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MBBS - Year 2 > Cardiology - Arryhthmias > Flashcards

Cardiology - Arryhthmias Flashcards

1
Q

Definition of AF

A

SVT
Uncoordinated atrial contraction
Irregular and frequently fast ventricular rate

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2
Q

Epidemiology of AF

A

Commonest cardiac arrhythmia - 1.2%

Prevalence increases with age - 10% > 70yrs, 23% > 80 yrs

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3
Q

ECG appearance in AF

A

No distinct P wave

Irregularly irregular

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4
Q

Classification of AF

A 
First-diagnosed AF 
Paroxysmal AF 
Persistent AF 
Long standing persistent AF 
Permanent AF
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5
Q

First-diagnosed AF

A

AF that hasn’t been diagnosed before

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6
Q

Paroxysmal AF

A

Self-terminating, usually in 48 hrs

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7
Q

Persistent AF

A

AF lasting longer >7 days

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8
Q

Long-standing persistent AF

A

Continuous AF lasting >1 yr when its decided to adopt a rhythm control strategy

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9
Q

Permanent AF

A

AF accepted by pt and Dr

Rhythm control interventions aren’t pursued

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10
Q

AF symptoms

A 
Palpitations 
Dyspnoea 
Chest tightness 
Fatigue/ lethargy 
Sleeping disturbances 
Psychological effects
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11
Q

Modified EHRA symptoms scale

A

1 - 4

No symptoms to disabling symptoms

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12
Q

Aetiological factors of AF

A 
Aging (structural remodelling)
Heart failure 
HTN and DM 
Valvular heart disease (esp mitral)
CAD
Alcohol excess 
Hyperthyroidism (trigger)
Obesity and sleep apnoea 
Autonomic activation
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13
Q

Autonomic activation of AF

A

Sympathetic - increased ectopic activity

Vagal - reduced APD and increased spatial heterogeneity

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14
Q

Target BP for AF pts

A

130/80 mmHg

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15
Q

Mx of wt in AF pts

A

10% reduction in body wt (BMI < 25)
Increased physical activity
Diet (low-calorie food)

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16
Q

Mx of lipids in AF pts

A

Lifestyle measures if LDL >100mg/dL after 2/12 started on statins

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17
Q

Glycaemic control in AF pts

A

HbA1c > 6.5% after 2/12 - metformin

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18
Q

Mx of OSA in AF pts

A

Sleep study

Nocturnal CPAP

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19
Q

OSA

A

Obstructive Sleep Apnoea

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20
Q

Diagnostic workup for AF

A 
12 lead ECG 
BP 
Bloods 
Echo 
Holter monitoring
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21
Q

Bloods for AF

A 
FBC 
U&Es 
LFT 
TFT 
Coagulation
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22
Q

Why do we measure U&Es for AF

A

Abnormal K can ppt AF

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23
Q

Holter monitoring

A

Symptoms/ rhythm correlation
AF burden
Ventricular rate control

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24
Q

Potential consequences of AF

A

Morbidity associated w/ symptoms
AF +/- tachycardia mediated CM
Stroke
Increased mortality

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25
Q

Rship between AF and stroke

A

Blood pools in atria –> blood clot forms –> whole/ part of blood clot breaks off –> travels to brain occluding cerebral artery

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26
Q

Mechanisms of AF

A 
Ectopic activity (trigger + AF driver)
Re-entry - can be single or multiple circuit
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27
Q

Ectopic activity in AF

A

Enhances automaticity

Early or delayed after depolarisations

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28
Q

What tissue properties are required before re-entry can cause AF

A

Shortened & heterogenous ARPs
Areas of slow conduction - fibrosis
Conduction barriers - anatomical vs iatrogenic (scars from catheter ablation/ surgery)

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29
Q

AF induced remodelling

A

Electrical remodelling
Contractile remodelling
Structural remodelling - irreversible

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30
Q

Mx for AF

A
  1. Rhythm control
  2. Rate control
  3. Anti-coag
  4. L atrial ablation and/or ICD placed
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31
Q

Rhythm control for AF

A

Flecanide is 1st line (Class Ic)
Amiodarone (class III) w/ structural heart disease
Ablation (once drugs have failed)

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32
Q

Rate control for AF

A

BB - LVEF <40%
Rate-limiting Ca channel blockers (Class IV) - LVEF > 40%
Digoxin (used in combination w/ another drugs as 3rd line)
Cardioversion

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33
Q

What must be considered before anticoagulating an AF pt

A

CHADVASC (2 for women and 1 for men)

HASBLED/ORBIT

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34
Q

Main anticoagulants given in AF

A

Apixiban

Dabigatran

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35
Q

CHADVASC score

A 
Congestive heart failure 
HTN 
Age >75yrs  - 2 points
DM 
Stroke/ TIA - 2 points 
Vascular disease (MI. PVD, aortic plaque)
Age (65-74 yrs)
Sc - sec category (female)
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36
Q

HASBLED Score

A 
HTN 
Abnormal renal/liver function - 1/2 points 
Stroke 
Bleeding tendency 
Labile INR
Age > 65
Drugs - 1/2 points

