Cardio Winter 1 Chapter 7 Objec.

Front 1

what are the possible mechanisms by which abnormal automaticity is suppressed? (3)

Back 1

1) lower the RMP
2) decreasing the slop of phase 4 in diseased cells, lowering the rate that AP's occur
3) raise the threshold potential

Front 2

What are the mechanisms that can be utilized to interrupt reentry circuits? (4)

Back 2

1) getting rid of the unidirectional block
2) turning the unidirectional block into a bi-directional block
3) altering the conduction velocity around the circuit and within the damaged tissues
4) altering the time the surrounding normal cardiac tissues take to repolarize

Front 3

what are class 1a, sodium channel blockers? (2)

Back 3

1) Quinidine
2) procainamide

Front 4

How do class 1a sodium channed blockers work?

Back 4

prolonging the action potential duration and decreasing the slope of phase 0.

Front 5

When would you use Class 1a sodium channel blockers? (4)

Back 5

1) suppression of ventricular tachycardia
2) VPC
3) reentry pathways
4) supraventricular tachys such as a fib.

Front 6

what are contraindications for using class 1a sodium channel blockers? (3)

Back 6

1) AV blocks
2) digoxin toxicity
3) known hypersensitivity

Front 7

what are class 1b, sodium channel blockers? (2)

Back 7

1) lidocaine
2) mexiletine

Front 8

how do class 1b sodium channel blockers work?

Back 8

decreasing the slope of phase 4 which slows automaticity and also shortens the action potential duration

Front 9

what are the indications for using a class 1b sodium channel blockers? (3)

Back 9

1) ventricular arrhythmias
2) reentry pathways
3) high vagal tone causing a fib

Front 10

which drugs has the highest effect on damaged myocardial tissues?

Back 10

lidocaine

Front 11

what drug would you use if you had a ventricular arrhythmia that you needed long term control for and is responsive to lidocaine?

Back 11

mexiletine

Front 12

what are the contraindications for lidocaine? (2)

Back 12

1) AV blocks
2) liver dz

Front 13

What is the drug of choice for ventricular arrhythmias?

Back 13

lidocaine

Front 14

what are the contraindications for mexiletine? (2)

Back 14

1) AV block
2) renal dz

Front 15

what are some signs of class 1b sodium channel blocker toxicity? (3)

Back 15

1) Gi
2) CNS
3) tremors

Front 16

what are class 2 beta-adrenergic receptor blockers? (2)

Back 16

1) Propranolol
2) Atenolol

Front 17

How do class 2 beta-adrenergic receptor blockers work?

Back 17

decreases automaticity by blocking sympathetic tone, interrupts reentry by prolonging refractory periods of the AV node and decreases node refractoriness, slowing ventricular response to atrial tachys.

Front 18

what are the indications for using class 2 beta-adrenergic receptor blockers? (3)

Back 18

1) atrial tachycardia and fib (if refractory to digoxin)
2) ventricular arrhythmias in combination with class 1 antiarrhythmics
3) occasionally in cats with sinus tachycardia or ventricular arrhythmia from hyperthyroidism

Front 19

what are contraindicaitons for using class2 beta-adrenergic receptor blockers? (6)

Back 19

1) underlying myocardial dz
2) AV blocks
3) asthma
4) CHF
5) diabetes
6) pulmonary disorders (less of a concern with atenolol)

Front 20

what are your class 3, potassium channel blockers? (1)

Back 20

Sotalol

Front 21

how do class 3 potassium channel blockers work?

Back 21

works by prolonging the AP duration which will interrupt reentry pathways and increase the ventricular fibrillation threshold.

Front 22

what other types of receptors does sotalol block?

Back 22

beta-adrenergic receptor

Front 23

when would you use sotalol?

Back 23

life-threatening ventricular arrhythmias in dogs with underlying heart disease, such as DCM in boxers and dobies

Front 24

what are the contraindications for sotalol?

Back 24

do not combine with class 2 or 1a antiarrhytmics
heart failure

Front 25

what are you class 4 calcium channel blockers? (2)

Back 25

1) diltiazem
2) verapamil

Front 26

How do class 4 calcium channel blockers work?

Back 26

slow ca++ entry into smooth muscle, producing vasodilation and BP and slows Ca++ entry into myocardial tissue, slowing conduction and reducing contractility.

Front 27

what phases are depressed in calss 4 ca++ channel blockers?

Back 27

4 and 0

Front 28

what are the indications for class 4 Ca++ channel blockers? (5)

Back 28

1) reentry pathways that use the AV node
2) decreases AV node refractoriness
3) anti-hypertensive
4) terminates supraventricular tachy such as AF or atrial flutter
5) slows rapid ventricular rates

Front 29

what are the contraindications for class 4 ca++ channel blockers? (4)

Back 29

1) AV block
2) sick sinus syndrome
3) use of class 2 anti-arrhythmics
4) CHF

Front 30

what are the MOA of digoxin? (6) (this is a f***ing terrible card. I broke it into smaller bits.)

