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Unit 12 > Physiological Mechanisms of Arrhythmia > Flashcards

Physiological Mechanisms of Arrhythmia Flashcards

1
Q

What is the action potential pattern of the sinus nodal cell?

A

Regulated by autonomic tone, is automatic (self generating pace maker)
Phase 4:
Background currents - Na+ influx
Funny currents activated in hyperpolarised cells - HCN - Na+ influx
Ca2+ channel recover, the rate of this step determines the heart rate.
Phase 0: depolarisation
T type calcium ion channels - bring to threshold
L type Ca2+ channels are activated bring to action potential
Phase 3: repolarisation
Ca2+ influx stops and K+ efflux starts.

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2
Q

What are the phases of action potential in a contractile cell?

A

Phase 0 - Na+ passes through gap junctions into contractile cell from neighbouring cells from SA node, VGNa+C open Na+ ion influx causes depolarisation,
Phase 1 - K+ efflux
Phase 2 - L type channel Ca2+ influx and K+ efflux are equal - this causes a plateau phase - this is when the cells contract
Depolarisation passes down T tubeles through conformational change in dihydropyridine and ryanodine channels causes Ca2+ efflux from SR into cytoplasm.
phase 3 - K+ efflux is greater than Ca2+ influx - causes repolarisation, may become hyperpolarised
Phase 4: resting membrane potential action of Na+K+ pump.

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3
Q

What is a cardiac arrhythmias?
What are the two main types?

A

An abnormality of cardiac rhythm, can originate in patients with apparently normal hearts, diseased tissue or underlying structural heart disease
Two main types are bradycardia (below 60bpm at day and 50bpm at night) and tachycardia (above 100bpm)

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4
Q

What are the potential symptoms of cardiac arrhythmias?

A

Sudden death
Syncope
Heart failure
Chest pain
Dizziness
Palpitations
No symptoms at all.

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5
Q

What are the different types of tachycardias?

A

Supraventricular trachycardias - arise from atrium or AV junction
Ventricular tachycardia - originate from ventricles

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6
Q

What can cause an arrhythmia to be more symptomatic than normal?

A

Tachy -when sustained and fast
When mycoardial function is poor - can be potentially life threatening.

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7
Q

What is meant by a sinus arrhythmia?

A

Fluctuations in autonomic tone result in phasic changes in sinus discharge rate
Causes irregularities of pulse
For example during inspiration PANS tone decreases and heart rate increases then decreases during expiration
This variation is normal and tends to have predictable causes
Typically occurs in children and young adults.
Have a normal P wave and PR interval.

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8
Q

What is sinus bradycardia?

A

A sinus rate of less than 60bpm during day or 50bpm at night
Usually asymptomatic unless very slow
Is normal in athletes due to increased vagal tone.

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9
Q

What are the main mechanism of arrhythmogenesis?

A

Disordered impulse generation:
1) Increased automaticity - reduced threshold potentaion or increased phase 4 depolarisation
2) triggered activity due to early or deleted after depolarisation reaching threshold potential
Disturbances in impulse propagation:
3) Re-entry pathway
4) conduction block
5) both - atrial flutter

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10
Q

What are different potential causes of sinus bradycardia and bradycardia?

A

Sinus - Abnormally slow automaticity (still generated by SAN so normal PR and P)
Bradycardia - AV block or abnormal AV conduction or intraventricular conduction

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11
Q

What is accelerated automaticity as a mechanism of arrhythmia?

A

Accelerate heart rate by - decreasing threshold or increasing diastole depolarisation (funny current influx)
This will trigger an action potential in the pacemaker faster
For example - SANS stimulate noradrenaline inc automaticity

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12
Q

What types of arrhythmia is accelerated automaticity associated with?

A

Sinus tachycardia
Escape rhythms
Accelerated AV nodal (junctional) rhythms.

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13
Q

What is triggered activity as a cause of arrhythmia?

A

Myocardial damage results in oscillation of the transmembrane potential at the end of an action potential
(hence are always preceded by an AP)
These oscillations are called as after-depolarisation
If these reach action potential they can cause an arrhythmia

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14
Q

What are the two different types of after-depolarisations?

A

Early after depolarisations EADs - occur before the end of phase 3 (before threshold reached in repolarisation)
Delayed after-depolarisations - occurs after threshold has been passed in repolarisation

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15
Q

**What can exaggerate the effects of a after depolarisation arrhythmia?

A

Pacing
Catecholamines
Electrolyte disturbances
Hypoxia
Acidosis
Digoxin - medication

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16
Q

What pathology is after depolarisations thought to underpin?

