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Pharmacology Test #3 > 11.05 Dysrhythmias > Flashcards

11.05 Dysrhythmias Flashcards

0
Q

what is the “pacemaker” of the heart (node)? and what is the pathway of the depolarization?

A 
the Sinoatrial (SA) node
SA node (atrial contraction)-->AV node-->perkinje system/bundle of HIS--> depolarization of ventricles
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1
Q

What are the front line agents for treatment of dysrythmias? (Arrhythmia)

A
  • Beta blockers
  • Ca channel blockers
  • Na+ channel blockers
  • K channel blockers
  • (cardiac glycosides can be used, but aren’t very effective bc they can also cause dysrthytmia)
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2
Q

what is the QT interval on the ECG?

A

ventricle repolarization duration,

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3
Q

spontaneous depolarization

A

something about phase 4, SA and AV nodes

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4
Q

what drugs can increase the QT interval?

A 
Sotalol, it's a beta blockers used to treat Arrhythmia
-also Amiodarone and Qunidine (class IA)
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5
Q

what determines the conduction velocity of the cardiac cells?

A

the number of Na+ channels

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6
Q

abnormal heart tissue usually has what electrical status?

A

it is usually depolarized

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7
Q

if the resting membrane potential is more depolarized, what does that do to the number of available Na+ channels?

A

the more depolarized, the less Na+ channels available, thus the slower the conduction velocity

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8
Q

what do antidysrhythmic drugs do to the number of available Na+ channels?

A

they decrease the available sodium channels (shifts the curve to the left) and thus slow their recovery from excitation

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9
Q

what is the definition of dysrhythmia?

A
  • arrhythmia; any abnormality of firing rate, regularity or site of origin of cardiac impulse or disturbance of conduction that alters the normal sequence of activity of atria and ventricles
  • normal is 60-100 bpm and the SA node is the origin
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10
Q

phase 0

A

Na+ ion channels open(Na flows into cell)=fast depolarization, ends with Na channels closing

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11
Q

phase 1

A

starts with sodium channels closing, then rapid opening and then closing of the K channels, not that important of a phase

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12
Q

phase 2

A

also called the ‘plateau phase’

  • calcium channels open, calcium goes inside the cell
  • K leak out
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13
Q

phase 3

A

the repolarization phase

Potassium (K) channels open (Ca channels close) K flows out of the cell

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14
Q

phase 4

A

K channels close and the Na/K pumps correct the ion concentration
-“spontaneous depolarization” caused by the ion leak of Na and Ca into the cell and K out of the cell

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15
Q

where is the slope of phase four the highest (what part of the heart?)

A

Sinoatrial node, then next in the AV node, then the perkinje fibers, but in the atrial and ventricular tissues, the line is generally flat

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17
Q

what is the major cause (mechanism) of dysrhythmias?

A

-abnormal impulse conduction
=could lead to a total AV block, which would leave the ventricles to start their own pacemaker rhythm) or
=Re-entry: re-excitation around a conducting loop which produces tachycardia (major), unidirectional block leading to extra contractions

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18
Q

Re-entry

A

re-excitation around a conducting loop, which produces tachycardia

  • unidirectional conduction block
  • establishment of new loop of excitation
  • conduction time that outlasts refractory period
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19
Q

what drugs can cause lupus?

A

hydralazine and procainamine

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20
Q

phenytoin

A
  • class 1B, anticonvulsant
    1. Non-sedative anticonvulsant used in treating epilepsy (‘Dilantin’)
    2. Limited efficacy as antidysrhythmic (second line antiarrythmic)
    3. Suppresses ectopic activation by blocking Na and Ca channels
    4. Especially effective against digitalis-induced dysrhythmias
    5. T1/2 = 24 hr – metabolized in liver
    6. Gingival hyperplasia (40%)
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21
Q

gingival hyperplasia

A

Phenytoin-anticonvulsant

  • CCBs (nifedipine)
  • cyclosporine
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22
Q

Flecainide

A

-class 1C prototype
Depress rate of rise of AP without change in refractoriness or APD
1. Decreases automaticity, conduction in depolarized cells.
2. Marked block of open Na channels (decreases Ph. 0); no change repolarization.
3. Used primarily for ventricular dysrhythmias but effective for atrial too
4. No antimuscarinic action
5. Suppresses premature ventricular contractions (PVCs)
6. Associated with significant mortality; thus, use limited to last resort applications
like treating ventricular tachycardias
7. Significant negative inotropic effect

