Arrythmias 1 Flashcards
Normal Electrocardiogram (ECG)
PQRST
- Normal PR interval
- Normal QRS complex
- Normal QT interval
- 0.12-0.2 sec
- 0.04 - 0.14 sec
- < 0.42 sec
Ventricular AP : WHats the influx, whats the efflux?
Nodal Tissue : Whats influx, whats efflux?
- Sodium influx, Potassium Efflux
- Calcium influx, Potassium Efflux
Abnormal Impulse Generation –Automatic Tachycardias
- What can cause this?
- If the rate of impulse generation from “latent” pacemaker cells is > rate of SA node, what starts?
- What are some causes of Incr Phase 4 Slope?
- Incr in phase 4 slope causing heightened automaticity of “latent” pacemaker cells
- An arrhythmia
- Digitalis, or catecholamines
Hypoxemia
Electrolyte imbalance (hypokalemia)
Fiber stretch (Cardiac dilation)
Abnormal Impulse Generation - Triggered Automaticity
Occur prior to phase 4 :
1) During repolarization (Early after depol , EADS)
-Caused by ? (3)
2) After repolarization (Delayed after depolarization , DADs)
-Caused by ? (2)
- hypokalemia
class 3 and 1a AAD’s
-Slow stimulation rates - Digitalis or catecholamines
-can be suppressed by Calc Channel Antags
Name 4 ways that AAD’s can slow automatic Rhythms ?
- Altering phase 4 slope
- increasing threshold potential
- Incr maximum diastolic potential
- incr AP duration
Class 1 AAD (1A, 1B, 1C)
1. Predom effect is to ?
2. Slows ___
3. How does each class affect the ventricular AP?
- block the fast inward Na+ channels leading to a decr in the depolarization rate of phase 0
- intra-cardiac conduction
- 1a has moderate Na channel block, and prolonged repolarization
-1b has mild Na channel block, and shortened repolarization
-1c has MARKED Na channel block, and no change in repolarization
Which drugs are in class 1A, 1 B and 1C?
1A : Disopyramide, Quinidine, Procainamide
1B : Lidocaine, Mexiletine
1C: Flecainide, Propafenone
Class 1 A
1. Broad spectrum AAD meaning it can help with which 2 Arrhythmias ?
2. CLass Electrophys effects ?
-Widen ___
-Lengthen ____
-Lengthen ____
-No or slightly lengthen ___
3. Part of EP effects can be attributed to ?
4. ALL are effective in suppressing ?
5. In re-entrant tachycardias, they produce ?
- Supraventricular and ventricular
- QRS
-QT interval (may induces TdP)
-Refractory period
- PR interval - K+ channel blockade
- Automatic tachycardias
- bidirectional block (by depressing conduction and prolonging refractoriness)
Disopyramide :
1. Used to maintain ___ in ___ or __
2. Used to prevent recurrence of ___ or ___
3. Prolongs __ and ___
4.Prominent ___ action = AE’s
5. Signif AE’s ? (6)
- Sinus rhythm, atrial flutter, fibrillation
- ventricular tachycardias , fibrillation
- QRS and QT interval
- anticholinergic action
- HYPOTENSION
-ANTICHOLINERGIC SYNDROME (Dry mouth, constipation, urinary retention, precip glaucoma)
-Gi upset
-Hypoglycemia
-PROARRHYTHMIAS (TdP )
-HF (Depression of cardiac contracility)
Quinidine
1. Maintains ___ in Afib or flutter and prevents recurrence of ?
2. Blocks ___ and multiple __
3. Prolongs ___, due to ?
4. Produces ___ and ___ **
5. AE’s (7)
- sinus rhythm , ventricular tach or fibrillation
- Na+ current, K+ currents
- Cardiac AP duration, K+ blocking
- Beta receptor blockade and vagal inhibition
- Cinchonism (D/N/Tinnitus, Visual changes, dizzi, HA)
-HYPOTENSION
-THROMBOCYTOPENIA
-Hemolytic anemia
-QT INTERVAL PROLONG AND TDP
-Proarrhythmia
-DIARRHEA
Procainamide
1. Used to treat ?
2. FOr acute tx? WHats no longer commerically available?
3. Procainamide (PA) and its Metab (NAPA)
-PA decreases ___, increases ___, slows __, and prolongs __ and ___
-NAPA lacks ___ but is equally potent in blocking ___
- Why must you use in caution with HF pt’s with reduced EF?
- Monitor PA and NAPA levels… wat are those levels?
- SUPRA and ventricular arrhythmias
- IV, PO version
- automaticity
-refractory periods
-conduction
-QRS and QT intervals
-NA+ blockade, outward K+ - Negative Inotrope
- PA = 4-8 mcg/mL
NAPA = 4-10 mcg/mL
Procainamide :
1. Eliminated rapidly by ?
2. AE’s ? (7)
- renal excretion , hepatic metabolism
- HYPOTENSION (IV USE)
-Nausea
-TDP! Particularly with NAPA accum
-LUPUS LIKE SYNDROME!!!!! (Test question) , this occurs more often and earlier during tx in “Slow acetylators”
-Bone marrow aplasia
-QT prolongation (less than quinidine)
-Fever
Class 1B : Lidocaine and Mexiletine
- COnsiderably more effective for ?
- Class EP effects
-No effect on __ and ___
-Decr in ___
-No effect on ___ - WHat accentuates its effects?
-Changes in pH alter time that lidocaine is bound to ? - Attractive for which pt’s?