High score is 3/3+

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37
Q

Features of L Bundle of His

A

Large, diffuse structure

Rare to be damaged unless underlying heart disease

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38
Q

Features of R Bundle of His

A

Smaller, discrete structure

More commonly damaged without sig underlying heart disease

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39
Q

What part of the cardiac conduction system is supplied by sympathetic nerves

A

All of it - so drugs that stimulate SNS can increase HR even in heart block

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40
Q

What part of the conduction system is supplied by parasympathetic nerves

A

SAN

AVN

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41
Q

Hierarchy of pacemakers

A

Cardiac cells that polarise fastest will drive HR (60 - 100bpm)
SAN is usually fastest then AVN (40-60bpm) then Purkinje network in ventricles (20-40 bpm)

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42
Q

Bradycardia definition

A

HR <60 bpm

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43
Q

Physiological causes of bradycardia

A

High vagal tone (sleep, athletes)

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44
Q

Pathogical causes of bradycardia

A

Fibrosis - occurs in aging
IHD - a/c (MI) and c/c
Drugs - BB, CCB, digoxin, antiarrhytmics
Electrolyte/ metabolic disturbance - esp K
Post cardiac surgery (esp aortic valve surgery)
Infection e.g. IE

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45
Q

What symptoms do pts with bradycardia present with

A 
Dizziness 
Fatigue 
Difficulty concentrating 
Exercise intolerance 
Falls 
Syncope 
Breathlessness
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46
Q

Where is the SAN found

A

Under epicardium at junction of SVC and RA

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47
Q

What are SA nodal cells set in

A

Dense, fibrous tissue

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48
Q

Why is the SAN easily damaged in cardiac surgery

A

Its superficial location

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49
Q

What can go wrong at the sinus node

A

It can fail to generate an impulse or conduct an impulse at the atrium

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50
Q

Sinus bradycardia

A

Fewer impulses generated than usual

Pts are usually asymptomatic

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51
Q

Sinus arrest

A

No impulse is generated at SAN

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52
Q

Sinus arrest on ECG

A

Period with no wave

Escape rhythm from AVN

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53
Q

Types of escape rhythms

A

Junctional - normal QRS
Ventricular - broad QRS

Both have no p waves present

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54
Q

Sinoatrial block

A

Impulse generated but not conducted out of SAN to atrium

Pause is longer than P-P interval

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55
Q

Tachycardia- bradycardia syndrome

A

Sick sinus syndorme
Alternating bradycardia and tachycardia
Usually seen in AF and another bradycardia

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56
Q

How many types of AV block are there

A

3

1st to 3rd degree

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57
Q

1st degree AV block

A

PR interval is prolonged, but all impulses are conducted to the ventricle

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58
Q

2nd degree AV block

A

Some (but not all) impulses are conducted to the ventricles

Two types - Mobitz type I, Mobitz type II

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59
Q

3rd degree AV block

A

No impulses are conducted to ventricles

AV dissociation

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60
Q

1st degree heart block on ECG

A

Prolonged PR interval

Rship between every P wave and QRS complex

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61
Q

3rd degree heart block on ECG

A

Rship between QRS complexes
Rship between P waves
NO rship between p waves and QRS

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62
Q

AV dissociation

A

Any situation in which atria and ventricles beat independently
Can be caused by complete heart block

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63
Q

Mobitz type I heart block on ECG

A

PR interval gets more and more prolonged until one P wave isn’t followed by QRS complex

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64
Q

What is Mobitz type I caused by

A

Block in AVN

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65
Q

Mx for Mobitz type I

A

No mx required

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66
Q

Mobitz Type II heart block on ECG

A

Sudden loss of AV conduction - one P wave isn’t followed by a QRS but PR interval doesn’t get progressively more prolonged

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67
Q

What is Mobitz type II caused by

A

Block in His-Purkinje system

Can lead to complete heart block

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68
Q

Mx of Mobitz Type II heart block

A

Mx with pacemaker required even if asymptomatic

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69
Q

Symptoms of Mobitz Type I

A

Lightheadedness/ dizziness

Syncope

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70
Q

Symptoms of Mobitz Type II

A

Chest pain
SOB
Postural hypotension

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71
Q

Symptoms of 3rd degree heart block

A

Feeling faint
SOB
Extreme tiredness, sometimes w/ confusion
Chest pain

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72
Q

2: 1 AV block

A

Type of 2nd degree AV block

Every other P wave is conducted

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73
Q

Treatment of 2:1 AV block

A

Pacemaker

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74
Q

Advanced AV block

A

AV conduction ratio of 3:1 or higher

Always needs a pacemaker

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75
Q

Emergency treatment of bradycardia

A

ABCDE approach
Atropine 500 mcg IV
If not responding to atropine, give drugs that stimulate SNS
If haemodynamically instable, pace pt

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76
Q

Which bradycardia condns have a risk of asystole

A

Mobitz II AV block

Complete heart block w/ broad QRS

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77
Q

What does atropine do

A

Blocks effect of vagus nerve on heart - increases HR in sinus bradycardia and AVN disease caused by block within AVN

