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Block 4 > L7 Physiology: autonomic nervous system > Flashcards

L7 Physiology: autonomic nervous system Flashcards

1
Q

Cardiac output (CO)

A

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

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2
Q

Cardiac output formula

A

HR x SV

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3
Q

Stroke volume (SV)

A

The volume of blood ejected per contraction

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4
Q

Formula of stroke volume

A

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

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5
Q

Heart rate (HR)

A

Number of contractions per minute

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6
Q

Heart rate is determined by?

A

SA node

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7
Q

SA node is regulated by?

A

Autonomic nervous system

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8
Q

Venous return

A

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

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9
Q

Athletes with large hearts have?

A

Large EDV and SV.

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10
Q

At rest, athletes’ CO and HR?

A

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

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11
Q

Beta-blockers does what?

A

(Negatively ionotropic) reduces contractility of ventricles

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12
Q

Calcium channel blockers function?

A

Negatively ionotropic - slows down the heart.

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13
Q

Ivabradine function

A

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.

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14
Q

Beta agonist function?

A

binds to muscarinic receptors, increases heart rate.

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15
Q

Adrenaline and noradrenaline acts on?

A

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

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16
Q

Sympathetic activation increases HR by?

A

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

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17
Q

Parasympathetic activation decreases HR by?

A

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

18
Q

Atropine acts on?

A

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

19
Q

Which changes contractility and therefore stroke volume?

A

SNS and hormones

20
Q

What changes after-load of stroke volume?

A

Blood pressure required to eject blood and open aortic valve

21
Q

What changes pre-load of stroke volume?

A

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

22
Q

What lvl of bpm until CO begins to decline?

A

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

With compliant vessels, the bpm is lower.

23
Q

Describe Frank starilng law (preload)

A
  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
24
Q

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

A

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

25
Q

Preload ensures consistent ____ despite daily variation in aortic pressure.

A

Cardiac output

26
Q

End diastolic volume correlates with?

A

Venous return

27
Q

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

A

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).

28
Q

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

A
  • Myosin and actin molecules interact more.

- Also increases calcium ion sensitivity of contractile proteins, which increases force of contraction.

29
Q

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

A
  • 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.
30
Q

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

A

Increase venous pressure peripherally with respect to centrally.

31
Q

How do you increase venous pressure peripherally?

A
  • Sympathetic innervation of veins
  • Skeletal muscle pump
  • Respiratory pump
32
Q

Respiratory pump increases ?

A

VPc

33
Q

Describe skeletal muscle pump

A

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

34
Q

Describe sympathetic innervation of veins

A

Venoconstriction of peripheral veins reduces venous compliance (increases VPp)

35
Q

Describe work of a pump

A

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

36
Q

Angina/cardiac ischaemia is due to?

A

Excessive cardiac work and oxygen consumption

37
Q

Drugs which cause peripheral vasodilation are very effective at?

A

Effective at treating hypertension and heart failure (Afterload reduction).

E.g. ACE inhibitors and Ca channel blockers

38
Q

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

A

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

39
Q

Noradrenaline/adrenaline activates?

A

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.

40
Q

Effect of noradrenaline/adrenaline on myosin cross bridge cycling

A

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.

41
Q

Why is noradrenaline/adrenaline advantageous?

A

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

42
Q

Cardiac vagal stimulation

A

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

Block 4 (8 decks)

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