Inhalation Agents2--Pharm Test 3

Front 1

What does oxygen and CO2 attach to on the RBC?

Back 1

Hemoglobin

Front 2

Does Oxygen or CO have a higher affinity for Hemoglobin?

Back 2

CO

Front 3

Does NO (Nitric Oxide) have a short or long half life? How long is it?

Back 3

SHORT; gone in 6-10 seconds

Front 4

What 2 things manufacture NO?

Back 4

Nitrates and Endothelial Cells

Front 5

What protein must NO bind to to become activated?

Back 5

Guanylyl Cyclase

Front 6

What is the end product of the NO pathway and what is its effect?

Back 6

Myosin-LC; causes relaxation

Front 7

What is the intermediate step in the NO pathway between Guanylyl Cyclase and Myosin-LC?

Back 7

cGMP

Front 8

Can NO be pathalogical? Why or why not?

Back 8

YES; can create superoxides which can cause DNA Fragmentation and Mutations and Cell Death

Front 9

In relation to mechanism of action, what is the "Meyer-Overton Hypothesis?"

Back 9

Proposes that IAs acted in hydrophobic portion of the neurons; argues that anesthetic potency correlates closely with the affinity of the anesthetic for a lipid phase and thus implies an action in a lipid-like phase

Front 10

What "nonspecific action" on neuronal lipid bilayers did IAs perform as proposed by the Meyer-Overton Hypothesis?

Back 10

Expansion or fluidization of the membrane by the presence of the anesthetic molecule

Front 11

Where do most investigators NOW believe the site of IAs action is?

Back 11

on portions of membrane PROTEINS

Front 12

How does MAC relate to the affinity of the anesthetics for a lipid phase and how does this support the Meyer/Overton Hypothesis?

Back 12

MAC for conventional anesthetics correlates INVERSELY with the affinity of the anesthetics for a lipid phase, i.e. correlates with the lipid/gas partition coefficient--adding support for the hypothesis

Front 13

Which IA is the most POTENT and has the highest Oil-Gas Partition Coefficient(most lipophilic or hydrophobic)

Back 13

Methoxyflurane (Penthrane)

Front 14

Which IA is the least POTENT and has the lowest oil-gas partition coefficient (least lipophilic or hydrophobic)

Back 14

Nitrous Oxide (N2O)

Front 15

MOST investigators believe that inhaled anesthetics act by effects at ______ sites. What is this concept called?

Back 15

Multiple; "Multisite Theory of Narcosis"

Front 16

FEW investigtors believe that the inhaled anesthetics act on no more than _____ or _____ specific sites to produce a specific effect. What is this concept called?

Back 16

Two or Three; "Unitary Theory of Narcosis"

Front 17

GABA-A and Glycine Receptors are both (excitatory or inhibitory)?

Back 17

Inhibitory

Front 18

How are GABA-A and Glycine receptors inhibitory? What is their specific mechanism of action?

Back 18

Increased Chloride permeability; membrane hyperpolarization; inhibition of excitability

Front 19

How does activation of the GABA-A receptor affect a person?

Back 19

Enhanced activity associated with anxiolysis, sedation, amnesia, myorelaxation, anticonvulsant action

Front 20

What does activation of the Glycine receptors affect?

Back 20

Spinal reflexes and startle responses; major inhibitory receptor in the spinal cord

Front 21

What are the cellular roles of the Neuronal Nicotinic Acetylcholine receptor?

Back 21

High permeability to cations and calcium; release of NTs

Front 22

What are the cellular roles of Muscle Nicotinic Acetylcholine receptors?

Back 22

Neuromuscular transmission

Front 23

What are the behavioral and/or physiological roles of activation of the Neuronal Nicotinic ACh receptors?

Back 23

Association with memory nociception; mutations linked with seizure disorders; autonomic functions

Front 24

What are the behavioral and/or physiological roles of activation of the muscle nicotinic ACh receptors?

