Physiology

Question 1

What is the CVS?

Answer 1

A bulk flow system for O2 and CO2, nutrients, metabolites, hormones and heat.

Question 2

Why must output be equal?

Answer 2

Pumps are arranged in series (Starling’s law). Most vascular beds are arranged in parallel, which means all tissues get oxygenated blood and there can be regional re-direction of blood.

Question 3

Give 2 examples of shunts in the body.

Answer 3

1) Releasing factors go straight from the hypothalamus to the anterior pituitary without entering the blood supply. 2) Nutrient rich blood from the gut goes straight to the liver via the hepatic portal vein.

Question 4

Flow = delta P / R … what does this mean?

Answer 4

Darcy’s law. Flow = the difference in pressure over resistance. There needs to be a pressure difference to drive resistance. The pressure difference is equal to MAP - CVP (which is usually 0) and so MAP drives pressure differences. Resistance is controlled by radius^4 of vessels and selectively redirects blood flow - small changes in radius can mean big changes in resistance.

Question 5

Which vessels control resistance?

Answer 5

Arterioles.

Question 6

What are the different classification of blood vessels?

Answer 6

1) Elastic arteries: aorta and pulmonary arteries; elastic walls; wide lumen; low resistance to make it easier for blood to flow through. 2) Muscular arteries: all other arteries; wide lumen; non-elastic walls; low resistance condiut. 3) Arterioles: resistance vessels; narrow lumen; thick, contractile wall; control resistance and therefore flow; allow regional redirection of blood. 4) Venules and veins; capacitance vessels; thin, distensible walls; wide lumen; low resistance; blood reservoir.

Question 7

What to veins and venules allow?

Answer 7

Fractional distribution of blood between veins and the rest of the circulation. 2/3 of blood is in veins and venules.

Question 8

Briefly describe gross structure of the heart.

Answer 8

L and R sides separated by septum. All valves are passive. Aortic and pulmonary valves are both SL. R side tricuspid and L side bicuspid/mitral - AV valves. Chordae tendinae are connected to papillary muscle to stop valves turning inside out when they close. Papillary muscle contracts at the same time as the heart.

Question 9

Describe the cardiac cycle.

Answer 9

1) Late diastole: both atria and ventricles are relaxed and fill passively. 2) Atrial systole: atrial contraction pushes a small amount of additional blood into the ventricles. 3) Isovolumic ventricular contraction: first phase of ventricular contraction. Force of ventricular contraction pushes AV valves shut but is not high enough to open SL valves. Pressure inside ventricles exceeds pressure inside atria. 4) Ventricular ejection: ventricular pressure rises and exceeds pressure inside the arteries which opens SL valves. Blood is ejected into aorta and pulmonary arteries. 5) Isovolumic ventricular relaxation: as ventricles relax, pressure inside ventricles falls. Blood flows back into cusps of SL valves and snaps them closed.

Question 10

How long is the cardiac interval?

Answer 10

0-0.8 seconds: the time is takes for the heart to beat.

Question 11

Which processes make up the cardiac interval?

Answer 11

1/3 systole and 2/3 diastole. As HR > systole takes up more of cardiac cycle. Diastole limits CO.

Question 12

Describe pressure inside the aorta during cardiac cycle.

Answer 12

Mitral valve closes and 0.2 seconds later aortic valve opens - peak aortic pressure (120 mmHg - systolic BP). At this point, pressure inside LV and aorta is the same. Pressure then drops - dicrotic notch when aortic valve closes at 0.25 seconds. After this, pressure falls in the aorta during diastole as Ca2+ stops being taken up.

Question 13

What causes the dicrotic notch?

Answer 13

Sudden drop in pressure after systolic contraction causes back flow of blood into the arteries while the valve is still closing. Aortic valve bounces shut at 0.25 seconds.

Question 14

Describe pressures inside the ventricle.

Answer 14

Rises as more Ca2+ is being taken up and more X-bridges are being taken up. Then follows aortic pressure until dicrotic notch. Continues to drop after systole and pressure is the same as in the atria during diastole.

Question 15

What is pulse pressure?

Answer 15

Difference between systolic and diastolic pressure: 120 - 80 = 40.

Question 16

What is BP?

Answer 16

Peak pressure and minimum pressure in the aorta which is 120/80.

Question 17

What is MAP?

Answer 17

Average pressure during a single cardiac cycle - 90 mmHg.

Question 18

Describe pressures in the atrium.

