Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CV Block > CV Stimulant and Cholinergic Antagonists > Flashcards

CV Stimulant and Cholinergic Antagonists Flashcards

1
Q

Muscarinic M2 receptors are coupled with which type of G protein? What does activation of this receptor in the heart DIRECTLY cause?

(mechanism by which it slows the heart)

A

Gi (inhibitory) /Go (PTX sensitive)–> inhibition of adenylyl cyclase causes a decrease in cAMP.

  1. Activation of inward K+ channels.
  2. Inactivation of L-type (voltage gated) Ca2+ channels
  3. Net result = HYPERPOLARIZATION and inhibition of action potential generation.

Decreased contractility/HR/conductivity!

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

What effects does cholinergic stimulation have on the heart and vasculature?

A

Heart: Decrease contractility and HR

Vasculature –> causes synthesis of EDGF (endothelin-derived growth factor), a VASODILATORY intermediate.

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

Where on the heart do parasympathetic neurons go?

A

SA and AV node.

Very little to no effect on the ventricle.

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

What effects does parasympathetic innervation have on the:

  1. SA node
  2. Atrial Myocardium
  3. AV node
A

Parasympathetic innervation causes:

  1. Decreased rate of spontaneous depolarization (Ik+ channel activation and Ca2+ channel inhibition) ….AKA…. phase 4 prolongation.
  2. Atrial Myocardium: Causes hyper polarization and decrease in AP duration (Ik+ channel activation)
  3. AV node –> slows conduction velocity and increases refractory period
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

M3 receptors have what G protein mechanism?

A

DAG/IP3, and increased intracellular Ca2+

DEPOLARIZATION AND EXCITATION! –> increase sEPSP –>

Leads to the synthesis and release of Nitric Oxide (NO) for VASODILATORY EFFECTS

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

What compensatory mechanism tries to negate excessive parasympathetic stimulation of the heart and vasculature?

A

Barreceptors –> sense a decrease in BP or Po2, decrease their firing rate to the brain, and cause the NTS to send out sympathetic stimulation to start the heart back up.

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

There are 4 primary effects Acetylcholine has on the CV system. Name them.

A
  1. Vasodilation
  2. Decreased HR (negative CHRONOTROPIC effect)
  3. Decreased AV node conduction velocity
  4. Decreased contractility ( negative INOTROPIC effect)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What effect does Ach release have on NE?

A

It inhibits NE release from sympathetic nerve terminals by binding to M2 or M3 heteroreceptors (located on the sympathetic neurons).

NE can do the same thing to Ach in parasympathetic neurons.

The release of one causes inhibition of release of the other.

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

Explain the effect of Acetycholine on intact vascular tissue vs. endothelial damage tissue.

A

M3 stimulation by Ach in INTACT endothelium causes NO production and vasodilation.

M3 cholinergic stimulation in DAMAGED endothelium causes smooth muscle cell contraction (vasoconstriction)

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

Where in the body is lacking cholinergic innervation?

A

Human skeletal muscle

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

MOA of Atropine at low levels.

A

Low –> blocks the presynaptic M1 receptor (negative feedback loop) of Ach, resulting in increased Ach release. Transient decrease in HR.

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

MOA of Atropine at high levels.

A

High –> Blocks M2 receptors in SA nodal cells, blocking Ach’s activation of them. (no vagal tone in heart…so heart can run away with itself)

Increased resting heart rate! Tachycardia!

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

Atropine’s effect on the circulation.

A

At low doses: Completely counteracts peripheral vasodilation caused by Ach stimulation.

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

What is Atropine Flush? Why does it occur?

A

High doses of Atropine can cause cutaneous BV dilation, making a flushed face appearance.

Why does it happen? Atropine is a parasympathetic (muscarinic) antagonist, and our body temp is controlled by Eccrine sweat glands under parasympathetic control.

Without them, we overheat, and the cutaneous vasodilation is our body’s way of trying to release that heat.

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

When do you use ATROPINE?

A

Asystole and Bradycardia –> removes ALL vagal tone from the heart, allowing sympathetic tone to take over and re-start the heart.

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

REMEMBER: High doses of Atropine remove parasympathetic stimulation, and low doses allow it to work a little better. HIGH DOSE SAVES YOU LIFE IN ASYSTOLE. Low dose will just make you… more dead.

A

Yep.

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

Stimulation of cardiac function can be accomplished either through stimulation of the _________ nervous system, or inhibition of the __________ nervous system.

A

Stimulation of sympathetic, inhibition of parasympathetic.

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

How do direct-acting CV stimulants work?

A

Stimulate the post-synaptic membrane to gain a sympathetic response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How do mixed CV stimulants work?

A

Stimulate the post-synaptic membrane to gain a sympathetic response, and act on the pre-synpatic membrane to cause release of endogenous transmitter as well.
Double whammy.

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

How do Indirect CV simulates work?

A

Increase the availability of existing NE or Epi via inhibition of their metabolism, greater release, or reuptake inhibition.

21
Q

A1 receptor mechanism.

A

Gq

DAG/IP3 –> increased intracellular Ca2+ (easier contractility)

22
Q

A2 receptor mechanism

A

Gi

Inhibits adenylyl cyclase, decreases cAMP levels

23
Q

B1/B2/B3 receptor mechanisms.

A

G2

Activates adenylyl cyclase

Increase cAMP levels, with different effects in each tissue

24
Q

D1/D5 receptor mechanism.