Back 24

Skeletal muscle contraction

Front 25

What are the cellular roles of Serotonin 3 receptors?

Back 25

Enhance excitability by inhibiting resting potassium-leak currents

Front 26

What are the behavioral/Physiological roles of activation of the Serotonin type 3 receptors?

Back 26

Arousal; possible role in emesis

Front 27

What are the cellular roles of the Glutamate receptors?

Back 27

Fast excitatory neurotransmission; cation conductance for calcium and magnesium

Front 28

What are the Behavioral/Physiological roles of activation of the Glutamate receptors?

Back 28

Perception; learning and memory; nociception

Front 29

What are the cellular roles of Non-Voltage gated potassium channels?

Back 29

Modulation of Cell resting potential and excitability; role in chemical, mechanical and pH sensitivity

Front 30

What are the cellular roles of Voltage-activated Potassium Channels?

Back 30

recovery from action potentials

Front 31

What are the behavioral/physiological roles of activation of Non-voltage gated Potassium channels?

Back 31

Nonspecific role; most likely widespread

Front 32

What are the behavioral/physiological roles of activation of Voltage-gated Potassium Channels?

Back 32

Nerve conduction; cardiac action potentials; mutations associated with cardiac arrhythmias

Front 33

What are the Cellular roles of Sodium channels?

Back 33

Generation and propagation of action potentials

Front 34

What are the Behavioral/Physiological roles of activation of Sodium channels?

Back 34

Nerve conduction; cardiac action potentials (arrhythmias)

Front 35

What are the cellular roles of Voltage-gated cardiac calcium channels?

Back 35

generation of pacemaker potentials in neurons (T-Type)

Front 36

What are the behavioral/Physiological roles of activation of Voltage-gated cardiac calcium channels?

Back 36

Cardiac inotropy and chronotropy; vascular tone

Front 37

What are the cellular roles of voltage-gated neuronal Calcium channels?

Back 37

Presynaptic localization; NT release

Front 38

What are the behavioral/physiological roles of activation of Voltage-gated neuronal calcium channels?

Back 38

nonspecific role; most likely widespread

Front 39

What are the roles of Calcium-induced calcium release (Ryanodine receptor, Inositol Triphosphate receptors)?

Back 39

Intracellular channels; release on intracellular calcium stores after stimulation of surface receptors; production of calcium oscillations

Front 40

What are the behavioral/physiological roles of activation of calcium-induced calcium release receptorts (Ryanodine and Inositol Triphosphate receptors)?

Back 40

Excitation-contraction coupling

Front 41

GABA receptors are made of many combinations of subunits. What is the GABA-A primary subunit composition?

Back 41

Made up of 2-alpha, 2-Beta and 1-gamma subunit(s)

Front 42

Anesthetics _____ the inhibitory action

Back 42

potentiate

Front 43

Gases are _____; cannot compete off of channels

Back 43

Non-competitive

Front 44

IAs ____ the NMDA receptor and thus inhibits _____ flow

Back 44

Inhibit; Calcium

Front 45

What ion channels/receptors does Nitrous Oxide inhibit?

Back 45

Neuronal Nicotinic ACh receptors, and N-methyl-D-Aspartate Glutamate receptors

Front 46

What ion channels/receptors do Halogenated Alkanes and Ethers (most all IAs) ENHANCE?

Back 46

GABA-A receptor, Glycine receptor, Ryanodine-activated calcium channels (enhance AND inhibit), ATP-activated potassium channels, background potassium channels

Front 47

What ion channels/receptors do Halogenated Alkanes and Ethers (most all IAs) inhibit?

Back 47

Muscle Nicotinic ACh receptors, Glutamate receptors, Voltage-activated Potassium channels, Ryanodine-activated calcium channels (enhance AND inhibit)

Front 48

What ion channels/receptors do Halogenated Alkanes and Ethers (most all IAs) inhibit WEAKLY?

Back 48

Serotonin Receptors, Voltage-activated Sodium channels, and Voltage-activated Calcium channels

Front 49

What ion channels/receptors do Halogenated Alkanes and Ethers (most all IAs) inhibit STRONGLY?

Back 49

Neuronal nicotinic ACh receptors

Front 50

What is the primary receptor involved in Malignant Hyperthermia?

Back 50

RYR1

Front 51

What test is considered to be the "Gold Standard" in assessing for Malignant Hyperthermia?

Back 51

Halothane Caffeine Contracture test

Front 52

What causes the symptoms of Malignant Hyperthermia?

Back 52

the mutated RYR1 receptor is the site of action of IAs; the mutation causes an abnormal release of intracellular Calcium which causes the malignant hyperthermia cascade

Front 53

What type of malignant hyperthermia diagnostic tool is not the "Gold Standard" but becoming more common?

Back 53

Genetic Testing

Front 54

Which GABA-A receptor subunit is associated with Transmembrane (TM) 1,2,3 and 4?

Back 54

GABA-A (alpha 1)

Front 55

Which IA is associated with the GABA-A (alpha 1 subunit) receptor?

Back 55

Isoflurane (Forane)

Front 56

Which 4 amino acids link Isoflurane to the GABA-A (alpha 1 subtype) receptor?

Back 56

Ala291, Tyr415, Leu232 and Ser270

Front 57

Which GABA-A receptor subunit has 4 specific amino acids associated with it?

Back 57

GABA-A (alpha 1 subunit)

Front 58

Isoflurane (Forane) is associated with which GABA-A receptor subunit?

Back 58

GABA-A alpha-1

Front 59

Which drug is associated with the GABA-A Beta-2 subunit?

Back 59

Propofol

Front 60

Which GABA-A subunit is associated with 3 specific amino acids?

Back 60

GABA-A Beta-2

Front 61

Propofol is associated with which GABA-A receptor subunit?

Back 61

GABA-A Beta-2

Front 62

What are the 3 specific GABA-A Beta-2 amino acids that link Propofol to the receptor?

Back 62

Met286, Tyr445 and Asn265

Front 63

What are 3 physical properties of N2O (Nitrous Oxide)?

Back 63

Colorless gas, sweet odor and stored under pressure in a BLUE-COLORED steel cylinder

Front 64

What is the critical temperature of N2O?

Back 64

36.5 degrees C

Front 65

Definition of Critical Temperature: _____ temperature at which a substance can be _____ by any amount of pressure

Back 65

Highest; liquefied

Front 66

At a temperature of less than 36.5 C, how many atms does it take to liquefy N2O?

Back 66

74 atms

Front 67

To go from a solid to a liquid, a substance has to reach its ______ ______

Back 67

Melting Point

Front 68

To go from a liquid to a Vapor, a substance has to reach its ______ _______

Back 68

Boiling Point

Front 69

To go from a Vapor to a Gas, a substance has to reach its ______ ______

Back 69

Critical Temperature

Front 70

What is the primary difference between a vapor and a gas?

Back 70

Temperature

Front 71

What has to happen to a gas before it can be compressed back into a vapor?

Back 71

It has to be cooled below its critical temperature

Front 72

What degrees Celsius is room temperature?

Back 72

20 degrees C

Front 73

What is the pressure in a N2O cylinder at room temperature (20 degrees C)?

Back 73

745 lbs/sq. in or approx. 51 atms guage pressure

Front 74

How many lbs/sq.inch is 1 atm?

Back 74

14.7 lbs/sq.inch

Front 75

The pressure of the vapor above the liquid N2O varies with ________.

Back 75

TEMPERATURE

Front 76

What is the pressure of N2O at 0 degrees C?

Back 76

31 atms

Front 77

If temperature is above 36.5 (critical temperature), what phase will N2O be in?

Back 77

Gas

Front 78

At room temperature, N2O will stay at 51 atms until all liquid in the cylinder is ______.

Back 78

Vaporized

Front 79

Why can't you rely on the pressure guage of N2O on the cylinder to let you know when you need to replace it?

Back 79

Guage will remain at 51 atms until all the liquid N2O has been vaaporized and the tank is nearly empty; by the time you realize tank needs to be changed, it's already empty

Front 80

Is N2O flammable or explosive?

Back 80

NO

Front 81

Is N2O stable in soda lime?

Back 81

YES

Front 82

N2O is a ______ analgesic and a ______ anesthetic

Back 82

Potent analgesic; Weak anesthetic

Front 83

1 MAC of N2O is _____% at 37 degrees C in a 30-55 year-old; this is what makes it a weak anesthetic

Back 83

104%

Front 84

What's the only scenario in which you can give a full MAC (104%) of N2O? Why?

Back 84

Hyperbaric Chamber; can't give a full MAC under other conditions as it would not allow you to meet O2 requirements

Front 85

What is the Blood/Gas Partition Coefficient for N2O? IS this high or low?

Back 85

0.47; LOW

Front 86

N2O having a low Blood/Gas Partition Coefficient means it has a rapid ______ and rapid ______.

Back 86

Induction; Emergence

Front 87

Arterial blood will lose 75% of N2O in it within the first _____ minutes of emergence (after N2O is turned off)

Back 87

3 minutes

Front 88

What occurs in the Alveolus during emergence from N2O?

Back 88

Alveolar O2 is diluted by N2O that rushes in from arterial blood; this causes a subsequent drop in arterial O2

Front 89

In addition to alveolar O2 being diluted by N2O, what else is diluted? What effect does this have?

Back 89

Arterial CO2 is diluted; Stimulus to breathe is decreased

Front 90

What is the disadvantage of administering N2O to a patient with an already compromised arterial O2 level (such as lung dz)?

Back 90

N2O emergence diffusion hypoxia can aggravate an already depressed PaO2

Front 91

When is the greatest effect from diffusion hypoxia from N2O emergence seen?

Back 91

greatest effect in the first 5 minutes after turning N2O off

Front 92

What important intervention is necessary to prevent diffusion hypoxia from N2O emergence?

Back 92

Give 100% O2 for at least 5 minutes

Front 93

To prevent diffusion hypoxia, administer 100% O2 for at least 5 minutes after N2O turned off; would you administer 100% O2 to ALL people including those you wouldn't normally give 100% O2 to (COPD, etc)?

Back 93

YES; Give to everyone

Front 94

True/False: N2O will preferentially fill an air-filled cavity in the body

Back 94

TRUE

Front 95

How do the Blood/Gas Partition Coefficients of N2O and Nitrogen (N) compare? Based on these values, how much of each is carried in the blood?

Back 95

N2O=0.47;
Nitrogen (N)=0.015;
100 ml blood will carry 47 ml N2O; and 100 ml blood will carry 1.5 ml Nitrogen

Front 96

How many times greater is the Blood/Gas Partition Coefficient of N2O than Nitrogen?

Back 96

31 times greater

Front 97

Because the Blood/Gas partition coefficient of N2O is 31 times greater than Nitrogen, what is the overall effect of this?

Back 97

N2O is more able to flow INTO an air-filled cavity than Nitrogen (N) is able to flow OUT; Net effect=pressure or volume of cavity is increased/expanded

Front 98

Preferential transfer of Nitrous to air filled cavity increases ____ when walls are non-compliant

Back 98

Pressure

Front 99

Preferential transfer of Nitrous Oxide to air filled cavity increases _____ when walls are compliant.

Back 99

Volume

Front 100

What are 3 anatomical examples of N2O increasing PRESSURE in areas with non-compliant walls?

Back 100

Occluded Middle Ear, Cerebral Ventricles with air spaces (raises ICP), occluded sinuses (causes more pressure and pain)

Front 101

What are anatomical/physiological examples of N2O increasing VOLUME in areas with compliant walls?

