Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

1020: Physiology FM1020 (E) > P: Cardiac Output > Flashcards

P: Cardiac Output Flashcards

1
Q

Where do sympathetic pre-ganglionic fibres originate?

A

T1-T5 in spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What nerve passes to entire thoracic and abdominal regions of the body including the heart?

A

Vagus nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What parts of the heart do post-ganglionic sympathetic nerves innervate?

A
  • SA and AV nodes
  • Contractile atrial and ventricular tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What parts of the heart do post-ganglionic parasympathetic (vagus) nerves innervate?

A
  • SA and AV nodes
  • Some innervation of contractile atrial and ventricular tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What’s the effect of ANS on cardiac APs? What do sympathetic and parasympathetic nerves release to do so?

A
  • Regulates the heart rate by enhancing/inhibiting spontaneous generation of slow response APs of autorhythmic cells (heart generates its own APs, ANS modulates their rate and strength)
  • Modulates fast response APs in contractile myocytes
  • Sympathetic: noradrenaline (stimulatory)
  • Parasympathetic (vagus): acetylcholine (inhibitory)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does vagal nerve activity do to heart rate?

A

Reduces heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Explain vagal escape

A
  • Experimental electrical stimulation of vagus nerve: heartbeat stops for a few seconds
  • If HR = 0 —> cardiac output = 0
  • Reduction in CO triggers reflex stimulation of sympathetic nerves (baroreceptor reflex)
  • Simultaneous sympathetic (+) and vagal (-) nerve activity —> HR of 20-40 bpm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Modulating ___ nerve activity exerts a more immediate control and is physiologically more important than ___ activity

A
  • vagus nerve
  • sympathetic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Explain sympathetic regulation of heart rate

A

Increase of HR:
- Noradrenaline released from sympathetic nerve endings binds Beta1 adrenergic receptors on pacemaker cells
- cAMP levels rise, PKA activity increases
- cAMP binds to Na+ channels and PKA phosphorylates Ca2+ channels
- Increased opening of HCN channels and increase of ions flow through them —> increases rate of autorhythmic cell depolarizations —> increases HR (threshold is achieved more rapidly)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Explain vagal regulation of heart rate

A

Reduction of HR:
- Release of ACh from vagus (parasympathetic) nerves causes opening of K+ channels: increased K+ efflux during phase 4 causes membrane potential to become more negative (hyperpolarization)
- Release of ACh from vagus nerve causes closing of HCN channels on pacemaker cells (by binding M2 muscarinic receptors —> inhibits cAMP production)
- These 2 factors reduce generation of slow response APs —> reduces HR (threshold is achieved slower)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

SV is intrinsically (directly) proportional to ___ and ___
How?
What principle explains this?

A
  • EDV and contractility
  • Increase in EDV increases ventricular pressure (preload) —> stretches ventricular myocytes –> increases intrinsic contractility of myocytes –> increases SV
  • Frank-Starling Law of the Heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Definition of Frank-Starling mechanism

A

Ability of the heart to change its force of contraction and therefore stoke volume in response to changes in venous return

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Changes in ___ produce significant changes in ejection fraction (EF)

A

Contractility/inotropy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is ejection fraction (EF)? How to calculate it? Normal EF? Exercise EF? Severe heart failure EF?

A
  • % of EDV ejected from heart
  • EF = SV/EDV x 100
  • Normally EF > 60%
  • Exercise: EF > 90% (increased inotropy)
  • Severe heart failure: EF < 20%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Effect of increased EDV on contractile force and how?

A
  • Increased EDV increases sarcomere length to 2-2.4 µm
  • Optimum overlap of thick/thin filaments: maximizes number of cross-bridges formed + increases affinity of troponin C for Ca2+
  • Contractile force is increased
  • When sacromeres stretched beyond optimum length (2.4 µm) –> contractility diminished (only happens in heart failure)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is preload pressure in normal heart? At which pressure does contractility peak?

A
  • 12 mmHg
  • Peaks at 30 mmHg
17
Q

Explain how Frank-Starling mechanism acts to restore normal cardiac output in bradycardia

A
  • Bradycardia initially decreases cardiac output –> increases duration of diastole –> increased ventricular filling –> increased EDV or preload –> increased stretch + contractility –> increased SV
  • Reduction in HR is compensated by increase in SV –> CO remains constant (CO = HR x SV)
18
Q

Explain how Frank-Starling mechanism acts to restore normal cardiac output in afterload

A

Afterload: arterial pressure opposing opening of semilunar valves
- Increased BP (diastolic pressure) –> increased afterload
- Increased peripheral resistance –> increased afterload –> delays opening of valves and ventricular ejection –> ventricles contract for longer to open semilunar valves –> reduction in stroke volume + increase in ESV

Ventricles can adapt by increasing contractility:
- Decrease in SV = increased EDV in next cardiac cycle (constant venous return VR)
- ESV + VR = EDV in next cardiac cycle –> will cause subsequent contractions to be stronger –> increased contractility restores SV to normal

19
Q

What is Frank-Starling Mechanism characterized by?

