CVS Lecture 11/12 - Regulation of CVS and Responses to CVS stress Flashcards Preview

LSS 1 - Thorax anatomy, Respiratory and Circulatory system > CVS Lecture 11/12 - Regulation of CVS and Responses to CVS stress > Flashcards

Flashcards in CVS Lecture 11/12 - Regulation of CVS and Responses to CVS stress Deck (56)
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1
Q

How do you work out SV, CO, MBP?

A

SV= EDV-ESV, CO=HR*SV, MBP= CO*TPR

2
Q

What is venous volume distribution affected by?

A

Peripheral venous tone, gavity, skeletal muscle pump, breathing

3
Q

What does central venous pressure determine?

A

The amount of blood flowing back to the heart -> which determines stroke volume

4
Q

How is flow control controlled in veins and arteries?

A

Veins: constriction determines compliance and venous return. Arterioles: constriction -> flow changed by primarily altering vessel radius

5
Q

What does constriction in arterioles determine?

A

Blood flow to organs they serve, MABP, pattern of distribution of blood to organs

6
Q

What are the ways of regulating blood flow?

A

Local mechanisms (intrinsic to SM or closely associated - important for local blood flow regulation within an organ), Extrinsic: systemic regulation (hormones), ANS

7
Q

What is the primary function of extrinsic factors?

A

Regulate arterial BP by altering systemic vascular resistance that at any given time is determined by the balance of competing vasoconstrictor and vasodilator influences

8
Q

What is autoregulation in the vessels?

A

Intrinsic capacity to compensate for changes in perfusion pressure by changing vascular resistance

9
Q

How is autoregulation carried out in the vessels?

A

Myogenic theory -> SM fibres respond to tension in vessels wall. Metabolic theory -> as blood flow decreases, metabolites accumulate and vessels dilate, when flow increases metabolites are washed away. Injury -> serotonin release from platelets causes constriction

10
Q

Which substances are released from the endothelium which can regulate blood flow?

A

NO -> vasodilation; PGI2/TXA2 -> vasodilator/constrictor; Endothelins are potent vasoconstrictors

11
Q

What are the circulating hormones that affect the vascular system?

A

Kinins -> complex interactions with RAAS, relax VSM; ANP -> atrial natriuretic peptide secreted from cardiac atria, vasodilator; Circulating vasoconstrictors -> ADH, NA (from adrenal medulla), Ang II

12
Q

What is the difference in PSNS and SNS when it comes to role in CVS?

A

SNS controls circulation; PSNS regulates heart rate

13
Q

Which blood vessels and other CVS components are sympathetically innervated?

A

All vessels except capillaries, precapillary sphincters and some metarterioles; heart and large veins -> elsewhere distribution is variable: more in vessels to kidneys, gut, spleen and skin; less in skeletal muscle and brain

14
Q

Where does NA preferentially bind to?

A

Alpha-1 adrenoceptors to cause SM contraction, vasoconstriction

15
Q

What is the vasomotor centre and where is it located?

A

Bilaterally in reticular substance of medulla and lower 1/3 of pons -> composed of pressor, depressor and cardioregulatory inhibition area

16
Q

What does the VMC do and by what is it influenced?

A

Transmits impulses distally through the spinal cord to almost all blood vessels -> many higher centres of brain (hypothalamus) can exert powerful excitatory/inhibitory effects on VMC

17
Q

What do the lateral portions of VMC control?

A

Heart activity by influencing heart rate and contractility

18
Q

What do the medial portions of VMC do?

A

Send signals via vagus nerve to heart that tend to decrease HR

19
Q

How does the vasomotor centre control blood vessel diameter?

A

Blood vessels receive symp post-ganglionic innervation (NA) -> always some level of tonic activity so always tone in vessels and by changing it you can change vessel diameter -> primarily SNS response, as generally no PSNS innervation to vascular system

20
Q

How can you control blood vessel radius?

A

x

21
Q

How is the heart innervated?

A

HR is continually slowed in the body by PSNS

22
Q

How can we increase HR?

A

Increase: activity of SNS nerves to the heart and plasma adrenaline. Decrease activity of PSNS nerves to the heart

23
Q

How does SNS affect force of contraction of heart?

A

By binding to beta 1-adrenoceptor, which causes increase in cAMP, increasing PKA, which phosphorylates L-type Ca channel, which means more Ca2+ enters cells and also phosphorylates CaATPase which means more Ca are stored for the next contraction

24
Q

How is SV controlled?

A
25
Q

How do you increase CO?

A
26
Q

How is feedback given in the CVS?

A

Baroreceptors sense disturbance and which send it to medulla, which compares it to set point and change the output and control the variables

27
Q

What structures provide feedback in the CVS?

A

Baroreceptors are key pressure sensing devices in the aortic arch and in the carotid sinuses (stretch receptors) feeding back via the glossopharyngeal nerve (carotid sinus) or the vagus (aortic arch)

28
Q

How does the baroreceptor activity change depending on pressure?

A

Increased pressure = increased baroreceptor activity -> pressures between 60 and 180 mmHg and most sensitive at 90-100mmHg

29
Q

What is reciprocal innervation?

A

Afferent input -> stimulates PSNS to heart AND inhibits SNS to heart, arterioles and veins. If receptor sees ^ BP, feeds back via afferent nerve, identically relayed to PSNS -> slowing heart down as PSNS is stimulated and SIMULTANEOUSLY inhibits SNS -> more specifically inhibitory interneurone sends inhibitory signals which if it outweighs the tonic activity, dampens SNS activity

30
Q

What happens if there is increased BP sensed by the baroreceptors?

