Integrated Control of the Cardiovascular System Flashcards

1
Q

What is the ultimate goal of the cardiovascular system?

A

To maintain blood flow!

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2
Q

What is preload?

A

venous pressure that results in the filling of the heart in diastole. depends on venous return
OR
the degree to which the ventricles are stretched prior to ejection.

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3
Q

What is afterload?

A

Pressure against which the heart must work to eject blood. depends on aortic pressure.

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4
Q

What is stroke volume?

A

The volume of blood ejected with each heart beat.

SV=EDV-ESV

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5
Q

What is the main regulator of TPR?

A

The resistance of the arterioles.

Note: this appears to only apply to the systemic circulation, not the pulmonic.

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6
Q

What does an increase in preload do to SV?

A

This implies an increase in venous return & therefore an increased stretching in the ventricles.
This increase the SV. This increase CO.

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7
Q

What do an increase in afterload do to SV?

A

This decreases SV.

It decreases it b/c it has to eject against a greater pressure.

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8
Q

If the venous return doesn’t equal the cardiac output–>then where does the extra blood go?

A

It is stored in the central venous pool. This is comprsied of the great veins in the thorax & the RA.

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9
Q

If heart rate is greatly increased…how does this affect diastolic pressure?

A

It increases it b/c there’s not enough time for relaxation b/w contractions/ejections.

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10
Q

Review: What is the equation for tissue perfusion/blood flow?

A

Q=P/R

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11
Q

What are the factors that determine systolic pressure?

A

stroke volume
aortic distensibility
ejecting velocity

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12
Q

What are the factors that determine diastolic pressure?

A

systolic pressure
heart rate
aortic distensibility
peripheral resistance

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13
Q

What is the main determinant of stroke volume? What are its 3 main determinants?

A

Venous Return.–>
Blood Volume
Skeletal Muscle Pump
Respiratory Pump

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14
Q

How does gravity affect the pressure of various blood vessels in the body?

A

Blood vessels that are below the level of the heart have higher pressure.
Blood vessels that are above the level of the heart have lower pressure.
*There is actually a negative intracranial pressure.

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15
Q

What’s the deal w/ orthostatic redistribution of blood?

A

So basically if there were increased compliance of our veins…more blood could pool in our lower extremities & maybe never make it back to our heart to be pumped out.
The only way we can stand up is that we have a proper amount of compliance of our veins & valves that prevent backflow.
Still…going from supine to standing decrease intrathoracic blood volume & decreases CO & Pulse pressure.

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16
Q

So when you move from supine to standing…you can experience this sudden drop in BP as blood moves to your lower extremities….but the body fights this. How does the body fight this mechanically? There are 3 ways.

A

Muscle Pump.
Respiratory Pump
Venous Valves

17
Q

What is another thing that happens with venous pooling in the lower extremities?

A

This increases local venous pressure & fluid is filtered into the interstitium.

18
Q

What is the neural response to postural change?

A

Blood pressure decreases.
Baroreceptors decrease frequency of firing.
Vasomotor Control Center increases sympathetic activity & decreases parasympathetic activity.
This increases HR, arterial constriction, venous constriction. This increases CO & BP.
RAAS also plays a long term role in this regulation.

19
Q

Why do people sometimes faint when they stand up too quickly?

A

B/c w/ venous pooling in lower extremities, BP decreases. If it gets low enough…then cerebral pressure will be low enough that you’ll faint.

20
Q

Why could prolonged standing theoretically lead to syncope?

A

B/c prolonged standing causes increased capillary hydrostatic pressure & therefore increased filtration & interstitial fluid volume buildup. This decreases venous return, CO & BP.
Low cerebral BP–>syncope.
But we have compensatory mechanisms…mainly baroreceptors that counteract this so we are usu good.

21
Q

T/F Abdominal & Limb resistance increases when standing up & therefore abdominal & limb blood flow decreases.

A

True.

22
Q

When you give blood why don’t you experience the symptoms of hemorrhage?

A

B/c they don’t take a detrimental volume of blood & they take it over a long period of time.
Also, they give you nutrients like chocolate or something afterwards to replenish you.

23
Q

Why does a patient with a hemorrhage present w/ tachycardia?

A

Their heart rate is increased b/c of increased sympathetic activity as a part of the compensatory mechanism signaled for by the baroreceptor reflex.

24
Q

What would you think happened w/ a patient who presents w/ hemorrhage & bradycardia?

A

Head trauma.
B/c a lower heart rate (increased parasympathetic tone) is a characteristic of the ischemic brain response, not the normal baroreceptor reflex.

25
Q

What is the order & the 3 compensatory mechanisms that seek to reestablish a healthy BP after hemorrhage?

A
  1. Fastest–Baroreceptor Reflex.
  2. Fluid reabsorption from the interstitial compartment b/c the capillary hydrostatic pressure is so low.
  3. Decreased renal excretion & increased ingestion of salt & water.
26
Q

How much of a blood loss can your body’s compensatory mechanisms counteract?

A

1-1.5 L of blood lost.

27
Q

What happens if you lose more blood than your body can handle?

A

Circulatory Shock.

Basically, tissue death.

28
Q

T/F Athletes & non-athletes can surprisingly achieve the same high HR & CO.

A

False.
Athletes & non-athletes can achieve the same HR. like 200 bpm.
However, athletes achieve a much higher CO (like 40L/min).

29
Q

What is the approx HR when you just remove vagal tone?

A

100 bpm.

30
Q

If athletes & non-athletes & cardiac patients can all achieve the same high HR…why are athletes so awesome?

A

B/c athletes can perform more activity @ a lower heart. Like at rest athletes may have a HR of significantly less than 50bpm.

31
Q

How is cardiac output increased during exercise?

A
Thru increase in HR (SNS)
But mainly thru an increase in SV.
SV is increased by:
Increasing Preload/EDV:
muscle pump
respiratory pump
splanchnic venoconstriction (b/c this shifts more blood to the heart)-->done by SNS
Decreased ESV:
Increased Contractility (done by SNS)
32
Q

Where does the cardiac output during exercise mainly redistribute to?

A

The muscle that is working
Skin (to get rid of extra heat)
Lungs (need to get that O2 & deliver that CO2)

33
Q

How can the blood flow to muscle cells increase SO much during exercise.

A

Almost entirely b/c of local control by massive metabolic vasodilation.
Low pO2, High pCO2, low pH
Adenosine, Potassium, Lactate
**also b/c of capillary recruitment.

34
Q

BP raises somewhat during exercise.

What happens to CO & TPR?

A

CO always raises during exercise.
TPR always decreases during exercise.
**This is so that the BP won’t get dangerously high & so that blood flow can get to the skeletal muscle.

35
Q

What happens to the systolic & diastolic BP during exercise?

A

Systolic increases significantly b/c of increased CO & SV & vasoconstriction to inactive tissues.
Diastolic may be relatively constant b/c of the reduced TPR b/c of the release of metabolic vasodilators to skeletal muscle.

36
Q

Why do people who are lifting super heavy weights or something w/ static exercise have a higher BP than ppl on the treadmill for a period of time?

A

B/c they have all of the same forces increasing their BP…
But they don’t have the vasodilation & increased blood flow to their muscles decreasing their BP b/c the tonic muscle contraction is obstructing this blood flow.

37
Q

What is the major determinant of pulse pressure (something that increases it)?

A

Decreased Arterial compliance.