Lecture 21 : Control of the Heart Flashcards

(34 cards)

1
Q

What are intrinsic or local controls?

A

Controls that originate entirely from within a system

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2
Q

What are extrinsic controls?

A

Controls that involve input from outside - in particular hormonal and nervous effects

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3
Q

How do intrinsic and extrinsic controls work together?

A

Both forms of control operate continuously to adjust the heart and vessels, so that both are always functioning appropriately

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4
Q

What is a chronotropic factor?

A

Anything affecting heart rate

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5
Q

What is an inotropic factor?

A

Anything affecting stroke volume

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6
Q

How is stroke volume calculated?

A

The difference between the end diastolic volume (EDV) and the end systolic volume (ESV)
* SV= EDV-ESV
* With every beat the heart pumps about 60% of the blood in its chambers (65-70 mL)

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7
Q

What are the 3 intrinsic and extrinsic controls of stroke volume?

A
  1. Preload
  2. Afterload
  3. Contractility
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8
Q

How is preload an intrinsic control?

A
  • Determines the intial (pre-contraction) muscle fibre length
  • Left ventricle - when EDV and EDP increase = preload increase
  • LVEDV and LVEDP will be used as the index of preload of the left ventricle
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9
Q

How is pre load related to ‘Starling’s law of the heart’ or ‘Frank-Starling mechanism’?

A

If LVEDV increases, the left ventricle responds by doing more work
- Extra work done by the left ventricle produces a larger stroke volume
- More fill = more empty

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10
Q

What accounts for the Frank-Starling mechanism?

A
  • Length-tension relationship
  • Increase in Ca2+ sensitivity
  • Increase in number and strength of cross-bridges
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11
Q

What is afterload?

A
  • Intrinsic control
  • The tension the fibres must generate before they can shorten
  • Afterload is the pressure that the ventricles must overcome to force open the aortic and pulmonary valves
  • Increase in arterial pressure = increase afterload (hypertension)
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12
Q

How is afterload determined?

A

Mean aortic or mean arterial pressure will be used as the index of afterload of the left ventricle

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13
Q

Describe the extrinsic control of contractility:

A
  • Catecholamines from the adrenal medulla, and sympathetic nerves in the heart, alter ventricular function without a change in LVEDV
  • Improve contractiliy
  • More “effective” pump
  • Causes contraction and relaxation to occur more quickly
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14
Q

If contractility increases what is the affect on stroke volume?

A

Stroke volume increases

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15
Q

What is the ejection fraction?

A

Blood pumped out of the heart per beat
- The ratio of stroke volume (SV) to end-diastolic volume (EDV)

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16
Q

What is the ejection fraction (EF) equation?

A

EF = SV/EDV
EF = 70/130
* Expressed as %, EF normally averages between 50-75% under resting conditions

16
Q

Describe the overall inotropic effect:

A
  • Increase sympathetic nerve activity to heart
  • Increase EDV
  • Increase plasma epinephrine
    -> Increase stroke volume
16
Q

If contractility increases what happens to EF?

A

Ejection fraction increases

17
Q

Which mechanism has the major control on heart rate?

A

Extrinsic mechanisms (nervous and endocrine)

18
Q

What role do intrinsic mechanisms play in controlling heart rate?

A
  • Very limited role
  • Right atrial pressure has small effect of AP generation by SA node
19
Q

How do extrinsic mechanisms of heart rate operate?

A
  • Tonic
  • Mostly active and control CV system by altering level of their control, rather than switching on/off
  • Without nervous control HR would be ~110bpm at rest
20
Q

What is a result of increasing parasympathetic nervous activity to the SA node?

A

Reduces HR: 110bpm-70bpm

21
Q

What is the result of increasing sympathetic nervous activity?

A
  • Increases frequency of AP generation in the SA node
    -> Increase HR: 110bpm-170bpm
22
Q

What effect do agents that alter heart rate have?

A

They have a chronotropic effect

23
How are chronotropic effect of the nervous system brought about?
Alterations to the slope of the slow diastolic pacemaker potential through changes in the permeability of the SA node cell membrane to K+, Na+ and Ca2+
24
What are 6 responses of the heart to increased sympathetic activity?
1. Increase heart rate 2. Increase conduction velocity 3. Reduction in duration of diastole 4. Small reduction in duration of systole 5. Synchronisation of contractions 6. Elevated contractility - SV maintained despite HR increase
25
What is cardiac work?
The work the heart has to do - Metabolic cost (O2 demand) is determined by tension development in the cardiac muscle (Law of laplace)
26
What is the law of laplace?
* Muscle tension (T) to develop ventricular pressure (P) depends on radius of the ventricle (r) and the thickness of the ventricle wall (u) * Tension = transmural pressure x radius/ 2 x wall thickness * 𝑻 =𝑷 𝑿 𝒓/ 𝟐 𝑿 u
27
What is the relationship between tension and pressure, radius and thickness?
T α P T α r T α 1/u
28
What affects metaboloic cost more, tension development or muscle shortening?
Tension development
29
What is needed in order for a constant afterload?
Tension that has to be generated by the ventricular muscle increases as the radius (LVEDV) increases
30
What is needed for a constant radius?
Tension that has to be generated by the ventricular muscle increases as the afterload increases
31
What is acute heart failure (preload)?
* Left ventricle unable to contract effectively at a normal LVEDV * It fills more - larger LVEDV - in order to generate a normal stroke volume - Continuously larger volume (radius) - Ventricle generates more tension - Dilated ventricle has thinner wall (u) = problem
32
What is arterial hypertension (afterload)?
* Ventricle has to generate higher pressure than normal - Requires greater tension development * Hypertrophy of the ventricular wall increases wall thickness, bringing wall tension development back towards normal * Larger mass of heart muscle will require more oxygen (and coronary blood flow reduced due to thick muscle)