Cardiac dysrhythmia

Question 1

Arrhythmia

Answer 1

Same as dysrhythmia
Benign variation or events, at rest or during exercise (eg sinus arrythmia, ectopic beats)
Abnormal heart rhythm either -
1. Pathological - unpleasant symptoms (palpitations), syncope (fainting), exercise intolerance, secondary consequences (increased risk of stroke with AF)
2. Immediately life threatening - eg ventricular fibrillation.

Question 2

Sinus arrhythmia

Answer 2

A cyclic irregular rhythm which varies with respiratory cycle.
Closer beats during inspiration.
Sinus bradycardia - p wave and QRS complex are normal but HR is 100bpm. Physiological effects can be seen durjng exercise/stress (due to infreased symp stimulation). Ischemic effect of SA and AV nodes.

Question 3

What is normal rhythm?

Answer 3

Heart beats fairly regularly, has intrinsic variability (sinus arrhythmia).
60-100bpm at rest.
HR increases with exercise and emotional stress.
Normal cardiac excitation process is AP conduction in heart tissue.
In normal sinus rhythm, rate of beating is determined by SA node. ECG reflects spread of activity and recovery I the whole heart.
Broad QRS complex (>0.14secs) indicates slow and ineffective myocardial activation (VPB/VEB).
VPB - ventricular premature beat
VEB - ventricular ectopic beat

Question 4

Aetiology and predisposing factors for arrhythmias

Answer 4

Congenital structural defects.
Congenital channelopathies.
Ischemic heart disease.
Myocardial infarction (congestive heart failure).
Hypertrophic cardiomyopathy.
Enlarged heart in athetes.
Infection (myocarditis).
Cardiac tumours (rare).
Drug side effects (including anti-dysrythmic drugs).
Electrolyte imbalance (hyperkalaemia, hypomagnesaemia)
Idiopathic (cause unknown)
Electric shock/ blow to the chest (commotio cordis)

Question 5

Diagnosis

Answer 5

Patient history / medical background / currdnt medication.
Primary diagnostic tool is ECG (3 or 12 lead ECG in clinic or holtor ambulatory monitoring for periods >24hrs).
Risk assessment (ie after MI) - by signal averaged ECG (SAECG), heart rate variability (HRV), repolarisation alternans (RPA), And EP lab/pacing clinic.

Question 6

Treatment

Answer 6

Treat underlying pathology, remove causes.
Surgery - radiofrequency catheter ablation, pacemaker implant.
Anti-arrhythmic drug therapy.
Defibrillation of VF.
Cardiaversion of AF - DC shock, adenosine/procainemide injection.

Question 7

Arrhythmia classification

Answer 7

Severity - benign/pathological/life threatening.
Longevity - transient/sustained.
Rate - bradycardia/tachycardia.
Origin - ventricular/atrial
Altered mechanism - altered impulse formation(cellular) /altered impule conduction (multicellular).

Question 8

Tachyarrhythmias

Answer 8

Increased firing rate
Increased automaticity of SA node
Increased automaticity of latent pacemakers.
Abnormal automaticity
Altered impulse formation leading to increased reentry.

Question 9

Bradyarrhrythmias

Answer 9

Decreased firing rate
Decreased automaticity of SA node due to altered impulse formation (cellular).
Conduction blocks due to altered impulse conduction(multicellular).

Question 10

What determines cell firing rate?

Answer 10

Reduced If gives a more negative maximum diastolic potential and a less negative threshold potential. This gives a reduced firing rate, therefore slowers HR.
Ivabradine is a drug that decreases Diastloic depolarisation by inhibition of If (used in stable angina where beta-Blockers can’t be used and pateint has normal sinus rhythm)

Question 11

Latent pacemakers

Answer 11

SA node (main pacemaker) - intrinsic rate 60-100bpm.
AV node - intrinsic rate 35-60bpm.
Pacemakers in ventricular muscle - intrinsic rate is less than 40bpm.
When SA is not working, others take over.

Question 12

How is pacemaker firing rate increased/defreased from normal?

Answer 12

Vagal stimulation decreases firing rate.
Overdrive suppression decreases or temporarily stops firing.
Reduced electrotonic interactions increase firing rate.

Question 13

Escape beats and rhythms

Answer 13

SA and AV nodes are most sensitive to vagal stimulation, followed by atrial tissue and then the ventricular conducting system.
Vagal stimulation may Supress SA node and allow pacemaker acyivity to shift to another site.
Junction escape rhythm - normal width QRS complexes at a slow constant rate are not preceded by p waves.

Question 14

Overdrive suppression

Answer 14

SA node activity supresses other pacemaker sites.
Cells are forced to fire faster than their intrinsic firing rate.
More sodium enters per unit time, sodium potassium pump becomes more active.
This generates a hyperpolarising current which hyperpolarises the cell (countering If current).
Prevents If reaching threshold, supresses spontaneous AP generation.

Question 15

Loss of electrotonic interactions

Answer 15

Loss of interconnections due to ischemia stops the suppression of automaticity in the AV node.
This is due to the nodal cell no longer being hyperpolarised by neighbouring cells, thus depolarising to threshold more easily.

