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31 Cards in this Set
- Front
- Back
- 3rd side (hint)
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Action potential for a Purkinje fiber in the ventricles. Name the phases, explain actions and Ion flux.
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Phase 0-Rapid depolarization-Rapid Na influx
Phase 1-Early repolarization-Cl influx Phase 2- Plateau- Ca influx Phase 3- Rapid depolarization-K efflux Phase 4-Resting Slow Na influx |
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What is the Effective(absolute Refractory Period(ERP). What phases are included?
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time when a second impulse cannot be initiated. Includes phase 0 through first half of phase three
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single common most stimulation for arrhythmia
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reentry
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What's going on in heart during:
p wave PR interval QRS complex T wave QT interval |
p wave-atrial depolarization
PR interval-conduction time from atria to ventricles QRS complex-Ventricular depolarization T wave-ventricular repolarization QT interval-Ventricular depol. and repol. |
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What are Two common mechanisms for arrhythmia formation
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1. Abnormal impulse initiation: Most common form is altered automaticity: For example, increased sympathetic drive may cause sinus tachycardia whereas decreased SNS drive causes Bradycardia.
2. Abnormal impulse conduction: Most common form is Reentry. Result from scar tissue due to MI or other structural disease |
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This arrhythmia originates in sinus node, atria or AV node. Give three examples.
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Supraventricular.
Sinus Bradycardia/tachycardia PSVT(usually self fixing) AFlutter and AFib |
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This class of arrhythmias originate below HIS bundle. Give three examples(which one includes Torsades)
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Ventricular
VPC VT(includes Torsades de Pointes) VFib |
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Name the conduction blocks
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First, Second or third degree AV block
RIght or Left Bundle Branch block |
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Morizicine is in what drug class?
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Na Channel Blockers
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Three Na Channel blockers that prolong repolarization. Class?
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Class IA
Quinidine Procainamide Disopyramide |
May cause Torsades
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Three Na Channel blockers that shorten repolarization
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1B
Lidocaine Mexiletine Tocainide |
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THese two Na channel Blockers have minimal effect on repolarization. Class?
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1C
Flecainide Propafenone |
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Class of Propranolol
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Beta blocker
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Four agents that block K efflux and prolong repolarization
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Amiodarone
Sotalol Ibutilide Dofetilide |
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Two CCBs
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Verapimil
Diltiazem |
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Two misc drugs that prolong AV conduction
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Digoxin
Adenosine |
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Drug of choice for PSVT
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Adenosine IV push
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Nonpharmacologic treatment for PSVT(done first)
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Physical maneuvers to increase Vagal Tone
a. unilateral carotid artery sinus massage b. Valsalva maneuver(hold breath and bear down) |
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Alternatives drugs besides DOC Adenosine for PSVT. For example, if pt has too much caffeine, cannot do adenosine.
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BB, or CCB
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Most common arrhythmia. What increases incidence?
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AFib. Age and presence of HRT disease
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Chaotic rhythm with multiple ectopic foci in atria firing randomly; multiple reentrant loops
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AFib
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No identifiable p wave. Which arrhythmia and what is atrial and ventricular rate?
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Afib. Atrial rate 350-600. Ventricular rate 130-180. Irregularly irregular
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Conditions associated with AF
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Coronary heart disease
HTN Valvular heart disease HF |
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Increases risk of stroke. Which arrhythmia?
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AFib
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Symptoms of Afib? Why?
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Palpitations, dizziness, fatigue, chest pain, heart failure, sycope. Rapid ventricular rate decreases filling time
Loss of atrial contraction("kick") also decreases ventricular filling |
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TREATMENT OF AF
If: Hemodynamic symptoms? What doesn't work? |
Electrical cardioversion. Digoxin, BB and 1 of 2 CCBs, Adenosine doesn't work due to short half-life
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Treatment of AFib in hemodynamically stable patient:
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Step 1: Slow ventricular rate w/ AV nodal blocking drugs
a. Digoxin b. Beta Blcoker c. Calcium channel antagonist Step 2. Attempt conversion to NSR a. Electrical cardioversion b. Pharmacological(IA,III) |
Note: if pt has been in AF>48 hours or of unk. duration, anticoagulation may be req/ to prevent stroke as a result of cardioversion procedure.
Step 3: If Cardioversion success keep at NSR a. Class III(amiodarone, sotalol) b. Group IA |
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Rapid-Acting Insulin
a. name three b. Peak c. Duration |
a. Lispro/Aspart/Glulisine
b. 0.5-2hours c. lasts 5 hours |
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Short-Acting Insulins
a. name them b. onset c. Peak d. Duration g. Injected how long before meals? |
a. Humulin R, Novolin R
b. onset: 0.5-1hr c. Peak: 2-3 hours d. Duration: 3-7 hours e. Injected 30-35 minutes before meals |
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Intermediate-Acting insulin
a. Route of admin b. Names c. Onset d. Peak e. duration |
a. SubQ only
b. NPH, Humulin N, Novolin N(Isophane insulin suspension) -lente(insulin zinc susp-removed) c. Onset. 2-4 hours d. Peak: 6-12 hours e. Duration: 12-20 hours |
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Long Acting insulin
a. names b. Duration c. Which one binds to albumin and has less peaks |
a. Glargine(Lantus) and Detemir(Levemir
b. 24 hours c. Detemir binds to albumin and less peaks, more truly basal |
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