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b. pharm exam 2 (w13) > antidysrhythmic drugs > Flashcards

antidysrhythmic drugs Flashcards

2
Q

drug classification: what are the different actions that classify antiarrhythmics:

A

can be sodium channel or calcium channel blockers : also beta blockers, amio, adenosine, bretylium (blocks K+ channels and NE)

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2
Q

factors causing dysrhythmias:

A 
electrolyte imbalnce
acid base balbnce
myocardial ischemia
altered sns
bradycardia
drug effects
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3
Q

classes of antiarrhythmics and names of each

  1. class I:
  2. class II:
  3. class III:
  4. class IV:
  5. (other..)
A
  1. class I: SODIUM CHANNEL BLOCKERS (block fast inward Na ion current and can decrease rate of phase zero (0) depolarization; further divided into class Ia,Ib,Ic)
  2. class II: BETA BLOCKERS
  3. class III: POTASSIUM CHANNEL BLOCKERS: (amiodorone, bertylium)
  4. class IV: CALCIUM CHANNEL BLOCKERS
  5. other: cardiac glycosides, adenosine
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4
Q

A. Do we need to treat all dysrhythmias?

B. when do we treat dysrhythmias (4 THINGS)

A

A. no, some people have dysrhythmias that are unmasked when asleep, stressed, or in pain.
B. 1. when hemodynamic function is compromised
2. disturbance predisposes to more serious dysrhythmias
3. CNS changes
4. when they cannot be corrected by removing precipitating cause

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5
Q
  1. volatile anesthetics cause dysrhythmias possibly by action on the… or development of …?
  2. what gas might your patient lose his p waves with?
A
  1. SA node (suppression) or development of re-entry circuits

2. forane (isoflurane)

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6
Q
  1. what does lidocaine do (action)

2. what is the class?

A 
1. decreases automaticity and shortens effective refractory period
and action potential duration of the HIS-Purkinje system
	-delays the rate of spontaneous phase 4 depolarization by preventing or diminishing the gradula decrease in potassium ion premeability 
2. class IB
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8
Q 
antiarrhythmics: sodium channel blocker:
lidocaine gtt:
1. dose- (bolus & infusion)
2. onset-
3. peak-
4. duration-
A
  1. Bolus: 1-1.5 mg/kg (1-2%) followed by 0.5 mg/kg every 2-5 minutes (max 200-300 mg in one hour); Infusion: 1-4 mg/min (15 mcg/kg/min)
  2. 45-90 seconds
  3. 1-2 minutes
  4. 10-20 minutes
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12
Q
  1. how are antidysrhythmics classified?

2. what are the major physiological mechanisms causing ectopy?

A
  1. actions on ion channels (sodium or calcium)

2. re-entry alterations or enhanced automaticity

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14
Q 
antidysrhythmics:
Lidocaine: side effects:
1. cardiovascular
2. pulmonary
3. CNS
4. at what plasma levels do these side effects occur
A
  • CV-decreased heart contractility, hypotension, bradycardia, arrhythmias, heart block
  • Pulm-respiratory depression, arrest
  • CNS-potentiates NMBs (succ), sedation (prolonged gtt), tinnitus, seizures, hearing loss, euphoria, anxiety, diplopia
  • s/e occur with plasma levels greater than 5 mcg/ml
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15
Q

How do the doses of lidocaine affect cardiovascular system?

  1. theraputic doses:
  2. higher doses:
  3. use caution in what patients?
A
  1. theraputic doses do not significantly decrease systemic arterial BP, myocardial contractility or C.O.
  2. higher doses decrease contractility and cause vasodilation resulting in decreased BP
  3. use caution in hypovolemia, chf, shock and complete heart block
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16
Q

antiarrhythmics: Lidocaine:
1. metabolism by what organ, what means and to what metabolite?
2. what is important about the metabolite?
3. what happens to the metabolite?

A
  1. metabolized by the liver by oxidative dealkylation to metabolite monoethylglycinexylidide
  2. monoethylglycinexylidide has about 80% of the antidysrhythmic prpoperties
  3. metabolite is hydrolyzed to xilidide
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17
Q

antiarrhythmics: procainamide:
1. action?
2. best uses?

