Flashcards in Drugs-Cardiac Rhythm Deck (68):
Class I drugs
Class II drugs
Class III drugs
Class IV drugs
Ca Channel Blockers
What channels does class IA block
What is a class IA drug?
What kinds of tissues do class I drugs work on?
What do class IA drugs do to AP duration?
What do class IA drugs do to resting potential?
What do class IA drugs do to excitability?
What channels does class IB block?
What is a class IB drug?
What does class IB do to excitability
Decrease, esp in depolarized tissue
What channels does IC block?
What is an example of IC drug?
What does class IC do to excitability?
What does class IC do to ERP?
Increase in fast tissue
What is an example of a class II drug?
What channel is affected by atenolol?
What kind of tissues do class II drugs work on?
Slow response tissue
What does atenolol do to sinus rate?
What does atenolol do to AV node ERP?
What does atenolol do to AV node excitation?
When are class I drugs most potent?
In cells with depolarized resting membrane potential (this determines sodium blocking effect-->recover with repolarization).
More potent at faster HR because there is less time to repolarize and knock off the drug
Rank class I drugs from most potent to least
IC-->IA-->IB (least potent)
What factors increase the effect of Ik blockade on action potential duration?
-Low extracellular K+ or Mg
What channels does class III drugs block?
Delayed rectifier K+
What is an example of a class III drug?
What kinds of tissues do class III drugs work on?
What do class III drugs do to the ERP?
Increase in fast tissue
What kind of tissue does class III drugs work on?
What do class III drugs do to the AP duration?
What channels do class IV drugs work on?
block Ca2+ channels
What types of tissues do class IV drugs work on?
What is an example of a class IV drug?
What does verapamil do to the sinus rate
What does verapamil do to the AV node ERP?
What does verapamil do to the AV node excitability?
What is digoxin?
Blocks Na/K pump, muscarinic receptor agonist, so it increases vagal tone
What does digoxin do to the Ca current?
What does digoxin do to the KAch current?
What are the consequences of digoxin's KAch current actions?
hyperpolarization of AV and SA nodes
What does digoxin do to the sinus rate?
What does digoxin do to the AVnode ERP?
What does digoxin do to the AVN excitability
What is adenosine?
Adenosine or purinergic receptor agonist
What channels does adenosine work on?
Dec Ca current and increases KAch current
What types of tissue does adenosine and digoxin work on?
Which classes of drugs work on fast response tissue?
II and IV
Which classes of drugs work on slow response tissue?
I and III (directly on Ca channels), digoxin and adenosine (work by enhancing parasympathetic/reduction of sympathetic stimulation)
Which drug has a positive inotropic effect?
Digoxin (all others have negative ionotropic effects)
Which drug is IV only?
Is digoxin slow or fast acting?
Which arrhythmias involve fast tissue?
-Some AV reentry
Which arrhythmias involve slow tissue?
-AV nodal reentry
What do we use class I drugs for?
Ventricular tachy, a fib, some AV reentry
What do we use class II drugs for?
AV reentry, AVN reentry
What do we use class III drugs for?
Vent tachy, a feb, AV reentry
What do we use class IV drugs for?
What do we use digoxin for?
What do we use adenosine for?
What is an excitable gap?
Amount of time tissue is excitable (ie if it's long, it has recovered and can form an AP)
What is a low safety factor?
Does not require much stimulation to cause an AP
What are 2 ways to cause block in a fast response re entrant circuit?
1. Prolong ERP to cause refractory block
2. Depress excitability to cause fixed block
What drugs do we use for AV re entrant tachy?
IA, III (block bypass tract by prolonging ERP)
Adenosine, atenolol, digoxin (prolong AV refractory)
How do we know if we blocked re entrant or AV node?
On EKG, the p wave associated with the last QRS will be before the QRS if blocked re entrant and after if blocked AVnode
(this makes sense! with reentry here, the impulse goes down the AV node and up the accessory pathway. If you block the AV node, the P wave will be after the accessory pathway up from the ventricles, if you block the accessory, the P wave comes before the ventricles contract)
Post Mi, what ERP and safety factors do the dead tissues have?
Longer ERPs and lower safety factors