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Physiology > Lecture 2-Exam 3 (cardiac) > Flashcards

Lecture 2-Exam 3 (cardiac) Flashcards

1
Q

What is the mean arterial pressure equation?

A
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2
Q
  • What drives blood flow?
  • What is systolic blood pressure?
  • What is diastolic blood pressure?
A
  • The pressure difference across the circulation from the arteries to the veins drives blood flow.
  • Systolic blood pressure (SBP) is the peak pressure recorded in the central arterial system and occurs during ventricular ejection.
  • Diastolic blood pressure (DBP) is the minimum pressure recorded in the central arterial system and occurs just before the start of ventricular systole.
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3
Q

What is pulse pressure? What is PP reflected by?

A

Pulse pressure (PP) is the difference between SBP and DBP. PP is reflected by the strength of the arterial pulse wave palpated in the peripheral arteries.

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4
Q

What is the MAP? How are the values weighted?

A

Mean arterial pressure (MAP) is a time- weighted average of SBP and DBP. Systole occupies about one-third of the cardiac cycle under resting conditions and diastole occupies about two-thirds, giving rise to the following estimate of MAP

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5
Q

Blood pressure measured by cuff inflation in the upper arm of a healthy person is 120/80 mm Hg
* What is the SBP, DBP and PP?

A

SBP = 120 mm Hg; DBP = 80 mm Hg; and PP = 120 – 80 = 40 mm Hg.

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6
Q

Fill in the values

A
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7
Q

What are the three determinants of SBP?

A

SV, Diastolic blood pressure and aortic compliance

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8
Q

Hoe does stroke volume affect SBP?

A

Increased SV (dt more stretch) increases SBP and PP

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9
Q

How does Diastolic BP relate to SBP?

A

The absolute value of SBP must be interpreted with respect to DBP, since this is the baseline pressure before systole. For this reason, PP is a useful guide to SV.

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10
Q

How does aortic compliance affect SBP?

A

If compliance is low (i.e., stiff aorta), the SV produces a large SBP.

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11
Q

What is aortic compliance?

A

Aortic compliance is not physiologically regulated but often declines with age due to loss of elastic tissue, atherosclerosis, and calcification; SBP typically increases 1 mm Hg for each year after age 60.

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12
Q

What are the three determinants of DBP?

A

Vascular resistance, runoff of blood from the aorta, diastolic time interval

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13
Q

How does vascular resistance affect DBP?

A
  • Main determinant of DBP
  • Blood flow through the circulation continues throughout diastole because the arterial pressure exceeds the venous pressure and due to recoil of the elastic aorta.
  • DBP is determined by the size of arteriolar resistance encountered by blood flow. Higher arteriolar resistance (vasoconstriction) increases DBP.
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14
Q
  • How does runoff of the blood from the aorta affect the DBP?
  • What is an example?
A
  • DBP decreases if blood flow into the circulation during diastole is reduced or decrease in diastolic blood pressure at a reduced heart rate due to increased run-off time (different ways to say it)
  • Aortic valve insufficiency is an example where aortic pressure rapidly decreases during diastole because backflow of blood into the left ventricle reduces forward flow into the circulation.
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15
Q

How does diastolic time interval affect DBP?

A
  • Aortic pressure decreases with time between heart beats because blood continues to flow into the circulation from the aorta throughout diastole.
  • DBP is lower when the HR is slow because more time elapses between beats. DBP is higher at faster heart rates because there is less time for a decline in aortic pressure between beats aka increases DBP with increase HR dt reduced run off time
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16
Q

What happens when there is a slower HR? (What happens to SV, PP, DBP?)

A

CO is the same

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17
Q

What happens when there is a faster HR? (What happens to SV, PP, DBP?)

A

CO is same

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18
Q

What is total peripheral resistance?

A

The collective resistance to blood flow presented by the systemic vasculature is called systemic vascular resistance, or total peripheral resistance (TPR).

MAP=CO X TPR

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19
Q

Systemic vascular resistance is mainly determined by what?