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78
Q

What is atropine not effective for

A

AVN disease caused by block in His-Purkinje

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79
Q

Drugs that stimulate SNS

A

Adrenaline

Isoprenaline

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80
Q

Types of temp pacing

A

Central vein - internal jugular, subclavian, femoral

Transcutaneous

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81
Q

Performing transcutaneous pacing w/ defibrillator

A

Attach pads and connect defibrillator lead
Set defibrillator to pacer
Set pacer rate and output
Conform electrical capture
Confirm mechanical capture - feel femoral (R brachial) pulse

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82
Q

Cardiac devices

A

Devices implanted for dx or treatment of cardiac arrhythmias or unexplained syncope

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83
Q

Example of a diagnostic cardiac device

A

Loop recorder

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84
Q

Cardiac devices that treat and dx

A

Pacemaker (low heart rhythm)
Defib (treat fast and slow heart rhythm)
Cardiac resynchronisation therapy (treat heart failure - either pacemaker or defibrillator)

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85
Q

Pacemaker

A

Electronic device implanted in body that regulates the heartbeat

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86
Q

Roles of pacemaker

A

Detect pts own intrinsic impulses (withhold pacing pulse) - capture
Depolarise the heart if there aren’t any impulses - capture

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87
Q

Limitations of traditional pacemakers

A

Device can become infected

Leads can fail over time

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88
Q

Leadless pacemakers

A

Only pace RV

Indicated mainly in pts with AF and slow HR

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89
Q

ICD

A

Implantable Cardioverter Defib

Specialised pacemaker that treats life threatening ventricular arrhythmias

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90
Q

Who needs an ICD - primary prevention

A

Severe LV impairment

Inherited cardiac condns

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91
Q

Who needs an ICD - secondary prevention

A

Survivors of a VF/VT cardiac arrest
Sustained VT with haemodynamic compromise
Sustained VT and severe LV impairment

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92
Q

ICD vs anti arrhythmic drugs in SCD

A

ICD is superior to drugs in preventing Sudden Cardiac Death

Anti-arrhythmics are still important to reduce need for ICD therapies

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93
Q

How does an ICD recognise arrhythmias

A

ICD looks at HR

If above certain threshold, delivers shock

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94
Q

What do ICDs do in ventricles

A

Anti-tachycardia pacing
Cardioversion
Defib

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95
Q

Limitations of conventional ICDs

A

Leads can become damaged and may not be straightforward to remove

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96
Q

What can ICDs NOT do

A

Treat bradycardia
Provide anti-tachycardia pacing
Prevent death from progressive heart failure

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97
Q

Where are conventional ICDS implanted

A

Venous system

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98
Q

CRT

A

Treatment for pts with severe systolic heart failure and a broad QRS who remain symptomatic despite medical therapy
Also used in CRT
Improves symptoms and survival

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99
Q

Indications for pacemaker

A

Either symptomatic bradycardia or high risk e.g. advanced/ complete heart block (but asymptomatic) bradycardia

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100
Q

Indications for ICD

A

Ventricular arrhythmias e.g. VT/ VF

High risk of ventricular arrhythmias e.g. severe LV impairment

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101
Q

Indication for CRT

A

Severe heart failure w/ broad QRS (>120 ms) continuing symptoms despite meds

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102
Q

Mx of sick sinus syndrome (tachycardia-bradycardia)

A

Treat w/ pacemaker for Brady
Rate lowering drug (BB) for tachycardia
Anticoagulants

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103
Q

Types of cardiac cells

A

Pacemaker cells - conducting cells (SAN)

Non-pacemaker cells - contracting cells

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104
Q

What does the resting membrane potential of cardiac cells depend on

A

K ions as the membrane is semi permeable to K

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105
Q

Atrial vs ventricular action potential

A

Channels in atria are slower and Ca2+ drives depolarisation
Channels in ventricles are faster and Na+ drives depolarisation
Ventricular ap has plateau phase

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106
Q

How many stages does the ventricular ap have

A

5

0 - 4

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107
Q

Starting membrane potential of atria

A

-70 mV

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108
Q

Starting membrane potential of ventricles

A

-85/90 mV

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109
Q

Stage 0 of ventricular ap

A 
K+ outflux (-ve cell) triggers:
Rapid influx Na+
Slow influx of Ca+ 
Via VG ion channels 
Causes depolarisation to +20mV
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110
Q

Stage 1 of ventricular ap

A

VG Na+ channels close quickly
VG K+ channels open for K+ outflux
Causes repolarisation

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111
Q

Stage 2 of ventricular ap

A

Ca+ continues influx
K+ outflux
Membrane potential remains steady = plateau

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112
Q

Stage 3 of ventricular ap

A

VG Ca2+ ion channel closes
K+ outflux continues
Membrane potential repolarises

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113
Q

Stage 4 of ventricular ap

A

VG K+ channel closes however a steady flux of K+ remains

Resting membrane potential is restored

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114
Q

Main methods of pharmacological intervention for arrhythmias

A

Interfere with ap by blocking certain ion channels

Block sympathetic effects of ANS on heart

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115
Q

ERP

A

Effective Refractive Period
Time within which a new ap cannot be released by same cells (stages 0 - 3)
Acts as protective mechanism

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116
Q

ERP as a protective mechanism

A

Keeps HR in check
Prevents arrhythmias
Coordinates muscle contraction

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117
Q

Classification of anti arrhythmic agents

A 
Class Ia/ Ib/ Ic - Na channel blockers 
Class II - BB
Class III - K blockers 
Class IV - Ca blockers 
Class V - misc

