CPB (Neuro/Endo) Flashcards

1
Q

What is the incidence of stroke during surgery?

A

2-8%

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2
Q

Does CPB alone increase the risk of minor post-op neurologic dysfunction?

A

Yes, especially during the early post-op period

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3
Q

What are the sources of microemboli while on CPB?

A

Air (from oxygenator, heart, temperature gradients, IV solutions, arterial line filter) + Oxygen + Lipid globules (from cardiotomy suction) + muscle/connective tissue fragments + platelet/leukocyte fibrin aggregates + plastic + calcific particles (from aorta, cannulation sites)

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4
Q

What are the major sources of macroemboli during cardiac surgery?

A

Large air bubbles or atheromatous/calcific debris from valvular lesions or plaques on the aorta; most often occurs during clamping and cannulation of the aorta

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5
Q

What is an air embolus made primarily of?

A

Nitrogen (doesn’t desolve rapidly); this is why a CPB circuit is flushed with highly disssolvable CO2

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6
Q

What are signs of an air embolus?

A

Seizures, arrhythmias, and ventricular dysfunction

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7
Q

How can you decrease the risk of air embolism while on CPB?

A

Arterial filters/pre-bypass filters (decreases pump debris and gas/particular matter)

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8
Q

What are common sources of air embolisms?

A

Aorta, pulmonary vessels, and intracardiac negative pressure vents + unexpected, open contracting heart + pressured cardiotomy circuit + reversal of vents

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9
Q

Where does most air end up in the heart?

A

LAA + ventricular apex + spaces between chordae tendinae, pap muscles, and trabeculae carinae + cardiac chamber cul-de-sacs + aortic root

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10
Q

What are independent risk factors for neurologic dysfunction after cardiac surgery?

A

Advanced age (>75yo are 2x more likely to have a neurologic event) + duration of CPB (>2 hrs) + DM, history of CVA, and calcified aorta

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11
Q

What are ways to monitor the CNS during cardiac surgery?

A

EEG + transcranial doppler (measures blood flow velocity through MCA - can detect embolic events) + jugular venous O2 sat (measures cerebral O2 delivery)

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12
Q

What is the formula for cerebral perfusion pressure and what is the normal range?

A

CPP = MAP - ICP (or CVP); normal is 60-80 mmHg

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13
Q

What does pH stat generally do to the CNS during hypothermia?

A

Keeps patients more acidotic (adding CO2 to preserve pH of 7.4 and PCO2 of 40) which leads to cerebral vasodilation and increased CBF; loss of cerebral autoregulation and mismatch of CBF and CMRO2

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14
Q

Which method of acid-base management has been associated with improved neurologic outcomes in adults?

A

Alpha stat; possibly due to decreased risk of microemboli (since there is hypocarbia and cerebral vasoconstriction) while pH stat adds CO2 so increased CBF and higher risk of emboli

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15
Q

Which method of acid-base management has been associated with improved neurologic outcomes in children?

A

pH stat; less risk of emboli so you get better balanced brain cooling with cerebral vasodilation (CBF and CMRO2 are dissociated) + right-shift of oxy-hemoglobin dissociation curve

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16
Q

How much of your CO does the splanchnic circulation receive and why is it at risk during CPB?

A

20% of CO and is unable to autoregulate at extremes of blood pressure so it is more vulnerable to flow changes while on CPB

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17
Q

What are factors that contribute to splanchnic ischemia?

A

Systemic inflammation from the CPB machine + non-pulsatile blood flow + hypothermia

18
Q

What is the minimum flow needed for hepatic O2 consumption to be maintained?

A

2.2 L/m2/min

19
Q

What can you see after bypass with the hepatic system?

A

Transient increased LFTs + jaundice (from hepatic injury, excessive bilirubin 2/2 blood transfusions or trauma from the pump itself and hemolysis)

20
Q

What can you to do reduce the risk of GI complications while on CPB?

