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42 Cards in this Set
- Front
- Back
Class 1a agents
1)Conduction velocity 2)refractory period 3)automaticity |
1) decrease
2) increase 3) decrease |
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Class 1b
1)conduction velocity 2)refractory period 3)automaticity |
1)0/decrease
2)decrease 3)decrease |
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Class 1c
1)conduction velocity 2)refractory period 3)automaticity |
1)decrease
2)0 3)decrease |
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Class II
1)conduction velocity 2)refractory period 3)automaticity |
1)decrease
2)increase 3)decrease |
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Class III
1)conduction velocity 2)refractory period 3)automaticity |
1)0
2)increase 3)0 |
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Class IV
1)conduction velocity 2)refractory period 3)automaticity |
1)decrease
2)increase 3)decrease |
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Supraventricular arrhythmia
SINUS BRADYCARDIA Causes |
1)excesive vagal stimulation from vomiting or straining during a bowel movement
2)drugs such as beta-antagonists, calcium antagonists, and digoxin 3)sinus node abnormalities due to an inferior wall AMI or open heart surgery |
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SINUS BRADYCARDIA
Treatment (symptomatic) |
1)Atropine
2)TCP 3)dopamine 4)epinephrine 5)isoproterenol |
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SINUS BRADYCARDIA
Cautions |
1) do NOT give doses smaller than 0.5mg of atropine to adults due to paradoxial bradycardia
2)excessive tachycardia may worsen ischemia or the extent of myocardial infarct in AMI patients |
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Supraventricular arrhythmia
SINUS TACHYCARDIA Causes |
1)decrease vagal tone
2)increased sympathetic tone 3)AMI 4)fever 5)stress 6)hypotension 7)CHF 8)drugs |
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SINUS TACHYCARDIA
Treatment (symptomatic) |
Propanolol, Verapamil, Diltiazem, Digoxin
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SINUS TACHYCARDIA
Treatment (symtomatic patient with CHF) |
Digoxin
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SUPRAVENTRICULAR TACHYCARDIA
a)PAT Cause b)PSVT Cause |
a)AMI, chronic lung dx, drug intoxication
b)healthy individuals or WPW |
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SUPRAVENTRICULAR TACHYCARDIA
goal of treatment |
interupt the AV nodal re-entry loop by slowing condution through this node
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PSVT
Treatment (severe hemodynamic compromise) |
Synchronized cardioversion
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PSVT
Treatment (hemodynamically stable) |
1)vagal maneuvers
2)Adenosine 3)Verapamil/Diltiazem 4)Propanolol/digoxin |
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Adenosine drug interactions
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Dipyridamole - prolongs effect (start with 1/2 dose)
Theophylline - decreases efficacy |
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Adenosine adverse effects
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Transient flushing and SOB
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Adenosine precautions
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1)asthmatics
2)wide QRS complex tachycardias 3)2 OR 3rd degree AV blockade |
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Delay in AV conduction manifested by a prolonged PR interval
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First degree AV block
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First degree AV block causes
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1)increase vagal tone
2)drugs 3)hypoxia |
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First degree AV block tx
|
none
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Progressive prolongation of AV nodal conduction and PR interval until an atrial impulse is completely blocked by the AVN and a QRS complex is dropped
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Second degree AV block
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Second degree AV block causes
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1)inferior AMI
2)increased vagal tone 3)drugs |
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Second degree AV block treatment
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Usually transient and does not require tx
Atropine if sx'matic of hypoperfusion that may occur if ventricular rate is excessively slow |
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None of the atrial stimuli are transmitted through the AVN, no P waves conducted to the ventricles
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Third degree AV block (complete heart block)
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Third degree AV block causes
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1)anterior AMI
2)cardiomyopathy 3)sarcoidosis |
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Third degree AV block treatment
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1)temporary pharmacological pacing with isoproterenol may be of benefit until (2) a permanent pacemaker can be inserted
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PREMATURE VENTRICULAR CONTRACTIONS (PVCs)
Causes |
1)common post AMI
2)CHF 3)hypoxia 4)digoxin toxicity 5)sympathomimetic drugs |
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PVCs
Treatment |
Amiodarone or Lidocaine for multifocal, paired PVCs, R-on-T, but NOT unifocal PVCs
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Lidocaine toxicities
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Paresthesias, respiratory arrest, seizures, muscle fasciculations, diz and drows
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Agents for chronic PVC suppression
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Class 1a's and propanolol
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Life-threatening arrhythmia defined as 3 or more consecutive PVCs
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Ventricular tachycardia
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Ventricular tachycardia
Causes |
Post AMI
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Ventricular tachycardia treatment in the unstable patient (SBP <80-90
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Cardioversion
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Ventricular tachycardia (monomorphic) treatment in the stable patient (SBP>80-90) with a poor EF
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Amiodarone IVP or Lidocaine IVP THEN use synchronized cardioversion
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Ventricular tachycardia (monomorphic) treatment in the stable patient (SBP>80-90) with a normal EF
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Procainamide or Sotalol
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A life-threatening arrhythmia, totally disorganized depolarization of the ventricles-caused by many ventricualr ectopic focii, there is no pulse or blood pressure.
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Ventricular fibrillation
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VF causes
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After AMI, chest trauma, drug toxicity, or electrolyte abnormalities
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VF treatment
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3 shocks -> epinephrine or vasopressin -> 1 shock -> lidocaine or amiodarone -> 1 shock -> Mg -> 1 shock -> procainamide
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Defined as no ventricular activity and appears as a flat line on ECG
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Asystole
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Asystole treatment
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Transcutaneous pacing -> epinephrine -> atropine -> decide whether to cease resuscitative efforts
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