinus rhythm

57
Q

Describe permanent atrial fibrillation

A

Normal sinus rhythm cannot be restored

58
Q

Describe the appearance of atrial fibrillation on an ECG (4)

A

irregularly irregular QRS complexes
Absence of P waves
Presence of F waves
Atrial rate > 300bpm

59
Q

how does atrial fibrillation affect the cardiac cycle (2)

A

Diastole time decreased
Therefore cardiac output is decreased

60
Q

What treatment is used to restore rhythm in the event of atrial fibrillation (2)

A

anti-arrhythmic drugs
Direct current cardioversion (DCCV)

61
Q

What treatment is used to maintain rhythm in the event of atrial fibrillation (3)

A

Anti-arrhythmic drugs
Catheter ablation (of atrial focus/pulmonary veins)
Surgery

62
Q

What is used to control heart rate in the event of atrial fibrillation (4)

A

digoxin
Beta blockers
Verapamil
Diltiazem

64
Q

What class of drug must be used in atrial fibrillation if there is a high risk for stroke

A

anticoagulants

65
Q

What is atrial flutter(2)

A

a rapid and regular form of atrial tachycardia
Sustained by a macro-re-entry circuit (usually confined to right atrium)

66
Q

what does atrial flutter carry the risk of

A

Thromboembolic stroke

67
Q

What can chronic atria flutter often progress to

A

atrial fibrillation

68
Q

How is atrial flutter treated (4)

A

radiofrequency ablation
Pharmacological therapy
Cardioversion
Oral anti-coagulant

70
Q

How does supraventricular tachycardia present on an ECG

A

Narrow QRS complex

71
Q

How is acute supraventricular tachycardia treated

A

increasing vagal tone and slowing atrioventricular node conduction
Us using IV adenosine and IV verapamil

72
Q

How is chronic supraventricular tachycardia treated (4)

A

avoiding stimulants
Elecrophysiological study (and radiofrequency ablation)
Beta blockers
Anti-arrhythmic drugs

73
Q

What are the types of atrioventricular tachycardia (2)

A

atrioventricular nodal re-entrant tachycardia
Atrioventricular re-entrant tachycardia via accessory pathway

74
Q

Where may ventricular tachycardia originate (2)

A

ventricular myocardium
Fascicles of the conducting system

75
Q

How does ventricular tachycardia show up on an ECG and why

A

wide QRS complex
As arrhythmia pathway is outside His-PK system - depolarisation takes longer

76
Q

How is acute ventricular tachycardia treated (3)

A

stable: pharmacological cardioversion with anti-arrhythmic drugs
Unstable: direct current cardioversion (DCCV)
Correct triggers

77
Q

What is involved in long-term treatment of ventricular tachycardia (2)

A

Implantable cardiovertor defibrillator (if life threatening, high risk of recurrence)
Ventricular tachycardia ablation

78
Q

What are triggers of ventricular tachycardia (4)

A

electrolytes
Ischaemia
Hypoxia
Pro-arrhythmic drugs

79
Q

Describe ventricular fibrillation (2)

A

Fast and irregular contractions
Heart loses ability to function as a pump

80
Q

Describe heart block (bradycardia)

A

delayed/no conduction via atrioventricular node

81
Q

What are the degrees of heart block

A

first - slow conduction
Second - intermittent conduction
Third - non-conduction

82
Q

How does first degree heart block show up on an ECG

A

Long PR interval

83
Q

How does second degree heart block show up on an ECG

A

varied PR interval

84
Q

How + when is sinus bradycardia treated

A

atropine
Pacer
If symptomatic or unstable

85
Q

What are clinical causes of arrhythmias (6)

A

Abnormal anatomy
Autonomic nervous system
Metabolic
Inflammation
Drugs
Genetics

86
Q

How can abnormal anatomy cause arrhythmia (2)

A

congenital heart disease
Accessory pathways

87
Q

What are example metabolic causes of arrhythmias (3)

A

hypoxia
Ischaemic myocardium
Electrolyte imbalances

88
Q

How can genetics link to arrhythmias

A

Mutations can occur in genes that encode cardiac ion channels

89
Q

What are the mechanisms of arrhythmias (2)

A

ectopic beats
Re-entry

90
Q

What are ectopic beats (3)

A

beats/rhythms originating in places other than the sino-atrial node
Triggered activity
Altered automaticity

91
Q

What does re-entry require (2)

A

multiple connected conduction pathways with different speeds of induction/recovery of excitability
Central blocking by a core block of issue so impulse can loop around via surrounding excitable tissue

92
Q

When does re-entry occur

A

When an action potential fails to extinguish itself and re-activates a region that has recovered from refractoriness

93
Q

What are substrates

A

electrophysiological abnormalities that pre-dispose to re-entry

94
Q

What does arrhythmia propagation require (2)

