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001 Respiratory Therapy > Anesthesia Pharmacology > Flashcards

Anesthesia Pharmacology Flashcards

1
Q

Intravenous Anesthetics

A

The drug will be injected into the arterial (rare) or venous circulation which allows for

  • Rapid distribution to the site of action (usually the brain/CNS)
  • Quick onset of action
  • Titration of “dose to effect”
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2
Q

Disadvantages of Intravenous Anesthetics

A

Possible severe side effects

Anaphylaxis

Phlebitis, thrombophlebitis, PTE

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3
Q

Dose to Effect

A

Intravenous Anesthetics

Dose can be slowly increased until the desired effect is achieved and then will be maintained through a slow continuous infusion

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4
Q

Tissue Up-Take

A

The rate and amount of the drug absorption is proportional to blood flow and tissue mass

High perfusion or vessel rich organs will receive peak concentrations of a drug within 30 to 60 seconds.

As time passes, the concentration of the drug in the large muscle mass can exceed that of the brain (5 to 10 minutes) therefore continuous infusion is necessary

Lipid soluble agents (Thiopental etc.) will also be taken-up by fat tissue.

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5
Q

Lipid Soluble Agents

A

Ex. Thiopental

Will also be taken-up by fat tissue

The rate may be slow (poorly perfused) but the high mass will cause continued absorption by this tissue, and later, expect slower recovery or more residual effect after administration is discontinued.

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6
Q

Regional Blood Flow

A
  • Vessel Rich Viscera-70%
    • Brain, heart, liver, kidney
  • Muscle-25%
  • Adipose Tissue-4%
  • Vessel Poor Tissue-1%
    • Skin, cartilage, bone
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7
Q

Elimination

A

The removal of intravenous drugs from the body is achieved by

Metabolism: Liver has mixed function oxidase that convert the drug to inactivate variants (Ex. Cytochrome P450)

Excretion: Activated by the normal kidney or through the bile/feces pathway

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8
Q

Isopropyl Phenols

A

Propofol

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9
Q

Barbiturates

A

Thiopental

Methohexital

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10
Q

Benzodiazepines

A

Midazolam, Diazepam etc.

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11
Q

Phencyclidines

A

Ketamine

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12
Q

Carboxylated Imidazoles

A

Etomidate

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13
Q

Propofol Trade Name

A

Diprivian

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14
Q

Propofol Dose

A

Loading Dose of 1.5-2.5mg/kg

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15
Q

Propofol Use

A

Used in outpatient procedures due to rapid redistribution and elimination

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16
Q

Propofol Advantages

A

Anti-Emetic

Lack of sumulative effect is helpful for total anesthesia (TIVA)

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17
Q

Propofol Side Effects

A

May cause vivid dreams and sexual fantasies during emergence

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18
Q

Propofol Respiratory Effects

A

May cause transient apnea with a reduced response to O2 and CO2

Will not cause bronchospasm

May cause bronchodilation

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19
Q

Propofol Duration of Action

A

3-8 min

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20
Q

Propofol Elimination Half Life in Hours

A

4-23

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21
Q

Thiopental Trade Name

A

Sodium Pentothal

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22
Q

Thiopental

A

Slow acting

No analgesic action

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23
Q

Thiopental Dose

A

3-5 mg/kg is used for the initial induction

Slow injection allows for dose to action titration

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24
Q

Thiopental Duration of Action

A

5-10 min redistribution sends more agents to muscle mass

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25
Q

Thiopental Half Life

A

11 hours

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26
Q

Thiopental Uses

A

Induce Unconsiousness

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27
Q

Thiopental Side Effets

A

Decreased cerbral oxygen demand

Decreased myocardial function

Possible decrease in vascular tone which will lead to hypotension

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28
Q

Thiopental Respiratory Effects

A

Due to it association with an increased airway reactiveness this is not used with asthmatics

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29
Q

Diazepam Trade Name

A

Valium

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30
Q

Diazepam

A

Widely used tranquilizer

Causes pain at peripheral injection site

Better to infuse through a central line

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31
Q

Diazepam Dose

A

0.3 to 0.6 mg/kg dose can achieve induction

Metabolized by the liver and excreted by the kidney (70%) & bile/feces (30%).

Prolonged effect due to first metabolites having nearly as strong an effect as the original drug.

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32
Q

Diazepam Duration of Action

A

15-30

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33
Q

Diazepam Elimination Half Life

A

20-50

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34
Q

Diazepam Uses

A

Pre anesthetic sedation

Mild muscle relaxant and anti-convulsant

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35
Q

Diazepam Respiratory Effect

A

Can cause the loss of airway reflexes at high doses and a decrease in tidal volume at lower doses

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36
Q

Midazolam Trade Name

A

Versed

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37
Q

Midazolam Dose

A

0.1 to 0.3 mg/Kg dose.