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23
Q

Propranolol

A
  • class II, beta-adreno blocker
  • main action on phase four, it will decrease the slope and thus decrease the conduction velocity
  • some have membrane stabilizing properties that can also block Na channels to some degree
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24
Q

esmolol

A

arrthymia treatment (esp during surgical procedures)

25
Q

sotalol

A

-beta blocker, and it also is a K channel blocker

26
Q

beta-Blockers: Untoward Effects, Cautions

A

Supersensitivity: Rebound effect with

27
Q

Amiodarone

A

Class III

  • a. New DOC for ventricular dysrhythmias (Lidocaine, old DOC)
    b. prolongs refractory period by blocking potassium channels
    c. also member of Classes IA,II,III,IV since blocks Na, K, Ca channels and alpha and beta adrenergic receptors
    d. serious side effects (cardiac depression, pulmonary fibrosis, thyroid)
    e. effective against atrial, A-V and ventricular dysrhythmias
    f. widely used, very long acting (>25 d)
28
Q

Cardiac effects of Amiodarone

A

a. Block Na channels (1A), but low affinity for open channels; mainly blocks inactivated Na channels
b. Block is most pronounced in tissues with long action potentials
c. Weak Ca channel blocker also (Class IV activity)
d. A powerful inhibitor of abnormal automaticity, decreases conduction, increases refractory period and APD.
e. Has antianginal effects (blocks alpha/beta receptors and Ca channels)
Extracardiac effects: Vasodilation via block of Ca channels and alpha receptors

29
Q

Adverse effects: Amiodarone

A

A. Cardiac
**i. Sinus bradycardia, increase QT interval –>risk TdP
ii. Negative inotropic action due to block of Ca channels and beta receptors; but can improve heart failure via vasodilation.
iii. A-V block, paradoxical VTs.
B. Non-cardiac:
i. Deposits into almost every organ
ii. Reduces clearance of drugs like procainamide, flecainide, digitalis, quinidine and diltiazem.
**iii. Thyroid dysfunction (hypo or hyperthyroidism)
***iv. Pulmonary fibrosis is most serious adverse effect
v. Paresthesias (tingling, pricking, or numbness)
**vi. Photosensitivity Prolonged QT interval vii. **Corneal microdeposits and blurred vision
viii. Ataxia, dizziness, tremor
ix. Anorexia, nausea

30
Q

Ibutilide

A

class III

  1. Prolongs cardiac action potential without additional effects.
  2. Administered I-V. Most effective current agent to convert atrial fibrillation and flutter of recent onset to normal rhythm. Low incidence of Torsades de Pointes (TdP, about 2%), compared to other drugs.
  3. More effective for flutter than fibrillation
  4. Generally well tolerated
31
Q

Sotalol (Class III and Class II)

A

Sotalol (Class III and Class II)

  1. Non-selective beta blocker,
  2. Increases AP duration, increase QT interval
  3. Uses: dysrhythmias of supraventricular (very effective) & ventricular origin
32
Q

beta blockers can only be used for … not for both

A

supraventricular, but not ventricular tachycardia

33
Q

Verapamil

A

class IV, CCB

a. Blocks active and inactivated Ca channels, prevents Ca entry
b. More effective on depolarized tissue, tissue firing frequently or areas where activity dependent on Ca channels (SA node; A-V node)
c. Increases A-V conduction time and refractory period; directly slows SA and A-V node automaticity
d. suppresses oscillatory depolarizing after depolarizations due to digitalis
e. Dihydropyridine CCBs are generally poor antiarrhythmics

34
Q

constipation (side effect of:)

A

CCBs

35
Q

which anit-arrthymic agent has vagal stimulation?

