O2 Demand Flashcards
1
Q
what makes up O2 demand?
A
metabolic demands - temp, physical activity, and stress
2
Q
what are the two subdivisions of the autonomic nervous system?
A
1) parasympathetic nervous system (cholinergic receptors; rest and digest)
2) sympathetic nervous system (adrenergic receptors; fight or flight)
3
Q
what receptors are responsible for vasoconstriction of arterioles in skin/gut/kidneys when the SNS is activated?
A
alpha adrenergic receptors
4
Q
beta 2 receptors
A
- located in lungs and skeletal muscle
- cause bronchodilation and vasodilation
5
Q
beta 1 receptors
A
- in heart (SA node, AV node, and myocardium)
- increased HR, conductivity, automaticity, force of contraction
6
Q
in the healthy person, the SNS is designed to?
A
support increased cellular metabolism and energy production for the increased work the body has to do to respond to the threat of stress (short term)
7
Q
SNS short facts
A
- fight or flight meant for short term
- critical illness can be longer term therefore puts SNS in overdrive
- huge increase in cellular metabolism and oxygen demand
- in critical illness not everyone has O2 supply to meet demand
8
Q
what state are we in during critical illness?
A
state of hypermetabolic demand
9
Q
what is cellular metabolism?
A
- the chemical tasks of maintaining essential cellular fx
- provides the cell with the energy it needs
- ATP is produced as intracellular energy and is used as primary energy source
- specific metabolic pathway are used for prod of ATP
10
Q
for most efficient ATP production ____ is needed which is ____
A
oxygen, aerobic metabolism
11
Q
when oxygen delivery to cell is insufficient or delayed, the cell switches to ____
A
anaerobic metabolism
12
Q
what makes up ATP
A
food and oxygen
13
Q
how much ATP does aerobic metabolism produce?
A
36 ATP
14
Q
how much ATP is created from anaerobic metabolism?
A
2 ATP
15
Q
what happens when critically ill patients remain in a state of constant SNS activation over days, weeks?
A
prolonged massive increase in cellular metabolism and O2 demand
16
Q
what leads to hypermetabolic demand?
A
critical illness > activation of SNS > increased metabolic demands > increased O2 demands
17
Q
interventions to reduce demand
A
- intubation
- mechanical vent
- sedatives
- paralysis
- bedrest
- cooling
18
Q
activities that increased demand
A
- bath
- dressing change
- assessments
- ECG
- position change
- weighing in a sling scale
- CXR
- ETT suctioning
19
Q
conditions that increase demand
A
- burns
- sepsis
- severe infection
- head injury, pt not sedated
- skeletal injuries
- chest trauma
- MODS
- fever
- increased WOB
20
Q
assessing O2 supply and demand balance
A
- assess end organ perfusion (comprehensive ax, signs of poor EOP, evidence of imbalance)
- assess global oxygenation parameters (lactate, ABGs, ScVO2 + O2ER)
21
Q
end organs
A
- brain
- heart
- lungs
- GI tract
- liver
- kidneys
- skin
- global
22
Q
brain
A
LOC is most sensitive parameter for evaluating cerebral perfusion and O2 supply
- decreased LOC
- restlessness
- agitation
- coma
23
Q
heart
A
signs of ischemia alert us to imbalance
- chest pain
- SOB
- ECG changes
- increased cardiac biomarkers
24
Q
lungs
A
inadequate pulm perfusion will result in poor gas exchange and decrease SaO2 and PaO2
- poor gas exchange, decreased resp muscle fx r/t perfusion to resp muscles
25
GI tract
decreased gut fx will result from poor gut perfusion
- decreased GI motility
- abdo pain
- nausea/vomiting/high gastric residuals
- ischemic bowel
26
liver
responsible for metabolic, filtration, detox and storage functions
- increased INR and PTT
- increased LFTs (ALT - high specificity for liver)
27
kidneys
renal lab tests and urine output provide info about renal perfusion
- BUN/urea
- creatinine
- urine output
28
skin
observation and palpation can provide info about perfusion to skin
- skin temp: cool, cold
- colour: cyanosis, mottling, pallor
- pulse strength: +1, by doppler, absent
- cap refill: >= 3 seconds
29
overall markers of EOP
markers of global EOP such as lactate, O2ER, and ScVO2 reflect that overall ability of O2 supply to meet O2 demand