Metabolized by liver—excreted by kidneys

Duration of action is 15 minutes—longer than thiopental but less than valium.

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38
Q

Midazolam Duration of Action

A

15-20

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39
Q

Midazolam Uses

A

Cardio-version

Intubation

Bronchoscopy

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40
Q

Midazolam Respiratory Effect

A

Little effect on RR

Can cause the loss of airway reflexes at high doses and a decrease in tidal volume at lower doses

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41
Q

Midazolam

A

A stronger cousin of Diazepam (X2-3)

Will have the same pharmacological action as diazepam, but also has anterograde amnesia effects. The patient will appear awake but will have no memory of the event afterwards

Little effect on BP, cerebral blood flow, ICP

No pain at injection site

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42
Q

Ketamine Trade Name

A

Katalar

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43
Q

Ketamine Dose

A

Given IV or IM in 1-2 mg/kg dose over 1 minute

Duration of action is 5-10 minutes

Converted in liver and exreted by kidneys

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44
Q

Ketamine Duration of Action

A

5-10 min

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45
Q

Katamine Elimination

A

2-4 hours

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46
Q

Katamine Uses

A

Will Create a dissociative mental state

Used in burns, pediatrics, etc

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47
Q

Dissociative Mental State

A

Catalepsy-Trance like state with muscle rigidity

Sedation

Amnesia

Analgesia

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48
Q

Ketamine Side Effects

A

Increased BP (20-40 mmHg)

Increased HR

Increased ICP

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49
Q

Ketamine Respiratory Effects

A

Patient can maintain airway

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50
Q

Ketamine

A

Pts need dark, quiet room to recover as can cause hallucinations/bad dreams (emergence delirium)

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51
Q

Etomidate Dose

A

Loading dose: 0.2 to 0.3 mg/kg

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52
Q

Etomidate Duration of Action

A

3-8 min

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53
Q

Etomidate Half Life

A

2.9-5.3 Hour

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54
Q

Etiomidate Side Effect

A

Some adrenal suppression, (which may be advantageous in some pts).

Potent cerebral vasoconstrictor.

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55
Q

Etiomidate

A

No Analgesia effects

Minimal cardio vascular effects

Possible alternative to Propofol or Thiopental

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56
Q

Thiamylal

A

Ultra short acting pentothal

Being phased out

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57
Q

Methohexital

A

Cousin of thiopental

Faster hepatic extraction therefore less residual drowsiness and less cumulative effect

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58
Q

Lorazepam

A

Cousin of valium

Long Duration and Action and Half-Life

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59
Q

Inhalation Anesthetics

A

Major role is the maintance of anesthesia after the patient has been induced through another means (ex. IV Thiopental)

Induction can be indicued by these agents when there is contraindications (ex. small children)

These agents are introduced to the body via the respiratory tract and distributed by normal circulation

As vapours these agents will behave according to normal gas laws

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60
Q

DALTONS’ LAW

A

Ptotal = P1 + P2 + P3 + P4 etc.

The total pressure in a gas mixture is equal to the sum of all the partial pressures.

The partial pressure of each gas is proportional to the volumetric percentage of each gas.

The partial pressure of each gas is the pressure it would exert if it were alone in the container.

Eg. A gas mixture of 10 litres total, containing 100 mL of Halothane vapour is a 1% concentration. (FiHalothane= 0.01)

At BTPS, that 1% in a gas would exert a pressure equal to;

(760-47) * 0.01) = 7.13 mmHg.

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61
Q

COMPARTMENTS

A

Compartments can be considered as the different spacesagents need access to, to achieve their desired effect.

For inhaled agents the first compartment is the lung.

Agents need to traverse the A/C membrane to get to the second compartment — the blood.

The blood–brain barrier needs to allow agents in to get to the usual site of action in the brain (CNS) — the third compartment.

Partial pressure is the primary determinant of diffusion.

If pressure equilibrium is achieved, and therefore no pressure gradient exists, movement of agent will stop.

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62
Q

Minimum Alveolar Concentartion (MAC)

A

A measure of a drugs potency and is the minimum concentration that is needed in order to prevent the movement of 50% of pt when an incision is made—

The lower the MAC, the more potent the agent.

