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Pharmacotherapy > Anesthesia > Flashcards

Anesthesia Flashcards

1
Q

What is the induction and maintenance dose of propofol?

A

Induction 1-2.5 mg/kg iv

Maintenance 20-200 ug/kg/min

Half life = 2-8 minutes for redistrobution and 4-7H for elimination

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2
Q

What opiate is potently synergistic with propofol?

A

remifentanyl

A drug that is 2.5 times stronger than fentanyl or 250 times stronger than morphine

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3
Q

What are the main side effects of propofol?

A
  • greatest reduction in systolic and diastolic BP compared to other IV anesthetics (20-40%) due to reduced SVR and reduced stroke volume
  • reduced baroreceptor response (decreased compensation
  • reduced respiratory drive and periods of apnea in 25% of patients
  • decreased CBF, CMR, ICP, IOP
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4
Q

What is the target of propofol?

A

Propofol is an alkylphenol GABA receptor agonist

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5
Q

What other sedation drugs are in the same class as propofol?

A

Barbituates- Thiopental
Benzodiazepines ( Midazolam, Diazepam, Lorazepam)
Imidazole derivatives- etomidate

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6
Q

What class of drugs is Ketamine?

A

NMDA receptor antagonist

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7
Q

What is the context sensitive half-time?

A

It is the time required for a drugs plasma concentration to decrease to level compatible with awakening following cessation of a continuous IV infusion

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8
Q

What is the MAC

A

The minimum alveolar concentration

This is the concentration necessary to prevent movement in 50% of people from a surgical stimulus

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9
Q

What is the typical total MAC that is aimed for?

A

1.2-1.3 MAC

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10
Q

What is the induction and maintenance dose of Ketamine?

A

Induction 0.5-2 mg/kg IV or 3-5 mg/kg IM

Maintenance 2-6mg/kg/hr
Analgesia 0.15-0.25 mg/kg iv

1/2 life to distribution is 11-16 minutes, to elimination is 2-4 hours

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11
Q

What are the side effects of Ketamine?

A
  • causes impaired norepinephrine uptake–> increased sympathetic tone–> transient increase in BP, HR, CO, SVR
  • can cause direct negative inotropic effect when sympathetic system is blocked or exhausted (shock, sepsis, prolonged illness)
  • no significant respiratory depression
  • induction may cause loss of airway reflexes–> increased risk of aspiration
  • Increased cerebral vasodilation, increased CMR, increased CBF
  • unpleasant dreams, hallucinations, frank delerium
  • increased blood sugar due to increased sympathetic tone
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12
Q

What is the dose of midazolam?

A

sedation - 0.01-0.1 mg/kg IV

co-induction 0.02-0.04 mg/kg iv

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13
Q

What are the side effects of midazolam?

A

-minimally reduced cardiac output and blood pressure

  • apnea and severe respiratory depression
  • reduced CMR and CBF to a lesser extent than propofol
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14
Q

What is dexmedetomidine and what is the dose?

A

intravenous alpha 2 agonist

  1. 5-1 meg/kg over 10 minutes as bolus
  2. 2-0.7 meg/kg/hr
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15
Q

What are the side effects of demedotomidine over the other IV anaesthetics?

A

It has very little respiratory depression like ketamine, but does produce the hallucinations, dreams and other issues as in ketamine.

  • biphasic cardiac curve with transient hypertension and reflex bradycardia with initial bolus followed by decrease in SVR
  • can cause severe bradycardia, heart block, asystole (can reverse with atropine or glycopyrolate)
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16
Q

What are the ASA classification categories?

A

ASA 1- healthy patient, no medical problems
ASA 2-mild systemic disease with no functional limitation (treated hypertension)
ASA 3-severe functional disease with definite functional limitation (emphysema)
ASA 4- severe systemic disease a constant threat to life (unstable angina)
ASA 5- moribund patient that is not expected to survive for 24 hours with or without surgery
ASA 6- a clinically brain dead patient
E- emergency case

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17
Q

What are the components of the airway exam?

A

Thyromental distance
Cervical motion
Bitting upper lip
Malampati score

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18
Q

What are the malampati categories?

