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Anesthesia Pharm II > Antidysrhythmics Study Guide > Flashcards

Antidysrhythmics Study Guide Flashcards

1
Q

How many classifications of antidysrhythmics drugs are there?

A

4 classifications

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2
Q

What is the mechanism of action for Class I?

A

Class I: sodium channel blockers

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3
Q

What is the mechanism of action for Class II?

A

Class II: beta blockers

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4
Q

What is the mechanism of action for Class III?

A

Class III: potassium channel blockers

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5
Q

What is the mechanism of action for Class IV?

A

Class IV: non-dihydropyridines

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6
Q

Class I antidysrhythmics have 3 subclasses. What is the MoA for each of them and name a drug or two that falls into the categories?

A

Class IA: prolong the action potential duration (quinidine, procainamide)

Class IB: shorten the action potential duration (lidocaine, phenytoin)

Class IC: decrease the rate of phase 0 depolarization (flecainide, propafenone)

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7
Q

What are some Class II drugs?

A

propranolol

esmolol

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8
Q

What are some Class III drugs?

A

amiodorone

sotalol

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9
Q

What are some Class IV drugs?

A

verapemil

diltiazem

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10
Q

What occurs during phase 0 of the ventricular myocyte?

A

Na rapidly enters the cell (AKA depolarization)

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11
Q

What occurs during phase 1 of the ventricular myocyte?

A

K and Cl move out of the cell the inward Na current rapidly decays (AKA the start of repolarization)

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12
Q

What occurs during phase 2?

A

Ca enters the cell, moving slowly K exits the cell these two balance out the membrane potential and cause the “plateau”

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13
Q

What occurs during phase 3?

A

Ca current decays K continues to exit the cell, eventually getting the cell back to its resting membrane potential

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14
Q

What occurs during phase 4?

A

slow K leak that keeps the membrane at its resting potential

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15
Q

What do all the phases look like?

A
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16
Q

What is the MoA of procainamide?

A
  • Class IA antidysrhythmic drug
  • Decreases the slope of phase 0 depolarization
  • Lengthens the action potential duration and the effective refractory period (Na channel action) and lengthens the repolarization period (K channel blockade).
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17
Q

What is the indication for procainamide?

A

ventricular tachydysrhythmias and atrial tachydysrhythmias

(though not as effective as quinidine)

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18
Q

What are side effects of procainamide?

A

Hypotension (due to myocardial depression)

Ventricular asystole or fibrillation (when administered in the presence of heart block)

Ventricular dysrhythmias (in excess plasma levels)

Lupus like syndrome (present in slow acetylators)

Fever, rash, nausea, vomiting

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19
Q

What are the EKG changes seen with procainamide?

A

QRS prolongation

ST-T wave changes on the EKG

Prolongation of the QTc (similar but less than with quinidine)

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20
Q

Procainamide dose?

A

Titrate to effect IV: 100-200 mg loading dose or 15-18 mg/kg infused slowly (over 15-20 minutes), may repeat q 5 minutes to effect.

Then a rate of 1-6 mg/min (Therapeutic levels are 4-8 micrograms/mL)

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21
Q

What is the MoA of lidocaine?

A
  • delays the rate of spontaneous phase 4 depolarization by preventing or diminishing the gradual decrease in potassium ion permeability that normally occurs during this phase.

(Does not alter spontaneous phase 4 depolarization in atrial cardiac cells) [this was in S&H]

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22
Q

Indication for lidocaine?

A
  • Suppression of ventricular dysrhythmias (having minimal effects on supraventricular tachydysrhthmias)
  • Suppresses reentry cardiac dysrhythmias such as PVCs and VTach.
  • Efficacy of prophylactic lido therapy for preventing early vfib after acute MI has not been documented and is no longer recommended.
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23
Q

Side effects of lidocaine?

A
  • Bradydysrhythmias and asystole.
  • Toxic doses (>5mcg/ml) produce peripheral vasodilation and direct myocardial depression, resulting in hypotension
  • Seizures are possible at high doses
  • CNS depression, apnea, and cardiac arrest at greater than 10mcg/ml
  • Conculsive threshold is decreased during arterial hypoxemia, hyperkalemia, or acidosis
  • If toxic, start IV lipid therapy. (per the book, but we know that this probably won’t work)
24
Q

EKG changes seen with lidocaine?

A
  • No significant effect on QRS or QTc or on AV conduction
  • May decrease conduction in AV node as well as bundle of HIS. (prolonged PR, widened QRS if toxic)
25
Q

Dose for lidocaine?