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63
Q

MAC and Solubility of Sevoflurane

A

2% in 100% O2

1.1 in 70% N2O

B/G Sol CoEf 0.69

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64
Q

MAC and Solubility of Enflurane

A
  1. 70% in 100% O2
  2. 57% in 70% N2O

B/G Sol CoEf 1.9

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65
Q

MAC and Solubility of Isoflurane

A
  1. 15% in 100% O2
  2. 5% in 70% N2O

B/G Sol CoEf 1.4

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66
Q

MAC and Solubility of Halothane

A
  1. 77% in 100% O2
  2. 29% in 70% N2O

B/G Sol CoEf 2.4

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67
Q

MAC and Solubility of Methoxyflurane

A
  1. 16% in 100% O2
  2. 07% in 70% N2O

B/G Sol CoEf 1.9

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68
Q

MAC and Solubility Coefficient of Desflurane

A

6% in 100% O2

3.50% in 70% N2O

B/G Sol CoEf 0.6

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69
Q

MAC and Solubility Coefficient of Nirtous Oxide

A

104%

Sol CoEf 0.47

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70
Q

Stacking MACs

A

The different MACs of agents can be combined for greater effects, but combing them is not precise and there can be a range of reactions

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71
Q

What Are Factors That Will Increase MAC

A

—Hyperthermia

—Drug use

—Chronic alcohol abuse

—Amphetamines

—CNS stimulants

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72
Q

What Are Factors That Will Decrease MAC

A

—Advanced age

—Hypothermia

—Severe hypotension

—Other agents; opiates,valium

—Acute drug or ETOH intox.

—Pregnancy

—High PCO2, Low PO2

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73
Q

What Factors Will Not Influence MAC

A

Gender

Duration of anesthesia

Mild hypercapnia

Hypocapnia

Mild anemia

Mild acid-base imbalance

Hypertension.

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74
Q

Cumulative Effect

A

—Patient may well have been given:

  • Pre-operative sedation.
  • Induction agent—Propofoletc.
  • Intra operative opioids.
  • Muscle relaxants.
  • Halogenated hydrocarbons.

—All agents can contribute to the depth of anesthesia. Repeated assessment of the depth of anesthesia is mandatory.

Vital signs, tearing, obvious movement, etc.

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75
Q

Alveolar Uptake is Determined By

A
  • —Inspired concentration ( [] effect)
  • —Washout of alveolar gas
    • –Alveolar ventilation
    • –Functional residual capacity
  • —Uptake by pulmonary blood flow
    • –Solubility of agent in blood
    • –Cardiac output
    • –Alveolar-mixed venous tension gradient
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76
Q

Oil to Gas Solubility

A

The more soluble the gas the more potent it is

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77
Q

Second Gas Effect

A

Because nitrous oxide has a low blood solubility it will equlilbrate very fast, it also has a large MAC meaning you can use a lot of it before you will ever see the affects. Due to this we can combine nitrous oxide with other inhaled drugs to help them equalibrate faster —

Solubility is related to the speed at which a drug will enter the blood/brain

Potency is how much you need of a drug to see effect

So second gas effect is combining drugs with low solubility (nitrous oxide) with drugs with high potency allowing for quicker induction and less quantity of any particular component.

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78
Q

Drug / receptor affinities.

A

Different drugs will have different affinities for one type of receptor OR the same drug may have different affinities for similar but different receptors.

—Drugs can be active on enzyme function and not receptors. General anesthetic inhaled agents seem to have no specific receptor site but are highly lipid soluble and cause some CNS cell membrane changes.

—Generally speaking, drugs that excite the CNS (amphetamines), will increase the MAC; drugs that depress the CNS (sedatives/hypnotics, tranquilizers, narcotics) will decrease the MAC.

—If a drug like valium was to decrease the MAC by 20% it could be said to contribute a MAC fractionof 20%.

79
Q

General Anesthesia Therories

Meyer Overton

A

—Critical volume hypothesis, cell membrane volume swelling or expansion may obstruct ion channels and therefore electrical activity.

80
Q

General Anesthesia Therories

Membrane Fluidization

A

—Lipids surrounding an ion channel that are normally a semi-rigid gel, may liquefy and block the channel.

81
Q

General Anesthesia Therories

GABA

A

—GABA = gamma-aminobutyric acid

A neurotransmitter that binds to receptors on CNS neurons, to inhibit their action may be potentiated by anesthetic agents. The GABA binding/blocking is strengthened.

82
Q

Nitrous Oxide

A

Blue Tank Shoulder

—Mac of 104%.

Very lowsol CoEf.

—Often used as a 70% strength with balance O2.

—Weak anesthetic, good analgesic. ‘Entonox’ 50/50.

—Used in combination with a narcotic analgesic and muscle relaxant, and a stronger anesthetic.

Some respiratory and myocardial depression

83
Q

Enflurane

A

Orange Tank Color

Pleasant odor

Good muscle relaxant

Muscle relaxant properties similar to IsoF.

84
Q

Isoflurane

A

Purple Tank Color

—Dose related decrease CNS, slight increase ICP (Tx w/hypervent)

Potentiates non-depolmuscle relaxants ( decreased by 1/3).

85
Q

Desflurane

A

Blue Tank Shoulder

Least potent (MAC 6%)

Least soluble (rapid induction and recovery)

—Sympathomimetic Properties: Dose related tachycardia / hypertension, very resistant to biodegradation therefore little chance of systemic toxicity.

