Clinical Pk Exam 2- Procainamide

Front 1

2 indications for proacinamide
for v-arrhythmia- what line is it?

Back 1

Supraventricular and ventricular arrhythmias
Management of cardiac arrest

2nd

Front 2

procainamide properties vs quinidine (4)

Back 2

Less hypotensive
Less antimuscarinic
Less cardiotoxic
Can be given safely by I.M. or I.V.

Front 3

procainamide metabolite (2)

Back 3

active- N-acetylprocainamide
(NAPA) renally

take into consideration (renal)

Front 4

2 things monitored on procainamide

Back 4

Blood pressure and EKG monitored during dosing

Front 5

procainamide- when to stop (3)

Back 5

Increase
in QRS or QT intervals by >25% or hypotension necessitate
discontinuation of loading infusion
Assess for proarrhythmia (e.g., Torsades de Pointes)

Front 6

IR vs. SR use for proacainmade (2)

Back 6

• Use immediate release formulation in the acute setting
• Use sustained release formulation for chronic therapy to
improve compliance

Front 7

procainamide metabolism

Back 7

first pass

Front 8

prmiacinade efficacy

Back 8

Adequate even after resection of large portions of small intestine

Front 9

when dose procainamide peak

Back 9

1 hr

Front 10

relative half life of procainamide and what this suggests for what formulation to use

Back 10

short half life = use SR
but make sure to counsel on ghost matrix

Front 11

IM Absorption of procainamide

Back 11

IM absorption is rapid and complete, with peak in about 25 min

Front 12

Distribution after IV- compartments of procainamide

approximate half life? it takes to distribute?

Back 12

2 compartment

5 min??

Front 13

Protein binding for procainamide

Back 13

10-20%

Front 14

effects of obesity of procainamide on distribution

Back 14

Obesity does not appreciably affect V. Distributes
poorly into fat tissue

Front 15

CHF effect on PK of procainamide

Back 15

V reduced in CHF

Front 16

metabolism of procainamide- metabolite
mechanism

Back 16

Acetylation to NAPA in liver and extrahepatic sites
• NAPA is the major and only metabolite of PA - lupus

Front 17

fraction of PA as NAPA in fast vs. slow acetylators (general)

Back 17

Fraction as NAPA averages 0.33 and 0.20 in fast and slow
acetylators, respectively

bigger in fast acetylators

Front 18

3 minor metabolic ptahways of PA? or NAPA?

Back 18

• Desethylation by N-dealkylation by microsomal mixedfunction
oxidases (DENAPA, DEPA) - not important
• Hydrolysis of amide of PA = p-aminobenzoic acid (PABA);
0-10% of PA dose in urine

deacetylation of NAPA to PA

Front 19

major pathway of PA

Back 19

NAT-2

Front 20

elimination of PA (3)

Back 20

• About 50 % of PA and 85 % of NAPA excreted in urine
unchanged
• Glomerular filtration with proximal tubular secretion
• Hemodialysis effectively removes both PA and NAPA

Front 21

therapeutic range of PA for most pt and those with resistant v tachycardia

Back 21

• 4-10 μg/ml for most patients
• 10-20 μg/ml may be required for select patients with resistant
ventricular tachycardia

Front 22

NAPA properties (3)

Back 22

not used (with PA) for monitoring

CLASS III anti-arr
less potent than PA

Front 23

look up when to use IBW and ABW-

Back 23

something about obese pt use ABW, underweight use ABW

but the drug distribution matters too?

Front 24

Two infusion method --> outpatient (3)

Back 24

Infuse L.D. over 1 h (not faster than 25 mg/min), while
monitoring the blood pressure, heart rate and EKG.

This is immediately followed by the maintenance infusion.

then Converting IV to oral therapy

Front 25

when is loading dose decreased (to 12 mg/kg) ? (what factors would cause this) (2)

Back 25

The loading dose is decreased to 12 mg/kg in the presence of
severe renal insufficiency or decreased cardiac output (HF)

Front 26

maint. doses for renal failure/CHF (3)

Back 26

3 mg/kg/hr - Normal
o 2 mg/kg/hr - Moderate renal failure / CHF
o 1 mg/kg/hr - Severe renal failure / CHF

Front 27

IR or SR use for oral therapy

Back 27

The immediate release product must be used

Front 28

how to give loading dose (oral?)

Back 28

The loading dose should be split into 2 fractions, given 1 h
apart

Front 29

Oral maintenance dose for procainamide- for normal, CHF/liver failure, and renal failure

Back 29

o Normal - 50 mg/kg/day
o CHF & liver failure - decrease dose by 25%
o Renal failure - decrease dose by 50%

Front 30

freq of maintenance oral dose (IR)

Back 30

The total daily maintenance dose is divided, and
given every 4-6 h

Front 31

when to switch to oral SR

Back 31

Conversion to sustained release should be done once
the arrhythmia is controlled

Front 32

rapid vs sustained release graph over time

Back 32

more frequency with IR- Two humps per hump of SR
reach SS after 5-8 half lives

Front 33

AE of procainamide (4)

Back 33

Systemic lupus erythematosus like syndrome**** (slow acetylators...)
GIT: Nausea, diarrhea
Torsade de pointes
Hypotension

Front 34

drug interactions with procaineamide (5)

Back 34

amiodarone
cimetidine
drugs prolonging QT
ranitidine
trimethoprim

all increase serum levels of drug/NAPA except QT drugs, which is more of a synergistic issue

Front 35

what to remember about procainamide (4)

Back 35

Short T1/2- need for maitenence doses with high frequency
NAT2 PG: Fast and slow metabolizers
Renal impairment/CHF
Start low approach because low therapeutic ratio

Front 36

NAPA

Back 36

active metabolite with longer half life

Front 37

bioavailability for oral doses

Back 37

F = 0.83 for immediate release capsules; sustained release
approximates regular capsules