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

1/109

Click to flip

109 Cards in this Set

  • Front
  • Back
An _________ is a disruption of the normal sequence of impulse initiation &/or propagation.
ARRHYTHMIA
________ terminate an ongoing arrhythmia or prevent recurrence of an arrhythmia.
ANTIARRHYTHMICS
IS THIS ACTION POTENTIAL FROM A PURKINJE FIBER OR A PACEMAKER CELL?
-
In the VAUGHAN-WILLIAMS CLASSIFICATION SCHEME FOR ANTIARRHYTHMICS, CLASS I are _______ CHANNEL BLOCKERS
FAST Na+
CLASS I have a a local ______ effect
anesthetic
Class I drugs preferentially bind to the ____ or inactivated state of the Na+ channel.
open
All CLASS 1 antiarrhythmics decrease the ____ of depolarization
Vmax
All CLASS 1 antiarrhythmics decrease the the slope of phase ___
0
with class 1 antiarrhytmics the faster heart rate, more ______ the drug, therefore they are good at treating _____ arrhytmias
effective
tachy
CLASS IA preferentially bind to ____ channels
OPEN
In perkinge cells Class Ia drugs result in a _______ Na+ channel block, And also blocks K+ channels which slowes down _______(phase 3)
moderate
repolarization
This class IA drug is a cinchona alkaloid. It is used for atrial & ventricular arrhythmias
QUINIDINE (generic)
Quinidine has the additional effect of being a mild ___-blocker (this receptor exists in the vascular smooth mm) The vasodilation it induces can result in vasodilaton, a drop in blood pressure and ultimately reflex ______
alpha

tachycardia
Quinidine has the additional effect of causing a decrease in ___release (anti- muscarinic effect) This increase conduction through the AV node and can also result in ______
Ach

tachycardia
increase contuction through the AV node is a problem with _______.
ATRIAL FLUTTER
High dose of quinidine can cause fatal ______.
V-FIB
High dose of quinidine can cause _____block or _____
SA/AV
asystole
QUINIDINE ______the Q-T interval causing 2-8% of patients to develop _______.
prolongs
Torsades de pointes
Torsades de pointes is a polymorphic ventricular tachycardia common to Rxs that blocks ____ channels.
K+
_______ - the most common non-cardiac side effect of quinidine
DIARRHEA
the hypokalemia caused by the diarrhea can increase the risk of developing _______
Torsades de pointes
Qunidine can also cause ________ which includes: Blurred vision, tinnitus, headache, disorientation & psychosis
CINCHONISM
Quinidine nhibits cyp 2d6, the enzyme that converts _______ to morphine. Morphine actually carries out analgesic activity.
codeine
Quinidine displaces _______– increasing the risk of toxicity
digoxin
This type IA antiarrythmic drug is an analog of procaine with effects similar to quinidine but with less antimuscarinic activity
PROCAINAMIDE (Procanbid) -
PROCAINAMIDE (Procanbid) is an alternative to quinidine for various ________ arrhytlunias
ventricular
PROCAINAMIDE (Procanbid)is metabolized to _______
N-ACETYLPROCAINAMIDE (NAPA)
(NAPA) is a ____ channel blocker (Class III antiarrhythmic) that enhances procainamide's effect on phase 3 repolarization.
K+
The effect of NAPA will vary depending if the patient is a fast or slow _________.
acetylator
In _____ acetylators NAPA hangs around longer & can reach toxicity
slow
Rapid IV administration of PROCAINAMIDE (Procanbid) can cause ________
hypotension
PROCAINAMIDE is better tolerated than quinidine but chronic use increases the incidence of side effects: -______ /_______ / _______
Depression
hallucinations
psychoses
PROCAINAMIDE can cause a ___-like syndrome (25-50% of patients) - T ANAs, rash, arthralgias & possible _________ with tamponade (potentially fatal).
SLE
pericarditis
Rare but potentially fatal _______
agranulocytosis
PROCAINAMIDE (Procanbid) can also induce________
Arrhythmias
This type IA drug is reserved for life threatening ventricular arrhythmias.
It has the most antimuscarinic effects of the type IAs.
DISOPYRAMIDE (Norpace)
Common side effects with DISOPYRAMIDE (Norpace) include _________(4)
Constipation, blurred vision, dry mouth, urinary retension
Dont use DISOPYRAMIDE (Norpace) if patient has _______ because the antimuscarinic effect will relax the ciliary mm and decreases the opening to the canal of sclemm
glaucoma
DISOPYRAMIDE (Norpace)also depresses myocardial ________ & can precipitate heart failure! This Rx carries the same caution as quinidine regarding its use with atrial flutter.
contractility
This Rx has properties of Class IA & IC antiarrhythmics. Class IC properties ↑ the mortality rate when used post Ml.
USES only for life threatening ventricular arrhythmias
MORICIZINE (Ethmozine)
CLASS lB anti-arrythmics bind ____& ______channels
open

