Cardio 8 Flashcards

1
Q

In cardiac cells, what is the force generated during a contraction proportional to?

A

It is proportional to the stretch imposed on a cell before contraction (ventricular volume)

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2
Q

According to the Frank-Starling mechanism, if ventricular filling is_____, the muscle is _____ , increasing the force of contraction, resulting in ________

A

increased
More stretched
a higher stroke volume

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3
Q

What is preload in the Frank-Starling mechanisms?

A

The amount of ventricular wall stretch

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4
Q

When is the Frank-Starling mechanism important? Why?

A

during exercise

When CO increases, Preload increases, and the amount of blood pumped per beat automatically increases.

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5
Q

Which variable of the MAP formula does the F-S mechanism affect?

A

Stroke volume to then influence the CO

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6
Q

What are the names of the two local control of the heart?

A

F-S mechanisms
Autoregulation

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7
Q

Where does autoregulation occur?

A

At the levels of individual organ tissues

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8
Q

How does autoregulation work at the heart?

A

To respond to a sudden drop in perfusion pressure, the coronary vessels will reduce resistance to compensate and maintain/regain a stable flow

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9
Q

Why is it called autoregulation?

A

Because it is not under neural control

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10
Q

What is the autoregulatory range?

A

he range of blood pressures that can be at least partially compensated for by autoregulation

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11
Q

What is autoregulation mediated by if there is no neural control?

A

Myogenic autoregulation or Metabolic autoregulation

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12
Q

What is the difference between Myogenic and metabolic autoregulation?

A

Myogenic: stretch-activated channels get activated in the heart walls

Metabolic: a build-up of waste or lack of O2 will bring on autoregulation

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13
Q

Regarding the CV system, what will the autonomic nervous system have effects on?

A

The heart, vessels and the adrenal glands

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14
Q

If a neural response changes heart rate, what else will be affected?

A

CO (flow) and MAP

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15
Q

In general, what do the PS and Symp nerves to at the level of the heart?

A

PS: Decreases activity of the SA node
S: Increases activity of the SA node

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16
Q

Describe the pathway of the PS nerves from the medulla oblongata to the heart to decrease HR.

A

Pre-ganglionic axon reaches ganglion
Releases ACh onto nicotinic receptors
Postganglionic axon reaches sinus node
Releases Ach onto muscarinic receptors

Result: Increase in neural activity –> decreases HR (PANS)

17
Q

Describe the pathway of the Symp. nerves from the spinal cord to the heart to increase HR.

A

Pre-ganglionic axon reaches the ganglion, close to the spinal cord
Releases ACh onto nicotinic receptors
Postganglionic axon reaches sinus node
Releases NE onto B-androgenic receptors

Result: Increase in neural activity –> increase HR (SANS)

18
Q

Explain how the SANS controls contractility.

A


post-ganglionic axon reaches ventricular muscle cells.
NE increases contractility by changing channel conductances, which ultimately increase cytoplasmic Ca
Increase in maximal force produced with each contraction (increases SV)
And reduction in the duration of contraction.

19
Q

Why is controlling contractility of the heart during a SANS response important?

A

The reduction in duration reduces the action potential duration, and ultimately the refractory time, which allows the heart to support a higher beating frequency (which is done at the sinus node)

20
Q

Is the SV change the same during the F-S mechanism and the SANS response?

A

No, the F-S mechanism is dependent on the end-diastolic volume whereas the SANS response will increase SV for a same end-diastolic volume (not the same curve)

21
Q

In addition to HR and SV, what else can the SANS response affect?

A

vessel diameter (vessel tone) to ultimately affect resistance and perfusion pressure.

22
Q

Describe the pathway for Adrenal gland activation and the result.

A

Pre-ganglionic neuron reaches the gland
Releases ACh
The Adrenal gland releases E and NE
Because both are alpha and beta agonists, they affect heart rate (HR), contractility (SV) and TPR, and therefor affect MAP (decrease and increase respectively depending on receptor)

23
Q

What are baroreceptors?

A

Receptors in carotid arteries that sense pressure via the stretch of the vessel walls

24
Q

What is the Baroreceptor reflex?

A

A FAST response to blood pressure changes

25
Q

How will the baroreceptors react to Normal, Elevated and Reduced MAP?

A

Normal: Baroreceptors fire at a moderate rate

Elevated: baroreceptor firing increases –> activates the parasympathetic system

Reduced: baroreceptor firing is minimal –> triggers a sympathetic response

26
Q

What kind of feedback is the baroreceptor?

A

They provide negative feedback

27
Q

Standing up results in a large shift of blood and a drop in central blood volume, what would be the immediate effects? Where do those effects come from?

A

Increase in HR (S and PS)
Increase in SV by incresing contractility(S)
Increase in TPR via vessel tone (S)

28
Q

Which variable do each have an affect on?
1. PS
2. S

A

PS: HR
S: HR, contractility, constriction, adrenal gland activation

29
Q

What would happen if the glossopharyngeal and the vagus nerve were cut from the baroreceptors? What is that called?

A

The MAP would stay the same but would be unstable/ unregulated –> Labile hypertension