Chapters 106-114 Preoperative and Postoperative Issues Flashcards

1
Q

What active cardiac conditions that in surgeries other than emergencies that mandate preoperative evaluation?

A

unstable angina
decompensated heart failure (systolic or diasystolic)
significant arrhythmias
severe valvular disease

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2
Q

What 5 clinical risk factors are independent risks for poor outcomes postoperatively?

A
history of ischemic heart disease
prior decompenstated heart failure
history of stroke OR TIA
DM- insulin dependent
renal insuffiency (crt >2.0)
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3
Q

According to ACC/AHA guidelines what is the only category of high risk surgery?

A

vascular surgery (aortic and PVD surgeries)

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4
Q

In terms of oxygen consumption, what is 1 MET?

A

3-5 mL/kg/min O2 consumption

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5
Q

Look over ACC/AHA guidlines

A

“patients with poor or indeterminate functional capacity fo intermediate or high risk surgery should have additional evaluation (IF IT WILL CHANGE MANAGEMENT) and if they have >1 risk factor (CAD, CHF, stroke, DM-insulin, CKD

  • **need to look at the clinical risk factors to determine this-with only 1 risk factor you can proceed to surgery with heart rate control. 2 risk factors, consider preoperative evaluation IF it will change management and >3 DO IT.
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6
Q

Who should get beta blockers preoperatively?

A

1) Already on it for treatment of: angina, HTN, arrhythmicas, CHF
2) Patients undergoing vascular surgeries who are at high risk of ischemia (as determined by preop eval)
3) PROBABLY recommended for: patients intermediate to high risk factors undergoing intermediate to high risk surgeries

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7
Q

Time delay for elective procedures after PCI without stent? bare metal stent? DES?

A

without stent- 2 weeks
BMS- 4-6 weeks after dual-antiplatelet therapy
DES- at least 12 months

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8
Q

In-stent thrombosis mortality rate when you prematurely discontinue dual anti-platelet therapy?

A

20-45%

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9
Q

What is MOA of cocaine?

A

Stimulant that stimulates dopaminergic neurons and inhibits norepi reuptake

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10
Q

What is MOA of LSD?

A

It is a hallucinogen that binds to dopamine and serotonin receptors in the CNS

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11
Q

What is MOA of methamphetamine?

A

stimulation of Beta and alpha receptors in CNS and periphery with increase catecholamine release and decrease in reuptake

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12
Q

How is EtOH metabolized?

A

90% through liver, 10% through pulmonary or excreted in secretions (sweat, urine)

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13
Q

What is MOA of EtOH?

A

At low levels it binds to GABA-A receptors. At higher levels it acts as an antagonist to NMDA receptors.

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14
Q

What are signs and symptoms of DTs and how would you treat it (delirum tremens)

A

usually 24-72 hours after the last drink,

s/s= tremulousness, disorientation, hallucinations, autonomic hyperactivity (tachycardia/hypertension)

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15
Q

How does disulfuram work? Why is it important in perioperative period?

A

blocks the acetaladehyde dehydrogenase. This can block the conversion of dopamine to norepi– hypotension.

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16
Q

What are some anesthetic agents to consider in DDx with delayed emergence?

A

scopolamine/atropine==> central anticholinergic syndrome

opioids==> decrease response to hypercarbia and cause hypoventilation and decrease in clearance of gases

17
Q

What are some pharmacokinetic/dyanmic factors to consider in DDx for delayed emergence?

A
  • low cardiac output decreases profusion to kidneys/liver
  • hypoproteinemia or competition of binding site with other drugs causes higher than expected drug levels
  • decreased liver metabolism in extremes of age
  • hypothermia causes decrease in drug metabolism and can also cause “cold narcosis” and directly suppress CNS activity
18
Q

What are some endocrine disorders to consider on DDx for delayed emergence?

A

hypothyroid, adrenal insuffiency, hypoglycemia

19
Q

What are some electrolyte abnormalities to consider in DDx of delayed emergence?

A

hypo-osmolarity and hyponatremia (TURP) or from SIADH

Hypercalcemia/hypocalcemia, hypermagnesium/hypomagnesemia

20
Q

What are some neurologic problems to consider in DDx of delayed emergence?

A

global or regional ischemia; hypoxia, increased ICP, cerebral hemorrhage