A

changes in the diameter of the arterioles

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20
Q
  • What is vaccular tone?
  • What is arteriolar tone affected by?
  • How is TPR increased?
A

i. Arterioles are partially constricted under normal physiologic conditions, called vascular tone, and are the sites of active regulation of blood flow in the circulation.
ii. Arteriolar tone is affected by many factors, including sympathetic tone and hormones and endothelial and metabolic factors.
iii. Systemic vascular resistance is increased by vasoconstriction and reduced by vasodilation.

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21
Q

Large compliance in veins allows what?

A

Large compliance in the veins allows them to accommodate high volumes with little change in pressure.
o Systemic veins are ~20 times more compliant than systemic arterie

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22
Q

What happens in arteries when there are changes in volume and pressure?

A

In arteries, small changes in volume cause large changes in pressure…and large changes in pressure result in a small degree of expansion

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23
Q

What is venous return?

A

is the volume of blood returning to the central venous compartment (i.e., thoracic venae cavae and right atrium) per minute.

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24
Q
  • What is central venous pressure?
  • What does low CVP promotes?
  • CVP has a strong influence on what?
A

Central venous pressure (CVP) is the pressure of venous blood in the thoracic vena cava and the right atrium.
* Low CVP promotes venous return into the central venous compartment, whereas high CVP reduces venous return.
* CVP has a strong influence on cardiac preload and, through the Frank-Starling mechanism, determines ventricular SV.

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25
Q
  • What drains the blood from the head and neck regions? Low pressure gradient from arms, abdomen and lower extremity requires what?
A
  • Gravity drains blood from head and neck regions
  • Low pressure gradient from arms, abdomen, and lower extremity, thus other mechanisms also required
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26
Q

Low pressure gradient from arms, abdomen, and lower extremity, thus other mechanisms also required. What are the 4 mechanisms?

A
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27
Q

What increases venous return?

A
  • Dynamic exercise increases venous return
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28
Q

When described using cardiac and venous function curves, dynamic exercise increases venous return and cardiac output for three reasons. Explain

A
  1. Activation of the sympathetic nervous system increases cardiac contractility (shifting the cardiac function curve left).
  2. Sympathetic activation (release NE) increases venous return due to venoconstriction (shifting the vascular function curve right).
  3. Release of local metabolites in working muscle causes vasodilation (increasing the slope of the vascular function curve).
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29
Q

What alters arterial pressures?

A

Interactions among stroke volume, heart rate, and systemic vascular resistance

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30
Q

If an increase in HR is balanced by a proportional and opposite change in SV, what happens to MAP and why?

A

MAP does not change because CO remains constant

MAP= TPR X CO

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31
Q
  • The influence of a change in CO on MAP is _ of the cause of the change - whether it comes from HR or SV.
  • In contrast, the effect of a change in CO on PP greatly depends on what?
A
  • Independent since both HR and SV can be affected
  • In contrast, the effect of a change in CO on PP greatly depends on whether and how SV or HR change
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32
Q

Dynamic exercise
* Produces little change in MAP because why?
* What causes the increase in CO?
* Increase to SV results in what? How does this effect PP?

A
  • Produces little change in MAP because ↑ CO is balanced by ↓ SVR (systemic vascular resistance).
  • The ↑ CO is caused by ↑ in both HR and SV
  • ↑ SV results in a ↑ SBP, whereas DBP is ↓ because the fall in SVR allows greater runoff from the aorta during diastole. – thus PP increases
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33
Q

What happens during static exercise to SVR, SBP, DBP, PP?

A

Increases SVR, increased systolic pressure and diastolic pressure – thus PP constant

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34
Q

Compliant arteries does what do cardiac work?

A

reduce cardiac work

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35
Q
  • Arteries in the human body are neither what?
  • This example serves to demonstrate that decreased arterial compliance increases what?
A
  • Arteries in the human body are neither totally rigid nor infinitely compliant.
  • This example serves to demonstrate that decreased arterial compliance increases cardiac work and oxygen demand

Increase in afterload=increase contraction so increase in metabolic pro.

