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Flashcards in CV basic Deck (10):
1

describe the effects of enhanced Cardiac Late Na+ current

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

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2

describe the voltage-gated Na+ channels gating mechanisms

- 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

3

Describe the differences between cardiac conduction tissue and cardiac muscle

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

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

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4

describe Early After-Depolarization (EADs)

- 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

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5

describe Delayed after-depolarization (DAD)

- 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

 

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6

describe re-entry circuties

- 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

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7

what are the consequences of arrhythmias

- 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

8

describe the general mechanisms of action of antiarrhythmic drugs

- Decrease phase 4 slope

- increase threshold potential (B)

- increase maximum diastolic potential (C)

- Increase APD (D)

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9

describe the two ways of increasing refractoriness

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

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10

Class 1 agents: general

- 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