A

Down vagus nerve to cardioinhibitory vasomotor centres which then sends the information up the vagus nerve to the heart, slowing it and decreasing the pressure AND at the same time the VMC instructs the sympathetic side to decrease activity -> decrease HR and contractility and SV; also symp drive in vessels lessens, dilating the vessels and decreasing the BP

31
Q

How is the pressure reflex controlled by carotid sinus nerve activity?

A
32
Q

How do we control venous return?

A
33
Q

What is the overall feedback of blood pressure control from haemorrhage?

A
34
Q

How do we maintain arterial pressure after a haemorrhage?

A
35
Q

What is the problem of change in posture?

A

Movement from supine to standing position is a severe challenge to human circulation due to (primarily) gravity -> in the vertical position the forces acting on the blood are: usual pressure resulting from cardiac contraction and effect of gravity on column of blood -> in foot capillary reaches 105mmHg

36
Q

What is a problem for the CVS when gravity is added?

A

Massive increase in hydrostatic pressure in blood vessels of lower limbs;

37
Q

Why is hydrostatic pressure increase due to gravity such a problem?

A

Veins are distensible, expand to hold the blood -> stretch and retain the blood, which means there is less blood in arteries so less pressure is in the arteries so BP falls. Pressure in capillaries are greater, so more fluid is going to leak out of capillaries, reducing effective circulating blood volume

38
Q

Why does an increase in hydrostatic pressure pushing fluid out of the blood cause a hypotensive effect?

A

Decreased EDV, so less stroke volume so BP decreases -> transient hypotension occurs when standing in most people

39
Q

How does the body compensate for change in posture?

A

Arterial baroreceptors firing rate decreases which causes decrease PSNS activity so decreases the inhibitory interneuron in the CNS, so there is decreased inhibition of SNS nerve, so increased SNS activity, which leads to increased HR (20bpm) and conctractility, so increased CO, and increased splanchnic and renal vasoconstriction of arterioles and venoconstriction of veins to squeeze blood back up

40
Q

What is the overall effect of change in posture and how is it compensated?

A
41
Q

What happens if any of the compensatory mechanisms for posture fail?

A

Faint -> if hypotension remains for any length of time, brain becomes hypoperfused -> brain switches off, collapses and brain regains blood due to lack of gravity pull

42
Q

What is the problem with haemorrhage?

A

Reduction in ACTUAL circulating blood volume

43
Q

What are the compensatory mechanisms for haemorrhage?

A

Same as posture -> decreased baroreceptor firing, which increases HR/heart contractility which helps maintain CO and there is organ specific vasoconstriction to increase TPR. Autotransfusion, hormone release

44
Q

How does autotransfusion help with haemorrhage?

A

Decreased hydrostatic pressure occurs due to less fluid in the vessel -> so when blood volume reduces, the oncotic pressure over the whole capillary exceeds hydrostatic pressure -> so vessels absorb fluid from tissues -> very effective short term strategy to preserve BP

45
Q

Which hormones are released as a compensatory mechanism for haemorrhage?

A

Ang II (decrease renal flow), aldosterone (increase Na/H2O retention), ADH (increases H2O reabsorption). DECREASE URINE OUTPUT

46
Q

How effective are the compensatory mechanisms at maintaining BP when blood is lost?

A

10% = same BP, 20-30% = decrease in BP but keeps you alive, 30-40% = shock (when tissues are inadequately perfused)

47
Q

What don’t you do if someone is in shock?

A

Keep them warm and give them alcohol -> DO put them in an ice bath

48
Q

What is the problem with exercise?

A

Increase blood flow is needed in the periphery, skeletal muscle is a very large organ and highly perfused -> so this leads to massive drop in TPR which would cause a hue drop in BP

49
Q

What occurs when skeletal muscle begins working?

A

Active hyperaemia -> increased blood flow is recruited via increased metabolism and increased O2 usage, so vasodilation occurs

50
Q

What are the control mechanisms that compensate for the increased blood flow to the skeletal muscles during exercise?

A

Muscle chemoreceptors -> which signal to brain that tissue has become more active AND preprogrammed patterns of exercise can cause the brain to activate the CV centre in the medulla which dampens PSNS and increases SNS

51
Q

Why does the TPR decrease during exercise?

A

Heart, lungs and skeletal muscle have massive locally mediated dilation due to active hyperaemia inducing dilation -> skin lose SNS stimulation, as body wants to lose heat

52
Q

How does the body try to compensate for decrease in TPR during exercise?

A

Increased SNS stimulation to GIT and Kidneys causing vasoconstriction, which reduces the massive decrease so there is less decrease (still some occurs)

53
Q

Due to slight fall in TPR, what needs to occur to bring BP up during exercise?

A

CO needs to increase, either via SV or HR -> HR increases due to increases SNS activity and decreased PSNS activity

54
Q

How is SV increased during exercise?

A

Skeletal muscle pump, which during exercise would work more, so increases venous return to the heart, increasing ventricular EDV which increases SV

55
Q

What factors can decrease CO during exercise?

A

Plasma volume can decrease due to increased hydrostatic pressure across muscle walls and loss of water/salt due to sweat -> however this is compensated by the increased venous return, so the CO doesn’t fall, it increases

56
Q

What is the overall effect of exercise and how is it compensated for?

A

CO is increased by increased HR, contractility and venous return. TPR is decreased by increased vasodilation of skeletal muscles/lungs/heart, and increased vasoconstriction of kidneys/GIT prevents a big fall -> so overall CO increases more than TPR decreases so BP increases during exercise

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