Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/42

Click to flip

42 Cards in this Set

  • Front
  • Back
Class 1a agents

1)Conduction velocity
2)refractory period
3)automaticity
1) decrease
2) increase
3) decrease
Class 1b

1)conduction velocity
2)refractory period
3)automaticity
1)0/decrease
2)decrease
3)decrease
Class 1c

1)conduction velocity
2)refractory period
3)automaticity
1)decrease
2)0
3)decrease
Class II
1)conduction velocity
2)refractory period
3)automaticity
1)decrease
2)increase
3)decrease
Class III
1)conduction velocity
2)refractory period
3)automaticity
1)0
2)increase
3)0
Class IV
1)conduction velocity
2)refractory period
3)automaticity
1)decrease
2)increase
3)decrease
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
SINUS BRADYCARDIA
Treatment (symptomatic)
1)Atropine
2)TCP
3)dopamine
4)epinephrine
5)isoproterenol
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
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
SINUS TACHYCARDIA
Treatment (symptomatic)
Propanolol, Verapamil, Diltiazem, Digoxin
SINUS TACHYCARDIA
Treatment (symtomatic patient with CHF)
Digoxin
SUPRAVENTRICULAR TACHYCARDIA
a)PAT
Cause
b)PSVT
Cause
a)AMI, chronic lung dx, drug intoxication

b)healthy individuals or WPW
SUPRAVENTRICULAR TACHYCARDIA
goal of treatment
interupt the AV nodal re-entry loop by slowing condution through this node
PSVT
Treatment (severe hemodynamic compromise)
Synchronized cardioversion
PSVT
Treatment (hemodynamically stable)
1)vagal maneuvers
2)Adenosine
3)Verapamil/Diltiazem
4)Propanolol/digoxin
Adenosine drug interactions
Dipyridamole - prolongs effect (start with 1/2 dose)

Theophylline - decreases efficacy
Adenosine adverse effects
Transient flushing and SOB
Adenosine precautions
1)asthmatics
2)wide QRS complex tachycardias
3)2 OR 3rd degree AV blockade
Delay in AV conduction manifested by a prolonged PR interval
First degree AV block
First degree AV block causes
1)increase vagal tone
2)drugs
3)hypoxia
First degree AV block tx
none
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
Second degree AV block
Second degree AV block causes
1)inferior AMI
2)increased vagal tone
3)drugs
Second degree AV block treatment
Usually transient and does not require tx

Atropine if sx'matic of hypoperfusion that may occur if ventricular rate is excessively slow
None of the atrial stimuli are transmitted through the AVN, no P waves conducted to the ventricles
Third degree AV block (complete heart block)
Third degree AV block causes
1)anterior AMI
2)cardiomyopathy
3)sarcoidosis
Third degree AV block treatment
1)temporary pharmacological pacing with isoproterenol may be of benefit until (2) a permanent pacemaker can be inserted
PREMATURE VENTRICULAR CONTRACTIONS (PVCs)
Causes
1)common post AMI
2)CHF
3)hypoxia
4)digoxin toxicity
5)sympathomimetic drugs
PVCs
Treatment
Amiodarone or Lidocaine for multifocal, paired PVCs, R-on-T, but NOT unifocal PVCs
Lidocaine toxicities
Paresthesias, respiratory arrest, seizures, muscle fasciculations, diz and drows
Agents for chronic PVC suppression
Class 1a's and propanolol
Life-threatening arrhythmia defined as 3 or more consecutive PVCs
Ventricular tachycardia
Ventricular tachycardia
Causes
Post AMI
Ventricular tachycardia treatment in the unstable patient (SBP <80-90
Cardioversion
Ventricular tachycardia (monomorphic) treatment in the stable patient (SBP>80-90) with a poor EF
Amiodarone IVP or Lidocaine IVP THEN use synchronized cardioversion
Ventricular tachycardia (monomorphic) treatment in the stable patient (SBP>80-90) with a normal EF
Procainamide or Sotalol
A life-threatening arrhythmia, totally disorganized depolarization of the ventricles-caused by many ventricualr ectopic focii, there is no pulse or blood pressure.
Ventricular fibrillation
VF causes
After AMI, chest trauma, drug toxicity, or electrolyte abnormalities
VF treatment
3 shocks -> epinephrine or vasopressin -> 1 shock -> lidocaine or amiodarone -> 1 shock -> Mg -> 1 shock -> procainamide
Defined as no ventricular activity and appears as a flat line on ECG
Asystole
Asystole treatment
Transcutaneous pacing -> epinephrine -> atropine -> decide whether to cease resuscitative efforts