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Y1 Cardiovascular > Conditions - ACS and Arrhythmias > Flashcards

Conditions - ACS and Arrhythmias Flashcards

1
Q

Points of auscultation

A

Aortic valve - right side second intercostal space, next to sternum
Pulmonary valve - left side second intercostal space, next to sternum
Tricuspid valve - Left side, 4th intercostal space, near the sternum
Mitral valve - Left side, 5th intercostal space, mid clavicular line

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2
Q

What is ACS

A

3 acute states of myocardial ischaemia which can lead to infarction and necrosis
Unstable Angina / STEMI / NSTEMI

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3
Q

Difference between unstable angina and angina

A

UA not relieved by GTN spray
UA occurs at rest / no specific triggers
UA lasts for 30 mins or longer whereas SA lasts for 15 mins only
UA due to rupture of atherosclerotic plaque whereas SA due to formation of atherosclerotic plaque narrowing the vessel

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4
Q

Difference between STEMI and NSTEMI

A

STEMI due to complete occlusion of blood vessel whereas NSTEMI is due to severe occlusion of blood vessel

STEMI causes ST elevation / new left bundle branch block on ECG whereas NSTEMI does not

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5
Q

What is the cause of ACS

A

Acute rupture of atherosclerotic plaque -> exposes collagen in the plaque to platelets -> blood clot forms and occludes the vessel

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6
Q

What are the reasons for rupture of atherosclerotic plaque

A

Young, fatty plaques are more likely to rupture
Bending and twisting of vessels during heart contraction
Change in intraluminal pressure
Injury

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7
Q

Which type of MI is due to acute coronary artery event

A

Type 1

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8
Q

What causes type 2 MI

A

oxygen supply / demand mismatch

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9
Q

Which type of MI are most NSTEMI and STEMI part of

A

Type 1

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10
Q

How can acute MI lead to heart failure

A

Myocardial ischaemia can lead to myocardial infarction hence necrosis
This causes the heart to lose muscle and eventually it may mean that the heart can no longer pump sufficient CO = heart failure

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11
Q

Symptoms of MI

A

Unstable angina
Sweating / clammy
Pale
May show heart failure symptoms

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12
Q

What are the symptoms of unstable angina

A

Severe pain
pain may radiate to neck and arms
Pain is 30 mins or longer
Occurs at rest
Not relieved by GTN spray

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13
Q

Diagnosis of MI

A

History
Urgent ECG
Measure troponin level

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14
Q

What may the results from ECG and troponin level be for NSTEMI and STEMI

A

STEMI - ST elevation and reciprocal ST depression or new LBBB + elevated troponin level

NSTEMI - non-ST elevation; T wave inversion and ST depression + elevated troponin level

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15
Q

Why isn’t troponin the definitive diagnosis of MI

A

Because other conditions can cause myocardial necrosis hence elevated troponin level

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16
Q

When should you start treatment for STEMI

A

Immediately after ECG diagnosis. Do not wait for troponin level results as ECG diagnosis is sufficient to indicate STEMI

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17
Q

Which troponin levels indicate myocardial necrosis

A

Troponin I and C

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18
Q

What is the management of STEMI

A

Immediate management - MONA
IV diamorphine
Oxygen
GTN
Aspirin + ticagrelor / clopidegrol
Anti-emetics
Immediate PCI within 120 mins of ECG diagnosis
Fibrinolysis if PCI not available promptly -> refer to PCI center -> angiography +/- PCI

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19
Q

What is the dosage of aspirin given to STEMI patients

A

300mg

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20
Q

Which antiplatelet should be used instead for STEMI patients going for immediate PCI

A

Prasugrel / clopidogrel (not ticagrelor)

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21
Q

What is the management of NSTEMI or UA

A

Calculate GRACE score
MONA
IV diamorphine
Oxygen
GTN
Aspirin + fondaparinux

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22
Q

What does GRACE score show

A

6 months mortality risk

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23
Q

What is the management for patients with very high GRACE risk score

A

immediate invasive angiography +/- PCI within 2 hours

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24
Q

What is the management for patients with high GRACE risk score

A

Early invasive angiography (<24 hour)

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25
Q

What is the management for patients with intermediate GRACE risk score

A

Invasive angiography (<72 hours)

