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IC > Tx of Cardiac Arrythmias > Flashcards

Tx of Cardiac Arrythmias Flashcards

1
Q

Cardiac arrythmias

A

Abnormal electrical activity in the heart

-heart beating too fast or slow, regular or irregular

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2
Q

Underlying causes of arrythmias

A

cardiovascular- htn, abn valve fxn, cad, hf
noncardio- hyperthyroidism, autonomically mediated, alcoholism, sleep apnea, obesity, drug induced

-due to: disturbance of impulse formation, disturbance of impulse conduction or both

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3
Q

What type of arrythmia should be treated

A

asymptomatic or minimally symptomatic arrythmias should not be treated

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4
Q

Premature (extra) beats

A
  • most common type of harmless arrhythmias
  • fluttering in chest
  • no need for tx
  • atria- premature atrial contractions
  • ventricles- PVC

-can be due to exercise, caffeine, heart disease

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5
Q

Supraventricular arrythmias

A

tachycardias that start in atria or SA node

-AF, atrial flutter, PSVT, WPW syndrome

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6
Q

AFib

A

-most common serious arrythmias
-irregularly irregular
-electrical signals start in other parts of atria or pulm vein–> irregular fast heart rate
-can cause stroke
pts need blood thinner

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7
Q

AFlutter

A

Atria beating faster than ventricles- regular fast hb

If ventricular rate is less than 120 bpm people normally have no symptoms

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8
Q

Paroxysmal supraventricular tachycardia (PSVT)

A
  • regular hr at 150-250 bpm
  • begins and ends suddenly
  • signals beginning in atria travel to vventricles and can reenter atria- resulting in extra heart beats
  • due to alcohol, caffeine, nicotine
  • Wolff Parkinson White syndrome is also a case
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9
Q

WPW Syndrome

A

-Bundles of kent which can take signal back to atria

Can cause PSVT

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10
Q

Ventricular arrythmias

A

Tachy starts in ventricles

-dangerous

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11
Q

ventricular tachycardia

A

fast but regular beat of ventricles that may last only for few seconds

  • short episodes (few seconds) are normal
  • longer episodes can be dangerous and can turn into VFib
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12
Q

Vfib

A

Uncontrolled, irregular beats up to 300 bpm

  • little blood pumped
  • medical attention needed immediately
  • must be converted with defibrillator
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13
Q

Bradycardia

A
  • HR <60 bpm
  • impulse not formed by SA node or not conducted properly to ventricles- mainly in elderly
  • CNS not signaling properly
  • SA node might be damaged or could be due to drug use
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14
Q

Factors precipitating arrythmias

A

ischemia, hypoxia, acidosis, alkalosis, electrolyte abn, excess catecholamines, drug tox, overstretching of muscle fibers

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15
Q

Pace maker rate depends on

A

AP duration and duration of diastolic interval

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16
Q

Diastolic interval depends on

A

slope of phase 4 depol

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17
Q

What slows pacemaker rate

A

-vagal discharge and b blockers reduce phase 4 slope–> slow pacemaker rate

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18
Q

What can increase pacemaker rate

A

b receptor stimulation, hypokalemia, positive chronotropic drugs, fiber stretch, acidosis, partial depol–> inc phase 4 depol and inc pace maker rate

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19
Q

early after depolarization

A

EAD- usually at slow heart rates

  • interrupt phase 3
  • can contribute to long QT related arryhtmias
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20
Q

Delayed afterdepolarization

A
  • interrupt phase 4
  • fast heart rate
  • digoxin excess, catecholamine, MI
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21
Q

disturbance of impulse conduction can be caused by

A
  • blocking impulse at any pt in normal pw

- reentry or circus movement- EAD or DAD

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22
Q

3 conditions for reentry to occur

A
  • conduction has to be blocked by anatomic or physiologic obstacle
  • block must be unidirectional
  • conduction time around block must exceed refractory period
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23
Q

