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Year 2 > Case 13 > Flashcards

Case 13 Flashcards

1
Q

How long is the PR interval normally?

A

120-200 ms

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2
Q

Which area of the heart has the fastest firing rate?

A

SAN normally 60-100bpm

Fastest intrinsic rate - pacemaker

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3
Q

When are palpitations more common?

A

Puberty
Pregnancy
Menopause

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4
Q

What may exacerbate palpitations?

A

Stress, alcohol, caffeine

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5
Q

Breathlessness can present in both tachy and bradyarrhythmias, what causes the breathlessness and how many tachy/bradyarrhythmias lead to this?

A

Breathlessness = reduced cardiac output
CO = SV x HR
Bradyarrhythmias reduce heart rate
Tachyarrhythmias reduce stroke volume (insufficient time to fill/ empty)

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6
Q

Chest pain can present in both tachy and bradyarrhythmias, what causes the chest pain and how many tachy/bradyarrhythmias lead to this?

A

Myocardial oxygen demand exceeds supply
Increased demand from increased hear rate - tachyarrhythmia
Decreased demand from decreased cardiac output - brady/ tachyarrhythmia

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7
Q

What is the equation for blood pressure?

A

BP = CO x total peripheral resistance

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8
Q

How do the arrhythmias that lead to sudden cardiac death arise?

A

1/3 - primary arrhythmias, structurally normal heart

2/3 - structurally abnormal heart, 80% with CAD, 20% cardiomyopathy

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9
Q

How do the arrhythmias that lead to sudden cardiac death arise?

A

1/3 - primary arrhythmias, structurally normal heart
2/3 - structurally abnormal heart, 80% with CAD, 20% cardiomyopathy
So most fatal arrhythmias are secondary to coronary artery disease

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10
Q

What is a primary arrhythmia?

A

Hear rhythm abnormality that develops out of the blue, not secondary to anything

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11
Q

What does the ECG look like in atrial fibrillation?

A

No p waves - chaotic baseline of fibrillation waves

Irregularly irregular rhythm

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12
Q

What is the most common sustained arrhythmia?

A

Atrial fibrillation

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13
Q

What are the risks of atrial fibrillation?

A

Cerebral thromboembolic event - stroke, transient ischaemic attack
Ventricular tachycardia if accessory pathway present - death

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14
Q

What differentiates paroxysmal, persistent and permanent atrial fibrillation?

A

Paroxysmal - episode lasts less than 48 hours
Persistent - episode lasts more than 48 hours but less than a week
Permanent (fewer symptoms observed by patient as get used to it)

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15
Q

Which rhythm control drugs can be given for atrial fibrillation?

A 
VW class Ic - flecainide, propafenone 
VW class III - amiodarone, dronedarone
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16
Q

How useful is aspirin in stroke prevention in atrial fibrillation?

A

No role

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17
Q

What happens in 1st degree heart block?

A

Pathological slowing of conduction from atria to ventricles

Long PR interval >200ms on ECG

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18
Q

What usually causes 1st degree heart block?

A

Slow conduction within the AVN

Often caused by AVN blocking drugs

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19
Q

What are the consequences of 1st degree heart block?

A

Doesn’t usually cause symptoms or need drugs

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20
Q

What may be the symptoms of 2nd degree or complete heart block?

A

Dyspnoea, T-LOC, chest pain from reduced CO

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21
Q

What happens in complete heart block?

A

Conduction from atria to ventricles fail

Heart continues to beat due to escape rhythm e.g. from ventricles if AVN blocked from them

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22
Q

What happens in complete heart block?

A

Conduction from atria to ventricles fail

Heart continues to beat due to escape rhythm e.g. from ventricles if AVN blocked from them

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23
Q

What is the most life threatening regular broad complex tachycardia?

A

Ventricular tachycardia

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24
Q

What is the most life threatening regular broad complex tachycardia?

A

Ventricular tachycardia

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25
Q

What kind of patient has ventricular tachycardia?

A

History of structural heart disease e.g. ischaemic heart disease
Inherited heart problems - cardiomyopathies, long QT syndrome

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26
Q

What family history might be alarming to VT?

A

Young ischaemic heart disease
Death younger than 40
Known heritable heart disease

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27
Q

What family history might be alarming to VT?

A

Young ischaemic heart disease
Death younger than 40
Known heritable heart disease

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28
Q

What past medical history might be alarming to VT?

A

MI
Heart failure
Ischaemic, congenital, valvular heart disease
Cardiac surgery

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29
Q

What clinical findings might be alarming to VT?

