Cardiac Drugs and Drug Classes Flashcards
SA node rate
70-80
AV node rate
40-60
Purkinje fibers rate
15-40
classification of arrhythmias (4)
- site of origin (atrial/junctional/ventricular)
- complexes on ECG (narrow/broad)
- heart rhythm (regular/irregular)
- heart rate is increased or decreased
mechanisms of arrhythmia production: altered automaticity
latent pacemaker cells take over the SA node’s role ex) escape beats
mechanisms of arrhythmia production: delayed after depolarization
normal action potential of cardiac cell triggers a train of abnormal depolarizations. main cause: increased calcium with train action potentials, called an “R on T phenomenon”
mechanisms of arrhythmia production: re entry
refractory tissue reactivated repeatedly and rapidly due to unidirectional block, which causes abnormal continuous circuit. ex) wolf parkinson white syndrome is an example, caused by accessory pathway conduction
mechanisms of arrhythmia production: conduction block
impulse fail to propagate in non conducting tissue. ex) LBBB, RBBB. usually due to ischemia, scarring, and fibrosis
factors underlying cardiac arrhythmias
arterial hypoxemia electrolyte imbalance acid base abnormalities myocardial ischemia altered SNS activity bradycardia administration of certain drugs enlargement of failing ventricle
causes of intraoperative rhythm disturbances: transient imbalances
stress: electrolyte or metabolic imbalance
laryngoscopy, hypoxia, hypercarbia
device malfunction, micro shock
diagnostic or therapeutic interventions (pacers, ICD)
surgical stimulation
CVC
when do cardiac arrhythmias require treatment (3)
- cannot be corrected by removing precipitating cause ex) fluid for FVD
- hemodynamic instability
- disturbance predisposes to more serious cardiac arrhythmias or co morbidities
non pharmacological treatment options
acute: vagal maneuvers, cardioversion
prophylaxis: ablation (EP lab), implanted defibrilator
pacing: external, temporary, permanent
Vaughan Williams Classification of Antiarrhythmic Drugs
Class 1 (A, B, C): sodium channel blockers (Phase 0) Class 2: beta adrenergic blockers (Phase 4) Class 3: potassium channel blockers (Phase 3) Class 4: calcium channel blockers (Phase 2) Class 5: unclassified drugs (unknown mechanisms)
Class 1 Agents MOA, ion targeted, and uses for tx
Class 1 agents are characterized by how quickly they dissociate from Na channel (A, B, C)
Block Na Channels with depresses phase 0 in depolarization of cardiac AP.
Decreases AP propagation, decreases depolarization rate, slows conduction velocity
Binds to sites on alpha subunits
Binds most strongly when Na channels are either in the open or activated state. Less strongly in the inactivated state.
Tx: SVT, Afib, WPW syndrome
Class 1A Agents MOA, ion targeted, elimination, SE, uses
slows conduction velocity and pacer rate
intermediate Na channel blocker (intermediate dissociation)
direct depressant effects on SA and AV node
decreased depolarization rate (phase 0)
prolonged repolarization (because also blocks K channels to some degree)
increased AP duration and effect of refractory period
decreased automaticity, increased QT duration (phase 0 to end of phase 3 in ventricular AP)
elimination: hepatic
se: reversible lupus like syndrome
used for: atrial and ventricular dysrhythmias
Class 1A Agents (3) and note*
Quinidine, Procainamide, Disopyramide. (these drugs are not commonly used due to toxicity and may precipitate heart failure)
Disopyramide class, use, route of administration, SE
class 1A, suppresses atrial and ventricular tachyarrhythmias, oral agent, has significant myocardial depressant effects and can precipitate congestive HF and hypotension. SE can include anticholinergic effects
Procainamide class, use, dose, therapeutic window, T1/2, protein binding, SE
class 1A, used in treatment of ventricular tachyarrhythmias (less effective with atrial)
dose: loading 100mg IV every 5 minutes until rate controlled (max 15mg/kg), then infusion 2-6mg/min
therapeutic window, 4-8mcg/ml
T1/2 2 hours
15% protein bound
SE: myocardial depression leading to hypotension, syndrome that resembles lupus erythematous
Class 1C agents (2)
flecainide (prototype), propafenone (oral)
Class 1C Agents MOA, uses
slow Na channel blocker (slow dissociation), so does not vary much during the cardiac cycle.
potent decrease of the depolarization rate of phase 0 and decreased conduction rate of cardiac impulses with increased AP
markedly inhibit conduction of AP through his-purkinje system
uses: atrial arrhythmias, PVC’s, vtach
flecainide chemical structure, class, use, route of administration, SE
fluorinated local anesthetic analogue of procainamide
class 1C
effective in tx of suppressing vtach, atrial tachyarrhythmias, WPW syndrome, delays conduction in bypass tracts so its good for reentry rhythms and therefore good for afib prophylaxis
PO
has pro arrhythmic SE
propafenone class, use, route of administration, SE
class 1C
suppression of ventricular and atrial tachyarrhythmias
PO
has pro arrhythmic SE’s (torsades, vfib)
Class 1B agents (3)
lidocaine (prototype), mexiletine, phenytoin
class 1B agents MOA, uses, unique characteristic of these agents
fast Na channel blocker (fast dissociation) alters AP by inhibiting Na ion influx via rapidly binding to and blocking sodium channels (fast) produces little effect on maximum velocity depolarization rate, but shortens AP duration and shortens refractory period decreases automaticity shortens repolarization and refractory period, decreases AP binds to open channels and dissociates quickly, in time for the next AP but premature beats still blocked little effect on max velocity and depolarization use: ventricle arrhythmias but not vfib post MI this class is unique because it also binds to ischemic cells to decrease activity in these cells while others dont.
Lidocaine class, uses, dose, route of administration, protein binding, metabolism, elimination
class 1B, used in tx of ventricular arrhythmias, particularly effective in suppression reentry rhythms, vtach, PVC’s, delays phase 4. not good for SVT, vfib after acute MI.
dose: 1-1.5mg/kg IV, infusion 1-4mg/min (max dose 3mg/kg)
extensive 1st pass PO so only given IV
50% protein binding
hepatic metabolism
active metabolite, prolongs elimination T1/2, 10% renal elimination
not pro arrhythmic but dissociates so quickly
Lidocaine metabolism considerations
metabolism may be impaired by drugs such as cimetidine and propranolol, or physiologic altering conditions such as CHF, acute MI, liver dysfunction, GA, or can be induced by drugs like barbiturates, phenytoin, or rifampin (CYP450)