A

Class 1- can see the entire soft palate including the pillars, the uvula, fauces

Class 2- The entire uvula is visible, but not the pillars of the soft palate

Class 3- The base of the uvula visible, but not fauces

Class 4- soft palate not visible at all

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19
Q

What is the active form of a local anaesthetic, and what is the mechanism of action?

A

The mechanism of action is to block the sodium channels, which prevents depolarization

The injected form in the LAH, and the LA- free basic form is able to cross the plasma membrane into the cell, and the LAH form is the active form in the cell

20
Q

What are the two kinds of local anaesthetics

A

Ester and amides

21
Q

What does adding bicarbonate to the local anaesthetic solution do to the efficacy?

A

It increases the proportion of free base, and increases the sedation

22
Q

What are the different kinds of nerve fibres, what do each of them do, and which ones do local anaesthetics work on?

A

A group are large diameter and are myelinated and control muscle contraction
(A alpha, beta, gamma, delta)
-some sensation of nociception, touch, tempearture

Beta- small diameter myelinated preganglionic fibres of the autonomic nervous system

C- unmyelinated postganglionic small diameter nerves and dorsal root nerves that transport nociception, temperature, touch, pressure, itch

Most sensitive to local anaesthetics are the B fibres, and then the C fibres, and then A delta

Thus local anaesthetics have very little effect on motor function

23
Q

What are the symptoms of local anaesthetic toxicity?

A

In order are

1) CNS depression leading to excitation
- numbness, paresthesia, dizziness, tinnitis, blurred vision, metallic taste
2) respiratory depression
3) Cardiac abnormalities–> PR interval increase, prolonged QR complex, dysrhythmias, ventricular fibrillation

24
Q

What is the maximum concentration of lidocaine and bupivacaine with and without epinephrine?

A

lidocaine (xylocaine) 4mg/kg without epinephrine, 7mg/kg with epinephrine

bupivocaine (marcaine) 2.5mg/kg with or without epinephrine

25
Q

Where in the peripheral nervous system is acethycholine the neurotransmitter, and where is it not?

A

ganglion–> acetycholine is the neurotransmitter for both the sympathetic and parasympathetic

postsynaptic cleft

  • Sympathetic–> norepinephrine
  • Parasympathetic–> acetycholine
26
Q

What is the difference between muscarinic and nicotinic receptors?

A

they are both parasympathetic

Muscarinic- on organs that receive parasympathetic innervation ( lung, heart, bladder, GI, eye (contraction of circular muscle –> pupillary constriction and cilliary muscle–> focus for near vision, glands, sphincters)

Nicotinic- nerve to nerve and nerve to muscle communication–> neuromuscular junctions

27
Q

How can you increase parasympathetic tone?

A

1)stimulate the vagus ( primary parasympathetic nerve) –> give a vagotonic –>
2)decrease the rate of acetycholine breakdown
(cholinesterase inhibitor) like neostigmine, physostigmine, insecticides (malathion and parathion)

28
Q

How can you decrease parasympathetic tone?

A

Give a vagolytic

29
Q

What are common muscarinic antagonists and their function

A

muscarinic antagonists–> decrease parasympathetic tone

Glycopyrolate–> decrease oral secretions
atropine–> increase the heart rate
Dilate the bronchioles–> ipratroprium
Treating incontinence and spasms of the bladder–> tolteridine

30
Q

What are common muscarinic agonists and antagonists?

A

Muscarinic agonists–>muscarine, pilocarpine, methacholine, bethanechol

muscarinic antagonists–>Glycopyrolate–> decrease oral secretions
atropine–> increase the heart rate
Dilate the bronchioles–> ipratroprium
Treating incontinence and spasms of the bladder–> tolteridine

31
Q

What are the common beta blockers and their B1 and B2 activity?

A

cardioselective ( B1 activity only)-> Metoprolol, atenolol, nebivolol, esmolol

Non-cardioselective (Mixed B1 and B2 activity)-propranolol, nodal, timolol

Mixed alpha and beta–> labetolol, carvedilol

32
Q

What are the contraindications to neuraxial anesthesia?

A

Absolute contraindications

  • patient refusal
  • coagulopathy
  • anticoagulation therapy
  • increased ICP
  • Allergy
  • lack of familiarity or resuscitative equipment

Relative contraindications

  • uncooperative patient
  • neurological deficit
  • significant hypovolemia
  • sepsis or local infection
  • fixed cardiac output states
  • previous spinal instrumentation
  • spinal deformities
33
Q

What is Tuffier’s line and what does it represent?

