23 - Arrhythmias Flashcards
1
Q
Describe the myocardial action potential
A
- Phase 4 = small amount K+ exiting cell & Na+ & Ca2+ entering cell
- Phase 0 = lots of Na+ & little Ca2+ entering cell
- Phase 1 = lots of Ca2+ entering cell w/ some K+ exiting
- Phase 2 = some Ca2+ entering w/ more K+ exiting
- Phase 3 = lots of K+ exiting; slowly decreasing as getting closer to phase 4
2
Q
Pathogenesis of tachyarrhythmias
A
- Most common arrhythmias are combinations of both automaticity & re-entry
- Automaticity = abnormality in impulse generation; often starts arrhythmia
- Re-entry = abnormality in impulse conduction; often maintains arrhythmia
3
Q
Classification of anti-arrhythmic drugs
A
- 1a (sodium med) = quinidine, procainamide
- 1b (sodium fast) = lidocaine, mexiletine
- 1c (sodium slow) = flecainide, propafenone
- 2 (beta blockers) = metoprolol, atenolol
- 3 (potassium) = amiodarone, sotalol, ibutilide
- 4 (CCB) = diltiazem, verapamil – don’t really affect refractory pathway, so can’t take someone out of an arrhythmia, more so prevent arrhythmias
4
Q
Pharmacology of rate control agents
A
- Reduce automaticity to prevent or slow arrhythmias
- Class 2 (beta blockers) – reduce adrenergic stimulation of SA/AV nodes & decrease adrenergic stimulation of myocardial contractility
- Class 4 (non-DHP CCBs) – reduce calcium current & recovery in SA/AV nodes
- Digoxin (Na/K/ATPase blocker) – increase myocyte Na/Ca, decrease K, increase AV node refractory period; increases vagal tone & decreases SA/AV activity
5
Q
Pharmacology of rhythm control agents
A
- Reduce re-entry to prevent or stop arrhythmias
- Class 1 (sodium channel blockers) – decrease in conduction velocity; re-entry loop loses “steam” & SA node takes over
- Class 3 (potassium channel blockers) – prolonged refractory period; re-entry loop “catches its tail” & SA node takes over
6
Q
Which drugs are pure rhythm control agents?
A
- Quinidine – class 1a & potassium blocker (class 3)
- Sotalol – class 3 & beta blocker (class 2)
- Amiodarone – class 3 & Na, Ca, beta blocker (class 1, 2)
- Propafenone – class 1c & beta blocker
- Flecainide – pure class 1c, but high risk for VT in CAD
- Ibutilide/dofetilide – pure class 3, but high risk of Torsade de Pointes
7
Q
EKG of atrial flutter
A
Saw tooth pattern
8
Q
Describe what happens during atrial fibrillation
A
- Rhythm looks irregularly irregular (distance between QRS complexes is not the same) and no clear P waves on EKG
- Extremely fast (400-600 atrial beats/min) and disorganized atrial rhythm (irregularly irregular)
- AV node controls the pulses sent from atria to ventricles, so prevents 400-600 beats/min being sent to ventricle; if this didn’t happen then A. fib would be life-threatening
9
Q
Categories of A. fib
A
- Acute = first 48 h
- Paroxysmal = terminates spontaneously w/in 7 days
- Persistent = continues for > 7 days
- Permanent = doesn’t terminate even w/ cardioversion attempts
10
Q
Factors that may precipitate A fib
A
- High adrenergic tone (temporary) – alcohol withdrawal, sepsis, post-surgery, excessive physical exertion, digoxin toxicity
- Atrial distention (permanent & chronic) – ischemia, HTN, valvular disorder, cardiomyopathy, pulmonary embolism/HTN, obesity
11
Q
Signs & sx of A fib
A
- Signs = irregular pulse, HR > 100 bpm, hypotension, EKG
- Sx = asymptomatic, palpitations, dizziness, syncope, angina, HF
12
Q
Serious complications of A fib
A
- Tachycardia induced HF
- Severe hypotension/HF
- Embolic stroke
13
Q
Major goals of therapy for A fib
A
- Control rapid ventricular response (ventricular rate control)
- Restore normal sinus rhythm (atrial rhythm control)
- Prevent thromboembolic complications
14
Q
Drugs for ventricular rate control. What are the efficacy endpoints?
A
- If px has HF – beta blockers +/- digoxin
- If px has CAD – beta blockers (preferred) and/or non-DHP CCBs
- If px has no HF or CAD – beta blocker, non-DHP CCB, digoxin, or combination
- Efficacy endpoints – HR < 100 bpm & decrease in palpitations, dizziness, & SOB
15
Q
Safety endpoints for rate control
A
Bradycardia, AV block
16
Q
Safety endpoints for diltiazem/ verapamil
A
- BP < 100/60, HR < 60, CHF, edema, nausea, constipation, anorexia
- Interactions = 3A4 & P-GP inhibitors
17
Q
Safety endpoints for metoprolol/ atenolol
A
BP < 100/60, HR < 60, CHF, asthma, diabetes, weakness, fatigue, PVD, abrupt d/c
18
Q
Safety endpoints for digoxin
A
- GI – anorexia, N/V, diarrhea
- Neurological – headache, fatigue, confusion
- Visual – blurred vision, halos around bright objects
- Cardiac – arrhythmias (when levels are too high)
19
Q
Digoxin drug-drug interactions
A
- *If pt is already on digoxin & need to start any of these drugs, decrease digoxin dose by 50%
- Amiodarone, propafenone, quinidine/quinine, verapamil, itraconazole
- Cholestyramine, Al-Mg antacids, kaolin-pectin, dietary fibre, sucralfate – 2 h interval between administration
20
Q
Options for restoration of normal sinus rhythm (to stop A fib)
A
- Electrical cardioversion (done in hospital)
- IV amiodarone controls rate & 30-40% effective for cardioversion
- For new onset A fib in hospital – amiodarone 300 mg IV bolus, then 30-60 mg/h infusion for 24-48 h
- If not cardioverted, then can use electrical cardioversion
- “Pill in the pocket” (must be rate controlled first) – flecainide 200-300 mg PO x 1 or propafenone 450-600 PO x 1