Back 101

Bowel Gas (increases), Loops on intestine in obstruction, Pneumothorax (makes bigger), Pulmonary Blebs (N2O can rupture Blebs), Air Emboli (can extend), Pneumoperitoneum, Intraocular Pressure

Front 102

The magnitude of increase in pressure or volume to various cavities due to N2O admin depends on what 3 factors?

Back 102

Partial pressure of Nitrous, Blood flow to cavity, Duration of anesthetic

Front 103

50% N2O may _____ size of cavity

Back 103

DOUBLE

Front 104

75% N2O may ______ size of cavity

Back 104

QUADRUPLE

Front 105

What % of N2O admin can Double the size of a cavity?

Back 105

50%

Front 106

What % of N2O admin can quadruple the size of a cavity?

Back 106

75%

Front 107

What's important to remember regarding Nitrous admin after inserting a central line?

Back 107

Don't start N2O until after CXR has confirmed placement of central line; if Pneumothorax is present, N2O could extend it

Front 108

N2O is _______ in the presence of a Pneumothorax

Back 108

contraindicated

Front 109

Bowel gas expands slowly; why?

Back 109

because it's not part of the Vessel Rich Group (VRG); there is less blood flow to the Bowel

Front 110

In a sitting/standing position, the pressure in the Sagittal Sinus is _______.

Back 110

-10 mmHg

Front 111

When considering N2O, what is critical to remember regarding the negative venous intracranial pressure when a Posterior Fossa Craniotomy is being performed?

Back 111

The negative venous pressure in the surgical area will place the patient at risk for an air embolism due to the fact that the negative pressure will actually drawn air in from the environment; N2O can extend this air embolism

Front 112

What test is considered to be the most sensitive and the "Gold Standard" in detecting an air embolism?

Back 112

TEE

Front 113

What are 3 non-anatomical things N2O can diffuse into and cause problems?

Back 113

ET tube cuff (cuff could get bigger and could perforate), Swan-Gantz Balloon tip catheter (could rupture pulmonary artery), and LMA

Front 114

How does N2O contribute to post-op hearing loss?

Back 114

Because of expansion of the middle ear; pressure can increase by 20-30 mmHg (and can perforate at these pressures)

Front 115

Which auditory procedure should you NOT use N2O for?

Back 115

Tympanoplasty

Front 116

During maintenance of anesthesia, N2O causes positive middle ear pressure but N2O causes _____ middle ear pressure upon emergence

Back 116

negative

Front 117

How is the negative middle ear pressure obtained during emergence from N2O? What negative effect can this cause?

Back 117

Due to N2O moving OUT of ear faster than Nitrogen (N) is moving back in; this negative pressure can cause drainage from the ear

Front 118

What 2 unfavorable conditions can ensue from negative middle ear pressure upon emergence from N2O?

Back 118

Serious otitis (drainage from ear) and Post-op N/V

Front 119

What unfavorable thing can occur to a COPD patient with N2O administration?

Back 119

Rupture of Blebs

Front 120

Does N2O cause analgesia?

Back 120

YES

Front 121

Does N2O depress the CNS?

Back 121

YES

Front 122

Will N2O produce unconsciousness in ALL patients? Why or why not?

Back 122

NO; some people will lose consciousness; others will not; there are individual differences; also dependent on physical status of patient

Front 123

What Cerebral/CNS effects does N2O produce?

Back 123

Increases CMRO2 and increases Cerebral Blood Flow (CBF), which increases ICP

Front 124

N2O has less effect on Cerebral O2 supply/demand than other IA; Why is this?

Back 124

Unlike many other IAs, CMRO2 and CBF are coupled (with N2O); this means they both increase or decrease together (not in opposite directions like other IAs)

Front 125

When N2O is given alone, it causes a _____% increase in Cerebral Blood Flow (CBF)

Back 125

35%

Front 126

With N2O, the CBF response to CO2 is ______.

Back 126

Preserved

Front 127

If N2O causes an increase in ICP, what is one way you can bring the ICP down?

Back 127

hyperventilate the patient; blowing off CO2 causes cerebral vasoconstriction with a subsequent decrease in CBF and ICP

Front 128

Does N2O have vasodilatory action?