A
  • For people with normal cardiac and liver function 2mg/kg IV followed by a continuous infusion of 1-4 mg per minute.
  • Decreased CO or hepatic blood flow (as with anesthesia, acute MI, CHF) decrease the dose by 50%.
26
Q

What is the MoA of phenytoin (dilantin)?

A
  • Class IB antidysrhythmic
  • Reduces the slope/slows phase 4 depolarization by interfering with K+ permeability.
  • Also reduces the slope/slows Phase 0 (phase characterized by RAPID influx of Na+) by preferentially blocking Na+ channels in rapidly-firing/depolarized myocardial tissue. This action slows the rate of myocardial depolarization. [per the book]
27
Q

Indication for phenytoin?

A
  • Classically used for ventricular dysrhythmias r/t digoxin toxicity*
  • Paradoxical V-tach or torsades de pointes (prolonged QT)
  • Ventricular dysrhythmias due to other causes (although less effective for this compared to quinidine, procainamide, or lidocaine)
28
Q

Side effects of phenytoin?

A

hypotension when delivered rapidly in high doses

nausea

pain at injection site (very alkaline)

increased blood glucose d/t inhibition of insulin secretion

megaloblastic anemia

thrombocytopenia d/t depression of bone marrow

phenytoin toxicity typically at levels >18mcg/mL (symptoms: CNS/cerebellar disturbances – ataxia, nystagmus, vertigo, slurred speech, sedation, confusion)

29
Q

EKG changes with phenytoin?

A

Shortens QT interval more than any other antidysrhythmic drug No significant effect on ST waves or QRS complex.

Improved AV node conduction SA node depression (volatile agents also depress SA node so be mindful of this if phenytoin is administered under general anesthesia)

30
Q

Phenytoin dose?

A

1.5mg/kg (or 100mg) q5min

up to 15mg/kg (max 1000mg) IV

31
Q

What is the MoA of amiodarone?

A
  • Class III antidysrhythmic
  • prolongs the effective refractory period in ALL cardiac tissue, as well as an antiadrenergic effect (noncompetitive blockade of alpha & beta receptors)
  • minor negative inotropic effect as well as potent vasodilation properties (antianginal by dilating coronaries)
32
Q

Indication for amiodarone?

A

Supraventricular & ventricular tachydysrhythmias (suppression of SVT, AFib, VT, VF, WPW) {depresses conduction in AV node & accessory bypass tracts}

33
Q

Side effects of amiodarone?

A
  • Pulmonary toxicity (is worse with either acute or slow insidious onset) (odd, i know)
  • CV: atropine resistant bradycardia* (due to depression of the automaticity of the SA node, negative dromotropy & decreased sensitivity to catecholamines & SNS stimulation 2nd to inhibition of alpha & beta receptors)
  • Inhibits P-450 thus increased serum levels of Digoxin, Warfin, etc. As well as displaced medications off protein binding sites to further increased serum drug levels (i.e. Dilantin)
  • affects the thyroid by either hypo or hyperthyroidism due the iodine (37% of the medication)
  • Other stuff: photosensitivity, neurological toxicity, peripheral neuropathy, sleep disturbances, HA, skeletal muscle weakness
34
Q

EKG changes with amiodarone?

A
  • May prolong Q-T
  • May develop AV heart block with IV administration
  • Bradycardia due to the depression of the automaticity of the SA node
35
Q

Dose of amiodarone?

A

IV – Acute: 300mg in presence of VT or VF; 150mg load over 10 min them gtt 1mg/min x 6 hours then decrease to 0.5 mg/min for 18hours (recurrent atrial or ventricular tachydysrhythmias)

(PO - 200mg QD suppression of supraventricular tachydysrhythmias; 400mg QD for suppression of ventricular tachydysrhythmias) PO for knowledge!!

36
Q

What is the MoA of digitalis?

A
  • Cardiac glycosides selectively and reversibly inhibit the sodium-potassium adenosine triphosphate (ATP) ion transport system (sodium pump) located in the sarcolemma of cardiac cell membranes.
  • The resulting increase in sodium ion concentration in cardiac cells leads to decreased extrusion of calcium ions by the sodium pump mechanism.
  • It is presumed that this increased intracellular concentration of calcium ions is responsible for the positive inotropic effects of cardiac glycosides.
37
Q

Indication for cardiac glycosides, such as digitalis?

A

congestive heart failure (increases inotropy, decreases chronotropy and dromotropy)

38
Q

Side effects of digitalis?

A
  • hypokalemia*
  • trigeminal neuralgia*
  • N/V - anorexia
39
Q

EKG changes with digitalis?