Anti-arrhythmic drugs have cross-class activity

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118
Q

What do Class I anti arrhythmic do

A

Bind to and block Na channels responsible for depolarisation

  • Slower depolarisation
  • Increased ERP
  • Reduced AV conduction
  • Reduced automaticity
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119
Q

Example of Class Ia anti-arrhythmic

A

Disopyramide

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120
Q

Effects of Class Ia anti-arrhythmic

A

Prolongs ERP
Reduced cardiac excitability
Increases AP duration

Prolonged repolarisation can increase risk of arrhythmia - torsades de pointes

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121
Q

Indications for Class Ia anti-arrhythmic

A

Maintain sinus rhythm after MI

Prevent and treat ventricular and SV arrhythmias

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122
Q

Example of Class Ib anti-arrhythmic

A

Lidocaine

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123
Q

Indication for Class Ib anti-arrhythmic

A

Cardiopulmonary resuscitation

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124
Q

SE of Class Ib anti-arrhythmic

A

Bradycardia

Convulsion

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125
Q

What are Class Ib anti-arrhythmics contraindicated in

A

AV block

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126
Q

Effects of Class Ib anti-arrhythmic

A

Reduced ERP

Decreases AP duration

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127
Q

Example of Class Ic anti-arrhythmic

A

Flecanide - most potent Na+ channel blocker

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128
Q

Effects of Class Ic anti-arrhythmic

A

Normal ERP
Normal AP duration
Reduced contractibility

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129
Q

Indication of Class Ic anti-arrhythmics

A

Tachycardia
Paroxysmal AF
Ventricular tachycardia resistant to other therapy

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130
Q

Using Flecanide and amiodarone together

A

Flecanide dose needs to be halved

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131
Q

Examples of Class II anti-arrhythmics

A

Sotalol
Propanolol
Atenolol

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132
Q

What do Class II anti-arrhythmics do

A

Block effects of norephedrine and epipharine (SNS) action on SAN

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133
Q

Monitoring required for Class II anti-arrhythmic

134
Q

What can Class II anti-arrhythmics cause

A

Prolonged QT interval

AV blocks

135
Q

Examples of Class III anti-arrhythmics

A

Amiodarone
Dronedarone
Sotalol

136
Q

What do Class III anti-arrhythmics do

A

Block K+ channels

137
Q

Effects of Class III anti-arrhythmics

A

Slow depolarisation
Longer ERP
Longer AP duration
Reduced cardiac excitability

138
Q

Effects of Class II anti-arrhythmics

A

Slowed pacemaker activity
Decrease cardiac conduction and contractibility
Increased ERP
Increased PR interval

139
Q

Why is there a risk of arrhythmias w/ Class III anti-arrhythmics

A

Can increase QT interval

140
Q

What do Class IV anti-arrhythmics do

A

Ca channel blockers

141
Q

Examples of Class IV anti-arrhythmics

A

Verapamil

Diltiazem

142
Q

Effects of Class IV anti-arrhythmics

A

Increased PR interval
Increased ERP
Slow rise of AP and prolonged depolarisation through AVN
Reduce contractility

143
Q

Contraindications of Class IV anti-arrhythmics

A

Pts with heart failure

Pts on BBs

144
Q

Examples of Class V anti-arrhythmics

A

Digoxin

Adenosine

145
Q

Adenosine as an antiarrhythmic

A

K+ channel activator = repolarisation
Slow pacemaker activity
Used in a/c therapy - half life is 10s

146
Q

Digoxin as an anti-arrhythmic

A

Inhibits Na, K & ATP - +ve inotropic effects
Increases myocardial contraction
Slows AV conduction and HR

147
Q

What are the main ion channels in cardiomyocytes

148
Q

What is the funny current in pacemaker activated by

A

Hyperpolarisation instead of depolarisation

Mainly carried by Na+ channels

149
Q

Example of parasympathetic stimulation on pacemaker cells

A

Acetylcholine

150
Q

The effects of parasympathetic stimulation on pacemaker potential

A

Hyperpolarisation

Reduced slope of pacemaker potential

151
Q

The effect of sympathetic stimulation on ventricular action potential and contraction

A

HR approx doubles
Shortening of AP
Contraction is stronger, quicker and relaxation more rapid

152
Q

Basic Q’s for arrhythmias

A

Is it brady or tachycardia
Are the QRS complexes broad or narrow
Is it regular or irregular
P waves?

