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Cardio/Resp > Cardiac Arrythmias > Flashcards

Cardiac Arrythmias Flashcards

1
Q

The electrical journey (6)

A

1) SAN
2) RA
3) AVN - junction point (rhythmically active - needs a poke = AP)
4) LA
5) Bundle of His
6) Pukinje fibres

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2
Q

What are the specialised conductive pathways?

A

pathways that take the electrical activity to LV + A

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3
Q

why does the AVN have a delay/ is a junction box?

A

allows for the filling of blood by the contraction of the ventricles

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4
Q

Where + what are the low resistance gap junctions? (3)

A

Heart is joined by them = heart is called syncytia

they are LR = pathway that does not impede the movement of electrical activity, membrane potential (made of connexons) = allows electrical activity to go through heart (sweeping motion)

connexons come together = connexins

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5
Q

what happens to the AP’s when you have myocardial ischaemia or myocardial infarction?

A

The non-decaying/decremental process of depolarisation + action potentials (sweeping motion) disappears.

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6
Q

what 3 things in the heart have inherent rhythmic system/pacemaker potential + what generates it? (4)

A
  • SAN : 60-110bpm
  • AVN: 40-55bpm
  • Bundle of his/purkinje fibres: 25-40bpm

SAN generates/dominant one- fastest

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7
Q

But what happens if the SAN gets damaged?

A

different pacemaker takes over = but then there’s an imbalance b/w SAN + others

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8
Q

Nodal cells vs myocytes (5)

A

Nodal (SA/AV):
- cannot contract (because no myosin)
- small ca2+ store SR
- approx -55mV MPV
-unstable MPStability
-relatively slow AP dev

myocyte (atria/ventricle):
- can contract
- well dev SR
- approx -80-90 MPV
-stable MPstability
-fast AP dev

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9
Q

Ventricular action potential graph (5)

A

Phase 4: Baseline or resting membrane potential

Phase 0: Fast depolarisation

Phase 1: Notch or transient repolarisation.

Phase 2: Plateau depolarisation

Phase 3: Complete repolarisation

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10
Q

what is ion conductance/permeability?

A

Testing how open a channel is

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11
Q

Phase 4 - Baseline or resting membrane potential (3)

A
  • Dominated by open k+ channels

-No other channels open (@rest)

-Pumps active to restore ionic balance

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12
Q

Phase 0- fast depolarisation (4)

A
  • Depolarisation from adjacent cells produces depolarisation
  • Opening of voltage sensitive sodium channels
    [encoded by SCN5a gene]
  • Large influx of sodium {why?} = further depolarisation
  • Channels inactivate leading to reduced conductance
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13
Q

Phase 1– Notch or transient repolarisation (3)

A
  • Coincident with NaV1.5 channel inactivation =
    Opening of potassium channels
  • Transiently open Kv channels
    [Kv4.2 / 4.3 – why transient?]

Transient repolarisation

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14
Q

Phase 2- Maintained depolarisations (3)

A
  • Voltage-gated calcium channels [CaV1.2] open
  • Limited opposing Kv channels as Kv4.3 is transient
  • Plateau phase determined by CaV
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15
Q

Phase 3: Complete repolarisation (5)

A
  • CaV and NaV are inactivated
  • Kv channels [Kv7.1 and Kv11.1] open to repolarise cell
  • Kv7.1 is encoded by KCNQ1

-Kv11.1 is encoded by KCNH2 a.k.a ERG (ether-a-go-go related gene)

  • Kv11.1 is susceptible to block by MANY drugs
    [consequence?]
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16
Q

What drugs can induce cardiac arrythmias + ventricular fibrillation? (5)

A

Cardiac arrhythmia and ventricular fibrillation is
rare in the population

-astemizole (deworming)

-ketoconazole (antifungal)

  • tefenadine (MOST POP ANTIHIST) = Vfib
  • helopredole (psychotic disorders)
  • Crisapride brouwer (bowel movements)
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17
Q

How do these drugs cause Arr + Vfib? - ECG (2)

A

they block the ERG channels

ECG = Vfib: Torsade de pointes (twisting of the points)

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18
Q

Ventricular Ion channel summary image

A

phase 0-3
Phase 0-3
Phase 1
Phase 3
Phase 3
Phase 4

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19
Q

Action potential of the atria vs ventricle - WHY??? (3)

A

images

ion channel complex in atria

  • atria expresses more K+ = brings it back down into the negative
    (IKur, IKAch, etc.)

