Ch 13/14 Cardiovascular Physiology (Day 5) Flashcards

1
Q

What are resistance vessels?

A

steepest pressure drop

–> there are pressure differences throughout systemic circulation

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2
Q

What is Total Peripheral Resistance?

A
  • Sum of all vascular resistance in systemic circulation
  • Blood flow to organs runs parallel to each other, so a change in resistance within one organ does not affect another (see next slide [96] )
  • Vasodilation in a large organ may decrease total peripheral resistance and mean arterial pressure.
  • Increased cardiac output and vasoconstriction elsewhere make up for this.
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3
Q

What are the extrinsic regulators of blood flow?

A
  1. sympathetic nerves (adrenergic)

2. parasympathetic nerves (cholinergic)

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4
Q

Sypathetic Nerves

A

ADRENERGIC

  • Increase in cardiac output and increase total peripheral resistance through release of norepinephrine onto smooth muscles of arterioles in the viscera and skin to stimulate vasoconstriction (alpha-adrenergic).
  • During “flight or fight”, blood is diverted to skeletal muscles
  • Adrenal epinephrine stimulates beta-adrenergic receptors for vasodilation
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5
Q

Parasympathetic Nerves

A

CHOLINERGIC

  • Acetylcholine stimulates vasodilation.
  • Limited to digestive tract, external genitalia, and salivary glands
  • Less important in controlling total peripheral resistance due to limited influence
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6
Q

What is arteriole diameter determined by?

A

tonic release of norepinephrine

  • increased release = constriction
  • decreased release = dilation
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7
Q

Paracrine Regulation of Blood Flow

A
  • Molecules produced by one tissue control another tissue within the same organ.
  • ->Example: The tunica interna produces signals to influence smooth muscle activity in the tunica media.
  • Smooth muscle relaxation influenced by bradykinin, nitric oxide, and prostaglandin I2 to produce vasodilation
  • Endothelin-1 stimulates smooth muscle contraction to produce vasoconstriction and raise total peripheral resistance.
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8
Q

Intrinsic Regulation of Blood Flow

A

Used by some organs (brain and kidneys) to promote constant blood flow when there is fluctuation of blood pressure; also called autoregulation.

Two types:

  1. Myogenic control mechanisms
  2. Metabolic control mechanisms
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9
Q

Myogenic control mechanisms

A

Vascular smooth muscle responds to changes in arterial blood pressure.

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10
Q

Metabolic control mechanisms

A

e.g. local vasodilation controlled by changes in:

↓PO2 /↑ PCO2 due to increased metabolism

↓ tissue pH (due to CO2, lactic acid, etc.)

Release of K+ and paracrine signals

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11
Q

Active hyperemia matches blood flow to increased metabolism.

A
  1. increased tissue metabolism
  2. increased release of metabolic vasodilators into ECF
  3. arterioles dilate
  4. decreased resistance = increased flow
  5. O2 and nutrient supply to tissues increases (as long as metabolism is increased)
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12
Q

Reactive hyperemia follows a period of decreased blood flow.

A

1, decreased tissue blood flow due to occlusion

  1. metabolic vasodilators accumulate in ECF
  2. arterioles dilate, but occlusion prevents blood flow
  3. REMOVE OCCLUSION
  4. decreased resistance = increased blood flow
  5. as vasodilators wash away, arterioles constrict and blood flow returns to normal
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13
Q

Blood Flow to the Heart and Skeletal Muscles: Aerobic Requirements of the Heart

A

Coronary arteries feed large # of capillaries (2,500–4,000 per cubic mm tissue).

  • Unlike most organs, blood flow is restricted during systole (due to compression by squeezing during contraction). Thus cardiac tissue has myoglobin to store oxygen during diastole to be released in systole.
  • Cardiac tissue is metabolically very active (↑ mitochondria and respiratory enzymes)
  • Large amounts of ATP produced from the aerobic respiration of fatty acids, glucose, and lactate.
  • During exercise, blood flow through coronary arteries increases from 80 to 400 ml/minute/100 g tissue.
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14
Q

Blood Flow to the Heart and Skeletal Muscles: Regulation of Coronary Blood Flow

A
  • Norepinephrine from sympathetic nerve fibers (alpha-adrenergic) stimulates vasoconstriction (recall sympathetic tone, slide #97), raising vascular resistance at rest.
  • Adrenal epinephrine (beta-adrenergic) stimulates vasodilation and thus decreases vascular resistance during exercise.
  • Vasodilation is enhanced by intrinsic metabolic control mechanisms – increased CO2, K+, paracrine regulators
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15
Q

Blood Flow to the Heart and Skeletal Muscles: Effect of exercise training on coronary blood flow

A
  • Increased density of coronary arterioles and capillaries
  • Increased production of NO to promote vasodilation
  • Decreased compression of coronary arteries during systole due to lower cardiac rate (in highly trained athletes)
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16
Q

Blood Flow to the Heart and Skeletal Muscles: Regulation of Blood Flow Through Skeletal Muscles

A
  • Arterioles have high vascular resistance at rest (α-adrenergic effect) (recall sympathetic tone, slide #97)
  • -> Even at rest, skeletal muscles still receive 20−25% of the body’s blood supply (due to their total mass over the entire body).
  • Blood flow decreases during contraction (squeezing of arterioles, as in heart) and can stop completely beyond 70% of maximum contraction (result pain, fatigue during sustained isometric contraction).
  • Vasodilation stimulated by both adrenal epinephrine (β-adrenergic effect) and cholinergic acetylcholine.
  • Intrinsic metabolic controls enhance vasodilation during exercise
17
Q

Circulatory changes during dynamic exercise

A
  • Vascular resistance through skeletal and cardiac muscles decreases due to:
    1. Increased cardiac output
    2. Metabolic vasodilation
    3. Diversion of blood away from viscera and skin
  • Blood flow to brain increases a small amount with moderate exercise and decreases a small amount during intense exercise.
  • CO can increase 5X due to increased cardiac rate.
  • SV can increase due to increased venous return from skeletal muscle pumps and respiratory movements
  • Ejection fraction increases due to increased contractility (Frank-Starling effect)

C.O. & muscle blood flow increase
Reflex: working muscles–>motor cortex–>CV
–> control center in medulla–> cardiac contractility & heart rate
↑ S.V. x ↑ H.R. = ↑C.O.

Vasodilation in muscle + vasoconstriction in other tissues
–> diversion of up to 90% of C.O. to the working muscle

18
Q

Endurance Training

A
  • Lower resting cardiac rate due to greater inhibition of the SA node by vagus
  • Increase in resting stroke volume because of the -increase in blood volume (almost 10% increase after only 8 days of training)
  • Improved O2 delivery to skeletal muscle:
    • -> because resting HR is lower, can achieve larger proportionate increase in CO & higher absolute CO during exercise