86
Q

Sevoflurane

A

Yellow Tank Color

Non pungent odor, (is used for induction)

87
Q

Des Cardiovascular Effects

A

BP: Increase

CO: No Change

SVR: Increase

HR: Increase

88
Q

Sevo Cardiovascular Effects

A

BP: Decrease

CO: No change

SVR: Decrease

HR: Increase

No PVC’s.

89
Q

IsoFl Cardiovascular Effects

A

Mild Cardiac Depressant

Few PVR, will not cause MI but may contribute to “coronary steal”

90
Q

EnFl Cardiovascular Effects

A

Although PVCs are less common, circulatory depression is greater than others.

91
Q

Des Respiratory Effects

A

Decrease Vt

Increase RR

Bronchodilation

Coughing and breath hold if given quickly

92
Q

Sevo Respiratory Effects

A

Decrease Vt

Increase RR

Bronchodilation

Dose related resp depression of both central and peripheral chemoreceptors.

93
Q

IsoFl Respiratory Effects

A

Decrease Vt

Small Increase RR

Decrease MV

Good Bronchodilation

94
Q

EnFl Respiratory Effects

A

Decrease Vt

Increase RR

Increase Upper Airway Irritability

Potent respiratory depressant

95
Q

EnFl Cautions

A

CO Decrease

Abnormal EEG and may cause seizures during hypocapnia

Potential nephro-toxic to pts with kidney disease.

96
Q

IsoFl Cautions

A

Uterine relaxant, may incidence of and severity of post-partum hemorrhage.

97
Q

Des Cautions

A

MAC of 6%

98
Q

Sevo Cautions

A

MAC of 2%

99
Q

Servo Drug Interactions

A

Decrease dose of muscle relaxant needed

100
Q

IsoFl Drug Interactions

A

Decrease dose of muscle relaxant needed

101
Q

Des Drug Interactions

A

Decrease dose of muscle relaxant needed

102
Q

EnFl Drug Interactions

A

Decrease dose of muscle relaxant needed

103
Q

Enfl Comments

A

Potential nephron toxic to kidney patients

104
Q

IsoFl Comments

A

Good for neuro-surgery, stable ICP, low Sol CoEf

105
Q

Servo Comments

A

Plesant smell

Low Sol-Coef

106
Q

Des Comments

A

Irritating smell

Low sol-coef, boils at 23.5oC

Dispensed as a gas from a heated vaporizer.

107
Q

Inhaled Gases Solubility

A

HE IS Dumb N2O

Halothane

Enflurane

Isoflurane

Sevoflurane

Desflurane

Nitrous Oxide

108
Q

Halogenated Hydrocarbons and Respiratory Effects

A

Both hypercapnic and hypoxic systems are depressed (EnFl is worst)

—Bronchodilationis caused by all, best with Halo.

—Hypoxic vasoconstriction is depressed by IsoFl.

—Halo and EnFlcan cause decreased cilliary function.

109
Q

Halogenated Hydrocarbons and Hepatic and Renal Effects

A

—All will reduce liver perfusion, Halo the most.

—Renal blood flow is decreased by all

—High concentrations of EnFl has caused nephro-toxicity.

110
Q

Halogenated Hydrocarbon and Metaboism, Toxicity, and Carcinogenicity

A

—Halothane undergoes the most extensive reductive metabolization (up to 40%) —- Isoflurane+ Des the least.

TOXIC in high doses: Halo—hepato, EnFl—nephro​

—Avoid all inhaled agents where the pt may be in the first trimester of pregnancy. (TIVA)

111
Q

Muscle Relaxants

A

Paralyzers

Muscle relaxants must NEVER, EVER, be given without sedation.

112
Q

Muscle Relaxant Caution

A

—Profound muscle relaxation is necessary during intubation and many operative procedures.

—Neuromuscular blocking agents have occasionally been used as a substitute for adequate anesthesia or for pharmacological restraints for combative patients.

—It should be remembered that these drugs can cause total muscle paralysis and therefore the ability to intubate and ventilate the patient must be available before indiscriminant use is contemplated.

