Arrhythmia Flashcards
Function of AV node
Delay - to allow ventricles to fill up
Decremental property - protect from high atrial rates
Intrinsic pacemaker rates of
SA
AV
Ventricular Muscles
60-100
40-60
20-40
Transplanted heart HR is higher/lower
Higher due to lack of parasympathetic control
- still responses to exercise but delayed
Cells ICF higher/lower than ECF
Sodium
Potassium
Calcium
Sodium lower
Potassium higher
Calcium lower
Describe Phases of Cardiac Muscle Action Potential
Phases 4 0 1 2 3
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
Absolute Refractory Period
- phase 0 1 2 3
- whats the function
Prevent second action potential initiation
- protect against tetanus
Whats sinus rhythm
Normal regular rhythm
- P wave followed by QRS
What arrhythmia causes are there
Too Slow [2]
Too Fast [4]
- subcategories
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
Drugs which can cause Bradycardia and their MOA
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
Whats atropine
Anticholinergic - nonselective muscarinic blocker
- block vagus nerve - block M2 @ heart increases SA increases HR
Whats abnormal automaticity
Other cells firing spontaneously other than SA node
- giving ectopic beats - giving tachycardia
Whats triggered activity
Heart cells contract twice - afterdepolarizations - tachycardia
Whats re-entry
Scar related or Abnormal AV connections
Whats fibrillations
Very rapid irregular contractions
- disorganized activity;
- AF, VF - tachycardias
How does TC and BC lead to decreased CO
BC: decreased HR
TC: increased HR but decreased SV due to filling time
Whats depolarization and whats + current
Depolarization - more positive membrane potential
+ Current - exiting cell
Whats QT interval
Start of Q to end of T wave
- ventricular systole including ventricular depolarization and repolarization
Major Drug Classes
I, II, III, IV
I - Sodium block
II - beta blocker
III - K+ block
IV - Ca2+ block
Class I drugs
MOA
- effect on APD, ERP
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
Whats automaticity
Induction of action potential wo stimulation
Class II
MOA
Use
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
Class III
MOA
AE
K+ blocker - Amiodarone
Prolong Phase 3
- Long ERP, AE of heartblock
Class IV
MOA
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
Class V/other
Adenosine
- Suppresses AV conduction - AV block
- Stimulates K+ channel - to block Ca2+ channels
USE: SVTC/ATC
Whats Procainamide
IA
Whats Lidocaine
IB
- Local anesthesia
- IV arrhythmia
Whtas Flecanide
IC
Whats Propanolol
BB
Whats Amiadarone
K+ blocker; Class III
Whats Verapamil
Ca2+ blocker; Class IV
Whats adenosine
AV blocker;
Whats Minoxidil
K+ channel opener - for vasodilating @ Blood Vessels
Normally…
- K+ depolarizes cell, Ca2+ enters
- Ca-Cadmodulin
- MCLK activated
- Vasoconstriction
