Inhaled Anesthetics 2 (exam 3) Flashcards

1
Q

Name (4) jobs of the Anesthesia Circuit

A
  1. Delivers Oxygen
  2. Delivered inhaled Drugs
  3. Maintains Temperature/humidity (body temp)
  4. Removes carbon dioxide and exhaled drugs
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2
Q

Name (3) Type of Anesthesia Circuits

A
  • Rebreathing (Bain)
  • Non-breathing (self-inflating BVM)
  • Circle Systems
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3
Q

Name this circuit

A

Bain Circuit

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4
Q

Does the Bain Circuit allow you to adjust PEEP?

A
  • No
  • only contains tubing, bag, oxygen and 1 escape valve
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5
Q

Name this circuit

A
  • Non-rebreathing (Ambu or BVM)
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6
Q

Does the Ambu allow you to adjust PEEP?

A
  • Yes
  • PEEP, Expiratory valve, pressure release valves.
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7
Q

Name the (6) parts of the Circle System

A
  1. Fresh gas inlet
  2. Inspiratory and Expiratory limbs
  3. Reservoir bag
  4. CO2 Absorbent
  5. One way valve
  6. Y piece
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8
Q

Inhalation Anesthesia: High Flow

A
  • FGF exceeds minute ventilation
  • Rapid changes in anesthetics
  • Prevents Rebreathing
  • Wasteful
  • Cools/dries delivered volume
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9
Q

Inhalation Anesthesia: Low Flow

A
  • FGF less than Vm
  • Low Cost
  • Less Cooling/drying
  • Very slow changes in anestheic
  • Concerned with Compound A production
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10
Q

Name (3) factors of the price of anesthetics

A
  • Cost of liquid/ml
  • Volume % of anesthetic delivered ( Potency)
  • FGF Rate
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11
Q

Pathology to Relax airway smooth muscle

A
  • Block Voltage-gated Ca++
  • Depleted Ca++ in SR
  • Requires intact epithelium
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12
Q

If the endolthelium is damaged or inflammed, will bronchodilation occur?

A
  • No
  • Requires an intact endothelium
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13
Q

Bronchodilation without bronchospasm

A
  • Baseline pulmonary resitance unchanged by 1-2 MAC
  • Need Histamine release or vagal afferent stimulation
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14
Q

Name (3) Volatiles that cause Bronchodilation with bronchospasm

A
  • Sevoflurane>Isoflurance
  • Desflurane may worsen, especially in smokers d/t pungency/irritation.
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15
Q

Name (4) Risk Factors for bronchospasm with bronchodilation

A
  1. COPD
  2. Cough response w/ ETT
  3. age <10
  4. URI
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16
Q
A

Respiratory Resistance Comparison
* More spastic and narrowed
* Thiopental is bad
* Sevoflurane is good

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17
Q

How Volatiles affect Neuromuscular

A
  1. Dose dependent skeletal muscle relaxation
  2. Potentiate depolarizing and non-depolarizing NMBDs.
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18
Q

Name (1) Volatile that does not have a relaxant effect on skeletal muscles.

A

Nitrous Oxide

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19
Q

How do volatiles potentiate depolarizing and non-depolarizing NMBD.

A
  • nAch receptors at NMJ
  • Enhance glycine at spinal cord
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20
Q

Define Ischemic Preconditioning with Volatiles

A
  • Brief periods of ischemia prior to longer periods.
  • Mediated by adenosine
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21
Q

How does Adenosine mediate Ischemic Preconditioning?

A
  • Increases protein Kinase C activity
  • Phosphorylates ATP sensitive K Channels
  • Production at reactive oxygen species (ROS)
  • Better regulated vascular tone
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22
Q

What dose of MAC can ischemic preconditions occur?

A
  • 0.25 MAC
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23
Q

Name (3) “ reperfusion injuries” Volatile Ischemia precondition can prevent.

A
  1. Cardiac dysrhythemias
  2. Contractile dysfunction
  3. Clinically apparent in delaying MI for PTCA , CABG
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24
Q

Volatile Effects on CNS activity

A
  • Dose Dependent ⬇️ CMRO2 and cerebral activity
  • Iso = Sevo = Des
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25
Q

At what MAC does wakefulness change to unconciousness?

A
  • 0.4 MAC
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26
Q

At what MAC does burst suppression occur right before brain death?

A
  • 1.5 MAC
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27
Q

At what MAC does does electrical silence or brain death occur?

A
  • 2 MAC
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28
Q

Name (3) Volatiles that have anticonvulsant activity

A
  1. Des
  2. Iso
  3. Sevo
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29
Q

At what dose will volatiles have anticonvulsant activity?

A
  • At high concentrations and with Hypocarbia
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30
Q

Name (1) Volatile that has Proconvulsant activity

A
  • Enflurane
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31
Q

At what dose and PaCO2 will Enflurance have Proconvulsant activity?

A
  • > 2 MAC
  • PaCO2 < 30 mmHg
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32
Q

Volatile Evoke Potential (2) Types

A
  • SSEP’s (Somatosensory Evoked Potential)
  • MEP (Motor Evoked Potential)
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33
Q

Define Evoked Potential

A
  • Dose related ⬇️amplitude and ⬆️ latency (0.5-1.5 MAC)
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34
Q

What dose of Volatile will you use for evoked potentials? Why?

A
  • Nitrous 60% and >0.5 MAC
  • Tell difference between surgeon induced and anesthesia induced.
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35
Q

Do Volatiles effect Cerebral Blood Flow?

A
  • Yes
  • Dose Dependent
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36
Q

Cerebral Blood Flow:Dose Dependent

A
  • ⬆️ CBF due to decreased cerebral vascular resistance
  • May increase ICP
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37
Q

Dose and onset of Volatile effect of Cerebral Blood Flow.

A
  • > 0.6 MAC
  • Occurs within minutes despite lack of BP changes
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38
Q

Does Iso or Des cause more changes in cerebral blood flow?

A
  • Neither.
  • They are equal
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39
Q
  • What volatile is a potent vasodilator, but unable to give at high enough doses?
A
  • Nitrous
  • give < 1 MAC
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40
Q

What Volatile is the worst at decreasing cerebral blood flow?

A
  • halothane
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41
Q

Auto Regulation

A
  • Halothane lost by 0.5 MAC
  • Sevo preserves to 1 MAC
  • Iso and Des lost 0.5 - 1.5 MAC
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42
Q

What parallel increases in Cerebral Blood Flow with volatiles?

A
  • ICP
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43
Q

What patients are most at risk for an increase in ICP?

A
  • Patient with space- occupying lesions
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44
Q

How can you oppose ICP?

A
  • Hyperventilation
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45
Q

Dose at which volatiles increase ICP? How much of an increase in ICP?

A
  • Onset > 0.8 MAC
  • ICP increases 7 mmHg
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46
Q

Pathology of Respiratory Depression with Volatiles

A
  • Direct depression of medullary Ventilatory center
  • Interfere with intercostal muscle (Diaphrams descends, chest wall collapses inward.)
  • Rate change insuffiencent to maintain Vm or PaCO2
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47
Q

At what dose do volatiles cause apnea?

A
  • 1.5 - 2.0 MAC
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48
Q

Name (2) Ventilatory Response with Volatiles

A
  • Blunt hypoxic response
  • Blunt hypercarbia response
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49
Q

What mediates the Blunt hypoxic response?

A
  • Carotid bodies
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50
Q

What MAC dose causes a 50 - 70% depression for blunt hypoxic response

A

*0.1 MAC

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51
Q

What MAC dose causes a 100% depression for blunt hypoxic response

A
  • 1.1 MAC
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52
Q

What Volatiles can cause a Blunt hypoxic response

A
  • All volatiles
  • including Nitrous
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53
Q

For how long can the blunt hypoxic response occur with volatiles

A
  • Several hours post-op
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54
Q

What mediates the blunt hypercarbic response to volatiles?

A
  • Dose dependent
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55
Q

What volatile has no blunt hypercarbic response?

A
  • Nitrous– does not increase PaCO2
  • substitute it for part of MAC: less depression.
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56
Q

Which volatiles will cause an increase in CO2?

