CV basic

Question 1

describe the effects of enhanced Cardiac Late Na+ current

Answer 1

• causes electrical instability, giving rise to after depolarizations and arrhythmias, and mechanical dysfunction (abnormal contraction and relaxation

Question 2

describe the voltage-gated Na+ channels gating mechanisms

Answer 2

• contains two gates that respond in opposite ways to depolarization
• resting (closed) state

–> actiavtion gate is closed and the inactivation gate is open

• Depolarization

–> rapid opening of activation gate allows Na+ to flow through the channel

–> As the inactivation gate close, Na+ channels enter the inactivated (closed state)

• repolarization

–> first the activation gate closes, then the inactivation gate opens as the channel returns to the resting state

Question 3

Describe the differences between cardiac conduction tissue and cardiac muscle

Answer 3

• phase 0 of AP in nodal tissues is controlled by Ca2+ entry

–> phase 0 in non nodal tissue is controlled by Na+ entry

Question 4

describe Early After-Depolarization (EADs)

Answer 4

• Prolongation of the cardiac AP, such as occurs as the result of slow heart rate, hypokalemia or drugs that prolong APD

–> Phase 3 repolarization may be interrupted

–> induced mroe readily in purkinje cells than in epicardial or endocardial cells

• EADs trigger FUNCTIONAL REENTRY across the ventricular wall
• can cause torsades de pointes

Question 5

describe Delayed after-depolarization (DAD)

Answer 5

• under conditions of intraellular or sarcoplasmic reticulum Ca2+ overload, a normal action potential may be followed by a Delayed afterdepolarization (DAD)

–> If DAD reaches threshold, a secondary triggered beat or beats may occur

–> DAD-medaited triggered beats are more frequent when the underlying heart rate is rapid

Question 6

describe re-entry circuties

Answer 6

• occurs when the existence of conduction routes with different conduction velocity
• A-V nodal reentrant tachycardia (AVNRT)

–> premature atrail impuse finds the fat pathway refractory, allowing conduction only down the slow pathy.

–> by the time the impulse reaches the His bundle, the fast pathway may have recovered, allowing retrograde conduction back up to the atria

–> RESULTS in “circus movement” gives rise to slow-fast atrioventricular nodal re-entrant tachycardia

Question 7

what are the consequences of arrhythmias

Answer 7

• Compromise of mechanical performance

–> affect ventricular stroke volume directly leading usually to decreases in cardiac output

• Proarrhythmic/arrhythmogenic

–> many arrhythmias, when not corrected, may lead to more severe forms of arrhythmias

• Thombogenesis

–> facilitate the formation of thrombi in the heart chambers (assocaited with endocardial lesisons

Question 8

describe the general mechanisms of action of antiarrhythmic drugs

Answer 8

• Decrease phase 4 slope
• increase threshold potential (B)
• increase maximum diastolic potential (C)
• Increase APD (D)

Question 9

describe the two ways of increasing refractoriness

Answer 9

• Increased by drugs that block Na+ channels or drugs taht increase APD

Question 10

Class 1 agents: general

Answer 10

• Block fast inward Na+ channels to varying degrees in CONDUCTIVE TISSUES of the heart

–> Decrease max depolarization rate (Vmax of phase 0)

• -> Reduce automaticity, delay conduction
• -> Prolong ERP –> ERP/APD INCREASED
• Useful in varying degrees for vetnricular dysrhythmia and/or digitalis or MI-INDUCED ARRHYTHMIA