O2 Supply and Demand Flashcards
Which receptors utilize the neurotransmitters epinephrine and norepinephrine
adrenergic
What receptors are responsible for vasoconstriction when the SNS is activated
alpha adrenergic receptors
stimulation of alpha adrenergic receptors causes vasoconstriction of arterioles in what 3 things
skin
gut
kidneys
what receptors are responsible for bronchodilation and vasodilation
Beta 2
what are beta 1 adrenergic receptors responsible for (4)
increased HR
speed of conduction
force of contraction
automaticity of the heart
what is the first stage of cellular respiration
glycolysis
how much does sepsis increase resting O2 demand
50-100%
how much does a head injury increase O2 demand
138
how much does MODS increase O2 demand
20-80%
how much does shivering inc O2 demand
50-100%
how much does inc WOB inc O2 demand
40%
3 numeric values to help access O2 supply and demand
lactate
svO2
O2 ER
what is the end product of anaerobic cellular metabolism
lactate
where is ScVO2 drawn from and what does it measure
superior vena cava
represents O2 supply and demand from upper body as SVC drains head and upper body
Where is SvO2 drawn from and what does it measure
drawn from a PA line measures oxygen saturation returning from the whole body
what 4 factors influence ScvO2 and SvO2
arterial o2 saturation
hemoglobin
CO
tissue metabolism and O2 consumption
what does a high ScO2 SCVO2 mean
increased O2 delivery and decreased demand
what does a low ScO2 ScVO2 mean
decreased supply, increased demand
what is the normal value for ScO2 and ScVO2
60-80%
how much lower is SvO2 the ScvO2
5%
what does an oxygen extraction ratio represent
systemic balance between supply and demand
what is the extraction ratio formula
((SaO2 - SvO2)/ SaO2 )x 100
what is the normal ER
25%
what ER do we air for in critical illness
25-35%
what is the process by which the liver produces glucose from noncarbohydrate sources primarily amnio acids
gluconeogenesis
what is the process in the liver in which glycogen is broken down into glucose
glycogenolysis
What is the role of cortisol (6)
glucose metabolism anti-inflammatory action fat metabolism protein metabolism psychic effect permissive effect
What does cortisol do in terms of glucose metabolism
stimulates gluconeogenesis to increase blood glucose levels
What does cortisol do in terms of protein metabolism
increases breakdown of proteins and plasma protein levels
What does cortisol do in terms of fat metabolism
incrases mobilization and utilization of fatty acids
What does cortisol do in terms of anti-inflammatory actions (5)
prevents release of inflammatory mediators
decrease capillary permeability
Decreases WBC fn
suppresses the immune response
reduces fever
What does cortisol do in terms of psychic effect
contributes to emotional stability
What does cortisol do in terms of permissive effect
facilitates the response of tissues to catecholamines during extreme stress
i.e contractility, vascular tone, BP
the primary source for gluconeogenesis during critical illness is
protein
T or F hypoglycemia is common in critical illness
F
hyperglycemia is common
6 factors contributing to hyperglycemia in the critically ill
increased cortisol levels catecholamines glucagon levels gluconeogenesis and glycogenolysis insulin resistance develops in critically ill
2 benefits of cortisol in critical illness
facilitates response of tissues to epi and norepi
promotes maintenance of contractility, vascular tone and BP
what type of receptors are involved in the SNS and PNS
SNS - adrenergic
PNS - cholinergic
name 2 catecholamines
epinephrine and norepinephrine
what is the purpose of the neuroendocrine system
hypothalamus maintains homeostasis and regulates metabolism, energy utilization BP etc
what are we focusing on for the neuroendocrine system
HPA axis
what does HPA axis stand for
hypothalamic-pituitary-adrenal axis
How is the HPA axis activated
by stress
what are the 3 steps invovled in the HPA axis to produce cortisol
(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
what can happen to cortisol in critical illness
prolonged stress response can cause adrenal exhaustion/insufficiency
what can cause adrenal insufficiency
Ca
trauma
infections
how does adrenal insufficiency present
hemodynamic instability unresponsive to inotropes or pressers
what tests can you do to test for adrenal insuffiency
random cortisol level
ACTH test to evaluate adrenal fn
how is adrenal insufficiency treated
hydrocortisone
what is important to remember when giving a pt hydrocoritone
to taper doses as it suppresses HPA axis reducing endogenous supply of cortisol
what is ADH do and where is it released from
Antidiuretic hormone (vasopressin) released from posterior pituatrary after stimulation from hypothalamus
what are the 2 fn of ADH
increases H2O reabsorption in kidneys (preload)
vasoconstriction (afterload)
what does aldosterone do
regulates fluid balance by retaining Na in nephron - fluid retention (preload)
where is aldosterone released from and what is it stimulated by
adrenal cortex
ACTH and RAAS
Where is glucagon released from
alpha cells in pancreas
what does glucagon do
stimulates liver to release glucose from glycogen reserves and gluconeogenesis