A

Gs

Activates adenylyl cyclase

Increase cAMP levels

25
Q

D2 receptor mechanism

A

Decrease adenylyl cyclase.

INCREASE K+ CONDUCTANCE

26
Q

All of the CV stimulants cause an increase in BLOOD PRESSURE EXCEPT:

A

Isoproterenol

Only works on B receptors, so if anything it decreases BP.

27
Q

You give reserpine to a 3 patients before administering one of the following to each of them:

  1. Direct-Acting CV stimulant
  2. Mixed-acting CV stimulant
  3. Indirect CV stimulant

What happens?

A

The direct acting drug is effective. Increases BP and HR.

The Mixed acting drug’s action blunted, but not gone.

The indirect acting drug is negated. No effect when reserpine is administered. Indirect CV stimulants are entirely dependent on endogenous stores of catecholamines

28
Q

MOA of reserpine.

A

Binds VMAT and inhibits it (VMAT is responsible for vesicular storage of NE and Epi)

There is no storage of NT for release, no matter how much the brain wants it.

29
Q

Where is Epinephrine released from?

A

Adrenal medulla

30
Q

Norepinephrine’s action on the body.

Specifically on pulse pressure as well

A

Increased TPR due to A1 agonism (vasoconstriction)

This causes an increase in BP (systolic AND diastolic).

NO EFFECT ON PULSE PRESSURE because it equally increases systolic and diastolic BP’s

Increase in BP elicits a baroreceptor response, which slows down the heart rate.

31
Q

Epinephrine’s effect on Pulse Pressure, and the body.

A

Epi’s action on B2 receptors in the smooth muscle causes diastolic pressure decrease.

A1 agonism causes systolic pressure to raise, due to vasoconstriction of the other vessels.

B1 agonism causes increased contractility, increasing systolic pressure as well. Also, increased Renin release.

PULSE PRESSURE IS INCREASED

TPR decreases due to B2 action.

32
Q

Isoproterenol’s effect on the body and pulse pressure.

A

B1 agonism = increased HR/contractility, which increases CO, very slightly increasing systolic pressure

(slight systolic pressure increase is secondary to increased CO)

B2 agonism promotes vasodilation, decreased TPR, and LOWER diastolic pressure.

INCREASES THE PULSE PRESSURE mainly due to significantly decreased diastolic pressure.

33
Q

Why can’t you take Epinephrine orally? What other route of delivery is contraindicated?

A

Take Epi orally and it will be metabolized.

Must be given IV, inhaled or IM.

Can’t take it Subcu because of slow absorption. Epi will cause local vasoconstriction at application site and take forever to reach the heart.

34
Q

Which is more sensitive to stimulation by Epi: Alpha1 or B2 receptors? What does this mean for Epi’s effects at low doses?

A

B2 receptors.

This means the effects of Epi on B2 receptors will linger once its other effects have waned.

At low concentrations, Epi may cause a decrease in BP (not normal) cause of greater B2 receptor affinity.

35
Q

Increase in SYSTOLIC BP is always due to what, when we’re talking about CV stimulants?

A

Systolic BP increase is due to cardiac stimulation, and increased contractility. This increases the cardiac output, which causes increased systolic BP.

Even happens from minor stimulation like NorEpi’s slight B1 affinity.

36
Q

Which CV stimulant causes an increase in the MAP?

A

NorEpi (raises both systolic and diastolic pressures)

37
Q

FACT: Dopamine is the metabolic precursor to Epi and NE.

A

Tyrosine –> Dopamine –> Norepinephrine –> Epinephrine

38
Q

Where is dopamine synthesized?

A

Kidney proximal tubule

39
Q

Describe the Dose-Dependent effects of Dopamine.

A

Low doses: D1 activation (vasodilation, and improved GFR)

Moderate: D1+B1 vasodilation and increased cardiac inotropic and chronotropic effects.

High: Alpha receptors : vasoconstriction

40
Q

Can Dopamine and NE be administered via any other route than IV?

A

NOPE

41
Q

Dobitamine MOA

A

Dobutamine has NO effect on dopaminergic receptors.

It’s a B1 and A1 agonist/antagonist racemic mixture.

Increases CO and SV without marked effect on HR.

42
Q

When do you use Dobutamine?

A

Short term treatment of cardiac decompensation (post MI or CHF)

Only in hospitals by IV infusion, because the T/2 is so short. (2 min)

43
Q

A patient has bradycardia. THey didn’t respond to atropine. (Remember atropine blocks vagal parasymp stimulation and allows sympathetic to take over).

What do you give them now, to stimulate the heart?

A

ISOPROTERENOL

Used in Atropine-unresponsive bradycardia, particularly in anticipation of pacemaker implantation.

44
Q

What CV stimulant is a direct acting alpha agonist with barely any B-adrenergic activity?

A

Phenylephrine

45
Q

Give Phenylephrine to a patient. what happens?

A

Increase in TPR increases BP.

Reflexive decrease in HR.

46
Q

You give Norepinephrine to a patient. What happens to their heart rate?

A

It decreases in reflexive response to an increase in both diastolic and systolic BPs.

47
Q

MOA of Ephedrine

A

MIXED sysmpathomimetic.

Directly acts at both A and Beta receptors, and causes increased release of NE from presynaptic neurons.

48
Q

What is Ephedrine used for?

A

Hypotension.

CV Block (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions