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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
Drugs for Rate control
B-blocker (metoprolol and atenolol), Ca channel blockers (verapamil and diltiazem), and digoxin
26
Drugs for rhythm control
Na channel blockers (procainamide, quinidine, disopyramide, flecainide, lidocaine, mexiletine, propafenone) K channel blockers (amiodarone, ibutilide, sotalol, dofetilide)
27
Class I Na+ channel blockers
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
Class IA-Procainamide
- 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
Toxic effects of Class IA- Procainamide
Cardiotoxic- QT prolongation- torsades de points - Lupus like syndrome with long term therapy - Does not elevate digoxin levels
30
Therapeutic use of Procainamide
- 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
Class 1A Quinidine
- Similar to procainamide - QT prolongation due to K channel blocking - blocks a-adrenergic receptors causing vasodilation--> reflex tachy, marked hypotension
32
Quinidine toxicity
- Class IA Na blocker - precipitate digoxin toxicity - thrombocytopenia - syncope due to torsade de point - rarely used
33
Class IA Disopyramide
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
Lidocaine
Class IB - blocks activated and inactivated Na channels - minimal effect on atrial tissues - No effect on K channels
35
Lidocaine toxicity
- 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
Lidocaine uses
- 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
Mexiletine
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
Class IC Antiarrythmics
All given orally | -inc mortality from cardiac arrest or arrythmic sudden death in pts with recent myocardial infarct
39
Flecainide
Class IC Na blocker - Blocks Na and K channels, no QT prolongation - No antimuscarinic effects - Tx for supraventricular arrythmias
40
Propafenon
Class IC Na blocker - Blocks Na channels - Similar to propranolol so weak b-blocker - may exacerbate arrythmias and cause constipation - Supraventricular arrythmias
41
Moricizine
-Withdrawn from US market | Potent Class IC Na channel blocker
42
B blockers
Propanolol (nonselective) and acebutolol (B1 selective) - Supraventricular and ventricular arrythmias caused by sympathetic stimulation - prevents Vfib - can be used for rate control
43
Propranolol
nonselective beta blocker
44
Acebutolol
b1 selective beta blocker
45
Esmolol
b1 selective beta blocker given IV for tx of acute arrythmias occuring during surgery
46
Beneficial effects of b blocker
- diminished sym activity - diminished cardiac workload reduces oxygen demand - reduced vasoconstriction BAD effect:-Negative inotrop- induce precipitate HF -
47
Amiodarone
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
Amiodarone toxicities
- 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
Dronedarone
structural analog of amiodarone - no iodines - blocks K and Na channels - No thyroid dysfunction or pulmonary toxicity - LIVER TOXICITY! -2 cases needed transplantation
50
Sotalol
- 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
Dofeltilide and ibutilide
- 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
Verapamil and diltiazem
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
Nifedipine
not used as antiarrythmic bc of reflex tachycardia and pronounced vasodilation
54
Adenosine
- 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
Digoxin
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
Magnesium
mechanism unknown | used to prevent torsades and digoxin induced arrythmias
57
antiarrythmic therapy
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
Contraindication for disopyramide
prostatism bc of urinary retention due to anticholinergic activity
59
contraindication for procainamide
chronic arthritis because it causes lupus like syndrome
60
contraindication for amiodarone
advanced lung disease because it causes pulmonary fibrosis

IC (31 decks)

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