SM 119a - Integrative Function Flashcards

1
Q

List the central and local cardiovascular responses to exercise

A

Central: Mediated by increased sympathetic and decreased parasympathetic outflow

  • Increase cardiac output
  • Splanclinc and renal constriction of arterioles
  • Constriction of veins

Local: Mediated by increases in vasodilator metabolites

  • Dilation of skeletal muscle arterioles
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2
Q

How does cardiac function change in response to exercise?

What mediates these changes?

A
  • Increased Heart Rate
  • Increased Contractility
  • Increased Cardiac Output
  • Increased Stroke Volume

Mediated by central command: decreased parasympathetic input (decreased vagal tone) and increased sympathetic input

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3
Q

What are the three mechanisms that increase stroke volume in response to exercise

A
  • Increased preload -> Increased strength of contraction
    • Due to increased venous return, due to constriction of veins and pumping of skeletal muscles
  • Increased contractility
    • Due to increased adrenergic tone
      • Increased Ca2+ in the SR
      • Increased myogenic sensitivity to Ca2_
    • Treppe/Bowditch/Force-frequencey effect
      • Increased HR leads to increased intracellular Ca2+
  • Increased Lusitropy
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4
Q

How does venous constriction affect the strength of cardiac contraction?

A

Venous constriction increases venous return, which increases preload, thus increasing the strength of cardiac contraction

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5
Q

In splanchnic/renal beds, what kind of adrenergic receptors would you expect to find?

Why?

A

Alpha-1 receptors, causing arterioles supplying these areas to constrict in response to sympathetic input

These areas are non-essential to running away from predators, so they do not need blood flow during a sympathetic response

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6
Q

In veins, what kind of adrenergic receptors would you expect to find?

Why?

A

Alpha-1 receptors, causing constriction in response to sympathetic input

During a sympathetic response (ex: exercise or running away from predators), constriction of venules decreases the unstressed volume and increases venous return. This forces blood into the arteries and exercising muscles and increases the strength of cardiac contraction by increasing preload

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7
Q

In exercising myocytes, what mechanism increases the hemoglobin concentration in the blood?

A

Increased myocyte metabolism leads to…

  • Increased metabolic byproducts
  • -> Increased oncotic pressure in the extracellular space
    • More force sucking fluid out of the capillary into the extracellular space
  • -> Increased H2O in the extracellular space, from the capillary
  • -> Increased concentration of hemoglobin in blood (due to decreased solvent)
    • This increases the pO2 in the blood to allow for better oxygen delivery
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8
Q

What are the vasodilator metabolites produced by exercising myocytes?

A
  • Lactate
  • Adenosine
  • K+
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9
Q

What are the two major short-term goals in repsonse to hemorrhage?

A
  1. Mitigate blood loss due to hemorrhage
  2. Maintain CO and BP to perfuse tissues and brain
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10
Q

What are the major changes to the cardiovascular circulation in immediate response to hemorrhage?

A
  1. Venous return decreases
  2. Central blood volume decreases

But short-term physiologic responses function to restore both, in order to maintain CO and BP

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11
Q

In immediate response to hemorrhage, venous return decreases.

What is the effect on central and peripheral chemoreceptor?

A

Decreased venous return -> Decreased CO ->
Decreased regional blood flow

  • Peripheral chemoreceptors activate in response to
    • Decreased pO2
    • Increased pCO2
    • Decreased pH
  • Central chemoreceptors activate in response to
    • Decreased pH in the brain ECF
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12
Q

In immediate response to hemorrhage, venous return decreases.

What is the effect on cardiac function? On MAP?

A
  • Decreased Stroke Volume
  • Decreased Cardiac Output
  • Decreased MAP
    • Decreased blood flow to all areas
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13
Q

List the 4 major inputs to the medullary cardiovascular control center in response to hemorrhage

A
  • High pressure baroreceptors are deactivated
    • Decreased cardiac function -> less stretch in the carotid and aorta -> No firing
  • Peripheral chemoreceptors are activated
  • Central chemoreceptors are activated
  • Low pressure baroreceptors are deactivated
    • Decreased blood volume -> Decreased atrial filling
  • > Decreased atrial volume -> No firing
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14
Q

In response to hemorrhage, the medullary CV control center receives input and then sends efferent signals.

What is the effect of these signals on the kidney?

