Integration Flashcards

1
Q

SNS nerves innervating the adrenal gland cause what?

A

Secretion of epi and norepi into the blood

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2
Q

What normally happens to norepi and what can sometimes happen?

A

Normally the norepi released is taken back up by the nerves, but some can diffuse into the capillary blood and enter the systemic circulation

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3
Q

What happens to epi and norepi levels during exercise?

A

The circulating levels of norepi and epi can become very high so that the net effect is vasoconstriction (but remember that metabolic trumps sympathetic)

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4
Q

What factors influence CV response to exercise?

A
  1. Type of exercise significantly affects CV responses
  2. Body posture
  3. Level of physical conditioning
  4. Environmental factors
  5. Increased age
  6. Gender
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5
Q

How does the type of exercise affect CV responses?

A
Dynamic exercise (aerobic) results in joint movement and muscles contract rhythmically
Isometric/static contraction (heavy weight lifting) elicits a different CV response
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6
Q

With physical conditioning what can a trained individual achieve over an untrained individual?

A

A higher overall CO, whole body O2 consumption, and workload….. while resting CO is the same, the trained person has a lower resting HR and a higher SV… so trained person has a wider HR range to operate through than the lazy person on the couch eating chips

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7
Q

What does high alt. do?

A

Decrease maximal SV and CO from reduced O2 levels

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8
Q

By how much does maximal O2 consumption decrease between 20 and 70 years of age?

A

40%

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9
Q

What is the anticipatory response for exercise?

A

SNS activity primary the SV system for the upcoming workout

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10
Q

What is steady-state HR?

A

This is the initial increase in HR seen when starting exercise that plateaus … this plateau is the HR at which CO matches the body’s needs

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11
Q

What is cardiac drift?

A

This is the increase of HR seen to maintain CO from a steady-state position. As a person exercises longer the body’s metabolic demands increases. The heart increase its HR to try and maintain CO and this HR increase is cardiac drift

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12
Q

At which level does SV plateau and is it a linear relationship to exercise intensity?

A

SV may increase only up to 40-60% of maximal capacity at which point it plateaus. SV increases proportionally with exercise intensity

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13
Q

What happens to the a-vO2 difference with exercise?

A

As exercise intensity increases the difference in pressure between the arteriolar and venular end of the capillary bed increases. This increases the filtration through the capillary bed and more fluid moves into the muscles.
This increases the difference in O2 conc. between the two and can be 3x that of a resting level when at maximal exertion levels

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14
Q

With training what happens to the heart?

A

Hypertrophy WITH an increase in chamber size

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15
Q

What happens to SV with exercise?

A

SV increases at rest, during submaximal training, and maximal exercise following training. SV at rest averages 50-70mL/beat in untrained vs. 70-90mL/beat in trained and 90-110mL/beat in world-class endurance athletes

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16
Q

What mechanisms maintain SV at high HR during exercise?

A

Increased venous return prompted by thoracic and skeletal muscle pumps
Venous constriction maintains central venous pressure
Increased atrial inoptropy augments atrial filling of ventricles
Increased ventricular inotropy decreases ESV, which increases SV and ejection fraction
Enhanced rate of ventricular relaxation (lusitropy) aids in filling

17
Q

What is lusitropy?

A

An enhanced rate of ventricular relaxation

18
Q

What is greater blood flow to skeletal muscle following training a result of?

A

Increased number of capillaries
Greater opening of existing capillaries
More effective blood redistribution
Increased blood volume

19
Q

How is CO primarily maintained during pregnancy?

A

Increased SV

20
Q

Why does MAP generally fall in pregnancy despite elevated CO?

A

A disproportionate decrease in systemic vascular resistance

21
Q

What happens to blood volume during pregnancy?

A

Increases progressively from 6-8 weeks (6-7L/min) and reaches a maximum at 34 weeks with little change thereafter (8-9L/min)

22
Q

How does CO change with pregnancy?

A

Increases to a similar as blood volume. During the 1st trimester CO is 30-40% higher than the non-pregnant state

23
Q

What positional and size changes does the heart undergo during pregnancy?

A

Heart is enlarged by both chamber dilation and hypertrophy.
Dilation across the tricuspid valve can initiate mild regurgitant flow causing a normal grade I or II systolic murmur.
Upward displacement of the diaphragm by the enlarging uterus causes the heart to be moved left and anteriorly so that the apex beat is moved outward and upward.

24
Q

What do the size and positional heart changes seen in pregnancy result in on an ECG?

A

Left axis deviation
Sagging ST segments
Frequently inversion or flattening of the T-wave in lead III

25
Q

How does BP change during pregnancy?

A

Systemic arterial pressure is never increased during normal gestation.
By midpregnancy a slight diastolic decrease can be seen.
Pulmonary arterial pressure also maintains a constant level
Vascular tone is more dependent on sympathetic control than in the nonpregnant state

26
Q

What is aortocaval compression?

A

From mid-pregnancy onward the enlarged uterus compresses both the inferior vena cava and the lower aorta when the pt. is supine

27
Q

What changes are seen in venous distension during pregnancy?

A

Venous distension increases approx. 150% during the course of gestation and the venous ends of capillaries become dilated, causing reduced blood flow