Lecture 14: Contractility and Cardiac Output Flashcards

1
Q

What factors affect cardiac output?

A

Heart rate
Contractility
Preload
afterload

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2
Q

How is cardiac muscle contraction different from skeletal muscle contraction?

A

More responsive to adrenergic inputs and relies more heavily on Ca2+ since it allows heart to contract stronger

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3
Q

How are cardiac glycosides used to treat heart failure?

A

Blocks the Na/K ATPase and Ca/Na exchanger to keep Na and Ca inside the cell for depolarization and stronger contraction

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4
Q

What is the formula for cardiac output?

A

CO = HR x SV

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5
Q

How does length tension (stretching) relate to contraction?

A

The higher the length tension the stronger the contraction

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6
Q

What does preload mean? How is this measured?

A

How much blood is ready to be pumped into the system by the left ventricle (left ventricular end-diastolic volume). Measured by the tension (stretch) on the walls of the left ventricle

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7
Q

What is the Frank Starling relationship?

A

The LVEDV determines the volume pumped by the left ventricle

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8
Q

What is afterload?

A

Pressure needed to be overcome to open the valve and release the blood into the next vessel

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9
Q

What are the equations for calculating these? What are the normal numbers?
Stroke volume
Ejection fraction
Cardiac output

A

SV (70 mL) = EDV (120 mL) - ESV (50 mL)
EF% (55%)= SV / EDV
CO (5 mL/min) = SV x HR

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10
Q

If you increase preload, what happens to CO?

If you increase afterload, what happens to CO?

A

Increases (along with contractility)

Decreases (along with contractility)

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11
Q

How does the heart overcome decreased CO?

A

Increasing contractility and HR

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12
Q

How does HR affect contractility? What is this effect called?

A

Increased HR = increased Ca2+ stored in SR since there is no time to clear Ca2+ = stronger contraction.
Positive staircase effect

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13
Q

What are the characteristics of the positive staircase effect?

A

Since there are more Ca2+ stored in cardiac myocyte, the next contraction is much stronger

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14
Q

By which mechanism does activation of the sympathetic B-adrenergic receptors affect cardiac output?

A

Phosphorylation of Ca2+ channels, phospholamban and inhibitory troponin I produces a positive ionotropic effect

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15
Q

How does activation of parasympathetic muscarinic receptors affect cardiac output? Which type of cardiac myocytes do they mostly affect?

A
  • Decreases influx of Ca2+ and increases efflux of K+ via K+-Ach channels
  • Atrial myocytes
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16
Q

On the Ventricular pressure-volume loop, what happens at points 1-4? What represents the stroke volume?

A
  1. Isovolumetric contraction (pressure rises rapidly)
    1. Ventricle overcomes the pressure and ejects the blood
    2. Isovolumetric relaxation
    3. Ventricular filling

Distance between the vertical lines

17
Q

What happens to the stroke volume (and thus the pressure-volume loop) when preload increases?

A

Increases EDV = increased stroke volume

18
Q

What happens to stroke volume and the ejection fraction of the afterload is increased? What medical conditions does this happen?

A
  • Increased pressure needed to open the valve = decreased stroke volume and ejection fraction
  • Aortic stenosis, HTN
19
Q

What happens to stroke volume and the ejection fraction if contractility is increased?

A

Increased SV and EF. Release more blood so less is left in the heart

20
Q

What does Volume work mean?
Pressure work?
Minute work?
Stroke work?

A

Cardiac output
Aortic pressure
CO x aortic pressure
SV x aortic pressure

21
Q

Why is increased aortic pressure (as in aortic stenosis or HTN) bad?

A

Higher pressure to overcome to pump the blood = decreases the stroke volume. Heart increases contractility and overworks itself to keep the stroke volume the same = hypertrophy of the heart

22
Q

What is the Fick Principle equation?

A

O2 consumption = CO x [O2] in PV - [O2] in PA

23
Q

What is the vascular function curve? What is the normal level?

A

Circulatory filling pressure when there is no blood flow (0 cardiac output)
+7-8 mmHg

24
Q

What happens to cardiac and vascular function curves if you increase or decrease contractility?

A

Cardiac function curve:
Increase: Increases CO (y axis) and decreases RAP (x axis)
Decrease: decreases CO (y axis) and increases RAP (x axis)

Vascular function curve: no effect

25
Q

What happens to cardiac and vascular function curves if you increase or decrease TPR (resistance?)

A

Cardiac function curve:
Increase: Decreases CO (y axis) and maintains RAP (x axis)
Decrease: Increases CO (y axis) and maintains RAP (x axis)

Vascular function curve:
Increase: Decreases CO (y axis) and maintains RAP (x axis)
Decrease: Increases CO (y axis) and maintains RAP (x axis)

26
Q

What happens to cardiac and vascular function curves if you increase or decrease blood volume?

A

Vascular function curve:
Increase: Increases CO (y axis) and increases RAP (x axis)
Decrease: decreases CO (y axis) and decreases RAP (x axis)

Cardiac function curve: no effect

27
Q

What happens during cardiac failure? What is increased and decreased?

A

Decreased inotropy and compliance
Increased blood volume and resistance

Body tries to increase the possible amount of blood to be pumped by holding on to fluids (like water) via kidneys - edema during CHF