O2 and metabolic demand Flashcards
1
Q
Receptors that utilize norepi and epi
A
Adrenergic receptors
2
Q
Adrenergic receptors
A
Alpha, Beta 1 and Beta 2
3
Q
Alpha-adrenergic receptors cause
A
Vasoconstriction
4
Q
Beta 2
A
Bronchodilation
5
Q
Beta 1
A
Heart rate
Conduction
Contractions
6
Q
Stress is controlled by which system
A
Autonomic nervous system
7
Q
Autonomic nervous system 2 sub divisions
A
Parasympathetic nervous system
Sympathetic nervous sytem
8
Q
Parasympathetic nervous system
A
Rest and digest
9
Q
Sympathetic nervous system
A
Fight or flight
10
Q
Interventions to reduce demand
A
Intubation Sedatives paralysis Bed rest Mechanical ventilation
11
Q
How do we assess oxygen supply and demand
A
End organ perfusions
Lactate
SvO2 and ScvO2
Oxygen extraction (O2ER)
12
Q
Oxygen Demand
A
The amount of O2 cells needs to provide energy (ATP) for their function
13
Q
Increased cellular work means
A
Increased cellular oxygen demand
The need for increased fuel for cells to functions
14
Q
Assessing end-organ perfusion HEART
A
Angina pain
shortness fo breath
ECG changes
Increased cardiac bio markers
15
Q
Assessing end-organ perfusion LUNGS
A
Poor gas exchange
Decreased muscle function
16
Q
Assessing end-organ perfusion GI
A
Decreased gastric motility abd pain nausea vomiting Ischemia to the bowel
17
Q
Assessing end-organ perfusion BRAIN
A
Decreased LOC
REstlessness
Agitation
Coma
18
Q
Assessing end-organ perfusion LIVER
A
Changes in Labs
19
Q
Assessing end-organ perfusion KIDNEYS
A
ddecreased output
BUN CR and GFR
20
Q
Assessing end-organ perfusion Skin/ Tissue perfusion
A
skin warmth colour pulse strength cap refill
21
Q
Assessing GLOBAL end-organ perfusion
A
Increased lactate Poor perfusion ScVO2 EOP ABG O2ER
22
Q
Lactate
A
Produced when cells switch from aerobic to anaerobic metabolism- lactate is generated as a by-product
Tells us that tissues don’t have enough oxygen
<2 is normal
23
Q
ScvO2
A
central venous oxygen saturation
Percentage of oxygen bound to hemoglobin in venous blood returning to heart from top of body (drawn from superior vena cava) -usually drawn from IJ
Tells us about our demand- what is left over
24
Q
Where is ScvO2 drawn from
A
drawn from the distal port in CVC (IJ)
25
SvO2
Mixed venous oxygen saturation
percentage of oxygen bound to hemoglobin in venous blood returning to the lungs from the entire body
Sampled from Pulmonary Artery catheter (PA cath or PA line also known as Swan-Ganz catheter)
26
Normal values for ScvO2 and SvO2
60-80%
| SvO2 typically trends 5% lower due to inclusion if myocardial demand oxygen consumption
27
ScvO2 and SvO2 high
body isn't using the O2
28
ScvO2 and SvO2 low
high demand or low O2
29
How often do we check gastric residuals
Q4H
30
Key points for feeding
Feed as early as possible
Give protein packs
Enertal feeding is better than parenteral
reduce interruption (If you pause it pause insulin as well)
think about motility agents
stay on top of bowel care
31
Adrenal insufficiency
Adrenal insufficiency results in the decreased production of adrenal hormones, including
cortisol. Causes can be primary (involving the adrenal gland) and secondary (involving the
pituitary gland), and include various cancers, infections, or traumas. Reversible causes that are often present during critical illness include systemic inflammatory
response syndrome (SIRS) and sepsis and adrenal exhaustion.
32
Anxiety
is a subjective experience that occurs in response to a perceived or actual threat to self-
integrity e.g. critical illness and pain. It elicits changes in the neuroendocrine system (via the
HPA axis) that result in increased metabolic and oxygen demand
33
Basal energy expenditure (BEE)
Calculation of BEE (using a formula) is the most frequently used method of determining
nutritional requirements of critically ill patients. It is not a particularly accurate assessment
of nutritional need, but is easy to complete.
34
Base deficit or excess
Base deficit/ excess is a calculated value that reflects total concentration of all buffer
systems in the blood that are involved in acid-base balance (i.e., bicarbonate, ammonia,
phosphate buffer systems). A deficit indicates an acidosis and excess indicates an
alkalosis
35
Central venous oxygen saturation
s a measured parameter that provides information about oxygen supply and demand
balance. ScvO2 reflects the amount of oxygen bound to hemoglobin, in the blood returning
to the heart. It is affected by both oxygen supply and oxygen consumption and so offers an
indication of oxygen supply and demand balance for the whole body (global tissue
oxygenation). ScvO2 is typically measured from a specimen taken from a CVC, which
includes blood predominately from the head and upper body. Normal value is 60-80%.
