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unit 4 pharm > arrhythmia > Flashcards

arrhythmia Flashcards

1
Q

cardiac AP (non nodal tissue)

A
  • phase 0= fast sodium influx (QRS complex)
  • phase 1= overshoot –>Na inactivated, transient outward K current
  • phase 2= plateau phase (slow Ca and Na “window” current influx balanced by delayed rectifier K current)
  • phase 3= repolarization –> delayed K rectifier current increases as Ca current dies out
  • phase 4: return to resting membrane potential via Na/K ATPase
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2
Q

SA and AV node AP vs atria, ventricle, HP AP

A
  • Nodal: slow, mediated by calcium, sponatenous depolarization (via If)
  • Non-nodal: fast, mediated by Na, refractory period
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3
Q

1st degree AV block

A
  • slow conduction from A to V (not a true block)
  • PR interval > 200 ms
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4
Q

2nd degree AV block type I

A
  • wenchebach
  • lengthening of PR interval utnil conduction is blocked
  • block w/i AV node
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5
Q

2nd degree AV block type II

A
  • consistent PR interval with occasional blocking
  • block below AV node
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6
Q

3rd degree AV block

A
  • complete block
  • atrial and ventricles arent communicating with each other
  • none of the p waves are conducted
  • ventricular rate depends on escape pacemakers
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7
Q

focal atrial tachycardia

A
  • increased automaticity (impulse coming from atrial tissue other than SA node)
  • rate > 100 bpm
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8
Q

mutlifocal atrial tachycardia

A
  • numer of different clusters of cells outside the SA node take over control of firing
  • 3 or more kinds of P waves with rate > 100 bpm
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9
Q

ventricular tachycardia

A
  • rhythmathat originates in ventricle with rate >100 bpm
  • most common mechanism is due to reentry
  • wide QRS
  • regular
  • “big,wide, regular and fast”
  • atrial activity doesnt precede ventricular
  • can’t treat with CCB (Class IV)
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10
Q

3 mechs of arrhythmias

A
  1. increased automaticity (ectopic pacemakers)
  2. triggered automaticity (ie: EAD and DAD)
  3. reentry
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11
Q

Early after Depolarization (EAD) and Delayed after Depolarization (DAD)

A
  • both are types of triggered automaticity
  • EADs interrupt phase 3 of AP (long QT syndrome)
  • **get EAD with hypokalemia (prolonged phase 3–> greater excitability –> greater risk of arrhthymia
  • DADs interrupt phase 4 of AP (digoxin toxicity)
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12
Q

AV Nodal reentry Tachycardia (AVNRT)

A
  • reentry is the most common mechanism for arrhythmias
  • fast pathway quits 1st
  • normally the fast pathway conducts the rhythm but if it gets blocked the slow pathway will conduct
  • reentrant current by the time the fast pathway has recovered
  • anterograde pway = slow –> contraction of ventricles –> QRS
  • retrograde pway = fast –> contraction of atria –> inverted p wave
  • simultaneous contraction of A and V (p wave may be buried in QRS)
  • reentrant circuit is faster than SA firing –> SVT
  • **also occurs in ischemia where the slow pway is the ischemic tissue and the fast pway quits due to an ectopic beat the catches the fast pway in its refractory phase)
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13
Q

Wolff Parkinson White Syndrome

A
  • presence of abnormal accessory electrical conduction pathway between atria and ventricles –> premature ventricular contraction down abnormal pway
  • short PR interval (conduction via AP doesnt produce a delay in conduction to ventricles –> immediate depolarization)
  • delta wave (slurred upstroke of QRS complex)
  • can result in reentrant tachycardia (antidromic: impulse spreads down AP and then back up HP in retrograde fashion; orthodromic: reentrant loop runs in opp direction)
  • can also result in afib or futter (AP pway not associated with a delay in conduction to ventricles)
  • don’t give AV nodal drug bc this will cause all conductionto go through the aberrant pway
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14
Q

atrial fibrillation

A
  • lack of organized atrial activity
  • cardiac muscle extends into the sleeves of the vein (which is the source of firing)
  • SA node is overwhelmed by erratic atria –> ventricles drive the rhythm (normal QRS)
  • ventricular response is **irregularly irregular **
  • undulating baseline
  • risk of thrombi (via blood stasis) –> need anticoagulants
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15
Q

atrial flutter

A
  • arises from circuit within RA
  • anatomic barriers within RA sustain macro-reentry circuit (it is a type of reentry circuit that is anatomically determined)
  • initiated by electrical impulse arising in atria and propagated due to diffs in refractory periods of atrial tissue –> creates self-perpetuating loop of electrical activity
  • AV nodes plays no role (can’t used AV blocking drug)
  • ventricular response is fast but regular
  • sawtooth
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16
Q

Class IA

A
  • blocks fast Na channel (open state)
  • blocks Ikr (delayed rectifier current)
  • Double Quarter Pounder
  • Quinidine, Procainamide, Disopyramide
  • prolong QRS and QT
17
Q

Quinidine

A
  • class 1A
  • INa, Ik, Ito channel blocker
  • prolong AP duration, prolong QRS
  • causes muscarinic receptor blockade too –> increase HR and AV conduction –> proarrhythmic (potential lethal arrhythmia!)
  • extra cardiac effects: nausea, diarrrhea
  • went out of favor due to SE and potential lethal arrthymia
  • tx for Brugada’s
18
Q

Procainamide

A
  • class 1A
  • Na channel blocker –> prolong QRS
  • non-specific K channel block –> increase APD and suppress SA and AV node
  • NAPA is the active metabolite (Class III)
  • ganglionic block leads to hypotension
  • oral form went out of favor due to development of Lupus
  • tx: acute settting for afib and ventricular arrhythmia
  • DOC for pre-excited afib
  • **Procainamide = naPa,luPus, hyPotension
19
Q

Disopyramide

A
  • Class 1A
  • vagolytics effects –> good choice for PT with bradycardia
  • used in tx of vagally-mediated afib and VT
  • anticholinergic effect –> urinary retention, blurred vision, glaucoma
20
Q

Class 1B

A
  • Na channel blockers (block “window” current)
  • greater blockade in inactivated state (ie: ischemic tissue)
  • don’t work in atrial tissue (can’t give in atrial arrhthymia!)
  • shorten QT and APD due to blockage of slow Na “window” currents (influx current in plateau phase that prolongs repolarization) –> increases diastole and extends recovery time
  • Lidocaine and Mexiletine (Lettuce and Mayo)
21
Q

Lidocaine

A
  • class IB
  • Na channel blocker (inactivated state- ischemia)
  • **least cardiotoxic **
  • CNS SE: tremor, paresthesia, seizure
  • DOC in ischemic related arrhythmia (non atrial) ie: ischemic VT
  • only available IV
22
Q

Mexiletine

A
  • Class IB
  • Na channel blocker (inactivated, ischemic)
  • oral lidocaine (tx VT)
  • GI SEs
23
Q

class 1C

A
  • the most potent Na channel blockers
  • block fast Na channels
  • no effect on APD (bc they block any Na channel)
  • negative inotrope –> depress LV function –> worsen HF
  • proarrhythmia in ischemic tissue
  • used to treat atrial arrhythmia in structurally normal heart with preserved LV function, no active ischemia and no hx of CAD or hypertrophy
  • Flecainide and Propafenone (Fries Please)
24
Q

Flecainide

A
  • Class IC
  • very potent Na channel blocker
  • can only be used in PTs with structurally normal heart with preserved LV function, no ischemia, CAD or hypertrophy
25
Q

Propafenone

A
  • Class 1C
  • similar in action to Flecainide but has active metabolite
26
Q

Class II

A
  • beta blockers
  • decrease SA and AV nodal activity
  • negative inotropes
  • SE: bronchospasm and bradycardia
  • Metropolol, Atenolol, Nadolol (MAN)
27
Q

Class III

A
  • K+ channel blockers
  • **class III works at phase 3
  • Sotalol, Amiodarone, Dronedarone, Dofetilide (SADD)
  • prolong APD/QT
28
Q

Sotalol

A
  • class III
  • K+ channel blocker
  • non-selective Beta Blocker (-“alol”)
  • increase APD, prolong QT
  • renal excretion –> monitor liver function
29
Q

Amiodarone

A
  • Class III but action of all 4 classes (good! but many SE)
  • 40x daily required dose of Iodine is ingested daily –> end organ toxicities
  • pulmonary fibrosis, hepatic necrosis, thyroid dysfunction, blue “smurf skin” and others (CNS, ocular, GI)
  • many drug interactions
30
Q

Dronedarone

A
  • Class III
  • “softer” Amiodarone (less organ toxicities but less efficacious)
  • no Iodine substituents
31
Q

Dofetilide

A
  • Class III
  • highly selective IKr blocker but proarrhthymic effects –> strong regulations (must hospitalize PT to dose this drug)
32
Q

Class IV

A
  • non-dihyrdopyridine Ca channel blockers
  • decrease nodal activity
  • other effects: negative inotrope action on heart, sinus arrest, hypotension, AV block
  • Verapamil and Diltiazem
  • tx: SVT (won’t work on Vtach because that is below the AV node)
33
Q

Adenosine

A
  • activates adenosine receptors in atrium, SA and AV nodes
  • activates K+ current –> hyperpolarizes tissue –> decreases automaticity and AV conduction
  • shortens APD
  • short half-life (IV administration)
  • DOC for paroxysmal SVT (acute settings)

unit 4 pharm (8 decks)

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