cardiac arrhythmia

Question 1

what are the two different types of cardiac myocytes

Answer 1

non-specialised and specialised conducting myocytes

Question 2

what is the difference between non-specialised and specialised myocytes

Answer 2

the difference is electrophysiological ie the difference in the character of the action potentials (which are distinct bc of different types and populations of cardiac ion channels)

Question 3

QRS

Answer 3

the summation of all action potentials in the ventricles

Question 4

P wave duration (atrial conduction), PR interval (ANV conduction) and the QRS (ventricular depolarisation)

Answer 4

reflects the speed and sequence of depolarisation and cardiac conduction

Question 5

describe the anatomy of cardiac conduction

Answer 5

the SA node is located near the RA next to the atrial appendage, and this is where the rhythm of the heart originates, the SA node conducts through intranodal tracks to the atrioventricular node, this passes through ht fibrous layer dividing the atria from the ventricles and it connects to the ventricles through the Bundle of His, the Bundle of His then progresses into the ventricles and the conducting fibres divide into two main sections - the left and R bundle - the left bundle consists of two fascicles (the left posterior fascicle and the left anterior fascicle) and these primarily supply the left ventricle
the fascicles then further divide into the purkinje fibres that supply the rest of the myocardium

Question 6

ectopy

Answer 6

when arrhythmia occurs as single beats

Question 7

arrhythmia can occur continuously

Answer 7

as persistent/sustained or paroxysmal/non-sustained

Question 8

SVT

Answer 8

supraventricular arrhythmias
ie happens anywhere above the AV node
> the ECG shows a narrow QRS
» include SVT tachycardia ie AF, atrial flutter, ectopic atrial tachycardia
»bradycardia ie sinus bradycardia and sinus pauses

Question 9

ventricular arrhythmias

Answer 9

include ventricular ectopics or premature ventricular completes (PVC)
>ventricular tachycardia VT
>ventricular fibrillation VT
>asystole (ie no contraction at all)

Question 10

AV node arrhythmias

Answer 10

> AVn re-entry tachycardia (AVNRT)
AV reciprocating or AV re-entrant tachycardia (AVRT)
AV block (from 1-3 degrees)

Question 11

clinical causes of arrhythmias (6)

Answer 11

> abnormal anatomy that allows re-entrant circuits
-accessory pathways
-congenital HD
autonomic nervous system (ANS)
-sympathetic stimulation ie stress, exercise, hyperthyroidism, increased vagal tone causing bradycardia
metabolic
-hypoxia ie PE or chronic pulmonary disease
-ischaemic myocardium ie acute MI / angina
-electrolyte imbalance
inflammation : viral myocarditis - causing scarring on tissue
drugs
genetics
-mutations of genes encoding cardiac ion channels ie the congenital long QT syndrome

Question 12

electrophysiological mechanisms of arrhythmia (1)

Answer 12

ectopic beats (focal activity)

• beats or rhythm that originate in places other than the SA node
• altered automaticity ie ischaemia /catecholamines (adrenaline)
• triggered activity ie digoxin / long QT syndrome

Question 13

electrophysiological mechanisms of arrhythmia (2)

Answer 13

re entry : require more than one conduction pathway with different speed of conduction (depolarisation) and recovery of excitability (refractoriness)
-accessory pathway tachycardia, previous MI, congenital heart disease

Question 14

how abnormal physiology and pathology causes arrhythmia - ones that increase phase 4

Answer 14

the following are ectopics .. hyperthermia, hypoxia, hypercapnia, myocardial stretch, SNS all increase the phase 4 slope causing an increase in HR

Question 15

how abnormal physiology and pathology causes arrhythmia - ones that decrease phase 4 slope

Answer 15

hypothermia, hyperkalaemia, RNS

these decrease the phase 4 slope causing slowed conduction ie bradycardia and heart block

Question 16

triggered activity

Answer 16

they are caused when there are premature depolarisations, that occur in the terminal phases of the AP during phase 2/3 (early after depolarisation EAD) or after the AP in phase 4 (delayed after depolarisation DAD)
> if there is sufficient magnitude and reach the depolarisation threshold there is a sustained train of depolarisations and this is termed triggered activity
» this is what underpins the ventricular arrhythmia in digoxin toxicity, long QT syndrome etc

Question 17

re - entry

Answer 17

occurs when an action potential fails to extinguish itself and reactivates a region that has recovered from refractoriness
- can occur in the presence of an obstacle around which an action potential can travel and result in a self-perpetuating circuit
but !! need more than one conducting pathway and the pathways mist have different speeds of conduction, central blocking by a core of tissue that is completely blocked allows re circulation of the excitation

Question 18

2 types of re-entry

Answer 18

> bidirectional conduction = conduction is the same so the wavelets confront each other and cancel each other out essentially
unidirectional block = one pathway is slower and so allows the other pathway to recover from refractoriness which can therefore be re-excited and create a circuit