A
  1. increases the effective refractory period and reduces impulse conduction velocity in the atria, HIS- Purkinje fibers and ventriclar muscle
  2. antiarrhythmia control in:
    • malignant hyperthermia
    • lidocaine resistant ventricular arrhythmias
    • a-fib
    • paroxysmal atrial tachycardia
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17
Q

antidysrhythmics:
procainamide:
1. contraindications:
2. use caution in:
3. reduce dose in what patients?
4. patients with what___cardiac issues should have what___ ___before receiving procainamide?
5. what cardiac symptom signifies toxicity (possibly)?
6. what should be monitored with patients receiving procainamide?

A
  1. in patients with complete heart block, torsades and lupus
  2. use caution in 1st degree heart block and arrhythmias form dig toxicity
  3. reduce dose in CHF or renal failure
  4. patients with afib or aflutter should have RATE CONTROLLED prior to receiving procainamide.
  5. QRS widening of greater than 25% of baseline
  6. plasma levels, vital signs and ekg
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17
Q

antiarrhythmics:
procainamide:
1. what may occur with rapid administration?
2. ___ (condition)caused by the toxicity of ____(what drug)mixed with procainamide can cause ___&___?
3. procainamide potentiates the effects of what anesthesia meds?
4. what GI meds cause increased serum levels?

A
  1. hypotension may occur
  2. heart block caused by dig toxicity mixed with procainamide can cause v fib or asystole
  3. potentiates effect of NDMRs
  4. cimetidine (tagament) and ranitidine (zantac) cause increased serum levels
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18
Q

antiarrhythmics: procainamide
1. half life increases with what conditions?
2. how prolonged is it with these conditions?

A
  1. Half life of NAPA is prolonged in patients with CHF and renal insufficiency
  2. 7-70 hours
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18
Q

antiarrhythmics:
procainamide:
1. what plasma levels are theraputic for antidysrhythmia?
2. what effects on myocardium can be seen and at what levels?

A
  1. theraputic range=4-12 mcg/ml

2. myocardial depression is seen at greater than 8 mcg/m

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18
Q

antiarrhythmics: procainamide:
1. onset:
2. peak effect:
3. duration:

A
  1. onset: immediate
  2. peak: 5-15
  3. duration: 2.5 hours in fast acetylators
    5 hours in slow acetylators
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19
Q

antiarrhythmics: Procainamide:
1. loading dose:
2. max dose:
3. maintainance:
4. theraputic level:

A

1 Loading dose: 100 mg slow IV push every 5 min until arrhythmia is suppressed or hypotension occurs

  1. max: 1 gm; dilute 1000 mg in 50 ml of D5W
  2. maintainance: infusion 2-6mg/min
  3. theraputic level: 4-12 mcg/ml
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20
Q

antiarrhythmics:
1. adenosine: aka?
2. what is the action of adenosine
3. what dysrhythmias is it good for/ what is it a substitute for?
4. what dysrhythmias is it not good for?
5. what happens when vascular adenosine receptors are activated?
6. what else does it prevent the heart from doing?

A
  1. adenocard
  2. metabolite of an endogenous (made in our body) nucleotide that slows conduction thru SA & AV node by stimulating adenosine receptors to INCREASE K+ ion currents which SHORTENS the ACTION POTENTIA DURATION and hyperpolarizes the cardiac cell (slowing the depolarization rate down)
  3. Treatment for PSVT and WPW, (alternative to Ca+blocker).
  4. not good for a-fib, a-flutter, or v-tach
  5. vasodilation (thus decrease in SVR/ BP).
  6. prevents heart rom responding to endogenous sympathetic activity
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22
Q

antiarrhythmics: adenosine
1. dose?
2. what commonly will occur with infusion?
3. how should it be fast flushed?
4. what is the best line or best location for instillation?

A
  1. 6-12 mg can be repeated q 1-2 minutes
  2. chest pain, temporary cessation of rhythm, flushed skin
  3. follow with 20 ml saline
  4. best if given via central line (second best is AC iv)
23
Q

antiarrhythmics: adenosine:
1. why is it so short lived?
2. main med used for “____” Cardioversion
3. what are side effects (definite and probable)?
4. what conditions is it contraindicated in?