Toxic doses of antiarrythmics can cause

A

drug induced arrythmias because it can affect normal tissues

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24
Q

basic mechanisms for antiarrythmic drugs

A
  • slow down heart
  • rhythm control- sinus rhythm
  • cannot speed up heart rate (need pacemaker for bradycrrdia)

-Na, K, Ca channel blockage, blockage of sympathetics, prolongation of refractory period (Lidocaine prolongs inactivation of Na channel)

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25
Q

Drugs for Rate control

A

B-blocker (metoprolol and atenolol), Ca channel blockers (verapamil and diltiazem), and digoxin

26
Q

Drugs for rhythm control

A

Na channel blockers (procainamide, quinidine, disopyramide, flecainide, lidocaine, mexiletine, propafenone) K channel blockers (amiodarone, ibutilide, sotalol, dofetilide)

27
Q

Class I Na+ channel blockers

A

Decrease HR by elevating threshold for excitation, decreasing slope of phase 4 depol in SA node

  • Class IA, IB, IC
  • All block Na and K channels and can induce Torsade de pointes
28
Q

Class IA-Procainamide

A
  • moderate Na channel block
  • prolonged repolarization- prolongs APD by nonspecific blocking K channels (QT prolongation- fatal- torsades de pointe)
  • procainamide
  • inc effective refractory period of atria and ventricles (supra and ventricular arrythmias)
  • directly suppress SA and AV nodes
29
Q

Toxic effects of Class IA- Procainamide

A

Cardiotoxic- QT prolongation- torsades de points

  • Lupus like syndrome with long term therapy
  • Does not elevate digoxin levels
30
Q

Therapeutic use of Procainamide

A
  • Class IA Na Channel blocker
  • atrial and ventricular arrythmias
  • short 1/2 life- less useful for long term
  • use 2nd line after lidocaine or amiodarone
31
Q

Class 1A Quinidine

A
  • Similar to procainamide
  • QT prolongation due to K channel blocking
  • blocks a-adrenergic receptors causing vasodilation–> reflex tachy, marked hypotension
32
Q

Quinidine toxicity

A
  • Class IA Na blocker
  • precipitate digoxin toxicity
  • thrombocytopenia
  • syncope due to torsade de point
  • rarely used
33
Q

Class IA Disopyramide

A

Similar effects to quinidine and procainamide

  • More antimuscarinic- accelerates heart rate
  • Adverse effects (atropine like)- urinary retention, dry mouth, blurred vision, worsening of preexisting glaucoma
  • not used often
  • in USA only approved for ventricular arrythmias
34
Q

Lidocaine

A

Class IB

  • blocks activated and inactivated Na channels
  • minimal effect on atrial tissues
  • No effect on K channels
35
Q

Lidocaine toxicity

A
  • low toxicity
  • least cardiotoxic of current Na blockers
  • large doses in pts with HF can cause hypotension by depressing myocardial contractility
  • neurologic AE
  • seizures after rapid IV administration
36
Q

Lidocaine uses

A
  • IV because of high first pass metabolism
  • used for digoxin toxicity
  • relatively ineffective in normally polarized tissues as in atrial flutter of afib
  • terminates vtach and prevents vfib
37
Q

Mexiletine

A

Class IB Na blocker

  • lidocaine analog- resistant to first pass metabolism so can be given orally
  • AE effect neurologic- tremor, blurred vision, lethargy
  • Varrythmias tx
  • relief of chronic paifor diabetic neuropathy and nerve injury (off label)
38
Q

Class IC Antiarrythmics

A

All given orally

-inc mortality from cardiac arrest or arrythmic sudden death in pts with recent myocardial infarct

39
Q

Flecainide

A

Class IC Na blocker

  • Blocks Na and K channels, no QT prolongation
  • No antimuscarinic effects
  • Tx for supraventricular arrythmias
40
Q

Propafenon

A

Class IC Na blocker

  • Blocks Na channels
  • Similar to propranolol so weak b-blocker
  • may exacerbate arrythmias and cause constipation
  • Supraventricular arrythmias
41
Q