A

Long QT syndrome

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17
Q

What factors increase the risk of an early after depolarisation?**

A

Slow HR
Prolonged action potentials
Cartain antiarrhythmic drugs like quinideine

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18
Q

What factors increase the risk of a delayed after depolarisation?**

A

Increased serum calcium - activate Na+/Ca2+ exchanger
Increased adrenaline
Drug toxicity like digoxin
Myocardial infarction

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19
Q

What are sone consequences of a Early after depolarisation on heart function?

A

Nothing
Prolong QT
Sustained arrhythmia (torsades de pointes)

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20
Q

What are the consequences of a delayed after depolarisation?

A

Nothing
Ectopic beat
Sustained arrhythmia (ventricular tachycardia)

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21
Q

What is the re-entry or circus movement as a mechanism of arrhythmia?

A

Requires a ring of cardiac tissue around an inexcitable core (scarred myocardium)
Has two pathways around it - one fast with a longer recovery period (refractory limb)and one slower with a faster recovery period (excitable limb)
Ectopic beats is required
Conduction through the excitable limb is slow enough that the other limb will have recovered allowing retrograde activation to complete the re-entry loop.
If movement around the ring is slower than recovery period, will continue to reach excitable tissue causing a continuous circus movement producing a tachycardia.

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22
Q

What are the causes of the slower pathway in re-entry tachycardia?

A

Central area of block - e.g scar tissue, refractory cells
Area/path of variable blocking e.g dead mycoyte, myocytes with different refractory periods/conduction speeds.

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23
Q

What are the different categories of narrow complex tachycardia?

A

Sinus tachycardia
Paroxysmal supraventricular tachycardia including Atrial tachycardia (automatic cause), AVNRT and AVRT.
Atrial Flutter
Atrial Fibrillation

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24
Q

What is the cause of atrial tachycardia and how does this present on an ECG?

A

Is unifocal
A focus point outside the SAN fires off automatically at a rapid rate.
This normally occurs in patients with structural heart disease or following extensive ablation within atria.
Shows on an ECG with organised atrial activity with P wave morphology different from sinus rhythm (but same in all complexes) and PR is an isoelectrical line preceding QRS.

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25
Q

What is the cause of an AVNRT (atrioventricular Nodal re-entrant tachycardia)?

A

Cardiac stimulus originates as a wave of excitation that spins around the AV nodal area.
Ectopic beat occurs whilst the fast pathway in the AVN in refractory resulting in impulse travelling down the slow conduction pathway, this takes longer than the fast refractory period allowing to travel back up the fast pathway and enter a circus like rhythm.
Results in retrograde P waves that be by hidden within, just after or rarely just before the QRS complex.
This is due to near-simultaneous contraction of the atria and the ventricles.

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26
Q

What AVNRT look like on an ECG?

A

Narrow but normal QRS complexes
Absent P wave
Tachycardia

Im my mind appears as more depressed segment at S.

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27
Q

What is AVRT (atrioventricular re-enterant tachycardia)?

A

A re-enterant movement occurs by a concealed bypass tract due to abnormal separation of the atria and the ventricles during embryology.
Large circuit made from the AVN, His Bundle, ventricles and an abnormal bypass tract.
Is a macro-renetry - each part of the circuit is activated sequentially.
Atria activation tends to occur after ventricular depolarisation, resulting in an inverted P wave before the T wave.

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28
Q

What does AVRT look like on an ECG?

A

Narrow QRS complex
Tachycardia
Inverted P wave between QRS and T wave.

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29
Q

What is an example of an AVRT?

A

Wolff-Parkinson-White Syndrome

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30
Q

What does Wolff-Parkinson-White Syndrome?
What does it look like on an ECG?

A

Accessory pathway can conduct from atria to ventricles during sinus rhythm
The electrical impulse conducts quicker over the accessory pathway
Results in pre-excitation of the ventricles as begin to depolarise early
This presents as a slurred beginning to the QRS complex known as a delta wave.
Also a shortened PR interval

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31
Q

What are the potential causes of a sinus bradycardia?

A

Extrinsic factors that influence a relatively normal sinus node
Intrinsic sinus node disease

32
Q

What are some of the external factors that can cause a sinus bradycardia?

A

Hypothermia
Hypothyroidism
Cholestatic jaundice
Raised intracranial pressure
Drugs - beta blockers, digitalis and other anti-arrhythmic drugs.
Neurally mediated syndromes - carotid sinus syndrome, vasovagal attacks.

33
Q

What are some on the intrinsic causes of sinus bradycardia?

A

Acute Ischemia and infarction of the sinus node (complication of MI)
Chronic degeneration changes such as fibrosis of the atrium and sinus node - results in sick sinus syndrome.

