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RT-131B - FInal Sem > Sedatives, Paralytics, Analgesics > Flashcards

Sedatives, Paralytics, Analgesics Flashcards

1
Q

What are the goals of Analgesics and Sedatives?

A

Patient Comfort
Reduce Anxiety/Agitation
Provide Pain Relief
Retrograde Amnesia

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2
Q

What are the goals of Paralytics?

A

Facilitate Procedures
Minimize Movement
Control Ventilation

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3
Q

What is the side effect that we are most concerned about when giving Analgesics, Sedatives, Paralytics?

A

A drop in BP

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4
Q

What are the drug classes in Sedatives?

A

Benzodiazepines
Neuroleptics
Anesthetic Agents

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5
Q

What are the drug classes in Analgesics?

A

Opioids

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6
Q

What drugs are under Benzos?

A

Diazepam - Valium
Midazolam - Versed
Lorazepam - Ativan

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7
Q

What is Haldol?

A

Neuroleptics
Treatment for agitation and delirium

Onset 3 – 20 minutes
Duration 18 – 54 hours

Potential side effects
Drowsiness/Lethargy
Muscle rigidity
QT prolongation
Torsades de Pointes
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8
Q

What is the reversal agent for Benzos?

A

Flumazanil

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9
Q

What is the commonly used low cost sedative?

A

Benzos

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10
Q

What are concerns with using Benzo’s in ICU patients?

A

ICU delirum when combined with Sleep disruption

Depression of Respiratory drive when mixed with Opioids in COPD

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11
Q

Tell me about Diazepam/Valium (onset, duration, elimination)

A

Rapid onset
2 – 5 minutes
Lipid soluble – can build up in the tissues for longer release
Easily crosses blood brain barrier

Long duration
Long half life of up to 120 hours!

Eliminated by kidney
Patients with renal impairment will have difficulty clearing

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12
Q

Tell me about Midazolam/Versed (onset, duration, elimination)

A

Rapid onset
2 – 5 minutes
Lipid soluble – can build up in the tissues for longer release
Easily crosses blood brain barrier

Shorter duration
Short half life of 3 – 11 hours

Eliminated by kidney
Patients with renal impairment will have difficulty clearing

Anterograde amnesic effect

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13
Q

Tell me about Lorazapam/Ativan (onset, duration, elimination)

A

Slower onset
5 – 20 minutes
Less lipid soluble
Does not easily crosses blood brain barrier

Longer duration
Longer half life of 8 – 15 hours

Metabolized by liver to inactive metabolites

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14
Q

What are side effects of Lorazapam/Ativan?

A

Lactic acidosis – Propylene Glycol used in manufacturing!
Hyperosmolar coma
Nephrotoxicity

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15
Q

Tell me about Propofol (onset, duration, Who its best used for)

A

Onset is very rapid

Duration is short when discontinued

Drug of choice for TBI patients
Ease of neuro assessment
Reduction of ICP

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16
Q

What are side effects of Propofol?

A

Significant and immediate hypotension can occur!
Bradycardia
Elevated Pancreatic Enzymes – Pancreatitis
Elevated Kcal
Pediatric Patients – Lactic Acidosis and hyperlipidemia
Propofol induced hypoxemia – dilute o2

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17
Q

What is the reversal agent for Opioids?

A

Nalaxone

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18
Q

What are side effects of Opioids?

A

Respiratory Depression
Bradycardia/Hypotension
Histamine release
Dependence

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19
Q

Tell me about Morphine (onset, duration, elimination)

A

Naturally occurring opioid agonist

Slow onset due to low lipid solubility
Slower transit across Blood Brain Barrier

Long acting due to active metabolites

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20
Q

What are side effects of Morphine?

A 
Hypotension
Hypoventilation
Decreased CPP/ICP
Drowsiness
Constipation/Vomiting
Bronchospasm!  (histamine release)
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21
Q

Tell me about Fentanyl/Sublimaze (

A

Synthetic opioid 150 times more potent than MSO4

Increased lipid solubility
Decreased onset and longer half life

Better choice for unstable cardiovascular patients
No histamine release

Respiratory depression with increased doses

22
Q

What are the uses of Paralytics?

A

Facilitation of less conventional mechanical ventilation strategies (e.g., inverse I:E ratios, high-frequency ventilation, permissive hypercapnia)

Facilitation of intubation, ensuring stability of the airway during transport or repositioning

Dynamic hyperinflation that cannot be corrected

Adjunctive therapy for controlling raised ICP

Reduction of oxygen consumption and carbon dioxide production

23
Q

What is minimal sedation?

A

Patients can respond to verbal commands, although cognitive function may be impaired.

