CV Control 2: Reg. of Cardiac Output Flashcards

0
Q

Normal cardiac index range?

A

2.5-3.5 L / min / m^2

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1
Q

Is oxygen demand the sole determinant of blood flow?

A
Nope. It's important, but...
For kidney, filtration rate.
For skin, heat dumping.
For GI, absorption.
etc. can also determine blood flow.
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2
Q

What is the indicator dilution technique?

What is “diluted”?

A

To measure CO, tracer is injected into bloodstream, and its “concentration” is measured downstream.
Tracers include oxygen and heat.

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3
Q

What’s the formula for measuring CO with O2 concentrations?

A

CO = VO2 (total O2 usage) / AVO2D (aterio-venous oxygen difference)

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4
Q

How is thermal diffusion for CO measured?

A

Temp probe in pulmonary artery, cooled saline injected into RA via catheter.
CO can be derived… with calculus.

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5
Q

Normal mixed venous O2 sat. at rest?

What’s a theoretical minimum necessary mixed venous O2 sat at rest without change in CO?

A

75%
Theoretically this could go down to 25% without any change in CO (though if you see this, your patient is very very sick).

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6
Q

Review: 3 factors affecting SV?

A

Preload
Afterload
Inotropic state

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7
Q

With increasing HR, there’s less time for ventricular filling. What fact about ventricular filling in diastole makes helps faster heart rate produce a net increase in CO?

A

Most of the filling happens in the first 1/3 of diastole, so abbreviating diastole doesn’t decrease SV that much. (unless HR is at extremes, maybe > 200bpm)

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8
Q

What’s the problem with trying to boost CO with drugs that increase HR and inotropic state? (i.e. “whipping” the heart)

A

This increases the metabolic demands of the heart, so if patient has disorders from CAD, or certain valve disorders, this can actually cause ischemia.

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9
Q

2 ways to modulate preload?

A

Vasomotor tone.

Renal regulation of intravascular volume.

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10
Q

How to modulate afterload?

A

Altering systemic vascular resistance.

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11
Q

How to modulate inotropy?

A

beta adrenergic input

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