113
Q

Parasympathetic Autonomic Pathway

A

Natural Agonists: Noreepinephrine (no effect), Epinephrine (no effect), and Acetylcholine (strong effect)

Artifical Agonists: Muscarine Pilocarpine

Heart and Blood Vessel Effect: Decrease HR and Force vasodilation

Antagonists: Atropine and Scopolamine

Degradation Blockers: Anti-cholineresterase

114
Q

Beta Adrenal Autonomic Pathway

A

Natural Agonists: Noreepinephrine (weak effect), Epinephrine (strong effect), and Acetylcholine (no effect)

Artifical Agonists: Isoproterenol (B1 and B2)

Heart and Blood Vessel Effect: Increased HR and Force vasodilation

Antagonists: Propranolol

Degradation Blockers: Monoamiine Oxidase Inhibitros and CCMT Inhibitors

115
Q

Alpha Adrenal Autonomic Pathway

A

Natural Agonists: Noreepinephrine (strong effect), Epinephrine (Weak effect), and Acetylcholine (no effect)

Artifical Agonists: Phenylephrine

Heart and Blood Vessel Effect: Constriction

Antagonists: Phentolamine

Degradation Blockers: Monoamiine Oxidase Inhibitros

116
Q

Synaptic Architecture

A

—->Action potential travels to synaptic end bulb ►ACh(or other) neurotransmitter spills out ► Post synaptic receptor takes up ACh, yields an action potential which

117
Q

Types of Muscle Relaxants

A

—Non-depolarizing:Blocks action potential without depolarizing post-synaptic neuron.

—Depolarizing:Blocks action potential by depolarizing post-synaptic neuron and preventing effective re-polarization.

118
Q

Long Acting Non-Depolarizing Agents

A

d-Tubocurarine

Pancuronium

119
Q

d-Tubocurarine

A

Original Gold Standard

Quick onset

Last 30-45 min

–Loading dose 0.4 mg/Kg, depolarizing and anesthetic agents will potentiate effect.

–Histamine release and sympathetic block result in hypotension

Caution with asthma

120
Q

Pancuronium

A

Trade Name: –Pavulon®

Duration of Affect: Quick acting, lasting 45-60 minutes

Loading Dose: 0.08 mg/kg

Depolarizing and anesthetic agents will potentiate effect.

Small histamine release

Action on vagus nerve (parasympatholytic) and catecholamine reuptake depression causes tachycardia and perhaps BP.

121
Q

Long Acting Non-Depolarizing Agent

A

Metocurine

Pipecuronium

Doxacurium

Alcurnium

122
Q

Metocurine

A

Similar to d-tubo

0.2 mg/kg

no histamine release

Can cause hypotension

Avoid renal failure

123
Q

Pipecuronium

A

Derivative of pabcuronium

0.05 mg/kg

Minimum cardiac effect

124
Q

Imtermediate Acting Non-Depolarizing Agents

A

Gallamine

Atracurium

Vecuronium

Cisatracuriumaka NimBex

125
Q

Gallamine

A

Strength = d-Tubox 0.2, 2.0 mg/Kg

–Quick acting, lasts 20+ minutes, little or no histamine release, cardiac vagal blockade causes sinus tachycardia.

Contraindicated in renal failure.

126
Q

Atracurium

A

0.4 mg/Kg

–Quick acting

Lasts 20+ minutes

Relative cardiac stability

127
Q

Vecuronium

A

0.08 mg/Kg

–Quick acting

Last 25+ minutes

128
Q

Cisatracuriumaka NimBex

A

4-5 times more potent than Rocuronium

–Rocuronium has a faster onset, shorter duration, and faster recovery when compared to cisatracurium.

129
Q

Rocuronium

A

Trade Name: Zemuron

Loading Dose: 0.3-0.5 mg/min

Onset Time: 60-90 seconds (ideal for RSI)

Intermediate Duration of Action: 35-45 min

Continuous Infusion (seldom done): 4-16 mcg/kg/min

130
Q

Neostigmine

A

Used with atropine to end the effects of non-depolarizing neuromuscular blocking medications

131
Q

Pyridostigmine

A

10 – 20 mg given with a half dose of Atropine

Slower onset but longer duration

132
Q

Short Acting Non-Depolarizing Agents

A

Mivaurium

133
Q

Mivacurium

A

Dose 0.15 mg/kg

Very short acting (15 min)

May cause hypotension due to histamine release

134
Q

Reversal Mechanisms & Drugs

A
  • How long a drug works for will depend upon amount used, distribution throughout the body, and metabolic and excretion pathways
135
Q

Anticholinesterase Drugs

A

Neostigmine

Pyridostigmine

Edrophonium

136
Q

Anticholinesterase

A

Using anticholinesterase allow concentration of ACh to build up which will complete with the drug at the neuromuscular junction ​

If the block is severe, the clinician will wait until some degree of muscle function has returned.

137
Q

Edrophonium

A

Tensilon®

1 mg / Kg (Small doses are ineffective in that they may allow relaxation to return)

Quicker onset and less muscarinic side effects. (like bradycardia, salivation etc

138
Q

Sugammadex

A

Reversal of neuro bloackade without inhibition of acetycholinesterase meaning it will not cause autonomic instability

Atropine do not need to be co-administered

Greater cardiovascular and autonomic stability than the traditional reversal agents

139
Q

Factors Effecting Action of Non-depol MR

A

—Priming

—Age

—Hypothermia

—Acid-Base Status

—Electrolyte Imbalance

—Renal Failure

—Myasthenia Gravis

—Eaton-Lambert (myasthenic-Oat Cell CA)

—Other Drug Interactions

140
Q

Priming

A

—A 10% dose of MR given prior to the actual need for anesthesia allows a much smaller dose to be given later.

