Antiarrhythmics Flashcards
(46 cards)
1
Q
sodium channel types
A
- M gate = activation
- H gate = inactivation gate
- resting membrane potential = -90
- Both activation and inactivation gates have to be open for there to be flow
2
Q
Phases of Action Potential
A
- phase 0: Na into cell through activated Na channel (m gate open, h gate open) - corresponds to QRS complex
- phase 1: Cl exit (overshoot)
- phase 2: plateau - Ca in, K out (CONTRACTION OCCURS)
- phase 3: rapid polarization - K out; corresponds to T wave
- phase 4: resting - Na out and K in
- depolarization is more dependent on Ca than Na
3
Q
SA and AV node vs atrial and ventricular tissue
A
- slow depolarization through Ca channels, slow response action potentials
- rapid depolarization through Na channels and gates
4
Q
pacemaker cells
A
- depolarization due to funny channels (hyperpolarization activated ion channels
- occurs in both normal and ectopic pacemaker cells
- High potassium slows or stops pacemaker
- Low potassium facilitates pacemaker
5
Q
effect of elevating the threshold potential
A
- Na+ inactivation gates close between –75mV and –55 mV
- APD evoked at –60mV have less Na+ channels “available” than at –80mV
- Vmax: slope or rate of rise of phase 0
- less negative threshold → slower Vmax (slope or rate of rise of phase 0) → decreased AP amplitude → decreased excitability → decreased conduction velocity; also prolonged recovery time
6
Q
Action potential duration (phases)
A
phases 0-3
7
Q
Effective refractory period
A
-ERP - will not propagate another stimulus
8
Q
Mechanisms of arrhythmias
A
- impulse FORMATION disturbance
- impulse CONDUCTION disturbance
- both
9
Q
Factors that will slow HR
A
vagal stimulation, beta blocker → slope of phase 4 decreases (also potentially more negative repolarization) - bradycardia because it takes longer to reach threshold
10
Q
Factors that will increase HR
A
hypokalemia, beta stimulation, fiber stretch, acidosis → slope of phase 4 increases
11
Q
early after depolarization
A
- during phase 2 or 3
- d/t reduced membrane potential
- worse with low K, low Ca, acidosis
- exacerbated by bradycardia (torsades de pointes)
12
Q
delayed after depolarization
A
- during phase 4
- d/t excess intracellular Ca
- exacerbated by tachycardia; arrhytmias d/t digitalis, catecholamines, myocardial ischemia
13
Q
factors that exacerbate arrhythmia
A
- ischemia
- hypoxia
- acidosis, alkalosis
- electrolyte abnormalities
- excessive catecholamine
- drug toxicity (digoxin, other antiarrhythmics)
- overstretching of cardiac tissue
- scarred/diseased cardiact tissue
14
Q
MOA of antiarhythmic drugs
A
- reduce ectopic pacemaker activity
- decrease conduction, excitability, and increase APD in depolarized cells (moreso than normally polarized cells)
- done by blocking Na and Ca channels of depolarized cells
- high affinity for activated (phase 0) and inactivated (phase 2) channel - poor or no drug-binding during “rested” state
- prolong channel recovery time (increase refractory period)
- early extrasystoles unable to propagate or do so more slowly → bidirectional block
- most reduce phase 4 slope
- at higher doses, these drugs can also affect NORMAL tissue!! → drug induced arrhythmias
15
Q
MOA of Class 1
A
- Na channel blockage → inhibit Na transport, membrane stabilizer, decrease Vmax
- 1A: lengthen APD, intermediate action on Na channels
- 1B: Shorten APD, rapid binding to Na channels
- 1C: No effect or small increase APD, slow binding to Na channels
16
Q
MOA of Class 2
A
-Sympatholytic - reduce adrenergic activity; beta blockade
17
Q
MOA of Class 3
A
-Prolongs effective refractory period; prolongation of action potential duration by blocking outward or augmenting inward currents; most block potassium currents
18
Q
MOA of Class 4
A
-Block calcium currents; slows conduction and increase refractory period in Ca-dependent tissues
19
Q
How do B blockers work for arrhythmias
A
- decrease slope of phase 4
- membrane stabilizing effects (propranolol)
20
Q
B blocker uses
A
- Post-MI: reduce death rate and sudden death rate (atenolol, metoprolol, propranolol)
- tx of thyrotoxicosis, pheochromocytoma, surgery, catecholamine excess
- afib/flutter: reduces the ventricular response rate (metoprolol, propranolol) → RATE CONTROL, block primarily at AV node
21
Q
hyperkalemia effects
A
- resting potential depolarizing action
- membrane potential stabilizing action due to increased K+ permeability
- end result: depressed ectopic beats, slow conduction (severe hyperK slows SA node)
22
Q
hypokalemia effects
A
-increased EAD and DAD, and ectopic pacemakers (esp with digoxin)
23
Q
Magnesium MOA, Use, and dose
A
- MOA: not well understood
- Use: digoxin-induced arrhythmias if Mg low; TdP and AMI, including with normal Mg
- Dose: 1-2gm diluted in 50-100cc given over 20 minutes
24
