Trachte/Nordgren Week 3 Flashcards

(49 cards)

1
Q

What do sympathetic nerves innervate to elevate HR, SV and TPR?

A

atria, ventricle, arterioles and veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the major effect of the sympathetic nervous system?

A

elevate blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the equation for BP?

A

HR x SV x TPR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Steps to synthesis of norepinephrine?

A

Tyrosine to DOPA to Dopamine to Norepinephrine to Epinephrine (adrenal medulla)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the rate limiting step in norepinephrine production?

A

tyrosine hydroxylase (cystolic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is an inhibitor of DOPA carboxylase?

A

carbidopa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the 3 deviations that can cause an arrhythmia?

A

change in rate of impulse, impulse site of origin or conduction of the impulse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the equilibrium potential of K?

A

-90mv (wants to move out of cell)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the equilibrium potential of Na?

A

+70mv (wants to move into cell)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the key factor in pathophysiology of arrhythmias and the drugs that treat them?

A

relation between RESTING potential of a cell and the number of ACTION POTENTIALS that can be evoked

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the range where Na channel inactivation gates close?

A

75 to -55mV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the time between Phase 0 and sufficient recovery of Na+ channels in Phase 3 to allow another action potential?

A

Refractory Period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

In what phase do Na channels recover from inactivation and become available?

A

During repolarization in phase 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What happens at optimal conditions when you add a drug that blocks Na channels?

A

total number of channels available at optimal conditions will be decreased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What happens at suboptimal conditions when you add a drug that blocks Na channels?

A

Na channels will be unavailable dt inactivation gate closure AND drug blockade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What happens to Na channel recovery time with depolarization of membrane potential? Why?

A

Increases; depolarized cells recover more slowly and increases the refractory period of the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What phase of a pacemaker cell is the more important factor of the two on HR?

A

diastolic interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What 2 things can you do to slow the pacemaker?

A
  1. alter slope of diastolic interval 2. hyperpolarize diastolic interval
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What can you do to speed the pacemaker?

A

alter slop of diastolic interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are membrane voltage oscillations that result in transient, abnormal depolarizations of cardiac myocytes during phase 2, 3, or 4 of the cardiac AP

A

Afterdepolarizations

21
Q

Define an early afterdepolarization

A

occur during action potential and interrupt orderly repolarization of myocyte

22
Q

What is the cause of a late phase 2 early afterdepolarization?

A

opening of more Ca channels

23
Q

What is the cause of a late phase 2 early afterdepolarization?

A

opening of sodium channels

24
Q

What can happen dt inhibition of K channels?

A

early afterdepolarization

25
If early afterdepolarization is exacerbated at slow heart rates what can occur?
torsades des pointes and tachycardias
26
Define a delayed afterdepolarization
occur after action potential, when nearly or fully repolarized, but before another action potential would normally occur
27
What causes a delayed afterdepolarization?
elevated cytosolic Ca levels dt overload of SR spontaneous release of Ca and leads to depolarizing current
28
When is a delayed afterdepolarization exacerbated?
at fast heart rates
29
When do blocks occur?
if the electrical signal is slowed or disrupted as it moves through the heart
30
Define a partial blockage of impulse conduction?
electrical impulses are delayed and/or occasionally stopped
31
Define a complete blockage of impulse conduction?
electrical impulses are completely stopped
32
Define reentry impulse conduction disturbance? What is another name for this?
impulse reenters and excites areas of the heart more than once; aka circus movement
33
What type of block prevents passage of an impulse when it approaches form one direction but not from the other?
unidirectional block
34
What type of block prevents passage of an impulse in both directions?
bidirectional block
35
What 3 things must happen in order for reentry to occur?
1. obstacle (anatomic or physiologic) to homogenous conduction 2. unidirectional block at some point in the circuit 3. conduction time must exceed the effective refractory period
36
Name an abnormal electrical accessory connection b/w atria and ventricle
bundle of kent
37
A form of reentry that is strictly anatomical?
Wolff-Parkinson-White Syndrome
38
What happens dt Bundle of Kent?
allows for impuls to be conducted without going through AV node, causing ventricle to prematurely contract; conduit for reentry to the atria
39
How does slow conduction lead to no reentry?
bidirectional block
40
How does too fast conduction (almost normal) lead to no reentry? why?
bidirectional block; impulse travels around unidirectinoal block too quickly and reaches tissue that is still refractory so no reentry
41
What causes slowing conduction?
decreased Ca current or decreased Na current
42
What is the action of Na channel blockade (Class 1 drugs)?
alters AP duration and kinetics of Na channel blockade
43
What is the action of B-adrenoceptor blockade (Class II drugs)?
blockade of SNS effects in the heart
44
What is the action of K channel blockade (Class III drugs)?
prolongation of the effective refractory period
45
What is the action of Ca channel blockade (Class IV drugs)?
slows conduction where depolarization is Ca dependent
46
When do use or 'state dependent' drugs bind?
bind to activated (phase 0) or inactivated (phase 2); bind poorly or not at all to rested channels
47
When do 'use' or 'state dependent' drugs block electrical activity?
fast tachycardia (many channel activations), significant loss of resting potential (many inactivated channels during rest)
48
What happens as a result of Na and Ca channel blockade?
slow conduction speed to bidirectional block to no reentry (steady state reduction in # of available unblocked channels which reduces excitatory currents to a level below that required for propagation)
49
What happens as a result of K channel blockade?
slow conduction speed to bidirectional block to no reentry (prolongation of recovery time of the channels still able to reach the rested and available state, which increases refractory period)