Control of Peripheral Circulation Flashcards

(45 cards)

1
Q

What values can be used as preload?

A

EDV, EDP, LAP, RAP, pulmonary capillary pressure

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2
Q

What is the little sharp blip in the curve of aortic pressure? What causes this?

A

Dicrotic notch; result of aortic valve closure where a small volume of aortic blood flows backward to fill the space behind the aortic valve leaflets as they close

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3
Q

How can mean arterial blood pressure be calculated using Pulse pressure?

A

MABP= Diastolic pressure + (1/3) x pulse pressure

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4
Q

Why is MABP not simply the average of diastolic and systolic blood pressures?

A

We spend more time in diastole

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5
Q

Why is it important to have sufficient pressure in the aorta?

A

To provide sufficient blood flow to the systemic organs

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6
Q

What serves as local (intrinsic) control for peripheral circulation?

A

Tissue cells, endothelium, vascular smooth muscle

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7
Q

What exerts extrinsic control of peripheral circulation?

A

SNS and PSNS

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8
Q

What ANS system has more influence over peripheral circulation?

A

SNS

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9
Q

What is the capacity for cardiac output to increase?

A

CO can increase 4-fold overall

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10
Q

What kind of vascular smooth muscle cells respond more to central (extrinsic) control?

A

Multiunit cells

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11
Q

What type of peripheral circulation control is unitary vascular smooth muscle more sensitive to?

A

Local control

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12
Q

What is the effect of Rho kinase phosphorylating MLC phosphatase?

A

It is inactivated, which leads to maintained smooth muscle contraction

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13
Q

What does tone refer to in vessels?

A

The contractile state of the vessel

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14
Q

How is myosin light chain kinase inhibited? What is the physiologic effect of this in blood vessels?

A

Phosphorylation by PKA, leading to vasodilation

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15
Q

How does the sympathetic nervous system mediate vasodilation?

A

SNS activates PKA, which phophorylates MLCK and inhibits it

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16
Q

In what type of cell are mechanical coupling-stretch activated Ca2+ channels found?

A

Unitary type smooth muscle cells

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17
Q

How is membrane potential linked to force development?

A

Via a relationship between K+ channels and Ca++ channels: Opening K+ channels allows K+ efflux, decreasing the membrane potential, which closes the L-type voltage-gated Ca+ channels –> less Ca++ influx and less smooth muscle contraction

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18
Q

How is smooth muscle contraction affected by ATP/ADP?

A

ADP opens K+ channels so that less contraction will occur to conserve energy

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19
Q

How does the SNS mediate both vasoconstriction and vasodilation?

A

NE is released from nerves with binds to alpha adrenergic receptors, resulting in calcium inflex and contraction; Epinephrine released from the adrenal medula via SNS stimulation binds to beta 2 adrenergic receptors, causing phosphorylation of MLCK, relaxing smooth muscle tone

20
Q

What is the afferent limb of the baroreceptor reflex?

A

CN IX and CN X

21
Q

Where is the control center for the baroreceptor reflex?

22
Q

How is vasodilation mediated by the PSNS? What vasodilations are under PNS control?

A

Vasodilation is mediated by NO and in the PSNS it controls coronary and cerebral vessels and erection

23
Q

How do local mechanisms affect blood flow?

A

Changing the radius of vessels

24
Q

What local factors mediate vasocontriction as a response to increased work of the tissue?

A

CO2, H+, K+, Lactic acid, adenosine

25
What is reactive hyperemia?
A higher than normal blood flow that occurs transiently after the removal of any restriction that has caused a period of lower than normal blood flow
26
What is active hyperemia?
Occurs in organs with a highly variable metabolic rate and results from local metabolic vasodilator feedback on arteriolar smooth muscle
27
What caues reactive hyperemia?
Increased concentration of vasodilators in the interstitial space surrounding the vessel bc they are not being washed out with bf
28
How is blood flow to a particular organ maintained during a sharp increase in blood pressure?
Increased vascular resistance via myogenic response and decreased vasodilator concentration
29
What is the myogenic response of vascular smooth muscle?
When unitary smooth muscle is stretched, it wants to contract. As blood flow increases in a vessel, it stretches and opens Ca++ channels allowing for contraction, bringing blood flow back down
30
How much blood flow does the brain receive?
750 mL/min
31
What formula can be used to calculate a person's exact cardiac output?
CO= (MABP-RAP)/ SVR
32
Unless explicitly stated what should the assumed value of RAP be?
0 mmHg
33
What region/ oragn system receives the most blood flow during rest?
GI tract
34
In what state are the kidneys most active?
Resting
35
What is the best organ at local control? The 2nd best?
The brain; heart
36
What is the impact on the exercise state on HR, CO, SV, EF, SVR, and MABP?
Increase in HR, CO, SV, EF; slight increase in MABP; decreased SVR
37
How is stroke volume increased in the exercise state?
Increased contractility and the Frank-Starling mechanism
38
How is GI blood flow affected in the exercise state? How is this response mediated?
GI blood flow is significantly decreased in the exercise state. SNS releases NE which binds to large amount of alpha receptors in vsm, increasing Ca++, leading to stonger contraction and vasoconstriction
39
How does blood flow to the heart change in going from a resting state to an exercise state?
It increases in the exercise state
40
Which organ system has the greatest capacity to increase its blood flow?
Skeletal muscle
41
How does blood flow to the skin change in going from a resting state to an exercise state? What is the importance of this?
During exercise there is an increase in blood flow to the skin because the heat produced during exercise is dissapated through the skin
42
What is the relative degree of SNS activation during the hemorrhage state compared to the exercise state?
Approximately the same
43
What is the effect of hemorrhage on HR, CO, SV, pulse pressure, contractility, SVR, and MABP?
Decrease in CO, massive decrease in SV, weakened pulse pressure, increased contractility (compensatory), tremendous increase in SVR, slight decrease in MABP
44
What can the tremendous increase in SVR during the hemorrhage state be attributed to?
Massive vasoconstriction occuring in the GI and renal systems and in skeletal muscle
45
What is the blood flow to skin in the hemorrhage state relative to other states?
Decreased