Answer 18

3 waves: a, c and v. A wave occurs just after P wave on ECG and is due to atrial contraction. C wave: occurs after the QRS complex and coincides with ventricular contraction. Pushes mitral valve shut and increases pressure inside the atrium. V wave: increases gradually during systole and is due to continuous venous return from the lungs. This drops when the mitral valve opens and blood can flow through to the ventricle. Small rise at the end of diastole when the last bit of blood is pushed into the ventricle. Atria generally low pressure.

Question 19

Describe volumes inside the LV.

Answer 19

Isometric contraction at time 0. Rapid ejection phase occurs at 0.05 seconds. Once the aortic valve opens most blood leaves during the 1/3 systole. Then slower ejection phase when the remainder of the blood leaves. Isometric relaxation phase. Rapid filling phase - most filling occurs here and this takes place during the 1/3 of diastole. Then slower filling phase.

Question 20

Why are the filling phases important at high HR?

Answer 20

Most filling occurs in 1/3 of diastole and so > HR doesn’t affect this as it only cuts into slow filling phase.

Question 21

What is ESV?

Answer 21

End systolic volume: 60 ml blood.

Question 22

What is EDV?

Answer 22

End diastolic volume: 140 ml blood.

Question 23

What is SV?

Answer 23

Stroke volume which is EDV - ESV. This is not clinically important as it varies from person to person. SV is the amount of blood ejected from the heart in one contraction.

Question 24

What is more clinically important than SV?

Answer 24

Ejection fraction which is SV/EDV. This should be 2/3.

Question 25

Is there any difference between the L and R side of the heart?

Answer 25

SV is the same. Smaller pressures on R side but volumes are the same. ESV and EDV can be different.

Question 26

Describe the pressure-volume loop.

Answer 26

Ventricular diastole and filling: volume increases but pressure stays the same. Then mitral valve closes –> EDV. Ventricle starts to contract and pressure inside the ventricle exceeds pressure inside the aorta which closes the mitral valve. Volume doesn’t change. This is isovolumic contraction. Aortic valve opens and volume falls. Pressure increases as X-bridges are being formed then Ca starts to fall. Ventricular ejection: aortic valve closes so volume doesn’t change but pressure drops –> ESV. Mitral valve opens and cycle starts again.

Question 27

What causes the sounds heard when listening to the heart?

Answer 27

Turbulence in the blood that occurs when the valves close. No noise when aortic and pulmonary valves open, only when they close.

Question 28

What is the name for the period between lub and dub?

Answer 28

Systole.

Question 29

What are the 2 systolic murmurs?

Answer 29

Pulmonary/aortic stenosis or mitral/tricuspid regurgitation.

Question 30

What are the 2 diastolic murmurs?

Answer 30

Mitral/tricuspid stenosis or pulmonary/aortic regurgitation.

Question 31

What noise does septal defect produce?

Answer 31

A murmur throughout the full cycle.

Question 32

Which factors regulate HR and SV?

Answer 32

HR: neural. SV: preload, afterload, neural and pathological.

Question 33

Describe the regulation of HR.

Answer 33

In a normal heart, there are pacemakers in the SA node.

Sympathetic: releases NA plus circulating A from adrenal medulla. These act on B1 receptors on pacemaker cells in SA node. Cells get to threshold quicker and fire AP’s. Increases slope of pacemaker potential and > HR –> tachycardia.

Parasympathetic: vagus nerve releases ACh which acts on muscarinic receptors on SA node. This hyperpolarises cells which decreases slope of pacemaker potential and bradycardia. Cardiac interval is longer (time between each heart beat).

Question 34

Name the 4 ways in which SV is regulated.

Answer 34

Preload, afterload, neural and pathological.

Question 35

How does preload regulate SV?

Answer 35

Preload is the filling pressure of the heart at the end of diastole - EDV. If there is > venous return, > EDV and > SV. If there is Preload is determined y venous return.

An increase in EDV increases preload on the heart which increases the amount of blood ejected from the heart during systole (SV).

Question 36

How does afterload regulate SV?

Answer 36

The pressure in the wall of LV during contraction (load against which muscles contract to eject blood). Afterload is set by arterial pressure against which blood is expelled - depends on TPR. If TPR > then SV

Question 37

Which factors affect aortic pressure?

Answer 37

1) How much blood is pushed into the aorta (CO). 2) How easy it is for that blood to get out of the aorta (TPR).

If TPR increases, aortic pressure will increase. Ventricle has to work harder to push open aortic valve and will have less energy to eject –> decrease in SV.

If an arteriole is really dilated it is easier for blood to get out as there is less pressure.

Question 38

Which has the most important effect on SV, preload or afterload?

Answer 38

Preload. Venules and veins are capacitance vessels and so effect preload. They can squeeze more blood back to the heart which > EDC and makes the heart bigger due to venous constriction. Arterioles affect afterload. They don’t actually do anything to the heart, just make it more difficult for blood to get out.

Question 39

Describe neural regulation of SV.

Answer 39

Sympathetic nerves release NA plus circulating A from adrenal medulla. Acts on B1 receptors on myocytes and increases contractibility. Gives a stronger, but shorter contraction regardless of what preload and afterload were. Whole Starling curve shifts upwards.

Parasympathetic: little or no effect, probably as the vagus nerve does not innervate ventricular muscle.

Question 40

Describe pathological control of SV.

Answer 40

Hypercalcaemia: curve up and left, more Ca2+ in extracellular fluid means more X-bridges –> higher SV.

Hypocalcaemia: shifts curve down and right, less Ca2+ means less X-bridges –> lower SV.

Ischaemia: shifts curve down and right, loss of blood supply to part of muscle means less muscle available to contract –> smaller SV.

Barbiturates (sleep-inducing drugs): shifts curve down and right –> lower SV.

Question 41

Why is SV not a good indication of heart health?

Answer 41

If there is a reduced pumping ability in the heart it works around a bigger EDV. Ejection fraction is more important.

Question 42

What is CO?

Answer 42

CO = SV x HR

Question 43

What happens to CO with a pacemaker?

Answer 43

Increasing HR with an electronic pacemaker causes a small increase in CO, but then SV decreases. Heart rates at 150 bpm cut into the rapid filling phase - reduced EDV reduces preload and so, by Starling’s law, reduces SV.

Question 44

Which factors act to produce an increase in CO?

Answer 44

1) HR increases: via vagal and sympathetic tone; vagal activity is turned down during exercise which causes HR to rise.
2) Contractility increases: via increased sympathetic tone; alters ionatropic state and shortens systole.
3) Venous return increases: via venoconstriction and skeletal/respiratory pumps; increases preload.
4) TPR falls: due to arteriolar dilation in muscle, skin and heart which reduces afterload.
5) CO increases 4-6 times: breathing faster and deeper during exercise pushes blood out of the veins and increases EDV.

Question 45

What are the 3 different structures of capillaries?

Answer 45

1) Continuous: no clefts (endothelial cell junctions) or channels; eg. brain
2) Fenestrated: clefts and channels; eg. muscle
3) Discontinuous: clefts and massive channels; eg. liver as it produces proteins that need to get out

Question 46

How does clotting occur in the endothelium?

Answer 46

Formation of a platelet plug then formation of a fibrin clot. Thrombin turns fibrinogen into fibrin which makes a clot.

Question 47

Name anti-clotting mechanisms of the endothelium.

Answer 47

Stops blood contacting collagen, produces prostacyclin and NO: all inhibit platelet aggregation.

Produce tissue factor pathway inhibitor (TFPI): stops thrombin production by inhibiting part of the pathway that produces thrombin.

Expresses thrombomodulin: binds to thrombin and inactivates it.

Expresses heparin: inactivates thrombin.

Secretes tissue plasminogen activator (t-PA): plasminogen –> plasmin and digests clot (clot buster).

Question 48

Why is diffusion non-saturable?

Answer 48

It is not reliant on a pump system that could become saturated.

Question 49

How is glucose transported in the brain?

Answer 49

Carrier-mediated transport.

Question 50

Describe bulk flow.

Answer 50

Hydrostatic pressure pushes water out of capillaries and leaves solutes behind - they are too big. Increased solute concentration inside the vessel builds up oncotic pressure. This draws water back into the capillary.

–> Capillary hydrostatic pressure vs ISF hydrostatic pressure

–> Plasma oncotic pressure vs ISF oncotic pressure

Question 51

How much fluid is lost through bulk flow?

Answer 51

20L/day. 17L is regained through oncotic pressure drawing fluid back into capillary. The remaining 3L is now called lymph and enters the lymphatic system.

Question 52

Describe the lymphatic system.

Answer 52

Lymph drains into lymph capillaries which are blind ended and go back through lymph vessels and nodes. This drains back into the CVS through the vena cava. Lymph vessels have smooth muscle around them to push fluid.

Question 53

What is oedema?

Answer 53

Accumulation of excess fluid for many reasons.

Lymphatic obstruction (filariasis or surgery), raised CVP (due to ventricular failure), hypoproteinaemia (liver failure, nephrosis, kwashiorkor), increased capillary permeability (inflammation) etc.