153
Q

Ddx for narrow complex tachycardia

A

Atrial flutter
Atrial tachycardia
AVNRT
AVRT

154
Q

What does AVNRT stand for

A

Atrioventricular nodal re-entrant tachycardia

155
Q

What does AVRT stand for

A

AV re-entrant tachycardia

156
Q

Appearance of atrial flutter on ECG

A

Saw tooth appearance
Narrow complex
Irregular

157
Q

What is the usual atrial rate

A

300 cycles/ min

158
Q

Atrial rate with 2:1 conduction

A

2 flutter waves: 1 QRS complex

HR is 150 bpm

159
Q

How many bpm with a 4:1 conduction block

160
Q

How many bpm with a 5:1 conduction block

161
Q

Curing atrial flutter

A

Ablation - breaks spp anatomical short circuit

162
Q

Using adenosine for dx

A

Increases degree of AV/ AVN block, unmasking flutter waves

Breaks short circuit in AVNRT/ AVRT and returns pt to sinus rhythm

163
Q

Physiology of inverted P waves

A

Electrical activity starting low in atrium and spreading upwards

164
Q

Retrograde P waves

A

Inverted P wave is superimposed on the end of the QRS complex
Atria and ventricles are depolarising at the same time

165
Q

What do delta waves indicate

A

Pre-excitation

Seen in extra electrical connection or accessory pathway

166
Q

Tachycardias occurring above AVN

A

AF
Atrial flutter
Focal atrial tachycardia

167
Q

Tachycardias occurring below AVN

168
Q

Examples of narrow complex tachycardias

A 
Sinus tachycardia 
AF 
A flutter 
Focal atrial tachycardia 
AVNRT 
AVRT
169
Q

Examples of broad complex tachycardia

A

VT - suspect until proven otherwise
SVT w/ aberration
Pre-excited tachycardia
Pacemaker associated tachycardia

170
Q

General mx of tachycardia

A

Mx of thromboembolic risk in AF and AFl
Rate control - BB, rate slowing CCB, digoxin
Termination of re-entrant arrhythmia
Antiarrythmics - Class I, II, III
Interventional electrophysiological procedures

171
Q

Indications for interventional electrophysiological procedures

A

Ablation - AVRT/ AVNRT, A flutter, fibrillation

172
Q

Magnitude of sudden cardiac arrest in UK

A

~100,000 per yr
1 every 5 mins
20-25% - first px of cardiac disease

173
Q

Possible causes of collapse

A 
Cardiac 
Cardiovascular 
Catastrophic vascular event 
Neurological 
Pyschogenic
174
Q

Potential causes of cardiac arrest

A

Tachycardic

  • VT - most likely
  • VF
  • PMVT/ Torsades

Bradycardic

  • AV block
  • SA block
175
Q

Underlying causes of cardiac arrest

A

IHD
Cardiomyopathy
Structural heart disease
Ion channel abnormalities

176
Q

IHD causing cardiac arrest

A

A/c - ACS/ MI

C/c - ventricular scarring

177
Q

Acquired CM causing cardiac arrest

A 
IHD 
HTN 
Viral 
Alcohol 
Chemo
178
Q

Inherited CM causing cardiac arrets

A

HCM
DCM
ARVC

179
Q

Relevant hx of cardiac arrest

A

Hx of event
PMH
Fhx

180
Q

Relevant tests for cardiac arrest

A

ECG
Echo
Monitoring
Imaging - angio/ CT/ MRI

181
Q

Treatment of cardiac arrest directly attributable to an ACS

A

Treatment is of underlying cause

Usual coronary 2’ preventative measures

182
Q

When is late arrhythmias in ACS more likely to occur

A

In setting of impaired LV function

The longer post MI, the more likely they are to be at risk

183
Q

Types of CM

A

Hypertrophic
Dilated
Arrhythmogenic (Right ventricular)

184
Q

Causes of acquired long QT

A 
Drugs 
Ischaemia 
Hypothyroidism 
Hypothermia 
Bradycardia
185
Q

Triggers of lethal cardiac events in long QT syndrome

A

Exercise
Emotional stress
Sleep

186
Q

Where are the leads in transvenous ICDs

A

Intracardiac

187
Q

Which type of ICD would be used for VT

A

Transvenous (conventional) ICD

188
Q

Which types of ICD would be used for VF

189
Q

Mx of A flutter

A

Ablation

BB

190
Q

Who do SVTs usually present in

A

Younger pts (150-200 bpm)

191
Q

Vasovagal manoeuvres

A

Blowing into syringe
Blowing on thumb
Carotid sinus massage
Valsalva manouvre

192
Q

S/e of digoxin

A

Blurry vison
Insomnia
Dizziness

193
Q

What can amiodarone be used to treat

A 
SVT 
Paroxysmal SVT 
AF 
A flutter 
VT 
VF
194
Q

Amiodarone and preventing AF

A

Use after open heart surgery

195
Q

S/e of amiodarone

A

Thyroid dysfunction
Parasthesia
May also cause pulmonary fibrosis

196
Q

Which antiarrhythmic can also treat cluster headaches

197
Q

Common causes of atrial flutter

A

R atrial dilatation - PE, congestive heart failure
Ischaemic heart disease
Idiopathic

198
Q

For how long should pts not drive after a VT/VF episode

199
Q

Mx of Torsades de Pointes

A

IV Magnesium sulfate (slow infusion)

200
Q

What is VF usually a progression from

201
Q

Shockable rhythms

A

VF

Pulseless VT

202
Q

Px of long QT syndrome

A

Hx of syncope and blackouts
Seizures
Heart palpitations

203
Q

Causes of long QT syndrome

A 
Hypokalemia 
Hypomagnesia 
Hypocalcaemia 
Hypothermia 
Congenital long QT syndrome 
A/c MI 
Subarachnoid haemorrhage 
Drugs
204
Q

Causes of short QT syndrome

A

Hypercalcaemia

Congenital short QT syndrome

205
Q

Drugs causing long QT syndrome

A

AT A CAFE

Antihistamines 
TCAs (tricyclic antidepressants)
Anticholinergics/ Antidepressants 
Chloroquine 
Antiarrhythmics (esp quinidine and sotalol)
Fluoroquinolones
Erythromycin
206
Q

Mx of long QT syndrome

A

BB as rate control
ICD or pacemaker may be implanted
Lifestyle changes - not exercising strenuously, avoiding stressful situations
Foods high in K

207
Q

Presentation of cardiorespiratory arrest

A

Sudden collapse
No pulse
No breathing

208
Q

Initial ix for cardiac arrest

A

ABCDE assessment

209
Q

Mx of cardiac arrest

A 
CPR and give oxygen 
Gain IV access 
Give adrenaline every 3-5 mins 
Give amiodarone after 3 shocks 
Defib if pt is in shockable rhythm 
Treat reversible causes
210
Q

Evaluating palpitations

A 
Continuous or intermittent?
Regular or irregular?
Approx HR
Associated symptoms 
Precipitating factors (exercise or alcohol)
Structural heart disease
211
Q

Discrete attacks of tachycardia

A

Can happen w/ heart palpitations

>120 bpm

212
Q

Examinations for blackouts and faints

A

Pulses = problem with BP
Lying and standing bp = postural hypotension
Murmurs = AS
Carotid sinus massage = carotid sinus syndrome (neurocardiogenic cause)

213
Q

Neurocardiogenic mx of blackouts

A

Reassure
Educate about triggers and warning signs
Lifestyle changes - increase fluid intake to 3L/ day and increase salt intake
Stop BP meds if causing bradycardia

214
Q

Function of cytokines

A

Mediate communication between cells of immune system and direct cell movement

215
Q

Structure of cytokines

A

Small proteins/ glycoproteins (<30 kDa)

Generally soluble

216
Q

Examples of biological effects produced by cytokines

A

Activation
Proliferation
Differentiation
Apoptosis

217
Q

Why is only a low conc of cytokines required

A

Most cytokines act over short distance

218
Q

Why do cytokines have short half-lives

A

Ensures localised effect

219
Q

Autocrine action

A

Cell produces cytokine and receptors

220
Q

Paracrine action

A

Cytokine acts on nearly cells

221
Q

Endocrine action of cytokines

A

Circulates in blood stream to reach distant targets cells

Uncommon

222
Q

Different modes of action of cytokines

A

Pleiotropy
Redundnacy
Synergy
Antagonism

223
Q

Pleiotropy

A

1 cytokine has several functions e.g. IL4

224
Q

Benefit of cytokines having different modes of action

A

Antagonism and synergy allows us to modulate immune response

225
Q

What are the majority of cytokines secreted by

A

Th cells
Dendritic cells
Macrophages

226
Q

What are cytokines mainly involved in

A

Cellular and humoral response
Infl
Haematopoiesis
Wound healing

227
Q

Where do cytokines mature in

228
Q

Where do cytokines migrate to

A

2’ lymphoid tissue

229
Q

Examples of APC

A

Macrophages
Dendritic cells
B cells

230
Q

What do T cells differentiate into

A

CD4 - Th cells (MHC II)

CD8 - cytotoxic T lymphocytes (MHC I)

231
Q

When are Th1 cells created from CD4 cells

A

When IL-12 is secreted by APC

232
Q

When are Th2 cells created from CD4+ cells

A

When IL-4 is secreted by APC

233
Q

What do Th1 cells secrete

234
Q

What are Th1 cells involved in

A

Macrophage activation
Cellular immunity against intracellular pathogens
Autoimmunity
Delayed type hypersensitivity

235
Q

What do Th2 cells secrete

A

IL-4
IL-5
IL-10
IL-13

236
Q

What are Th2 cells involved in

A

Ig class switching
Humoral immunity against extracellular pathogens
Allergy

237
Q

When are Treg cells created from CD4

A

When TGFbeta is secreted by APC

238
Q

What do Treg cells secrete

239
Q

What are Treg cells involved in

A

Inhibition of infl

Immune tolerance

240
Q

Why do cytokines not activate all immune cells

A

Tightly regulated surface expression of cytokine receptors e.g. only cells activated by spp antigen express certain cytokine receptors
Immune synapses

241
Q

Immune synapses

A

Close cell-cell

Directional cytokine secretion so cytokines restricted to one area

242
Q

Types of cytokines

A 
Interleukins (IL)
Tumour Necrosis Factors (TNF)
Interferons (IFN)
Colony Stimulating Factors (CSF)
Chemokines
243
Q

Pro-infl cytokines

A

IL-1alpha
IL-1beta
IL-6
TNF-alpha

244
Q

Anti-infl cytokines

A

IL-10
IL-4
TGFbeta

245
Q

What does IL-2 cause

A

T cell proliferation and differentiation into memory and effectors CD4 or CD8 cells in peripheral tissues

