Regulation of the CVS

Question 1

Which organs can autoregulate blood flow and why?

Answer 1

• Brain, heart, kidneys
• Don’t have stores of fuel, depend on aerobic respiration => must be provided with O2 and fuel, waste must also be taken away
• Will regulate the flow of blood through them if there’s a change in bp

Question 2

What are coronary arteries?

Answer 2

1st arteries to come off the aorta and feed the cardiac muscle (there is a left and right coronary artery)

Question 3

How can coronary artery autoregulation be tested and what were the results?

Answer 3

• cannulation of coronary arteries so that they are connected to an external pump, perfusion pressure depends on pump and not aortic pressure
• We have the aortic pressure which is constant, the perfusion pressure which is the pressure in the pump and coronary flow
• we suddenly drop the perfusion pressure from 130 mmHg to about 90 mmHg so flow drops but it comes back up to the same level about 12 seconds later, perfusion pressure does not change, the only other possible variable is resistance (flow = perfusion pressure/resistance) so flow is maintained thx to resistance falling thanks to the dilation of resistance vessels (small arteries/arterioles)

Question 4

What is the autoregulatory range?

Answer 4

• Broad
• Determined by repeating the cannulation experiment and systematically dropping pressure each time even lower and seeing if flow is restored, they could also bring pressure up and see if flow goes back down
• As an immediate effect if pressure drops, flow drops and if pressure increases, flow increases but there is a steady state effect where flow is restored in between a range of about 60 mmHg to 160 mmHg thanks to regulation of resistance (vasodilation or vasoconstriction)
• Beyond that range, there is a steep slope and flow cannot be restored

Question 5

What are the two mechanisms or components of autoregulation?

Answer 5

Metabolic and Myogenic
- Operating at the same time, used by heart, brain and kidneys (important baddies), arterial vasodilation

Question 6

Describe the metabolic mechanism of autoregulation

Answer 6

• Down arterial pressure in organ (perfusion pressure falls), down blood flow to organ but since organ working, accumulation of waste products (down O2 and up metabolites) since flow in drops and flow out will drop soon, this will have an effect on smooth muscle to relax => arteriolar and small artery dilation in organ => restoration of blood flow toward normal in organ

Question 7

Describe the myogenic mechanism of autoregulation

Answer 7

• Down arterial pressure in organ (perfusion pressure falls) so arteriolar pressure in organ falls (in all vessels down the vascular tree), so the vessel-wall stretch in organ will fall since the transmural pressure is down (Pin-Pout), wall stretch is less if transmural pressure is down, this also alerts the smooth muscle to relax, arteriolar and small artery dilation in organ and restoration of blood flow toward normal in organ

Question 8

What is local metabolic control?

Answer 8

The purpose is to adjust flow to metabolic need following mechanical work (skeletal muscle, cardiac muscle) or physio-chemical work (brain, kidney pumping ions and making neurotransmitters)
- Up metabolic activity of organ, so down O2 and up metabolites in organ interstitial fluid, arteriolar and small artery dilation in organ (relaxation in smooth muscle), up blood flow to organ
- This is active (due to work) hyperemia (change in blood flow)
- Same mechanism of autoregulation but different goal

Question 9

What is the difference in stimulus and output between autoregulation and local metabolic control?

Answer 9

• Autoregulation: stimulus is a change in bp, output bp comes back
• Local metabolic control: stimulus is change in amount of activity or metabolic activity of organ, output is change in flow through organ

Question 10

What does autonomic mean in the autonomic innervation of CVS? What does it allow?

Answer 10

Involontary nervous system (allows us not to faint when we stand and increase cardiac output in exercise)

Question 11

What are the two branches of the autonomic innervation of CVS?

Answer 11

Parasympathetic and sympathetic

Question 12

Why is heart rate and its control important?

Answer 12

Determines CO and MAP since CO = HR x SV and MAP = CO x TPR = HR x SV x TPR
- If we want to increase CO => increase HR (increase during exercise) or SV
- If car accident, lose volume, drop pressure => autonomic nervous system can change 1 or 2 or 3 to increase MAP (during exercise or when standing all 3 change)

Question 13

What is the autonomic innervation of the SA node?

