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CRAAB 5 > Nordgren: CV Reflex Demonstration > Flashcards

Nordgren: CV Reflex Demonstration Flashcards

1
Q

What is Ps?

A

Highest pressure reached in systemic arteries during a cardiac cycle

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2
Q

What is Pd?

A

Lowest pressure reached in systemic arteries during a cardiac cycle

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3
Q

What is Pp?

A

Ps-Pd

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4
Q

What is MAP?

A

Systemic arterial pressure over a complete cardiac cycle

Pd +Pp/3

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5
Q

What are the two direct determinants of Pa?

A

CO x TPR

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6
Q

What 2 influences directly affect HR?

A
  1. Sympathetic- beta adrenergic receptors on SA node

2. Parasympathetic- muscarinic cholinergic receptors on SA node

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7
Q

P wave on an ECG?

A

atrial depolarization

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8
Q

QRS on a ECG?

A

Ventricular depolarization

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9
Q

T wave on a ECG?

A

ventricular repolarization

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10
Q

How does CVP compare to systemic arterial pressure?

A

Usually MUCH lower (5 to 100)

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11
Q

What happens to CVP during inspiration?

A

Temporarily DECREASES!

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12
Q

Does respiration affect HR?

A

YES!

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13
Q

How does respiration affect cardiovascular variables (3 ways)?

A
  1. Inspiration > decreased CVP > Increased VR and EDV
  2. Fluctuations in intrathoracic pressure> affect stretching forces on walls of aortic arch> fluctuations in firing rate of aortic arch baroreceptors
  3. Changes in stretch of low pressure cardio-pulmonary baroreceptors affect input into the medullary center and affects the sympathetic outflow to the heart, blood vessels and kidneys.
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14
Q

What determines the average value of CVP?

A

It takes on whatever value necessary to make VR = CO.

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15
Q

Central venous pressure has three fluctuations with each heart beat. What are these?

A

a wave- atrial contraction
c wave- onset of ventricular contraction and closure of tricuspid valve
v wave- sudden decrease in central venous volume as blood rushes from the central venous pool through the opened tricuspid valve and into the right ventricle

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16
Q

How are CVP, cardiac filling pressure and cardiac preload related?

A

All three terms are synonymous!

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17
Q

How are Pa and afterload related?

A

MAP = afterload

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18
Q

What does common carotid occlusion do to the firing rate of carotid sinus baroreceptors?

A

Bilateral carotid occlusion>
lower pressure in carotid sinuses (bifurcation of CCA)>
decrease stretch of carotid sinus walls>
decrease firing rate w/in them

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19
Q

How does common carotid occlusion affect the sns and pns nerve activity?

A

decreases in arterial barorecetpor input>
medullary center>
increase SNS activity and decrease PNS activity

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20
Q

What does carotid occlusion do to HR, contractility, arteriolar tone and venous tone?

A
  1. Decreased PNS> increased HR

2. Increased SNS> increased HR, contractility, arteriolar tone, venous tone

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21
Q

What directional changes are expected in TPR, SV, CO and MAP following a carotid occlusion?

A

incresesd arteriolar tone> increased TPR
increased contractility> increased SV
Increased HR/SV> increased Co
incraesed CO/TPR> increased MAP

22
Q

During the peak of a response to carotid occlusion are the aortic arch baroreceptors signaling the medullary cvc to increase SNS activity?

A

NO

The baroreceptors are seeing a HIGH p and firing more rapidly and therefore blunting the medullary CVCs response to the loss of input from the carotid sinus baroreceptors.

23
Q

How are the cardiac output curve and the venous return curve shifted during carotid occlusion?

A

increased SNS activity> shifts cardiac fxn curve upward

increased SNS activity to peripheral veins> shifts venous curve upward

24
Q

Why doesn’t central venous pressure change much during an occlusion?

A

Both VR and cardiac fxn curves are shifted upward and intersect at the same CVP.

25
Q

How does EPI affect the heart?

A

Epi>
alpha and beta recptors>
increase in HR, contractility, arteriolar constriction, venous constriction

26
Q

What does EPI do DIRECTLY to TPR, SV, CO and MAP?

A

It increases all of them

27
Q

What does an increase in MAP do to the firing rate of arterial baroreceptors and therefore sns and pns activity?

A

It INCREASES firing and therefore reflexively decreases SNS activity and INCREASES pns

28
Q

Will injecting a large dose of epi (a pressure raising disturbance) elicit reflex rxn aimed at counteracting that disturbance?