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26
Q

What is the management for patients with low GRACE risk score

A

Non-invasive testing
If symptoms worsen -> invasive angiography

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27
Q

What are the non-invasive testing methods for NSTEMI

A

Cardiac MRI
Transthoracic echocardiogram
Stress echocardiogram
CT angiography

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28
Q

What antiplatelets should be given to patients with intermediate to very high GRACE risk score

A

Prasugrel or ticagrelor

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29
Q

What should be given to NSTEMI patients that are going to have invasive angiography

A

LWMH

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30
Q

What is the post MI management

A

Beta Blockers - bisnoprolol
ACEi - ramipril
Aspirin + clopidogrel or ticagrelor
Statin
Cardiac rehabilitation
ECHO

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31
Q

What are the complications of MI

A

Ventricular fibrillation
HF
Left ventricular free wall rupture
Mitral regurgitation
Cardiogenic shock
Ventricular septal defects
Acute pericarditis
Aneurysm

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32
Q

Which type of infarct most commonly causes heart block

A

Inferior infarct

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33
Q

What is supraventricular tachycardia

A

Tachycardia originating above ventricles; including atrial flutter, atrial fibrillation, ectopic atrial tachycardia, AVNRT, AVRT

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34
Q

What does ectopic atrial tachycardia mean

A

Abnormal electrical signal started from within the atrium and takes over the SA node

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35
Q

What are Junctional rhythms

A

AV node takes over SA node and propagates impulses to atria and ventricles at the same time so atria and ventricles contract simultaneously

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36
Q

What are the ECG findings for junctional rhythms

A

Narrow QRS complex
Absent P wave, masked by QRS complex

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37
Q

What does re-entrant circuit mean

A

A continuous wave of depolarisation in a circular path; as the depolarisation travels to its site of origin, it reactivates that site

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38
Q

Which arrhythmias uses reentrant circuit

A

Atrial Flutter
Atrial Fibrillation
AVNRT
AVRT

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39
Q

What are the requirements for re-entrant circuits to occur

A

1) require 2 conduction pathways
2) 1 pathway is slow but short refractory period ; the other pathway is fast but long refractory period

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40
Q

What is an accessory pathway

A

Abnormal connection between atria and ventricles, faster conduction than through AV node

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41
Q

What are the common symptoms of arrhythmia

A

Palpitations
Dizziness
Syncope / pre syncope
dyspnea

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42
Q

Mechanism of atrial flutter

A

Normal impulse from SA node passes to the circular circuit in atria and AV node at the same time

This causes the atria to contract rapidly

The reentrant circuit also stimulates the AV node every time it passes but not all impulses will be conducted to the ventricles

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43
Q

Not all impulses generated in reentrant circuit in atria passes into ventricles. Why is that

A

Due to AV node block - normal AV node has a delay in conducting impulse from atria to ventricles

Depends on the degree of AV node block

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44
Q

What is the common ratio between atrial flutter waves and QRS complex

A

2:1

2 flutter waves to 1 QRS complex due to AV node delay

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45
Q

Where does atrial flutter occur

A

Common in right atrium but can spread in left atrium

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46
Q

Which type of reentrant circuit does atrial flutter use

A

Macro-re entrant circuit

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47
Q

What are the ECG findings for atrial flutter

A

Narrow QRS complex
2:1 (but can be 3:1 / 4:1 as well)
saw-tooth baseline
Regularly irregular

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48
Q

Regularly irregular vs irregularly regular

A

Regularly irregular - recurrent pattern of irregularity
Irregularly irregular - completely disordered

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49
Q

Which type of arrhythmia increases risk of stroke

A

Atrial fibrillation

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50
Q

Mechanism of atrial fibrillation

A
  1. multiple spontaneous waves of excitation leading to atrial muscles contracting independently and ineffectively
  2. the abnormal electrical impulses are intermittently passed down to the ventricles through AVN
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51
Q

Ventricular rate in AF is variable between people. Why is that

A

Due to variable AVN conduction speed
This means that young patients with fast AVN are very symptomatic

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52
Q

What can be caused by chaotic contractions of the atria

A

Blood stasis, increasing risk for blood clots to form

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53
Q

Risk factors for AF

A

Mitral regurgitation
Atrial / ventricular dilation
Atrial / ventricular hypertrophy
Wolff-Parkinson syndrome
Hypertension
Obesity
Thyroid dysfunction
Infections

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54
Q

Where does the arrhythmia of AF often originate from

A

left atrial myocytes

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55
Q

Why is it important to measure all apical, radial and carotid pulses

A

Because sometimes the abnormal ventricular contractions may not be strong enough to transfer fast pulses to the radial artery.