A

Tuftier’s line is an imaginary horizontal line at the level of the iliac crests

This line passes through the L4 vertebrae

Above this line is the L3/4 space
Below this line is the L4/5 interspace

34
Q

What is the mechanism of action of acetominophen?

A

1) direct and indirect inhibition of central cyclooxygenases
2) activation of the endocannabinoid system
3) activation of the spinal serotonergic pathway

35
Q

What are the typical products of the cyclooxygenase pathway and where are they important?

A

cyclooxygenase catalyze the conversion of arachidonic acid to prostaglandins and thromboxanes and prostacycline( which is important for protection of the stomach)

COX-1 is responsible for the baseline physiological production of these molecules

COX-2 is responsible for the production of prostaglandins for inflammatory pathways

36
Q

How do NSAIDS affect renal function?

A

They inhibit prostaglandins responsible for the vasodilatation of the afferent glomerular arterioles

37
Q

What are the contraindications to NSAIDS

A 
Allergy to ASA or NSAID
ASA exacerbated respiratory disease
PUD
Renal insufficiency
CHF
Active inflammatory bowel disease
Pregnancy
Bleeding disorders
Wound or bone healing may be impaired in high risk patients
38
Q

What is the Apfel score, and what is it helpful to predict?

A

The Apfel score is helpful to predict the risk of PONV (post operative nausea/vomitting)

There are four components to the Apfel score

1) Female
2) non smoker
3) history of PONV
4) Postoperative opioids

With each risk factor, the risk of developing PONV is
10%, 20%, 40%, 60%

39
Q

What are some strategies to reduce PONV?

A

1) use local or regional and not GA
2) Use propofol
3) Avoid Nitrous oxide
4) Avoid volatile organics
5) minimize opioid use
6) Ensure adequate hydration

40
Q

What is ondansetron, what is the dose, and what are the side effects?

A

Ondansetron (Zofran) is a serotonin (5-HT3) receptor antagonist

The prophylactic dose of Zofran is 4mg IV

Ondansetron works by blocking serotonin both peripherally (on vagal nerve terminals) and centrally in the chemoreceptor zone

The most important potential side effect is that there is a risk of QT prolongation with Zofran use

Other SE include headache, fatigue and malainse

41
Q

What is the dose of diphenhydrinate?

A

Diphenhydrinate (gravol) is an H1 antagonist with anticholinergic activity

Its dose is 50-100mg PO or IV q4H

42
Q

What other medications can be used to treat PONV?

A

Haloperidol

Propofol

43
Q

What is the cause of malignant hyperthermia, and what is the treatment?

A

It occurs in people who are susceptable in response to a trigger.

The trigger is a volatile anaesthetic or succcinylcholine.

The key features of MH include rise in end tidal CO2, muscle rigidity, rhabdomyolysis, hyperthermia, acidosis, hypoxemia, hyperkalemia

The temperature can rise 1 Degree Celsius every 5 minutes

The pattern of inheritance is autosomal dominant and it is due to a defective calcium channel in the sarcoplasmic reticulum (the rayinodyne receptor)

Gold standard for testing is the in vitro contracture testing (not used for screening), and no standardized genetic testing is availble because there are so many possible mutations (> 100).

The initialtreatment for MH includes dantrolene 2.5-30 mg/kg, and to cease any causitive agents

See the full treatment guidlines, but the involve cooling with IV and other cooling methods, treatment of acidosis and hyperkalemia

44
Q

What is the differential diagnosis for MH

A

Cardioresp– atelectasis, sepsis
Neuro- meningitis, ICH, TBI
Toxins- amphetamines, salicylate, serotonin, anticholinergic, cocaine, NMS
Misc- iatrogenic overheating, heat stroke

45
Q

What are the risk factors for aspiration?

A

Decreased LOC- EtOH, anesthesia, head injury, cns pathology
Impaired airway reflexes-prolonged intubation, CVA, decreased LOC
Abnormal anatomy-zenkers diverticulum, esophagael stricture
Decreased GE competence-
Increased intragastric pressure-
Delayed gastric emptying- narcotics, anticholinergics, sympathetic tone, pregnancy, renal failure, diabetes

Pharmacotherapy (14 decks)

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