Question 19

presentation of arrhythmia

Answer 19

palpitations 'pounding heart' 'skipped beat"
dysopnea
faintness 'presyncope'
syncope 
shock
sudden cardiac death
angina
HF
anxiety

Question 20

investigation for arrhythmia

Answer 20

> 12 lead ECG - important to do in sinus rhythm
bloods (fbc, biochemical, thyroid function)
CXR
echocardiogram
stress ECG
24 hour ECG
event recorder
electrophysiological study (deliberate onset of arrhythmia)

Question 21

function of the ECG

Answer 21

assesses heart rhythm

but can also reveal if there has been a previous MI and if there has been pre-excitation

Question 22

function of exercise ECG

Answer 22

reveals if there is ischaemia / exercise induced arrhythmia

*exercise release the catecholamines and some arrhythmias are triggered by the releases of these

Question 23

function of the echocardiogram

Answer 23

assesses for structural heart disease ie enlarged atria in AF

Question 24

sinus bradycardia

Answer 24

<60 beats per min

• commonly seen in athletes, if on beta blockers, or if there is ischaemia
• the treatment = atropine (acute) , or pacing (chronic) if haemodynamic compromise ie hypotension

Question 25

sinus tachycardia

Answer 25

>100 bpm can be physiological ie anxiety/fever or drugs - the treatment is to treat the underlying cause and also Bblockers can be prescribed as well

Question 26

atrial ectopic beats

Answer 26

present with palpitations or nothing at all !! there is not really any treatment B-adrenergic blockers may help and also avoiding stimulants such as caffeine

Question 27

AVNRT vs AVRT // micro circuit vs macro circuit

Answer 27

they are both re-entry tachycardia using the AV node but in the AV node re-entrant tachycardia - the circuit is within the AVn itself whereas AVRT circuit uses AVn and another pathway

Question 28

SVT arrhythmia management

Answer 28

acute: increase vagal tone - valsalva, carotid massage slow conduction in the AVN - IV adenosine, IV verapamil chronic: avoid stimulants, electrophysiologic study and radiofrequency ablation, antiarrythmic drugs, beta blockers

Question 29

RFCA

Answer 29

radio frequency catheter ablation it is the selective cautery of cardiac tissue to prevent tachycardia, targeting either an automatic focus or part of a re-entry circuit

Question 30

causes of AVn conduction disease (heart block)

Answer 30

``` ageing acute MI myocarditis infiltrative disease ie amyloid/sarcoidosis drugs calcific aortic valve disease post-aortic surgery genetics ```

Question 31

1st degree av block

Answer 31

conduction following P wave takes longer

Question 32

2nd degree av block

Answer 32

intermittent block at the av node (dropped beats) - mobitz 1 = progressive lengthening of the PR interval eventually resulting in mobitz 1 - mobitz 2 = pathological (ie caused by scarring of the av node) and need a pacemaker

Question 33

3rd degree av block

Answer 33

= complete heart block ie your life is on the line | no action potentials from the SA node/atria can get though to the AV node >> ASYSTOLE AND THEN DEATH

Question 34

function of the pacemaker

Answer 34

can get single chamber pacemakers ie pacing the RA or RV only can get dual chamber (paces both) >maintains AV synchrony >used for AVN disease

Question 35

causes of ventricular ectopics - VEs

Answer 35

structural causes include LVH, HF, myocarditis metabolic causes include ischaemic heart disease, electrolytes ... may be a marker for in hearted cardia conditions if worse on exercise, need to investigate further beta blockers, ablation of focus

Question 36

causes of ventricular ectopics - VEs

Answer 36

structural causes include LVH, HF, myocarditis metabolic causes include ischaemic heart disease, electrolytes ... may be a marker for in hearted cardia conditions if worse on exercise, need to investigate further treatment = beta blockers, ablation of focus

Question 37

causes of VT

Answer 37

usually have significant heart disease ie coronary artery disease a previous MI HF .. less frequent causes include inherited cardiomyopathy inherited channelopathy

Question 38

treatment of VF

Answer 38

defibrillation, cardiopulmonary resuscitation

Question 39

treatment of VT

Answer 39

acute : direct current cardio version (DCCV) if stable, consider pharmacological cardio version with AAD >if unsure of VT administer adenosine to make a diagnosis

Question 40

treatment of VT

Answer 40

acute : direct current cardio version (DCCV) if stable, consider pharmacological cardio version with AAD >if unsure of VT administer adenosine to make a diagnosis correct triggers - look for the causes ie electrolytes, ischaemia, hypoxia, pro-arrhythmic medications chronic : revascularisation if possible optimise CHF therapies implantable cardioventor defibrillators if life threatening VT catheter ablation

Question 41

CIEDs

Answer 41

cardiac implantable electronic devices ie pacemakers and ICDs

Question 42

VT/VF s need to know !!

Answer 42

> A WIDE QRS TACHYCARDIA WITH HISTORY OF CAD/HF = VT UNTIL PROVEN OTHERWISE >>MOST VENTRICULAR ARRHYTHMIAS OCCUR IN THE SETTING OF STRUCTURAL HEART DISEASE IE CHF,CAD >>>ANTIARRHYTHMIC DRUGS ARE INEFFECTIVE ON SURVIVAL, BUT ARE OFTEN USED TOGETHER WITH ICDs TO REDUCE SYMPTOMs >>>>OPTIMAL MANAGEMENT OF THE UNDERLYING CONDITION REDUCES RISK OF PATIENT DEVELOPING ARRHYTHMIA >>>>>PRIMARY ARRHYTHMIC CONDITIONS ie when vt/vf is in a structurally normal heart and so could be genetic and their could be a risk for their relatives and also lots of arrhythmias are drug induced

Question 43

patterns of AF

Answer 43

>paroxysmal - is paroxysmal and lasts less than 48 hours, is often recurrent >persistent - an episode of AF lasting greater than 48 hours, which can still be cardioverted to NSR, unlikely to spontaneously revert to NSR >permanent - inability of pharmacological or non-pharmacological methods to restore NSR

Question 44

causes of AF

Answer 44