IKach: opened by the vagus releasing ACh = activating M2r = HR reduces

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20
Q

Myocytes vs Nodal cells - SAN + V’s (3)

A

images

SAN:
-Low resting K permeability
low/no Kir2.1 expression
-Funny current present High HCN expression
- No NaV low SCN5a expression = sluggish

Ventricles:
- High resting K permeability High Kir2.1 expression
- Negligible funny current Low HCN expression
- Prominent NaV High SCN5a expression = high energy

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21
Q

Regional differences

A

created by the expression of different ion channels

22
Q

Q’s to ask: (6)

A

What are the phases of
an action potential and
what is the main
characteristics ?

What determines
the AP in nodal v
myocyte cells?

What might cause
the cardiac rhythm
alter?

What is a funny
current and why is it
called that?

What is the order of
depolarisation in a
healthy heart?

What would you
target if rhythm is
altered?

23
Q

2 types of arrthmias:

A

bradycardia - slow
tachycardia - fast

24
Q

AHA arrythmia def’s (4)

A

The term “arrhythmia” refers to any change
from the normal sequence of electrical impulses.

The electrical impulses may happen too fast, too
slowly, or erratically – causing the heart to beat
too fast, too slowly, or erratically.

When the heart doesn’t beat properly, it can’t
pump blood effectively.

When the heart doesn’t pump blood effectively,
the lungs, brain and all other organs can’t work
properly and may shut down or be damaged”

25
Q

Atrial (a.k.a supra-ventricular) arrhythmias (2)

A

Atrial flutter (Aflut)
Afib

26
Q

Ventricular arrhythmias
(2)

A

ventricular tachycardia (Vtach)

Vfib =killer (pumping no blood)

27
Q

Vfib =killer = why? (3)

A

not pumping blood
- because of contractions being too fast

no blood to brain = fainting
no blood to itself

28
Q

Normal process of electrical pathway (5)

A

1) APs generated in nodal cells

2) Propagate through gap
junctions to myocytes

3) Activation and
inactivation of sodium
channels = upstoke

4) Balance of calcium and
potassium channels
=plateau

5) Repolarisation and
sodium channels
available

29
Q

Effective refractory period (2)

A

3) Activation and
inactivation of sodium
channels = upstoke

4) Balance of calcium and
potassium channels
=plateau

  • cannot be stimulated in this specific time frame - don’t respond (dictated by ion channel properties)
  • tells you when the cell can be reactivated again
30
Q

Relative Refractory period

A

images

some ion channels have started to recover and they’re able to respond to another input ( just before full recovery)

31
Q

what are arrythmias caused by? + why (4)

A

Cardiac arrhythmias are generated by abnormal
impulse formation or impulse propagation.

  1. Changes in the repetitive SAN activity, depending on its pacemaker currents.
  2. Creation of subsidiary pacemaker formation
    in specialized conducting AVN or Purkinje fibres.
  3. Ectopic activity in normally nonautomatic
    atrial and ventricular cardiomyocytes when they
    are depolarized by some pathological processes (- assuming heart disease)

-usually as a consequence of defective ion channels,
exchangers or ion handling

32
Q

images of cardiac arrythmia causes images (3)

A

Exaggeration of normal cellular capacity to fire.
Increase in funny current = faster SAN depolarisation

Failure to repolarise results in an EARLY after depolarisation that
stimulates adjacent cell

DELAYED after depolarisation induces AP sooner than expected.
Calcium release = NCX current = depolarisation

33
Q

Maintenance of arrhythmias (3)

A

Heterogeneities generate obstacles to AP conduction,
around which the AP circulates with slowed conduction velocities.

May reflect altered ion channel or myocardial tissue electric properties

Re-entrant excitation is also facilitated by abnormalities leading to heterogeneities in AP recovery

34
Q

Re-entrant or circus activity 1 (3)

A
  • Abnormal impulse formation or abnormal
    automaticity
  • Pathological conduction

images:
1) Normal wave of propagation

2) Injury - region of slow conduction

3) Re-entry: Slow retrograde
conduction , Wave split

35
Q

Re-entrant or circus activity 2 (3)

A

1) Normal wave of propagation

2) Unidirectional block: Ragged wave front

3) Re-entry

36
Q

Focal activity def

A

an abnormal site is generating impulses (WHY?). This site is
often called “ectopic”, which
really means outside the
normal location (i.e. the sinus node)

37
Q

circus movement def

A

In re-entry, the impulse
turns around in a loop or a
circuit (a.k.a circus
movement). These can also
occur in the atria or in the
ventricles.

