L7 Physiology: autonomic nervous system

Question 1

Cardiac output (CO)

Answer 1

The volume of blood pumped out of the heart (left or the right ventricle) per minute.

Question 2

Cardiac output formula

Answer 2

HR x SV

Question 3

Stroke volume (SV)

Answer 3

The volume of blood ejected per contraction

Question 4

Formula of stroke volume

Answer 4

End diastolic volume (EDV) - End systolic volume (ESV)

Question 5

Heart rate (HR)

Answer 5

Number of contractions per minute

Question 6

Heart rate is determined by?

Answer 6

SA node

Question 7

SA node is regulated by?

Answer 7

Autonomic nervous system

Question 8

Venous return

Answer 8

The volume of blood returning to the heart (right or left atrium) per minute

Question 9

Athletes with large hearts have?

Answer 9

Large EDV and SV.

Question 10

At rest, athletes’ CO and HR?

Answer 10

Low HR and adequate CO e.g. 40 bpm. Only the normal CO at rest is needed.

Question 11

Beta-blockers does what?

Answer 11

(Negatively ionotropic) reduces contractility of ventricles

Question 12

Calcium channel blockers function?

Answer 12

Negatively ionotropic - slows down the heart.

Question 13

Ivabradine function

Answer 13

Not negatively ionotropic, safe in overdose as complete block of it does not stop SA node from firing. It blocks funny channel which is partly responsible for slow depolarisation towards AP threshold slows.

Question 14

Beta agonist function?

Answer 14

binds to muscarinic receptors, increases heart rate.

Question 15

Adrenaline and noradrenaline acts on?

Answer 15

Acts on adrenergic receptors (beta-1), increases HR in same way as sympathetics.

Question 16

Sympathetic activation increases HR by?

Answer 16

By causing an increase in rate of rise of pacemaker potential, threshold reached rapidly, more action potentials generated.

Question 17

Parasympathetic activation decreases HR by?

Answer 17

By reducing rate of rise of pacemaker potential.
Also some hyperpolarisation (moving potential down a bit), threshold is reached later, greater intervals between potentials.

Question 18

Atropine acts on?

Answer 18

Acts on muscarinic receptors, blocking the parasympathetic vagal cholinergic system faster.

Question 19

Which changes contractility and therefore stroke volume?

Answer 19

SNS and hormones

Question 20

What changes after-load of stroke volume?

Answer 20

Blood pressure required to eject blood and open aortic valve

Question 21

What changes pre-load of stroke volume?

Answer 21

Determined by venous return, which is major factor of controlling stroke volume.

Increases calcium sensitivity of contractile proteins.

Stretching the ventricle (within limits) places the contractile proteins in a more favourable arrangement by generating more cross-bridge formation

Question 22

What lvl of bpm until CO begins to decline?

Answer 22

180bpm, because there is inadequate time for ventricular filling during diastole.

With compliant vessels, the bpm is lower.

Question 23

Describe Frank starilng law (preload)

Answer 23

1. Increase in venous return
2. Increase end-diastolic ventricular volume
3. Increased force of ventricular contraction.
4. Increased stroke volume.
5. Increased cardiac output

Question 24

The greater the filling of the ventricle (end-diastolic ventricular volume), the greater the?

Answer 24

Greater the force of contraction (and hence stroke-volume).

Question 25

Preload ensures consistent ____ despite daily variation in aortic pressure.

Answer 25

Cardiac output

Question 26

End diastolic volume correlates with?

Answer 26

Venous return

Question 27

Change in return of blood to right or left ventricle is immediately followed by?

Answer 27

By a change in output (e.g. on changing posture venous return suddenly decreases or increases, or due to gravity, decrease in venous return decreases in SV and CO).

Question 28

Why does stretching ventricles favours arrangement and generates more cross-bridge formation?

Answer 28

- Myosin and actin molecules interact more. | - Also increases calcium ion sensitivity of contractile proteins, which increases force of contraction.

Question 29

During exercise, which following changes occur that lead to increased venous return?

Answer 29

- Decreased total peripheral resistance + Increased skeletal muscle activity - Above leads to increased peripheral venous pressure - This leads to increased pressure gradient. - Increased venous return - Increased respiratory activity leads to decreased right atrial pressure which leads to increased venous return. - Increased cardiac output increases end-diastolic ventricular volume which increases venous return.

Question 30

To increase end systolic ventricle blood volume, you need to increase?

Answer 30

Increase venous pressure peripherally with respect to centrally.

Question 31

How do you increase venous pressure peripherally?

Answer 31

- Sympathetic innervation of veins - Skeletal muscle pump - Respiratory pump

Question 32

Respiratory pump increases ?

Answer 32

VPc

Question 33

Describe skeletal muscle pump

Answer 33

Alternate contraction and relaxation of skeletal muscles, one-way valve preventing backflow, increasing venous return during dynamic exercise (increases VPp)

Question 34

Describe sympathetic innervation of veins

Answer 34

Venoconstriction of peripheral veins reduces venous compliance (increases VPp)

Question 35

Describe work of a pump

Answer 35

SV x Pressure. Therefore work of the heart is increased by hypertension.

Question 36

Angina/cardiac ischaemia is due to?

Answer 36

Excessive cardiac work and oxygen consumption

Question 37

Drugs which cause peripheral vasodilation are very effective at?

Answer 37

Effective at treating hypertension and heart failure (Afterload reduction). E.g. ACE inhibitors and Ca channel blockers

Question 38

Effect of sympathoadrenal neuronal stimulation (exercise, emotional excitement) leads to?

Answer 38

Increase in intracellular calcium in myocardial fibres activation of cardiac sympathetic nerves, or an increase in circulating adrenaline, increases cardiac contractility.

Question 39

Noradrenaline/adrenaline activates?

Answer 39

Activates B1 adrenergic receptor so ATP is converted to cAMP which activates protein kinases which phosphorylate slow calcium channels, promoting more calcium entry from extracellular space. Also SR releases more calcium ions, which increases intracellular concentration.

Question 40

Effect of noradrenaline/adrenaline on myosin cross bridge cycling

Answer 40

Increases rate of myosin cross bridge cycling, which ultimately increases force of contraction of the heart and that's independent of end diastolic ventricular volume.

Question 41

Why is noradrenaline/adrenaline advantageous?

Answer 41

It does not reduce diastolic filling time as it otherwise may be.

Question 42

Cardiac vagal stimulation

Answer 42

Activation of cardiac vagal nerves leads to a decrease in myocardial intracellular calcium ions, resulting in a reduced cardiac contractility