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FHB Exam 1 - Cardiovascular Physiology > Lecture 18 - Autonomic Regulation > Flashcards

Lecture 18 - Autonomic Regulation Flashcards

1
Q

What is the difference between Basal Tone & Resting Sympathetic Tone? In which case is resistance higher?

A

Basal tone: amount of stimulation under RESTING conditions w/o extrinsic influences

Resting Sympathetic Tone:
- amount of vascular CONSTRICTION resulting to tonic sympathetic stimulation

  • resistance is higher under RESTING SYMPATHETIC Tone due to tonically released NE
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2
Q

Mechanisms that induce a change AWAY from basal arterial tone are called what? Mechanisms that induce a change back TOWARD basal arterial resistance are?

A
  1. ACTIVE

2. Passive

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3
Q

Withdrawing sympathetics results in what?

A

Passive Vasodilation

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4
Q

What is the affect of sympathetic CHOLINERGICS? (muscarinic) What occurs when this is removed?

A

ACTIVE vasodilation

  • passive vasoconstriction
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5
Q

What are 3 effects of Sympathetic cholinergics?

A
  1. Piloerection
  2. Sweat glands
  3. Vascular Smooth muscle VASODILATION
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6
Q

Name 3things that stimulate Adrenergic receptors:

A
  1. Isoprotenerol
  2. Norepinephrine
  3. Epinephrine (hormone from adrenal cortex)
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7
Q

What is the function of the following receptors:

  1. Alpha
  2. Beta -1 Cardiac
  3. Beta - 2 cardiac
  4. Beta - 2 - smooth muscle
A
  1. VASOCONSTRICTION (except coronary & cerebral)
    - on smooth muscle
  2. HR & Contractility stimulated
    - on cardiac muscle
  3. Beta 2: secondary - HR & contractility
  4. Beta 2 - Smooth muscle:
    VASODILATION
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8
Q

What type of receptors are Sympathetic Cholinergic? What do they cause?

A

MUSCARINIC- post-ganglionic sympathetic fibers that release acetylcholine

VASODILATION
ex: sweat glands, piloerection, smooth muscle

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9
Q

What are the affects of Parasympathetic Cholinergics on the heart?

A

VASODILATE:

  1. Cerebral
  2. VIscera - splanchnic, genitalia, blader, large bowel
  • skeletal & cutaneous vessels not innervated
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10
Q

What are two ways that the sympathetic system works to increase diastolic pressure? What is one way to increase systolic pressure?

A
  1. Peripheral Vasoconstriction
  2. increase HR
  3. Increase CONTRACTILITY - systolic
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11
Q

Where are baroreceptor and chemoreceptor nerve terminals located?

A

Carotid Sinus & Aortic Arch

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12
Q

How do baroreceptors respond to changes in BP?

A
  • they feel VASCULAR stretch (mechanoreceptors)

- increase firing of parasympathetics to decrease BP

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13
Q

When does baroreceptor firing increase?

A

When there is an INCREASE in arterial pressure

& decrease firing when arterial pressure decreases

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14
Q

What is stimulated & inhibited during decreased BP?

A

Sympathetics increased, parasympathetics inhibited

  1. Vasoconstriction
  2. HR
  3. Contractility
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15
Q

What counteracts an increase in Mean Arterial Pressure?

Decrease?

A

Bradycardia & Vasodilation

  • Vasoconstriction, HR, Contractility
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16
Q

Baroreceptors respond more to which of the two changes:

Phasic (Pulsatile) or COnstant (static) Changes in Pressure?

A

Phasic!

  • activated in early systole at normal MAP
  • fewer impulses during late systole when pressure is still high and changing less
17
Q

When are there more/fewer baroreceptor firing:

  1. Early Systole
  2. Late systole?
A

EARLY systole

  • there are fewer impulses during late systole because PRESSURE IS STILL HIGH & changing less
  • when pressure falls during diastole, the receptors reduce firing rate even if pressure is above threshold

(RATE OF CHANGE MORE IMPORTANT THAN ABSOLUTE PRESSURE)

18
Q

How does the neural activity recorded from carotid sinus change when the Pulse Pressure is DAMPENED & MAP is held constant? What happens to the MAP? WHY?

