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NSCC 7320 > Oxygen Demand > Flashcards

Oxygen Demand Flashcards

1
Q

What receptor stimulation is involved with SNS? What are the outcomes?

A

Beta 1: inc HR, inc contractility
Beta 2: vasodilation in skeletal muscles, bronchodilation in lungs
Alpha: vasoconstriction of skin and peripheral muscles to shunt blood to vital organs

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2
Q

What occurs to the SNS in critical illness?

A

Put into overdrive over longterm resulting in a massive increase in cellular metabolism and O2 demand

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3
Q

What are some interventions to decrease O2 demand?

A

Intubation and mechanical ventilation, sedative, analgesics, NMBA, bed rest

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4
Q

What does lactate reflect?

A

Systemic O2 supply and demand, adequacy of tissue oxygenation.

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5
Q

What is a base deficit associated with in lab values?

A

Metabolic acidosis. Poor cellular oxygenation and predominance of anaerobic metabolism.

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6
Q

What does SCVo2/SVo2 reflect? What is the normal range? Where would each sample be obtained from? Which value will be slightly lower?

A

Systemic oxygen supply and demand balance and adequacy of tissue oxygenation. 60-80%.
SCvO2: CVC
SVO2: PA catheter, this value will be 5% lower as it includes blood that has been through the myocardial system in addition to head and upper body

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7
Q

What is the OER? What is the normal range? How is it calculated? What is something important to remember about this value?

A

Systemic oxygen supply and demand balance and adequacy of tissue oxygenation. Normal 24 - 35%. SaO2-SVO2/SaO2 x 100. It is time specific.

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8
Q

What is a high SCVO2 indicative of? A low value?

A

High: increased FiO2/increase O2 delivery, decreased O2 demand
Low: decreased O2 supply, increased demand

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9
Q

What is the role of the Hypothalamic Pituitary Adrenal Axis in stress? Walk through the process.

A

Stress stimulates hypothalamus to release corticotropin releasing hormone which situmulates the anterior pituitary to release ACTH and ACTH stimulates cortisol release

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10
Q

What is the role of cortisol?

A

Glucose metabolism (inc BG levels)
Protein metabolism (patients will metabolize their protein in critical illness with sustained cortisol levels)
Fat metabolism
Anti-inflammatory action (decrease capillary permeability, decrease WBC function, suppress immune response, decrease fever)
Permissive effect (facilitate tissues response to epidemic and norepinephrine, thereby increasing contractility, vascular tone and BP
Provides emotional stability

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11
Q

How might we know someone is in adrenal insufficiency in critical illness?

A

Low random cortisol level, failed ACTH stimulation test, hemodynamic stability that does not respond to inotropes or vasopressors.

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12
Q

Why is tapering required when hydrocortisone is administered?

A

It suppresses HPA axis which will no longer produce cortisol, therefore cortisol still needs to be provided to body

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13
Q

In addition to cortisol, list three other hormones that are released during the Neuroendocrine Response

A

ADH (vasopressin)
Aldosterone
Glucagon

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14
Q

What are the roles of ADH in the neuroendocrine response?

A

Increases water reabsorption by kidneys and has vasoconstrictive effects. Increases after load, increases preload which support MAP and increase O2 supply

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15
Q

What are the roles of aldosterone in neuroendocrine response?

A

Retain Na at the nephron (water follows) which leads to fluid retention and increased preload.

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16
Q

What are the roles of glucagon in the neuroendocrine response?

A

Stimulates gluconeogenesis, increases BG which allows for more available glucose for cellular metabolism

17
Q

What is the primary source of gluconeogenesis of a person in critical illness? Why?

A

Protein, because after glycogen stores run out the body will use protein (1st) and fat (2nd) for fuel.

18
Q

Why is early feeding so important in critical illness? What’s the range of protein someone in critical illness should receive daily?

A

To provide protein to these patients - to ensure they are not using their own protein sources for metabolism. 1.5-2 g/kg/day

19
Q

What are some consequences of not feeding early in ICU?

