Antiarrythmias Flashcards
How does heart contract?
Depolarization. Changes resting membrane potential via Na, Ca, Cl, K. K intracellular (-), Na Extracelluar (+). 3 Na out 2 K in= change in potential
What does M gate means?
m=Activation gate at channels (intramembrane protein or phosophlipid). h= inactivation.
RESTING m= closed, h = open or closed
What is speed of Na and Ca channels state?
Na- fast, Ca-slow L channel more +
During ventricular contraction what is gate status?
Phase 0-Na/Ca m and h gate= OPEN QRS on EKG
What ion do SA and AV node depend for depolarization?
Calcium channels
Atria and ventricular rely on NA channels
What are phases seen in purkinje fibers?
Phase 1- Cl exit.
Phase 2- plateau, Ca in K out= contraction
Phase 3- rapid repolarizations K out T wave
Phase 4- resting Na out K in, flat in ventricle
How do pacemaker cells contract?
Depolarize via special hyperpolization ion channels. HYPERKALEMIA= SLOW PACEMAKER. HYPOKALEMIA=FAST PACEMAKER
How do formation disturbance affect arrhythmia mechanisms?
Affects slope of Phase 4 by 1. DEC slope d/t vagal stimulation, B-blockade bradycardia 2. INC slove d/t HYPOkalemia, B-stimulation fiber stretch, acidosis, INC HR
How do conductance disturbance affect arrhythmia mechanisms?
HYPERKALEMIA- extracellular potassium DEC APD (AP duration), slow impulse, DEC pacemaker rate, flattens Phase 4. HYPOKalemia- INC APD, INC pacemaker rate, INC Slope of phase 4
What is seen in fibers related to disturbing impulse conduction?
Normally conduction meet and extinguish each other.
IF a block d/t damage, pulses re-enter into tissue where impulse bifurcates
What exaggerate arrhythmia?
Ischemia, Hypoxia, Acidosis-formation issue, Excessive catehcholimines- Ca issue, Electoryles, Drug toxics, scarred stretced cardiac tissue- dec impulse geneation (SIMIlar to MSK injury)
How do anti-arrhythmic drugs DEC ectopic (outside) pacemaker activity?
- DEC conduction, excitably, INC APD
- Block Na or CA channels
- Prefer Phase 0 upstroke and Phase 2 plateau. NO binding during resting phase
- Reduce Phase 4 slope
Why does the EBM state antiarrhymics are poison with therapeutic effects?
At higher does, ischemia, hyperkalemia, and INC HR- the drugs can affect normal tissue-
What Drug class are Na channel blocker lengthen APD?
CLASS 1A- Discopyramidine, Quinidine, Procainamide (Double Quarter Pounder)
What Drug class are Na channel blocker that Shorten APD?
CLASS 1B- Lidocaine and Mexiletene (w/ lettuce and mayo)
What Drug class are Na channel blockers that slow bind to NA channel no effect APD?
CLASS 1C- Flecaine and Propafenone (Fries please)
What Drug class is Sympatholytic- reduce SNS/adrenerig/Epi/NE activity?
CLASS II- Propanol, Beta Block
Which Class prolongs refractory period, Prolongs APD, most blocking of outward K+ channels, thus HYPOkalemia, (less K outward, INC slope of Phase 4, less repolarization) INC APD, INC pacemaker Rate. BUT arrythmia may occur.)
CLASS III-Ibutilide, Solatol, Amiodarone, Dronedarone
Mr. Heme was DX w/ Afib has NO CVD, but has COPD and HTN. What class drugs are ideal for him?
BB and CCB (Class 4)
Mrs. Hart has A. Fib with LV dyfs and HF. Which drug is ideal for her?
BB and Digoxin, Amiodarone
** AVOID CB
If a pt has A.fib what 2nd line drug is ideal, but with Caution d/t SE?
Amiodarone.
**AVOID w/ COPD
What are MC used anitarrythmics?
BB, CCB and amiodarone. LEAST- LIDOcaine
This drug is Class 1A, with a-blockade vagolytic and blocks K channels, used for Malaria IV. Rare for Afib. flutter, WPW, VT?
Quinidine: USE; RATE ADE- 1. Ears, 2. vision,3. HYPOtension. 4. INC HR in a.fib d/t AV node. treat-digoxin CCB, BB
This drug is Class 1A, with a-blockade vagolytic and **ganglionic blockade, with a **metabolite the prolongs APD?
PROCAINAMIDE- USE- RATE VT, post MI (2nd line). INJ ONLY. ADE: Lupus, Agranulocytosis, MDD, Psychosis
(PRO crazy)