A

YES

29
Q

In a situations where EPI is in high concentrations, the SNS are off, and PNS are on, how does this affect the heart?

A

increases contractility- direct effect of epi
increases arteriolar tone- direct effect of epi
increases venous tone- direct effect of epi
LOW Hr- epi increases HR but reflexive decrease by PNS

30
Q

Why does hte HR decrease in response to an epi injection?

A

reflex response to elevated arterial pressure

31
Q

What indicates that hte heart is beating with a ventricular rhythm 1 minute after the epi injection?

A

absence of p waves

32
Q

After an injection of epi, what causes the shift from a sinus to a ventricular rhythym?

A

Strong reflex parasympathetic influence can suppress atrial automaticity. Doesn’t happen in the ventricles b/c PNS nerves aren’t present.

33
Q

How does EPI stimulation differ at HIGH and LOW concentrations?

A

High- stimulates alpha and beta

LOW- only beta

34
Q

Is MAP higher or lower than normal 4 mins after an epi injection?

A

LOWER

circulating epi is reduced enough so that beta 2 receptors causing aretriolar vasodilation dominate hte response

35
Q

What relative activity levels of SNS and PNS nerves do you predict 4 mins after an epi injection?

A

SNS activity will be HIGH and PNS will be LOWER to compensate for the reduced arterial pressure

36
Q

Why is HR 4 mins after an epi injection above normal when it was below normal 1 min after injection?

A

At 4 mins, the decrease in TPR d/t beta 2 receptor activation> fall in MAP> reflex INCREASE in HR

At 1 min> TPR elevated and MAP elevated > reflex DECREASE in HR

37
Q

4 min after an injection of epi, is the CO higher or lower than normal? What purpose does this serve?

A

CO is HIGHER than normal

This counteracts the fall in arterial pressure that is being produced by the reduction in TPR

38
Q

How does ACh affect HR?

A

Lowers HR

39
Q

Why does an ACh injection cause a fall in MAP?

A

ACh injection>
reduces TPR>
fall in MAP

40
Q

Why does cutting the vagus nerves cause an increase in HR?

A

Cutting the vagus nerves removes the tonic parasympathetic activity on the heart which normally slows the HR

41
Q

Do afferent fibers from the aortic baroreceptors travel in the vagus nerves?

A

Yes

42
Q

After cutting the vagus nerves, what do the medullary cardiovascular cetners think teh pressure in the aortic arch is?

A

MCVCs no longer receive input from aortic arch barorecetpors, it’s interpreted as pressure being ZERO at that site.

43
Q

Why does a vagal section cause a RISE in MAP?

A
  1. Removal vagal tone> increased HR> increased CO> increased MAP
  2. Loss of input from AA barorecetpors> reflex increase in SNS activity
44
Q

Does vagal stimulation slow the heart?

A

Yes

45
Q

What is meant by the term vagal escape?

A

When atrial pacemakers are completely suppressed (by strong VAGAL activity), ventricular pacemakers gradually kick and increase their rate to reach a rate of 30bpm

46
Q

Why do people become unconsicous in vasovagal syncope?

A

Strongly activate PNS while DECREASE SNS>
reduced MAP> decreased blood flow to brain>
LOC

47
Q

Why does carotid occlusion cause a reflex increase in SNS activity after vagal section?

A

occlusion>
reduces pressure in carotid sinuses>
decrease in baro input to MCVC>
reflex increase in SNS activity

48
Q

Why does MAP reach a higher value during carotid occlusion with vagal section than without?

A

Since hte MCVC are sensing “no pressure” from the arterial baroreceptors there is a strong activation of hte SNS system.

Because the vagi are cut you don’t get a “brake” response.

49
Q

What direct effects of beta-adrenergic receptor blcokade would you expect on HR, contractility, arteriolar and venous tone?

A

Reduces HR and contractility

has NO effect on arteriolar/venous tone. These vessels have beta receptors but aren’t innervated nor normally active.

50
Q

What do you expect propanolol to do to MAP, SNS and PNS activity?

A

Decrease in MAP

Reflex increase in SNS and decrease in PNS

51
Q

What do you expect propanolol to do to the cardiac function curve and the venous return curve?

A

LOWER cardiac fxn curve d/t direct effects of beta blocker

RAISE venous return curve> reflex activation of SNS

CRAAB 5 (9 decks)

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