A
  1. it DECREASES
    - less firing from Carotid sinus
  2. SYSTEMIC ARTERIAL PRESSURE INCREASES
  3. due to less inhibition of sympathetic activity!!!
19
Q

If you restore pulse pressure, how does the systemic MAP change & the frequency of sinus nerve discharge change?

A
  1. MAP decreases to control

2. Frequency INCREASES

20
Q

How does the sensitivity of baroreceptors change during HYPERTENSION?

A
  • become LESS SENSITIVE to high pressures (lower frequency nerve response & smaller decrease in MAP)
  • but still sensitive to changes to BP
21
Q

When are chemoreceptors activated?

A
  • low pO2
  • high CO2
  • low pH (acidic)
  • mor involved with respiratory system than cardiovascular
22
Q

When do chemoreceptors play a role in the CARDIOVASCULAR system?

A
  • during severe HYPOXIA

not to normal changes in pO2

23
Q

What response do chemoreceptors stimulate in sympathetic & parasympathetic systems?

A
  1. Vasoconstriction

2. Bradycardia

24
Q

What does HYPOXIA induce in real life? WHY?

A

TACHYCARDIA!

  • increase in ventilation acts = via stretch receptors in the lung to INHIBIT EFFERENT VAGAL activity
25
Q

Because ventilation INCREASES during hypoxia, what happens to the HR?

A
  • INCREASES

- vagal activity is inhibited so HR increases

26
Q

What has the highest blood flow per gram of body? (BOARDS QUESTION)

A

Carotid Sinus

  • designed to sense oxygen in the blood
27
Q

As oxygen content decreases, which direction does the curve shift? Why?

A

RIGHT & Up

  • makes it more sensitive to drops in CO2
  • so as oxygen content decreases the RESPONSE INCREASES
28
Q

What is the result of Hyperventilation & Hypoventilation?

A
  1. Hyperventilation - blow off a lot of CO2 = ALKALOSIS

2. Hypoventilation - a lot of CO2 remains: ACIDOSIS

29
Q

What happens as the system attempts to respond to acidosis due to a drop in O2?

A

(ischemic & acidic)

1.inhibit parasympathetics

  1. Stimulate SYMPATHETICS
    - cause vasoconstriction
    to raise BP & bring more O2 to the ischemic area
30
Q

What happens to BP and HR during hypoxia?

A
  1. BP increases
  2. HR increases
    - sympathetics increased & parasympathetics inhibited because of the RESPIRATORY AFFECT

(increased ventilation)

31
Q

What is the purpose of the Renin-Angiotensin-Aldosterone Mechanism?

A

Mitigate Dehydration

not hemorrhage because this is not due to an ACUTE change
- hem. doesn’t last long enough to activate this

32
Q

What does renin do?

A

Convert Angiotensinogen to Angiotensinogen I

33
Q

What does ACE do?

A

Angiotensinogen Converting Enzyme

  • Convert Angio. I to ANgio II
34
Q

What are the 3 actions that result with the production of Angiotensinogen II?

A
  1. Vasoconstriction of Renal & Systemic vessels
  2. ALDOSTERONE release
    - increase Na reabsorption
    (water follows)
  3. Hypothalamus: increase thirst & secrete ADH
    - which increases permeability of collecting duct to reabsorb WATER as well
35
Q

What is the final result of the Renin-Angiotensin-Aldosterone pathway?

A

INCREASE IN BP & Blood volume

  • stimulated during hypovolemia (dehydration)
36
Q

Why is the Renin-Angiotensin-Aldosterone System stimulated during CHF? What is the TX to prevent this from happening?

A
  • body senses decrease in cardiac output (heart is congested with blood)

SO it stimulates this pathway to increase Blood volume

  • BAD: only worsens the issue

TX: ACE Inhibitors to lower blood volume

(also given for hypertension)

37
Q

What is the function of aldosterone? ADH?

A

Aldosterone
- increase Na reabsorption which increases water uptake

ADH: (anti-DIuretic Hormone)
- makes the collecting duct more permeable and REABSORBS water

FHB Exam 1 - Cardiovascular Physiology (26 decks)

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