A
  • All
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57
Q

What is Hypoxic Pulmonary Vasoconstriction?

A
  • Normal contration of pulmonary smooth muscle
  • Beneficial means of diverting blood flow
  • Can occure with volatiles
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58
Q

When is Hypoxic Pulmonary Vasoconstriction the most concerning?

A
  • 1 lung ventilation
59
Q

Hypoxic Pulmonary Vasoconstriction: Beneficial means of diverting blood flow

A
  • Optimize V/Q
  • 5 minutes …. regional blood flow is 1/2
  • Maximal response lasts 2-4 hours
60
Q

Hypoxic Pulmonary Vascoconstriction with Volatiles

A
  • Dose dependent decrease in response
  • 50% depression at 2 MAC
61
Q

Volatiles Cardiovascular Depression: MAP

A
  • Direct myocardial depression
  • Dose Dependent
  • Greater significance in diseased hearts w/ already altered contractility.
62
Q

Pathology on how volatiles have a direct myocardial depression

A
  • Alters Ca++ entry and SR function
63
Q

Volatiles Dose Dependent cardiovascular depression:MAP

A
  1. ↓ contractility, SV and CO (more with Halothane)
  2. ↓MAP primarily due to ↓SVR
64
Q

Name (1) volatile that has no cardiac depression

A

Nitrous

65
Q

Volatiles effect on Heart Rate

A
  • Dose dependent
  • Confounding variable
66
Q

At what dose does Sevo affect heart rate?

A
  • > 1.5 MAC
67
Q

At what dose does Iso and Desflurane affect heart rate?

A
  • ISO: Lower concentrations
  • Desflurane: over-pressurization
68
Q

Name (4) Confounding Variables that can affect HR with volatiles

A
  • Anxiety
  • Opioids
  • Beta-blockade
  • Vagolytic administration(glycopyrolate)
69
Q

How do volatiles affect cardiac output?

A
  • Dose dependent ⬇️ CO (offset by mild ⬆️ in HR for most volatiles)
  • Coronary steal
70
Q

Name (1) Volatile that does NOT decrease CO

A
  • Nitrous
  • sympathomimetic…mild increase CO
71
Q

Define Coronary steal

A
  • rob ischemic vessels and give to normal vessels
72
Q

How do volatiles cause Coronary steal?

A
  • d/t coronary vasodilation
  • Preferentially in 20-50 micrometer vessels
  • Not clinically significant
73
Q
A
  • Halothane - huge decline in CI
  • Iso - small decline
  • Des and Sevo level off and increase slightly
74
Q

Name (1) cardiac dysrhythmia that occurs because of volatiles

A
  • Increased risk of Torsades’s
  • d/t Prolonged QT interval in healthy patients
  • Inhibition of K current
75
Q

Name (1) volatile that has miminal proarrythmic effect

A

Nitrous

76
Q
A
77
Q

Cardiac dysrhythmias: Ablation studies w/ ISO and SEVO

A
  • Iso ↑ refractoriness of accessory paths…..difficult interpretation
  • Sevo no effect…acceptable for ablation
78
Q

Immune Effects of Volatiles

A
  • Neuroendocrine stress response
79
Q

Define the Neuroendocrine stress response of Volatiles

A
  • ANS and HPA activated
  • Perioperative surge in catecholamines, ACTH, cortisol
  • Suppression of monocytes, macrophages, and T-cells
80
Q

Immune response: GA compared to neuraxial

A
  • Increase metastasis
  • increased mortality
81
Q

Volatiles effect on Hepatic Blood Flow: Total Hepatic Blood Flow

A

Maintained

82
Q

Volatiles effect on Hepatic Blood Flow: Hepatic Artery flow

A

Maintained

83
Q

Volatiles effect on Hepatic Blood Flow: Portal Vein flow

A
  • Increase d/t volatiles vasodilation
  • 1-1.5 MAC
84
Q

Name (1) Volatiles that decreases hepatic flow

A
  • Halothane
  • decrease hepatic flow –> decrease oxygen delivery
85
Q

Hepatotoxicity definition and consequences

A
  • Inadequate oxygenation of hepatocytes
  • ↓ blood flow, enzyme induction…↑ O2 demand
86
Q

