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CVS > Arrhythmia > Flashcards

Arrhythmia Flashcards

1
Q

Function of AV node

A

Delay - to allow ventricles to fill up

Decremental property - protect from high atrial rates

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2
Q

Intrinsic pacemaker rates of
SA
AV
Ventricular Muscles

A

60-100
40-60
20-40

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3
Q

Transplanted heart HR is higher/lower

A

Higher due to lack of parasympathetic control

- still responses to exercise but delayed

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4
Q

Cells ICF higher/lower than ECF

Sodium
Potassium
Calcium

A

Sodium lower
Potassium higher
Calcium lower

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5
Q

Describe Phases of Cardiac Muscle Action Potential

Phases 4 0 1 2 3

A

Phase 4: Resting

  • K+ channels closed / leaky
  • Ca2+ channel contributes abit

Phase 0: Depolarization [Intercalated disc signal]

  • VG Na+ channel opens, sodium enters, opening more VGNC - more sodium enters
  • rapid inactivation due to -ve Em needed to open

Phase 1: Early Fast Repolarization

  • VGNC closes
  • VGKC opens: K+ exits

Phase 2: Plateau

  • K+ exits, repolarization
  • Ca2+ enters (from ECM and SER)

Phase 3: Repolarization
- Ca2+ stops
- K+ continue to exit, Em approaches Ek;
at negative potential, sodium channel recovers

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6
Q

Absolute Refractory Period

  • phase 0 1 2 3
  • whats the function
A

Prevent second action potential initiation

- protect against tetanus

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7
Q

Whats sinus rhythm

A

Normal regular rhythm

- P wave followed by QRS

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8
Q

What arrhythmia causes are there

Too Slow [2]
Too Fast [4]
- subcategories

A

Too slow:

  • SA problem // generation problem
  • AV blocks

Too fast:

  • Re-entry - Scar
  • Abnormal automaticity + Triggered Activity - afterdepolarizations
  • Disorganized activity - Fibrillations - AF, VF
  • Sinus TC
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9
Q

Drugs which can cause Bradycardia and their MOA

A

Digoxin - block Na-K-ATPase of Myocardium - increase [Na] hence maintaining [Ca2+] from antiporter (less Na enters)

  • Decreases HR, Phase 4 lengthened
  • Increased Contractility
    • Vagus nerve stimulating effect, slow AV NODE, PR interval increases as antiarrhythmic drug
  • —- Use as HF, Atria arrhythmias

Beta Blockers - decrease HR + decrease Renin
- Propanolol, Atenolol

Non-Dihydropyridine Ca channel blockers - CLASS IV
- Verapamil

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10
Q

Whats atropine

A

Anticholinergic - nonselective muscarinic blocker

- block vagus nerve - block M2 @ heart increases SA increases HR

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11
Q

Whats abnormal automaticity

A

Other cells firing spontaneously other than SA node

- giving ectopic beats - giving tachycardia

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12
Q

Whats triggered activity

A

Heart cells contract twice - afterdepolarizations - tachycardia

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13
Q

Whats re-entry

A

Scar related or Abnormal AV connections

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14
Q

Whats fibrillations

A

Very rapid irregular contractions

  • disorganized activity;
  • AF, VF - tachycardias
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15
Q

How does TC and BC lead to decreased CO

A

BC: decreased HR
TC: increased HR but decreased SV due to filling time

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16
Q

Whats depolarization and whats + current

A

Depolarization - more positive membrane potential

+ Current - exiting cell

17
Q

Whats QT interval

A

Start of Q to end of T wave

- ventricular systole including ventricular depolarization and repolarization

18
Q

Major Drug Classes

I, II, III, IV

A

I - Sodium block
II - beta blocker
III - K+ block
IV - Ca2+ block

19
Q

Class I drugs

MOA
- effect on APD, ERP

A

Block sodium - Sodium involved in Phase 0

  • slower upstroke, make slope of Phase 0 gentler
  • hence both decreases automaticity

Procainamide -Ia

  • APD increased
  • ERP increased

Lidocaine - Ib

  • APD decreased
  • ERP ehhh

Flecainide - Ic

  • APD minor
  • ERP much increase
20
Q

Whats automaticity

A

Induction of action potential wo stimulation

21
Q

Class II

MOA
Use

A

Beta Blockers - Propranolol

  • beta - cAMP - PKA activation
  • in heart PKA increases Ca2+ conc
  • Diminishes Phase 4 depolarization
  • flattens and delays threshold before Phase 0 upstroke
  • Delays AV conduction, reduces automaticity

Decrease HR, contractility
USE: tachycardia, used to reduce mortality after MI

22
Q

Class III

MOA
AE

A

K+ blocker - Amiodarone

Prolong Phase 3
- Long ERP, AE of heartblock

23
Q

Class IV

MOA

A 
Non DHP (more cardiac than vasodilatory function) 
Ca blocker - Verapamil

Block Phase 4 spontaneous depolarization, Shorten Phase 2

  • slow conduction, decrease automaticity - SAME AS Beta blockes
  • prolong APD, ERP

USE of Verapamil - block all VG Ca channel in heart and vessels hence vasodilation too

  • HI, Angina
  • Atrial TC/ Supraventricular TC

AE:
- hypotension

Note Verapamil is a non-dihydropyridine CCB

24
Q

Class V/other

A

Adenosine

  • Suppresses AV conduction - AV block
  • Stimulates K+ channel - to block Ca2+ channels

USE: SVTC/ATC

25
Q

Whats Procainamide

A

IA

26
Q

Whats Lidocaine

A

IB

  • Local anesthesia
  • IV arrhythmia
27
Q

Whtas Flecanide

A

IC

28
Q

Whats Propanolol

A

BB

29
Q

Whats Amiadarone

A

K+ blocker; Class III

30
Q

Whats Verapamil

A

Ca2+ blocker; Class IV

31
Q

Whats adenosine

A

AV blocker;

32
Q

Whats Minoxidil

A

K+ channel opener - for vasodilating @ Blood Vessels

Normally…

  • K+ depolarizes cell, Ca2+ enters
  • Ca-Cadmodulin
  • MCLK activated
  • Vasoconstriction

CVS (7 decks)

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