Back 128

YES

Front 129

The CV effects of N2O are complicated by what 4 things?

Back 129

Volatile Anesthetics, Opioids, Other Anesthetic Adjuvants, with or without CV disease

Front 130

N2O creates a modest (increase or decrease) in HR?

Back 130

Increase

Front 131

Does the co-administration of N2O with Volatile agents cause a higher HR than if you just gave the volatile agent alone?

Back 131

YES

Front 132

N2O causes a DECREASED HR with what condition?

Back 132

Coronary Artery Disease

Front 133

Does N2O cause a small increase or decrease in arterial pressure?

Back 133

Increase

Front 134

What mechanism causes N2O to cause a small increase in arterial pressure?

Back 134

N2O has a mild sympathomimetic effect

Front 135

What effect on arterial pressure does co-administration of N2O with a volatile anesthetic have?

Back 135

NO effect or modest increase (Volatile agents DEPRESS BP)

Front 136

N2O causes a DECREASE in arterial pressure in what condition?

Back 136

Coronary Artery Disease

Front 137

60% N2O causes a small (increase or decrease) in cardiac output and Stroke Volume?

Back 137

Small increase

Front 138

Combining N2O with Volatile Agents causes a small (increase or decrease) in Cardiac Output and Stroke Volume?

Back 138

Small Increase

Front 139

N2O causes a DECREASED Cardiac Output and Stroke Volume in what 2 conditions?

Back 139

Concurrent admin of Opioids and Cardiac Disease

Front 140

Admin. N2O with volatile anesthetics makes the SVR (higher or lower) than if admin. volatile anesthetic alone?

Back 140

Higher

Front 141

Admin. of N2O with Opioids causes an (increase or decrease) in SVR?

Back 141

Increase

Front 142

N2O ____ venous tone and thus ____ venous capacitance in conscious volunteers

Back 142

Increases; Decreases

Front 143

N2O increases or decreases Pulmonary Artery Pressure (PAP)?

Back 143

Increases

Front 144

N2O increases or decreases Pulmonary Vascular Resistance (PVR)?

Back 144

Increases

Front 145

N2O increases or decreases Venous Return?

Back 145

Increases

Front 146

N2O increases or decreases Central Venous Pressure (CVP)?

Back 146

Increases

Front 147

Due to all the Cardiac parameters that are increased with the usage of N2O, what 3 conditions/populations must you be cautious with when admin. N2O?

Back 147

Pulmonary HTN, Neonates, and Congenital Heart Disease

Front 148

Does N2O offer any cardiprotective effects?

Back 148

NO

Front 149

Why might N2O exacerbate myocardial ischemia?

Back 149

Because it causes a reduction in arterial pressure in patients with coronary artery disease

Front 150

N2O is a (strong or weak) Sympathomimetic

Back 150

Weak

Front 151

Because N2O is a weak sympathomimetic, it causes pupillary ______.

Back 151

Dilation; this can be masked by admin. of Opioids

Front 152

What other effect (other than pupillay dilation) does N2O cause due to its weak sympathomimetic effect?

Back 152

Diaphoresis

Front 153

Is N2O good to give to asthmatics? Why or why not?

Back 153

NO; does NOT relax brocho smooth muscle; actually causes bronchoconstriction

Front 154

Which Volatile agent is best to give to asthmatics due to its bronch smooth muscle relaxation effects?

Back 154

Sevoflurane is best

Front 155

Describe the respiratory pattern that occurs with N2O during general anesthesia?

Back 155

Regular, rhythmic, rapid, shallow pattern of breathing

Front 156

What effect does N2O have on CO2?

Back 156

None; remains stable at approx. 40 mmHg

Front 157

What effect does N2O have on respiratory rate (RR)?

Back 157

Dose dependent increase in Respiratory Rate (RR)

Front 158

What effect does N2O have on Tidal Volume (TV)?