A

Abnormal ECG
Heart murmur
Signs of heart failure

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30
Q

Which inherited conditions can predispose to primary arrhythmias?

A

Long QT syndrome
Brugada syndrome
Wolff-Parkinson-White syndrome

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31
Q

What are the inherited cardiomyopathies that can predispose to arrhythmias?

A

Hypertrophic
Dilated
Arrhythmogenic RV

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32
Q

What helps the spread of excitation from SAN to LA?

A

Bachmann’s bundle

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33
Q

What electrically separates the atria from ventricles?

A

Anulus fibrosus

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34
Q

What causes depolarisation in a normal cell and cardiac pacemaker cell?

A

Normal cell - Sodium influx causes depolarisation

Cardiac pacemaker cell - Calcium influx causes depolarisation

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35
Q

Which phase of cardiac pacemaker cells does sympathetic/ parasympathetic stimulation effect?

A

Phase 4 - altering the rate of funny current (slow inward current of sodium)

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36
Q

What are the unipolar limb leads?

A

aVR/ Augmented vector right - lead on R wrist
aVL/ Augmented vector left - lead on L wrist
aVF/ Augmented vector foot - lead on L foot

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37
Q

What’s the PR interval?

A

Start of p wave to start of QRS

0.12-0.20 seconds

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38
Q

How do you convert seconds to milliseconds (ms)?

A

x1000

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39
Q

Which part of the ECG represents atrial systole?

A

P wave

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40
Q

Which part of the ECG represents electrical conduction through the AVN?

A

PR segment

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41
Q

Which part of the ECG represents ventricular systole and atrial repolarisation?

A

QRS complex

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42
Q

Which part of the ECG represents a time where the ventricles are entirely depolarised?

A

ST segment

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43
Q

Which part of the ECG represents ventricular repolarisation?

A

T wave

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44
Q

Which part of the ECG represents ventricular depolarisation and repolarisation?

A

QT interval

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45
Q

What is the sequence of the ECG?

A

P wave, PR segment, QRS complex, ST segment, T wave
or
PR interval, QT interval

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46
Q

How long is the QRS complex in order to be classed as:
A) Normal?
B) A broad complex?

A

A) Normal is less than 120ms

B) QRS duration >120ms

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47
Q

What is the QT interval?

A

Start of the QRS complex to the end of the T wave

Normal: less than 450ms

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48
Q

Which part of the ECG represents atrial depolarisation and the time take to pass through the AVN?

A

PR interval

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49
Q

How is an ECG recording calibrated?

A

Set to 1mV that is 1cm (10 small squares high)

Paper feeding in at 25mm/s

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50
Q

If paper is fed in at a rate of 25mm/s what does one large square represent?

A

0.2 seconds

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51
Q

If paper is fed in at a rate of 25mm/s what does one small square represent?

A

0.04 seconds

52
Q

How do you calculate the heart rate on an ECG?

A

300/ no. of large squares in R-R interval

53
Q

What is a tachycardic heart rate?

A

> 100bpm

54
Q

What is a bradycardic heart rate?

A

Less than 60 bpm

55
Q

Work out the heart rate for the following R-R intervals:
A) 4 large squares
B) 5 large squares
C) 6 large squares

A

A) 75
B) 60
C) 50

56
Q

What 2 things should be considered on assessing rhythm of the ECG trace?

A

R-R interval: regular, regularly irregular or irregularly irregular
Is every P wave followed by a QRS complex: sinus

57
Q

Which leads will be positive and negative in right axis deviation?

A

Positive: III and aVF
Negative: I and aVL

58
Q

What causes right axis deviation?

A 
Average depolarisation moves to the right 
Right ventricular hypertrophy
COPD
PE
lateral MI
Wolff-Parkinson-White syndrome (WPW)
59
Q

Which leads will be positive and negative in left axis deviation?

A

Positive: aVL and I
Negative: II, III and aVF
Only significant when II is negative

60
Q

What causes left axis deviation?

A

LVH
Inferior MI
WPW syndrome Left anterior hemiblock

61
Q

What should the INR of patients with atrial fibrillation be?

A

INR of 2 to 3

62
Q

What is the mechanism of atrial flutter?

A

Macro re-entry circuit in right atrium - area of slow conduction near the IVC
The AV node cannot conduct impulses at this rate leading to AV block - ventricles only beat once for every 2/3/4 atrial beats
The most common is a 2:1 block producing a ventricular rate of 150bpm

63
Q

What is typically the atrial rate in atrial flutter?

A

Atrial rate of around 300bpm

64
Q

What can cure atrial flutter?

