CV Packet 2 Questions Flashcards

1
Q

What is the difference between flow and velocity of flow? (HINT: recall what the units of
measurement are)

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2
Q

What is the functional consequence of the velocity of blood flow being the slowest in the capillaries?

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3
Q

When someone is at rest, is turbulent flow in a blood vessel normal? If there is turbulent flow in a blood vessel, this is a vascular murmur called __________.

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4
Q

What determines the blood flow within any given vessel? (HINT: there is an equation that provides the answer)

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5
Q

What are all the factors that determine resistance to blood flow? (HINT: there is an equation for this) (SECOND HINT: every year, many students miss this question on the final exam – not because they didn’t memorize the equation, but rather because they did not understand what the relationships in the equation mean, which are explained in the slide and were discussed in lecture on the board)

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6
Q

Define: SBP, DBP, MAP

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7
Q

What is the significance of MAP? What is typical minimal “healthy” value?

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8
Q

Describe cardiac output in words.

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9
Q

DRAW the “big equation” for cardiac output and all its contributors (i.e., the large equation written on the 2 white boards)

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10
Q

What is the Frank-Starling law? Why is it an intrinsic property of the heart?

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11
Q

Define and distinguish afterload from total peripheral resistance (TPR)

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12
Q

Where in the vasculature is TPR primarily regulated? How does this regulation occur?

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13
Q

Describe 2 ways that cardiac contractility can increase? (HINT: you’ve already done this in Packet 1, but we refined it in Packet 2!)

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14
Q

Describe excitation-contraction coupling in the heart

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15
Q

Where are L-type calcium channels located?

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16
Q

What drug class acts as an antagonist to L channels?

What is the effect of this drug class on blood vessels?

What is the effect of this drug class on cardiac contractility?

Given your answer for (b) and (c), what would be the medical indications for the use of this drug class?

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17
Q

The ANS provides background innervation “tone” to the heart. What is the effect of PNS “tone”?

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18
Q

What is the effect of SNS “tone”?

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19
Q

Beta blockers (the “-lols”) are beta adrenergic receptor antagonists that have what effect on the heart?

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20
Q

What are 2 common indications for beta blockers?

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21
Q

What is the effect of beta blockers on exercise capacity?

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22
Q

What is the most appropriate method to prescribe exercise intensity for someone taking a beta blocker?

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23
Q

Define orthostatic hypotension. What is another term for orthostatic hypotension?

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24
Q

Is orthostatic hypotension the same as hypotension? Why or why not?

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25
Q

What can we do to mitigate symptomatic orthostatic hypotension?

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26
Q

Digoxin has a low therapeutic index. What does this mean, and what should clinicians do about this?

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27
Q

Digoxin is a cardiac glycoside.
What is its effect?
How does the mechanism of action (MOA) for this effect?
What is the primary indication for this drug?

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28
Q

List 2 ways exercise affects cardiac output

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29
Q

List 3 effects of aerobic training on cardiac output.

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30
Q

If you were asked by a physician what a patient’s hemodynamic response to exercise was, what values would you be reporting?

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31
Q

What are the normal hemodynamic responses to exercise? Be sure you can list the actual values, or limits.

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32
Q

What are ACSM’s blood pressure cut-off points for when NOT to start exercise (testing) and when to STOP exercise (testing)?

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33
Q

What is the key difference between a symptom-limited exercise test and exercise tests that PTs typically perform?

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34
Q

Where is most of our total blood volume located at rest?

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35
Q

Which vessels have higher compliance (or, capacitance)? Why?

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36
Q

What are the 4 key regulators to blood volume?

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37
Q

What is the result of the RELEASE of anti-diuretic hormone (ADH) on blood volume and blood pressure? Describe the mechanisms of action to achieve these changes. (Refer to the flow diagram for your recall.)

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38
Q

What is the trigger for activation of the RAAS (renin-angiotensin-aldosterone system)?
What is the result of activation of the RAAS?
Describe the mechanisms of action to achieve these changes. (Refer to the flow diagram for your recall.)

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39
Q

What is ANP? Where is it released from? What is its action?

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40
Q

Describe the baroreceptor reflex. (What baroreceptors are sensing, where they are located, what happens to the firing rate of the afferent nerves when an increase or decrease in stretch is sensed, and what the final efferent output is)

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41
Q

List 3 factors that decrease the sensitivity of the baroreceptor reflex.

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42
Q

What is the result of a carotid massage? How does this effect occur?

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43
Q

When the carotid and aortic chemoreceptors detect decreased pH, decreased PO2, and/or increased PCO2, afferent nerves to the rhythmicity center trigger increases in RR and TV and also cause arteriolar _____________

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