- increased serum lactate
- decreased ScVO2
- elevated O2ER
- metabolic acidosis
30
assessment parameter: EOP
info provided:
physical ax data and system specific lab data provides indication of adequacy of fx in specific physiologic systems. adequate fx indicates O2 supply and demand balance
31
assessment parameter: serum lactate
info provided:
normal values:
info provided: reflects systemic O2 S+D balance and adequacy of tissue oxygenation
normal values: 0.9-1.8 mmol/LI
32
assessment parameter: ABG
info provided:
normal values:
info provided: metabolic acidosis reflects inadequate cellular oxygenation and O2 S+D imbalance
normal values: pH 7.35-7.45, base excess/deficit +/-2
33
assessment parameter: ScVO2 and Svo2
info provided:
normal values:
info provided: reflects systemic O2 S+D balance and adequacy of tissue oxygenation
normal values: 60-80%
34
assessment parameters: O2ER
info provided:
normal values:
normal values: 25-35%
35
lactate
- end product of anaerobic cellular metabolism
- elevated = O2 S+D imbalance; inadequate O2 supply and impaired cellular oxygenation; results in lactic acidosis
36
venous oxygen saturation
- % of O2 bound to Hgb in venous blood returning to the heart (leftover oxygen)
- affected by O2 supply and consumption
- a reflection of supply and demand balance and global tissue oxygenation
37
ScVO2 - venous gas
- sample is taken from distal tip of CVC line in the SVC
- SVC drains blood from brain and upper body
- represents O2 sats in central venous system
38
SVO2 - mixed venous
- sample is taken from distal tip of pulmonary artery catheter
- collects venous blood from entire body; mix of venous blood from all over body including coronaries
39
what is the normal value for ScVO2?
60-80% but goals for pt may vary depending on clinical site and presentation
40
is SVO2 typically higher or lower than ScVO2? why?
typically 5% lower b/c deoxygenated blood from coronary circulation
41
factors that influence venous oxygenation
- arterial O2 sats
- Hgb
- cardiac output
- tissue metabolism and O2 consumption
42
when might you have high SvO2/ScVO2 >80%?
- increased O2 delivery (increased FiO2)
- decreased O2 demand (heavy sedation, anesthesia, NMBA)
43
what would cause low ScVO2/ScVO2 <60%?
- tissues are extracting higher percentage than normal
- decreased O2 supply, CO, SaO2, Hgb
- increased O2 demand
44
oxygen extraction ratio
- reflects systemic balance between supply and demand
- relative to CO and SaO2 and is time specific
- takes into account O2 supply at a specific point in time when the sample is taken
- utilizes arterial O2 sats and venous O2 sats
- tells us how much O2 tissues are extracting
45
equation for O2ER
O2ER = (SaO2 - SvO2)
-------------------- x 100
Sao2
46
what value do we aim for with O2ER?
25-35%; need to determine if supply or demand is the issue
47
SaO2 and ScVO2 are used to...
calculate how much O2 is being extracted from the arterial supply by the end organs
48
how do you obtain an O2ER?
1. ensure pt has CVC in internal jugular or subclavian vein
2. draw a venous gas from the CVC at the same time as drawing an ABG from the ART line
3. when gases have resulted, pull the correct numbers (SaO2 and ScVO2)
*remember ratio represents a single point in time
49
with an O2ER >35%...
body requires more of the available O2 to meet demand
supply decreased, demand increased
50
with a low O2ER <25%...
the body requires less of the available O2 to meet demand
supply increased, demand decreased
51
what is important to do once you have your O2ER?
is there a problem with supply and demand? what is it? is it supply or demand that's an issue? look at comprehensive ax. do we need to intervene with supply or demand. trend values to determine if the interventions are effective.
52
neuroendocrine system
- network of cells throughout the body
- cell structure similar to neurons
- cells receive electrical/chemical signals from the nervous system and blood stream and produce hormones in response
- 8 glands
- hypothalamus is the master (maintains homeostasis; regulates metabolism, energy utilization, BP, mood, and other functions)
53
what is the neuroendocrine response?