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56
Q

What are the ECG findings of atrial fibrillation

A

Irregularly irregular
Narrow QRS complex
Absence of discrete P waves
Long RR interval -> short RR interval

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57
Q

What are the complications of AF

A

Ischaemic stroke
HF
Cardiogenic shock

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58
Q

What causes AVNRT

A

Micro re-entry circuit within the AV node

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59
Q

Mechanism of AVNRT

A

1) A normal impulse from SA node passes into AV node where there are 2 anatomical conduction pathways
2) The impulse travels to both slow and fast pathways but only the impulse from fast pathway travels down to ventricles
3) Another impulse (pre ectopic beat) travels down to slow pathway bc fast pathway is still in refractory period
4) This causes the ventricles to be excited again. The impulse then travels back up to fast pathway to re-excite atria

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60
Q

What are the ECG findings of AVNRT

A

Rapid, narrow QRS complex
regular tachycardia (>/ 100bpm)
Absent P waves

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61
Q

What causes AVRT

A

macro re-entry circuit - uses accessory pathway

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62
Q

Mechanism of AVRT

A

Impulses travel retrograde (ventricles -> atria) or antegrade (atria -> ventricles)

63
Q

Types of AVRT

A

Antidromic
Orthodromic

64
Q

What is antidromic AVRT and its ECG findings

A

Anterograde AVRT

Wide QRS complex
Shortened PR interval
Absent P waves

65
Q

What is antidromic AVRT and its ECG findings

A

Induced by premature atrial beat, the premature impulse travels down to the accessory pathway

broad QRS complex
Retrograde P wave after QRS complex

66
Q

What is ventricular tachycardia

A

Rapid recurrent ventricular depolarisation from a focus within the ventricles

67
Q

What can ventricular tachycardia cause

A

Syncope
Cardiac arrest
Decrease / loss of cardiac output

68
Q

What are the ECG findings of VT

A

Regular tachycardia
Rapid, broad QRS
Absent P waves

69
Q

What is Torsades de point

A

A type of VT due to depolarisation from multiple foci in ventricles

70
Q

What are the ECG findings of Torsades de Point

A

variable QRS complex
Prolonged QT

71
Q

What is ventricular fibrillation

A

When the ventricles start contracting independently and no longer meaningfully

72
Q

Pulseless is a common feature of which type of arrhythmia

A

Ventricular fibrillation

73
Q

Why is ventricular fibrillation so serious

A

Because the heart loses its ability to pump hence there is no cardiac output, leading to cardiogenic shock / cardiac arrest

74
Q

What are the classes of anti-arrhythmics

A

Class I - blocks Na+ channels
Class II - Beta blockers
Class III - blocks K+ channels
Class IV - CCB

75
Q

Which classes are rate controlling anti-arrhythmics

A

Class II and Class IV

76
Q

Class I anti-arrhythmic subtypes

A

Ia - disopyramide; intermediate rate
Ib - lignocaine; fast rate
Ic - flecainide; slow rate

77
Q

Example of class III drug

A

Amiodarone

78
Q

Mechanism of action of amiodarone

A

Blocks K+ channels to prolong action potential duration

79
Q

Why isn’t amiodarone used for long term rhythm control

A

Long term use has high risk of
pulmonary fibrosis
thyroid disorders
photosensitivity
peripheral neuropathy

80
Q

Why may a diabetic not experience chest pain when he has STEMI

A

Due to diabetic neuropathy

81
Q

What CCB are used as anti-arrhythmic drugs

A

dilitiazem
Verapamil

82
Q

What treatment is required to prevent blood clots in patients with atrial fibrillation