38
Q

Causes (8)

A

Acute myocardial infarction (AMI) (no blood = cells ischaemic or die)

Heart failure (chamber remodelling = structural changes = easy to dev + main arrth)

Therapeutic (e.g. digitalis) and abuse drugs (xs na+ drive)

Inherited mutations of cardiac ion channels

Hyperthyroidism

Hypokalemia (especially in anorexia nervosa)

Autonomic dysfunction

Fever

39
Q

Anti-Arrhythmic mechanism (5)

A

Target the abnormal automaticity

Target the ectopic activity

Directly:
- Na channel blockers
- Ca channel blockers

Indirectly:
- K channel blockers

40
Q

Vaughan‐Williams Classification (VWC) (5) BKG

A

class I – Sodium Channel blockers

Class II – beta adrenoceptor blockers

Class III‐ Potassium channel blockers

Class IV‐ Calcium channel blockers

Others adenosine / digoxin

41
Q

Class I - function (3)BKG

A

Reduce ectopic ventricular/atrial automaticity

Reduce DAD‐induced triggered activity

Reduce re‐entrant tendency by converting unidirectional
to bidirectional block

42
Q

Class 1 - 3 drug types - dw about names (3) BKG

A

Block NaV1.5 Na+ channel

1a (Dissociation rate: quickly) : Quinidine, dysopyramide, procainamide, ajmaline:
Open channel block, APD duration prolonged due to K block

1b (Dissociation rate: not so quickly): Lidocaine, mexiletine
Rapid onset and dissoc mean little accumulated block, Fast depolarizing tissue or ischemic tissues - affected, Bind to inactive channel state

1c (Dissociation rate: slowly)
flecainide, propafenone
Depression of phase 0 by accumulated block

43
Q

Problems of Class I (3) BKG

A

Do not target the damaged tissues

Effectively make healthy tissue like ischaemic

Can stop conduction = asystole

Class Ia also affect K channels = increased risk of torsade de pointes

44
Q

Class II (3) BKG

A

Target the abnormal automaticity

Abnormal automaticity may be due to high β adrenergic drive (sympathetic).

β adrenoceptor blockers eg Atenolol or metoprolol

Class II VWC

45
Q

Class III (5) BKG

A

Potassium channel blockers
E.G Amiodarone, dronedarone, vernakalant, D‐sotalol,

Achieved by delaying repolarization anywhere in re‐ entrant pathway including healthy regions

This is because cells are inexcitable during AP (refractory to any arrhythmic wavefront)

Prolonging refractory period indirectly blocks Na channels and conduction

Increase in AP recovery time = increased refractory time =decreased re‐entrant tendency

46
Q

Problems of Class III (3) BKG

A

Possibility to precipitate LQT prolongation and TdP

Eg SWORD trial (Survival With ORal D‐sotalol) showed:
‐ increased one year mortality with D‐sotalol

Amiodarone decreases thyroid function

47
Q

Spectrum of class I and class III antiarrhythmics:
relationship with Na and K channel blocking (4) BKG

A

image
so Na+ and K+ block - work together (opposite levels)

Class1b = neurotoxicity
Class1C + a = good
Class III = tosardes de pointes

48
Q

Class IV (5) BKG

A

Reduce conduction in AV node by blocking Ca++
channels

Reduce DADs leading to ectopic activity in atria
/ventricle

Eg verapamil or diltiazem
Not dihydropyridines like nifedipine

Bolus i.v. converts re‐entry in the AV node to sinus
rhythm

High concentration arrives at AV node blocking
conduction in damaged section

49
Q

Caveats (5) BKG

A

Reduction inexcitability and prolongation of refractoriness are also
pro‐arrhythmic.pro‐arrhythmic.

Na+ channel block slows conduction thereby promoting re‐entry

β‐AR blockers and Ca2+ channel blockers cause bradycardia and
atrioventricular (AV) block

Extensive APD prolongation especially by selective hERG (K+) channel blockers increases the risk for early afterdepolarizations.

Torsade de pointes, a polymorphic ventricular tachyarrhythmia that
can easily turn into ventricular fibrillation

50
Q

Modified Vaughan Williams Classification (8)

A

Class O-rhythm generation

Class Id – late Sodium Channel blockers

Class II- Adenosine

Class III – Atria specific blockers

Class IV- Calcium-release modifiers

Class V- Stretched activated channels

Class VI-Gap junctions

Class VII-environmental remodelling

Cardio/Resp (34 decks)

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