- response to critical illness
- releases several hormones
- integration of the nervous system with NTs/and the endocrine system and their release of hormones
54
what hormone is produced by the adrenal glands and is essential for survival
cortisol
55
HPA axis
- hypothalamic-pituitary-adrenal axis
- mechanism by which hypothalamus maintains homeostasis and regulates metabolism, energy utilization, BP, mood and other functions
- designed for short term threats only
56
HPA axis steps
1. stress
2. threat is processed through signals starting in amygdala then hypothalamus
3. hypothalamus releases CRH to the pituitary gland
4. pituitary gland is stimulated to release ACTH into the bloodstream
5. adrenal glands are stimulated to release cortisol as well as epi/norepi
6. cortisol signals the hypothalamus to stop producing CRH (negative feedback loop)
7. cortisol mobilizes protein and sugar through gluconeogenesis in the liver
57
CRH and ACTH stand for
- corticotropin releasing hormone
- adenocorticotropin hormone
58
HPA axis - role of cortisol
increased cortisol production in critical illness beyond normal levels which is sustained
59
gluconeogenesis vs glycogenolysis
gluconeogenesis: liver produces glucose from noncarbohydrate sources, primarily amino acids
glycogenolysis: breaking down glycogen into glucose which takes place in liver and muscle cells
60
glucagon
- released from alpha cells in pancreas
- stimulates release of glucose from stores (glycogenolysis) and the creation of glucose from noncarb sources (gluconeogenesis)
- increase blood glucose
61
sources of fuel during the stress response: what does critical illness create a state of? what happens after glycogen stores run out? what is the primary source for gluconeogenesis?
- critical illness creates a state of hypermetabolism which increases the need for fuel
- Glycogenolysis is a short term response and not enough to sustain prolonged need for fuel
- After glycogen stores run out the body will use fat as fuel
HOWEVER
- The primary source for gluconeogenesis during critical illness is PROTEIN
62
contributing factors to hyperglycemia
- Increased cortisol level
- Catecholamines
- Glucagon levels
- Gluconeogenesis and glycogenolysis
- Insulin resistance also develops in many critically ill patients
63
permissive effect of cortisol: what does cortisol facilitate the response of? what does it promote? when does it become a problem?
- Cortisol facilitates the response of
tissues to epinephrine and
norepinephrine
- promotes maintenance of
contractility, vascular tone, and
blood pressure
- becomes a problem when
cortisol is depleted in critical
illness
64
adrenal insufficiency
- decreased production of adrenal hormones
- primary cause: issues with adrenal gland
- secondary cause: issues with pituitary gland
- caused by cancers, trauma, infection, SIRS, sepsis, adrenal exhaustion
65
adrenal insufficiency happens for a number of reasons:
- relative deficiency of cortisol
- damage to structures involved in HPA-axis
- suppression of HPA-axis through sustained
stimulation of HPA axis
*result is decreased cortisol
66
what do small changes in cortisol cause? hallmark sign?
alters pt's response to hemodynamic instability
Hallmark Sign: hemodynamic instability not responsive to inotropes/vasopressors, low cortisol, and if treated with hydrocortisone, an improvement seen
67
adrenal insufficiency: how to test/treat
test:
- random cortisol level (will be low)
- ACTH stimulation test to evaluate adrenal fx (lower than expected production of cortisol in response to stimulation)
treat:
- corticosteroids
- hydrocortisone IV (see fast response, may be able to titrate down on vasopressors)
- exogenous corticosteroids will suppress HPA axis and tapering is required to prevent glucocorticoid adrenal insuff.
68
what are other neuroendocrine hormones?