A

In general, the kidney responds to hemorrhage by working to conserve blood volume by conserving Na+ and H2O

  • Constriction of renal vascular beds
    • Decreased glomerular filration
      • Decreased excretion of Na+ and H2O
  • Decreased ANP secretion
    • Decreased excretion of Na+ and H2O
  • Increased renin secretion
    • Increased angiotensin II
      • Increased aldosterone
        • Increased reabsorption of Na+
  • Increased ADH
    • Increased reabsorption of H2O
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15
Q

What are the major goals of efferent signaling from the medullary CV control center in response to hemorrhage?

A

Mitigate blood loss, maintain CO and BP

  • Increase CO via…
    • Increased HR
    • Increased contractility
  • Increase TPR via…
    • Arteriolar constriction
    • Venous constriction
  • Conserve H2O and Na+ via…
    • Via signaling to the kidney
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16
Q

In response to hemorrhage, what are the longer-term adaptations in capillary absorption/filtration?

A
  • Decreased capillary pressure
    • Net absorption at the capillary level due to Starling forces (decreased hydrostatic pressure)
    • This leads to a relative decrease in hemoglobin concentration
  • Increased interstitial oncotic pressure (in response to absorption into the capillary)
    • This puts a brake on the amoutn of fluid that can get into the capillaries
17
Q

How are plasma proteins replenished after hemorrhage?

A
  • Short term
    • Enter the blood via fenestrated capillaries in the liver and mesentary
  • Long term
    • Synthesized in the liver
18
Q

List the 4 mechanisms that could cause irreversible hemorrhagic shock

A
  • Failure of the vasoconstrictor response
    • Neurotransmitter depletion at blood vessels or
    • Local metabolic signaling -> vasodilation
  • Failure of capillary refill mechanisms
    • Due to failed resistance at the precapillary sphincter
    • This increased capillary presssure anc causes inappropriate filtration out of the capillary
  • Heart failure
    • Due to prolonged ischemia when MAP is low
  • Failure of CNS response
    • Lack of sympathetic outflow -> loss of intensity of compensatory mechanisms
19
Q

What causes CNS failure in response to hemorrhage?

How does this lead to irreversible hemorrhagic shock?

A

CNS is caused by…

  • Decreased or absent sympathetic outflow

This leads to irreversible hemorrhagic shock because…

  • Intensity of compensatory mechanisms is lost
  • The body does not effectively mitigate blood loss or maintain CO/BP to perfuse tissues and brain
20
Q

What causes heart failure in response to hemorrhage?

How does this lead to irreversible hemorrhagic shock?

A

Heart failure is caused by…

  • Prolonged ischemia when MAP is low, due to hemorrage

This leads to irreversible hemorrhagic shock because…

  • Contractility decreases
  • This leads to even lower MAP
  • Tissues/brain cannot be perfused
21
Q

What causes failure of the capillary refill mechanism?

How does this lead to irreversible hemorrhagic shock?

A

Failure of the capillary refill mechanism is caused by…

  • Failure of resistance a the precapillary sphincter

This leads to irreversible hemorrhagic shock because…

  • Capillary pressure will stay high, promoting filtration out of the capillary
  • Fluid loss will continue
22
Q

What causes failure of the vasoconstrictor response?

How does this lead to irreversible hemorrhagic shock?

A

Failure of the vasoconstrictor response is caused by…

  • Neurotransmitter depletion at blood vessels

OR

  • Local metabolic signaling -> vasodilation

This leads to irreversible hemorrhagic shock because…

  • The blood vessels cannot constrict to prevent hemorrhage
  • Blood loss continues
23
Q

What is the main compensatory mechanism of the CV system in response to postural change? (Standing from sitting)

A

Baroreceptor reflex

(low volume/pressure is sensed in the heart, and the reflex works to restore both to normal)

24
Q

In immediate response to standing, how does arterial pressure change?

A

Arterial pressure decreases

The baroreceptor reflex works to restore arterial pressure to normal

25
Q

What efferent signals are mediated by the baroreceptor reflex in response to postural changes? (standing from sitting)

A

Upon standing, the baroreceptors sense decreased volume and pressure in the heart. Decreased firing of the baroreceptors signals to…

  • The heart to…
    • Increase HR
    • Increase contractility
    • Increase CO
  • The arteries to…
    • Constrict
    • Increase TPR
  • The veins to…
    • Constrict
    • Decrease unstressed volume
    • Increase venous return

All of these mechanisms work to restore arterial pressure

26
Q

What is the long term cardiovascular response to prolonged standing?

A

Filtration of fluid into the extracellular space in lower extremiteis (as a result increased hydrostatic pressure in capillaries because of gravity)

  • Decreased plasma volume
  • Edema in lower extremities