A

Radiofrequency catheter ablation - burn the area between the inferior vena cava and the tricuspid annulus so that it can no longer conduct impulses

65
Q

What does atrial flutter look like on ECG?

A

Saw-tooth appearance - regular flutter waves

66
Q

How would you describe a sequence of 3 flutter waves before every QRS complex?

A

3:1 AV block

67
Q

What would show left atrial enlargement on an ECG?

A

Bifid p wave called P mitrale

RA depolarises before the LA

68
Q

What may cause a bundle branch block, causing the QRS complex to be >120ms?

A

Conduction system fibrosis
Ischaemic/ Hypertensive/ Valvular heart disease (especially aortic stenosis)
Cardiac surgery
Cardiomyopathies

69
Q

Which type of bundle branch is always pathological?

A

Left

right can be present in normal hearts

70
Q

What can cause right bundle branch blocks?

A

MI
PE
Cor pulmonale
Normal variant

71
Q

What can cause left bundle branch blocks?

A

IHD, MI
Hypertension
Aortic Stenosis
Dilated cardiomyopathy

72
Q

What are the ECG changes in a STEMI?

A

ST elevation: >2mm in chest leads, >1mm in limb leads
ST elevation must be in at least 2 contiguous leads
First change: Tall peaked T waves
T wave inversion (immediate or delayed)

73
Q

ST elevation in which leads suggest an anterior infarction?

A

V2-5

74
Q

ST elevation in which leads suggest an inferior infarction?

A

III and aVF

75
Q

ST elevation in which leads suggest a lateral infarction?

A

I, aVL and V5-6

76
Q

What could happen do the ECG with an NSTEMI?

A

T wave flattening/ inversion
ST segment depression >0.5mm (up-sloping/ horizontal/ down-sloping)
ECG may be normal

77
Q

If an NSTEMI is suspected from ECG recording, what is required for confirmation?

A

Troponin rise

78
Q

What ECG changes are seen in pericarditis?

A

Widespread concave upwards ST elevation (saddle-shaped)
Widespread PR depression
Reciprocal ST depression and PR elevation in aVR
Later T wave inversion

79
Q

What are examples of broad complex tachyarrhythmias/ wide QRS complexes?

A

Ventricular tachycardia, torsades de pointes
Ventricular fibrillation
Supraventricular tachycardia with bundle branch block

80
Q

What are examples of narrow complex tachyarrhythmias/ narrow QRS complexes?

A 
Sinus tachycardia 
Atrial fibrillation 
Atrial flutter
AV node re-entry tachycardia (AVNRT)
AV re-entry tachycardia (AVRT)
Atrial tachycardia
81
Q

Which causes pre-excitation; AVNRT or AVRT?

A

AVRT

82
Q

Which leads would have inverted T waves in a left sided accessory pathway?

A

V1-3

83
Q

Which leads would have inverted T waves in a right sided accessory pathway?

A

V4-6

84
Q

What are the differences in QRS complex between AVRT causing orthodromic tachycardia compared to antidromic tachycardia?

A 
Orthodromic tachycardia (retrograde passage through accessory pathway, more common) - narrow QRS
Antidromic tachycardia (anterograde passage through accessory pathway, less common) - wide QRS
85
Q

What ECG changes are observed in AVNRT?

A

In sinus rhythm looks like a normal ECG
Supra-ventricular tachycardia with narrow QRS complexes
May have inverted P waves

86
Q

What ECG changes are observed in AVRT?

A

In sinus rhythm there is a delta wave
Short PR interval
Orthodromic tachycardia – looks like a SVT
Antidromic tachycardia – looks like VT

87
Q

How are ANVRT and AVRT treated?

A

Vagal manoeuvres
If this fails then adenosine
In haemodynamically compromised patients, DC cardioversion is indicated

88
Q

What are the reversible causes of cardiac arrest?

A 
(4 H's) 
Hypoxia 
Hypovolaemia 
Hyper/ hypo kalaemia/ hypocalcaemia/ hypoglycaemia
Hypothermia
(4 T's) 
Thromboembolic 
Tamponade (cardiac) 
Tension pneumothorax 
Toxins
89
Q

What’s the antidote for heparin?

A

Protamine sulphate

90
Q

What’s the antidote for warfarin?

A

Vitamin K

91
Q

What’s the antidote for novel oral anticoagulants?

A

Idarucizumab

92
Q

What is the name of the accessory pathway in Wolf-Parkinson-White syndrome?

A

Bundle of Kent

93
Q

What is the difference between Mobitz type 1 and 2 2nd degree heart block?