—This will cause some paralysis in a small number of patients but allow easier reversal in the majority.

141
Q

Age and Non-Depolarizing Muscle Relaxants

A

—The very young (neonates and premies) have underdeveloped synaptic architecture.

—The very old may have decreased muscle mass and slower renal function.

—These conditions may dictate less MR needed to gain desired effect therefore less reversal agent.

142
Q

Hypothermia and Non-Depolarizing Muscle Relaxants

A

—Although cooler tissue is somewhat resistant to MR (more needed), the renal function is also slowed (more retained).

—Net result is a prolonged duration of action.

—

—

143
Q

Electroylte Imbalance and Non-Depolarizing MR

A

—Acute onset hypokalemia, potentiates MR action and depresses Neostigmines’ ability to reverse.

144
Q

Acid-Base Imbalance and Non-Depolarizing MR

A

—Respiratory acidosis, metabolic alkalosis potentiate the MR, but metabolic acidosis seems to decrease the action of MR.

145
Q

Renal Failure and Non-Depolarizing MR

A

—Drugs whose primary detoxification pathway is renal, will obviously stay in relatively high concentration in the patient with renal failure.

—The counterbalance is that the reversal drugs like neostigmine will also have a prolonged effect.

—Drugs with a high hepatoclearance pathway will not be as effected and the clinician may need less reversal agent if its’ main clearance route is nephro.

146
Q

Myasthenia Gravis and Non-Depolarizing MR

A

There will be antibodies that compete with ACH and will block or depress the action of ACH

—

147
Q

Eaton-Lambert Syndrome and Non-Depolarizing MR

A

Impaired Ach release mechanisms.

More susceptible to both depolarizing and non-depolarizing agents.

148
Q

Inhaled Agents Drug Interactions

A

All inhaled agents will potential non depl MR—

—

149
Q

Succinylcholine Drug Interactions

A

—Succinylcholine can before intubation to potentiate MRs by up to 20%. Therefore pts hould be showing signs of recovery from ‘Succs’ before more MRs are given.

—

150
Q

—Magnesium Sulfate Drug Interactions

A

—Magnesium Sulfate (for seizures) antagonizes the action of calcium at the motor end plate therefore enhancing the blockade.

—

151
Q

—Calcium channel blockers Drug Interactions

A

—Calcium channel blockers like verapamil will enhance the neuromuscular block.

—

152
Q

—Aminoglycosides Drug Interactions

A

—Aminoglycosides (streptomycin and others) potentiate non-depolMRs.

153
Q

——Anti-convulsants Drug Interactions

A

—Anti-convulsants like phenytoin and carbamazepine will actually depress the action of non-depol MRs.

154
Q

Depolarizing Muscle Relaxants

A

—Normally all muscles have some tension.

—They will increase tension if stretched.

—Peripheral surgery may require little relaxation.

—Deeper procedures need complete muscle flaccidness.

155
Q

Succinylcholine (Anectine)

A

Dose: 1-2 mg/kg

Duration of Action: 3-5 min

Produces a constant depolarization resulting in isotonic contractions and fasciculations

Rapid paralysis and vagal stimulation may lead to cardiac arrhythmias

—Broken down by plasma (or pseudo)-cholinesterase.

156
Q

Succinylcholine Side Effects

A

Arrhythmia

Salivation

Muscle pain and spasm—

Increased pressures (ex. gastric, ICP, ocular)

Increased potassium which is why it is not used with burns

157
Q

Succinylcholine Factors Effecting Action

A

◦Pre-curarization, small pre-dose of NonDepol

◦Self-taming,small pre-dose of Succs

◦Myotonia, succsmay aggravate, see next slide

◦Myasthenia Gravis, IgG antibodies block site

◦Atypical Plasma Cholinesterase, ↓breakdown

◦Others

158
Q

Myotonia

A

—Fainting Goats

—The inability to relax a muscle group, common to MD pts.

159
Q

Narcotic Analgesics

A

Morphine and derivatives allow good hemodynamic stability (but reduced ventilatory drive) and have been used as sole agents in anesthesia.

Analgesics are generally used to relieve pain with no loss of consciousness. (normal dosages)

160
Q

Mechanism of Action: Multiple Sites

A

Triggers a recpetor on a CNS neuron which will activate a G protein and become an inhibitory force

The action of Ca ion channels will become depressed

Substance “P” from sensory neurons in the spinal cord is involved in sending painful sensations to the brain. Opioids inhibit this transfer.

There are changes in nociception in the forebrain as well.