- Ventricular arrhythmias
- QRS, QT length
- refractory period
- PR interval - Acidosis
- Na+ channel - Post -MI pt’s
Lidocaine
1. Reduces ___ and alters ___
2. It’s not really effective as ___ only 15-20% effective in pt’s with ___
3. Minimal effects on __ or __
PK
1. How is it metabolized ?
2. What affects Vd and CL?
3. WHat causes reduced CL?
4. Therapeutic levels?
- slope of Phase 4, threshold for excitability
- monotherapy. Monomorphic VT
- CO or BP
- Liver metabolized
- Heart failure
- Hepatic disease
- 1.5-5 mcg/mL
Lidocaine AE’s
- Levels > 5 mcg/mL
C,S,D,D,V,M,P,N,T - Levels > 9mcg/mL
P,S,R,S,B,C
- Confusion
slurred speech
dizziness
drowsiness
vertigo
muscle twitching
perioral numbness
Nausea
tinnitus - Psychosis
seizures
respiratory suppression
sinus arrest
bradycardia
complete heart block
Mexiletine
1. oral analog of ?
2. Modifed to reduce __ allowing for ?
3. EP effects are?
4. Approved for treating ?
5. NOT EFFECTIVE FOR ?
6. Often used in combo with other AAD’s such as ?
7. AE’s (4) or 2 major ones
- lidocaine
- first pass metab, chronic oral therapy (F = 90%)
- Similar to lidocaine
- Ventric arrhythmias
- atrial arrhythmias
- Sotalol or quinidine to incr efficacy while limiting ae’s
- CNS (Dizzi, tremor, ataxia, slurred speech, blurred vision , mem impairment, rarely psychosis or seizures)
-Pro arrhythmia
-GI upset
-Thrombocytopenia (rare)
Class 1C : Flecainide, Propafenone
- Class EP effects?
-Widen ___
-Lengthens?
-Decr?
-Lengthens? - Profoundly slows __
- Cannot be used in pt’s with ?!!!
- QRS interval
-QT interval (primarily via qrs widening)
-Conduction velocity
-PR interval - conduction velocity because of Slow association and dissociation with Na+ Channel
- Structural heart disease (LVH, CHF, CAD , s/p MI and to a lesser extent heart valvular lesions)
Flecainide (Tambocor)
1. Derivative of procainamide that does what?
2. Negative ___
3. effective for ?
4. CAUTION WHEN?
5. Currently used in ?
6. It profoundly slows ___
7. It blocks 3 currents (what r they)
8. In atrial tissue, What’s prolonged?
9. EP effects : Prolongs duration of ? (3)
- Na+ channel blocker
- Inotrope
- BOTH supra and ventric arrhythmias
- used for life threatening venrtric arrhythmias (Pro arrhytmic)
- in absence of structural hd, for maintenance of sinus rhythm in supraventric arrhythmias (AFIB)
- conduction velocity
- Na+current, Delayed rectifier K+ current, and Ca2+ currents
- AP duration prolonged at fast rates
- PR, QRS, and QT
Flecainide AE’s
1. P
2. B, D, L
3.n/v
4. Exacerbates ___ in pt’s with ___
5. __ in pt’s with pre existing conduction disease
- Proarrhythmic
- blurred vission , drowsiness, lightheadedness
- heart failure, depressed LEFT ventric function
- Heart block
Propafenone
- What channel blocker? some ___
- Structurally similar to ? but has weaker ___
-CI in ? - EP effects?
- ECG effects?
- Used primarily to maintain ??
- How is it eliminated ?
- Na+ channel blocker (Slow recovery)
-Some K+ channel blocker - Beta blockers
-Beta blocker activity
-COPD or Asthma - Slows conduction in fast response tissues
- prolongs PR and QRS duration
- Sinus rhythm in pt’s with SUPRAventricular arrhythmias (AFIB)
- Renal and hepatic (CYP2D6)
Propafenone AE’s
-P
-Worsening ___
-B
-C
-G
-M
Propafenone would better charlie’s general mind
Proarrhythmia
-CHF
-Bronchospasm
-CNS effects (blurred vision, dizzi , pre syncope)
- GI upset
-Metallic bitter taste
Class 2 AAD’s
1. Beta ADrenergic blocking agents like ?
2. Reduces inflow of ?
3. Increases AV nodal __ and prolongs AV nodal ___
- ____ in AFIB or flutter
- Class EP effects
-No effect on ?
-Incr ___On atrial and AV nodal tissues
-Decr __
-WIdened ___
- Propanolol , esmolol, metoprolol, carvedilol, acebutolol
- ca2+ into cell
- conduction time, refractoriness
- Ventricular RATE control
- QRS or QT interval
-Refractory period
-Conduction velocity
-PR interval
Esmolol
1. Selective ?
2. What admin method?
3. Used primarily to ?
4. Dosing ? LD, MD, Rebolus
- Beta 1 blocker
- IV only
- control ventric response in AFIB (rate control)
- Loading dose 500 mcg/kg IV over 1 minute
– maintenance dose 50 mcg/kg/min to start and may increase by 50 mcg/kg/min every 4 minutes until a maximum of 300 mcg/kg/min
– may rebolus w/ 500 mcg/kg before each dose increase
Class 3 : Name the 5 drugs
- Delays repolarization by ?
- Lengthens ___
-Increases ___
-Prolongs ____
Amiod, Dronedarone, Ibutilide, Dofetilide, Sotalol
- blocking k+ channels
- QT interval!!!
-refractory period
-cardiac AP