A

digoxin

36
Q

digoxin

A

used to treat atrial flutter and fibrillation

  • AV node decr. conduction (vagal stimulation)
  • myocardium decr. refractory period
  • Purkinje fibers incr. refractory period, decr. conduction
37
Q

occurrence of dysrhythmias

A
  • 80% of patients with acute myocardial infarctions
  • 50% of anaesthetized patients
  • about 25% of patients on digitalis
38
Q

unidirectional block

A

impulse travels in retrograde direction and reenters the conduction pathway causing an extra or irregular heart beat

39
Q

Actions of Quinidine: cardiac effects

A

a. decrease automaticity, conduction velocity and excitability of cardiac cells.
b. Preferentially blocks open Na channels
c. Recovery from block slow in depolarized tissue;
lengthens refractory period (RP)
d. All effects are potentiated in depolarized tissues
e. Increases action potential duration (APD) and prolongs AP repolarization via block of K channels; decreases reentry
f. Indirect action: anticholinergic effect (accelerates heart), which can speed A-V conduction.

40
Q

Actions (extracardiac) & Toxicity of Quinidine

A

Extracardiac
a. Blocks alpha-adrenoreceptors to yield vasodilatation.
b. Other strong antimuscarinic actions
Toxicity
- “Quinidine syncope”(fainting)- due to disorganized ventricular tachycardia
- associated with greatly lengthened Q-T interval; can lead to Torsades de Pointes (VT, precursor to ventricular fibrillation)
- negative inotropic action (decreases contractility) - GI - diarrhea, nausea, vomiting
- CNS effects - headaches, dizziness, tinnitus (quinidine “Cinchonism”)

41
Q

prolonged QT interval

A

quinidine

42
Q

what drug should be avoided in conjunction with quinidine?

A

digoxin, quinidine displaces digoxin from plasma binding sites

43
Q

what drug has these adverse effects:

  • sinus bradycardia: increase QT interval–>incr. risk TdP
  • thyroid dysfunction (HYPO or hyperthyroidism)
  • pulmonary fibrosis (most serious adverse effect)
  • photosensitivity
  • corneal microdeposits and blurred vision
A

Amiodarone

44
Q

Ca++ Channel Blockers - Actions extracardiac

A

a. Peripheral vasodilatation via effect on smooth muscle
b. Used as antianginal / antihypertensive
c. Hypotension may increase HR reflexively

45
Q

CCB toxicity

A

a. Cardiac
- Too negative inotropic for damaged heart, depresses contractility
- Can produce complete A-V block
b. Extracardiac
- Hypotension
- Constipation, nervousness - Gingival hyperplasia

46
Q

Acute Supraventricular

A

adenosine, digoxin, CCBs

47
Q

Acute, Ventricular

A

Amiodarone Procainamide Sotalol, Bretylium Lidocaine

48
Q

chronic supraventricular

A

Beta-blocker Calcium antagonist

49
Q

chronic ventricular

A

Amiodarone Sotalol Flecainide

50
Q

Drugs affect different parts of the heart: Beta- blockers and CCBs used for

A

SVT

51
Q

Ca channel blockers (Class IV) are selective for

A

A-V and S-A nodes, where Ca action potentials predominate.

52
Q

Lidocaine (Class IB) has been useful for treating

A

PVCs in Purkinje fibers, since longer APDs in Purkinje yield more inactivated Na channels. Lidocaine selectively blocks inactivated state and some open Na channels.
Lidocaine has little effect, in contrast, on atrial tissue.

53
Q

Quinidine affects which dysrthymias?

A

both atrial and ventricular dysrhythmias (but has been mostly used to treat atrial fibrillation).

54
Q

group IB agents (Lidocaine, phenytoin) act on which phase of the cardiac cycle?

A 
phase III (shorten phase III repolarization) and decreases the duration of the action potential
-they block the open or inactivated Na channels
55
Q

what channels does lidocaine act on?

A

Exclusively acts on Na channels in depolarized tissue by blocking open and inactivated (mainly) Na channels

56
Q

Suppresses ventricular tachycardia; prevents fibrillation after acute MI; rarely used in supraventricular dysrhythmias

A

Lidocaine

57
Q

Propranolol contraindicated in

A

ventricular failure; can lead to A-V block.

58
Q

Group III drugs (amiodarone) prolong what phase?

A

prolong phase 3 repolarization without altering phase 0

59
Q

DOC for ventricular dsyrhythmias

A

amiodarone (dronedarone)

Pharmacology Test #3 (9 decks)

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