A
  • prolonged PR interval
  • degrading block
  • atrial tachycardia with block
  • V-fib arrest***
40
Q

What is the MoA for Class II beta blockers? (propranolol, esmolol, and metoprolol)

A
  • Decrease the rate of spontaneous phase 4 depolarization resulting in decreased ANS activity, which may be important in suppression of ventricular dysrhythmias during MI and reperfusion.
  • Slow the speed of conduction of cardiac impulses through the atrial tissues resulting in prolongation of the PR interval.
  • Blockade of the responses of beta receptors in the heart to SNS stimulation and effects of catecholamines
41
Q

Indications for Class II beta blockers?

A
  • Cardiac dysrhythmias related to enhanced activity of the SNS (perioperative stress, thyrotoxicosis, pheochromocytoma)
  • Propranolol and esmolol are effective for controlling the rate of ventricular response in pts with Afib and A Flutter.
  • May also be used for controlling Torsades (esp Propranolol)
42
Q

Side effects of Class II beta blockers?

A
  • bradycardia
  • hypotension
  • myocardial depression
  • bronchospasm
  • patients with CHF may have worsening of symptoms d/t blockade of SNS
  • use with preexisting AV block not recommended
43
Q

EKG changes with Class II beta blockers?

A
  • Decreased conduction velocity
  • Increased refractory period
  • Increased PR duration
  • Decreased QT duration
44
Q

Doses of Class II beta blockers? (propranolol, esmolol, and metoprolol)

A

Propranolol: 10-80 mg Q6-8Hours

Esmolol: HTN - 0.5-2 mg/kg; SVT loading dose 500 mcg/kg over 1 minute followed by 50-200 mcg/kg/min infusion

Metoprolol: HTN/Angina100-450mg daily, Acute MI -15mg IV then switch to 100mg PO twice daily

45
Q

What is the MoA for Class III beta blockers? (sotalol)

A
  • Blocks Potassium channels resulting in prolongation of cardiac depolarization, action potential, and refractory period.
  • Nonselective Beta Blocker at low doses, and at higher doses, it prolongs the cardiac action potential in the atria, ventricles, and accessory bypass tracts.
  • Usually used for patients with life-threatening Ventricular dysrhythmias.
  • Does not bind to plasma proteins, is not metabolized, and does not cross the BBB. Use carefully in pts with renal dysfunction.
46
Q

Indication for sotalol?

A
  • Sustained VT or VF.
  • May also be used to treatment of atrial tachydysrhythmias.
47
Q

Side effects of sotalol?

A
  • Torasades de pointe**
  • Decreased myocardial contractility
  • bardycardia
  • delayed conduction through the AV node
  • others: fatigue, dyspnea, vertigo and nausea.
48
Q

EKG changes with sotalol?

A
  • Prolongs QT interval
  • Torsades*
  • decreases conduction velocity
  • Increases action potential
  • Increases P-R and QRS duration
49
Q

Sotalol dose?

A

240-320mg PO twice daily

50
Q

What is the MoA of calcium channel blockers? (class IV: verapamil and diltiazem)

A
  • Blocks L-type Ca Channel
  • decreases heart rate by decreasing contractility
  • Depresses AV node
51
Q

Indications for non-dihydropyridines?

A
  • Afib with RVR
  • SVT (First line med)
  • Vasospastic angina
  • HTN
  • symptomatic hypertophic cardiomyopathy
  • may be useful for idiopathic VT
52
Q

Side effects of non-dihydropyridines?

A

(-) chronotropy

(-) ionotropy

(+) coronary artery dilation (min)

(+) peripheral dilation (min) (the side effects with Diltiazem are not as impressive as with Verapamil)

53
Q

EKG changes with non-dihydropyridines?

A
  • AV block
  • Bradycardia
  • Effect P-R duration
  • No effect on QT, QRS duration. (the EKG changes with Diltiazem are not as impressive as with Verapamil)
54
Q

What considerations need to be made before patients undergo anesthesia while they are taking antidysrhythmic medications?

A
  • Drugs administered for the chronic suppression of cardiac dysrhythmias pose little threat to the uneventful course of anesthesia and should be continued up to the time of induction.
  • The majority of cardiac dysrhythmias that occur during anesthesia do not require therapy.
  • Cardiac dysrhythmias, however, do require treatment when (a) they cannot be corrected by removing the precipitating factor, (b) hemodynamic function is compromised, (c) the disturbance predisposes to more serious cardiac dysrhythmias.
55
Q

Which antidysrhythmics have active metabolites and do these contribute to the antidysrhythmic action of the medication?

A

Active metabolite that contributes:

  • procainamide
  • verapamil
  • amiodarone (active metabolite with a longer elimination half time than parent drug)

Active metabolite that has weak skillz:

  • propranolol
  • lidocaine

Anesthesia Pharm II (19 decks)

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