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HTLH 2511 > Module C: Drugs for Cardiac Dysrhythmia > Flashcards

Module C: Drugs for Cardiac Dysrhythmia Flashcards

1
Q

Pacemaker cells

A 
-have automaticity (depolarize spontaneously), located in:
SA node (R atrium, natural pacemaker)
AV node
Bundle of His
Bundle branches
Purkinje fibres
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2
Q

Depolarization of SA node

A
  • resting membrane potential approx. -55- -60 mV (phase 4)
  • depolarization primarily by influx of Na+ and K+ as efflux of K+ subsides
  • RMP becomes less negative
  • at threshold potential (TP) of -40mV, depolarization occurs (phase 0) and impulse conducted through heart
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3
Q

Resting Membrane Potential (RMP)

A

difference in ion concentration between inside of cell compared to outside

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4
Q

Threshold potential (TP)

A

critical level when all activation gates open instantaneously and there will be a large influx or efflux of an ion

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5
Q

RMP of ventricular myocyte

A

-85 to -90 mV

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6
Q

Phase 0-4 ventricular polarization

A

0: SA impulse changes RMP to less negative; when TP o f-65mV is reached, Na+ channels open to max. and Na+ rushes inside until +30mV
-depolarization of ventricles = QRS of EKG
1-2: repolarization of ventricles begins = ST segment
-K+ channels open, K+ exits cells
-this phase slowed by influx of Ca++ (isoelectric potential)
3: inward flow of Ca+ stops, outward flow of K+ increases=inside of cell is negative = T wave
-repolarization complete
4: ion distribution (K+ and Na+) different across cell membrane
-Na+/K+ ATPase pump and Ca2+/Na+ exchanger restore ions to initial and correct compartments (Na+ outside, and K+ inside)

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7
Q

Refractory Periods

A
  • time when cell cannot accept new action potential until repolarization of cell has occurred
  • two periods:
    1: Absolute or Effective Refractory Period (ERP)- cell cannot conduct action potential, no matter how strong (Phase 0-middle of phase 3)
  • on EKG = beginning of Q wave to middle of T wave
    2: Relative Refractory Period (RRP)- strong stimulus may result in conduction but may not be normal
  • on EKG = middle of T wave to end of T wave
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8
Q

Arrhythmias

A
  • disturbances to normal rhythm of heart
  • caused by coronary schema or hypoxia, electrolyte imbalances, increased sympathetic activity, drugs, etc.
  • leads to abnormal impulse formation or abnormal impulse conduction
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9
Q

Abnormal Impulse Formation

A
  • often leads to tachycardia

- due either to increased automaticity or afterdepolarization

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10
Q

Increased Automaticity

A

-diseases or drugs (ie. sympathomimetics) can make cells depolarize more rapidly

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11
Q

Afterdepolarization

A
  • occurs due to abnormal Ca++ influx into cardiac cells
  • occurs during, or immediately after, Phase 3 of ventricular action potential
  • can be provoked by Digitalis toxicity
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12
Q

Abnormal Impulse Conduction

A
  • occurs due to reentry (reexcitation of a particular area of cardiac tissue by the same impulse)
  • primary cause is a unidirectional block in a bifurcating pathway, where reexcitation happens due to retrograde impulse
  • often leads to tachycardia, in particular, paroxysmal supra ventricular tachycardia (PSVT)
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13
Q

Tachycardias

A
  • caused by fever, increased sympathetic activity, stimulants, and pathological conditions
  • may be constant or paroxysmal
  • ex. PVST (atrial originated), afib, aflutter, vtach,vfib
  • flutter - little blood pumped
  • fib - no blood pumped
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14
Q

Bradycardias

A
  • not always pathological, (ie. athletes)
  • may be caused by a stroke or abnormal electrical impulses
  • serious if associated with hypotensive symptoms such as LOC, dizziness, etc.)
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15
Q

Irregular Rhythms

A
  • due to atrial or ventricular ectopic foci taking over SA node normal function resulting in:
  • > premature or extra contractions (PAC- premature atrial contractions)
  • > blockade of impulse transmission (AV block)
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16
Q

Non-pharmacological therapies

A
  • defibrillation or implantable cardioverter-defibrillator (ICD)
  • transcatheter ablation (uses high frequency wavelengths, freezing or heat)
  • pacemaker implantation
17
Q

Purpose of Antiarrhythmic Drugs

A
  • suppress ectopic impulse generation and restore control to normal pacemaker cells
  • normalize heart rhythm as much as possible
18
Q

classifications of antiarrhythmic drugs

A
  • based on mechanism of action
  • Vaughan-Williams (V-W) classifications: Class I,II,III,IV
  • 3 drugs do not meet classifications: Adenosine, Mag Sulfate, Digoxin (sometimes known as class V)
19
Q

Class I Antiarrhythmics

-basic mode of action

A

SODIUM CHANNEL BLOCKERS

  • greatest effect on myocardial cells actively firing (where Na+ channels are open)
  • blockade of channels results in reduced action potential or amplitude of myocardial cells (delayed conduction and prolonged refractory time)
  • minimal effects on pacemaker cells
20
Q

Subclasses of Sodium Channel Blockers

A
  • Class IA Pronestyl (Procainamide)
  • Class IB Xylocaine (Lidocaine)
  • Class IC Rythmol (Propafenone)
21
Q

Class IB agent: Xylocaine (Lidocaine)

A
  • greater effect on inactivated Na+ channels (non-firing cells), especially ventricular myocardial cells
  • used for refractory ventricular arrhythmias
  • local anesthetic with anti arrhythmic properties that slows down reentry impulses in ischemic tissue, so normal impulses can “take over”
  • has low toxicity and high degree of effectiveness
  • used for vtach/vfib in cardiac arrest situations where Amiodarone is ineffective
22
Q

Class II Antiarrhythmics

A

B-ADREERGIC BLOCKERS

  • block B adrenergic receptors, inhibiting physiologic response that would normally occur with stimulation of B receptor, by Norepi or by B agonists
  • result in decreased automaticity (decreased HR), decreased AV node conduction (prolonged PR), increased AV node refractory time, and decreased inotropic effect
  • used for non-life threatening arrhythmias, in particular atrial arrhythmias
  • useful in preventing cardiac modelling post MI

-selective B blockers, non-selective B blockers, or combination of a+B blockers

23
Q

Selective B blockers

A

Tenormin (Atenolol)
Brevibloc (Esmolol)
Lopressor (Metoprolol)

24
Q

Non-selective B blocker

A

Inderal (Propanolol)

25
Q

a+B blockers

A

Coreg (Carvedilol)

26
Q

Class III Antiarrhythmics

A

POTASSIUM CHANNEL BLOCKERS

  • primarily affect K+ channel, but also block Na+, Ca++ channels and B1 receptors
  • block efflux of K+ = slowed repolarization or increased ERP and decreased HR
  • aka increased refractory time agents
  • drug ex. Cordarone (Amiodarone)
27
Q

Cordarone (Amiodarone)

A
  • slows down both atrial and ventricular rates
  • long onset of action and extremely long T1/2 (weeks)
  • can have serious toxic effects: hypothyroidism, neuropathy, hepatic dysfunction, pulmonary fibrosis
  • has replaced Lidocaine as first-line anti arrhythmic in ventricular arrhythmias
28
Q

Class IV Antiarrhythmics

A

CALCIUM CHANNEL BLOCKERS

  • block entry of Ca+ ions into cell, especially at SA and AV nodes = decreased HR
  • little effect on ventricular conduction and QRS duration = more useful for atrial or supra ventricular tachycardias
  • drugs ex. Cardizem (Diltiazem) and Isoptin (Verapamil)
29
Q

Cardizem (Diltiazem)

A
  • slows rise of Phase 4 and 0 of SA node = increased P-P interval and slows AV node conduction velocity so PR interval is increased, HR decreased
  • used as antiarrhythmic, antianginal, and as vasodilatory
30
Q

Adenosine

A
  • endogenous nucleoside, A1 receptors on myocytes in atria, SA and AV node
  • ENDOGENOUS levels increase during hypoxia = vasodilation and decreased cardiac work = promotes increased O2 supply and decreased cardiac work (antiadrenergic effect)
  • as EXOGENOUS, similar effects, stimulates A1 receptors = decreases HR, decreased SV, decreased response to Epi
  • at A2 receptors, causes vasodilation especially of coronary arteries
  • short T1/2 (10 sec) with minimum side effects
  • very useful in Tx of PSVT, but no effect on ventricular tachycardias and therefore is often used to Dx arrhthmia
31
Q

Magnesium Sulfate

A
  • 2nd most common intracellular ion
  • used in various cardiac functions, such as ATPase pump (used to pump Na+ and K+ into its respective compartments)
  • deficiency can result in arrhythmias and CHF
  • used to Tx various life-threatening ventricular arrhythmias
32
Q

Digoxin

A

-increases parasympathetic stimulation of SA and AV node, and decreases sympathetic activity =decreased HR and AV node conduction (dromotropic effect)

HTLH 2511 (10 decks)

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