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Physiology Block 1- Cardiovascular Physiology > Control of Peripheral Circulation > Flashcards

Control of Peripheral Circulation Flashcards

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?

A

Medulla

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
Q

What is reactive hyperemia?

A

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
Q

What is active hyperemia?

A

Occurs in organs with a highly variable metabolic rate and results from local metabolic vasodilator feedback on arteriolar smooth muscle

27
Q

What caues reactive hyperemia?

A

Increased concentration of vasodilators in the interstitial space surrounding the vessel bc they are not being washed out with bf

28
Q

How is blood flow to a particular organ maintained during a sharp increase in blood pressure?

A

Increased vascular resistance via myogenic response and decreased vasodilator concentration

29
Q

What is the myogenic response of vascular smooth muscle?

A

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
Q

How much blood flow does the brain receive?

A

750 mL/min

31
Q

What formula can be used to calculate a person’s exact cardiac output?

A

CO= (MABP-RAP)/ SVR

32
Q

Unless explicitly stated what should the assumed value of RAP be?

A

0 mmHg

33
Q

What region/ oragn system receives the most blood flow during rest?

A

GI tract

34
Q

In what state are the kidneys most active?

A

Resting

35
Q

What is the best organ at local control? The 2nd best?

A

The brain; heart

36
Q

What is the impact on the exercise state on HR, CO, SV, EF, SVR, and MABP?

A

Increase in HR, CO, SV, EF; slight increase in MABP; decreased SVR

37
Q

How is stroke volume increased in the exercise state?

A

Increased contractility and the Frank-Starling mechanism

38
Q

How is GI blood flow affected in the exercise state? How is this response mediated?

A

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
Q

How does blood flow to the heart change in going from a resting state to an exercise state?

A

It increases in the exercise state

40
Q

Which organ system has the greatest capacity to increase its blood flow?

A

Skeletal muscle

41
Q

How does blood flow to the skin change in going from a resting state to an exercise state? What is the importance of this?

A

During exercise there is an increase in blood flow to the skin because the heat produced during exercise is dissapated through the skin

42
Q

What is the relative degree of SNS activation during the hemorrhage state compared to the exercise state?

A

Approximately the same

43
Q

What is the effect of hemorrhage on HR, CO, SV, pulse pressure, contractility, SVR, and MABP?

A

Decrease in CO, massive decrease in SV, weakened pulse pressure, increased contractility (compensatory), tremendous increase in SVR, slight decrease in MABP

44
Q

What can the tremendous increase in SVR during the hemorrhage state be attributed to?

A

Massive vasoconstriction occuring in the GI and renal systems and in skeletal muscle

45
Q

What is the blood flow to skin in the hemorrhage state relative to other states?

A

Decreased

Physiology Block 1- Cardiovascular Physiology (17 decks)

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