Back 30

1) slows conduction through the AV node
2) increases parasympathetic and reduces sympathetic tone on the AV node
3) positive inotrope, in contrast to class 2 and 4 anti-arrhythmics
4) indicated for CHF or myocardial dz, prevention of supraventricular arrhythmias

Front 31

MOA of digoxin:
_______ conduction through the AV node
_______ parasympathetic tone and _________ sympathetic tone on the ______ ______

Back 31

slows conduction through the AV node
INCREASES parasympathetic and REDUCES sympathetic tone on the AV NODE

Front 32

MOA of digoxin:
_________ inotrope, in contrast to class ___ and _____ anti-arrhythmics

Back 32

POSITIVE inotrope, in contrast to class 2 adn 4

Front 33

MOA of digoxin:
indicated for ______ or __________ _________
prevention of ____________________ arrhythmias

Back 33

indicated for CHF or MYOCARDIAL DZ
prevention of SUPRAVENTRICULAR arrhythmias

Front 34

what are the side effects and toxicities of digoxin? (3)

Back 34

1) Gi
2) heart block
3) ventricular arrhythmias

Front 35

what do you have to be cautious about when using digoxin?

Back 35

patients with kidney disease

Front 36

what do anticholinergics increase? (2)

Back 36

1) automaticity of the SA node
2) conductivity through the AV node

Front 37

what are anticholinergics and sympathomimetics used for? (3)

Back 37

1) bradycardia
2) heart blocks
3) other conditions that will most likely require a pacemaker

Front 38

what do sympathomimetics increase? (2)

Back 38

1) automaticity
2) rate of escape beats

Front 39

what do you use for bradycardias when pacemakers are not available?

Back 39

sympathomimetics

Front 40

When would you treat bradycardia? (4)

Back 40

1) sick sinus
2) high grade 2nd degree AV block
3) 3rd degree AV block
4) atrial standstill

Front 41

what would you use as MEDICAL treatment to treat bradycardia? Drugs you would use for chronic cases vs short term?

Back 41

1) sympathomimetic drugs (chronic=terbutaline, short term= dopamine)
2) parsympatholytic drugs (atropine, isoproterenol)

Front 42

when would you use emergency medical management for bradycardia? What would you use?

Back 42

atrial standtill/complete heart block. You could use atropine (rarely works), then go to isoproterenol, dopamine.

Front 43

what would be a surgical option for long term control of bradycardia?

Back 43

pacemaker

Front 44

how would you treat sick sinus/ 2nd AV block?

Back 44

Theophylline, terbutaline, atropine
(Most end up needing a pacemaker)

Front 45

when would you treat supraventricular arrhythmias? (4)

Back 45

1) when you need to eliminate cx signs or reduce risk of heart failure
2) sustained atrial or junct tachycardia
3) SVT dt accessory pathways
4) atrial fib or atrial flutter

Front 46

what are the tx goals for supraventricular arrhythmias? (2)

Back 46

1) acute tx for termination
2) long term to prevent recurrence

Front 47

How can you cause acute termination of supraventricular arrhythmias? (4)

Back 47

1) vagal maneuver (carotid sinus massage, HEAD IN WATER (WTF??!!) "diving reflex"

Front 48

what usually follows vagal maneuver for acute termination of supraventricular arrhythmias? (what meds would you use after apparently drowning your patient)

Back 48

propranolol
esmolol diltiazem
procainamide

Front 49

what are drugs you are going to use for chronic oral maintenance for supraventricular arrhythmias?

Back 49

procainamide, quinidine, or diltiazem to restore sinus rhythm
can go to sotolol

Front 50

what can you use if procainmide, quinidine, diltiazem or sotolol aren't working in supraventricular arrhytmias?

Back 50

can slow ventricular rate with digoxin or add diltiazem/altenolol if rate not controlled

Front 51

what drug can you give to treat a fib? If that doesn't work, what drugs can you add?

Back 51

digoxin
can add diltiazem or atenolol if inadequate response with just digoxin

Front 52

what is your first choice of drug for acute termination of ventricular premature beats?

Back 52

can cause acute termination with lidocaine IV

Front 53

what can you use to treat ventricular premature beats if lidocaine doesn't work? What can you top off with?

Back 53

procainamide
top off with esmolol or propranolol or amiodarone/quinidine IV

Front 54

what do you use for chronic oral maintenance of ventricular premature beats?

Back 54

sotalol

Front 55

what do you have to do for V fib?

Back 55

defibrillate!!!

Front 56

what is the process you would do for v fib?

Back 56

defib, external massage, defib again etc. Can administer lidocaine/epi.

Front 57

what does epi do in v fib?

Back 57

improve myocardial perfusion