Moricizine

A

-Withdrawn from US market

Potent Class IC Na channel blocker

42
Q

B blockers

A

Propanolol (nonselective) and acebutolol (B1 selective)

  • Supraventricular and ventricular arrythmias caused by sympathetic stimulation
  • prevents Vfib
  • can be used for rate control
43
Q

Propranolol

A

nonselective beta blocker

44
Q

Acebutolol

A

b1 selective beta blocker

45
Q

Esmolol

A

b1 selective beta blocker given IV for tx of acute arrythmias occuring during surgery

46
Q

Beneficial effects of b blocker

A
  • diminished sym activity
  • diminished cardiac workload reduces oxygen demand
  • reduced vasoconstriction
47
Q

Amiodarone

A

Class III Antiarrythm ic
-Orally or IV to maintain normal sinus rhyrhm
Pts with afib or prevention of recurrent vtach
-Prolongs AP duration and QT interval by blocking K channels
-decreases rate of firing in pacemaker cells by blocking Na channels
-Blocks alpha and beta receptors and Ca channels inhibiting AV node conduction to produce bradycardia
-causes peripheral vasodilation

48
Q

Amiodarone toxicities

A
  • bradycardia and AV block in pts with SA and AV node disease
  • pulm fibrosis
  • skin deposits- grayish blue skin in sun exposed areas
  • abn liver function
  • corneal microdeposits
  • Blocks conv from T4 to T3
  • hypo or hyperthyroidism
  • long half life- toxicity can continue long after its discontinued
  • affects virtually every organ system
  • metabolized by CYP3A4–> drug drug interactions
49
Q

Dronedarone

A

structural analog of amiodarone

  • no iodines
  • blocks K and Na channels
  • No thyroid dysfunction or pulmonary toxicity
  • LIVER TOXICITY! -2 cases needed transplantation
50
Q

Sotalol

A
  • Class III
  • Non selective b-adrenergic blocker prolongs APD
  • Prolongs repol resulting in torsade de points at high dose
  • use for life threatening vent arrythmias
  • maintain sinus rhythm in afib
  • supraventricular and vent arrythmias in peds
51
Q

Dofeltilide and ibutilide

A
  • Dofeltilide is oral and ibutilide is IV
  • blocks rapid component of delayed rectifier K current to slow cardiac repol
  • restores normal sinus rhythm in afib or aflut
  • prolongs QT and torsades in 10% of pts
52
Q

Verapamil and diltiazem

A

Class IV antiarrythmics

  • Blocks L type Ca channels
  • depress SA and AV nodes by decreasing contractility and reduce SA node automaticity, slow AV node conduction
  • used for supraventricular arrythmias and rate control in afib
53
Q

Nifedipine

A

not used as antiarrythmic bc of reflex tachycardia and pronounced vasodilation

54
Q

Adenosine

A
  • opens inward rectifier K channels- hyperpolarization
  • Inhibits L type calcium chanels
  • inhibits pacemaker current- decreases HR
  • Affects AV node, not SA node
  • IV to convert PSVT to sinus rhythm
  • causes flushing, sob, headche, hypotension, nausea
55
Q

Digoxin

A

Inhibitor of Na/K/ATPase–> inc Ca–> positive inotrope

  • stimulates vagus nerve and decreases HR
  • afib to decrease hr
  • narrow therapeutic window and other drugs can enhance toxicity
  • toxicity: GI and cardiac
56
Q

Magnesium

A

mechanism unknown

used to prevent torsades and digoxin induced arrythmias

57
Q

antiarrythmic therapy

A

rate vs rhythm control + warfarn for AFib

  • inc mortality from cardiac arrest in pts with recent MI with most drugs (except b blockers)
  • narrow margin of safety
58
Q

Contraindication for disopyramide

A

prostatism bc of urinary retention due to anticholinergic activity

59
Q

contraindication for procainamide

A

chronic arthritis because it causes lupus like syndrome

60
Q

contraindication for amiodarone

A

advanced lung disease because it causes pulmonary fibrosis

IC (31 decks)

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