34
Q

What is sick sinus syndrome?

A

Idiopathic fibrosis of the sinus node
Fibrosis may also be caused by ischaemic heart disease, cardiomyopathy or myocarditis.
Patients develop episodes of sinus bradycardia or sinus arrest
Commonly experience paroxysmal atrial tachyarrhythmias (tachy-brady syndrome) due to diffuse atrial disease.

35
Q

What are the features of sick sinus syndrome on an ECG?

A

Sinus arrest - only occasional P waves
Bradycardia (may show tachy-brady)
Junctional escape beats (no p wave as originate from elsewhere (norm AVN) not the SAN)

36
Q

What are the different types of heart blocks?

A

AV block - block in conduction in AV node of His bundle
Bundle branch block - block is lower in the conduction system
Blocks can be classified as:
1. First degree
2. Second degree
3. Third degree.

37
Q

What is a first degree AV block?

A

Regular but prolonged PR intervals
More than 0.2 seconds (more than 5 mini squares)
All atrial depolarisations are conducted to the ventricles but with delay.

38
Q

What is a second degree heart block?

A

When some P waves are conducted and others are not
Have many different presentations:
Mobitz-1 block
Mobitx 2 block
2:1 or 3:1 (advanced) block

39
Q

What is a mobitz 1 block?

A

Also known as Wenckebach block phenomenon
Sinus rhythmy is present
PR interval lengthens progressively with each successive beat
Eventully one P wave is not conducted through (QRS dropped)
Process repeated with PR interval after drop returning to normal.
Normaly due to block in the AV node.

40
Q

What is a mobitz 2 block?

A

Sinus rhythm is present
The PR interval is consistent
One P wave in not conducted (dropped QRS)
Usually QRS complex is wide (>0.12 seconds)
Is normally due to a block at the infranodal level such as His bundle.

41
Q

What is a 2:1 or 3:1 heart block?

A

The ratio of P waves to QRS complexes
The PR interval is always the same
Is different to mobitz 1 and morbitz 2.

42
Q

What is third degree heart block?

A

When there is no communication between the atria and the ventricles.
Atrial rate (appearance of P waves) tends to be faster than the appearance of QRS complexes
P wave rate and QRS rate is independent of each other.
Some P waves fall on the T wave distorting it other may be in the QRS complex and be lost
QRS complex may be normal, wide or narrow depending on origin

43
Q

What are some potential causes a a third degree/complete heart block?

A

Congenital - transposition of great vessels
Idiopathic fibrosis: Levs (older) disease, Lenegres disease (younger)
IHD - acute MI, ischaemia cardiomyopathy
Non-IHD - calcific aortic stenosis, idiopathic dilated cardiomyopathy, infiltrations (neoplasia)
Cardiac surgery - aortic valve replacement
Iatrogenic - pacemaker implantation, radiofrequency AV node ablation
Drug induced - digoxin, beta blockers, amiodarone, non-dihydropyridine Ca2+CB
Infections - endocarditis, lymes disease, chagas disease
Autoimmune - SLE and RA
Neuromuscular disease - Ducheenes muscular dystophy.

44
Q

How might ischemic heart disease cause AV block?

A

Right coronary artery most commonly supplies the SAN and the AVN
This is an inferior myocardial infarction (most cases)
Occlusion of this artery =
1) Damaged SAN - sinus bradycardia
2) Damaged AVN - AV block.

45
Q

What causes the ventricular contractions in a third degree heart block?
How can we differentiate between these?

A

Escape rhythm
His Bundle - narrow QRS complex, rate 50-60bpm, often from transient ischaemia or IV atropine only requires pacing if chronic not acute,
His-Purkinje system - Broad QRS complex, slowest rate less than 40bpm, associated with dizziness and blackouts (Stokes-Adam attacks), Levs and Lenegres disease, requires a permanent pacemaker to be put in place.

46
Q

What is an escape rhythm?

A

When the SA node fails to generate an impulse
Rhythm is generated from an alternative site, atrial, AV node or ventricular.

47
Q

What are the ECG features of a generic bundle branch block?

A

Complete block often results in a wide QRS complex and an abnormal pattern to the QRS
Is normally asymptomatic
The specific shape of the QRS depends on if the right or left bundle branch block.

48
Q

What are the features of a right bundle branch block on an ECG?

A

Secondary R wave R’ in V1 gives a M like appearance
Slurred S wave in V5 and V6 due to replayed depolarisation of the right bundle block. Gives a W like appearance

49
Q

Who tends to be affected by right bundle branch block?