ADH and aldosterone - both increase preload
69
ADH
- Hypothalamus stimulates posterior
pituitary to release ADH
- Increases water reabsorption in the
kidneys (decreased UO)
- Increase circulating volume
- Improve EOP
- Some vasoconstrictive effects
70
aldosterone
- Released from adrenal cortex
- Stimulated by ACTH and RAAS
- Regulates fluid balance by retaining
sodium in the nephron
- Water follows salt
- Increases circulating volume
71
what happens when there is a massive neuroendocrine response?
increased consumption of protein as fuel
72
how can we meet protein requirements?
through enteral or parenteral nutrition or the body will use its own sources of protein which are used for support of vital functions, organs and tissues
73
consequences of not feeding: loss of tissue
- delayed wound healing
- wound dehiscence
- decubitus ulcers
- sepsis
- inability to wean from mechanical ventilator
- longer hospital stays
- significant weakness requiring months long rehab
- death
74
guiding principles for feeing in critical care
- pts need to be fed as early as possible (best within 24-72hrs)
- overall caloric and protein
requirements are often greater than
normal
- d/t ongoing gluconeogenesis,
we must provide extra protein, so
the body does not rob from its own
tissue
75
why do we want to avoid overfeeding?
produces excessive CO2 from carbs
and can also produce insulin resistance and hyperglycemia
76
refeeding syndrome
- significant and severe (sometimes fatal) shifts in fluid and electrolytes
when nutrition is introduced to undernourished patients (cancer,
ETOH, NPO ++, elderly); can cause cardiac and neuro changes
- hallmark sign: significant drop in serum Phosph when feeds are
introduced (may also see low Mg and K)
77
when a malnourished pt is given aggressive nutritional support, such as PN, a number of events ensue, primarily driven by....
the change in insulin secretion as a result of the shift from protein metabolism to carb metabolism. The increase in glucose levels, which results from the
composition of the nutritional support formula, increases insulin release by the pancreas ->
promotes cellular uptake of glucose along with electrolytes, primarily phosphorus, magnesium, and
potassium -> can be a life-threatening depletion of these vital electrolytes
78
how to prevent refeeding syndrome
- Monitor electrolytes and aggressively replace as needed
- Ensure electrolyte balance prior to initiation of feeds
- Decrease feeding and caloric intake until stabilized
- Closely monitor for complications
(neuro, neuromuscular dysfunction, resp dysfunction, cardiac dysfunction/arrhythmias, increased intravascular volume-heart failure
- give thiamine, Vit B complex, and multivitamin
79
routes for feeds
parenteral, NG, nasoduodenal, PEG
80
if a pt has high aspirates, what do you do?
don't stop feeding. they need the calories. begin a motility agent, consider a small bore feeding tube placed in small bowel
81
high residuals are not good - why?
- increased risk for VAP from vomiting
- not getting enough nutrition and d/t hypermetabolism, needs nutrition or will start to metabolize own proteins
- need to treat (motility agent, small bore feeding tube)
82
propofol: how does it help with nutrition?
its lipid based, high calorie
83
pain
- one of worst memories for pts who have survived critical illness
- subjective
- often undermedicated
- CC pts are hypersensitive to pain
- assume that all critically ill pts may be experiencing pain or at high risk for pain
84
are vital signs a reliable indicator of pain?
no - used to cue us to do a pain assessment
85
pharmacological approach to pain management
Opioids
* Fentanyl
* Hydromorphone
* Morphine
Non-opioids:
* Tylenol (don’t forget!)
* Gabapentin
* Ketamine
86
nonpharmacological approach to pain management
- warm blankets
- repositioning
- massage
87
anxiety
- subjective experience in response to
perceived or actual threat
- Psychological
- Common causes: illness, pain,
hospitalization, critical illness, intubation
88
agitation
- hyperactive movements that range from small
restless hand movements to physical aggression
- Behavioural
- Common causes: pain, anxiety, delirium, sleep
deprivation, critical illness, etc.
89
RASS
- Scored on behaviours
- RASS goal will be ordered
- Your role is to: try and achieve RASS
goal, increase/decrease sedation, advocate for a different
RASS goal (“can we wake this
patient up?”; “should we deepen
sedation for this
patient?)
90
what should you do when managing agitation meds wise?
