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.

25
What causes phase 0 in the SA node AP? How does this compare to the ventricular tissue?
- Ca++ current in SA node | - Na+ in ventricular myoctye
26
What phases are missing from the SA node AP?
No phase 1 and 2
27
What do Na+ channel blockers effect more, nodal or ventricular tissue? Why?
Ventricular/ myocyte b/c these tissues have a fast inward Na+ current that causes depolarization
28
What is the ERP/ADP ratio? Why is this important?
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
Draw the cardiac action potential and the effective/ relative refractory periods.
N/A
30
What are the two major categories of mechanisms of arrhythmogenesis?
1) Disorders of impulse formation | 2) Disorder of impulse conduction
31
List the disorders of impulse formation.
- No change in pacemaker site e.g. sinus tachy or bradycarida - Ectopic foci - Early and delayed after-depolarizations
32
List the disorders of impulse conduction.
- AV Block - Ventricular re-entry - AV re-entry
33
How is atrial tachycardia manifested on ECG?
Change in shape and rate of p-waves
34
What is an early after-depolarization?
Depolarization in the relative refractory period, during a prolonged plateau phase
35
What is a common consequence of an early-after depolarization?
Torsades De Pointes
36
What is a delayed after-depolarization?
- Occurs in high intracellular Ca++ concentrations - Normal upstroke followed by abnormal depolarization that leads to a secondary uptroke - Abnormal rhythm results
37
What is the difference between a 1st, 2nd, and 3rd degree AV block?
``` 1st= prolonged PR interval 2nd= not all p-waves followed by QRS 3rd= no P/QRS relationship i.e. AV dissociation ```
38
What is AV Nodal Reentrant Tachycardia?
- 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
What are the manifestations of re-entry?
- A-flutter - AVNRT - Accessory SVT - Ventricular re-entry