Anti Arrhythmics

Front 1

4 classes of antiarrhythmics

Back 1

Class 1: Na ch blkrs
Class 2: B-blkrs
Class 3: K ch blkrs
Class 4: Ca ch blkrs

"No Bad Boy Keeps Clean"

Front 2

3 subsets of Class I

Back 2

a: Procainamide, Desipramide, Quinidine
b: Tocainide, Phenytoin, Lidocaine, Mexiletine
c: Flecainide, Propafenone, Encainide

"Police Dpt Questioned- The Phunny Little Mexican- For Pushing Ecstasy"

Front 3

Class I
MOA:
uses:
S/E:
effects on HR, CO, BP, SV
effects of EKG

Back 3

MOA: by blocking Na ch, dec slope of phase 4 depolarization
uses: primarily vent arrhythmias
S/E: LLTD everywhere except atrium (constipation, n/v bc food is sitting there, visual disturbance, CNS depression, cardiovascular depression)
HR dec, CO dec, BP dec, SV inc
EKG: wider QRS, wider QT (predispose to arrhythmias)

Front 4

Quinidine S/E's

Back 4

1) sinchinism (tinnitis, hearing loss, low pltlts)
2) strongly anti-Cholnrgc (SNS symps + dry)
3) induce P450
4) Torsade

Front 5

In cinchinism
-what causes tinnitis and hearing loss?
-what causes low pltlts?
- why does quinidine cause low pltlts?

Back 5

-damage to CN 8
-sequestering by spleen (so you'll see splenomegaly)
-quinidine acts as a hapten for platetelets

Front 6

Why does Desipramide cause GABA side effects?

Back 6

its an amine (bc it has the suffix amide)
amines are metabolized by liver to NH3

NH3+ H --> NH4 + alpha KG + NAD --> glutamate --> GABA

Front 7

Any drug with the word cain in it is ____

Back 7

anesthetic

Front 8

some anesthetics are esters
some are amides
whats the rule to tell the difference?

Back 8

no I before cain = ester
yes I before cain = amide

Front 9

esters are metabolized by _____
amides are metabolize by _____

Back 9

esters by pseudocholinesterase
amides by liver

Front 10

Procainamide is an amide/ester?
S/E:

Back 10

ester
S/E: neuropathy, drug induced lupus

Front 11

Lidocaine is an amide/ester

Back 11

amide (metabolized by liver, fat soluble, distributes fast so must give it IV)

Front 12

Tocainide: amide/ester
S/E:

Back 12

ester (metablized by pseudocholinesterase)

S/E: pulm fibrosis

Front 13

Phenytoin
S/E

Back 13

LAD,
Induce P450,
Gingival hyperplasia,
Hirsutism,
Teratogenic,
SLE-like synd,
Ataxia,
Nystagmus,
Diplopia,
Malignant hyperthermia,
Megaloblastic anemia (interferes with folate metabolism),
Peripheral neuropathy,
Sedation

"LIGHTS AND MMPS"

Front 14

Mexiletine
S/E:

Back 14

most GI upset

"mix it all up"

Front 15

Class 1c Na ch blockers (Encainide, Flecainide, Propafone)
S/E:
uses:
CI:

Back 15

S/E: blocks 90% of Na ch's; inc mortality
uses: tachyarrhythmia, only as a last resort, when pt about to die.
CI: post-MI

Front 16

CI for all class I drugs

Back 16

hypERk

Front 17

Which class I drugs came from lidocaine?

Back 17

Tocainide, Mexiletine

Front 18

Which class I drug is the quickest acting Na ch blocker?

Back 18

Lidocaine

Front 19

Which class I drugs have both Na ch blkr and Ca ch blkr properties?

What arrhythmia are these drugs ideal to treat?

Back 19

Quinidine, Procainamide, Phenytoin

Rx: WPW (bc half its fibers are in atria, half its fibers are in ventricle)

Front 20

Which class I drug effects ischemic tissue ONLY?

Back 20

Lidocaine

Front 21

Which subset of Class I can be used as local anesthetics?

Back 21

Class I b "The Phunny Little Mexican"

Front 22

Class II
MOA:
effects on HR, CO, BP, SV
EKG changes:
uses:
S/E:
CI:

Back 22

MOA: decrease cAMP, thus decreasing Ca currents, thus decrease slope of phase 4.
***AV node particularly sensitive
HR dec, CO non, BP dec (by dec renin sec from JGA), SV none
EKG changes: inc PR
uses: any tachy, fib or flutter
SE: depends on what site is blocked
CI: asthma, DM, CHF, elderly

Front 23

Beta- 2 rec locations and stimulation

Back 23

arteriole: dilation
CNS: inc activity
Beta cells: inc insulin
ventricles: inc contractility
broncho: dilation
bladder: relax
CNS: stimulate
uterus: relax (beta 2 agonists can be used to delay preterm labor)
ventricles: inc contractility

