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NSCC 7320 - Critical Care Theory 3 > O2 Supply and Demand > Flashcards

O2 Supply and Demand Flashcards

1
Q

Which receptors utilize the neurotransmitters epinephrine and norepinephrine

A

adrenergic

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2
Q

What receptors are responsible for vasoconstriction when the SNS is activated

A

alpha adrenergic receptors

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3
Q

stimulation of alpha adrenergic receptors causes vasoconstriction of arterioles in what 3 things

A

skin
gut
kidneys

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4
Q

what receptors are responsible for bronchodilation and vasodilation

A

Beta 2

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5
Q

what are beta 1 adrenergic receptors responsible for (4)

A

increased HR
speed of conduction
force of contraction
automaticity of the heart

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6
Q

what is the first stage of cellular respiration

A

glycolysis

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7
Q

how much does sepsis increase resting O2 demand

A

50-100%

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8
Q

how much does a head injury increase O2 demand

A

138

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9
Q

how much does MODS increase O2 demand

A

20-80%

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10
Q

how much does shivering inc O2 demand

A

50-100%

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11
Q

how much does inc WOB inc O2 demand

A

40%

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12
Q

3 numeric values to help access O2 supply and demand

A

lactate
svO2
O2 ER

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13
Q

what is the end product of anaerobic cellular metabolism

A

lactate

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14
Q

where is ScVO2 drawn from and what does it measure

A

superior vena cava

represents O2 supply and demand from upper body as SVC drains head and upper body

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15
Q

Where is SvO2 drawn from and what does it measure

A

drawn from a PA line measures oxygen saturation returning from the whole body

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16
Q

what 4 factors influence ScvO2 and SvO2

A

arterial o2 saturation
hemoglobin
CO
tissue metabolism and O2 consumption

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17
Q

what does a high ScO2 SCVO2 mean

A

increased O2 delivery and decreased demand

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18
Q

what does a low ScO2 ScVO2 mean

A

decreased supply, increased demand

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19
Q

what is the normal value for ScO2 and ScVO2

A

60-80%

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20
Q

how much lower is SvO2 the ScvO2

A

5%

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21
Q

what does an oxygen extraction ratio represent

A

systemic balance between supply and demand

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22
Q

what is the extraction ratio formula

A

((SaO2 - SvO2)/ SaO2 )x 100

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23
Q

what is the normal ER

A

25%

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24
Q

what ER do we air for in critical illness

A

25-35%

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25
Q

what is the process by which the liver produces glucose from noncarbohydrate sources primarily amnio acids

A

gluconeogenesis

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26
Q

what is the process in the liver in which glycogen is broken down into glucose

A

glycogenolysis

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27
Q

What is the role of cortisol (6)

A 
glucose metabolism
anti-inflammatory action
fat metabolism
protein metabolism
psychic effect
permissive effect
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28
Q

What does cortisol do in terms of glucose metabolism

A

stimulates gluconeogenesis to increase blood glucose levels

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29
Q

What does cortisol do in terms of protein metabolism

A

increases breakdown of proteins and plasma protein levels

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30
Q

What does cortisol do in terms of fat metabolism

A

incrases mobilization and utilization of fatty acids

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31
Q

What does cortisol do in terms of anti-inflammatory actions (5)

A

prevents release of inflammatory mediators

decrease capillary permeability

Decreases WBC fn

suppresses the immune response

reduces fever

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32
Q

What does cortisol do in terms of psychic effect

A

contributes to emotional stability

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33
Q

What does cortisol do in terms of permissive effect

A

facilitates the response of tissues to catecholamines during extreme stress
i.e contractility, vascular tone, BP

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34
Q

the primary source for gluconeogenesis during critical illness is

A

protein

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35
Q

T or F hypoglycemia is common in critical illness

A

F

hyperglycemia is common

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36
Q

6 factors contributing to hyperglycemia in the critically ill

A 
increased cortisol levels
catecholamines
glucagon levels
gluconeogenesis and glycogenolysis
insulin resistance develops in critically ill
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37
Q