Answer 13

Parasympathetic and sympathetic

Question 14

Describe the parasympathetic control of heart rate

Answer 14

Cell body in brain in medulla oblongata sends AP through pre-ganglionic axon in vagus nerve (huge nerve, many axons to organs in thorax and abdomen) causing a release of acetylcholine in the ganglion (localized accumulation of cells outside the CNS) in fat just outside the heart and it hits the nicotinic receptor on the ganglion cell so then it goes through post-ganglionic axon which causes the release of acetylcholine onto the muscarinic receptor on the SA node (neuron-muscle cell synapse) this triggers the opening of a special class of ion channel and slows heart rate because slows the SA node firing

Question 15

What is a drug related to the parasympathetic control of heart rate and how does it work?

Answer 15

• Atropine
• acetylcholine antagonist, emergency medicine given to block muscarinic receptor => parasympathetic blocker => increase heart rate => increase CO and MAP

Question 16

Describe the sympathetic control of heart rate

Answer 16

• When activated or increased activation => AP, more NE, increased HR
• Cell body is in spinal cord instead, pre ganglionic axon, ganglion, ACh, nicotinic receptor, post ganglionic axon but instead releases NE to SA node on B adrenergic receptor, opens ion channels, several currents affected, speeds heart rate

Question 17

What are some drugs associated with sympathetic control of heart rate and how do they work?

Answer 17

• B agonist mimics effect of NE => increase HR and CO and MAP (given if CO too low or HR falling)
• B antagonist (is a B blocker, main class of drug given to treat high blood pressure), block NE, decrease HR and CO and MAP (antihypertensive agent)

Question 18

What chamber of the heart is most influenced by the neural control of contractility of the heart?

Answer 18

• Really bestie ventricle since atrium not the most involved in CO

Question 19

Describe the sympathetic control of contractility

Answer 19

• control of force of contraction
• same as SA node but receptor is on the ventricular muscle and not an increase in rate since not a pacemaker but increase in force of contraction => increase in SV => increase MAP

Question 20

What drugs are associated with the sympathetic control of contractility and how do they work?

Answer 20

• B agonist => increase in contractility, SV and MAP
• B antagonist (B blocker): 2 actions but still working to decrease MAP, here reduces contractility, antihypertensive drug

Question 21

What are the effects of an increase in contractility?

Answer 21

• Maximal force is increased
• Rate at which the force is developed increases
• Duration of systole is shorter
  All during stimulation of sympathetic nerves to heart or anything else to increase contractility

Question 22

Increased contractility is often confused with which mechanism of increasing SV?

Answer 22

With the Franck starling mechanism if increase in EDV, increase SV or increased contractility to increase SV but no effect on EDV (no extra filling of the heart)
- Moving along the Frank-Starling curve is not the same as shifting to operation on a different curve (change in contractility) (2 curves one control one increased contractility)

Question 23

Why would we change vessel diameter?

Answer 23

• To set appropriate flow for each organ (might involve redistribution of flow)
• To maintain MAP

Question 24

What is Poseuille’s law?

Answer 24

• R is proportional to 1/r^4, small changes in r make huge changes in R and r is changed by the contraction or relaxation of smooth muscle on walls of vessels, in all vessels except capillaries
• Resting tone = basal tone + neurogenic tone

Question 25

How change r to change R?

Answer 25

• neural
• hormonal
• local (metabolic)
• endothelial (all kinds of compounds that go to smooth muscle to constrict/dilate)

Question 26

Describe the sympathetic control of vessel tone

Answer 26

• All vessels except capillaries are innervated by sympathetic (no smooth muscle in capillaries)
• high tone when constricted, low tone when relaxed
• Cell body is in spinal cord
• Same neural path but ends up releasing NE onto alpha adrenergic receptors on vessels causing constriction

Question 27

What drugs are associated with the sympathetic control of vessel tone?

Answer 27

• Alpha agonist given when low bp, last ditch intervention when trying to increase bp, constriction of all vessels (except capillaries duh), TPR goes up and CO and MAP
• alpha blocker too

Question 28

Describe the sympathetic control of adrenal glands

Answer 28

• Cell body in spinal cord, no ganglion, no postganglionic axon
• neural hormonal control
• ACh on nicotinic receptor of adrenal medulla secreting Epi and NE which are both alpha and beta agonists that go all over the body to increase HR, SV (both beta), TPR (alpha) and increase MAP

Question 29

In conclusion, overview of the autonomic control of heart rate?

Answer 29

• Plasma Epi and NE go up, go beta on SA node, increase HR, symplathetic upregulated, parasympathetic downregulated less ACh, and most of the time if HR increases because of all the other stuff going on, the other variables are changed as well