Q
Epinephrine
A
-For VF/pulseless VT arrest; vasoconstrictor; may cause tachy, HTN
25
Vasopressin
-potent vasoconstrictor at high doses
26
Atropine
-for bradycardia; parasympatholytic effect; may cause dry eyes, dry mouth, urinary retention, tachycardia
27
dopamine
-effect depends on dose; increases renal blood flow → increases heart rate, + inotrope → HTN; may cause tachy, HTN
28
isoproterenol
-B 1 and 2 agonist; may cause tachy
29
Drugs for post-MI
- beta-blockers improve survival
| - amiodarone reduces arrhythmic death but NOT overall mortality
30
Drugs for HF - sudden cardiac arrest or sustained VT
- ICD > surgical ablation, antiarrhythmic alone
- amiodarone
- sotalol or mexilitine
31
AF etiology
- structural cardiac defect, CAD, HF
- holday heart, caffiene, sympathomimetics, COPD, PE, thyrotoxicosis, electrolyte abnormalities
- AF: atria 350-600 bpm, ventricle 120-180 bpm
- mortality increased; risk for CVA without valvular disease 5x increase, with valvular disease 17x increase
32
AF sx
-palpitations, exertional fatigue, lightheadedness, dyspnea, exercise intolerance
33
Paroxysmal AF
- self-terminating or intermittent
- recurrent AF (greater than/equal 2 episodes) that terminates spontaneously in seven days or less, usually less than 24 hours
34
Persistent AF
- AF that fails to self-terminate in 7 days
| - episodes often require pharmacologic or electrical cardioversion to restore NSR
35
Permanent AF
-individuals with persistent AF where a decision has been made to no longer pursue a rhythm control strategy
36
most common and devastating complication of atrial fibrillation
STROKE
37
3 important aspects of AF care
- ventricular rate control
- consider conversion to NSR
- Stroke risk - anticoagulation
38
CHADS2 score
-stroke risk in AF
39
rate vs rhythm control: which is more important
- rhythm control strategy not superior to rate-control strategy
- therapy based on each patient's symptoms and disease
- management options for AF include rate control, stroke prevention, and maintenance of NSR
40
goals of rate control
- reduce symptomatic palpitations
- improve ventricular performance, exercise capacity, hemodynamics
- prevent (reverse) tachycardia-related cardiomyopathy
41
Ventricular rate goals
- 60-80 bpm at rest or >20% decrease from baseline with symptoms relief
- 90-115 bpm with exercise
- if no structural heart dz, resting HR <110 bpm
42
Drugs for Rate control
- digoxin:may convert AF → NSR
- BB: control rate via slow AV node conduction; both at rest and exercise; DOC thyrotoxicosis and post-cardiac surg; not good for HF
- CCB: effect on slow Ca channels; control at rest and exercise; can reduce BP, can pre-tx with IV calcium if low BP or LV dysfxn; pretx with Ca not affect chronotropic effects
- long-term control goals: resting < 90bpm, exercise < 140bpm, < 60 - excessive tx
43
goals of rhythm control
- restore NSR
- maintain NSR, prevent recurrence of AF
- Reduce frequency of AF episodes, suppress symptoms, improve tolerability of recurrence, improve exercise capacity, hemodynamics
- prevent (reverse) tachycardia related cardiomyopathy
- limit drug toxicity
44
Acute rhythm control
- direct cardioversion
- flecainide, dofetilide (hosp only d/t prolonged QT), propafenon, and IV ibutilide; oral amiodarone reasonable alternative (less EBM)
- propafenon or felcainide (pill in the pocket) in addition to BB or nondihydropyridine CCB is reasonable to terminate AF outside hospital once tx has been observed to be safe
- dofetilide: APD prolongation less at higher freq, increased at lower; therefore, convert Aflut > afib, must convert in hosp, ltd use
- role in AV-nodal ablation and pacing can produce good results in sx pts, but could lead to pacemaker dependency and leave pt in permanent AF
45
Conversion to NSR if Afib present > 48hrs
- warfarin, maintain at therapeutic INR x3 wks prior, and 4 weeks after
- ~25% of pts convert from persistent AF → NSR at 1 yr. 50% revert within first week, 90% by 6 mos
- anti-coag - 4 weeks prior bc takes time for atrial fxn to return
46
Conversion to NSR
- electrical and structural remodeling over time: PAF → AF
- electrical cardioversion 80-90% convert: less likely to convert with AF long duration, pts with greater weight, idiopathic dilated cardiomyopathy
- chemical conversion more effective if AF recent onset (<7 days; best if <24hrs)
- PSVT: Ca antagonists and adenosine (usu re-entry via AV node)
- Afib: class I
- Aflutt: Class 3
- termination of arrhythmia: shock, drugs if shock fails
- maintenance: decreasing use
- stable VT: monomorphic: procainamide, sotalol; poor EF: amiodarone, lidocaine
- stable VT: polymorphic: normal QT: BB, lidocaine, amiodarone, procainamide, sotalol
- stable VT: polymorphic: prolonged QT: isoporterenol, phenytoin, lidocaine
- prevention sudden death: BB, amiodarone
