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FM1020 > P: Cardiac Output > Flashcards

P: Cardiac Output Flashcards

1
Q

What is Stroke volume

A

EDV - ESV
Volume of blood ejected by each ventricle during systole

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2
Q

Cardiac output

A

stroke volume x cardiac rate
Normal at rest = 5-5.5 litre/min

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3
Q

Cardiovascular control centres

A

Sensory information relayed to hypothalamus, which regulates activity in CV control centres located in reticular regions of pons and medulla oblongata.

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4
Q

Sympathetic pre-ganglionic fibres originated in:

A

T1-T5 segments

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5
Q

Post-ganglionic sympathetic nerves innervations

A
  • Innervate SA and AV nodes
  • Innervate contractile atrial + ventricular tissue
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6
Q

Post-ganglionic parasympathetic (vagus) innervations

A
  • Innervate SA and AV nodes
  • Some innervation of contractile atrial + ventricular tissue
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7
Q

Vagal escape

A
  • Reduction of heartrate making the HR = 0 triggers reflex stimulation of sympathetic nerves (baroreceptor reflex)
  • Simultaneous sympathetic and vagal nerve activity results in a HR of 20-40bpm.
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8
Q

Sympathetic regulation of heart rate

A
  • Sympathetic stimulation of pacemaker cells increases ion flow through ifNa+ channels and iCa Ca2+ channels.
  • This increase rate of autorhythmic cell depolarizations and thus HR.
  • Noradrenaline released from sympathetic nerve endings binds B1-adrenergic receptors on pacemaker cells.
  • cAMP levels and PKA activity increases
  • cAMP binds to ifNa+ channels and PKA phosphorylates iCa2+ channels
  • Results in opening of these channels.
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9
Q

Vagal regulation of heart rate

A
  • Release of acetylcholine from vagus nerves causes opening of K+ channels and closing of ifNa+ and iCa Ca2+ channels (HCN) on pacemaker cells
  • Ach binds directly to and activates Ach-sensitive K+ channels
  • Ach also minds M2 muscarinic receptors which inhibits cAMP production.
  • Opening of ifNa+ and iCa Ca2+ channels is decreased, reducing their permeability.
  • Increase K+ efflux during phase 4 causes Vm to become more negative –> dampens rate of generation of slow response Aps in autorhythmic cells + HR is reduced.
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10
Q

Regulation of conduction rate

A
  • Vagal stimulation also decreases excitability of AV node cells, slowing transmission of cardiac impulse into ventricle: hyperpolarization slows generation of successive Aps required to Conduct electrical activity through AV node –> longer duration of diastole and ventricular filling.
  • Sympathetic stimulation: increased sodium-calcium permeability makes It easier for AP to excited successive AV node cells, decreasing conduction time from atria to ventricles. Shortens duration of diastole and ventricular filling.
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11
Q

Frank-starling mechanism

A

ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return.
- Increased EDV increases resting sarcomere length in ventricular myocytes
- Allows optimum overlap of thick/thin filaments: maximum no. of cross bridges formed + increased affinity of troponin C for Ca2+

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12
Q

Ejection fraction

A
  • EF = SV/EDV * 100
  • % of EDV ejected from heart
  • Normally EF > 60%
  • Exercise EF > 90% due to increased inotropy (contractility)
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13
Q

How does an increase in EDV result in an increase of SV

A
  • Increase in EDV increases ventricular pressure (preload) which stretches ventricular myocytes
  • Increased stretch increases intrinsic contractility of myocytes
  • Myocytes contraction is stronger –> increases SV
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14
Q

Preload in normal heart:

A

12mmHg

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15
Q

Contractility will peak at preload of:

A

30mmHg

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16
Q

Optimum length of sarcomeres:

A

2.4µm

17
Q

Brachycardia effect on CO

A
  • Brachycardia decreases CO initially
  • Increased duration of diastole –> increased ventricular filling, so increased EDV
  • Increased stretch + increased contractility results in increased SV
  • Reduction of HR is compensated by increase in SV
  • CO remains constant
18
Q

Increase in afterload

A
  • Increase in blood pressure increases afterload
  • Increase in afterload delays opening of valves and ventricular ejection
  • Ventricles have to contract for longer to open semilunar valves
  • Reduction in stroke volume + increase in ESV.
19
Q

How does increased heart rate increase contractility?

A
  • Increased heart rate causes an increase in intracellular calcium in contractile myocytes.
  • Calcium enters cell during each AP plateau phase –> more AP/min = rise in [Ca2+]
  • Increased number of depolarizations also increases opening of Ca2+ channels.
  • Increased intracellular calcium increases contractility.
20
Q

Bowditch effect / Treppe phenomenon:

A

increased heart rate increases intracellular calcium, which increases contractility.

21
Q

Intrinsic mechanism of an increase in HR

A
  • Shortens diastolic time
  • Reduces duration of ventricular filling
  • Reduces EDV (preload)
  • Reduces SV
22
Q

Why does SV decrease as HR increases?

A
  • Reduced time for ventricular filling
  • Reduced EDV
  • Reduced SV
23
Q

Increasing influx of Ca2+ has 2 effects on fast response:

A
  • Prolongs plateau phase of AP
  • Increase i[Ca2+] induces stronger contraction of sarcomeres in myocytes.
24
Q

Sympathetic regulation of contractility:

A
  • Sympathetic nerves release noradrenaline which bind to B1 adrenergic receptors on myocytes
  • cAMP levels increase, resulting in activation of PKA
  • Phosphorylation of L-type Ca2+ channels increases opening time
  • Contractile strength increases
  • SV increases
25
Q

Mechanisms of a stronger + more rapid ventricular contraction:

A
  • Shortened systole
  • Faster relaxation
  • Diastole is longer
  • Promotes increased ventricular filling
26
Q

How vagus nerves regulate contractility:

A
  • Vagus nerves release Ach which closes L-type Ca2+ channels by either:
  • Ach binds to M2 muscarinic receptors + inhibits cAMP production, resulting in down-regulation of cAMP 2nd messenger system. Phosphorylation and opening of Ca2+ channels is reduced.
  • Release of ACH from vagal endings inhibits release of noradrenaline from neighbouring sympathetic nerves.
  • Contractile strength is decreased
  • SV is decreased.
27
Q

Cardiac output equation

A

(O2 absorbed per minute by the lungs)/(Arteriovenous O2 difference)

28
Q

Doppler echocardiography

A

Measures cardiac output non-invasively.
Determines direction + velocity of blood flow; SV and therefore CO is calculated from velocity of blood + area of aorta.

29
Q

Cardiac factors vs coupling factors

A

Cardiac factors: intrinsic to heart (e.g. heart rate + myocardial contractility)
Coupling factors: interaction of heart with blood vessels (preload + afterload)

30
Q

____ stimulation also decreases excitability of __ node cells, slowing transmission of cardiac impulse into ___:
_____ slows generation of successive Aps required to Conduct electrical activity through AV node –> ___ duration of ___ and _____.

A

Vagal
AV
Ventricle
Hyperpolarization
Longer
Diastole
ventricular filling.

31
Q

Increase in ____ increases afterload
Increase in afterload delays opening of ____ and ventricular ejection
Ventricles have to contract for longer to open ____ valves
Reduction in ____ + increase in ____

A

Blood pressure
Valves
Semilunar
Stoke volume
ESV

FM1020 (21 decks)

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