Back 158

Decreased TV

Front 159

Does N2O effect the ventilatory response to CO2?

Back 159

NO

Front 160

ALL IAs including N2O profoundly depress ventilatory response to _______. This occurs due to action on peripheral _______.

Back 160

Hypoxemia; Chemoreceptors

Front 161

______ is normally mediated by Carotid Bodies.

Back 161

Hypoxemia

Front 162

1 MAC causes ____% to ____% depression of carotid bodies response to hypoxemia

Back 162

50%-70%

Front 163

1.1 MAC causes ____% depression of carotid bodies response to hypoxemia

Back 163

100%

Front 164

With N2O, the synergistic effect of hypoxia and hypercapnia on ventilatory drive is _______.

Back 164

Depressed

Front 165

Nitrous (increases or decreases) FRC?

Back 165

Decreases

Front 166

The effect of decreased FRC caused by N2O admin. may be exaggerated by what?

Back 166

Nitrous-induced skeletal muscle rigidity

Front 167

Is N2O safe to use in regards to Malignant Hyperthermia?

Back 167

YES; this is an advantage of N2O

Front 168

Does N2O produce muscle relaxation?

Back 168

NO; in fact may see clonus (Posturing) and Opisthotamus (spasticity), especially in children

Front 169

Does N2O augment NM blockers?

Back 169

NO

Front 170

How does Nitrous interact with Vitamin B-12?

Back 170

Disrupts several pathways; inactivates Methionine Synthase (this is an enzyme involved in the metabolism of Vitamin B-12)

Front 171

The inactivation of Methionine Synthase (the enzyme involved in the metabolism of Vitamin B-12) by N2O causes a condition resembling ______ ______.

Back 171

Pernicious Anemia

Front 172

Why is it important for dental personnel to be cautious with the use of N2O?

Back 172

higher rate of infertility and spontaneous abortion with chronic N2O exposure

Front 173

What specific hematological effect does N2O have?

Back 173

depresses Megoblastic bone marrow activity

Front 174

When admin. 50% N2O for 12-24 hours, when is Megoblastic bone marrow suppression typically seen in healthy patients?

Back 174

At about the 12th hour

Front 175

When admin. 50% N2O for 12-24 hours, when is Megoblastic bone marrow suppression typically seen in critically ill patients?

Back 175

in about 2-6 hours (much more susceptible than healthy patients)

Front 176

What is the NIOSH standard for N2O concentration?

Back 176

OR not >25 ppm

Front 177

What concentration (in ppm) is CNS depression seen with N2O admin?

Back 177

1000 ppm

Front 178

With "Sleeper" C-sections why is it good to use N2O with Volatile agents?

Back 178

Volatile agents relax uterine muscle (no tone) and cause more bleeding; 1/2 MAC N2O + 1/2 MAC Volatile agent decreases the amount of bleeding

Front 179

Since N2O exposure can cause potential for adverse reproduction and development, how can you reduce your exposure via leaks in the anesthetic system?

Back 179

check for proper fitting of masks, high-pressure fittings (tightly screwed on) and exhalation valves

Front 180

Why is it good to avoid N2O admin. until after ET tube is in place?

Back 180

Limits exposure to N2O and potential for reproductive/development problems

Front 181

What 2 areas of the hospital have the highest incidence of Postoperative exposure to N2O (exposed as it's breathed off)?

Back 181

PACU and ICU

Front 182

In summary, what are the major adverse effects of N2O administration?

Back 182

Expansion of closed gas spaces (Bowel gas, Air embolism, Pneumothorax, ET Cuff), Diffusion Hypoxia, Post-op N/V, Minimum to trivial effect on greenhouse gases, Polyneuropathy from Vitamin B12 Oxidation, effects DNA synthesis (decreases RBC and Leukocyte production), increased incidence of spontaneous abortion and developmental delay

Front 183

What are the advantages of N2O admin?