A

Increased EDV –> increased inotropy

20
Q

Changes in cardiac contractility also occur ___ of preload —> unique to cardiac muscle, skeletal muscle can’t alter its ___ state

A

independently, intrinsic inotropic

21
Q

Increase in frequency of contraction increases ___ of myocardial fibres

A

Contractility (frequency of contraction is determined by HR, increased HR increases contractility)

22
Q

Explain Bowditch effect/Treppe phenomenon

A

Increased HR —> increased intracellular [Ca2+] —> increased contractility
- Ca2+ enters cell during each AP plateau phase —> increases # of AP/min –> rise in [Ca2+]
- Increased number of depolarizations also increases opening of Ca2+ channels

23
Q

As HR increases, ___ progressively decreases. Why?

A
  • SV decreases
  • Increase in HR shortens diastolic time —> reduced time for ventricular filling —> reduced EDV (preload) —> reduced SV
    (CO = HR x SV)
24
Q

Explain relation between HR and cardiac output from 50-250 bpm

A
  • 50-100 bpm: initial increases in HR elevate CO (effect of reduction in SV is less than effect of increase in HR)
  • 100-200 bpm: CO is constant (effect of reduction in SV balances effect of increase in HR)
  • > 200 bpm: CO decreases (ventricular filling time severely restricted)
25
Q

What happens during excessively slow HR/profound bradycardia concerning CO and how to fix it?

A
  • Slow sinus rhythm —> AV block
  • EDV and SV increase can’t compensate for slow HR (overstretch of ventricular sarcomeres + pericardium limits ventricular filling)
  • CO falls substantially
  • Artificial pacemaker
26
Q

Opening of L-type Ca2+ channels is regulated by the ___ to control the degree of Ca2+ influx and regulate ___ of the heart

A

ANS, contractile strength

27
Q

Effects of increasing influx of Ca2+ on fast response:

A
  • Prolongs length of plateau phase in AP
  • Stronger contraction of sarcomeres in myocytes
28
Q

Explain sympathetic regulation of contractility

A
  • Sympathetic nerves release NA –> binds to B1 adrenergic receptors on myocytes –> cAMP levels increase –> activation of PKA –> phosphorylation of L-type Ca2+ channels –> increases opening time
  • Contractile strength increases
  • SV increases
29
Q

Mechanism of stronger and more rapid ventricular contractions:

A
  • Systole duration is shorter
  • Relaxation happens earlier
  • Diastole duration is longer
  • Ventricular filling increases
30
Q

Explain vagal regulation of contractility

A

Vagus nerves release ACh which promotes closure of L-type Ca2+ channels in 2 ways:
- ACh binding to M2 muscarinis receptors inhibits cAMP production —> down-regulation of cAMP 2nd messenger system —> phosphorylation + opening of Ca2+ channels is reduced
- ACh inhibits release of NA from neighbouring sympathetic nerves
- Contractile strength decreased —> SV decreased

31
Q

Are vagus or sympathetic effects more important in regulating ventricular myocyte contractility?

A

Sympathetic

32
Q

Describe positive and negative inotropic effect

A
  • Positive: at the same EDV, sympathetic nerves increase contractility –> larger SV
  • Negative: at the same EDV, vagus nerves reduce contractility –> smaller SV
33
Q

What are factors increasing inotropy

A
  • HR (Bowditch Effect)
  • Parasympathetic (vagal) inhibition
  • Sympathetic activation
  • Afterload (Anrep Effect)
  • Circulating catecholamines
34
Q

Measurement of cardiac output (Q)

A
  • q1 = rate of O2 delivery to lungs from RV
  • q2 = O2 consumption by body
  • q3 = rate of O2 transport to LA from lungs
  • Q = CO
  • q1 = Q[O2] pulm artery
  • q2 = Q[O2] pulm vein
35
Q

How is CO calculated nowadays?

A

Doppler echocardiography:
- Ultrasound utilizes Doppler effect to determine direction and velocity of blood flow
- SV and CO is calculated from velocity of blood and area of aorta

1020: Physiology FM1020 (E) (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions