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_MS2 Cardio > 8/20- Anti-arrhythmics > Flashcards

8/20- Anti-arrhythmics Flashcards

1
Q

What is an ectopic arrhythmia?

A

Originates outside normal conduction system

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2
Q

What is sinus tachycardia?

A

Originates from normal AV node

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3
Q

Define: paroxysmal

A

Sudden onset

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4
Q

What is normal EDV? SV?

A

EDV = 140 mL

ESV = 70 mL

SV = 70 mL (normal is 50-65%)

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5
Q

Describe the membrane potential changes that occur in cardiac myocytes

A

0: Rapid depolarization due to Na influx

1: Early repolarization (due to Na closure?)

2: Plateau due to Ca influx with K efflux

3: Repolarization due to K efflux

4: Resting potential maintained by diastolic Na (and Ca) influx

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6
Q

What are the different targets for anti-arrhythmic drugs?

A
  • Na channels
  • K channels
  • Ca channels
  • Resting membrane potential (beta blockers)
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7
Q

What is If (funny current)?

A

Mediated by HCN channels (Hyperpolarization-activated Cyclic Nucleotide-gated)

  • Non-selective cation channels (Na and K)
  • Activated by hyperpolarization of cell as well as increased levels of cAMP
  • HCN channels close during depolarization
  • Responsible for increasing resting potential in nodal cells (Na influx and K efflux?)
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8
Q

Differences between SA node and ventricular myocytes?

A

Resting membrane potentials:

  • SA node: -55 mV
  • AV node:-65 mV
  • Vent myocytes: -85 mV

Threshold

  • Same (as well as the ions responsible for AP)

Big difference:

  • Ca current important in SA node depol (why CCBs will reduce heart rate more than contractility)
  • Na current is the key depolarizing current in myocytes
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9
Q

What is the result of potassium imbalance in regards to depol/rhythm?

A

Increased tendency to depolarize

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10
Q

What is the result of hypoxia in regards to depol/rhythm?

A

Hypoxia -> higher Ca inside cells -> increased tendency to depolarize from ectopic loci

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11
Q

What is an escape beat/what causes it?

A

SA nodal firing is too slow and latent pacemaker fires an escape beat

  • A series of escape beats may -> arrhythmia
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12
Q

What is an ectopic beat/what causes it?

A

Latent pacemaker starts beating faster than SA node

  • SA node firing is suppressed by faster-paced latent pacemaker
  • Series of ectopic beats -> arrhythmia
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13
Q

What increases the possibility of early afterdepolarization?

A

QT prolongation

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14
Q

What is early afterdepolarization?

A
  • Generally occur during repolarizing phase of action potential
  • Repetitive can trigger arrhythmia (“torsades de pointes”)
  • Increased by QT prolongation
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15
Q

Prolonged QT interval leads to what?

A

Ventricular arrhythmias

  • QT interval corresponds to ventricular depol and repol
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16
Q

What drugs can convert unidirectional block to bidirectional block?

How is this clinically useful?

A

Some Class 1 drugs

  • Lidocaine

(This prevents conduction through the damaged area and interrupts the reentrant arrhythmias)

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17
Q

What does a bypass tract result in?

Prevalence in normal population?

A
  • Bypass tract (bundle of Kent) will depolarize early and -> arrhythmias (WPW)
  • 0.1-0.3% in general population (1-3/1000)
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18
Q

What are the 4/5 classes of antiarrhythmic drugs?

A
  1. Na channel blockers (class Ia, Ib, Ic)
  2. Beta blockers (class II)
  3. K channel blockers (class III)
  4. Ca channel blockers (class IV)
  5. Other mechanisms (class V)
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19
Q

What are mechanisms of antiarrhythmics?

A
  1. Alter (lower) resting membrane potential
  2. Alter the rate of phase 4 depolarization
  3. Alter the threshold potential
  4. Alter the duration of AP (refractory period)
20
Q

What is the mechanism behind Lidocaine?

Difference between Ia, Ib, Ic?

A

Na channel blocker

Rate of drug binding and refractory period in subtypes:

Ia:

  • Intermediate binding
  • Increases refractory period

Ib:

  • Rapid binding
  • Decreases refractory period

Ic:

  • Slow
  • Unchanged refractory period

Note: some Na channels open during diastolic phase (“diastolic sodium current”; these are different from the VG-Na channels)

21
Q

All channels come in at least what 3 conformations?