2 benefits of cortisol in critical illness

A

facilitates response of tissues to epi and norepi

promotes maintenance of contractility, vascular tone and BP

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38
Q

what type of receptors are involved in the SNS and PNS

A

SNS - adrenergic

PNS - cholinergic

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39
Q

name 2 catecholamines

A

epinephrine and norepinephrine

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40
Q

what is the purpose of the neuroendocrine system

A

hypothalamus maintains homeostasis and regulates metabolism, energy utilization BP etc

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41
Q

what are we focusing on for the neuroendocrine system

A

HPA axis

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42
Q

what does HPA axis stand for

A

hypothalamic-pituitary-adrenal axis

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43
Q

How is the HPA axis activated

A

by stress

44
Q

what are the 3 steps invovled in the HPA axis to produce cortisol

A

(1) stress stimulates the hypothalamus to release corticotrophin-releasing hormone (CRH)
(2) CRH stimulates the anterior pituitary gland to release adrenocorticotrophic hormone (ACTH)
(3) ACTH stimulates the adrenal cortex to release cortisol

45
Q

what can happen to cortisol in critical illness

A

prolonged stress response can cause adrenal exhaustion/insufficiency

46
Q

what can cause adrenal insufficiency

A

Ca
trauma
infections

47
Q

how does adrenal insufficiency present

A

hemodynamic instability unresponsive to inotropes or pressers

48
Q

what tests can you do to test for adrenal insuffiency

A

random cortisol level

ACTH test to evaluate adrenal fn

49
Q

how is adrenal insufficiency treated

A

hydrocortisone

50
Q

what is important to remember when giving a pt hydrocoritone

A

to taper doses as it suppresses HPA axis reducing endogenous supply of cortisol

51
Q

what is ADH do and where is it released from

A 
Antidiuretic hormone (vasopressin)
released from posterior pituatrary after stimulation from hypothalamus
52
Q

what are the 2 fn of ADH

A

increases H2O reabsorption in kidneys (preload)

vasoconstriction (afterload)

53
Q

what does aldosterone do

A

regulates fluid balance by retaining Na in nephron - fluid retention (preload)

54
Q

where is aldosterone released from and what is it stimulated by

A

adrenal cortex

ACTH and RAAS

55
Q

Where is glucagon released from

A

alpha cells in pancreas

56
Q

what does glucagon do

A

stimulates liver to release glucose from glycogen reserves and gluconeogenesis

57
Q

T or F in critical illness the body is in a state of hypermetabolism

A

true

58
Q

t or f glycogenolysis is a long term response

A

false

short term response once stores run out begins to use fat and protein (skeletal muscle) as fuel

59
Q

what time frame does evidence suggest is best with regards to feeding the critically ill

A

need to be fed as early as possible within 24-72 hours

60
Q

what is the difference between the overall caloric and protein requirements between a healthy adult and a critically ill adult

A

healthy .8g/kg/day

critically ill 1.5-2g/kg/day

61
Q

what can happen if we overfeed our pts

A

excessive CO2 production from carbohydrates
insulin resistance
hyperglycemia

62
Q

what is the goal CBG for critically ill patients on insulin infusion

A

4-10

63
Q

what volume ideally should gastric residuals be maintained below

A

100

64
Q

what common motility agent is given to critically ill patietns

A

metoclopramide

65
Q

what patients are at risk for refeeding syndrome when starting feeds

A

malnourished pateints

66
Q

what occurs in refeeding syndrome

A

glucose levels increase as pt begins receiving nutrition
insulin secretion increases to reduce glucose, increasing uptake into cells
glucose takes PO4, Mg, and K along with it resuling in low Mg, PO4 and K

67
Q

what are complications of refeeding syndrome to monitor for what are they caused by

A 
neurological dysfunction
neuromuscular dysfunction
respiratory dysfunction
cardiac dysfunction/arrhythmias
increased intravascular volume/heart failure

fluid and lyte shifts

68
Q

how is refeeding syndrome treataed

A

thimaine, vit B complex, MV

replace lytes aggressively

69
Q

What acronym is used for metabolic increase in O2 demand in critical care

A

PADS

70
Q

what does PADS stand for

A

pain
anxiety
delirium
sleep issues

71
Q

T or F critically ill patients are often hypersensitive and undermedicated for pain