A

triggers
Substrates

95
Q

What are the symptoms of arrhythmias (7)

A

palpitations
Dyspnoea
Pre-syncope
Syncope
Angina
Heart failure
Anxiety

96
Q

What investigations are performed form arrhythmias (5)

A

ECG/ 24hr ECG/ stress ECG
Bloods (FBC< biochemistry, thyroid function)
CXR
Event recorder
Echocardiography

97
Q

What is CXR used to assess (2)

A

heart size and heart failure

98
Q

What feature on an ECG shows abnormal repolarisation

A

a long QT interval

99
Q

What can echocardiography be used to identify

A

structural heart disease

100
Q

What is radiofrequency ablation

A

Selective localised cautery of cardiac tissue to prevent tachycardia

101
Q

What can radiofrequency ablation target (2)

A

autonomic focus
Part of a re-entry circuit

102
Q

What can radiofrequency ablation be used to do (2)

A

restore rhythm
Control rate

103
Q

What is ablated to maintain sinus rhythm

A

Atrial fibrillation focus

104
Q

What is ablated to control rate

A

Atrioventricular node
Prevents rapid conduction to ventricles

105
Q

What are the four types of anti-arrhythmic drugs

A

reducing Na channel current
Beta blockers
Prolonging action potentials
Calcium channel blockers

106
Q

Which drugs reduce sodium channels current (3)

A

lignocaine
Quinidine
Flecainide

107
Q

Which drug is a beta blockers and anti-arrhythmic

A

propranolol

108
Q

Which drugs prolong action potentials (3)

A

amiodarone
Sotalol
Dronedarone

109
Q

Which drugs are calcium channel blockers (2)

A

verapamil
Diltiazem

110
Q

What are the types of pacemakers (2)

A

single chamber (pace either right atrium or ventricle)
Dual chamber (pace both right atrium and ventricle)

111
Q

Describe electrophysiological studies (2)

A

trigger clinical arrhythmias to study mechanisms
Radiofrequency ablation to extra pathway can be delivered

112
Q

What is heart failure (2)

A

the state in which the heart is unable to pump blood at an adequate rate to meet the requirements of tissue/is only able to do so at high pressures
Due to impaired filling or ejection

113
Q

What is ejection fraction and what should it be in a health individual

A

the percentage of blood pumped out of the heart during each beat
50%

114
Q

What are the two types of heart failure

A

HRrEF - heart failure with reduced (40%) ejection function
HRpEF - heart failure with preserved ejection fraction

115
Q

What is the impairment associated with HRrEF

A

Left ventricle is unable to eject enough blood during systole

116
Q

What is the impairment associated with HRpEF

A

Less blood is able to fill the ventricle during diastole due to myocardial stiffness

117
Q

What are the symptoms of heart failure (6)

A

SOB
Difficulty breathing at night
Reduced exercise tolerance
Fatigue
Tiredness
Ankle swelling

118
Q

What investigations/examinations are used to diagnose heart failure (6)

A

neck exam
Auscultation of lungs and heart
Checking for oedema
ECG
Chest C-ray
Echocardiography

119
Q

What lifestyle medications can be made to manage heart failure (4)

A

reduced water and salt intake
Regular exercise
Updated vaccinations
Mental health management

120
Q

What pharmacological treatment can be used to prolong survival in the event of heart failure (6)

A

RAS inhibition (ACEi, ARII antagonists)
Beta blockers
Aldosterone antagonists
vasodilators
Sinus node blockers
SGLT2 inhibitors

121
Q

What drugs can be used to improve symptoms of heart failure (2)

A

digoxin
Frusemide

122
Q

What are the four pillars of therapy in heart failure

A

ARNII
Beta blockers
MRA - aldosterone receptor antagonists
SGLT2 inhibitors

123
Q

What management is used for patients with refractor end-stage heart failure (3)

A

control of fluid retention
IV inotropics/vasodilators
Consideration of resynchronisation, mechanical assist devices, or heart transplant

124
Q

What is cardiac resynchronisation therapy (2)

A

a method to manage left bundle branch block in heart failure
Pacing of left ventricle form left lateral wall to increase synchronous contraction and improve left ventricle haemodynamics

125
Q

What changes can alter direction and magnitude of fluid movement across capillary walls

A

Increased capillary hydrostatic pressure
Decreased capillary oncotic reassure
Increased capillary permeability
Decreased lymphatic drainage

126
Q

what is oedema

A

accumulation of fluid in interstitial spaces

127
Q

what are the types of oedema (2)

A

pulmonary
Peripheral

128
Q

how is oedema managed

A

with diuretics

129
Q

What is the most common mechanism resulting in heart failure in patients with myocarditis

A

Systolic dysfunction

130
Q

Which cells migrate from the tunica media into the tunica intima forming a fibrous capsule over a plaque

A

smooth muscle cells