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PHYSIOLOGY Exam 3 (Lauren) > Exercise and Shock > Flashcards

Exercise and Shock Flashcards

1
Q

Is homeostasis disrupted during exercise?

A

Yes, and the body must make adjustments

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2
Q

What is VO2?

A

Oxygen consumption

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3
Q

Is maximum HR a function of age or training?

A

Age

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4
Q

Does HR increase linearly with exercise?

A

Yes

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5
Q

SV ____ at low intensity, but _____ at highest work loads

A

Increases, plateaus

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6
Q

What causes the plateau in SV at high intensity exercise?

A

Reduced ventricular filling time

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7
Q

What is the a-v difference?

A

It is the difference between the volume percent of blood that is O2 when it leaves the heart vs when it returns to the heart.

(Ex: at rest, it is usually 20% O2 by volume when it leaves the heart, and it is 15% O2 when it returns to the heart)

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8
Q

What does exercise do to a-v difference?

A

It increases it

More O2 gets transferred to the tissues

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9
Q

At rest, skeletal muscle receives 20% of CO. What happens during exercise’

A

Blood gets redistributed to the muslce and skin at the expense of the viscera (May gets up to 85% of CO)

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10
Q

Does blood ever get redirected away from the heart and brain during exercise in order to supply the muscle?

A

No, it will actually increase

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11
Q

Why does the skin get more blood flow during exercise

A

So that we can release heat

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12
Q

What effect does exercise have on TPR?

A

It drops! This is becasue the skeletal muscles are vasodilated due to all the local metabolites they release

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13
Q

As metabolic rate increases, TPR ______

A

Decreases

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14
Q

Exercise causes decreased TPR, but MAP increases! Why?

A

Due to the increased CO

MAP= CO x TPR

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15
Q

What happens to diastolic pressure during exercise?

A

Doesn’t change much

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16
Q

What happens to systolic and MAP during exercise?

A

Increase

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17
Q

Why does diastolic pressure stay the same during exercise? Increased HR should increase DP due to less time for runoff between beats!

A

The decreased TPR cancels out the effects of the increased HR, so DP stays about the same

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18
Q

What happens to resting HR in a trained athlete?

A

Decreases due to greater vagal tone and reduced SNS tone

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19
Q

If resting HR is lower in trained athletes, does their CO decrease?

A

No, it is maintained by an increased SV

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20
Q

Why does endurance training increase stroke volume both at rest and during exercise?

A

Increased heart size

Decreased HR which allows for greater filling

Increased contractility due to enhanced Ca++ release

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21
Q

What happens to total blood volume with endurance training?

A

Increases

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22
Q

Why does total blood volume increase in trained athletes ?

A

Increase in plasma volume

+minor increases in cell volume

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23
Q

Why would a trained athlete have a LOWER hematocrit than a nontrained person?

A

They have increased plasma volume, so therefore the percent of their blood that is RBCs is decreased

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24
Q

What is the benefit for trained athletes to have increased blood volume if its just plasma?

A

It provides cardiovascular stability during exercise:
-reduces cardiovascular drift

-fluid volume lost through sweat doesn’t impact venous return too much

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25
Q

Sweatinf during exercise has what effect on venous return?

A

Decreases venous return which reduces SV, and HR must increase even more to maintain CO

(Trained athletes with more plasma will be affected by this less)

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26
Q

Who will have a higher VO2 max and CO: sedentary person or athlete?

A

Athlete

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27
Q

How do people’s bodies acclimatize to high altitudes?

A

Respiratory: hyperventilation

Circulatory: polycythemia and an increase in 2,3 DPG in RBCs

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28
Q

What does 2,3 DPG do?

A

It enhances unloading of O2 in tissues

Decreases Hb’s affinity for O2

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29
Q

Who has lots of 2,3 DPG

A

People at high altitudes

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30
Q

What causes an increased RBC concentration in the blood?

A

EPO release by the kidney

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31
Q

What is the downside to polycythemia?

A

Increased blood viscosity

32
Q

What effect does blood viscosity have on afterload on the heart?

A

Afterload increases

33
Q

What happens to capillary density in peripheral tissues at high altitudes?

A

Increases

Via atrophy of muscle mass not increase of capillaries

34
Q

Do people at high altitudes have pulmonary hypertension?

A

Yes and it develops right away

35
Q

What causes pulmonary hypertension at high altitudes?

A

Hypoxic vasoconstricion of pulmonary vasculature

36
Q

What is one of the problems that can happen due to chronic pulmonary hypertension?

A

Right heart hypertrophy

37
Q

What is meant by hypoxic vasoconstricion in the lungs?

A

Blood is directed away from poorly ventilated alveolar units toward the better ventilated units

At high altitudes though, ALL of the alveolar units are poorly ventilated, so ALL of them get decreased blood flow via vascular constriction

(Can you see why this would cause pulmonary hypertension??)

38
Q

What is meant by a global hypoxic vasoconstriction at high altitudes?

A

Normally hypoxic vasoconstriction would happen if you had a mucus plug or something, but at high altitides, ALL of your alveolar units are “poorly ventilated” so the body will decrease blood flow to all of them via vasoconstriction

=pulmonary hypertension

39
Q

Other than high altitudes, when else might we see global hypoxic vasoconstriction to all the alveoli?

A

COPD

Fetuses (needs minimal blood flow to the lungs while they’re in the womb)

40
Q

What is circulatory shock?

A

Failure of the circulation with decreased perfusion and/or inadequate oxygenation of the vital organs and cells of the body

41
Q

What is the cardinal feature of circulatory shock?

A

Inadequate tissue perfusion

42
Q

What is carcinogenic shock?