"aBbbcuv"

Front 24

Beta- 1 block would cause

Back 24

CNS: depression
SA: dec HR and contractility
JGA: dec renin, thus BP
alpha cells: absence of release of glucagon in response to hypoglycemia

Front 25

Beta 1 specific antagonist

Back 25

A-M (except C & L)

Front 26

Non-specific beta blockers

Back 26

N-Z (also C & L)

Front 27

Beta- 1 rec locations and stimulation

Back 27

CNS: inc activity
SA: inc HR and contractility
JGA: inc renin (thus, aldosterone and BP)
alpha cells: secrete glucagon

Front 28

longest acting B blkr

Back 28

Propanolol

Front 29

Beta- 2 rec locations and stimulation

Back 29

CNS: inc activity
ventricles: inc contractility
broncho: dilation
Beta cells: inc insulin
uterus: relax (beta 2 agonists can be used to delay preterm labor)
bladder: relax
arteriole: dilation

Front 30

shortest acting B blkr (used alot by anesthesia)

Back 30

Esmolol

Front 31

Beta- 1 block would cause

Back 31

CNS: depression
SA: dec HR and contractility
JGA: dec renin, thus BP
alpha cells: dec response to hypoglycemia

Front 32

Beta-2 block would cause

Back 32

CNS: depression
vent: dec contractility (CHF exac)
broncho: constrict (asthma exac)
beta cells: dec insulin sec
uterus: contract
bladder: contract
arteriolar: constrict (musc cramps, impotence)

Front 33

longest acting B blkr

Back 33

Propanolol

Front 34

shortest acting B blkr (used alot by anesthesia)

Back 34

Esmolol

Front 35

beta blockers that treat glaucoma

Back 35

Timolol, Butexolol, Nadolol

Front 36

B blockers that also block K
S/E:

Back 36

Sotalol
QT prolongation (Torsades)

Front 37

Propanolol
uses:

Back 37

uses: arrhythmias, HTN, essential tremor, panic attacks, akathesia

Front 38

DOC for HTN in MI pt

Back 38

Esmolol

Front 39

DOC for thyroid strom

Back 39

Esmolol

Front 40

Which beta blockers also block alpha 1 recs?

Back 40

Labetalol, Carvedilol

Front 41

Which beta blockers can be used for hypertensive crisis?

Back 41

Labetalol, Carvedilol
(the ones that block alpha-1 rec's too)

Front 42

Which beta blockers have PARTIAL Beta AGONIST activity?

Back 42

Acebutelol, Atenolol, Pindolol

Front 43

Which are the ONLY beta blockers that can be used in asthmatics, DM, CHF, PVD, elderly, heart-block?
Why would you put these pts on a beta blocker at all?

Back 43

Acebutelol, Atenonol, Pindolol
(the ones with PARTIAL Beta AGONIST activity)

these pts would REQUIRE a B-blocker post MI bc they prolong life.

Front 44

Afib can be treated with 5 classes of drugs
1st line- 5th line:
If youre going to use a B blocker, use

Back 44

1st l: Ca ch blkr
2nd l: B- blkr (Labetalol)
3rd l: K ch-blkr
4th l: cAMP blkr (Adenosine)
5th l: digitalis (inc vagal tone)

Front 45

Class III drugs
MOA:
EKG changes:
uses:
S/E:

Back 45

MOA: blocks efflux of K, prolonging depolarization
EKG changes: peaked T wave, followed by prolonged T wave (thus prolonging QT)
uses: any arrhythmia, last resort
S/E: prolonged QT predisposes to new arrhythmias, effects all cells in body!!!

Front 46

Name Class III drugs

Back 46

K ch blockers
1) Bertylium
2) Amiodarone
3) Sotalol
4) Ibutelide

Front 47

Amiodarone
S/E:

Back 47

corneal/skin deposits
(gray/blue skin)
photosensitiviy
neuro defects
cardiosuppress
inh p450***
hepatotoxic*****
hypo/hyperthyroid*****
pulmonary fibrosis*****

"Check PFTs, TFTs, LFTs"

Front 48

Class IV drugs
MOA:
EKG changes
effects on HR, CO, BP, SV
uses:

Back 48

MOA:
1) by blocking Ca at SA node it slows phase 0 depolarization, slows SA node firing
2) by blocking Ca at AV node it slows conduction velocity
EKG: PR prolong (SA and atrium), ST prolonged (vent contrxn)
dec HR, CO?, dec BP (by dec TPR), SV?
uses: 1st line for atrial arrhthmia (also angina and HTN)

Front 49

Which 2 Ca ch blockers used to treat atrial arrhythmias?
which are used to treat HTN and angina?