246
Q

What does IL-4 cause

A

B cell activation and differentiation into antibody-secreting plasma cells

247
Q

What does IL-5 activate

A

Eosinophils

248
Q

Most common TNF

249
Q

What do TNFs do

A

Key regulator of infl response produced by activated macrophages

250
Q

Levels of TNF in healthy individuals

A

Undetectable

251
Q

When are TNF serum and tissue levels elevated

A

Infl and infectious condns

252
Q

What are anti-TNFs used for

A

Treatment of infl condns

253
Q

Types of IFN

A

Type 1

Type 2

254
Q

Type 1 IFN

A

1st line defence in viral infections - IFN alpha and beta

255
Q

Mechanisms of Type 1 IFN

A

Destroys viral RNA –> inhibits protein synthesis
Up-regulate MHC Class I presentation
Activation of cytotoxic CD8

256
Q

Most predominant Type 2 IFN

257
Q

What do Type 2 IFN do

A

Upregulate MHC expression –> clearance of intracellular pathogen

258
Q

TNFalpha in macrophages

A

Increased infl through pro-infl cytokine and chemokines

259
Q

TNFalpha in endothelium

A 
Increased cell infiltration 
Increased angiogenesis (VEGF)
260
Q

TNFalpha in hepatocytes

A

Increases CRP in serum

261
Q

TNFalpha in synoviocytes

A

Articular cartilage degradation

262
Q

What do CSFs do

A

Mediate growth and differentiation of immature leukocytes in bone marrow (haematopoiesis)

263
Q

Examples of CSFs

A

M-CSF - macrophage CSF
G-CSF - granulocyte CSF
GM-CSF - macrophage/granulocyte CSF

264
Q

What are chemokines

A

Small cytokines (7.5 - 12.5 kDa)

265
Q

What do chemokines do

A

Induce movement of leukocytes along conc gradient

266
Q

Chemotaxis

A

Cell movement directed by soluble factors

267
Q

Nomenclature of chemokines

A

According to structure

CCL
CXCL
XCL
CX3CL

268
Q

Example of chemokine

A

CXCL8 (IL-8)

Powerful chemo-attractant of neutrophils

269
Q

Cytokine-related diseases

A

Septic shock
Cytokine storm
T2DM
Cancer

270
Q

Septic shock caused by cytokines

A

Release of bacterial products (e.g. lipopolysaccharide) during systemic infections (Staph a, E.coli etc) causes overproduction of pro-infl cytokines

271
Q

Symptoms of cytokine storm

A

Pyrexia
Circulatory collapse
Diffuse intravascular coagulation
Haemorrhagic necrosis

All these lead to multiple organ failure

272
Q

What can cause cytokine storms

A 
Dilation of blood vessels 
Leakage of fluid into body tissues 
Pertubation of blood supply 
Tissue injury 
Widespread blood clotting 
Organ failure
273
Q

Infections inducing cytokine storms

A

Viral e.g Spanish influenza, SARS, bird flu, COVID-19

274
Q

T2DM and cytokines

A

Constitutive expression of TNF-alpha by adipose tissue of obese individuals –> decreased cellular response to insulin and glucose uptake

275
Q

Cancer and cytokines

A

IL-6 overexpression in most types of tumours –> enhanced proliferation, angiogenesis, invasiveness, and metastasis —> increased metabolism –> cachexia

276
Q

Cytokine-based therapies

A

Modulation of immune response by purified cytokines, soluble cytokine receptors and monoclonal antibodies against cytokines

277
Q

Main applications of cytokine-based therapies

A

Blocking of TNF-alpha, IL-1 or IL-2 signalling - dampening of immune response in autoimmune disease (RhA, Crohn’s) or after transplantation
Recombinant interferons - activation of immune reponse against cancers and c/c viral infections (Hep B & C)
Recombinant haemopoietic cytokines (CSFs, IL-11) – stimulate haematopoiesis during immunodeficiency, chemotherapy or certain types of anaemia

278
Q

Risks of cytokine-based therapies

A

Reduces cytokine activity —> increased risk of infection and malignancy
Targeted delivery (paracrine actions) vs systemic admin
V short t1/2 (mins) –> freq admin
Pleiotropic action of cytokines –> unpredictable and severe s/e

279
Q

How are AV valves reinforced

A

Chordae tendinae attached to papillary muscles

They contract & ‘brace’ during ventricular systole

280
Q

Why do SL valves not need to be reinforced

A

Blood they’re stopping is at a much lower pressure - passive back flow from arteries rather than high pressure being pushed out by ventricles

281
Q

Function of aortic sinus

A

Allows blood to pool after ventricular systole and from there flow into coronary sinus
Stops cusps from sticking to aortic walls when fully opens

282
Q

Why is the LV wall thicker than the RV wall

A

LV has to pump blood further so generates greater force in systole

283
Q

Blood flow over cusps in bicuspid valve

A

Blood flows over both in atrial and ventricular systole

Clinical relevance - more likely to wear down than other valves

284
Q

Cusps of pulmonary valve

A

Anterior
Left
Right

285
Q

Cusps of aortic valve

A

Left (coronary)
Right (coronary)
Posterior (non-coronary)

286
Q

Cusps of mitral valve

A

Anterior

Posterior

287
Q

Cusps of tricuspid valve

A

Anterior
Posterior
Septal

288
Q

Function of moderator bands

A

Conduct impulse from Bundle of His to base of anterior papillary muscle
Ensures impulse reaches papillary muscle at same time as apex of heart
Allows papillary muscle to contract, ‘bracing’ AV valves in advance of ventricular systole