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36
Q
  • By extension, myocardial oxygen demand will be increased by any factor that does what?
  • For this reason, because arterial compliance decreases as we age, the heart of an older person is confronted by what?
A
  • any factor that reduces arterial compliance, even if all other factors, such as arterial pressure, stroke volume, and heart rate, do not change.
  • For this reason, because arterial compliance decreases as we age, the heart of an older person is confronted by increased oxygen demand compared to a younger person even if all other variables affecting cardiac oxygen demand are the same between the two individuals.
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37
Q

DR. HOUSTONS NOTES

  • When cardiac output is held constant by what? What does this affect?
  • Effect of increased HR and stroke volume with no change in mean arterial pressure because why?
  • What increases around an unchanged MAP?
  • Systolic pressure is higher due to what? What is that associated with?
  • DBP is lower than the control becasue why?
A
  • When cardiac output is held constant by lowering HR, there is no change in mean arterial pressure (93 mm Hg), but systolic pressure increases while diastolic pressure decreases.
  • Effect of increased HR and stroke volume with no change in mean arterial pressure because of decreased SVR. After the first two beats, stroke volume and HR are increased
  • PP changes
  • Systolic pressure is higher due to higher ejection associated with the increased stroke volume
  • Diastolic pressure is lower than the control because the lower SVR allows more rapid runoff of blood out of the arterial system during diastole.
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38
Q

What are extrinsic and intrinsic regulations?

A
  • Extrinsic regulation (MAP, heart, brain flow)
  • Intrinsic regulation (individual flow
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39
Q

What does the microciculation regulates (4)

A
  • blood flow to individual organs
  • the distribution of blood flow within organs
  • diffusion distances between an organ’s blood supply and tissues
  • as well as the capillary surface area available for exchange of materials between the plasma and tissues.
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40
Q

In conjunction with cardiac output, microcirculation helps maintain what?

A

In conjunction with cardiac output, it helps maintain arterial blood pressure by altering total peripheral vascular resistance and diastolic filling of the heart.

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41
Q

If needed, the body will reduce blood flow to where? Why?

A

If needed, the body will reduce blood flow to most organs, such as the skeletal muscles and splanchnic organs, in order to sustain arterial pressure to preserve flow to the heart and brain.

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42
Q

What happens when you contract or relax precapillary sphincters?

A
  • Contract: Then blood flows via metarteriole
  • Relax: then the blood can flow through the capillary bed
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43
Q

Arterioles control what?

A

control blood flow into a region of tissue and, along with precapillary sphincters, control the distribution of blood flow within the capillary network

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44
Q

For capillaries:
* What are the endothelial cells held together by?
* What can pass through?
* What provides other pathways for exchange?

A
  • Adjacent endothelial cells are held together by tight junctions, which have occasional gaps.
  • Water-soluble molecules pass through pores formed where tight junctions are imperfect.
  • Vesicle formation and the diffusion of lipid-soluble molecules through endothelial cells provide other pathways for exchange.
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45
Q

What are the different factors (or characteristics) of capillaries

A
  • Surface area: increase or decrease
  • Velocity of flow: decreases in capilaries to have time to exchange
  • No vascular smooth muscle
  • RBC taco if vessel is really small
  • Fick’s law: Diffusion diameter
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46
Q

What are the different type of capillaries we have and where to find them? (3)

A
  • Contiunous capillary (regulated): Fat, muscle, NS
  • Fenestrated cap (semi-regulated): Intestinal villi (for absorbion), endocrine gland (to secrete) and kidney glomeruli (for filtration)
  • Discont. cap: Liver, BM and spleen
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47
Q

What is the lymphatic drainage across our body?

A
47
Q
  • The contraction–relaxation cycle of lymphatic bulbs is the fundamental process that does what?
  • Pressures along the lymphatics are generated by what?
A
  • The contraction–relaxation cycle of lymphatic bulbs is the fundamental process that removes excess water and plasma proteins from the interstitial spaces.
  • Pressures along the lymphatics are generated by lymphatic vessel contractions and by organ movements, which cause alternately external compression and relaxation stimuli.
48
Q

ransport across capillaries is enhanced by what?

A

increasing their collective surface area and reducing diffusion distances from capillaries to cells.

49
Q

Exchange between the interstitial fluid and capillaries occur via what three processes?

A

(1) diffusion
(2) filtration
(3) vesicular transport

50
Q
  • Increasing the number of microvessels does what?
  • Decreasing the number of perfused capillaries does what? Where can this result from?
A
  • Increasing the number of microvessels reduces diffusion distances and minimizes the dilution of molecules in ECF.
  • Decreasing the number of perfused capillaries increases diffusion distances, decreases exchange – threatens cell function and survival.
  • This can result from severely constricting arterioles or by destroying existing capillaries in disease states such as diabetes mellitus.
51
Q

At any given moment during resting conditions, only about 40% to 60% of the capillaries are what?

A

are perfused by red blood cells in most organs. The capillaries not in use do contain blood, but it is not moving.

52
Q

What is the effect of the number of perfused capillaries on the cell concentration of blood borne molecules

A

(A) With one capillary, the left side of the cell has a low concentration. (B)The concentration can be substantially increased if a second capillary is perfused. (C)The perfusion of three capillaries around the cell increases concentrations of blood-borne molecules throughout the cell.

53
Q

Diffusion of small molecules from the blood increased by increasing what ? (3)

A

i. vascular permeability
ii. surface area
iii. or blood flow

54
Q
  • What is Perfusion/Flow-limited transport?
  • What indictates rate?
A
  • Small solutes can diffuse rapidly, so transport is not limited by rate of diffusion
  • Instead, blood flow dictates rate of transport into cells
  • For a flow-limited transport substance, increasing blood flow increases the effective concentration of a substance in the capillary and thus accelerates its outward diffusion
55
Q
  • What is diffusion limited transport?
  • What does it exhibit?
A
  • larger lipophobic molecules, such as sucrose, polysaccharides, and proteins, have difficulty
    diffusing     across the capillary membrane or through capillary pores.
  • These substances may be delivered in large quantities into capillaries by blood flow but nevertheless
    exhibit low transcapillary flux.
  • Their transport between the bloodstream and tissues is therefore limited by their rate of diffusion into or out of capillaries and not appreciably altered by their rate of delivery into the capillary network by blood flow.
56
Q

In pathologic conditions, substances that otherwise exhibit flow-limited transport can become what? When does this happen?

A
  • can become diffusion limited.
  • This can occur when diffusion distances between capillaries and cells become too great to allow the rapid exchange of materials, as seen in the lungs when the transport of normally highly diffusible oxygen is impaired by infection or fluid accumulation in the pulmonary interstitium, which markedly increases diffusion distances
57
Q

The interplay between net hydrostatic and oncotic forces determines what?

A

Determines the net direction of fluid exchange across the capillaries

58
Q

What is the balance of starling’s forces along a normal systemic blood capillary?

A
59
Q
  • Capillary hydrostatic pressure decreases as what happen?
  • Net fluid filtration out of plasma typically occurs where, what about reabsorption?
  • he net driving force for filtration consists of what?
A
  • Capillary hydrostatic pressure decreases as blood flows from the arterial to the venous end of a systemic capillary.
  • Net fluid filtration out of plasma typically occurs at the arterial end of capillary beds, and net fluid reabsorption into plasma occurs toward the venous end
  • The net driving force for filtration consists of a gradient of hydrostatic pressure that pushes fluid out of plasma and is opposed by a gradient of oncotic pressure:
60
Q

What are the different starling forces?

A
61
Q

Where is there a larger and smaller hydrostatic pressure? Oncotic?

A
62
Q

What happens with edema and dehydration with tissue hydrostatoc pressure?

A
63
Q
  • Under normal conditions, tissue pressure is what?
  • But if there is increase in volume can cause what?
  • If the interstitial fluid volume exceeds the “safe range,” then what will present?
  • Tissue dehydration can cause what?
A
  • Under normal conditions, tissue pressure is slightly negative (subatmospheric), but an increase in volume can cause the pressure to become positive.
  • If the interstitial fluid volume exceeds the “safe range,” high tissue hydrostatic pressures and edema will be present.
  • Tissue dehydration can cause negative tissue hydrostatic pressures.
64
Q

What are ways to increase lymph flow? Increase edema formation?

A
65
Q

The most common causes of edema result from what?

A

result from increased venous pressure due to heart failure or venous obstruction.

66
Q

What is the difference between pul and systemic edema?