Ventilatory and cardiovascular functions are unaffected.

24
Q

What is moderate or conscious sedation?

A

The patient can perform purposeful response following repeated or painful stimulation. (Note: Reflex withdrawal from painful stimulus is not considered a purposeful response.)

Modification of painful and frightening experiences

Spontaneous ventilation is adequate, and cardiovascular function is usually maintained.

25
Q

What is deep sedation?

A

The patient is not easily aroused but can respond to painful stimulation.

Spontaneous ventilation and maintenance of patent airway may be inadequate.

Cardiovascular function is usually maintained.

26
Q

What does it mean for a patient to be under Anesthesia?

A

This level involves general anesthesia, spinal, or major regional anesthesia; local anesthesia is not included.

Patient cannot be aroused, even by painful stimulation.

Ventilatory assistance is typically required (i.e., artificial airway and positive-pressure ventilation).

Cardiovascular function may be impaired.

27
Q

What is the reversal agent to non-depolarizing agents?

A

Neostigmine followed by Atropine (for bronchospams, brady, and increased secretions)

28
Q

Tell me about Succinylcholine (onset, duration, side effects)

A

Quick onset; less than 60 sec, with short duration;
5 – 10 mins

Minimal cardiac effect

Side effects
Hyperkalemia
Increased ICP and intraocular pressures
Malignant hyperthermia
Tx: Dantrolene
CANNOT BE REVERSED!
29
Q

Tell me about pancuronium (onset, duration, side effects)

A

Long term continuous infusion for ICU
Prolonged paralysis

Due to metabolites maintaining 50% active

Side effects - Vagolytic
Tachycardia
Increased CO and MAP
Pulmonary Vasoconstriction

30
Q

Tell me about vecuronium (onset, duration, side effects)

A

Intermediate duration

Lack of Vagolytic effects makes it a better choice

Better for asthma patients

31
Q

Tell me about Atricurium/Cisatricurium (onset, duration, side effects)

A

Intermediate duration

Less hemodynamic effect than pancuronium

Can cause hypotension secondary to mast cell degranulation At increased doses

32
Q

How can you monitor the effect of paralytics?

A

Spontaneous breathing or train of four

33
Q

How can you assess pain relief?

A

Pain scale

34
Q

Who can benefit from an BIS monitor, what is the scale?

A

Anesthesia/sedation
Level of 40 – 60 shows adequate anesthesia
Controversial regarding efficacy

35
Q

How do you assess a train of four?

A

the # of twitches that a patient gives dictates the level of paralysis.

4 out of 4 is no paralysis

36
Q

Non-depolarizing agents block muscle contractions by what method?

A

Competitive inhibition

37
Q

when given a non-depolarizing agent is given, are patients still able to regain movement with their receptor sites still occupied?

A

yes

you can move with 75% of the sites occupied. >75% start to show effects.

38
Q

depolarizing agents block muscle contractions by what method?

A

Prolonged occupation and persistent binding

39
Q

what can you say about non-depolarizing agents with regards to dosages and effect

A

non-depolarizing drugs are dose dependent.

dosage are based on weight

40
Q

What do non-depolarizing reversal agents do at the neuromuscular junction?

A

they clear the NMJ of actylcholenesterase in order to flood the area with more ACH to knock out the drug.

Actylcholenesterase Inhibitors (AChEI)

41
Q

what is a test doctors use to measure ach production during non-depolarizing agent weaning?

A

head neck lift test.

the ability of the patient to lift the neck can burn ACH and see if the patient has enough ability to replace it.

42
Q

what is the onset and duration of a depolarizing agent?

A

60-90 secs with a duration of 10-15 mins

43
Q

Who do you NOT give a depolarizing agent to?

A

hyperkalemic patients (like burn patients and chest trama patients)

patients who have a full stomach
increased intraoccular pressure
increased intacranial pressure

44
Q

what are 2 alternative metabolism pathways for NMBAs?

A

hoffman degradation and plasma cholinesterase

45
Q

Atricurium/Cisatricurium are eliminated in the body by how?

A

nonenzymatic breakdown Hofmann degradation

46
Q

What is laudanosine?

A

breakdown product of Hofmann degradation in Atricurium.
Small amounts in Cisatricurium

Can cause neurostimulatory effects

47
Q

What are the effects of Prolonged propofol in PEDS parients?

A

Lactic Acidosis and Hyperlipidemia

48
Q

What drug should be avoided for patients with reye syndrome?

A

Aspirin

49
Q

What sedative has the least effect on blood pressure?

A

Etomidate

50
Q

Toxic levels of alcohol that affect the respiratory arrest are at what range?

A

400-600 mg/dl

RT-131B - FInal Sem (12 decks)

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