A
  1. metabolized rapidly in blood and tissue by ADENOSINE DEAMINASE (must be given fast flush)
  2. “CHEMICAL” cardioversion
  3. s/e: will produce: decreased SVR(pvr), and BP; may produce: bronchospasm, short lasting 1st, 2nd & 3rd degree heart blocks
  4. contraindicated in patients with 2nd & 3rd degree heart blocks or sick sinus syndrome (unless pacer is IN PLACE).
24
Q

antiarrhythmics: amiodorone:
1. what is it?
2. what is it used to treat?
3. class of drug? How does that work?

A
  1. potent antiarrhythmic with a wide spectrum of activity for refractory SVT and ventricular tachy-dysrhythmias; ALSO potent vasodilator.
  2. treatment of refractory v-fib, refractory a-fib or a-flutter, PSVT, prophylaxis of PSVT in patients with WPW.
  3. class III Potassium channel blocker –(prevents potassium from re-entering the cell prolonging refractory period (potassium influx ends refractory period)).
24
Q

antiarrhythmics: adenosine:
1. onset:
2. peak:
3. duration:
4. how should it be given
5. dont confuse it for what medication? used for?

A
  1. o:<20 seconds
  2. p: 20-30 seconds
  3. d: 20 seconds or so
  4. give fast flush, d/t quickly metabolized
  5. dont confuse with: adenosine PHOSPHATE; used for management of varicose venis
25
Q 
antiarrhythmics: amiodorone:
adverse effects:
1. cardiac:
2. respiratory:
3. nervous:
4. hepatic:
5. optic:
6. why are side effects so drastic with amiodorone
7. what drugs does it increase levels of?
A
  1. arrhythmias, chf, chest pain
  2. pneumonitis, alveolitis, pulmonary edema, dyspnea, cough, ards
  3. peripheral neuropathy, tremors
  4. hepatitis, elelvated LFTs
  5. blurred vision, optic neuropathy, photosensitivity, blindness
  6. because it is highly protein bound (hides in tissues) with a long half life (25-110 days). it is also highly lipid soluble and may have cardiac concentrations 50x plasma.
  7. coumadin, dig, procainamide (d/t inhibition of cp450 in liver).
25
Q

antidysrhythmics: amiodorone:
1. action (a,b,c,d)
2. why is amiodorone a “scary drug”?

A
  1. a-works directly on myocardium to prolong action potential duration and increase refractory period (by blocking K+ influx);
    b-has weak sodium channel blocking effect;
    c-noncompetitively inhibits alpha and beta receptors;
    d-vagolytic and Ca channel blocking effects;
  2. HIGHLY toxic drug, many adverse reactions occur in patients taking it for ventricular arrhythmias.
26
Q

antidysrhythmics: amiodorone:
1. dose (IV, PO)
2. onset: (IV, PO)
3. peak: (PO)
4. duration:

A
  1. 15 mg/min over 10 minutes; then infusion of 1 mg x 6 hours , than 0.5 mg x 18 hours (24 hrs total)
  2. iv-immediate: PO- 2-4 days
  3. PO-1-5 months
  4. months??
27
Q

what drugs are in the classes of the sodium channel blockers:

  1. class 1A
  2. class 1B
  3. class 1C
A
  1. class 1A: quinidine, procainamide
  2. class 1B: lidocaine, tocainide
  3. class 1C: flecainide, propafenone
28
Q

cardiac arrhythmia info:

  1. incidence of in patients undergoing cardiac and non cardiac major surgery?
  2. atrial fibrillation: seriousness?
A
  1. 16-84%

2. non serious but can lead to potentially fatal AV blocks/ V-fib

29
Q

antidysrhythmic check:

  1. what are the 2 major mechanisms of ectopy?
  2. name 6 factors involved in dysrhythmias?
  3. when do dysrhythmias require intervention?
A
  1. Re-entry and enhanced automaticity
  2. -lyte or acid base imbalances
    • hypoxemia
    • ischemia
    • altered SNS activity
    • bradycardia
    • drug effects
  3. -cannot be corrected by removing precipitating factor
    • hemodynamic instability
    • dysrhythmia can turn more serious
30
Q

antidysrhythmics: calcium channel blockers:
1. what are they also known as?
2. what is the action?

