Unit 3 Quiz 3 Material Flashcards

1
Q

What is cardiac output? how is it calculated? What is the normal value?

A

the volume of blood coming out of each ventricle per unit time, usually expressed as Liters/min
CO = HR x SV
5L/min

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2
Q

What are the typical effects of parasympathetic output?

A

-slows heart rate
-reduces cardiac output
-decreases SA frequency
-decreases AV conduction velocity
-decreases atrial kick

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3
Q

What are the typical effects of sympathetic output?

A

-increases HR
-increases SV and CO
-increases SA frequency
-increases conduction velocity– all cells
-increases atrial kick
-increases stroke volume (SV)

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4
Q

What is the Frank-Starling Relationship?

A

As you stretch the cardiac chamber, it gets stronger

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5
Q

What are the implications of the Frank-Starling Relationship?

A

-control EDV, prevent ESV from increasing (prevent clotting)
-matching of LV and RV output, output from right and left sides of the heart remain equal
-prevention of rise in venous pressure
-prevents blood from backing up into veins/capillaries

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6
Q

What determines EDV?

A

venous return

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7
Q

What leads to increased contractility in extrinsic vs. intrinsic?

A

adding NE and E

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8
Q

Describe the similarities and differences between extrinsic and intrinsic mechanism of regulation?

A

both have the same EDV but extrinsic has higher SV due to sympathetic stimulation

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9
Q

What is the ejection fraction and what does it represent?

A

EF = SV/ EDV
higher EF represents a more complete ejection of EDV

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10
Q

At rest, what percent of troponin is bound with Ca 2+? What does the addition of sympathetic output do?

A

30%
increased L-Ca2+ current, ie bigger trigger
more calcium into cytosol, more troponin saturation

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11
Q

What is THE POINT of the signal transduction pathway?

A

-faster and more calcium release
-faster calcium removal
-stronger, briefer contraction

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12
Q

Define Chronotropy

A

regulation of heart rate by autonomic NS

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13
Q

Define Dromotropy

A

conduction velocity through AV node

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14
Q

Define Inotropy

A

tension or force development (twitch)

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15
Q

Describe what a large artery consists of.

A

several elastic layers- allows for recoil
endothelium - smooth lining, commonly damaged
many layers of smooth muscle (radius and flow) and connective tissues (support and strength)
lumen

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16
Q

Describe what an arteriole consists of

A

endothelium
smooth muscle cells
lumen

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17
Q

Describe what a capillary consists of

A

single layer of endothelial cells
lumen

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18
Q

Describe what a venule consists of

A

endothelium
connection tissue
lumen

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19
Q

Describe what a large vein consists of

A

few elastic layers (floppy)
endothelium
wide lumen
few layers of smooth muscle and connective tissue

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20
Q

Name the 5 main types of blood vessels and what their main functions are

A
  1. Large artery- low resistance, conducting vessels
  2. Arteriole - flow regulators
  3. Capillary - functional unit of the CV system
  4. Venule - WBC’s released into tissues during inflammation and infection; capacitance vessels
  5. Large vein- low resistance, high-capacitance vessels, house 2/3 of blood in veins
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21
Q

What happens in response to pulsatile contraction of the heart?

A

waves of pressure move throughout the vasculature, decreasing in amplitude with distance

22
Q

What causes the dicrotic notch?

A

result of semilunar valve closing

23
Q

Where do oscillations stop or cease to exist?

24
Q

Define compliance

A

how easy to expand

25
What happens when blood is pumped into arteries?
the volume pumped out with single heart beat stretches out the arteries; their recoil then continues to push on the blood, keeping it moving during diastole
26
Describe elastic recoil
strength of snap back
27
Why are arteries described as a pressure reservoir?
very high in elastin
28
How is Pulse Pressure calculated?
pulse pressure = systolic - diastolic
29
How is Mean Arterial Pressure Calculated?
MAP = DP + (PP)/3
30
What happens to arterial compliance with increasing age?
decreases, ie arteries get stiff SP trends higher, DP trends lower PP trends higher MAP can stay the same
31
How does an increase in metabolism affect an artery?
increases radius, decreases resistance, increases flow, volume, and pressure in capillaries
32
How does a decrease in metabolism affect an artery?
decreases radius, increases resistance, decreases flow, volume and pressure in capillaries
33
What are the three main job of arterioles?
1. match flow to local tissue/cellular demand (default, get enough blood flow to cells) 2. maintain and protect MAP of whole system (protect brain, protect heart) 3. temperature regulation (skin)
34
Describe the histology of arterioles
thick smooth muscle layer, regulates pressure and flow to downstream capillaries
35
What is an example of a time where the arterioles would need to focus on protecting TPR cooperation and focus blood flow to the heart and brain?
loss of pressure in arteries, hemorrhage
36
What does active hyperemia mean?
more metabolism, increased blood flow
37
What are the factors that tell an arteriole to dialate?
rising CO2 levels, dropping O2, drop in pH, rise in metabolites
38
What is Myogenic Flow Autoregulaton?
protective mechanism against pressure-induced damage
39
What is reactive hyperemia?
high local blood flow after period of deprivation
40
What are local controls?
main regulators of flow to brain and heart muscle
41
Predict what happens must happen in the systemic arteriole for vasodilation to occur in regards to.. O2 CO2 pH ECF K+ Adenosine
decreasing increasing decreasing increasing increasing opposite is true
42
What are the extrinsic controls of the arterioles?
sympathetic innervation of vessels alpha 1 adrenergic receptor agonists induce constriction beta 2 adrenergic receptor agonists induce dilation NE stimulates alpha 1 strongly, causing constricton, reduced radius, reduced flow E stimulates beta 2 receptors strongly, causing dilation, increasing radius and flow (important in skeletal muscle)
43
Describe the effects of low dose vs. high dose of epinephrine
low dose (physiologic) causes vasodilation high dose (injection) causes vasoconstricton
44
Describe the neural controls that alter arteriolar smooth muscle
VASOCONSTRICTORS: sympathetic nerve that release NE, alpha1R VASODILATORS: neurons that release nitric oxide not dual innervation of vasculature: sympathetic only dilation from nitric oxide release, less NE applied
45
Describe the hormonal controls that alter arteriolar smooth muscle
VASOCONSTRICTORS: epinephrine high [] angiotensin II vasopressin = ADH VASODILATORS epinephrine low [] atrial natriuretic peptide = ANP
46
Describe the local controls that alter arteriolar smooth muscle
VASOCONSTRICTORS internal blood pressure (myogenic response) endothelin-1 VASODILATORS drop in O2 rise in K+, CO2, drop in H+ osmolarity adenosine substances released during injury nitric oxide
47
What is the most powerful constrictor measured?
endothelin-1, secreted by endothelial cells
48
Describe Arteriolar Smooth Muscle Control of the... 1.Heart 2. Skeletal Muscle 3. Brain 4. Lungs
1. coronary flow occurs mainly during diastole 2. controlled by local metabolic factors during excersize, Epinephrine causes vasodilation via Beta2-adrenergic receptors when present in low concentration, and vasoconstriction via alpha-adrenergic receptors when present in high concentration 3. influenced relatively little by the autonomic nervous system 4. constriction mediated by local factors in response to low oxygen-concentration- just the opposite of what occurs in the systemic circulation
49
What causes intrinsic mechanism of regulation in Frank Sterling?
change in EDV
50
What causes extrinsic mechanism of regulation in Frank Sterling?
sympathetic stimulation