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Cardiovascular > Week 4: anti arrhythmic drugs > Flashcards

Week 4: anti arrhythmic drugs Flashcards

1
Q

What are the sites of action of anti-arrhythmic drugs?

A

-They work on ion channels to interrupt: Na+permeability, K+ permeability, or both

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2
Q

What is the effect of inhibiting sodium permeability on the cardiac excitability and EKG waves?

A

-Slow Phase 0 depolarization (decreases slope)
-slows conduction
-prolongs P wave
-prolongs QRS complex
slows ventricular and atrial depolarization

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3
Q

What is the effect of inhibition of K+ permeability on cardiac excitability and EKG waves?

A
  • prolongs action potential duration (longer plateau phase 2)
  • prolongs refractory period
  • prolongs ST segment
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4
Q

Describe effective refractory phase and what phases it encompasses, where is spans on EKG.

A
  • is when cell can’t be stimulated
  • goes from phase 0 to half way into phase 3 depolarization
  • on EKG, from qrs to half of t wave
  • relative refractory period- not fully depolarized but may still be able to contract
  • with antiarrhythmic drugs, one goal is to prolong effective refractory period
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5
Q

Describe a unidirectional block.

A
  • As conduction travels down ventricles, orthograde conduction stops on one side with ischemic area that did not recover excitability
  • When impulse arrives retrograde from other side, the ischemic area has recovered excitability and impulse is conducted retrograde
  • causes reentry phenomenon or circus movement
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6
Q

What is the goal of anti-arrhythmic drugs in treating unidirectional block?

A
  • convert it into a bidirectional block so that it stops retrograde conduction
  • do so by inhibition of Na permeability (inhibits phase 0 depolarization) or increasing refractory period (inhibiting K+ permeability)
  • ectopic pacemakers are more sensitive to these drugs than SA node
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7
Q

What is the mechanism of anti-arrhythmic drugs that inhibit Na+ channels?

A
  • normal sodium channels: in resting state, M gate blocks channel, when activated, m gate is open, when inactivated h gate is closed (can’t be reactivated) until m gate is back in place
  • the drug binds to receptor and acts like a h gate
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8
Q

What are the 4 classes of anti arrhythmic drugs?

A
  1. Na channel blockade-affects phase 0
    - Ia, Ib, Ic
  2. blockage of sympathetic autonomic effects-affects phase 4
    - beta adrenoceptor antagonist
  3. prolong effective refractory period-affects phase 2
  4. Ca channel blockade-affects phase 2
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9
Q

Discuss class Ia anti arrhythmic drugs. List the drugs.

A
  • inhibits Na+ permeability, slow phase 0 depolarization, slows conduction
  • inhibits K+ permeability, prolongs APD
  • slows phase 4 depolarization in slow response, moves threshold potential up
    1. quinidine
    2. procainamide
    3. disopyrimide
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10
Q

Discuss class Ia drug Quinidine

A

Quinidine-don’t use anymore

  • effective for atrial and ventricular arrhythmias
  • side effects: GI, cinchonism (headaches, tinnitus, dizziness)
  • a1 blocking effect-postural hypotension
  • anticholinergic effect
  • torsades de pointes: excessive prolongation of refractory period–>increased QT, early after depolarization–>Vfib–>syncope or death
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11
Q

Discuss class Ia drug procainamide.

A

-Effective for ventricular»>arterial arrhythmias
-only IV in ER or ICU
-avoided due to toxic effects
ADVERSE
-Lupus like syndromes (long term therapy, reversible)
-hallucinations or psychosis
-Torsades de Pointes

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12
Q

Discuss class Ia drug disopyramide.

A

similar to quinidine and procainamide
-effective for all arrhythmias but only approved for ventricular ones
-oral formulation
ADVERSE
-anticholinergic effect: urinary retention, dry mouth, blurred vision, constipation
-marked depression of cardiac conduction, can precipitate clinical heart failure
-Torsades de pointes

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13
Q

Discuss in general class IB drugs.

A
  • shortens phase 3 depolarization
  • decreases the duration of the action potential
  • therapeutic effects only in ischemic cells
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14
Q

Discuss class IB drug Lidocaine.

A
  • effective for acute ventricular arrhythmias in setting of MI
  • IV formulation
  • clinical use limited, IV only , need to monitor serum levels closely
  • toxicity: neurologic
  • analogs: tocainide, mexiletine
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15
Q

Discuss in general class Ic anti arrhythmic drugs.

A
  • most powerful inhibitor of the fast sodium channel
  • slow phase 0 depolarization
  • prolong P wave and qrs complex
  • no significant effect on ST segment
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16
Q

Discuss class Ic drug flecainide.

A

-oral agent for atrial and ventricular arrhythmias
-proarrhythmic in setting of structural heart disease and ventricular arrhythmias
-only approved for supra ventricular arrhythmias in normal hearts
ADVERSE
-CNS: blurred vission, nausea, paraesthesia, dizziness, tremor, metallic taste
-proarrhythmic
-heart failure

17
Q

Discuss class IC drug propafenone.

A
  • indications similar to Flecainide

- adverse: metallic taste, constipation, proarrhythmic

18
Q

Discuss class II anti arrhythmic drugs.

A

Metoprolol and Esmolol
-beta adrenoreceptor blockers: block beta receptors and have direct membrane effects
-diminish phase 4 depolarization and decrease automaticity of SA node and ectopic pacemakers
-prolongs AV conduction, decease HR, decrease contractility, decrease ectopy
CLINICAL USE
-rate control of supra ventricular arrhythmias
-suppression of ventricular ectopy
-prevention of sudden cardiac death in patients with acute MI
ADVERSE
-fatigue, lethargy, hyperglycemia, hypotension, bradycardia

19
Q

Discuss class III anti-arrhythmic drugs in general.

A
  • prolong phase 3 depolarization without altering phase 0

- prolongs APD, increases ST segment, prolongs refractory period

20
Q

Discuss class III drug amiodarone.

A

-most widely used in in patient and outpatient
-oral and IV
-effective for atrial and ventricular arrhythmias
-broad spectrum of action, high efficacy and low incidence of acute toxicity
-long half life
-inhibits cytochrome p450
ADVERSE
-symptomatic bradycardia and heart block
-dose dependent toxicity (long term): pulmonary fibrosis, thyroid problems, hepatocelllar necrosis
-need PFTs, TFTs, and LFTs for baseline

21
Q

Discuss class III drug Dronedarone.

A

Structural analog to Amiodarone
Less effective than Amiodarone but favorable side effect profile (no risk of long-term pulmonary or thyroid toxicity and very low risk of liver toxicity)
An alternative for patients who would benefit from long-term Amiodarone therapy
Long-term studies showed an increased mortality risk in patients with NYHA III or IV hear failure or a recent heart failure exacerbation

22
Q

Discuss class III drugs Dofetilide, Ibutilide, Sotalol

A

Dofetilide: use for conversion of Afib and maintenance of normal sinus rhythm
Ibutilide: acute inpatient conversion of Afib and atrial flutter to normal sinus rhythm
Sotalol: maintenance of sinus rhythm in patients with Afib, suppression of ventricular ectopy/arrhythmias, alters defib thresholds
ADVERSE EFFECTS
-excessive QT interval prolongation and Torsades de pointes, not used in LVH
-less so for sotalol

23
Q

Discuss class IV anti arrhythmic drugs: Ca channel blockers

A

-Verapamil»diltiazem
-block inward Ca channel currents in AV and SA node
-diminish SA nodal phase 4 depolarization
-prolongs AV nodal conduction and refractory time
-decrease hr, contractility
CLINICAL use
-broadly used agent for rate control of supra ventricular tach, Afib, atrial fib, not used in ventricular arrhythmias
ADVERSE
-contraindicated in individuals with LV systolic dysfxn
-constipation, lethargy, bradycardia, peripheral vasodilation, heart failure

24
Q

Discuss the effects of adenosine.

A

-via G proteins, inhibit adenylate cyclase
-inhibits Ca2+ inward current
-slows conduction in AV node, and inhibits AV nodal reentry arrhythmias
-USES: paroxysmal SVT-reentry arrhythmia involving AV node
ADVERSE: flushing, dyspnea, chest pain, transient arrhythmias, contraindicated in asthma and heart block

25
Q

Discuss digoxin.

A

-cardiac glycoside
-inhibits Na/K ATPase pump of AV node
- increases intracellular Na and Ca, increases vagal activity
-increases cardiac conduction and slows AV conduction by increasing AV node refractory period
-used in control of ventricular rate in presence of A fib and atrial flutter
-improvement of symptomatic CHF exacerbations
ADVERSE: narrow TI, Arrhythmias, heart block, anorexia, nausea, diarrhea, xanthopsia, gynecomastia, confusion, agitation

Cardiovascular (29 decks)

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