A
  1. calcium entry blockers or calcium antagonists
  2. selectively interfere with calcium ion movement across myocardial smooth muscle; interfere with alpha subunit of the L-type slow channels
31
Q

antiarrhythmics: calcium channel blockers:
1. what class are calcium channel blockers?
2. what class is selective for AV node?
3. what class is selective for arteriolar bed?
4. what is the use of calcium channel blockers?

A
  1. class IV
  2. phenylalkylamines and benzothizepines are AV node selective
  3. 1,4-dihydropyrimidines are selective for arteriolar beds
  4. used for HTN, angina, arrhythmias, coronary artery spasm and migraine prophylaxis
32
Q

antiarrhythmics: calcium channel blockers:
1. how do ccbs work for BP? what is effect?
2. how do cccbs work as antiarrhythmics? what is effect?
3. how do cccbs work for heart rate? what is effect?

A
  1. selectively inhibit the transmembrane infulx of calcium ions into cardiac and smooth muscle-causing dilation of vessels and slowing rate
  2. antiarrhythmic effect d/t inhibition of calcium influx through the slow channels in cardiac conduction-interrups re-entry at AV nodes and restores NSR in PSVT.
  3. slows AV conduction and prolongs effective refractory period within the AV nodes. - reduces ventricular rate in atrial fibrillation and atrial flutter
33
Q

if calcium channel blockers vasodilate the peripheral vessels, what is happening to cerebral vessles?

A

cerebral dilation which increases cerebral blood flow and ICP

34
Q

antiarrhythmics: calcium channel blockers:
1. decreased clearance with what medications?
2. serum levels increased with what citrus fruit juice (deadly!!!)?
3. chemically incompatible with what solutions?
4. contraindicated with what conditions?

A
  1. decreased serum clearance with cimetidine
  2. grapefruit juice
  3. incompatible with bicarbonate and nafcillin
  4. sick sinus syndrome (sss), 2nd or 3rd degree AV block, acute MI, cardiogenic shock, V-tach, a-fib, a-flutter, WPW, short P-R syndromes
35
Q 
antiarrhythmics: calcium channel blockers:
what do calcium channel blockers do to each item?
1. myocardial contractility?
2. heart rate?
3. SA node?
4. AV node?
5. smooth muscle?
6. blood pressure?
A
  1. decrease myocardial contractility
  2. decrease heart rate
  3. decrease activity of SA node
  4. slow conduction thru AV node
  5. relax vascular smooth muscle
  6. decrease blood pressure
36
Q 
antiarrhythmics: calcium channel blockers
adverse effects:
1. cv?
2. pulm?
3. cns?
4. gi?
5. allergic?
A
  1. cv: hypotension, bradycardia, rebound tachycardia from decreased PVR
  2. pulm: bornchospasm, laryngospasm
  3. cns: dizziness, headache, seizures
  4. gi: nausea, abdomen discomfort
  5. allergic: urticaria, pruritis
37
Q

antiarrhythmics: verapamil:
1. classification
2. what does isomerization have to do with this drug?
3. 1.6 times stronger than what drug?
4. uses:

A
  1. classified phenylalanine
  2. -destroisomer devoid of activity at slow channels but acts on fast channels which accounts for local anestetic properties
    • levoisomre specific to slow channels predominantly, accounts for classification as calcium channel blocker
  3. than procaine (as a local anesthetic)
  4. PSVT, a-fib, a-flutter
38
Q

antiarrhythmics: verapamil:
1. metabolism:
2. excretion:
3. protein binding:

A
  1. almost completely metabolized in liver
  2. excretion mostly renal (approx 70% recovered in urine as active metabolites and 15% excreted in bile)
  3. major metabolite is norverapamil and is active enough to contribute to antidysrhythmic properties
  4. 90% protein bound
39
Q

antiarrhythmics: verapamil:
1. dose
2. onset
3. peak
4. duration

A
  1. 5-10 mg over 2 minuts, repeat in 30 min
  2. o: 2-5 min
  3. p: within 10 min
    d: 30-60 min
40
Q

antiarrhythmics: diltiazam
1. classification:
2. similar to what other antiarrhythmic in clinical use?
3. metabolized where? any metabolites?
4. excreted primarily where? (secondarily where?).
5. P.O. absorption (good or poor)?
6. protein binding (what %)?

A
  1. classified benzothiazepine
  2. similar to verapamil
  3. metabolized in liver into INACTIVE METABOLITES
  4. excreted primarily in bile (60%) and in urine to lesser extent (35%).
  5. well absorbed PO
  6. 70-80% protein bound
41
Q

antiarrhythmics: diltiazam:
1. onset
2. peak
3. duration
4. indications:
5. dosage

A
  1. o: less than 3 minutes
  2. p: 2-7 minutes
  3. d: 1-3 hours
  4. PSVT, A-fib, A-flutter
  5. d: 20 mg over 2 minutes, re-bolus after 15 minutes with 25 mg or begin infusion of 5-10 mg/hr.
42
Q

antiarrhythmics: Nifedipine:
1. what is the chemical structure (iupac) and action?
2. what is venous effect?
3. what about conduction (SA and AV node)
4. how does this medication decrease blood pressure?

A
  1. 1,4-dihydropyridine; has coronary and peripheral arterial vasodilator effects
  2. minimal effects on venous capitance
  3. little to no effect on SA and AV node conductance
  4. causes peripheral vasodilation with a decrease in systemic blood pressure
43
Q

antiarrhythmics: nifedipine:
1. uses:
2. po bioavailability:
3. protein binding:
4. metabolism:
5. elimination half time:

A
  1. used for angina especially d/t coronary artery vasospasm, HTN, pulmonary hypertension
  2. po bioavailability=40-60%
  3. protein binding=90%
  4. metabolism: 80% renal (15% hepatic)
  5. elimination half time: 2-5 hours
44
Q

antiarrhythmics: Nifedipine:
1. potentiates what meds?
2. what medication does it potentiate in pre-eclampsia?
3. sublingual administration causes what?
4. what does increased SNS cause (in brain, and heart)?

A
  1. potentiates NMBs
  2. potentiates magnesium in pre-eclampsia
  3. sublingual use for HTN causes a rapid decrease in BP which activates the baroreceptors which causes increased Sympathetic nervous system activity and heart rate
  4. SNS activity can result in cerebral ischemia, syncope, stroke, severe hypotension and heart block
45
Q

antiarrhythmics: nifedipine:
1. oral dose & onset
2. iv dose and onset
3. sublingual dose and onset

A
  1. 10-20 mg po ; 20 min
  2. 5-15 mcg/kg ; 1-3 minutes
  3. 10-20 mg sublingual ; 3 min
46
Q

antiarrhythmics: dilantin:
1. what is its primary use?
2. what class antiarrhythmic is it? what type arrhythmias?
3. metabolized by____ excreted by_____?
4. blood levels are increased in what organ disease?
5. what medications increase blood levels?
6. what medications decrease blood levels?

A
  1. used as anticonvulsant
  2. class 1B antiarrhythmic for ventricular arrhythmias
  3. metabolized in liver; excreted by kidneys
  4. liver disease
  5. warafin, phenylbutazone or isoniazid
  6. barbiturates
47
Q

antiarrhythmics: dilantin:
1. cns symptoms of toxicity?
2. what endocrine effects?
3. what effect on blood cells?
4. other signs of toxicity?

A
  1. cns symptoms include ataxia, nystagmus, vertigo, slurred speech, sedation, confusion
  2. inhibits release of insulin causing hyperglycemia
  3. bone marrow depression resulting in leukopenia, granulocytopenia, thrombocytopenia
  4. nausea, rash, megoblastic anemia
48
Q

Questions i got wrong: 5
1.Adenosine acton
2. Dobutamine dose:
3.

A
  1. K+ influx, Shorten refractoery period

2. 2-20mcg

b. pharm exam 2 (w13) (8 decks)

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