inactivated
in Purkinje Cells, 1Bs induce _____ Na+ channel block and ______ repolarization
Mild
Shorten
in Pacemaker Cells, 1Bs
______Slope of Phase 4, & __________threshold for firing
decrease
increase
This 1B drug is a local anesthetic used for ventricular arrhythmias
LIDOCAINE (Xylocaine)
LIDOCAINE (Xylocaine)has an extensive 1st pass metabolism so given ____ IV. Fast IV -> arrhythmia or seizures
slow
SIDE EFFECTS of LIDOCAINE (Xylocaine) include _______(4)
Nystagmus /altered consciousness
/Tremors / slurred speech /
This 1B drug is an Analog of lidocaine. Its given ORALLY for ventricular arrhythmias
MEXILETINE (Mexitil)
PHENYTOIN (Dilantin) is a 1B drug that blocks ____ influx & some ___ influx.
Na+
Ca2+
PHENYTOIN (Dilantin) is used for Ventricular & ____-induced arrhythmias
digoxin
Major SIDE EFFECTS of PHENYTOIN (Dilantin) are:
a)_______
b)_______
c)_______
Hirituism gingival hyperplasia
enzyme enducer
This drug reduces facial hair by inhibiting omithine decarboxylase in the synthesis of polyamines involved in hair cell growth & proliferation.
EFLORNITHINE (Vaniqa)
CLASS IC drugs were shown by the ________ study to cause excessive mortality or non-fatal cardiac arrest
CAST(cardiac arrhythmia suppression test)
In Purkinje Cells, 1Cs result in _____Na+ channel block and ____ change in repolarization
Marked
no
In Pacemaker Cells, 1Cs _______the Slope of Phase 4 and _______ the threshold for firing
decrease
increase
This class IC is limited to refractory ventricular arrhythmias
FLECAINIDE (Tambocor) -
This class IC is a broad spectrum antiarrhythmic. It
also produces significant β block (Class II activity).
It is extensively metabolized by CYP2D6 which is absent in 7% of patients. This can cause exaggerated effects & toxicity (mostly GI).
PROPAFENONE (Rythmol)
CLASS II ANTIARRHYTHMICS are ____ BLOCKERS
beta
ARE THEIR ANTIARRHYTHMIC EFFECTS FROM BLOCKING B1 OR B2 RECEPTORS?
B1 (heart)
The GOAL of B blockers is to decrease O2 demand on the heart by preventing or blocking the effects of endogenous ________
catecholamines
B blockers have NO EFFECTS on ______ Cells
Purkinje
In Pacemaker Cells, B blockers decrease the slope of _____ and Prolong repolarization of the ___ node
Phase 4
AV
PROPRANOLOL (Inderal) – nonselective - blocks ___ & ___ receptors
B1, B2
PROPRANOLOL (Inderal) is used for ______ & _____-induced arrhythmias
supraventricular
digoxin
B1 Block fromPropranolol can result in -> (-) inotropic/chronotropic effects that _______ CO. This can cause reflex _______to maintain BP.

CAUTION: Bronchoconstriction from 2 block can cause a respiratory crisis
decrease
vasoconstriction
This B1 SELECTIVE class II drug has some intrinsic sympathomimetic activity which limits its "approved” use to premature ventricular contractions (PVCs).
ACEBUTOLOL (Sectral)
This B1 SELECTIVE class II drug is given only IV b/c rapidly metabolized by plasma esterases.
ESMOLOL (Brevibloc)
Atenolol, metoprolol & pindolol have been used in select circumstances but they are not FDA approved as antiarrhythmics!
FDA
CLASS III ANTIARRHYTHMICS are ____ CHANNEL BLOCKERS
K+
CLASS III ANTIARRHYTHMICS show Marked ______of repolarization Purkinje Cells
prolongation
CLASS III ANTIARRHYTHMICS show ______ in pacemaker cells
no effect
This class III antiarrhythmic is structurally related to thyroid hormone. It has properties of all 4 classes of antiarrhythmics. Its DOMINANT EFFECT is Marked prolongation of the action potential
AMIODARONE (Cordarone)
AMIODARONE (Cordarone) is Highly _______ - accumulates in tissues & is slowly eliminated. This increases its risk of toxicity. T ½ up to 50 days!
lipophilic
USE of AMIODARONE (Cordarone) is ________ supraventricular & ventricular arrhythmias
Refractory
When given IV AMIODARONE (Cordarone) can cause ______ & ______ depression
Hypotension
myocardial
ORAL side effects of AMIODARONE (Cordarone) include _________(5)
- Pulmonary fibrosis - Hypo- or hyperthyroidism
- Hepatotoxicity
- Corneal deposits -> halos inperipheral fields
- Peripheral neuropathies- Photodermatitis (25%)
– blue skin discoloration (5%)
This class II drug a quarternary amine (must be given IV) used for life-threatening ventricular arrhythmias
BRETYLIUM (generic) -
DIRECTly BRETYLIUM (generic) Prolongs __________. INDIRECTly it
Displaces ____, causing an ionatropic effect and increaseing incidence of arrhythmia
action potential
NE
CAUTION when using BRETYLIUM (generic) Watch for an initial _____ BP & potential ventricular arrhythmias followed by a ______ in BP as NE stores deplete.
increase

This class III drug is a nonselective B blocker that also blocks the delayed rectifier. It is used for Supraventricular & ventricular tachyarrhythmias
3-4% of patients will experience Torsades de pointes.
SOTALOL (Betapace)
This class III drug is used to convert atrial fibrillation & atrial flutter to normal sinus rhythm
IBUTILIDE (Corvert)
IBUTILIDE's (Corvert) MAIN MECHANISMS activates a slow inward ____ channel

The MINOR mechanism blocks ________
Na+
delayed rectifier
IBUTILIDE (Corvert) carries with it 4-8 % Risk of ________ and can cause potentially fatal arrhythmias.
Torsades de pointes
This class III drug blocks delayed rectifiers. Used to convert atrial fibrillation or atrial flutter to normal sinus rhythm.
DOFETILIDE (Tikosyn)
CLASS IV ANTIARRHYTHMICS are _____ CHANNEL BLOCKERS
Ca2+
CLASS IV ANTIARRHYTHMICS block L-type Cat+ channels. They are most effective in the ____ node.
AV
CLASS IV ANTIARRHYTHMICS have ________ on Purkinje Cells
NO EFFECT
On Pacemaker Cells, CLASS IV ANTIARRHYTHMICS:

-_______ the Slope of Phase 4
-____ the rise in the action potential
- _____ repolarization
decrease
Slow
Prolong
This CLASS IV ANTIARRHYTHMIC is more selective for the heart
VERAPAMIL (Calan)
This CLASS IV ANTIARRHYTHMIC
acts on the heart & vascular smooth muscle
DILTIAZEM (Cardizem)
CLASS IV ANTIARRHYTHMIC bind best to open channels and are thus more effective vs ________ , particularly supraventricular arrhythmias.
tachyarrhythmias
With CLASS IV ANTIARRHYTHMICs Watch for _____ BP from vasodilation (mainly with diltiazem)
and a _____ inotropic effect
decrease
(-)
DIGOXIN is a misc antiarrythmic also used to treat _____ but by a different mechanism
CHF
digoxin ANTIARRHYTHMIC MECHANISMS are _______
vagomimetic:
) increase in potassion efflux—causes hyperpolarization
This hyperpolarizes the atria.
a decrease in ____ influx w/in AV node decrease slope of phase 0
Ca
digoxin causes an increase in _______ efflux which causes hyperpolarization of the atria.
potassion
digoxin is used for _____ fibrillation and flutter
Atrial
CAUTION: Carvedilol can _______ clearance of digoxin & thus _________ the risk of digoxin toxicity
decrease
increase
_______ increases the risk of digoxin toxicity & increases susceptability to Torsades de pointes
Hypokalemia
Digoxin preferentially binds to the ________ form of Na+-K+-ATPase and K+ promotes ________.
phosphorylated dephosphorylation
Decreased K+ promotes ________ of the pump thereby facilitating digoxin binding & digoxin _______ .
phosphorylation
toxicity
TREATMENT FOR DIGOXIN TOXICITY:
- Use a drug called ______
- give IV
digoxin immune FAB(digoxin Ab)
K+
FOR DIGOXIN-INDUCED ARRHYTHMIAS:
a)– use antiarrythmic
1)_____2) ____ 3)____
lidocain /phenotyn/mg
WHAT EFFECT WILL HYPERCALCEMIA HAVE ON DIG TOXICITY? WHY?
Enhance- w/ dig toxicity you get too much CA.
________Interferes with the actions of Cat+.
MAGNESIUM
WHAT EFFECT WILL HYPERMAGNESEMIA HAVE ON THE RISK OF AN ARRHYTHMIA?
slow down heart, slow down arrythmia
WHAT ABOUT HYPOMAGNESEMIA?
More prone to arrythmia’s cuz you have more Ca+
This misc. antiarrythmic Given IV for bradyarrhythmias
It is an Anti-muscarinic –-it blocks vagus from slowing the heart down
ATROPINE
This misc. antiarrythmic is a naturally occurring nucleoside It is given IV for acute reentrant supraventricular tachycardia
T'/2 - 15 seconds! Easy to control and reduces the risk of significant side effects.
ADENOSINE (Adenocard)
ADENOSINE (Adenocard)works by stimulating P1 receptors inducing a _____ in the atria and SA/AV nodes resulting in hyperpolarization, increased automaticity & transient AV block.
It also inhibits ____ currents which increases AVN refractoriness
K+ efflux
Cat+