161
Q

Opioid Receptors

Delta

A

Effects: Analgesic effects in CNS & spinal cord, changes in affective behavior, no sedation, some ventilatorydepression

Agonists: Enkephalins

162
Q

Opioid Receptors

Kappa

A

Effects: Analgesic effects in CNS & spinal cord, miosis(small & possibly unequal pupil size), sedation, littleventilatorydepression

Agonists: Dynorphins

163
Q

Opioid Receptors

Mu

A

Effects: Analgesic effects in CNS & spinal cord, respdepression, constipation, N&V, euphoria, physical dependence, bradycardia

Agonists: Endorphins, Morphine, Synthetic Opioids

164
Q

Opioid Receptors

Antagonists for All

A

Naloxone (Narcan)

Naltrexone (Revia; used in morphine and alcohol dependence therapies.)

165
Q

Opiods Absorption

A

•Morphine and other opiates are very well absorbed by the lungs, mucosa, subQ tissue or muscular injection and less well through the GI tract.

166
Q

Opiods Distribution

A

Morphine’s main action is in the CNS, but transport across the blood brain barrier is relatively slower than other lipid soluble narcotics. Dependent on the site of injection.

167
Q

Opoids Uses

A
  • For relief of pain during and after surgery.
  • Subcutaneous injection; 10–15 mg.
  • IV 1 –2 mg (­dose, titration against analgesia).
  • Can be used to induce anesthesia in larger doses.
  • As a premedication with atropine (vagolytic).
168
Q

Systemic Effects of Opioids

CNS

A
  • Both a stimulant and a depressant.
  • Stimulation—pupils constrict, N & V, spinal reflexes (muscle rigidity), convulsions.
  • Depression—analgesia, sedation, mood changes (tranquil, drowsy), hypoventilation.
  • Possible miosisin high doses.
  • Other Effects: No direct action on cerebral circulation if PCO2is controlled.

Depressedneuro-function and pupillary constriction hampers neuro-assessment.

169
Q

Systemic Effects of Opioids

Respiratory

A
  • The Mu effect will depress the respcenters in the brain stem.
  • Vtseems preserved but RR decreases. Overdose causes death by hypoventilation.
  • Use with great caution in asthmatic or COPD pts.
170
Q

Systemic Effects of Opioids

Cardiovascular

A

•Dose dependent bradycardia, contractility preserved.

Decreased SVR due to peripheral vasodilation (resistance and capacitance vessels) and peripheral histamine release.

Little worry with healthy, supine pt. in usual dosages

171
Q

Systemic Effects of Opioids

A
  • Stimulates the smooth muscle of the GI tract leading to ineffective peristalsis, increased transit time and constipation.
  • Spasm of Oddi’ssphincter (liver) and biliary backup can cause acute angina like pain.
  • Relieved by nitro-glycerin (relieves both biliary pain and angina) or naloxone (Narcanâ)

•

172
Q

Tolerance and Addiction

A
  • After repeated use, toleranceto these drugs requires increasing dose for the desired effect.
  • Usually reversible with 2-3 week abstinence.
  • Addictionis psychological and physical —- after 8 or more hours of abstinence, dependence presents as;

Restlessness, anxiety, tearing, rhinorrhea, N&V, diarrhea, hypertension, tachycardia, cramps and muscle ache.

173
Q

Potency

A

•Potency refers to the amount of drug (usually expressed in milligrams) needed to produce an effect, such as relief of pain or reduction of blood pressure. For instance, if 5 milligrams of drug A relieves pain as effectively as 10 milligrams of drug B, drug A is twice as potentas drug B.

174
Q

Efficiacy

A
  • refers to the potential maximum therapeutic response that a drug can produce.
  • For example, the diuretic LASIX eliminates much more salt and water through urine than does the diuretic DIURIL. Thus, LASIX has greater efficacythan DIURIL.
175
Q

Potency and Efficicay

A
  • , greater potency or efficacy does not necessarily mean that one drug is preferable to another.
  • When judging the relative merits of drugs for a patient, clinicians consider many factors, such as side effects, potential toxicity, duration of effect (which determines the number of doses needed each day), and even cost.
176
Q

Responsiveness

A
  • “Responsiveness”of a particular patient to therapy with opioids would then refer to the success of therapy (regardless of dose) in terms of reducing pain to an acceptable level with acceptable side effects.
  • Therefore the differences in potencies between different opioids becomes much less important than which drug produces the right balance between analgesia and side effects.
  • The relative potencies of various opioids becomes important only when trying to switch opioids while maintaining equipotent analgesic effects.
177
Q

IM vs PO

A
  • The standard accepted ratio of the relative potency of IM to PO Morphine is 1:6.
  • Interestingly, this ratio seems to change with chronic dosing such that the ratio of IM to PO becomes 1:2-3.
  • The ratio of potency of immediate release morphine to sustained or controlled-release of morphine remains 1:1.
178
Q

Other Opioid Like Drugs

A

Meperidine (Dermerol)

Fentanyl

Papaveretum

Alfentanil

Remifentanil

Carfentanil

179
Q

Meperidine

A

•Demerol

10-15mg IV, 75-125 mg IM

  • Synthetic morphine, dry mouth and blurred vision.
  • Less constipation, less pupillary constriction.
  • May¯myocardial function in high dose.
  • Shorter period of action than morphine.
180
Q

Fentanyl

A

•Fentanyl 100 times stronger than morphine (or Sufentanil which is 5x-10 stronger than fentanyl).

