Induction Agents and Adjuvants (Mod 3) Flashcards
1
Q
What is the MAC of Isoflurane?
A
0.0115 atm (low)
2
Q
What is the B/G coefficient of Isoflurane
A
1.4 (Large)
3
Q
What are common and adverse effects of Isoflurane?
A
Could depress CV (affects the myocardium) and the respiratory depression
- could lead to arrhythmias
4
Q
Is isoflurane dose dependant?
A
Yes; it has a high potency (low MAC) with low solubility (large b/G)
5
Q
Contraindications for Isoflurane?
A
susceptibility to malignant hyperthermia
6
Q
What is the relative potency and solubity of Sevoflurane?
A
High potency (low Mac) and low solubility (high b/g coefficient)
7
Q
What can Sevoflurane be used as?
A
A potent bronchodilator; has been used in treatment of status asthmatics
- Can be used for Asthma
- Sweet smell and well tolerated for inhalation induction
8
Q
Complications with Sevoflurane
A
Sevoflurane degrades into toxic compounds in the presence of a carbon dioxide absorber. Can cause nephrotoxitiy
- causing CV and resp depression (and arrhythmias)
- **Renal Toxicity)
9
Q
Desflurane relative potency and solubility?
A
Moderate potency (MAC 0.06 atm mod) and low b/g coefficient (0.45)
10
Q
Why is Desflruane a poor induction agent?
A
Pungency irritates the airway; increases risk of cough and laryngospasm
11
Q
Which anesthetic gas has a similar induction time as nitrous oxide?
A
Desflurane; much more potent though (oil/gas partition coefficient is higher)
12
Q
What occurs with increased/rapidly high concentration of anesthetics? -> think Desflurane
edit
A
Causes marked activation of the sympathetic nervous system
13
Q
Relative potency and solubility of Nitrious Oxide?
A
Low potency (High MAC:1.04) and low b/g coefficient (b/g = 0.47)
14
Q
Why is Nitrous oxide paired with other anesthetic agents?
A
Low potency means the need to maintain a acceptable partial pressure of O2 prevents the attainment of full anesthesia
- Can provide a analgesic effect in combo with other agents
- 2nd gas effect?
15
Q
What are some adverse effects and considerations for Nitrous Oxide?
A
2nd gas effect; diffusion hypoxia aka cana displaces other gases
- Can cause expansion of air collections (pneumothorax, bowel obstruction, obstructed middle ear, intracranial air)
16
Q
Which anesthetic gas does not require a vaporizer?
A
Nitrous oxide, it mixes in with regular O2
17
Q
What is Thiopental?
A
Barbiturate; ultra short acting; can induce anesthesia in seconds; BUT no reversal agent
18
Q
Dose for Thiopental?
A
3-4 mg/kg IV
19
Q
What are indications for Thiopental aside from
A
Reduction in elevated ICP (cerebral vasoconstriction) and seizures (increases the threshold for action potneitals in teh brain)
20
Q
General doses for IV anesthetics?
A
3-4 mg/kg IV
21
Q
Risk factor with Thiopental (barb)
A
Laryngospasm or Bronchospasm may occur with induction of light anesthesia and with airway manipulation (intubation).
- potent short acting drug with no reversal agent. subbed out with propofol
- indicated for elevated ICP or seizures, but benzos are preferred if available
22
Q
Why is Propofol preferred to short acting barbiturates?
A
Ultra short acting; rapidly metabolized, meaning faster recovery than barbiturates
23
Q
What is Propofol used for?
A
Induction and maintenance (sedation for mech. ventilation)
24
Q
Why could Propofol be a source of infection?
A
It’s a intralipid preparation; side note, its also a large caloric source
25
Why is Propofol generally not used for patients with low BP?
Could cause shock or cardiac arrest
1. Produces considerable decrease in BP w/reduction of up to 25-40% in systolic mean and diastolic pressures w/standard induction doses
2. Both arterial and venous dilation results in reduction in SVR
3. Inhibits baroreceptor response, limiting the normal increase in HR that occurs with decreased SVR
26
What does a inhibited or decreased baroreceptor response cause?