- Use the minimum effective dose required to achieve goal RASS or desired behaviour (e.g. safety)
- Try to stay away from benzodiazepines. Instead, use: propofol, dexmedetomidine (Precedex)
91
propofol for managing agitation: what is it, route for admin, side effects
- Short-acting anesthetic
- Hypnotic, anti-anxiolytic, amnesic properties (“milk of amnesia”, retrograde amnesia)
- NO analgesic effects
- Administration: IV push (mg/mL) (procedural, emergencies) or Infusion (mcg/kg/min) (ongoing sedation)
- Lipid emulsion
- Side effects: **Hypotension** (propofol and levophed are friends!), myocardial depression
- Adverse effect: Propofol Related Infusion Syndrome (PRIS)
92
dexmedetomidine (precedex) for agitation: what is it, routes for admin, side effects
- Sedative, anti-anxiolytics, hypnotic, analgesic properties
- Sedates pt. without making pt. unrousable
- Administration: IV infusion only (mcg/kg/hr); IV push for anesthesiologists only
- Used often to treat anxiety/agitation related to mechanical
ventilation. Allows patient to remain conscious but calm.
- Side effects: **bradycardia**-> this might limit how high you can
titrate; hypotension
93
benzos for managing agitation: what is it, routes for admin, side effects
- Anxiolytic, amnesic properties
- No analgesic properties
- Commonly used benzo in the ICU:
Midazolam
- Administration: IV push, infusion
(mg/hr) and PO/SL
- Side effects: withdrawal – need gradual
tapering if pt has been on it for
prolonged periods
- Can make delirium worse!
94
delirium
- experienced by 40-80% of ICU
pts
- Contributes to the continued activation
of neuroendocrine response to stress
- Results in increased metabolic and
O2 demand
- Can be scored: CAM or Intensive Care Delirium Screening
Checklist (ICDSC)
95
nonpharmacological approaches to managing delirium
- early mobilization
- using minimum effective dose of sedation infusions
- normalizing ICU environment
- reorientate pt frequently
- facilitate sleep
- treat pain
- encourage family participation in care
96
pharmacological approach to managing delirium
- antipsychotics (haldol)
- precedex
- in extreme cases: resedate pt while new meds/approaches are attempted; pt is at risk to themselves and others
97
what do you have to be careful of with haldol and managing delirium?
its a typical neuroleptic, can prolong QTI, cause arryhthmias and hypotension
98
what would indicate oversedation?
- poor cough/resp depression
- hypotension/ bradycardia
- GI tract paralysis
- immune depression
- renal failure
- immobility
- venous stasis
- failure to recognize cerebral insult
- delirium
- PTSD
99
what would undersedation look like?
pain, anxiety, HTN, tachycardia, hypoxia, hypercarbia, ventilator asychrony, agitation, PTSD
100
what could sleep deprivation cause?
- Linked to impaired healing and immune function
- Affects mood, memory, attention, concentration
- May be primary factor for delirium
- Linked to increased
morbidity and mortality in critically ill patient
101
what's important about mobilization?
- Usually safe to start once O2S&D balance is achieved
- Helps manage delirium
- Should be done as early as possible! Can be done on patients who are deeply sedated or who have a low GCS (if ordered)
- Reduces days on ventilator
- Reduces length of ICU stay
- Improves clinical outcomes
- You might need to titrate FiO2 and vasopressors up
during mobilization
102
what does paralysis do?
supports oxygen supply and demand balance AFTER maximal sedation has proven insufficient in minimizing O2 demand
103
common uses for paralysis
- Rapid sequence intubation (RSI) and
procedures (used to facilitate procedure
rather than to reduce demand)
- Prevent shivering during induced
hypothermia
- Promote ventilator synchrony
- Facilitate lying flat/still during scans
- Facilitate unconventional modes of
ventilation (e.g. single lung vent)
104
mechanism of action for non-depolarizing paralysis
Acetylcholine antagonist – binds competitively to muscle cells blocking acetylcholine from depolarizing the cell.
Rocuronium, vercuronium
105
mechanism of action for depolarizing paralysis
Acetylcholine agonist –binds to acetylcholine receptors and depolarizes the cell but does not allow for repolarization
succinylcholine– not seen often as has a tachy effect
106
NMBAs: what properties do they have? what do you need to ensure? what does it allow for?
- no sedative/analgesic properties
- ensure pt is properly sedated and analgesed prior to initiation of NMBAs
- Allows for use of unconventional methods of ventilation (e.g. single lung)
107
what should you avoid using when giving NMBAs
avoid concomitant use of corticosteroids – synergistic effects -> can cause severe and prolonged weakness (myopathy, critical illness acquired weakness) leading to long term ventilator weans and requiring extensive rehab)
108
how often should you evaluate use of NMBA?
daily; discontinuing asap, use lowest effective dose
109
what's important for pt care when using NMBAs?
