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Unit 12 Week 3 > Cardiac arrhythmias > Flashcards

Cardiac arrhythmias Flashcards

1
Q

Normal heart rhythm

A

i.e. normal sinus rhythm (NSR)

Impulses are coming from SA node

Regular P waves with similar morphology

Regularly followed by QRS complex

Normal rate

60-100 bpm

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2
Q

What is an arrhytmia

?

A

irregular heart rhythm (fast, slow, irregular)

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3
Q

Bradycardias and cause

A

<60

sinus bradycardias (physiological or sinus. node disease)

problems with AVN- atrioventricular block but not always

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4
Q

tachycardias

BPM

types and examples from the types

A

greater than 100 BPM

narrow comlpex tachycardias

AFib, A flut, AT and ST (atrial and sinus tach)

SVT

broad complex

Ventricular tachycardias

“horrible looking tachycardias”

VF and torsades

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5
Q

What things can cause arrhtymias

A
  • Electrolyte disturbances
  • Ion channel modification or defects
  • Structural/ anatomy abnormalities
  • Cell damage
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6
Q

Fundamentals of why arrhythmias occur

A
  1. Disturbances in impulse generation
  2. Disturbances in impulse propagation
  3. Bit of both
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7
Q

Who is at risk of arrhythmias

A

Cell/structural changes

Myocardial infarction

Myocarditis

Fibrosis

Toxins (ie alcohol)

Chemotherapy

Ion channels

Long QT syndromes

Drugs (i.e. antiarrhythmics, anti-epileptics)

Situational/Environmental factors can cause cellular dysfunction

Metabolic anomalies- K, Ca, Mg levels, temperature, acidaemia, hypoxia

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8
Q

Normal conduction process

A

Specialised conduction tissues run throughout key conduction areas of the heart.

Starts at the SA node in the top right of the right atrium.

Wave of depolarisation spreads across the atria, causing them to contract.

Electrical impulse reaches the AVN, in the bottom left of the right atrium. AVN is a specialised conduction tissue. It is the only one that allows depolarisation to spread to the ventricles.

The rest of the base of the atria is electrically isolated.

AVN directs impulse to the left and right bundle branches.

Impulse is passed onto the purkinje fibres in the bulk of the myocardium in the ventricles causing ventricular systole.

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9
Q

Disorders in pulse formation can be due to (2)

A

Disorders in automaticity

Triggered activity (EADs and DADs)

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10
Q

What is automaticity

A

“The property of a fibre to initiate an impulse spontaneously- without needing prior stimulation”

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11
Q

2 abnormalities in automaticity

A
  1. Inappropriate discharge rate (i.e. sinus tachycardia, sinus bradycardia)
  2. “ectopic” pacemaker takes over and controls atrial or ventricular rhythm
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12
Q

Increased or abnormal automaticity

A

Sinus tachycardia- SA node activating too quickly

Ectopic atrial tachycardia- abnormal focus of atrial cells that have automaticity, biphasic P waves

Junctional tachycardia- piece of tissue near AVN irregular

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13
Q

reason for decreased automatcity

A

Sinus node disease- presents as sinus bradycardia. Normal waveforms just too slow.

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14
Q

explain the cardaic pacemaker cells properties

A
  • Pacemaker cells have a pacemaker potential (phase 4) enabling them to self-generate their own action potentials
  • The rate of rise of ion influx at the pacemaker cell sets the intrinsic heart rate
  • The SA node rate is then influenced by the autonomic nervous system
  • A balance of sympathetic and parasympathetic tone sets the resting heart rate
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15
Q

What happens during phase 4 of a pacemaker potential

A
  • Reaches -60mV
  • Opening of slow inward (depolarising) Na+ funny channels
  • Small potassium out at decreasing level as channels close
  • -50 mV- opening of T-type Ca2+ channel (influx)
  • -40 mV- opening of L-type Ca2+ channels (long influx) and quick upsweep to depolarising
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16
Q

phase 4 of a normal cardiac cell

A

without the external stimulus of adjaecnt ion release an action potential would never be produced as the threshold potential would never be met

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17
Q

what are “triggered activities”

A

“after-depolarizations”

These are depolarising “oscillations” in the resting membrane voltage induced by one or more preceding action potentials

i.e. unstable depolarisations (activations) that occur when the heart should be repolarising (resting)

These oscillations can trigger (or be triggered by) extra heart beats

Can trigger arrhythmias like Torsades de Pointes (polymorhphic ventricular tachycardia) or VT

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18
Q

What is an EAD

A

Early After Depolarisations arise from an abnormal membrane potential during phase 2 and 3

Lots of “aborted” action potentials usually due to changes in the ion channels

i.e increased opening of Ca and Na channels

Mechanism:

Mini spike in phase 2 and 3 of the action potential

Manifestation: prolongs QT interval (time taken for ventricular depolarisation and repolarization- “resting”), prolonging how long it takes to return to electrical baseline.

If the depolarisation occurs at the right time it can be sufficient to trigger extra heartbeats.

Possible for one EAD to trigger another, then that one triggers another and so on and so on. This creates a sustained heart rhythm disorder like Torsades de pointes.

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19
Q

What are DADs

A

Late or Delayed After-Depolarisations occur after phase 4.

Due to an increased/ altered movement of calcium.

Activate a Na/Ca exchanger triggering an AP.

20
Q

what is the difference between LAD’s and DAD’s?