Inhibits the hypoxic respiratory drive and reduces the normal ventilatory response to hypercapnia
27
Induction dose of ketamine
0.5-2 mg/kg IV
28
Maintaince dose of Ketamine?
3-5 mg/kg IV
29
What are the desired affects of ketamine?
- Analgesia
- No effect on respiratory drive
- Cardiovascular stability; Increases cardiac output by inhibiting norepinephrine reuptake
30
What are secondary affects of Ketamine?
Produces dissociative anesthesia
- Patient may seem awake but is actually in an analgesic and amnesic state
31
Why could Ketamine increase CO?
Ketamine blocks receptors like norepinephrine from binding to synape sites
- thus MORE norepinephrine will reside in the space between, prolonging the affects on CO
- it inhibits norepinephrine reuptake
32
What are Adjuvants?
Provides additional effects that are desirable during surgery (help balanced anesthesia), but not necessarily provided by general anesthetics
33
3 classes of adjuvant drugs?
1. Benzodiazepines and other sedatives
2. Neuromuscular Blockades
3. Opiates and Opioids
- There are others tho
34
What is Glycopyrrolate (Robinul)?
Reduces secretion production and **treat bradycardias**
- sometimes used to help increase BP
- Adjuvant
35
How does Glycoprrolate indirectly help increase BP?
Helps with contractility (maintain CO)
36
What is Glycopyrrolate used with?
Used in conjunction w/neostigmine to mitigate the effect of bradycardias
37
What is Phenylephrine (neo synephrine)?
Alpha 1 agonist; which increases SVR via vasoconstriction
- Very potent aka quick onset of action
- Could cause reduction of organ perfusion
- Adjuvant
38
When is Phenylephrine used?
when low perfusion/severe hypotension is present via bonus
39
What is Ephedrine ?
General adrenergic medication: Chronotrope, inotrope, and vasopressor
- Stimulates both alpha and beta receptors
- **Stimulates norepinephrine release and reduces uptake**
40
what is Dexmedetomidine (precedex)?
Sedative; Short acting alpha 2 adrenergic agonist; **inhibits release of norepinephrine**
- Decreases activity of noradrenergic neurons in the brain and brain stem which leads to an increase in GABA (inhibitory) activity
- Mimics sleep by promoting an endogenous sleep pathway (mimics natural sleep more than most sedatives)
- **Does not impact respiratory drive**
41
When is Dexmedetomidine used?
Sedation of intubated patients; does not impact respiratory drive
42
Dose of Demetomidine
0.2-0.7 ug/kg/hr continuous infusion
43
What are Benzodiazpines?
Adjuvants used to modulate **Gabanergic** transmission aka inhibitory transmission (gaba agonist)
44
Clinical applications of Benzos?
- Anxiolytics
- Sedatives
- Anti-epileptics
- Muscle Relaxants
- Treatment of ethanol withdrawal symptoms
45
What does anterograde amnesia?
Helps reduce PTSD with remembering operations
46
What is midazolam?
Rapid onset and short acting (3-8 hours) anxiolytic/sedative/amnestic
- Synergistic potentiation with opiates
- Benzo
47
When is Midazolam used?
Used as a preanesthetic to reduce the requirement of anesthetic, to induce anterograde amnesia
48
Dose for Midazolam
Dose (Preanesthesia) 0.1 – 0.3 mg/kg every 2 mins as necessary for sedation
49
How do NMBs work?
Produce skeletal muscle paralysis by interfering with Acetylcholine at the neuromuscular junction
50
Onset for Pancuronium?
Quick onset, long acting NMB
Onset 60-90 seconds; Effects last 45-60 mins
51
Dose for Pancuronium?
Dose: 0.08 mg/kg; anesthetic agents will potentiate the effect
52
How are vitals affected by Pancuronium?