Pt will not be able to blink -> must protect corneas! Diligent eye-care, tape
eyelids closed
110
administering NMBAs by infusion
- Goal is usually not 100% paralysis, but rather around
50% paralyzed
- Use Peripheral Nerve Stimulator to assess “Train of
Four”
- PNS delivers small amounts of energy to a muscle
group (usually via ulnar nerve). 4 bursts of energy
are delivered and prior to paralysis patient should
have 4 corresponding muscle twitches
- Once paralysis onset has been achieved,
assessment is redone to determine percentage of
paralysis
111
admin of NMBAs by bolus
- preferred
- use smallest amount of drug to achieve results
- watch small movements when NMBAs wear off: eye or facial twitching, gagging, coughing, resp effort (seen on vent)
112
patient care you should always do if they are sedated +/- paralyzed
- Speak respectfully -> speak to them,
rather than about them
- Assume they can hear you: explain
what you are doing and why
- Introduce yourself and your plan every
time you enter the room
RASS -4/-5 and paralyzed patients:
- Provide eye care and oral care
regularly
- perform gentle ROM if indicated
113
things you should NEVER do if pts are sedated +/- paralyzed
use sedation to make work easier; think of it as sleep; delay weaning
114
fever
- 38 or higher
- hypothalamus in control
- caused by cytokines acting on hypothalamus
- cytokines triggered during infection, inflammation, drug reactions, neoplasm, autoimmune diseases, etc
- pyrogen (a protein) increases prostaglandin which increases the set point of the hypothalamus
115
hyperthermia
- Not regulated by the hypothalamus
(unless damaged)
- Results from body’s inability to vasodilate and sweat and help lose heat.
- Result is increase in body temperature
- some drugs can cause malignant hyperthermia
116
hypothermia
- Results from body’s inability to conserve or produce heat to maintain normothermia
- Can happen due to environmental factors, or can be induced
117
reasons not to treat fever
- increased resistance to infection when body temp is increased.
- Increased body temp is nature’s way of combating infection
- Increased immunologic response with fever (increased antibody production)
118
fever: reasons to treat
- 38% of critically ill pts experience fever
- 1 degree increase in temp = 10% increase in O2 demand
- HR/BP/CO increase to meet O2 demand
- if pt has rigors, O2 demand increases further
119
managing fever: nonpharmacological approaches
- Removal of blankets/gown
- Cool cloth
- Ice packs under armpits/groin (use with caution)
- Cooling blankets
- Decrease room temp
- Invasive: Thermaguard catheter
120
managing fever: pharmacological approaches
- acetaminophen (stops production of prostaglandins)
- clinical observations: drop in BP/MAP post admin in critical care population
- NSAIDs: not commonly used due to renal impairments/ r/o pre-renal AKI
121
what should you do when considering treating a fever?
explore immune benefits, risks of shivering, tylenol impact on BP
122
what can pts become hypothermic from?
- exposure to the elements (cold water immersion)
- long OR time
- cardiac surgery (induced hypothermia; to prevent tissue/brain ischemia during induced asystole)
- wound care
- purposeful induction of hypothermic protocols
123
when can a pt be declared dead?
when they have a core temp of 36
124
mild hypothermia
core temp is 32-35
125
moderate hypothermia
core temp is 28-32
126
severe hypothermia
less than 28
127
induced hypothermia: when is it used? what is the goal? what does it optimize? what is the target core temp?
- used in post cardiac arrest in pts with no return to consciousness after ROSC
- goal is to preserve neuro functioning
- optimizes O2 demand and supply balance for vital organs
- target core temp is 32-34
128
keeping a pt normothermic avoids the negative side effects of inducing hypothermia, which are...
decreased bowel motility
skin breakdown
paralytics required to treat shivering
129
phases of induced hypothermia
- induction (cooling to target temp)
- maintenance (maintain target temp)
- rewarming (rewarmed to normal body temp 0.2-0.5C/hr)