A

DAD’s happen at much more negative membrane potnetials

21
Q

Outcomes of an EAD (3)

A
  • Spike of sodium, nothing happens
  • Small action potential, prolongs QT interval
  • Sustained triggered activity (e.g. Torsades de Pointes) caused by early depolarisation. Influx of sodium is great enough to keep causing action potentials.
22
Q

outcomes of DAD (3)

A
  • Can sometimes do nothing- subthreshold
  • Just enough to trigger an action potential (ectopic/extra beat)
  • Sustained triggered activity (e.g. VT)- repeated DADs
23
Q

causes of EADs

A

Low serum K+

Slow HR

Drug toxicity ie quinidine

24
Q

Causes of DADs

A
  • Increased serum calcium
  • Increased adrenaline
  • Drug toxicity ie Digoxin
  • Myocardial infarction
25
Q

What are the 2 forms of impulse conduction disorder

A

re entry

conduction block

26
Q

What are the requirements for a re-entry tachycardia to take place (3)

A
  1. 2 possible routes for electrical impulse to flow down
  2. Two pathways must have different electrical properties, with one conducting faster- “Fast pathway” and “slow pathway”
  3. Impulse flows down one pathway, back up another and gets caught in a loop
27
Q

when is a re-entry circuit not a problem

A

differeent paces, the impulses arrive at the end together

28
Q

the slower pathway can be caused by:

A

central area of block e.g., scar tissue, refractory cells

area/ path of transient/ variable blocking e.g., dead myocytes, myocytes with different refractory period/ conduction velocity

29
Q

rhythms caused by re-entry

A
  • AV nodal Re-entrant tachycardia (AVNRT)
  • AV re-entrant tachycardia (AVNRT)
  • Atrial flutter
  • Atrial fibrillation
  • Ventricular tachycardia
30
Q

Explain supraventricular tachycardia

A
  • has 2 categories (will go into later)
  • Identified on ECG’s as a regular tachycardia 130-250 bpm
  • There is 1 P wave for each QRS, but they may not be visible
  • QRS duration is usually narrow (normal), as after the AVN the impulse is conducted normally through the ventricles
31
Q

How do accessory pathways lead to SVTs

A

(conductible breaks in the usually electrically insulated non-conducting strip at base of atria)

SA node fires as normal (P wave)

Reaches AVN as normal, however also reaches accessory pathway

Accessory pathways don’t have inbuilt delay so AP’s immediately pass through and activate ventricular systole.

The AVN then passes on its AP after its natural delay, remainder of ventricle catches up

Results in a slurring of the QRS complex- called delta wave

This means that there are 2 pathways for conduction; one of which is fast and one of which is slow. Therefore, a re-entry circuit can be set up.

32
Q

What are the 2 types of SVT

A

AVNRT- Extra wire near AVN that conducts slightly slower, creating a loop

AVRT-apparently it doesn’t matter, both look similar on ECG

33
Q

atrial fibrillation

A

Can be caused by smaller re-entry circuits above both atria

Common in those with small scarring or stretching on the atria- i.e. older people, high BP, diabetes

Wobbly and irregular baseline, no clear P waves

Electrical signals hit the AVN at random times, irregularly regular QRS complexes

34
Q

atrial flutter

A

(“macro” circuit- usually due to extra wiring by the tricuspid valve)

Electricity goes round the atrium- shown as a sawtooth baseline on ECG

35
Q

ventricular tachycardia

A

Most clinically prevalent when someone has had a large myocardial infarction, leaving a large section of scar tissue, some of these cells will be dead whereas others within it just conduct slower. Fast= purkinje fibre and slow = scar tissue.

Because this occurs in a large section of myocardium (ventricles), you get broad QRS complexes going round and round

36
Q

Disorders of impulse conduction

A

conduction blocks- block to conduction going from the atria to ventricles

e.g., 1st degree to 3rd degree heart block

37
Q

1st degree av block

A

ECG- normal activation of SAN (normal P wave), AVN has a greater delay (Prolonged PR interval)

Normal 200ms (5 small squares) here 6-7

38
Q

Second degree heart block (Type 1 av wenkebach)

A

Somewhat normal. AVN has normal delay/ break. In wenchebach, keeps applying the breaks harder nd harder until it applied them a. little too hard and it blocks the impulse entirely.

Gradual increase in PR interval until eventually, no QRS.

Next time, foot completely off the breaks so PR interval is normal.

Somewhat pattern like

39
Q

2nd degree heart block (type 2)

A

Randomly a P wave with occasional missing QRS. No PR interval prolongation.

40
Q

3rd degree av block

A

Essentially AVN is dead, allows no conduction

His purkinje system has to take over as pacemaker

Sinus rhythm normal (P wave) completely unrelated to QRS complex. May find P waves in the middle of QRS complexes.

41
Q

how might ischaemic heart disease cause AV block

A

Ischaemic heart disease is when you have atheroma (plaque) and eventual occlusion to the coronary arteries. Resultant ischaemia to myocardium.

Right Coronary Artery (RCA) usually supplies blood to critical electrical component of heart (i.e., AVN). Ischaemia to these areas can lead to sinus bradycardia or heart block

42
Q

Consequences of arrhythmias

A

haemodynamic compromise due to CO being affected

low HR causes direct drop in CO

high HR means that ventricles can’t fill as effectively so CO drops

43
Q

porlonged arrhythmia can cause

A

Prolonged arrhythmia can lead to

  • Heart failure- CO fails to meet end organ demand
  • Cardiac ischaemia and chest pain due to reduced coronary filling
  • Hypotension
  • Poor renal perfusion  renal failure
  • Poor liver perfusion  liver failure
  • Poor brain perfusion  syncope, confusion
44
Q

an inferior MI can affect from the RCA can affect what part of the ehart and cause what condition?

A

disrupt bf to the SA and AVN causing bradycardia and heart block

45
Q

If left atrial hypertrophy what would be seen on ecg

A

2 p wave peaks

46
Q

if right atrium hypertrophy what would happen to ecg

A

taller p wave

Unit 12 Week 3 (4 decks)

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