arrhythmia

Question 1

cardiac AP (non nodal tissue)

Answer 1

• 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

Question 2

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

Answer 2

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

Question 3

1st degree AV block

Answer 3

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

Question 4

2nd degree AV block type I

Answer 4

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

Question 5

2nd degree AV block type II

Answer 5

• consistent PR interval with occasional blocking
• block below AV node

Question 6

3rd degree AV block

Answer 6

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

Question 7

focal atrial tachycardia

Answer 7

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

Question 8

mutlifocal atrial tachycardia

Answer 8

• 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

Question 9

ventricular tachycardia

Answer 9

• 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)

Question 10

3 mechs of arrhythmias

Answer 10

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

Question 11

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

Answer 11

• 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)

Question 12

AV Nodal reentry Tachycardia (AVNRT)

Answer 12

• 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)

Question 13

Wolff Parkinson White Syndrome

Answer 13

• 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

Question 14

atrial fibrillation

Answer 14

• 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

Question 15

atrial flutter

Answer 15

• 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

Question 16

Class IA

Answer 16

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

Question 17

Quinidine

Answer 17

• 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

Question 18

Procainamide

Answer 18

• 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

Question 19

Disopyramide

Answer 19

• 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

Question 20

Class 1B

Answer 20

• 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)

Question 21

Lidocaine

Answer 21

• 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

Question 22

Mexiletine

Answer 22

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

Question 23

class 1C

Answer 23

• 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)

Question 24

Flecainide

Answer 24

• 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

Question 25

Propafenone

Answer 25

* Class 1C * similar in action to Flecainide but has active metabolite

Question 26

Class II

Answer 26

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

Question 27

Class III

Answer 27

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

Question 28

Sotalol

Answer 28

* class III * K+ channel blocker * non-selective Beta Blocker (-"alol") * increase APD, prolong QT * renal excretion --\> monitor liver function

Question 29

Amiodarone

Answer 29

* 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

Question 30

Dronedarone

Answer 30

* Class III * "softer" Amiodarone (less organ toxicities but less efficacious) * no Iodine substituents

Question 31

Dofetilide

Answer 31

* Class III * highly selective IKr blocker but proarrhthymic effects --\> strong regulations (must hospitalize PT to dose this drug)

Question 32

Class IV

Answer 32

* 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)

Question 33

Adenosine

Answer 33

* 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)**