A

Avoid hemodilution and severe anemia + use pulsatile flow + use filters to reduce emboli + use echo for aortic cannulation (decrease atheroemboli) + avoid IABP in patients with significant plaque

21
Q

How does CPB affect the catecholamine release?

A

Increases catecholamine release during CPB likely due to hypothermia, hypovolemia, hemodilution, hypotension, non-pulsatile flow and decreased perfusion of endocrine glands

22
Q

What can decrease the endocrine response to CPB?

A

Dexmedetomidine and neuraxial anesthesia has been shown to decrease the neuroendocrine response to CPB

23
Q

What is secreted from the posterior pituitary gland? When are these released?

A

ADH or vasopressin: released if increased plasma osmolality, decreased blood volume, hypoglycemia, stress and pain

24
Q

What happens to ADH levels while on CPB?

A

Increased ADH levels in the first 30 minutes of CPB independent of anesthetic technique

25
Q

What is secreted from the anterior pituitary gland?

A

ACTH, TSH, growth hormone, LH, FSH, and and prolactin

26
Q

What does ACTH do and what happens to ACTH levels while on CPB?

A

ACTH stimulates adrenal gland secretion of flucocorticoid and androgen hormones; levels increase with incision and fall during non-pulsatile CPB and increase again after bypass

27
Q

What does growth hormone do and what happens to GH levels while on CPB?

A

GH decreases protein catabolism and promotes protein synthesis (increases fat mobilization and glycogen deposition); GH increases with skin incision and CPB (peaks at 120 mins of CPB) and it rapidly decreases to preop levels 6 hours post CPB

28
Q

What is secreted from the adrenal cortex?

A

Cortisol and aldosterone

29
Q

What happens to cortisol levels during CPB?

A

Like all surgeries, cortisol increases with incision, it then decreases at the initiation of CPB (hemodilution and hypothermia) and then increases again post-op

30
Q

What is the role of aldosterone?

A

Helps regulate renal sodium reabsorption

31
Q

What happens to aldosterone levels during CPB?

A

Aldosterone levels increase with incision, then decreases with the start of CPB but increases 15 mins later

32
Q

How does hypothermia and CPB affect catecholamines released from the adrenal medulla?

A

Hypothermia delays metabolism of catecholamines while being on CPB decreases perfusion to the lungs, liver, and kidney which delays plasma clearance

33
Q

What happens to glucose and insulin levels on CPB for nondiabetic patients?

A

Glucose utilization decreases from hypothermia, cortisol/catechoaline release and suppression of insulin secretion; glucose levels increase during CPB due to decreased glucose utilization as above and increased hepatic glycogenolysis and gluconeogenesis from increased stress hormones

34
Q

When do glucose levels return to normal after cardiac surgery?

A

Usually post-op day 2

35
Q

What happens to glucose and insulin levels on CPB for diabetic patients?

A

During CPB, decrease in insulin and increase in glucose levels similar to nondiabetic patients; however, when rewarming, insulin requirements increase more for diabetic patients

36
Q

What does thyroid hormone do?

A

TSH from the anterior pituitary causes T4 (thryoxine) rleease from the thyroid gland which increases O2 consumption, cardiac output, contractility, and renal blood flow; T3 (thriiodothyonine) is more active and responsible for the hormonal effects

37
Q

What happens to thyroid hormone levels during CPB?

A

T3 levels decrease with the start of CPB, then increase slightly after CPB but still remain significantly lower than normal postoperatively

38
Q

What is euthryoid sick syndrome?

A

Low T3, low to normal T4, and normal TSH; can be seen in post CPB patients

39
Q

What happens to parathyroid hormone with CPB?

A

With CPB, there is a decrease in ionized Ca as well as a decrease in PTH; PTH initially decreases with CPB, then increases and peaks 60 min after the start of bypass

40
Q

Endocrine Effects Summary Table

A

See Excel Sheet