Lecture 7 Flashcards

1
Q

What regulates cerebral blood flow?

A
  • solely PCO2
  • not under the influence of the ANS
  • More PCO2 = higher blood flow
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2
Q

ECG anomalies due to hypokalemia:

A
  • globally present (all leads)
  • ST depression with flattened T waves
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3
Q

Ischemia due to angina on ECG:

A
  • ST depression
  • usually accompanied by T wave inversion
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4
Q

Renal circulation can accommodate about how much of CO?

A

20%

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5
Q

Hepatic circulation can accommodate about how much of CO?

A

25%

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6
Q

What is portal vein venous inflow set by?

A

splanchnic arteriolar tone (celiac trunk, SMA, IMA)

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7
Q

What gives the splanchnic arterial system a relatively low threshold for VSM activation/vasoconstriction?

A
  • large concentrations of α1 adrenoreceptors
  • will vasoconstrict in response to low levels of SNS tone
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8
Q

Pulse pressure equation:

A

PP = systolic BP - diastolic BP

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9
Q

What determines pulse pressure (3)?

A

SV, arterial compliance, and ejection force

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10
Q

As SV increases, arterial compliance must coordinately increase to maintain a normal pulse pressure. If arteries become less compliant, what occurs?

A
  • turbulent flow
  • systolic arterial BP elevates
  • greater work load on LV
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11
Q

Anticipatory phase of exercise:

A
  1. SNS becomes activated solely by cognitive output.
  2. HR increases via beta-1 activation, some inotropy as well.
  3. Increased TPR due to alpha-1 mediated vasoconstriction.
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12
Q

Cause of cardiac output increase during anticipatory and early stages of exercise:

A
  • mostly increase HR via beta-1 activation; little inotropy
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13
Q

What changes occur during the early phase of exercise?

A
  1. SNS increase.
  2. PSNS decrease.
  3. HR increase = CO increase.
  4. TPR increase (no vasodilation yet).
  5. Skeletal muscle vasodilatory factors increase.
  6. Skeletal muscle afferents reset high pressure baroreceptors and increase resipiratory drive.
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14
Q

During exercise, skeletal mechanoreceptor afferents cause two changes in the medullary cardio/respiratory centers:

A
  1. high pressure baroreceptors are reset so that the SNS can remain active.
  2. respiration drive increased due to increased PCO2. Chemoreceptors.
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15
Q

How does vasodilation due to vasodilatory metabolites increase heart efficiency during exercise?

A
  • decreases afterload
  • occurs in late phase of exercise
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16
Q

Differences in systolic and diastolic blood pressures during exercise:

A
  • systolic increases (dependent on CO) throughout.
  • diastolic decreases due to vasodilatory factors (dependent on TPR) in late stage.
17
Q

What changes during the late stage of vigorous exercise?

A
  • increased HR, EDV, EDP, CO (5X)
  • decreased ESV
  • increased systolic BP
  • diastolic BP stable or drops
18
Q

What happens to arterial blood gases (ABGs) during the late exercise stage?

A
  • PCO2 increases in the venous blood
  • Mild acidemia drives ventilation
19
Q

Anaerobic threshold:

A
  • level at which lactic acid production exceeds removal. Accumulates.
  • Mild acidemia drives ventilation.
20
Q

Draw cardiac function curve during the initial phase of exercise:

A
  • SNS tone increases.
  • Vasoconstriction and inotropy.
21
Q

Draw cardiac function curve during the late stage of physical exercise:

A

Vasodilation occurs due to skeletal muscle work metabolites