Name (1) Concern of hepatotoxicity

A
  • preexisting liver disease
87
Q

Hepatotoxicity: Type 1

A
  • 20% of patients
  • 1-2 weeks after exposure
  • Direct toxic effect or free radical effect
  • Nausea, lethargy, fever
88
Q

Hepatotoxicity: Type 2

A
  • Less commone
  • Immune- mediated response against hepatocytes: eosinophilia, fever
  • Prior exposure
  • 1 month after exposure
  • High mortality: acute hepatitis, hepatic necrosis
89
Q

Name (3) volatiles that are oxidized to acetyl halides metabolites. What enzyme?

A
  • Enflurane> isoflurane> desflurane
  • oxidized by P450
90
Q

What can acetyl halides metabolites cause?

A
  • antibody reaction
91
Q

Metabolism to acetyl halide is most common in patients……

A
  • sensitized by Halothane or Enflurane
92
Q

Sevoflurance can be metabolized into…..

A
  • vinyl halide
93
Q

Is vinyl halide capable of stimulating antibody formation?

A

No

94
Q

Name the Renal effects of Volatiles

A
  • Dose dependent
  • ↓ RBF, GFR and U/O
  • Not r/t to vasopressin release but CO
95
Q

How can the Renal effects be counteracted?

A
  • Preoperatively hydrate
96
Q

What cause nephrotoxity with volatiles?

A
  • Fluoride toxicity (metabolites)
97
Q

Name (3) s/s of Nephrotoxicity

A
  • Hyperosmolarity
  • Hypernatremia
  • increased creatinine
98
Q

Why are we not concerned about nephrotoxicity in newer volatiles

A
  • Newer volatiles have lower solubility
  • are exhaled prior to being metabolized and eliminated renally
99
Q

Name (1) Volatile that causes nephrotoxicity

A
  • Methoxyflurane
  • 70% metabolized
  • 1st noticed
  • Removed from market
100
Q

Compound A formation

A
  • Carbon dioxide absorbents and Sevo metabolism
  • ↑↑ levels of potassium and sodium hydroxide…
    Fluoromethyl-2,2-difluro-1-vinyl ether (compound A)
101
Q

Why are we not worried about Compound A today?

A
  • Absorbers are 75% or > calcium hydroxide
102
Q

Sevoflurane and fire

A
  • Reacts chemically with desiccated absorbent
  • Produces methanol and formaldehyde
  • Reaction→heat→faster reaction→more heat
  • to counteract this, additional water is added to Sevo
103
Q

If the absorbent canister is hot, what does this indicate?

A
  • absorbent is unable to absorb CO2
  • Switch out the canister
104
Q

When should a patient that has the possibility of Maliganant Hyperthermia be scheduled?

A
  • 1st case of the day
  • pre-run machines to scrub of volatiles
105
Q

Malignant Hyperthermia

A
  • Uncommon, inherited, genetic
106
Q

How is MH diagnosised?

A
  • Caffeine contracture test
107
Q

Triggers of MH

A
  • All volatiles
  • Succinylcholine
108
Q

MH: hypermetabolic state of skeletal muscle

A
  • Excessive Release of Ca++
  • Muscle Rigiditiy
  • Rhabdomyolysis
109
Q

MH: Symptoms

A
  • ↑ body temp, CO2 production, O2 consumption
  • 80% mortality untreated
110
Q

Treatment of MH

A
  • Dantrolene – blocks intracellular Ca++ release
  • Supportive care of rhabdomylosis
111
Q

Name the volatiles that cause PONV

A
  • All
112
Q

Name the (2) triggering agents with GA that can cause PONV

A
  • Volatiles and opioids
  • 25 - 30 %
113
Q

What volatile at >0.5 MAC causes PONV in all patients

A
  • Nitrous
114
Q

Name (3) Metabolic effects of Nitrous oxide

A
  • B12 deficiency
  • Megaloblastic bone marrow suppression
  • Increases plasma homocysteine levels
115
Q