Back 49

Verapamil, Diltiazam
(Verapamil is drug of choice for atrial arrhythm.)

the rest are used primarily for HTN and angina

Front 50

Ca ch blocker
S/E

Back 50

Ca is used in all smooth musc and neurons

Ca ch blockers on
1) neurons--> neuropathy
2) sm musc--> constipation, leaky vessels (edema, flushing)

Front 51

What is nimodapine used for?

Back 51

Ca ch blocker used for phx against vasospasm post-subarachnoid hemorrhage

Front 52

Which 4 drugs cause can cause digoxin toxicity?

Back 52

1) Amiodarone
2) Spirinolactone
3) Quinidine
4) Verapamil

Front 53

which 2 classes cause can cause bradycaria, CHF, and AV block

Back 53

B blocker, Ca ch blocker

Front 54

Which classes cause Torsades?
why?

Back 54

Class IA and Class 3 (specifically Quinidine, Procainamide, Sotalol)
bc they prolong QT

****Amiodarone RARELY-NEVER causes torsades (even if its a class 3)

Front 55

Which 4 drugs cause pulmonary fibrosis?

Back 55

1) Amiodorone
2) Tocainide
3) Busulfan
4) Bleomycin

"BBAT"

Front 56

Adenosine
MOA:
EKG changes:
uses:

S/E:

Back 56

MOA:
1) inh cAMP--> dec intracellular Ca
2) inc K efflux--> hyperpolarize
***primarily works on AV node

EKG: you'd expect to see prolonged PR, but since its half life is so short (<10s), any of its EKG effects are transient

uses: DOC in dx and rx of AV node arrhythmias; DOC for PSVT
S/E: TRANSIENT flushing, hypOtn, chest pain, SOB

Front 57

Which anti-arrhythmics inc AP duration?

Back 57

Class Ia, Class 3 (K ch blkr)

Front 58

Which anti-arrhythmics dec AP duration?

Back 58

Ib only

Front 59

How does class Ic affect AP?

Back 59

no effect

Front 60

Which anti-arrhythmics inc QT interval?

Back 60

Na, K,

Front 61

Which anti-arrhythmics inc PR interval, thus increasing chances of heart block, bradycardia and CHF?

Back 61

Beta blockers, Ca ch blockers, digoxin
(Adenosine, also, buts its half life is < 10 sec, so negligible)

Front 62

Which anti-arrhythmics inc ERP?

Back 62

IA, K , Ca ch blockers

Front 63

Digoxin
MOA:
effects on HR, CO, BP, SV
EKG changes
uses:
S/E:
CI:

Back 63

MOA:
1) competitive inh of K @ Na/K pumps to indirectly inh Na/Ca exchange; leads to inc intracellular
Ca--> positive ionotropy
2) stimulates vagus

uses
1) CHF: inc contractility via positive ionotropic effects
2) Afib: depress SA node and slows AV conduction via vagal effects
EKG: inc PR, dec QT (narrow QRS 2/2 inc contractility), scoop ST("j point" 2/2 compressing coronaries), T wave inversion
S/E: ANOREXIA, N/V, DIARRHEA, yellow/green vision, atrial arrhythmia (bc Ca staying inside cell), vent arrhythmia (bc Na staying inside cell)
***atrial arrhythmias more commone the ventricular
CI: **hypOk (more sites for dig to bind), hyPERCa (bc then you'll pull more Ca into cell then you bargained for), renal failure, quinidine, verapamil (dec clearance of digoxin)

Front 64

If quinidine induces P450, and digoxin is P450 dependent, how does quinidine magnify digoxin's effects?

Back 64

quinidine displaces digoxin from tissue binding sites

Front 65

Rx for digoxin toxicity

Back 65

slowly inc K,
class Ib,
Mg,
anti-dig Fab fragments,
cardiac pacer

Front 66

2 uses for Mg in correction of arrhythmias

Back 66

1) digoxin toxicity
2) torsades de pointes

Front 67

Which class is the ONLY class that prolongs action potential in cardiac MUSCLE cells (myocytes)?

Back 67

Class IA (P,D,Q)

Front 68

Which drug has very little effect on phase 0 depolarization, but SHORTENS phase 3 repol?

Back 68

Lidocaine

Front 69

Lidocaine is a Na channel blocker, why does it have such little effect on phase 0 depolarization?

Back 69

because its so fast acting (rapid binding, rapid release)

Front 70

Which drug is highly selective for rapidly depolarizing MYOCYTES?

Back 70

Lidocaine

Front 71

Which 2 classes only work on AV node and pacemaker cells (cells with automaticity)?

Back 71

Bblockers and CCblockers do NOT work on myocytes!

Front 72

Class Ic has its most prominent effect on....

Back 72

phase 0 (slows Na influx)

Front 73

What do we do if pt on Amiodarone gets hypOthroid?

Back 73

start levothyroxine, continue amiodarone

Front 74

sudden onset palpitations
dx:
Rx:

Back 74

Dx: PSVT
Rx: adenosine