Antidysrhythmics ppt Flashcards
Due to Mr. Boyd's inability to transpire his knowledge to the brains of the new and uprising stars study this to pass his section
what are 2 major physiologic mechanisms that cause ectopic cardiac dysrhythmias are what?
- reentry
- enhanced automaticity
What factors can cause cardiac dysrhythmias? This is a huge card don’t get overwhelmed look it through very important he and the book make a big deal about it.
- Arterial hypoxemia
- Electrolyte abnormality (hypokalemia or hypomagnesemia from diuretics predispose to ventricular dysrhythmias )
- Acid-base abnormalities (alkalosis more likely than acidosis to trigger cardiac dysrhythmia {i dunno I found that cool})
- Altered autonomic nervous system activity (increased activity predisposes to ventricular fibrillation)
- Bradycardia (predisposes to ventricular dysrhythmias)
- drugs (prolong QT-congenital or acquired) acquired (drugs)- hypoK, HypoMg, hypoCa, quinidine, amiodarone, metoclopramide, CCB, droperidol, haloperidol, R on T phenomenon
- Myocardial ischemia
- altered sympathetic activity (lowers fibrillatory threshold)
- Dilated cardiomyopathy (cells stretch)
All on pg 336 Nag
When to treat dysrythmias during anesthesia?
trick question…
the majority of cardiac dysrhythmias that occur during anesthesia DO NOT REQUIRE TREATMENT.
Treat only if
-can’t fix cause
-hemodynamic compromise
-can degrade to a more serious dysrythmia
classes of antidysrhythmics
I-IV for a bonus there is a class A B C for class I
Class I:
what group are they?
They work by inhibiting what?
- SODIUM CHANNEL BLOCKERS
- inhibit fast Na+ channels
MOA for ALL class I drugs (sodium channel blockers)
- Block fast inward Na+ current and can decrease the rate of phase 0 depolarization
- ALL CLASS I DRUGS-
1) depress automaticity
2) depress conduction in bypass tracts
3) have a depressant effect on phase 0 depolarization @ rapid heart rates
Class IA MOA
4
- depress phase 0 depolarization
- *prolong the action potential duration
- slow conduction velocity
- intermediate binding and dissociation from receptor
Class IB MOA
4
- *shorten the action potential duration
- little effect on phase 0 depolarization
- *** most rapid binding and dissociation
- *** bind in the inactive state- more effective for tachy
What is the main difference b/t Class IA and IB
- IA prolongs action potential duration
- IB shorten action potential duration
Class IC MOA
5
-Marked depress Phase 0 depolarization
** Minimal effect on the action potential duration
Profoundly slow conduction velocity
-slowest binding and dissociation
-Use dependent CV and QRS duration
If for every class I drug, you had to pick 4 main characteristics to differentiate them what are they? and then differentiate them
1) phase 0 depol
2) action potential
3) binding and dissociation
4) conduction velocity
1) phase 0 depol
- - IA -depresses
- - IB- little effect
- - IC- Marked depress
2) action potentials
- -IA- prolongs
- -IB- shortens
- -IC- minimally effects
3) binding and dissociation
- -IA- intermediate
- -IB- most rapid
- -IC- slowest
4) Conduction Velocity
- -IA-slow
- -IB-n/a
- -IC- profoundly
What is the most familiar class I group?
IB
which Class IA drug is very bad b/c it has active metabolites?
procainamide
Class IA drugs
Quinidine
Pocainamide
Disopyramide
The book adds -Moricizine
Class IB drugs
Lidocaine
Mexiletine
phenytoin
additional
Tocainide
Class IC drugs
Flecainide
Propafenone
additional
Lorainide
His chart has moricizine here??
Class II down and dirty MOA
decrease rate of depolarization
Class III down and dirty MOA
inhibit K+ channels
Class IV down and dirty MOA
inhibits slow Ca++ channels
Which Class IA drug increases SVR
Disopryamide
Class II drugs
remember they decrease the RATE of depolarization
- Propanolol
- Esmolol
Book also adds
Acebutolol
Class III drugs
- Amiodarone
- Ibutilide
- Sotalol (II and III)
book adds
Dofetilide
bretylium
Which drug is both class II and III
Sotalol
Class IV drugs
remember inhibits slow Ca++ channels
- verapamil
- Diltiazem
what are 2 unclassified antidysrhythmic drugs
Digoxin (lanoxin)
Adenosine (adenocard)
Procainamide
class?
analog of what LA?
treats what?
- IA
- Procaine
- Reentry and automaticity
- ——Atrial and Ventricular tachydysrhythmias
Procainamide
SE?
Active metabolite?
- Prolonged QT, QRS, ST-T changes (can develop heartblock) and Profound HYPOTENSION
- N-acetyl procainamide (NAPA)-contributes to antidyrhythmic effects (K+ channel blockade)
Procainamide
Metabolism
Renal 40%
hepatic 60%
–hepatic metabolism obviously causes active metabolites
Procainamide
odd or unique SE besides the HYPOTENSION
Lupus like syndrome
Procainamide
dose???
initial then titration
- 100 mg Q5 min until dysrhythmia controlled or total dose reaches 15mg/kg
- once controlled infuse 2-6mg/min
Lidocaine
class?
treats what?
- IB
- primarily reentry
- ——-Ventricular dysrhythmias
- ——- PVC, V-tach
Lidocaine
MOA
decreases the rate of phase 4 repolarization by diminishing the decrease in K+ permeability
-Decreases AV node and HIS conduction in high doses
Lidocaine
metabolism
hepatic- active metabolites
Lidocaine
SE:
- Toxic plasma concentration= vasodilation and myocardial depression
- SZ @ plasma levels > 5 mcg/ml
- CNS depression/apnea/arrest at plasma concentration > 10 mcg/ml
Lidocaine
Dose? both load and infusion
load- 1-2 mg/kg
Infuse- 1-4 mg/min
Phenytoin
class?
treats what?
effects are similar to what other drug?
- IB
- reentry and automaticity
- lidocaine
Phenytoin
treats Ventricular Dysrhythmias associated with _____ toxicity
digitalis
Phenytoin
1) Shortens QT more than_______
2) Hypotension occurs with ______
3) may depress ___ node activity, improves ___ node activity
1) any other
2) rapid administration
3) SA node / AV node
Phenytoin
metabolism
half time
hepatic
24 hours
Phenytoin
SE
- Ataxia
- nystagmus
- vertigo
- slurred speech
- Sedation
- mental confusion ( >18mcg/ml blood level)
- inhibits insulin secretion (hyperglycemia)
- Leukopenia
- agranulocytosis
- thrombocytopenia
- BM ( not poop, bone marrow) suppression
Beta Blockers
class?
actions?
- II
- decreased conduction velocity
- Increased refractory period
- Increased PR duration
- Decreased QT duration
Carvedilol
also blocks what?
Modestly prolong ______
chronic administration causes what?
- K+, Ca++, Na+
- APD ???? (action potential depolarization)
- increased # of Ca++ channel numbers
Class III
MOA?
- Block inhibitory K+ channels
- Prolong action potential, repolarization and refractory period
Amiodarone
class?
treat what?
- III
- reentry and automaticity
- —-SVT, VT, and A-fib
Amiodarone
suppresses tachydysrhythmias associated with what d/o?
WPW
Amiodarone
may decrease mortality after what?
MI
Amiodarone
decreases conduction in the __1__ __1__, and the __2__ __2__.
1) - AV node
2) - bypass tracts
Amiodarone
prolongs ______ ______ in all cardiac tissues?
Refractory period
Amiodarone
is made up of 37% what?
iodine
cool fact
Amiodarone
the antiadrenergic effect is due to blockade of what?
alpha and beta
- K+ and Ca++ channel blocking effects
Amiodarone
had minor __1__ inotropic effects, and potent __2__ properties
1) negative
2) vasodilating
Amiodarone
dilates _____ arteries, leading to questionable antianginal effects
Coronary arteries
Amiodarone
T 1/2 ?
metabolism?
29 days
hepatic
Amiodarone
SE?
- Pulm alveolities (5-15%) (acute or insidious)
- QT prolonged (brady, block, low CO)
- Antiadrenergic- accenuated under GA
- Depress Vit K factors
- corneal microdeposits, photosensitivity
- rash
- Cyanotic discoloration
- peripheral neuropathy
- weakness
- increased DIG levels (70%)
- thyroid abnormalities
Amiodarone
dose
150mg/100 mg over 10 min
gtt 900 mg/500 ml mix
1 mg/min x 6 hours
0.5 mg/min x 18 hours
Sotalol
Class
II and III
Sotalol
why is it 2 classes
- nonselective Beta antagonist (low doses) II
- prolongs action potentials of all tissues (high doses) III
Sotalol
excretion
Renal
Sotalol
Main SE
Torsade de pointes!!!!!
Digoxin
Class?
treats what?
Unclassified
- Atrial tachydysrythmias and Cardiac failure
Digoxin
MOA (basic)
positive inotrope- through inhibition of the NA-K ATPase ion transport system
- SLOWS CONDUCTION THROUGH AV NODE
- thus increase SV and decreases LVEDP
Digoxin
Bc we just learned that dig is positive inotrope- through inhibition of the NA-K ATPase ion transport system
-SLOWS CONDUCTION THROUGH AV NODE, what does this mean?????? only 2 correct answers!!!!! not 300 don’t try it
thus increase SV and decreases LVEDP
Digoxin
positive __1__
Negative __2__
Lusitrope (myocardial relaxation)
Chronotrope (speed on contraction)
Digoxin
narrow or wide therapeutic index (range)
Narrow
this was a gimme if you missed it stand up drop your pants, put on golf cleats and donkey kick yourself in your pathetic little nut sac that hangs off your little NP vagina full of crayons and feces, you dumb dumb dumb fucktard bastard
Digoxin
Hypokalemia is induced by what?
What occurs during this dig toxicity and hypokalemia?
-dig toxicity
-HypoK+- increased myocardial binding
- hyperventilation
-hyperCa++
-hypoMg
impaired renal function
Digoxin
symptoms of dig toxicity
–Early signs
Anorexia/ N/V/ pain stimulating trigeminal neuralgia
- other signs
- Prolonged PR
- degrading block
- atrial tachy with block
- V-fib- arrest