A

Mobitz type 1: progressive lengthening of PR interval until failure of conduction of an atrial beat
Mobitz type 2: Mostly constant PR interval, occasional atrial depolarisation whiteout subsequent ventricular depolarisation

94
Q

What happens in 2nd degree heart block?

A

Conduction from atria to ventricles is intermittent
ECG shows non-conducted p waves (not followed by QRS complex)
PR interval progressively lengthens in type 1
PR interval is constant in type 2

95
Q

Which direction does the septum normally depolarise ?

A

Left to right

96
Q

How can left bundle branch blocks be differentiated from right on ECG?

A 
(William Marrow)
LBBB: W in V1, M in V6
RBBB: M in V1, W in V6
W is a QRS complex
M is an RSR pattern
97
Q

Which leads would have tall, peaked P waves in P pulmonale? How tall?
Which leads must have a positive p wave? How tall?

A

Inferior - II, III and aVF >2.5mm

V1 and V2 >1.5mm

98
Q

What causes P pulmonale?

A

Right atrial enlargement from pulmonary hypertension (chronic lung disease/ PE) or tricuspid regurgitation

99
Q

Do regular narrow complex tachyarrhythmias increase the risk of sudden cardiac death?

A

No

100
Q

What is the valsalva manoeure and when should it be used?

A

Moderately forceful attempted exhalation against closed airway
For symptoms of tachycardia

101
Q

What does adenosine do to the conducting system of the heart?

A

Injected short acting AVN blocker

102
Q

What are beta 1 receptors coupled to?

A

Gs proteins

103
Q

What can encourage delayed after depolarisations?

A

Digoxin
Adrenaline (via GPCR)
through increasing intracellular calcium

104
Q

What happens in delayed after depolarisations?

A

Calcium is super threshold

Asynchronous action potentials are fired until the calcium runs out

105
Q

What is the threshold for action potential roughly?

A

-40mV

106
Q

What is an example of a Na+ channel blocker used for SVT?

A

Flecainide

107
Q

How do sodium channel blockers stop SVT?

A

They block fast path channels

108
Q

Give an example of a beta blocker used to treat SVT and state how beta blockers are effective

A

Bisoprolol

Block B1 adrenoceptors, reducing the slope of phase 4 potential

109
Q

Which phase of the action potential do potassium channel blockers affect?

A

Phase 3

110
Q

Example of a potassium channel blocker

and how do they work in treating VT, AF, atrial flutter and WPW?

A

Amiodarone
Blocking K+ channels slow repolarisation
Prolonging refractory period of cardiac action potential

111
Q

Name a calcium channel blocker used in treating arrhythmias and state the arrhythmias it is used to treat

A

Diltiazem

Paroxysmal SVT and reducing ventricular rate in atrial fibrillation

112
Q

How does adenosine stop AVNRT?

A

Activates alpha 1 receptors
Inhibiting adenylyl cyclase - decreasing cAMP
Triggers K+ efflux & inhibiting Ca2+ entry to SAN - cell hyperpolarisation

113
Q

How is heparin administered?

A

IV

114
Q

How would you monitor anticoagulation in a patient given heparin?

A

Measure prothrombin time compared against activated partial thromboplastin time (aPTT)

115
Q

What is the MOA of warfarin?

A

Vitamin K carboxylase inhibitor

Prevents formation of gamma-carboxylated blood clotting factors

116
Q

What is the MOA of heparin?

A

Activates anti-thrombin III

Inactivating thrombin and factor Xa

117
Q

What do low molecular weight heparin inhibit?

A

Factor Xa

118
Q

What does the NOAC dabigatran inhibit?

A

Thrombin

119
Q

What does the NOACs rivaroxaban and apixaban inhibit?

A

Factor Xa

120
Q

What are the phases of a normal action potential?

A 
0 Rapid depolarisation
1 Early repolarisation 
2 Plateau 
3 Rapid repolarisation 
4 Resting potential
121
Q

During phase 0 what does Ina occur through?

A

Ina (inward Na+ current)

Nav1.5 channels

122
Q

During phase 1 what does Ito occur through?

A

Ito (transiently outward K+ current)

Kv1.4

123
Q

During phase 2 what does Ikr occur through?

A

Ikr (Rapidly delayed rectifier K+ channel)

Kv11.1

124
Q

During phase 2 what does Iks occur through?

A

Iks (slowly delayed rectifier K+ channel)

Kv7.1

125
Q

During phase 2 what does Ica,L occur through?

A

Ica, L (SR Ca2+ release via L-type channels)

Cav1.2

126
Q

What’s the normal length of the QT interval?

A

0.35-0.43 seconds

Year 2 (13 decks)

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