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

Question 1

How do you work out SV, CO, MBP?

Answer 1

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

Question 2

What is venous volume distribution affected by?

Answer 2

Peripheral venous tone, gavity, skeletal muscle pump, breathing

Question 3

What does central venous pressure determine?

Answer 3

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

Question 4

How is flow control controlled in veins and arteries?

Answer 4

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

Question 5

What does constriction in arterioles determine?

Answer 5

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

Question 6

What are the ways of regulating blood flow?

Answer 6

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

Question 7

What is the primary function of extrinsic factors?

Answer 7

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

Question 8

What is autoregulation in the vessels?

Answer 8

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

Question 9

How is autoregulation carried out in the vessels?

Answer 9

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

Question 10

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

Answer 10

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

Question 11

What are the circulating hormones that affect the vascular system?

Answer 11

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

Question 12

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

Answer 12

SNS controls circulation; PSNS regulates heart rate

Question 13

Which blood vessels and other CVS components are sympathetically innervated?

Answer 13

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

Question 14

Where does NA preferentially bind to?

Answer 14

Alpha-1 adrenoceptors to cause SM contraction, vasoconstriction

Question 15

What is the vasomotor centre and where is it located?

Answer 15

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

Question 16

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

Answer 16

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

Question 17

What do the lateral portions of VMC control?

Answer 17

Heart activity by influencing heart rate and contractility

Question 18

What do the medial portions of VMC do?

Answer 18

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

Question 19

How does the vasomotor centre control blood vessel diameter?

Answer 19

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

Question 20

How can you control blood vessel radius?

Answer 20

x

Question 21

How is the heart innervated?

Answer 21

HR is continually slowed in the body by PSNS

Question 22

How can we increase HR?

Answer 22

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

Question 23

How does SNS affect force of contraction of heart?

Answer 23

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

Question 24

How is SV controlled?

Answer 24

Question 25

How do you increase CO?

Answer 25

Question 26

How is feedback given in the CVS?

Answer 26

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

Question 27

What structures provide feedback in the CVS?

Answer 27

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)

Question 28

How does the baroreceptor activity change depending on pressure?

Answer 28

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

Question 29

What is reciprocal innervation?

Answer 29

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

Question 30

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

Answer 30

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

Question 31

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

Answer 31

Question 32

How do we control venous return?

Answer 32

Question 33

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

Answer 33

Question 34

How do we maintain arterial pressure after a haemorrhage?

Answer 34

Question 35

What is the problem of change in posture?

Answer 35

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

Question 36

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

Answer 36

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

Question 37

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

Answer 37

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

Question 38

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

Answer 38

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

Question 39

How does the body compensate for change in posture?

Answer 39

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

Question 40

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

Answer 40

Question 41

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

Answer 41

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

Question 42

What is the problem with haemorrhage?

Answer 42

Reduction in ACTUAL circulating blood volume

Question 43

What are the compensatory mechanisms for haemorrhage?

Answer 43

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

Question 44

How does autotransfusion help with haemorrhage?

Answer 44

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

Question 45

Which hormones are released as a compensatory mechanism for haemorrhage?

Answer 45

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

Question 46

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

Answer 46

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

Question 47

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

Answer 47

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

Question 48

What is the problem with exercise?

Answer 48

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

Question 49

What occurs when skeletal muscle begins working?

Answer 49

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

Question 50

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

Answer 50

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

Question 51

Why does the TPR decrease during exercise?

Answer 51

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

Question 52

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

Answer 52

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

Question 53

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

Answer 53

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

Question 54

How is SV increased during exercise?

Answer 54

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

Question 55

What factors can decrease CO during exercise?

Answer 55

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

Question 56

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

Answer 56

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