Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Cardio/Resp > Cardiac Arrythmias > Flashcards

Cardiac Arrythmias Flashcards

(50 cards)

Start Studying
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the specialised conductive pathways?

A

pathways that take the electrical activity to LV + A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is ion conductance/permeability?

A

Testing how open a channel is

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Ventricular Ion channel summary image

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Regional differences

Study These Flashcards
A

created by the expression of different ion channels

22
Q

Q’s to ask: (6)

Study These Flashcards
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:

Study These Flashcards
A

bradycardia - slow
tachycardia - fast

24
Q

AHA arrythmia def’s (4)

Study These Flashcards
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
Atrial (a.k.a supra-ventricular) arrhythmias (2)
Atrial flutter (Aflut) Afib
26
Ventricular arrhythmias (2)
ventricular tachycardia (Vtach) Vfib =killer (pumping no blood)
27
Vfib =killer = why? (3)
not pumping blood - because of contractions being too fast no blood to brain = fainting no blood to itself
28
Normal process of electrical pathway (5)
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
Effective refractory period (2)
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
Relative Refractory period
images some ion channels have started to recover and they're able to respond to another input ( just before full recovery)
31
what are arrythmias caused by? + why (4)
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
images of cardiac arrythmia causes images (3)
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
Maintenance of arrhythmias (3)
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
Re-entrant or circus activity 1 (3)
* 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
Re-entrant or circus activity 2 (3)
1) Normal wave of propagation 2) Unidirectional block: Ragged wave front 3) Re-entry
36
Focal activity def
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
circus movement def
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
Causes (8)
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
Anti-Arrhythmic mechanism (5)
Target the abnormal automaticity Target the ectopic activity Directly: - Na channel blockers - Ca channel blockers Indirectly: - K channel blockers
40
Vaughan‐Williams Classification (VWC) (5) BKG
class I – Sodium Channel blockers Class II – beta adrenoceptor blockers Class III‐ Potassium channel blockers Class IV‐ Calcium channel blockers Others adenosine / digoxin
41
Class I - function (3)BKG
Reduce ectopic ventricular/atrial automaticity Reduce DAD‐induced triggered activity Reduce re‐entrant tendency by converting unidirectional to bidirectional block
42
Class 1 - 3 drug types - dw about names (3) BKG
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
Problems of Class I (3) BKG
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
Class II (3) BKG
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
Class III (5) BKG
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
Problems of Class III (3) BKG
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
Spectrum of class I and class III antiarrhythmics: relationship with Na and K channel blocking (4) BKG
image so Na+ and K+ block - work together (opposite levels) Class1b = neurotoxicity Class1C + a = good Class III = tosardes de pointes
48
Class IV (5) BKG
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
Caveats (5) BKG
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
Modified Vaughan Williams Classification (8)
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions