Dysrythmia and HTN Drugs Flashcards
Dromotropism definition
Ability to alter the rate of electrical conduction
Refractoriness
Inability of a cell to receive and transmit an action potential
Action potential duration
The time between phase 0 of one action potential to the next.
Increased length = decreased heart rate
Decreased length = increased heart rate
Effective refractory period
Time between phase 0- phase 3 in which the cells cannot initiate another action potential.
Relative refractory period
Time between phase 2-3 in which the cells cannot initiate another action potential except within the presence of an extreme stimulus
What is the normal threshold potential of an AV node action potential?
Approximately -65 mv
Sympathetics influence what cardio tissues?
All of them
- SA/AV nodes: epinephrine binds to B1 receptors, increasing the Ca2+ inward current causing an increasing rate of repolarization in phase 4 (funny current)
- causes tachycardia*
Atrial tissue: epinephrine binds to B1 receptors causing an increasing Ca2+ inward current which results in an increased conduction velocity and contractile
(Positive dromotropic and inotropic effects)
His/purkinje tissues: similar to atrial tissues
Delayed After Depolarizations (DADs)
Appear due to an abnormally elevated intracellular concentration of Ca2+.
At low rates of stimuli (brachycardia), the DADs skip ventricle depolarization since the threshold potential cannot be reached
At high rates of stimuli (tachycardia), the DADs produce spontaneous ventricle depolarizations causing v tachycardia.
Parasympathetics influence which cardiac tissues?
SA/AV node and atrial tissues
- SA/AV: acetylcholine produces a bradycardia effect by increasing phase 3 potassium out of the cell.
- decreases rate of repolarization during phase4*
Atrial tissues: acetylcholine increases the rate of conduction through the atrial muscle (positive dromotropic effect).
NOT ventricular tissues
What is the most common etiology of dysrhythmia?
Acute MI
Ventricular recently
A phenomenon that occurs when ischemic or scar tissue forms, or a boundless of Kent, along the normal conduction pathway.
Action potentials that are post-ERP cant go the normal pathway will ;try to redirect the pathway.
Class 1 dysrhythmic agents
Are all Na+ channel antagonists (blockers)
- blocks the non-nodal (ventricular) conductive tissue in phase 0
Effects:
- slows depolarization (lowers Vmax of phase 0)
- negative dromotropy
- lengthens QRS and QT intervals (1a especially increases QT)
- increases ERP/APD ratio (except lb)
Class 2 dysrhythmic agents
Are all B-blockers (B-adrenergic antagonists)
Class 3 dysrhythmic agents
Are K+ channel antagonists (blockers)
- block all types of cardiac tissue in phase 3
Class 4 dysrhythmic agents
Similar to class 2 except block calcium channels instead of B1 or B2 receptors
class 1a dysrhythmic agent effects (quinidine, procainamide, disopyramide, hydralazine)
moderate binding to the Na+ channels
- also block the potassium channels , delaying repolarization.
- can induce calcium blocking but only at very high doses
Effects:
- prolongs QRS complex
- prolongs QT intervals and valgus nerve effects
- slows phase 0
- increases ERP/APD ratio
Used to treat PVCs, V tach, atrial fibrilation (w/out WPW)
ADRs:
- can induce torsades
- cinchonism (tinnitis, hearing loss, blurred vision)
- hypotension
- SLE in slow acetylators of 1a drugs
Special populations to pay attention to:
- patients who are slow acetylators of 1a drugs
- renally impaired (must lower dosage)
Class 1b dysrhythmic agent effects
Lidocaine, tocainide
Weakest binding to the sodium channels. Actually accelerate the repolarization of conductive tissue (rapid “on-off” kinetics)
Effects:
- shortens the ERP/ADP ratio
- QT interval is shoterned
- no change in QRS
- positive inotropic and dromotropic effects
- MOST EFFECTIVE FOR DIGITALIS and MI INDUCED DYSRHYTHMIA
- also treat V tachycardia, premature ventricular beats and preventing V. Fibrillation
ADRs:
- hypersensitivity
Class 1c dysrhythmic agent effects
Encainide, flecainide, moricizine, propafenone
Strongest blockers of NA+ channels (“slow on-off” kinetics)
Effects:
- strong effects on phase 0 of the action potential of conducting tissues
- lengthen QRS and APD
- no change QT
- CAN STOP HEART THEREFORE ONLY LAST RESORT
MOST USEFUL FOR NON-MI INDUCED VENTRICULAR DYSRYTHMIAS
ADRs:
- prodysrthmic
- hypersensitivity
Class 2 agent effects
Propranolol, acebutalol, esmolol, metoprolol
Bind to B receptors and act as antagonists (also block calcium to a small degree since B-receptors are bound to calcium channels)
Effects:
- inhibit sympathetic activation (NE release)
- decrease Heart rate and cardiac output (negative chronotropic and inotropic)
- slight decrease on stroke volume
- AV nodal conduction is decreased (prolongs PR interval)
- AV nodal refractory is increased (prolongs PP interval)
MOST EFFECTIVE ON SUPRAVENTRICULAR AND DIGITALIS INDUCED DYSRHYTHMIAS AND HTN*
ADRs:
- hypotension
- asystole (@ high doses)
- bronchospasm
- rebound withdrawal (if not removed slowly will cause hypertensive crisis)
Specific patient populations to note:
- contraindicated in pregnant patients
- contraindicated in diabetics
Class 3 agent effects
Amiodarone, ibutilide, sortalol, dofetilide
Prolong repolarization by altering phase 3 of conducting cells and blocking potassium channels.
- amiodarone also can block sodium,calcium and B-receptors*
Effects:
- decrease effluent of K+ (prolonged ERP in all cardiac tissue)
- prolonged QT interval
- no effect on QRS complex
MOST USED FOR A/V FIB AND A FLUTTER.
ADRs:
- pulmonary toxicity
- elevated liver enzymes
- induces thyroid tumors/hypothyroidism
- photosensitivity
- can induce torsades
Certain populations to take note:
- contraindicated in liver impaired patients
- COPD patients (can still use just monitor)
Quinidine specifics
Class 1a drug
- used for atrial flutter/fibrillation, supraventriclar tachycardia, paroxysmal atrioventricular junctional rhythm, atrial/ventricle tachycardia
Effects:
- inhibit Na+ channels moderately (fastchannels only)
- increases ERP
- increases action potential duration
- prolongs QRS and QT intervals
- decreases membrane excitability and automaticity
Pharmacokinetics
- P.O 200-400mg every 4-6 hrs
Adverse effects: (33% of people will discontinue use)
- can causes cinchonism (tinnitis, hearing loss, blurred vision)
- excessive doses cause AV blocks, tachy dysrhythmia
- torsades de pointes via QT prolongation
- hypotension (blocks a1 receptors)
Procainamide specifics
Class 1a used primarily for PATs, A fib/ A flutter (especially prophylacticly)
- 2nd line behind Quinidine.
- can also be used for ventricular tachycardias however not the best
Effects:
- inhibits sodium channels moderately
- does not enter the CNS
PK: metabolized through hepatic N-acetyltransferase activity
- low acetylator activity patients will take longer to metabolize drug and can induce SLE
ADEs:
- arthralgia, fever, pericarditis, skin lesions, lymphadenopathy, anemia, hepatomegaly
- SLE like syndrome if slow acetylator
- torsades (prolongs QT) (less likely to happen compared to quinine)
Lidocaine specifics
Class 1b agent
MOA:
- inhibits sodium channels and inhibits reentry mechanisms (inhibits spontaneous depolarizations in ventricles) through fast sodium channels
- acts preferably on ischemic tissue and shortens the ERP (allowing the normal conduction pathways to work again)
- decreases excitability in ischemic tissue and increases excitability in healthy tissue
*Excellent use in post-MI or digoxin-induced tachycardia (especially if PVCs are present)
Pharmacokinetics
- IV dosage only and metabolized through liver. (be careful in patients with cirrhosis of liver since its half live is more than doubled)
Adverse side effects:
- mild CNS effects and hypersensitivity reactions only