A

Pump is broken due to heart attack

Might be a late development in hypovolemic and septic shock

43
Q

What is hypovolemic shock?

A

Fall in CO and MAP is due to a decrease in circulating blood volume

44
Q

What is septic shock?

A

Bacterial infection causes the release of mediators into the blood stream that ends up with blood flow to the tissues being maladjusted (too much in certain areas, too little in others)

45
Q

Can hypovolemic shock be causes by loss of plasma?

A

Yes, for example burns

46
Q

How do you fix hypovolemic shock

A

Blood/fluid transfusion

47
Q

What will happen to HR and contractility in hypovolemic shock?

A

Increased HR and heart contractility

48
Q

What will happen to the “unstressed” and “stressed” volumes of blood as the body tries to compensate for hypovolemic shock?

A

Veins will constrict to increase venous return, and therefor the unstressed volume of blood will decrease and the stressed volume of blood will increase

49
Q

What happens to the blood flow to the skin, gut, and kidneys as the body tries to compensate for hypovolemic shock?

A

Decreased

50
Q

Would action potential frequency from a baroreceptor to the NTS be increased or decreased in hypovolemic shock?

A

Decreased.

AP frequency increases with STRETCH***** Hypovolemic shock would do the opposite

51
Q

How does the NTS try to defend blood pressure in hypovolemic shock?

A

Via SNS

52
Q

When the body tries to compensate for slow blood loss, what happens to CO and MAP?

A

CO will fall (venous return is dimished)
MAP will remain stable due to increasing TPR

(MAP=CO x TPR)

53
Q

When would you see the CNS ischemic reflex?

A

When the MAP drops very low to about 50-60mmHg

It is a last ditch effort

54
Q

Since MAP may look normal with gradual blood loss, what should we look at instead?

A

HR, CVP, or urine output

55
Q

What is the CNS ischemic reflex?

A

It is a burst of SNS activity when blood pressure in the brain becomes too low.

CV centers in the NTS activate the SNS.

CO and TPR increase, leading to an increase in MAP

It is a last ditch effort to maintain cerebral perfusion

(Very bad sign because it happens when blood volume gets very low)

56
Q

In severe shock, TPR _____

A

Doubles

57
Q

What are the ways that the SNS response increase TPR to maintain CO during severe shock?

A
  • cutaneous blood flow decreased which results in pallor
  • renal vasoconstriction- oliguria/anuria
  • skeletal muscle and splanchnic vasoconstriction-mobilizes blood from these reservoirs
58
Q

What happens to the hydrostatic pressure in the capillaries during hemorrhage as a compensation mechanism?

A

It decreases in order to promote absorption from the interstitial fluid

59
Q

What are 2 effects of renal vasoconstriction during hemorrhage?

A

Reduces urine output

Activates the renin-angiotensin-aldosterone mechanism

60
Q

Does the body release vasopressin/ADH during hemorrhage?

A

Yes

61
Q

What are the two effects of vasopressin/ADH?

A
  1. Enhances water reabsorption from kidneys

2. Vasoconstrics

62
Q

What causes septic shock?

A

Profound Generalized Vasodilation in response to an infection*****

63
Q

How will someone in shock try to compensate for the decline in TPR?

A

Increased CO due to increased HR**

increased Central venous pressure

Hyperventilation

64
Q

Why do septic pts sometimes present with warm, flushed skin?

I thought they were in shock??!!

A

The cutaneous vessels are dilated initially

Skin will cool as shock progresses**

65
Q

What causes the widespread symptoms of septic shock?

A

Lipopolysachharides/endotoxins in the cell walls of the bacteria

66
Q

What are some of the specific effects of bacterial endotoxins that lead to the development of septic shock?

A
  • formation of kinins and prostaglandins that injure the vessel walls and increase permeability
  • cytokines stimulate the release of NO (local vasodilator)
  • direct myocardial depression (MDS) - suffering heart muscle! :(
67
Q

What are the 3 stages of shock?

A
  1. Nonprogressive
  2. Progressive
  3. Irreversible
68
Q

What happens in nonprogressive shock?

A

MAP returns to normal, body compensated on its own

69
Q

What is progressive shock?

A

Continued deterioration of the circulatory system. Positive feedback loops develop, and the patient requires some sort of intervention to recover BP and CO.

70
Q

What is irreversible/refractory shock?

A

Shock that is too far progressed, despite intervention to disrupt positive feedback loops, this person will die

71
Q

What happens in the fatal circulatory loop of progressive shock?

A

Severe shock -> severe hypotension and tachycardia —> coronary blood flow is reduced —> further depression of myocardial function —> severe hypotension and tachycardia and it keeps going

This death spiral is a Positive feedback loop**

72
Q

What is the fatal cerebral ischemic loop of progressive shock?

A

Severe shock —> MAP below 40mmHg —> severe cerebral ischemia —> depression of vasomotor areas —> vasodilation and lower HR —> further depression of BP and cerebral flow —> severe cerebral ischemia etc etc until you die

This death spiral is a positive feedback loop**

73
Q

What is the reason for irreversible shock despite intervention?

A

Underperfused tissues release substances that permanently damage the heart and vascular system

-myocardial depressant substances (MDS) basically kill the heart and have a negative inotropic effect

74
Q

What is the treatment of shock?

A
  • fluid replacement which increases central venous pressure and increases ventricular function via the starling mechanism
  • restoring tissue perfusion- pressors, supplemental O2,
75
Q

Which pressor is no longer used for shock?

A

Dopamine

76
Q

Which pressors are used in the treatment of shock?

A

Norepinephrine

May add epinephrine and vasopressin

PHYSIOLOGY Exam 3 (Lauren) (10 decks)

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