36
normal ScvO2
60-80%
37
Cortisol & HPA axis
is produced by the adrenal glands. The amount of cortisol produced is regulated by ACTH
(adenocorticotropic hormone) released from the pituitary gland. Production of ACTH is
controlled by the hypothalamus, via the hormone corticotrophin releasing hormone (CRH).
Production of CRH and ACTH is moderated by serum cortisol levels. This mechanism is
known as the hypothalamic-pituitary-adrenal (HPA) axis
38
Gluconeogenesis
Gluconeogenesis converts protein into glucose for cellular fuel. During critical illness, the
huge protein requirements for ongoing gluconeogenesis must be provided through either
enteral or parenteral nutrition, or the body will steal from its own tissues as a source of
protein.
39
Hypothalamic-pituitary-adrenal
central to stress response: moderates production of cortisol
40
Metabolic demand
Cells use oxygen and nutrients (especially glucose) to generate energy (ATP) required to
perform their function. The amount of energy they need at a given time is referred to as
metabolic demand. Increase in energy needs translates into increased metabolic demand:
decreased energy needs translates into decreased metabolic demand. Changes in
metabolic demand mean changes in oxygen demand.
41
Mixed venous oxygen saturation
a mixed venous oxygen saturation (SvO2) is measured from a specimen obtained via a
Pulmonary Artery catheter, the tip of which rests in the pulmonary artery. Blood in the in
pulmonary artery is a mix of venous blood returning from the whole body - hence the term -
“mixed venous”. Normal values are 60 -80%. SvO2 values are typically slightly lower than
ScvO2, due to the inclusion of heavily deoxygenated blood from the coronary sinus
42
Oxygen extraction ratio formula
O2ER = SaO2-SvO2 divided by SaO2
Times 100
43
Oxygen extraction ratio normal
25-35
44
Oxygen extraction ratio tell us...
how much oxygen the tissues are extracting (using)
45
LOW O2 ER
the tissues are extracting more oxygen
```
Causes:
Decreased O2 supply
Decreased CO
Decreased SaO2
Decreased Hgb
Increased O2 demand
```
46
High O2 ER
The tissues are extraction less oxygen
```
Causes
Increased O2 supply
Increased CO
Increased SaO2
Increased Hgb
decreased O2 demand
```
47
stress response in the body
Physiologically, the fight
or flight response involves the activation of the sympathetic
nervous system (SNS) which targets specific adrenergic receptors
with neurotransmitters called catecholamines (epinephrine and
norepinephrine)
48
Some interventions to reduce
| demand……
* Intubation
* Sedatives
* Paralysis
* Bed rest
* Mechanical ventilation
49
how do we assess oxygen supply &
| demand balance?
* EOP is a good place to start
* Lactate
* SvO2 & ScvO2
* Oxygen extraction (O2ER)
50
hypothalamic-pituitary-adrenal (HPA) axis.
HPA axis is the negative feedback loop responsible for controlling cortisol levels in the blood
Cortisol is produced by the adrenal glands and is essential for survival. The amount of cortisol produced is regulated by hormone (ACTH). ACTH is controlled by the hypothalamus, part of the central nervous system responsible for modulating both the SNS response and the other neuroendocrine responses to stress
Production of CRH and ACTH is moderated by serum cortisol levels (NEGATIVE FEED BACK LOOP)
51
Cortisol is responsible for
```
Glucose metabolism
Protein metabolism
Fat metabolism
Anti-inflammatory action
Permissive effect- facilitates the response of tissues to epinephrine and norepinephrine
```
52
Adrenal Insufficiency
result in suppression of the HPA axis and a decrease in production of cortisol. Regardless of the cause of acute adrenal insufficiency, it presents in many critically ill patients as hemodynamic instability that is not
responsive to inotropes or vasopressors
53
neuroendocrine response to stress increases...
cellular metabolism and oxygen demand, and mobilizes fuel for the increased metabolism.
54
Propofol
Propofol is a powerful sedative that is generally used as an anesthetic induction agent. It also has hypnotic, anxiolytic, amnestic, antiemetic and anticonvulsant properties, but no analgesic effects.
55
Dexmedetomidine (Precedex
It is a rapid acting, short-term sedative with analgesic/ opioid-sparing properties
allows patient to be sedated but still rousable, which means it is also associated with shorter time to extubation
56
Benzodiazepines
have anxiolytic and amnesic properties, but no analgesic effects.
57
Haloperidol
Haloperidol is a dopamine receptor antagonist, so its use results in higher levels of dopamine in the brain. It is used primarily to treat confused thinking and hallucinations in critically ill patients not associated with alcohol withdrawal.
58
Fever
caused by cytokines acting on the hypothalamus during
infection, inflammation, drug reactions, neoplasm, autoimmune
diseases, and vascular occlusive diseases
59
Induced Hypothermia-Rewarming Challenges
● Hypotension – due to vasodilation
● Electrolyte shifts: Serum K, Mg and Ca increase
● Hypoglycemia
60
Induced Hypothermia-Induction Challenges
● Electrolyte shifts: Serum K, Mg and Ca decrease
● Bradydysrhythmias, ECG changes (prolonged PR
interval, widened QRS)
● Coagulopathy