Question 16

Sick sinus syndrome

Answer 16

Variety of arrhythmic effects - sinus arrest, alternating sinus brady/tachycardia.
Cause is poorly understood - jutation in gene Cx40 for connexin which allows electrotonic interaction between sinus cells and neighbouring myocytes.

Question 17

Abnormal automaticity

Answer 17

Due to cardiac tissue damage/ischemia.
Effects cells outside specialised conduction system, which do not normally possess automaticity.
If current is not active in ventricular cells hut membranes become leaky, reducing the membrane potential.
AP shows a phase 4 depolarisation, producing ectopic beats.
Firing rate may even exceed thag of SA node thus overriding normal sinus rhythm.

Question 18

Triggered activity

Answer 18

Under certain conditions normal AP can trigger additional depolarisations leading to extra beats or tachycardia.

Question 19

Digitalis toxicity

Answer 19

Digitoxin (not the same as digoxin) is a cardiac glycoside derived from foxgloves.
Positive inotrope (increased cardiac contractility) used in heart failure.
Blocks sodium/potassium pump, increasing intracellular sodium, this then inhibits the sodium calcium exchanger, increasing intracellular calcium and theregore force of contraction.
Arrhythmic (inhibits Ica in AV node), usednin AF and AVRT.
Narrow therapeutic window.
Overdose casues - bradycardia due to AV node block, tachycardia due to triggered activity.
Metabolised hy liver (not kidneys like digoxin) so used in patients with decreased renal function.

Question 20

Disorders of impulse conduction

Answer 20

Multicellular
Factors affecting conduction velocity produce slow/blocked conduction. This leads to bradycardia ( ie AV block, 1st, 2nd, or 3rd degree).
Reentry and reentrant arrhythmia - gives rise to tachycardia, needs unidirectional conduction block and slowed conduction to initiate it, wolf-parkinson-white syndrome.

Question 21

What is conduction?

Answer 21

Movement of impulse (wave of depolarisation) through tissue.
At myocyte level - AP propagation from cells to cell via jap junctions (connexins).
Not conductance, which is how easily ion currents flow through ion channels.

Question 22

AP propagation

Answer 22

During AP propagation an excited cell serves as a source of electrical charge for depolarasation of neighboring cells towards threshold potential. The unexcited cell acts as a sink for the excited cell.
For propagation to succeed, excited cell must provide sufficient charge to bring the unexcited cell membrane to threshold.

Question 23

Determinants of conduction velocity

Answer 23

Cell to cell coupling - higher resistance between less well coupled cells means a smaller current flow from source to sink.
Cell excitability - less excitable cell takes longer to reach threshold and may wbe a weaker source for exviting other cells.
Celk to cell coupling is affected hy ischemia, fibrosis and remodelling in heart failure. These factors decrease celk to cell contact, gap junction density and conductance.

Question 24

Celk excitability

Answer 24

Completely inexcitable during AP (upstroke and refractory period).
Excitability between APs is reduced by - inhibition of sodium channels (due to hyperkalaemia, ischemia or class I anti-arrhythmic drugs).

Question 25

AV block (bradycardia)

Answer 25

AV node is particularly susceptible to conduction slowing and block (as conduction is already slow in this tissue).
Temporary causes include - indreased vagal tone, transient ischemia, digitalis, beta-blockers and calcium channel antagonists.
Permanent structural causes include - MI, degenerative disease.
1st degree - PR interval is prolonged.
2nd degree - mobitz I (PR interval progressively lengthens until QRS is completely blocked), mobitz II (QRS blocked without gradual lengthening of PR).
3rd degree - P wave and QRS rhythm are independant of one another. QRS widens, 2nd and 4th p waves superimpose on normal T waves.

Question 26

Reentrant arrhythmias (tachycardia)

Answer 26

A pattern of activation in which a wave of depolarisation reactivates the same region of cardiac tissue at leasg once (and possibly many times). Requires both a substrate for abnormal conduction and a trigger.
Can be atrial in origin (atrial flutter, atrial fibrillation), ventricular in origin (VT,VF,TdP), or due to accessory atrio-ventricular pathway (wpw syndrome).
VF lethal as it causes decreased cardiac output.

Question 27

Bypass tract

Answer 27

Bundle of Kent.
Can conduct impulses from the atrium directly to the ventricles, bypassing the AV node.
Causes a shortened PR interval and delta wave due to early excitation of ventricles.

Question 28

ECG diagnosis of WPW syndrome

Answer 28

PR interval of 100msec.

Question 29

Typical counter clockwise atrial flutter

Answer 29

Saw toothed P wave

Negative saw toothed P wave in leads II, IV and aVF.

Question 30

Flecainide (tambocor)

Answer 30

Class Ic anti-arrhythmic drugs
Used to treat WPW syndrome.
Blocks sodium channels, decreasing sodium current, excitability and conduction.
Use dependant.
More affective to terminate tachycardia but relatively little effect at normal HR.

Question 31

Functional reentry - VT vs VF

Answer 31

Transition from VT to VF thought to be due to splitting of singular wave into multiple smaller wavelets which continue to circulate in ventricle, producing characteristic complex polymorphic ECG.
Ordered waves = VT
Chaotic wavelets = VF