Nitrous Oxide: B12 deficiency

A
  • Oxidizes cobalt ion in B12
  • inhibits methionine synthase
  • inhibits DNA synthesis
116
Q

Name (2) adverse effects of Nitrous oxide B12 deficiency

A
  • Developing fetus at risk
  • Scavenging systems
117
Q

Nitrous Oxide: Megaloblastic bone marrow suppression

A
  • After 24 hours of exposure
  • Repeated exposures<3 day intervals cumulative
118
Q

Nitrous oxide: Increases Plasma homocysteine levels

A
  1. Associated with low B vitamins and > levels of atherosclerosis
  2. ↑ perioperative myocardial events
119
Q

Obstetric Effects of Volatiles

A
  • Dose-dependent (0.5-1.0 MAC)
  • ↓ uterine smooth muscle contractility
  • Useful with retained placenta
  • Worsen blood loss in uterine atony
120
Q

Obstetic Effects: Nitrous

A
  • No effect on contractility
  • Increase analgesia without opiods/BZD depression
121
Q

Halothane

A
  • Halogenated alkane
  • Compatible with inhalation induction
  • Lower risk of N/V
  • non-flammable
122
Q

Halothane Concerns

A
  • Catecholamine-induced arrhythmias
  • Occasional hepatic necrosis
  • Pediatric brady-arrhythmias
  • Decomposition to HCL acid….thymol preservative added
123
Q

Halothane Potency and Solubility

A
  • High potency
  • Intermediated solubility
124
Q

Isoflurane (Forane)

A
  • An isomer of enflurane
  • Highly pungent
  • Expensive to purify
125
Q

Isoflurane Potency and solubility

A
  • Highly potent
  • Intermediate solubility
126
Q

Isoflurane Stability

A
  • No deterioritation after 5 years
127
Q

Isoflurance (Forane) metabolism

A
  • Resistant to metabolism
  • Unlikely organ toxicity
128
Q

Desflurance (Suprane)

A
  • Fluorinated methyl ethyl ether
  • Identical to isoflurane (F sub for Cl-)
  • ↓ solubility and potency
  • ↑ vapor pressure
129
Q

What does Desflurance (Suprane) require on the anesthesia machine?

A
  • Special vaporizer (heated)
130
Q

Desflurance Pungent

A
  • The most pungent
  • Coughing, salivationm breathholding
  • Laryngospasm (w/ > 6% FI)
131
Q

Desflurane (Suprane) Over-pressurizing causes

A

SNS stimulation

132
Q

Desflurance (Suprane) degradation

A
  • Will degrade to CO (Carbon Monoxide) if absorbent dehydrated
  • Desflurane > Enflurane > Isoflurane > Sevoflurane (trivial)
133
Q

Sevoflurane (ultane)

A
  • Fluorinated methyl isopropyl ether
  • Low solubility
134
Q

Sevoflurance (ultane): Pungent

A
  • Sweet smelling; not pungent
  • Least airway irritation of modern volatiles
135
Q

Name the Volatile that has the least airway irritation of modern volatiles

A

Sevoflurane

136
Q

Sevoflurane (ultane): Metabolism

A
  • Inorganic fluride
  • Least like to form CO
  • Compound A –disproved
137
Q

Name the Volatile of choice for ↑ ICP

A
  • Sevo
138
Q

Sevoflurane: Cerbral vasodilation

A
  • DOC for ↑ ICP
  • Suppresses lidocaine induced seizure activity
139
Q

Nitrous Oxide

A
  • Usually not sole anesthetic
  • Low solubility, low potency
  • does not produce skeletal muscle relaxation
  • Can’t delived 1 MAC
140
Q

Odor of Nitrous

A
  • Sweet smelling/odorless
141
Q

Nitrous + spinals

A
  • Nitrous is a good to supplement with spinals when the spinal is wearing off.
142
Q

Positives of Nitrous

A
  • good analgesia
  • 2nd gas effect
143
Q

Negative of Nitrous

A
  • N/V > 50% (about 0.5 MAC)
  • ↑ PVR
144
Q

What can nitrous do in neonates

A
  • May increase right-to-left shunt
  • jeopardize arterial oxygenation