T or F in critical illness the body is in a state of hypermetabolism
true
t or f glycogenolysis is a long term response
false
short term response once stores run out begins to use fat and protein (skeletal muscle) as fuel
what time frame does evidence suggest is best with regards to feeding the critically ill
need to be fed as early as possible within 24-72 hours
what is the difference between the overall caloric and protein requirements between a healthy adult and a critically ill adult
healthy .8g/kg/day
critically ill 1.5-2g/kg/day
what can happen if we overfeed our pts
excessive CO2 production from carbohydrates
insulin resistance
hyperglycemia
what is the goal CBG for critically ill patients on insulin infusion
4-10
what volume ideally should gastric residuals be maintained below
100
what common motility agent is given to critically ill patietns
metoclopramide
what patients are at risk for refeeding syndrome when starting feeds
malnourished pateints
what occurs in refeeding syndrome
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
what are complications of refeeding syndrome to monitor for what are they caused by
neurological dysfunction neuromuscular dysfunction respiratory dysfunction cardiac dysfunction/arrhythmias increased intravascular volume/heart failure
fluid and lyte shifts
how is refeeding syndrome treataed
thimaine, vit B complex, MV
replace lytes aggressively
What acronym is used for metabolic increase in O2 demand in critical care
PADS
what does PADS stand for
pain
anxiety
delirium
sleep issues
T or F critically ill patients are often hypersensitive and undermedicated for pain
true
are VS a reliable indicator of pain
no
what 3 tools can be used in the critical care setting to assess pain
CPOT -critical care pain observation tool
BPS - behavioral pain scale
ventilation compliance
what is the difference between anxiety and agitation
anxiety - subjective experience
agitation - hyperactive movements, physical agression
what can be used to assess for anxiety and agiation in pts that are unable to self-reports
RASS - richmond agitation and sedation scale
what does a RASS score of +4 mean? 0? -5?
+4 - combaitve and immediate danger to staff
0 alert and calm
-5 no response to voice or physical stimulation
does propofol have an effect on pts diet
yes - has caloric effects as it is a lipid emulsion
what are two side effects of precedex
hypotension
bradycardia
what does delirium do to O2 demand? Why?
increase as it contributes to continued activation of neuroendocrine response to stress resulting in increased metabolic and O2 demand
how can you assess for delirium
CAM score or intensive care delirium screening checklist
what are some non-pharmolgical approaches to managing delirium
early mobilization
normalizing icu environment
what are some common pharacological approaches
haldol
queitapine
what can sleep deprivation activate
stress response - inc metabolic rate and catabolism
what are 3 things sleep deprivation can affect
memory
attention
concentration
what is a primary factor in delirium
loss of natural circadian rhythms
what are 3 ways we can help maintain natural circadian rhythms
promote regular day/night routines
limit care during night
limit noise
what is a depolarizing NMBA and how does it work
give an example
Acetylcholine agonist - binds to acetylcholine receptors and depolarizes the cell but does not allow for repolarization
ex. succinylcholine
what is a non-depolarizing NMBA and how does it work, give an example
acetylcholine antagonist - binds competitively to muscle cells blocking acetylcholine from depolarizing the cell
ex. rocc
what type of NMBA is contraindicated in severe renal impairment
depolarizing NMBA i.e. succ
what are 3 common situations in which NMBA are used
RSI
shivering
ventilator synchrony
what drugs should be avoided with NMBA
corticosteroids d/t synergistic effects
what test can be done to assess effectiveness of NMBA
train of four (TOF)
peripheral nerve stimulator which delivers shocks to stimulate thumb counting number of blocked stimuli tells you about effectiveness
T or F NMBA allos for unconventional methods of ventilation
T
T or F hyper and hypothermia are regulated by the hypothalamus
false
T or F Fever is regulated by the hypothalamus
true
what is fever caused by
cytokine release causing increase in hypothalamic temp set point
why does fever cause vasodilation
to radiate heat and cool off
how does tylenol cause hypotension
systemic vasodilation increases vasuclar space, decreases venous return
How does hyperthermia result
inability to vasodilate and sweat
is hyperthermia treatable with antipyretics
no
what does hypothermia result from
inability to conserve or produce heat
what are 3 non-phamalogical approaches to managing fever
fan
tepid sponge
removal of blankets
what are the 3 phases of induced hypothermia
induction
maintenance
rewarming
what are 4 challenges in induction of hypothermia
electrolyte shifting: serum K, Mg and Ca decreases
bradydysrhtmias prolonged PR and QRS
coagulopathy
shivering NMBA
what are 3 challenges in rewarming
electrolyte shifts inc K Mg and Ca
increased cellular metabolism - increase glucose in cell (hypoglycemia)
ST elevation from transiet acidosis from reperfusion
vasodilation –> hypovolemia