A

Anti-coagulants

83
Q

What anti coagulants are used to reduce risk of stroke in A fib patients

A

DOAC
Vitamin K antagonist such as Warfarin

84
Q

Examples of DOAC

A

Apixaban
Rivaroxaban

85
Q

What assessment tool is used to measure how likely it is for a A fib patient to get a stroke

A

CHA2DS2VASc tool

86
Q

What is the guideline for haemodynamically stable patient w acute Afib

A

If new onset -> rate or rhythm control
If not new onset -> rate control -> rhythm control

87
Q

What is considered as new onset atrial fibrillation

A

less than 48hrs

88
Q

What is the treatment for haemodynamically unstable patient w acute Afib

A

emergency synchronized DC cardioversion

89
Q

What is considered as haemodynamically unstable

A

Symptoms of shock
Syncope
signs of heart failure
Chest pain
Pulmonary oedema

90
Q

When should rate control not be used

A

If the patient
- has atrial flutter appropriate for ablation
- HF primarily caused by AF
- AF with a reversible cause

91
Q

What are the rate controlling drugs used for Afib

A

First line - Beta blockers except sotalol / CCB
Digoxin - for patients with heart faillure

92
Q

What are the rhythm controlling drugs used for AFib

A

flecainide or propafenone if no structural / ischaemic heart disease
Amiodarone if there is structural disease
Beta blockers for long term rhythm control

93
Q

What is the treatment guideline for haemodynamically unstable patient with atrial flutter

A

Emergency synchronized DC cardioversion

94
Q

What is the treatment guideline for haemodynamically stable atrial flutter

A

rate control

95
Q

When is ablation strategy used

A

recurrent atrial flutter despite drug treatment

96
Q

What is the guideline for ventricular fibrillation

A

1) ABCDE
2) defibrillation
3) chest compressions
4) inject adrenaline and amiodarone after 3rd shock
5) inject adrenaline every 3-5 mins (every alternate shock)

97
Q

What is the management for pulseless ventricular tachycardia

A

1) ABCDE
2) defibrillation
3) chest compressions
4) inject adrenaline and amiodarone after 3rd shock
5) inject adrenaline every 3-5 mins (every alternate shock)

98
Q

What is the management for VT with pulse

A

If haemodynamically stable -> amiodarone
If haemodynamically unstable -> synchronized DC cardioversion

99
Q

Is defibrillation synchronized or unsynchronized

A

Unsynchronized

100
Q

How to manage haemodynamically stable patient w torsades de point

A

magnesium sulfate

101
Q

How to manage regular narrow QRS tachycardia

A

Vagal manouevres - ice / valsalva
if fail -> adenosine

102
Q

Why shouldn’t adenosine be used in asthmatics

A

Because there is risk of bronchoscpasm

103
Q

What can left ventricular thrombus cause

A

Episodes of vision loss

104
Q

Why isn’t verapamil used with beta blockers

A

risk of complete heart block

105
Q

Which vein is associated with atrial fibrillation

A

Pulmonary veins

106
Q

Why is a loading dose of amiodarone needed

A

Because it has a long half life. A loading initial dose of amiodarone is needed to maintain the therapeutic concentration for a long half life

107
Q

What is the treatment for Mobitz Type 1

A

Nothing, as they are mostly asymptomatic and will not cause complete heart block

108
Q

Why is Mobitz Type II dangerous

A

patients are at risk of complete heart block

109
Q

What is the management for Mobitz Type II

A

Permanent pacemaker

110
Q

What is the management for third degree heart block (complete heart block)

A

Permanent pacemaker

111
Q

Indications for permanent pacemakers

A

Type II heart block
Complete heart block
Sick sinus syndrome
Atrial fibrillation
Bradycardia

112
Q

What does the P wave on ECG mean

A

Atrial depolarisation

113
Q

Where is PR interval and what does it mean

A

Start of P wave to the beginning of Q
It represents the time taken for depolarisation to conduct through the AV node

114
Q

What is not shown on ECG (depolarisation / repolarisation)