A

Ex) Na channel

  • Resting Na channel; fully repolarized (closed, ready to open)
  • Open Na channel
  • Inactivated Na channel (closed; cannot be opened)
22
Q

On what feature of ion channels does drug specificity depend?

A

Specificity of drugs is due to their higher affinity to open/inactivated conformations

23
Q

To which ion channel states do Na channel blockers have preference?

A

Drug binding is channel-state dependent

  • Open Na channel
  • Inactivated Na channel (closed; can’t be open)
24
Q

What are some adverse effects of Na channel blockers?

A

1. Many also cause arrhythmias

  • Class I drugs often used in hospital/under supervision

2. Class 1a: Quinidine (now low dose anti-malarial drug)

  • Cinchonism (ringing in ears, photosensitivity)
  • SA and AV block or asystole
  • Precipitate V fib (prolongs QT interval)
  • Increases digoxin levels by interfering with renal clearance

3. Class 1b: Lidocaine

  • CNS: drowsiness, slurred speech, paresthesia, agitation, confusion, convulsions

(- “caine” drug is local anesthetic)

4. Class 1c: Flecainide

  • Contraindicated in pts with CAD/CHF b/c of its proarrhythmic side effects
25
Q

Qunidine is a class 1a anti-arrhythmic drug. What is true:

A. Blocks Na channels and increases refractory period

B. Blocks ‘funny’ current (HCN channels) and increases refractory period

C. Blocks Na channels and decreases refractory period

D. Blocks Na channels and does not alter refractory period

A

Qunidine is a class 1a anti-arrhythmic drug. What is true:

A. Blocks Na channels and increases refractory period

B. Blocks ‘funny’ current (HCN channels) and increases refractory period

C. Blocks Na channels and decreases refractory period

D. Blocks Na channels and does not alter refractory period

  • Class 1a antiarrhythmic drugs block Na channels and increases refractory period
26
Q

What are class II anti-arrhythics?

A

Beta blockers

27
Q

Examples of beta blockers? Suffix?

A

End in “-olol”

  • Metaprolol
  • Propranolol
  • Esmolol
28
Q

How do beta blockers effect pacemaker cell APs?

A

Antagonize the tonic levels of E/NE and:

  1. Decrease slope of phase 4 depolarization (decreases HR) and:
  2. Prolongs repolarization (thus prolonged refractory period; especially important at AV node)
29
Q

Side effects/specifics of different beta blockers?

A

Propranolol- nonspecific; bronchospasm

Metaprolol- most common; extensively metabolized in liver; enters the CNS

Esmolol- very short acting; IV to treat acute arrhythmias in surgery or emergency

Sotalol- both a beta blocker and K channel blocker

30
Q

What are class III anti-arrhythmics? Examples?

How do they work?

A

Block repolarization K channels (prolongs refractory period and make it more difficult to initiate another depolarization cycle)

  • Target mostly cardiac myoctes

Examples)

  • Amiodarone (mostly class III, also I, II and IV)
  • Sotalol (class II and III)
31
Q

What are class IV anti-arrhythimcs? Examples?

How do they work?

A

Ca channel blockers

  • Slow the AP upstroke in SA and AV nodes
  • Arrhythmc impulses less likely to be transmitted via AV node
  • Targets mostly SA and AV node (Ca current is important in these)

Examples)

  • Verapamil (cardioselective)
  • Diltiazem (heart = vasculature)
  • Nifedipine (–dipine) = more selective to vascular smooth muscle
32
Q

Amiodarine and Sotalol are what class of antiarrhythmics? Mechanism?

A

class III

  • Block K channels
33
Q

Verapamil and Diltiazem are what class of antiarrhythmics? Mechanism?

A

class IV

  • Block Ca channels
34
Q

Adverse effects of Amiodarone?

A
  • Pulmonary fibrosis
  • Hypo/hyperthyroidism
  • Ocular and liver toxicity
  • Neuropathy
  • Optic neuritis
  • Blue-gray skin discoloration

Need to monitor lung and thyroid function before starting and during treatment

35
Q

Adverse effects of Beta blockers?