A

Normal healthy individuals
During PE
Right ventricular hypertrophy
Ischemic heart disease
Fallots tetralogy
ASD - atrial septal defect
VSD - ventricular septal defect

50
Q

What are the features of the left bundle branch block on an ECG?

A

RSR’ pattern giving an M shape in Leads 1 (AVL, V4-VR) - lateral side views on left ventricle
Slurred S waves in V1 and V2 (right ventricle) Gives a W shape

51
Q

What are the potential patholgy underlying left bundle branch block?

A

Has underlying cardiac pathology
Aortic stenosis
Hypertension
Severe coronary artery disease
Cardiac surgery.

52
Q

What is the difference in manging of a mobitz 1 and mobitz 2 block?

A

Mobitz 1 - monitored, pacing only required if chronic
Mobitz 2 - permanent pacing is required, has a greater risk of progression to a complete heart block

53
Q

What type of heart block is an MI most likely to cause?

A

Second degree heart block

54
Q

What are the difference in management of an anterior and inferior MI?

A

Anterior - risk of second degree heart block very likely to progress to complete heart block, temporary pacing replaced by permanent pacemaker is often required
Inferior MI - Close monitoring and transcutaneous temporary back-up pacing are all that is required.

55
Q

Where in the conduction system does damage cause a 2:1 heart block?

A

Either the AV node or the infranodal level.

56
Q

What is an atrial flutter?

A

Supraventricular tachycardia
Saw-tooth like atrial flutter waves between QRS complexes
Normally every fourth flutter wave is transmitted to the ventricles
Regular rapid atrial contraction 250-350bpm
Is normally a counter current circuit in the heart, maintained by an abnormal area of slow conduction often the cavotricupside isthmus allowing renetry.

57
Q

What clinical diagnosis has a better prognosis flutter or fibrillation?

A

Flutter
Due to lower thromboembolic risk, reduced stroke and heart failure risk

58
Q

What is an atrial fibrillation?

A

Irregular rhythm of choatic atrial contractoins tending to exceeding 300 bpm
With fine oscillation of the baseline (known as f waves) and no clear p waves.

59
Q

What are the symptoms of atrial flutter?

A

Palpitations, chest discomfort and fatigue

60
Q

What is the management for atrial flutter?

A

Rate control medications
Rhythm control such as ablation

61
Q

What are the symptoms of atrial fibrilation?

A

Palpitations
Dyspnoea
Dizziness
Fatigue

62
Q

What is the management of atrial fibrillation?

A

Rate control
Anti-coagulations
Rhythm control based on patient characteristics.

63
Q

What is ventricular tachycardia?
What does it look like on an ECG?

A

Broad QRS complex ventricular tachycardia (Mad child with crayon)
Originates in the ventricles
No clear P waves.
Can be caused be heart attack or heart failure.

64
Q

What is shown on the ECG?

A

Right bundle branch black
M in V1 - as RSR’
W in V6 - as slurred S wave

65
Q

What is shown on the ECG?

A

First degree heart block
Consistent but elongated PR intervals.
All QRS are present

66
Q

What is shown on the ECG?

A

Mobitz 1 second degree heart block
PR interval progressivly longer
Dropped QRS

67
Q

What is shown one the ECG?

A

Mobitz 2 second degree heart block
PR consistent but occasional QRS dropped.

68
Q

What is shown on the ECG?

A

2:1 heart block
Two P waves for every QRS complex

69
Q

What is shown on the ECG?

A

Complete heart block
The rate of p waves nad QRS complexes is independent of each other.

70
Q

What is shown on the ECG?

A

Left bundle branch block
RSR’ M shape on lateral leads V6
Slurred S wave on Anterior leads V1 V2 gives a W shape

71
Q

What is shown on the ECG?

A

AVRT
Tachycardia
Inverted P waves before T waves

72
Q

What is shown on the ECG?

A

AVNRT
Tachycardia
No clear p waves as merge into precedding QRS/T wave due to fast tachy
Some may show more depressed and curvy S

73
Q

What is shown on the ECG?

A

Wolff-parikinson-white syndrome in normal sinus rhythm
Delta wave - slow rise of R wave and short PR interval
As electrical activity passes through the accessory pathway faster than conducted through the AVN.

74
Q

What is shown on the ECG?

A

Atrial Flutter
Saw tooth appearance
Narrow complex tachycardia
Loss of isoelectric baseline

75
Q

What is shown on the ECG?

A

Atrial fibrilattion
Loss of isoelectric baseline
Squiggly.
Irregulalrly irregular
No p waves

76
Q

What is shown on the ECG?

A

Ventricular tachycardia
Mad child with crayon
Broad complex tachycardia
T wave and P wave hidden by larger QRS complexes.

Unit 12 (23 decks)

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