Nordgren: CV Reflex Demonstration

Question 1

What is Ps?

Answer 1

Highest pressure reached in systemic arteries during a cardiac cycle

Question 2

What is Pd?

Answer 2

Lowest pressure reached in systemic arteries during a cardiac cycle

Question 3

What is Pp?

Answer 3

Ps-Pd

Question 4

What is MAP?

Answer 4

Systemic arterial pressure over a complete cardiac cycle

Pd +Pp/3

Question 5

What are the two direct determinants of Pa?

Answer 5

CO x TPR

Question 6

What 2 influences directly affect HR?

Answer 6

1. Sympathetic- beta adrenergic receptors on SA node

2. Parasympathetic- muscarinic cholinergic receptors on SA node

Question 7

P wave on an ECG?

Answer 7

atrial depolarization

Question 8

QRS on a ECG?

Answer 8

Ventricular depolarization

Question 9

T wave on a ECG?

Answer 9

ventricular repolarization

Question 10

How does CVP compare to systemic arterial pressure?

Answer 10

Usually MUCH lower (5 to 100)

Question 11

What happens to CVP during inspiration?

Answer 11

Temporarily DECREASES!

Question 12

Does respiration affect HR?

Answer 12

YES!

Question 13

How does respiration affect cardiovascular variables (3 ways)?

Answer 13

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.

Question 14

What determines the average value of CVP?

Answer 14

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

Question 15

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

Answer 15

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

Question 16

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

Answer 16

All three terms are synonymous!

Question 17

How are Pa and afterload related?

Answer 17

MAP = afterload

Question 18

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

Answer 18

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

Question 19

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

Answer 19

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

Question 20

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

Answer 20

1. Decreased PNS> increased HR

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

Question 21

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

Answer 21

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

Question 22

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

Answer 22

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.

Question 23

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

Answer 23

increased SNS activity> shifts cardiac fxn curve upward

increased SNS activity to peripheral veins> shifts venous curve upward

Question 24

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

Answer 24

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

Question 25

How does EPI affect the heart?

Answer 25

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

Question 26

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

Answer 26

It increases all of them

Question 27

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

Answer 27

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

Question 28

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

Answer 28

YES

Question 29

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

Answer 29

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

Question 30

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

Answer 30

reflex response to elevated arterial pressure

Question 31

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

Answer 31

absence of p waves

Question 32

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

Answer 32

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

Question 33

How does EPI stimulation differ at HIGH and LOW concentrations?

Answer 33

High- stimulates alpha and beta | LOW- only beta

Question 34

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

Answer 34

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

Question 35

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

Answer 35

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

Question 36

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

Answer 36

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

Question 37

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

Answer 37

CO is HIGHER than normal This counteracts the fall in arterial pressure that is being produced by the reduction in TPR

Question 38

How does ACh affect HR?

Answer 38

Lowers HR

Question 39

Why does an ACh injection cause a fall in MAP?

Answer 39

ACh injection> reduces TPR> fall in MAP

Question 40

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

Answer 40

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

Question 41

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

Answer 41

Yes

Question 42

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

Answer 42

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

Question 43

Why does a vagal section cause a RISE in MAP?

Answer 43

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

Question 44

Does vagal stimulation slow the heart?

Answer 44

Yes

Question 45

What is meant by the term vagal escape?

Answer 45

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

Question 46

Why do people become unconsicous in vasovagal syncope?

Answer 46

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

Question 47

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

Answer 47

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

Question 48

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

Answer 48

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.

Question 49

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

Answer 49

Reduces HR and contractility has NO effect on arteriolar/venous tone. These vessels have beta receptors but aren't innervated nor normally active.

Question 50

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

Answer 50

Decrease in MAP Reflex increase in SNS and decrease in PNS

Question 51

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

Answer 51

LOWER cardiac fxn curve d/t direct effects of beta blocker | RAISE venous return curve> reflex activation of SNS