A
  • Contraindicated in pts with asthma
  • Conduction problems
36
Q

What classes of drugs are used for supraventricular arrhythmias?

A
  • Beta blockers (class II)
  • CCBs (class IV)
37
Q

What classes of drugs are used for ventricular tachycardia, V fib and SCD survivors?

A
  • Amiodarone (mostly class III)
38
Q

What classes of drugs are used to prevent SCD?

A
  • Amiodarone (class III)
  • Beta blockers (class II)
39
Q

When do we use class I drugs?

A

Rarely

40
Q

When is adenosine used? Mechanism?

A

Conversion of paroxysmal supraventricular tachycardia to normal sinus rhythm

  • Very short half life (under 10s); administered via IV
  • Hyperpolarizes the AV node (works in 90%)
41
Q

A 66 yo man has a Hx of myocardial infarction. Which one of the following would be appropriate prophylactic antiarrhythmic therapy?

A. Lidocaine

B. Metaprolol

C. Flecainide

D. Quinidine

E. Verapamil

A

A 66 yo man has a Hx of myocardial infarction. Which one of the following would be appropriate prophylactic antiarrhythmic therapy?

A. Lidocaine

B. Metaprolol

C. Flecainide

D. Quinidine

E. Verapamil

  • Want to use a beta blocker
42
Q

A 58 yo woman is being treated for chronic suppression of a ventricular arrhythmia. After 2 mo of therapy, complains of being tired. Exam reveals low heart rate and cool/clammy skin. Lab test results show thyroxin and high TSH levels. Which of the following anti-arrhythmic drugs is the likely cause of these signs and Sx?

A. Amiodarone

B. Flecainide

C. Propranolol

D. Quinidine

E. Verapamil

A

A 58 yo woman is being treated for chronic suppression of a ventricular arrhythmia. After 2 mo of therapy, complains of being tired. Exam reveals low heart rate and cool/clammy skin. Lab test results show thyroxin and high TSH levels. Which of the following anti-arrhythmic drugs is the likely cause of these signs and Sx?

A. Amiodarone

B. Flecainide

C. Propranolol

D. Quinidine

E. Verapamil

43
Q

Class III anti-arrhythmic drugs work by:

A. Inhibiting Na current

B. Inhibiting Ca current

C. Antagonizing E/NE

D. Inhibiting/repolarizing K current

E. Inhibiting hyperpolarizing Cl current

A

Class III anti-arrhythmic drugs work by:

A. Inhibiting Na current

B. Inhibiting Ca current

C. Antagonizing E/NE

D. Inhibiting/repolarizing K current

E. Inhibiting hyperpolarizing Cl current

44
Q

Which of the following arrhythmias can be treated effectively by IV adenosine?

A. Paroxysmal supraventricular tachycardia

B. Atrial fibrillation

C. Atrial flutter

D. Ventricular tachycardia

E. Ventricular fibrillation

A

Which of the following arrhythmias can be treated effectively by IV adenosine?

A. Paroxysmal supraventricular tachycardia

B. Atrial fibrillation

C. Atrial flutter

D. Ventricular tachycardia

E. Ventricular fibrillation

  • IV adenosine can be used to convert paroxysmal supraventricular tachycardia to normal sinus rhythm
45
Q

Most commonly used beta blocker to treat atrial flutter or atrial fibrillation is:

A. Sotalol

B. Carvedilol

C. Propranolol

D. Esmolol

E. Metoprolol

A

Most commonly used beta blocker to treat atrial flutter or atrial fibrillation is:

A. Sotalol

B. Carvedilol

C. Propranolol

D. Esmolol

E. Metoprolol

  • Metoprolol is beta-1 specific and is most commonly used beta blocker to treat arrhythmias that are atrial in origin
46
Q

Which one of the following is NOT an adverse effect associated with use amiodarone?

A. Cinchonism

B. Hypothyroidism

C. Hyperthyroidism

D. Pulmonary fibrosis

E. Blue skin discoloration

F. Optic neuritis

A

Which one of the following is NOT an adverse effect associated with use amiodarone?

A. Cinchonism

B. Hypothyroidism

C. Hyperthyroidism

D. Pulmonary fibrosis

E. Blue skin discoloration

F. Optic neuritis

  • Cinchonism is for quinidine

_MS2 Cardio (35 decks)

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