Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiovascular, renal and PNS > Cardiac arrhythmias + ionotropes > Flashcards

Cardiac arrhythmias + ionotropes Flashcards

1
Q

Anti-arrhythmic drugs - class I

A

[sodium channel blockers]

block sodium channels responsible for rapid depolarisation

slow down upstroke of cardiac AP + conduction

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

Anti-arrhythmic drugs - class II

A

[beta blockers]

block effects of adrenaline and cause heart to beat more slowly

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

Anti-arrhythmic drugs - class III

A

drugs that prolong AP duration by blocking voltage-activated K+ channels in depolarisation of phase 3 cardiac AP

reduces cardiac excitability + prevents abnormal heart rhythms

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

Anti-arrhythmic drugs - class IV

A

[calcium channel blockers]

slow down conduction at AV node

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

Anti-arrhythmic drugs - outside Vaughan Williams Classification

A

adrenaline - cardiac arrest

atropine - 2nd/3rd degree AV block

isoprenaline - 2nd/3rd degree block

adenosine - via adenosine A1 receptors in AVN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

supraventricular tachycardia (SVT)

A

condition where your heart beats faster than normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

types of SVT

A

atrioventricular nodal reentrant tachycardia (AVNRT)

Atrioventricular reciprocating tachycardia (AVRT)

atrial tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

causes of arrhythmias

A

congenial heart defects

hyperthyroidism

hypokalaemia

drugs - e.g. anti-arrythmic/hypertensive

stress

excess alcohol/drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

which genetic conditions can cause arrhythmias?

A

Mutations in channels

Long QT syndrome

Brugada syndrome

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

slow-fast AVRNT

A

impulse travelling along fast pathway will excite cells @ bundle of His AND slow pathway = cancellation of slow

next impulse enters slow pathway (fast refractory period)

excite fibres in both bundle of His and fast pathway
-> impulse travels rapidly backwards along fast pathway to atrium and re-enter slow pathway again (cycle)

= simultaneous atrial and ventricular contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what would appear on an ECG for AVRNT

A

narrow QRS and absence of P waves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Wolff-Parkinson-White (WPW) syndrome

A

extra conducting pathway between atrium and ventricle

[ECG]

  1. shorter PR intervals
  2. delta waves after QRS
  3. increased QRS duration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

main strategy for treated SVT

A

increase AVN delay to slow down conduction via AVN

rate control drugs - class II/IV (verapamil and digoxin)

rhythm control drugs - class I/III (Flecainide, sotalol, amiodarone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

macro re-entry

A

re-entry from atrium to ventricle (accessory pathway)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

micro re-entry

A

caused by ischaemic damage to Purkinje fibres in ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

early after depolarisation (EAD)

A

abnormality with depolarisation

slower HR - prolonged QT interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

delayed after depolarisation (DAD)

A

spontaneous Ca2+ overload during depolarisation

faster HR

18
Q

atrial fibrillation

A

fast, IRREGULAR heartbeat

19
Q

atrial flutter

A

fast, REGULAR heartbeat

20
Q

atrial fibrillation - common causes

A

EADs

AVRT

21
Q

atrial flutter causes

A

micro re-entry and EADs

22
Q

treatment for atrial flutter/fibrillation

A

[main cause of stroke]

rhythm control - electrical cardioversion

rate control - class II/IV drugs

23
Q

excitation-contraction coupling

A

regulation of Ca2+ homeostasis in cardiac myocytes

24
Q

what happens after the Na+ influx caused by depolarisation?

A

L-VACCs activated

influx of extracellular Ca2+

activation of RyR2 on SR = release of SR Ca2+ via NCX

25
Q

what happens once Ca2+ has been released from sarcoplasmic reticulum?

A

binds to troponin C of troponin-tropomyosin complex on actin filaments in sarcomere

= formation of cross-bridge between actin and myosin

26
Q

what happens to allow re-polarisation?

A

voltage-gated K+ channels open to allow outward current

relaxation occurs when Ca2+ is taken back up into SR via SERCA2a

forced out of cell by sarcolemmal NCX

27
Q

ryanodine receptor (RyR)

A

Large homotetrameric protein complex

intracellular Ca2+ release channel on SR

28
Q

isoforms of RyR

A

RyR1
RyR2
RyR3

29
Q

RyR mechanism of action

A

voltage change activates DHPR in T-tubule
-> signal transmitted to RyR1 channel by DHPR-RyR1 linkage

= opening of RyR1 channel and release of Ca2+ from SR

30
Q

SERCA’s role

A

uses energy stored in ATP to pump calcium back into SR

31
Q

NCX’s role

A

uses energy stored in sodium gradient to move calcium out of cell

32
Q

caffeine

A

low conc. increases sensitivity of RyRs to Ca2+

high conc. activates RyRs + leads to rapid Ca2+ release

33
Q

overview of Ca2+ removal

A
  1. reuptake into SR by SERCA
  2. forced out by NCX
  3. uptake by mitochondrial Ca2+ uniporter (MCU)
  4. forced out by sarcolemmal Ca2+ ATPase (Ca2+ pump)
34
Q

CaMKII catalyses phosphorylation of…

A
  • voltage-gated Ca2+ channels to increase Ca2+ entry
  • RyR2 to increase Ca2+ release
  • voltage-gated Na+ channels to increase sarcolemmal [Na+] which decreases driving force for Ca2+ by NCX
  • PLN to reduce inhibitory activity of PLN on SERCA2a
35
Q

what is the cardiac isoform of SERCA?

A

SERCA2a

36
Q

calcium removal by NCX

A

driven by increased cytosolic concentration of Ca2+ / Na+

exchanges 1 Ca2+ for 3 Na+

= ELECTROGENIC (produces change in electrical potential)

37
Q

SERCA + PLN

A

responsible for Ca2+ transport from cytoplasm to SR lumen

= muscle relaxation

38
Q

Catecholaminergic Polymorphic Ventricular Tachycardia, CPVT - cause

A

mutations in RyR2 and CASQ2 (triggered by exercise, emotion and drugs)

39
Q

Catecholaminergic Polymorphic Ventricular Tachycardia, CPVT - treatment

A

class II beta-blockers (reduces sympathetic input to heart)

class Ic (flecainide(

40
Q

iontrope

A

medicines that change the force of your heart’s contractions

41
Q

inotrope mechanism of action

A

Inhibition of Na+/K+ ATPase (Na-Pump) by binding to extracellular K+ binding site

Cardiovascular, renal and PNS (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions