EXAM #2: CV PHARM 1 Flashcards

1
Q

What is the definition of excitability?

A

Ability of a cell to respond to an electrical stimulus

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2
Q

What is the definition of automaticity?

A

Ability for a cell or group of cells to initiate an action potential

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3
Q

What is the definition of conductivity?

A

Ability of a cell or region of cells to receive and transmit an action potential

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4
Q

What is the definition of dromotropism?

A

Ability to alter the rate of conduction

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5
Q

What is the definition of refractoriness?

A

Inability of a cell to receive and transmit an action potential

E.g. during portions of the action potential

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6
Q

What phases of the cardiac action potential does the QRS complex correspond with?

A

Phase 0,2, and 3

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7
Q

What phases of the cardiac action potential does the p-wave correspond with?

A

Phase 0 of the atrial

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8
Q

What is the rule regarding electrical and mechanical activity of the heart?

A

Electrical activity ALWAYS comes before mechanical

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9
Q

What phase of the cardiac action potential does the T-wave correspond with?

A

Repolarization

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10
Q

Draw and label the phases of the cardiac action potential.

A

N/A

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11
Q

What ion channel mediates phase 0 if the cardiac action potential?

A
  • Na+
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12
Q

What is the difference between fast and slow Na+ current?

A

Fast= initial current for depolarization

Slow= maintained throughout action potential

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13
Q

What ion channels mediate phase 2 of the cardiac action potential?

A

1) Ca++ channels (L-type) inward

2) K+ outward

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14
Q

What maintains the plateau of phase 2?

A

Balance of Ca++ in an K+ out

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15
Q

What ion channels mediate phase 3 of the cardiac action potential?

A

K+ efflux

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16
Q

What happens to the cardiac action potential with K+ channel blockers?

A

AP is prolonged b/c of less efflux for phase 3

17
Q

What ion channel is responsible for phase 4 of the cardiac action potential?

A

Funny current

18
Q

What locations of the heart normally have phase 4 depolarization?

A

SA and AV node

19
Q

What are the three phases of the cardiac Na+ channel?

A

1) Resting
- Activation gate closed
- Inactivation gate open

2) Activated
- Both gates open

3) Inactivated
- Inactivation gate closed

20
Q

What is the effect of increased late Na+ current?

A

Prolonged cardiac action potential

21
Q

When is a prolonged Late Na+ current seen?

A

Ischemia
Heart Failure
Arrhythmia
Peripheral arterial disease

22
Q

Outline the pathophysiology associated with enhanced Late Na+ current.

A

1) Increased Na+ influx leads to elevated intracellular Na+
2) Elevated intracellular Na+ activates the Na+-Ca++ exchanged
- Exchange of Na+ (out)
- Ca++ into the cell
3) This causes increased intracellular Ca++
4) Ca++ overload develops

23
Q

What are the consequences cellular Ca++ overlaod?

A

1) Electrical instability–>after-depolarizations/ arrhythmia
2) Mechanical dysfunction–>abnormal contraction and relaxation

24
Q

Draw the SA node action potential.

A

N/A

25
Q

What causes phase 0 in the SA node AP? How does this compare to the ventricular tissue?

A
  • Ca++ current in SA node

- Na+ in ventricular myoctye

26
Q

What phases are missing from the SA node AP?

A

No phase 1 and 2

27
Q

What do Na+ channel blockers effect more, nodal or ventricular tissue? Why?

A

Ventricular/ myocyte b/c these tissues have a fast inward Na+ current that causes depolarization

28
Q

What is the ERP/ADP ratio? Why is this important?

A

This is the ratio of the “effective refractory period” to the “Total action potential duration”

The LOWER the ratio, the EASIER it is for depolarization by aberrant impulses i.e. the longer the APD is with a shorter ERP–>arrhythmia*

29
Q

Draw the cardiac action potential and the effective/ relative refractory periods.

A

N/A

30
Q

What are the two major categories of mechanisms of arrhythmogenesis?

A

1) Disorders of impulse formation

2) Disorder of impulse conduction

31
Q

List the disorders of impulse formation.

A
  • No change in pacemaker site e.g. sinus tachy or bradycarida
  • Ectopic foci
  • Early and delayed after-depolarizations
32
Q

List the disorders of impulse conduction.

A
  • AV Block
  • Ventricular re-entry
  • AV re-entry
33
Q

How is atrial tachycardia manifested on ECG?

A

Change in shape and rate of p-waves

34
Q

What is an early after-depolarization?

A

Depolarization in the relative refractory period, during a prolonged plateau phase

35
Q

What is a common consequence of an early-after depolarization?

A

Torsades De Pointes

36
Q

What is a delayed after-depolarization?

A
  • Occurs in high intracellular Ca++ concentrations
  • Normal upstroke followed by abnormal depolarization that leads to a secondary uptroke
  • Abnormal rhythm results
37
Q

What is the difference between a 1st, 2nd, and 3rd degree AV block?

A
1st= prolonged PR interval 
2nd= not all p-waves followed by QRS 
3rd= no P/QRS relationship i.e. AV dissociation
38
Q

What is AV Nodal Reentrant Tachycardia?

A
  • Patient has 2x conduction paths/velocities in the AV node*****
  • Ectopic ATRIAL PREMATURE BEAT finds fast pathway in refractory period (via normal SA nodal pathway)
  • Slow pathway depolarized and enters fast pathway b/c it is fast enough to repolarized enough for stimulation
  • Circular motion begins

Note that this does not have to occur just in the AV node.

39
Q

What are the manifestations of re-entry?

A
  • A-flutter
  • AVNRT
  • Accessory SVT
  • Ventricular re-entry