Modest increase (<15%) in HR and BP (due to inhibition of norepinephrine reuptake)
- Does not result in histamine release?
- risk of apnea tho
53
How is Rocuronium reversed?
With Sugammadex (think the febreeze affect)
- Acts as a chelating agent, encapsulating the free rocuronium to form a stable complex
54
Onsent of Rocuronium
Quick onset; intermediate acting
- 60-90 seconds; effects last 35-45mins
55
Dose for Rocuronium
0.3-0.5 mg/kg IV
56
What are the risks of using a NDMR like Rocuronium?
Hypertension;apnea -> need to confirm
57
Why is hyperkalemia bad?
High potassium in the blood and therefore the heart will prevent the heart from contracting -> cardiac arrest
58
Add slide 31 -> hinted to be tested material
59
What are some drawbacks of Morphine and opioids?
- general use?
Morphine and deriatives allow good hemodynamic stability **but** causes reduced ventilary drive
- Analgesics are generally used to relieve pain with no loss of consciousness. (normal dosages)
60
How do Opioids produce analgesia?
Analgesics are generally used to relieve pain with no loss of consciousness. (normal dosages)
- Sometimes they can be used as the sole agent in anesthesia
- Conspitation
61
Affects of Opioids in the brain?
alter mood, produce sedation, and reduced the emotional reaction to pain
62
Affect of Opioids in the brainstem?
opioids increase the activity of cells that provide descending inhibitory innervation to the spinal cord
63
Mechanism of Action for Opiates and Opioids?
Slide 34
64
Gold standard opiate/opioid used?
Morphine; used peripherally for long lasting analgesia
- Available by PO, IV, IM, SC, epidural, spinal, and rectal
65
Dose of Morphine?
2.5- 5mg IV slowly titrated to effect
66
Most potent opioid in clinical use?
Sufentanil; 10-15 times more potent than fentanyl; which is 100 times more potent than morphine
67
Induction dose of Sufentanil?
1.3-2.8 ug/kg
- doses of 0.3-1 ug/kg can be used to blunt the hemodynamic response of intubation can be associated w/muscle rigidity, especially when admin’d
68
Is Sufentanil dose dependent?
69
Contraindications for Depolarizing Muscle Relaxants like Succ?
- Burns (hyperkaliemia)
- Traumatic paralysis
- Myasthenia Gravis and NMB
70
Why is Pungency a factor for inhaled anesthetics?
Pungency irritates the respiratory tract therefore not typically used to induce a patient (for some gasses such as Isoflurane)
71
General contraindications for inhaled anesthetics?
Susceptible to malignant hyperthermia
72
Why should Nitrous Oxide always be administered with oxygen?
Diffusion Hypoxia (second gas effect)
73
Induction dose for Propofol?
1-2.5 mg/kg IV
74
Maintenance dose for Propofol?
5-50 ug/kg/min IV infusion
75
What do Alpha 1 agonists do?
Increase SVR via vasoconstriction
76
When would Phenylephrine (neo syneprhine) be used
When low perfusion or severe hypotension is present
- Typically given bolus
- very potent
77
What are neuromuscular blockades?
Introduction of a agent that produces skeletal muscle paralysis by interfering with Acetylcholine at the neuromuscular junction
78
How does a non depolarizing muscle relaxant work?
NDMR compete with acetylcholine at the nicotinic receptor. Non depolarizing NMB antagonize (inhibit) the effect of acetylcholine, preventing the action of muscle movement.
- Dose dependent; greater the dose the greater the intensity of muscle paralysis
79
What is the reversal agent for Rocuronium?
There is 2!
- Sugammadex
- Neostigmine
- Apparently anticholinesterase as well? 0->need to confirm
80
How do Depolarizing Muscle relaxants work?