``` can be structural, metabolic ... hypertension congestive HF sick sinus syndrome CHD obesity thyroid disease familia cardiac valve disease alcohol abuse congenital heart disease cardiac surgery COPD/pneumonia septicaemia pericarditis / tumours vagal cause ie high endurance athletes ```

Question 45

complications of AF

Answer 45

tarsi are no longer meaningfully contracting and contributing to CO, this lost 'atrial kick' and decreased filling time from shortened period in cardiac diastole results in reduced CO >>this can result in congestive HF .. reduces pressure in the capillaries in pulmonary vasculature leading to pulmonary oedema >> ventricular rates <60 mom suggest AV conduction disease and so caution with drugs and rate controlling drugs as could lead to complete heart block and ... may require permanent pacing

Question 46

management strategies - rate control

Answer 46

>goal is to maintain SR -drugs to slow down AVn conduction ie digoxin, betablockers, verapamil, diltiazem (can use these alone or in combination)

Question 47

management strategies - rhythm control

Answer 47

>goal is to accept AF and control ventricular rates -restoration of NSR = cardio version ie antiarrhythmic drugs - amiodarone / DCCV -maintenance of NSR = anti arrhythmic drugs, catheter ablation of atrial focus/pulmonary veins, surgery (maze procedure)

Question 48

management strategies - prevention of thromboembolism

Answer 48

oral and long term anti coagulation / antiplatelets | warfarin for mitral valve disease

Question 49

anti arrhythmic drugs (AADs) - mode of action

Answer 49

are classified according to the ion channels that they block and they work through electrophysiological mechanisms where they block these currents - Vaughan william classifications

Question 50

AAD - class 1

Answer 50

reducing sodium channel current | >lignocaine quinidine flecainide propafenone

Question 51

AAD - class 2

Answer 51

b adrenergic antagonists | >propranalol

Question 52

AAD - class 3

Answer 52

action potential prolongation >amiodarone, sotalol >dronedarone !!

Question 53

AAD class 4

Answer 53

calcium channel antagonists | >verapamil

Question 54

AAD - class 1

Answer 54

``` reducing sodium channel current >lignocaine, only IV quinidine flecainide, effective for treating AF but contraindicated with CAD propafenone " ```

Question 55

AAD - class 2

Answer 55

b adrenergic antagonists | >propranalol,

Question 56

AAD - class 3

Answer 56

action potential prolongation >amiodarone, sotalol >dronedarone !! ability to prolong the QT and if it does this excessively its really bad

Question 57

AAD class 4

Answer 57

calcium channel antagonists >verapamil slow HR

Question 58

AF can cause thrombosis-embolic stroke

Answer 58

``` more likely to happen if patient has .. thyrotoxicosis hypertrophic cardiomyopathy mitral valve disease non-valvular AF with 2 or more risk factors ```

Question 59

risk factors for AF

Answer 59

``` 75years+ hypertension HF precios MI / ischaemia CAD/ DM diabetes ```

Question 60

AF can cause thrombosis-embolic stroke

Answer 60

blood clot likely to form in the left atrial appendage due to stasis of blood flow associated with AF >more likely to happen if patient has .. thyrotoxicosis hypertrophic cardiomyopathy mitral valve disease non-valvular AF with 2 or more risk factors

Question 61

risk factors for AF

Answer 61

``` 75years+ hypertension HF precios stroke CAD/ DM diabetes being a woman ```

Question 62

atrial flutter

Answer 62

``` more organised AF >rapid and regular form of AF >paroxysmal or persistent pattern >sustained by a macro-reentrant circuit >confined to RA but can spread to LA >risk of stroke ```

Question 63

atrial flutter treatment

Answer 63

``` >RF ablation >slow the ventricular rate >restore sinus rhythm >maintain sinus rhythm >cardioversion >OACs ```