Arrhythmias Flashcards

1
Q

Two non-dihydropiridine CCB

A

Verapamil & Diltiazem

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2
Q

MOA CCB

A

work via effects on intracellular calcium ion influx at the AV node to decreases conduction velocity and increases refractory period

this produces a direct effect to the AV node and therefore actions persist during exercise or high stress to SLOW DOWN the ventricular rate (“ventricular response”)

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3
Q

What to monitor for while on CCB

A

blood pressure - diltiazem and verapamil are vasodilators

signs of congestive heart failure in susceptible patients due to negative inotropic effect
do not use in patient with decompensated heart failure

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4
Q

MOA BB

A

block beta-adrenergic receptors in heart

results in decreased conduction through A-V, increased refractory period at AV node

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5
Q

Name 3 non-selective BB

A

Propranolol, Nadolol, & Timolol

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6
Q

Name 2 main cardioselective BB (B1, which also affects kidneys and adipose tissue)

A

Atenolol and Metoprolol

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7
Q

What to monitor/AE of BB, and CI

A

bradycardia, hypotension, exacerbation of CHF

relative contraindicated in asthma due to bronchoconstriction

CNS adverse effects include fatigue, lethargy, depression, sexual dysfunction.

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8
Q

4 main classes to treat Atrial Fibrillation

A

CCB, BB, Digoxin, & Amiodarone

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9
Q

MOA for Digoxin

A

increases vagal tone to slow conduction at AV node

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10
Q

Name 2 situations that digoxin has advantages in treating A-fib.

A

Hypotension-no affect on BP

CHF exacerbation-dig improves heart contractility

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11
Q

Adverse effects of Digoxin & ae of chronic use

A

AE short: monitor for hypo -kalemia & -magnesia, new arrhythmia or A-fib

AE chronic: hallucinations, nausea/vomiting, AV block, sinus pauses, arrhythmias, vision changes

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12
Q

Amiodarone MOA/class and what it may do

A

BB and CCB that may convert A-fib to NSR

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13
Q

When to anticoagulate before converting A-fib?

A

> 48 hours

Need 3 weeks of Warfarin (INR 2-3) & 4 weeks post conversion

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14
Q

What main drug is used to treat Paroxysmal Supraventricular Tachycardia?

A

Adenosine. Verap/Diltiaz and BB also effective

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15
Q

Amiodarone MOA

A

Briefly interrupts conduction at AV node to break re-entry

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16
Q

What to monitor in Amiodarone, when to use with caution, and when CI?

A

peripheral vasodilation - hypotension, flushing, SOB, chest tightness, apprehension (all of short duration)

use with caution in patients with severe obstructive lung disease

contraindicated in heart transplant patients

17
Q

Main treatment of Ventricular arrhythmia

A

Defibrillators

18
Q

Unstable vs. Stable V-tach

A

Stable: adequate BP, mental status intact, & no CP
Unstable: SBP

19
Q

Treatment of acute V-tach non-emergent for both stable & unstable

A

Stable
1. Amiodarone:
150mg IV over 10 minutes,
then 1mg/min x 6 hours,
then continuous infusion 0.5 mg/min
2. Lidocaine, 1-1.5 mg/kg IV,
then 0.5-0.75 mg/kg every 5-10 minutes up to 3mg/kg,
then continuous infusion 1-4 mg/min
3. Procainamide (only if preserved heart function – EF > 40%),
17mg/kg IV no greater than 20-30mg/min.
a. Stop infusion if QRS widens > 50% or hypotension
4. Torsades de pointes with prolonged baseline QT interval
Correct electrolytes, Give Magnesium 1-2 gm IV, may repeat

Unstable
-Urgent Synchronized cardioversion

20
Q

First three things to do during cardiac arrest?

A

CPR, defibrillator, & maintain airway

21
Q

What drugs can be given to improve perfusion during CPR & what to do after giving them?

A

Epinephrine or Vasopressin

Flush with saline 20 ml

22
Q

What drugs are used to “fix” rhythm in v-fib/v-tach

A
  1. Amiodarone
  2. Lidocaine
  3. Procainamide
23
Q

Indications for Mag Sulfate

A

Torsades, suspected hypo magnesia, refractory ventricular arrhythmia, and dig tox

24
Q

What drug to give in asystole or pulseless electrical activity?

A

Atropine-it’s anti-cholinergic effects can reverse vagal stimulation on the heart to increase SA firing and AV conduction

25
Q

Do you shock asystole?

A

NO

26
Q

The potential causes of asystole (5 H’s & 5 T’s)

A

Hypovolemia Tablets (OD)
Hypoxia Tamponade
Hydrogen ion (acidosis) Tension Pneumothorax
Hyper-hypokalemia Thrombosis, coronary (MI)
Hypothermia Thrombosis, pulmonary (PE)