289
Q

Starting point of ventricular contraction

A

Apex of heart

290
Q

Clinical significance of moderator bands

A

Assist in stopping the valves everting, preventing back flow of blood into atrium during systole

291
Q

Why is jugular distension and RV heave seen in MS

A

MS decreases blood flow into LV

As LA pressure increases, flow is decreased in pulmonary vessels so RV distends and JVP rises

292
Q

Why is cardiomegaly a complication of MS

A

Heart attempting to decrease pressure

293
Q

Why is blood clot formation a complication of MS

A

Blood stuck behind stenotic cusp can clot

294
Q

What is fossa ovale an embryological remnant of

A

Foramen ovale

295
Q

What is the right auricle an embryological remnant of

A

Primitive atrium

296
Q

What is crista terminalis an embryological remnant of

A

Junction between sinus venosus and auricle

297
Q

What is Ligamentum venosum an embryological remnant of

A

Ductus venosum

298
Q

What is the smooth wall of atria an embryological remnant of

A

Sinus venosus

299
Q

What is Ligamentum arteriosum an embryological remnant of

A

Ductus arteriosum

300
Q

Which foetal structure acts as a shunt between pulmonary artery and aorta

A

Ductus arteriousm

301
Q

Which foetal structure acts as a shunt allowing blood to bypass liver

A

Ductus venosum

302
Q

Which foetal structures act as precursor of atrium

A

Junction between sinus venous and auricle
Sinus venosus
Primitive atrium

303
Q

Which foetal structure acts as a shunt between L and R atria

A

Foramen ovale

304
Q

How do oxygenated blood bypass the foetal lungs

A

Foramen ovale acts as shunt, thereby bypassing pulmonary circulation
Ductus arteriosus diverts blood from pulmonary trunk to arch of aorta, thus bypassing lungs

305
Q

Main processes occurring to facilitate change from foetal to postnatal circulation

A

Closure of umbilical arteries
Closure of umbilical veins & ductus venous - blood is now passing through liver
Closure of ductus arteriosus
Closure of foramen ovale

306
Q

Key factor in closure and fusion of septum premium and septum secundum

A

A relative increase within LA forces septum primum against the septum secundum associated with the first breath

307
Q

Cardioversion vs defibrillation

A

Cardioversion - one or more SMALL electrical shocks to restore rhythm
Defibrillation - one or more LARGE electrical shocks to restore rhythm

308
Q

Treatment of fast AF - acute px

A

Go trough ABCDE

Cardiovert electrically

309
Q

What can cause sinus bradycardia

A 
Hypothermia 
Hypothyroidism 
Vagal stimulation 
Drugs (e.g BB)
Raised ICP 
MI
310
Q

Infections causing sinus bradycardia

A

Legionnaires disease
Typhoid fever
Lyme disease

311
Q

Rhythm abnormalities seen in cardiac arrest

A

Pulseless VT
VF
PEA
Asystole

312
Q

PEA

A

Pulseless electrical activity

Organised electrical activity on ECG w/ no pulse or demonstrable BP

313
Q

Reversible causes of cardiac arrest

A

4 H’S & 4 T’s

Hypokalaemia
Hypothermia
Hypovolaemia
Hypoxia

Tamponade
Tension pneumothorax
Toxins
Thromboembolism

314
Q

What risk increases when the QT interval > 500ms

A

Ventricular arrythmias

315
Q

When do we see absent A wave in JVP

316
Q

When do we see a canon wave in JVP

A

Heart block

317
Q

Xanthopsia

A

Yellow vision

Can be caused by digoxin poisoning

318
Q

Which drugs reduce clearance of digoxin

A

CCBs and NSAIDs

319
Q

Inotropy

A

Looks at drug effect on cardiac contractility

320
Q

Chronotropy

A

Looks at drugs effect on HR

321
Q

What metabolic disturbance can hypothyroidism cause

A

Hyperkalaemia

322
Q

What type of heart block can an inferior MI cause

A

3rd degree

Can also be caused by combo of rate-limiting CCBs and BBs

323
Q

What can sudden cardiac death in the young be caused by

324
Q

Why can you not take verapamil or diltiazem with BB

A

Rate-limiting CCBs and BBs both reduce contractility and are -vely inotropic
Will cause slow conduction at AVN too much

325
Q

Inotropic vs chronotropic

A

+vely inotropic - increases contractility

+ve chronotropic - increases HR

326
Q

MOA of atropine

A

Vagus nerve inhibitor so increases HR

327
Q

Mx of sick sinus syndrome

A

BB
DOACs
Pacemaker

328
Q

Features of haemodynamic instability

A

HF
IHD
Shock
Syncope

Abnormal BP, HR etc

329
Q

How can an overdose of BB or CCBs be reversed

A

IV glucagon

330
Q

Synchronised vs unsynchronised shocks

A

Synchronised happens at certain point in cardiac cycle for haemodynamically compromised pts
Unsynchronised is used when contraction is random - defibrillator

331
Q

Digoxin effects on ECG

A

Widespread down sloping ST segment
T wave inversion
Flattened and shortened QT interval
Prominent U waves

MBBS - Year 2 (20 decks)

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