- 3 steps
- Succinylcholine
1. Activate cholinergic receptors at the neuromuscular junction to produce depolarization of the cell membrane
2. The result is a brief period of excitation, manifested by wide-spread fasciculations in muscle cells, followed by flaccid paralysis
3. Paralysis occurs because the agent maintains the cells in a depolarized condition, preventing repolarization and activation of muscle sarcomeres
81
What does Succinylcholine do?
Depolarizing muscle relaxant used for RSI
- No effect on consciousness or pain threshold
- Stimulates both nicotinic and muscarinic receptors; may cause bradycardia, dysrhythmias
- short term drug for conscious sedation
82
How does Succinylcholine affect ICP?
Succ can increase ICP up to 10mmhg
83
Dose for Succinylcholine?
0.5-1.5mg/kg IV
84
What risks are involved using Succinylcholine?
May cause bradycardia and dysrhythmias
- don't use on burns or trauma pts
- Could increase ICP as well
85
Why do patients with Myasthenia Gravis and NMB require a lower dosage for paralytics?
MG patients have fewer Ach receptors available due to destruction and down regulation by the body. MG patients have up to 80% fewer receptors available
86
Why is dosage important to be mindful of when administering a paralytic (NMB) for patients with conditions like Myasthenia Gravis?
Under normal conditions approximately 20% of receptors are required to be activated for neuromuscular transmission. **The remaining 80% of the receptors constitute a safety margin**
- **In MG, there is a decrease in functional receptors** with a subsequent decrease of the safety margin.
- Because there are **fewer receptors and a reduced safety margin, only a minimal amount required to be blocked to prevent neuromuscular transmission** due to marked sensitivity to Non-depolarixing NMB
87
Important consideration IV anesthetic
cannot easily be removed by ventilation, need to careful administration to avoid severe CNS depression. Hard to reverse
88
Distribution order of IV anesthetics
Blood (venous) - VRG - MG - FG
89
Depol NMBA in Myasthenia Gravis?
Increase dosage
90
Nondepol NMBA in myasthenia gravis
Decrease dosage (due to decrease in number of receptors available)
91
Succinylcholine contraindications?
Burns, Traumatic paralysis
- **May increase amount of potassium out of the muscle cells resulting in cardiac arrest**
- admin of succ will abnormally raise potassium out of the cells = cardiac arrest
92
Depolarizing muscle relaxants
Activate cholinergic receptors
producing depolarization but prevent re-polarization
- will see fasciculations during first seconds, demonstrating depolarizing. then muscles will relax
- compete for receptor sites
93
Non depolarizing muscle relaxants
compete with Ach at nicotinic receptors.
- Inhibit the effect of depolarization. preventing any muscle movement
- less receptors available
94
Rocuronium use
Used alot in ICU and OR>
no effect on pain or consciousness
- may result in apnea and HTN
95
Isoflurane usage
used for maintenance, but to to high potency, respiratory tract irritations causes it not to be used much
96
Contraindications to inhaled anesthetics (except N2O)
Malignant Hyperthermia
97
Desflurane characteristics
Very low BG coefficient
Need special vapourizer due to boiling point
Better balance and induction agent
98
Which inhaled anesthetics do NOT cause bronchospasm
Sevoflurane
N2O
99
How is paralytic dosing controlled to reach therapeutic affect for myasthenia gravis and neurological muscles disorders?
For depolarizing blockages, you need more of the drug because the receptors are competing
- competition for the receptors and how the drug works, trying to block it, few there and less of you need to
100
How do motor vehicle collisions affect succinylcholine?
Increases number of extra junctional receptors
101
Depolarizing vs non depolarizing
- DP: nicotine, polarize and create the action vasculations but prevents repolarization. Anti cholinergic.
- Non DP: Nicotinic; antagonist, prevent action potential of the neurons.
102
Why would you use non depolarizing agents like roc or pancuronium over succ?
Pancuronium and rocuronium allows for cardiac stability by potentially increasing heart rate and blood pressure by preventing reuptake of norepi
- heart keeps beating, but the skeletal muscles are impacted