Short duration of effect, severe respdepression.

181
Q

Papaveretum

A

50% Morphine

182
Q

Alfentanil and Remifentanil

A

reduced potency—rapid elimination —- quicker recovery

183
Q

Carfentanil

A

= Fentanyl x 100

200 ug is fatal.

184
Q

Opioid Reversal

A

Naloxone (Narcan)

  • Respiratory depression to the point of apnea is a hallmark of morphine overdose.
  • This opioid antagonist causes RR to increase, pupils to dilate, blood pressure to normalize and the patient to awake.
  • The adult dose of 100 mg IV, starts immediately and effects can be seen in 1 to 2 minutes. Short acting, repeat dose until desired effect is obtained, (ptcan return to lalaland).
  • Overdose of Narcanmay cause hypertension and agitation.

Naltrexone is an oral version given to addicts to blunt morphine euphoria and therefore desire.

185
Q

Codeine

A
  • natural opium alkaloid.
  • 10 to 15% the strength of morphine parenterally.
  • Low first pass hepatic clearance allows for oral delivery, liver converts some to morphine.
  • Eventual conjugation in liver and excretion by kidneys.
  • Usually used topically, IM or subQ. Has been used IV, in neurocases and ambulatory patients but is seldom used parenterally.

Semi synthetic derivatives: Oxycodone with ASA or acetaminophen—-orally; hydrocodone is also used with antitussive medications

186
Q

Analgesic Ladder

A

—When using the pharmacological approach please keep in mind the following recommendations:

—Use the simplest dosage schedules and least invasive pain management modalities first.

—For mild to moderate pain, use (unless contraindicated) aspirin, acetaminophen, or non-steroidal anti-inflammatory drug (NSAID; WHO ladder, Step 1).

—When pain persists or increases, add an opioid (WHO ladder, Step 2).

—If pain increases, increase the opioid potency or dose (WHO ladder, Step 3).

—Schedule doses regularly (i.e., “by the clock”) to maintain the level of drug that will help prevent recurrence of pain. Ask for patient and family cooperation in establishing the effective level.

—Administer additional doses “as needed” for breakthrough pain

NSAIDs reduce the production of prostaglandin E2 (PGE2) and prostacyclin (PGI2), which mediate pain and inflammation.

187
Q

Adjuvant Drugs

A

—Used off label in conjunction with opioids

◦Anti-depressants

◦Anti-seizure meds

◦Muscle relaxants

◦Sedatives

◦Anxiolytics

◦Marijuana (what label?)

◦Botulinum Toxins

188
Q

Botulinum Toxins

A

When injected in small amounts, it can effectively weaken a muscle for a period of three to four months.

It is used in the treatment of spasms and dystonias.

Botulinum is the most acutely lethal toxin known.

LD50 = 1-2 ng/kg IV-IM

189
Q

Distribution and Re-Distribution

A

First plasma will have the highest concentration

Next the viscera will reach peak concentration and the plasma concentration rapidly drops

Muscle mass takes longer to reach peak concentration and when it does the concentration in both the plasma and viscera will have dropped

As the muscle concentration begins to decrease adipose tissue will begin to gain concentration

190
Q

What drug is used as last attempt treatment for refractory status asthmaticus

A

Ketamine

191
Q

MAC From Lowest to Highest

A

Megan Has Isolated Evil Serious Dream Nightly

Methexyfluane (0.0016)

Halothank (0.0077

Isoflurane (0.115)

Enfluurance (0.0170)

Servo (0.02)

Des (0.06)

Nirtrous Oxide (1.04)

192
Q

Sevo CNS Effects

A

Dose related depression

Increased ICP which is the brains’ response to high PaCO2 (­increased RR decreased Vt) is preserved.

193
Q

Nociception

A

Ability to feel pain, caused by stimulation of a nociceptor.

Composed of four processes: transduction, transmission, modulation, andperception.

194
Q

—Halo Hepatitis

A

Post operative fever, eosinophilia and liver dysfunction (elevated enzymes) is very rare.

Pts with four of: age, femaleness, sepsis, obesity, biliary surgery, drug dependency, long procedures, multiple procedures, multiple allergies—-should be given another agent.

001 Respiratory Therapy (53 decks)

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