A

true

72
Q

are VS a reliable indicator of pain

A

no

73
Q

what 3 tools can be used in the critical care setting to assess pain

A

CPOT -critical care pain observation tool
BPS - behavioral pain scale
ventilation compliance

74
Q

what is the difference between anxiety and agitation

A

anxiety - subjective experience

agitation - hyperactive movements, physical agression

75
Q

what can be used to assess for anxiety and agiation in pts that are unable to self-reports

A

RASS - richmond agitation and sedation scale

76
Q

what does a RASS score of +4 mean? 0? -5?

A

+4 - combaitve and immediate danger to staff
0 alert and calm
-5 no response to voice or physical stimulation

77
Q

does propofol have an effect on pts diet

A

yes - has caloric effects as it is a lipid emulsion

78
Q

what are two side effects of precedex

A

hypotension

bradycardia

79
Q

what does delirium do to O2 demand? Why?

A

increase as it contributes to continued activation of neuroendocrine response to stress resulting in increased metabolic and O2 demand

80
Q

how can you assess for delirium

A

CAM score or intensive care delirium screening checklist

81
Q

what are some non-pharmolgical approaches to managing delirium

A

early mobilization

normalizing icu environment

82
Q

what are some common pharacological approaches

A

haldol

queitapine

83
Q

what can sleep deprivation activate

A

stress response - inc metabolic rate and catabolism

84
Q

what are 3 things sleep deprivation can affect

A

memory
attention
concentration

85
Q

what is a primary factor in delirium

A

loss of natural circadian rhythms

86
Q

what are 3 ways we can help maintain natural circadian rhythms

A

promote regular day/night routines
limit care during night
limit noise

87
Q

what is a depolarizing NMBA and how does it work

give an example

A

Acetylcholine agonist - binds to acetylcholine receptors and depolarizes the cell but does not allow for repolarization
ex. succinylcholine

88
Q

what is a non-depolarizing NMBA and how does it work, give an example

A

acetylcholine antagonist - binds competitively to muscle cells blocking acetylcholine from depolarizing the cell
ex. rocc

89
Q

what type of NMBA is contraindicated in severe renal impairment

A

depolarizing NMBA i.e. succ

90
Q

what are 3 common situations in which NMBA are used

A

RSI
shivering
ventilator synchrony

91
Q

what drugs should be avoided with NMBA

A

corticosteroids d/t synergistic effects

92
Q

what test can be done to assess effectiveness of NMBA

A

train of four (TOF)
peripheral nerve stimulator which delivers shocks to stimulate thumb counting number of blocked stimuli tells you about effectiveness

93
Q

T or F NMBA allos for unconventional methods of ventilation

A

T

94
Q

T or F hyper and hypothermia are regulated by the hypothalamus

A

false

95
Q

T or F Fever is regulated by the hypothalamus

A

true

96
Q

what is fever caused by

A

cytokine release causing increase in hypothalamic temp set point

97
Q

why does fever cause vasodilation

A

to radiate heat and cool off

98
Q

how does tylenol cause hypotension

A

systemic vasodilation increases vasuclar space, decreases venous return

99
Q

How does hyperthermia result

A

inability to vasodilate and sweat

100
Q

is hyperthermia treatable with antipyretics

A

no

101
Q

what does hypothermia result from

A

inability to conserve or produce heat

102
Q

what are 3 non-phamalogical approaches to managing fever

A

fan
tepid sponge
removal of blankets

103
Q

what are the 3 phases of induced hypothermia

A

induction
maintenance
rewarming

104
Q

what are 4 challenges in induction of hypothermia

A

electrolyte shifting: serum K, Mg and Ca decreases
bradydysrhtmias prolonged PR and QRS
coagulopathy
shivering NMBA

105
Q

what are 3 challenges in rewarming

A

electrolyte shifts inc K Mg and Ca
increased cellular metabolism - increase glucose in cell (hypoglycemia)
ST elevation from transiet acidosis from reperfusion
vasodilation –> hypovolemia

NSCC 7320 - Critical Care Theory 3 (5 decks)

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