A

Delayed wound healing, ulcers, sepsis, inability to wean from mech vent, muscle wasting, longer ICU admission, death

20
Q

What is the issue with overfeeding a critically ill patient?

A

Excessive CO2 from CHO breakdown can produce insulin resistance, inc BG, and make it difficult to wean from mech vent (lots of CO2 for patient to clear on own)

21
Q

Why is it so important to regulate BG in critical illness?

A

As very low BG and very high BG are associated with poor outcomes.

22
Q

What happens in Refeeding syndrome? What is the first electrolyte that will go out of balance that indicates this? What are the common electrolytes to see issues in?

A

Malnourished patient is fed, increased BG levels cause an increase release in insulin which promotes cellular uptake of glucose and electrolytes along with. Low PO4 as it is used to make ATP. Low PO4, K, Mg.

23
Q

What do we want to monitor for in refeeding syndrome?

A

Cardiac dysfunction/arrythmias, respiratory dysfunction, neuro, neuromuscular. Electrolytes are all important for muscle contraction. Increased intravascular volume, and heart failure.

24
Q

What is a benefit to using Ketamine?

A

Has analgesic and sedative/anesthetic effects.

25
Q

What is the benefit to using a propofol infusion in someone? What are the properties of propofol? What needs to be taken into consideration if someone is on propofol?

A

Short acting (patient will wake up quickly after it has been shut off).
Hypnotic, anxiolytic and amnesic
It is lipid based - enteral feeds will need to be adjusted based on this.

26
Q

What are the properties of precedex? Why is it valuable?

A

Sedative, anxyiolytic, analgesic.

Sedates patients without making them unarousable. Often used to treat mechanically vented patients in delirium.

27
Q

When would NMBAs be used? What is important to remember when administering these?

A

RSI, used only after maximum sedation is unsuccessful in decreasing O2 demand, facilitate unconventional mech vent, prevent shivering in induced hypothermia.
Ensure it is administered AFTER sedation and analgesia

28
Q

When would you want to avoid administering NMBA?

A

Concommitant use with steroids

29
Q

If you are giving your patient NMBA on a bolus basis, how would you assess if they need a PRN dose?

A

Triggering the vent, attempt to cough, any movement, facial twitching, gagging, blinking etc.

30
Q

If your patient is on a NMBA infusion, how would you check to determine if the infusion is enough?

A

Peripheral nerve stimulation (train of four TOF)

31
Q

What is an example of a depolarizing NMBA? What type of patient should this be avoided in?

A

Succinylcholine. Severe renal impairment.

32
Q

What is an example of non-depolarizing NMBA?

A

Rocuronium

33
Q

What are benefits to treating a fever?

A

Decreased O2 demand, avoid shivering

34
Q

What are benefits to not treating a fever?

A

Supports immune function, increased resistance to infection with increased body temperature

35
Q

After induced hypothermia, how slowly do we want to re-warm someone?

A

0.2 - 0.5 degrees per hour

36
Q

What are challenges with cooling someone? What are things that can be done?

A

Decreased serum K, Mg, Ca. Slowed cardiac depolarization can lead to bradydysrhythmias and ECG changes (wide QRS, wide PR). Vasoconstriction will increase preload and increase after load (increase cardiac workload), impaired platelet aggregation, shivering
Sedatives, opioids, Mg, NMBA

37
Q

What types of patients are good candidates for induced hypothermia? What will cooling them do?

A

Post cardiac arrest (pulseless VT, VF, PEA) with no return of consciousness after ROSC. Preserve neuro function. and optimize O2 supply and demand balance.

38
Q

What are challenges in re-warming someone?

A

Ca, Mg, K move out of cell, increase serum levels. Increased cellular metabolism leads to dec BG, vasodilation leading to hypovolemia.

39
Q

What can happen with someone’s volume status with cooling them?

A

Cold-induced diuresis, need to ensure adequate preload, give fluids PRN.

NSCC 7320 (7 decks)

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