A

Atrial repolarisation

115
Q

What is the normal length of PR interval

A

0.12 - 0.2 s

116
Q

What is the normal length of P wave

A

0.08 - 0.1 s

117
Q

What does T wave represent

A

Ventricular repolarisation

118
Q

What does ST interval represent

A

Ventricular contraction

119
Q

What does QRT represent

A

Ventricular depolarisation

120
Q

What is the normal duration of QRT

A

Less than 0.1s

121
Q

What does QT interval represent

A

The time taken for ventricles to depolarise and repolarise

122
Q

What is the normal duration of QT interval

A

0.35 - 0.44 s at a heart rate of 60
depends on the heart rate

123
Q

What does a small square on ECG represent

A

0.04s

124
Q

What does a large square on ECG represent

A

0.2s

125
Q

How to calculate heart rate from ECG (normal)

A

300 / number of large squares between 2 consecutive points (e.g. RR)

126
Q

How to calculate heart rate if the person has irregular heartbeat

A

Calculate the number of QRS complexes on rhythm strip x 6

127
Q

What are the colours for each limb electrode for ECG

A

Red - right wrist
Black - right limb
Yellow - left wrist
Green - left limb

128
Q

Where should you place the upper limb electrodes

A

on ulnar styloid process (wrist)

129
Q

Where should you place the lower limb leads

A

on medial or lateral malleolus

130
Q

Where should you place V1 - V4

A

V1 - 4th intercostal space, right sternal edge
V2 - 4th intercostal space, left sternal edge
V3 - placed between V2 and V4
V4 - left 5th intercostal space in midclavicular line

131
Q

Where should you place V5 and V6

A

V5 - left 5th intercostal space, anterior axillary line
V6 - left 5th intercostal space, mid axillary line

132
Q

What are the lateral leads

A

I , aVL , V5-V6

133
Q

What are the inferior leads

A

II , III , aVF.

134
Q

What are the anterior/ septal leads

A

V1 - V4

135
Q

What is the most common cause of death in the first hour of a patient having an acute MI

A

Ventricular fibrillation

136
Q

Post MI complications

A

1) HF -> cardiogenic shock
2) Ventricular fibrillation -> cardiac arrest
3) ventricular septal wall defect
4) ventricular free wall rupture
5) mitral regurgitation
6) left ventricular aneurysm
7) pericarditis
8) Dressler’s syndrome
9) Mural thrombus

137
Q

What are the complications that has a high risk of happening 0-24 hours post MI

A

Ventricular fibrillation -> cardiac arrest -> death

Heart failure -> cardiogenic shock

138
Q

Why does heart failure occur post MI

A

Because ischaemia causes necrosis of muscle fibres -> too much fibrosis means that there will be decreased contractility of the heart

139
Q

What are the histological findings of a heart 0-24hrs post MI

A

Early coagulative necrosis
Neutrophils
Wavy fibres
Hypercontracting myofibrils

140
Q

What are the complications that have a high risk of developing 1-3 days post MI

A

Pericarditis

141
Q

What are the signs and symptoms of pericarditis

A

Chest pain worsened by lying down and relieved by leaning forward

Pericardial rub

Pericardial effusion on CXR

142
Q

What are the histological findings 1-3 days post MI

A

Extensive coagulative necrosis
Neutrophils

143
Q

What are the complications that are at high risk of occurring 3 - 14 days post MI

A

Ventricular free wall rupture
Ventricular septal defect

144
Q

What are the histological findings 3-14 days post MI

A

Granulation tissues
Macrophages

145
Q

What causes acute mitral regurgitation post MI

A

Papillary muscle rupture

146
Q

Signs of left ventricular free wall rupture

A

Diminished heart sounds
Raised JVP
pulsus alterans

147
Q

What are the complications that are at high risk of developing 2weeks - months post MI

A

Dressler’s syndrome

148
Q

What causes Dressler’s syndrome

A

autoimmune reaction against antigenic proteins formed as the myocardium recovers

149
Q

Symptoms of Dressler’s syndrome

A

Signs of pericarditis
Fever

150
Q

What type of murmur is produced by ventricular septal wall defect patients

A

Pan-systolic murmur

151
Q

What conditions causes pan systolic murmur

A

Mitral regurgitation
Tricuspid regurgitation
Ventricular septal defect

152
Q

What condition is associated to persistent ST elevation

A

Left ventricular aneurysm

153
Q

Indications for permanent pacemakers

A

Type II heart block
Complete heart block
Sick sinus syndrome
Atrial fibrillation
Bradycardia

Y1 Cardiovascular (6 decks)

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