A
67
Q

Generalized edema may also result from what? What is this due to?
* Give example of this

A
  • Generalized edema may also result from low serum protein concentration due to reduced capillary oncotic pressure.
  • For example, this can occur in liver failure when insufficient albumin is synthesized and in nephrotic syndrome when plasma protein is excreted in the urine.
68
Q

In inflammation or sepsis, generalized edema may occur because why?

A

inflammatory mediators reduce protein reflection coefficient and proteins leak into the interstitium, thereby increasing interstitial fluid oncotic pressure.

69
Q

Lymphatic blockage causes what? Why?

A
  • Lymphatic blockage causes edema because the tissue fluid that has formed is trapped in the interstitium when the outflow pathway is blocked.
70
Q

HOUSTON NOTES

Starling equation, and the individual components of the net driving pressure are referred to as Starling’s forces: (4)

A

i. Capillary hydrostatic pressure (P c) is a force pushing fluid out of the capillaries. Hydrostatic pressure is usually about 35 mm Hg at the arteriolar end of a capillary, decreasing to about 15 mm Hg at the venous end of a capillary.

ii. Interstitial fluid hydrostatic pressure (P i) is usually near zero or is slightly subatmospheric, favoring fluid movement into the interstitial space.

iii. Capillary oncotic pressure (π c) is an osmotic force exerted by plasma proteins, and pulls fluid into the plasma from the interstitium and is approximately 25 mm Hg.

iv. Interstitial fluid oncotic pressure (π i) is normally low because proteins have reflection coefficients of 0.8–1.0 and interstitial protein concentration is low (see Chapter 1 for a discussion of reflection coefficient).

71
Q

The following sections consider the various physical and chemical conditions in tissues that affect the contractile state of VSM and, thus, affect what?

A

affect resistance in the microvasculature.

72
Q

Arteriolar smooth muscle maintains what?

A

maintains a constant amount of tone at all times, even without external stimulation to contract

73
Q

Arteriolar tone is increased or decreased for what two reasons? How does it happen?

A
74
Q

Intrinsic control mechanisms regulate what?

A

Figure X: Intrinsic control mechanisms regulate blood flow to each organ AND distribution of blood flow WITHIN organs (e.g., brain)

75
Q

Types of Intrinsic Regulation (a.k.a local control, autoregulation)

  • Most organs control their blood flow via what?
  • What is autoregulation of blood flow or simply autoregulation?
  • Changes in vessel diameter largely dictate what?
A
  • Most organs control their blood flow via local autoregulation.
  • The ability of an organ to maintain normal or near normal blood flow in the face of changes in the pressure driving flow is called autoregulation of blood flow, or simply autoregulation
  • Changes in vessel diameter largely dictate vessel resistance…smooth muscle relaxation vs. contraction
76
Q

What are the four types of intrinsic regulation?

A

i. Smooth muscle stretch (myogenic response)
ii. Metabolic activity (active hyperemia)
iii. Locally produced chemicals
iv. Changes in blood flow (reactive hyperemia)

77
Q
  • Myogenic regulation causes what?
  • Certain tissues contain arterioles with what?
  • When these fibers are under less than normal stretch (decreased MAP), then what happens?
A

*Myogenic regulation causes arterioles to actively contract or relax in response to changes in intravascular pressure.
* Certain tissues contain arterioles with stretch sensitive muscle fibers which contract when stimulated (vasoconstriction)
* When these fibers are under less than normal stretch (decreased MAP), they respond by relaxing (vasodilation)

78
Q

What is happening in active hyperemia?

A

Organ blood flow is increased by increased tissue metabolism through local, nonneurogenic mechanisms (active hyperemia)

79
Q

What produces factors that dilate microcirculatory arteries and veins?

A

Decreased organ perfusion or increased tissue metabolism

80
Q

Arteriolar contractile state is affected by what?
* Give an example

A
  • vasoactive chemicals released by endothelial cells
  • The mechanism of endothelium-dependent relaxation of vascular smooth muscle by nitric oxide (NO).
81
Q

What is reactive hyperemia? How is this different from active hyperemia?

A
  • When blood flow to any organ is stopped or reduced by vascular compression for more than a few seconds, vascular resistance dramatically decreases.
  • The absence of blood flow allows vasodilatory chemicals to accumulate while hypoxia occurs; the vessels also dilate as a result of decreased myogenic stimulation (low intravascular pressure).
  • As soon as the vascular compression is removed, blood flow is dramatically increased for a few minutes because the vessels became dilated during the stoppage of flow.
  • This phenomenon represents reactive hyperemia because it is a reaction to the previous period of ischemia.
82
Q

Both intrinsic and extrinsic control what?

A

mechanisms contribute to redistribution

83
Q

Explain the difference between heavy exercise and rest

A
84
Q

T/F: Systemic blood flow (i.e. CO) is kept relatively constant throughout a wide range of MAP

A

True

85
Q

The ability to maintain an adequate systemic blood flow by what?

A

by maintaining a sufficient driving force (MAP) is due to constant monitoring of MAP and the implementation of negative feedback mechanisms when MAP deviates out of homeostatic range

86
Q

The ability to maintain an adequate systemic blood flow by maintaining a sufficient driving force (MAP) is due to constant monitoring of MAP and the implementation of negative feedback mechanisms when MAP deviates out of homeostatic range
* How does this occur?

A
  • This occurs via extrinsic controls mechanisms called Neurohumoral Regulation
87
Q

Neural mechanisms elicit what?

A

Neural mechanisms elicit acute MAP changes, whereas hormonal mechanisms elicit more
chronic alterations to MAP.

88
Q

What is the neural control of MAP?

A

The Baroreceptor Reflex (a neural regulatory mechanism)

neg feed back mechanism

89
Q

The Baroreceptor Reflex:
* Protects against what?
* If a patient is moved from a supine to a standing position, the normal response is an initial decrease in MAP due to what?
* Decreased action potential frequency in the carotid sinus nerve results in what?

A
  • Protects against acute changes in the systemic
    arterial blood pressure.
  • If a patient is moved from a supine to a standing position, the normal response is an initial decrease in MAP due to venous pooling in the lower limbs, which reduces venous return and cardiac output.
  • Decreased action potential frequency in the carotid sinus nerve results in reduced parasympathetic tone and increased sympathetic tone.
90
Q

Several effector mechanisms restore MAP to prevent reduced brain perfusion and fainting: (4)

A
  • Heart rate is increased by withdrawal of vagal tone and by increased sympathetic stimulation of the SA node.
  • Ventricular contractility and SV are increased by sympathetic stimulation of cardiac myocytes.
  • Vasoconstriction, mediated by the sympathetic nerves, increases the systemic vascular resistance and thereby increases the DBP and MAP.
  • Venoconstriction, due to sympathetic stimulation, reduces vascular compliance, increasing venous return and restoring cardiac preload
91
Q

Fill in

A
92
Q
A
93
Q

What are the chemoreceptors?

A

Carotid body and aortic bodies

94
Q

Wall stretch provides information about blood pressures, which is used as an index of blood flow:
* Carotid sinus baroreceptor monitors what?
* Where are low pressure baroreceptors?
* The renal juxtaglomerular apparatus senses what?

A
  • Carotid sinus baroreceptors monitor arterial blood pressure.
  • Low-pressure baroreceptors in the venous system and cardiac atria monitor blood volume.
  • The renal juxtaglomerular apparatus senses effective circulating blood volume.
95
Q

DR.HOUSTON NOTES

  • An intervention that elevates arterial pressure (either mean arterial pressure or pulse pressure), does what? What does this result in?
  • Hormonal responses are what?
A
  • An intervention that elevates arterial pressure (either mean arterial pressure or pulse pressure), stretches the baroreceptors, and initiates the reflex. The resulting reduced systemic vascular resistance and cardiac output return arterial pressure toward the level existing before the intervention.
  • Hormonal responses (not shown in the figure) involving adrenal epinephrine and the renin–angiotensin system are also involved in the reflex but more so as a response to hypotension rather than to hypertension.
96
Q

Baroreceptor desensitivity

  • Where do you see baroreceptor adaptation?
  • What does this cause a patient to be susceptible in?
A
  • Chronic hypertension can result in desensitization of baroreceptors and a shift in baroreceptor reflex operating range
  • This may cause a patient to be susceptible to orthostatic hypotension
97
Q

DR. HOUSTON NOTES

  • With normal conditions, a mean arterial pressure of 93 mm Hg is near what?
  • Sustained hypertension causes what?
  • Aortic baroreceptors show similar what?
A
  • With normal conditions, a mean arterial pressure of 93 mm Hg is near the midrange of the firing rates for the nerves.
  • Sustained hypertension causes the operating range to shift to the right, putting 93 mm Hg at the lower end of the firing range for the nerves.
  • Aortic baroreceptors show similar relationships, except the point at which pressure activates the receptor and reaches maximum response is higher than that seen in carotid receptors
98
Q

What are other blood pressure reflexes?

A

i. - Chemoreflex
ii. - Medullary ischemic reflex

99
Q

Chemoreflex:
* What is the response to?
* Chemoreceptors are called what? Where are they located?
* Primary role in what?
* What is their secondary role? Because why?

A
100
Q

Medullary ischemic reflex:
* Response to what?
* Medulla oblongata monitors what?
* Activates what?

A
  • automatic response to a drop in perfusion of the brain
  • Medulla oblongata monitors its own blood supply
  • Activates corrective reflexes when it senses ischemia (insufficient perfusion)
101
Q

Medullary ischemic reflex
* Cardiac & vasomotor centers send sympathetic signals to heart & blood vessels and what does it cause?

A
  • Increases heart rate and contraction force
  • Causes widespread vasoconstriction
  • Raises BP and restores normal perfusion to the brain
102
Q

What are Other brain centers can affect vasomotor center?

A

– Stress, anger, arousal can also increase BP

102
Q

Input from sensors is coupled to changes in autonomic nervous tone and endocrine (hormonal) axes such as what?

A

as renin-angiotensin-aldosterone, atrial natriuretic peptide, and vasopressin.

103
Q

What is the ANS regulation of MAP?

A

Neurogenic control of the heart involves reciprocal activation of PSNS and SNS

104
Q
  • Vascular beds except the heart and brain contain more what?
  • There is no known parasympathetic innervation of what?
  • The primary site of cardiovascular control (cardiac and vasomotor) within the central nervous system is what?
  • What is spinal shock?
A
  • vascular beds except the heart and brain contain more α1- than β2-adrenergic receptors
  • There is no known parasympathetic innervation of blood vessels in systemic organs with the exception of those of the external genitalia
  • The primary site of cardiovascular control (cardiac and vasomotor) within the central nervous system is the medulla oblongata
  • Spinal shock: spinal cord is acutely transected, excitatory signals no longer reach sympathetic preganglionic fibers, their tonic firing is reduced and blood pressure falls.
105
Q

T/F: Circulating epinephrine exerts different cardiovascular effects from those caused by sympathetic nerves.

A

TRUE

106
Q

Epinephrine and NE have similar direct positive inotropic and chronotropic effects on the heart, but NE elicits what?

A

NE elicits a powerful baroreceptor reflex because it causes significant systemic vasoconstriction that increases SVR and thus mean arterial pressure.

107
Q
A
108
Q

The baroreceptor reflex also activates hormonal systems affecting blood pressure, explain

A
109
Q
A
110
Q
A
111
Q

What does intrinsic and extrinsic mechanisms do?

A

Intrinsic mechanisms (autoregulation)
* Distribute blood flow to individual organs and tissues as needed
Extrinsic mechanisms
* Maintain mean arterial pressure (MAP)
* Redistribute blood during exercise and thermoregulation

112
Q

What is circulatory shock?

A
  • A loss in blood pressure leading to hypoperfusion of organs and tissues
113
Q

What are the three types of shock? What are the causes of each?

A
114
Q

Severities of shock:
* What is compensated shock?
* What is progessive shock?
* What is irreversible shock?

A

i. Compensated shock = normal cardiovascular regulatory mechanisms will compensate for
the initial decrease in cardiac output and/or arterial pressure.
ii. Progressive shock causes a vicious cycle of cardiac and brain deterioration
iii. Irreversible shock, cardiac and cerebral function are so compromised that no intervention is
able to restore normal cardiovascular function. Death is inevitable.

Physiology (11 decks)

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