Back 183

N2O is cheap, it's a faster induction agent, it's a weak trigger for malignant hyperthermia, non-pungent odor (good for mask induction, esp. in children)

Front 184

Halothane (Fluathane) is a _____ ______ (not an Ether)

Back 184

Halogenated Hydrocarbon

Front 185

Halothane is an _____ derivative.

Back 185

Alkane

Front 186

Halothane is the (most,least) POTENT of the inhalation agents?

Back 186

MOST potent

Front 187

Chemically, what constitutes "Halogenation" of Hydrocarbons and Ethers?

Back 187

Substitution of a hydrogen atom with a halogen (Fluorine, Chlorine, Bromine, Iodine)

Front 188

Alkanes with 5 Halogens (such as Halothane) are more prone to induce arrhythmias than what?

Back 188

Ethers with 6 Halogens (such as Enflurane and Isoflurane)

Front 189

Is Halothane flammable?

Back 189

NO

Front 190

Is Halothane stable in light?

Back 190

NO

Front 191

How is Halothane stored?

Back 191

in amber colored bottles; clear bottles will break it down

Front 192

Does Halothane have a preservative?

Back 192

YES

Front 193

What is the preservative in Halothane and what is its purpose?

Back 193

Thymol; prevents spontaneous oxidative decomposition

Front 194

Halothane is absorbed in rubber more than what?

Back 194

Polyethylene

Front 195

Unlike N2O, the CMRO2 and CBF of Halothane are _____.

Back 195

Uncoupled

Front 196

How does Halothane effect CMRO2 and CBF?

Back 196

CMRO2 (demand) decreases (dose dependent) and CBF (supply) increases with Halothane

Front 197

1.1 MAC of Halothane increases CBF almost _____% (with BP support)

Back 197

200%

Front 198

Increased CBF with Halothane may also increase ______.

Back 198

ICP

Front 199

What can you do to prevent the increase in ICP (Secondary to the increase in CBF) with Halothane use?

Back 199

Hyperventilate patient BEFORE you turn on Halothane;

Front 200

When hyperventilating patient to avoid the increase in ICP with Halothane, what CO2 level should you hyperventilate to obtain?

Back 200

< 30 torr

Front 201

Under normal, awake conditions CBF is autoregulated between MAP of _____-_____ torr

Back 201

60-140-150 torr

Front 202

Under awake, HTN conditions CBF is autoregulated between MAP of ____-____ torr

Back 202

180-200 torr

Front 203

When patient is put to sleep with Halothane is the autoregulation of CBF lost or preserved?

Back 203

LOST

Front 204

Because autoregulation of CBF with Halothane is lost, CBF is ______ dependent

Back 204

Pressure

Front 205

Because CBF is pressure dependent with Halothane, as MAP increases, CBF ______.

Back 205

Increases

Front 206

What are Evoked Potentials used for?

Back 206

Used to monitor function of spinal cord, brain stem, and Cerebral Cortex

Front 207

BAEP monitors function of which cranial nerve?

Back 207

VIII (auditory)

Front 208

Does Halothane effect the ability to monitor BAEPs?

Back 208

NO

Front 209

VEP monitors function of which cranial nerve?

Back 209

Optic nerve

Front 210

Does Halothane effect the ability to monitor VEPs?

Back 210

YES

Front 211

SSEP monitors function of what?

Back 211

spinal cord

Front 212

What procedures would it be important to monitor VEPs?

Back 212

monitored during pituitary tumors or other lesions near the optic nerve or optic chiasm

Front 213

When would it be important to monitor SSEPs?

Back 213

Carotid, aortic or intracranial aneurysms

Front 214

Does Halothane effect the ability to monitor SSEPs?

Back 214

YES

Front 215

What effect does Halothane have on CSF production?

Back 215

decreased

Front 216

What effect does Halothane have on CSF absorption?

Back 216

decreased

Front 217

Why is Enflurane (Ethrane) bad to give to someone with increased ICP?

Back 217

It will cause further increase in ICP because it increases the secretion of CSF and decreases the absorption of CSF