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Interventions 3 > Specialty Gases (Mod 6) > Flashcards

Specialty Gases (Mod 6) Flashcards

Nitric Oxide and Heliox

1
Q

What functions does Nitric Oxide include?

A
  • Vasodilation (potent)
  • Neurotransmission
  • Long term memory
  • Immunologic defense
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2
Q

How could Nitric Oxide affect platelet adhesion?

A

Nitric Oxide would inhibit platelet adhesion

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3
Q

How could Nitric Oxide on the inflammatory response induced by mast cells?

A

Nitric Oxide would inhibit the inflammatory process by mast cells

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4
Q

What are expected physiological effects of Nitric Oxide?

A

Relaxation of smooth muscles

  • when inhaled = potent vasodilator
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5
Q

Why is it beneficial to inhale Nitric Oxide (NO) rather than admin percutaneously?

A

Nitric Oxide is a selective pulmonary vasodilator, it only affects ventilated alveoli. Meaning…

  • Vasodilation = Decreased PVR without decreasing SVR
  • NO increases blood flow only to ventilated alveoli by relaxing the smooth muscles of the capillaries supplying these alveoli
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6
Q

When Nitric Oxide has been admined, what does the subsequent pulmonary vasodilation result in?

A
  • Decreased intrapulmonary shunting
  • Improved oxygenation
  • Decreased PVR
  • Decreased pulmonary artery pressures
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7
Q

Why doesn’t Nitric Oxidie effect SVR?

A

The effects of NO are limited to pulmonary circulation because after diffusing into the capillaries NO immediately binds to hemoglobin

  • NO + hbg = nitrosylhemoglobin which is rapidly oxidized to methemoglobin (metHb)
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8
Q

Indications and potential uses for Nitric Oxide?

A

Look over, but don’t linger

Potential Uses
ARDS
PPHN
Primary pulmonary hypertension
Pulmonary hypertension post cardiac-Sx
Heart transplantation
Acute pulmonary embolism
COPD
Bronchodilation
Congenital diaphragmatic hernia
Congenital heart disease
Testing pulmonary vascular responsiveness

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9
Q

When would Nitric Oxide be used for Bronchodilation?

A

When bronchoconstriction results from histamine and/or methacholine challenges

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10
Q

What are the benefits of Nitric Oxide for pphn treatments?

A

NO reduces pulmonary pressure…therefore:

  • Systemic pressures > Pulmonary pressures therefore:
  • Shunting through PDA and PFO are stopped/reduced –> direct effect due to the reduced PAP (and decreased PVR)
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11
Q

Most common uses for Nitric Oxide?

A

NO is primarily used for its selective pulmonary vasodilator effects but

  1. Pulmonary Vasodilation
  2. Bronchodilation
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12
Q

When would pulmonary vasodilation be desired when using Nitric Oxide? (3)

  • what pathos?
A
  1. PPHN
  2. Congenital heart defects (maintain pfo and pda)
  3. ARDS
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13
Q

When would bronchodilation be desired when using Nitric Oxide? (3)

A

To reverse methacholine or histamine induced bronchoconstriction

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14
Q

Nitric Oxide Therapeutic dose range?

A

2-20 ppm (Neo-20ppm)

  • Beneficial effects peak at 10ppm in adult ARDS patients
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15
Q

When does the therapeutic dose of Nitric Oxide peak for adults with ARDS?

A

Around 10ppm

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16
Q

Nitric Oxide Starting dose in: Adults

A

Start at 10ppm followed by ABG 5 mins after initiation

  • optimize to the lowest dose w/favorable response
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17
Q

How is Nitric Oxide dosage optimized?

A

Wean NO by 2-4 pm while monitoring SpO2 and mean PAP

  • if SpO2 falls by >2% or mean PAP increases by > 5mmHg…return to last effective dose
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18
Q

P and P for Nitric oxide on adults

A
  1. Start at 10 ppm and do an ABG 5 min after initiation
  2. If no response (PaO2 increases <10 mmHg, SpO2 increases <2% or MPAP does not decrease by at least 5 mmHg) then increase to 20 ppm
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19
Q

After initiating Nitric Oxide for ARDS, what are the next steps if there is no response to treatment?

A

Discontinue NO (treatment failure)

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20
Q

After initiating Nitric Oxide for pulmonary hypertension, what are the next steps if there is no response to treatment?

A

10ppm (starting)–> 20 ppm–> 40ppm and assess response

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21
Q

Risk of high concentrations of Nitric Oxide?

A

NO Toxicity which can lead to acute pulmonary edema…than death

  • Most toxic effects are due to its by products: NO2, Nitric Acid, and Methemoglobin
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22
Q

What range would Nitric Oxide toxicity be a concern?

A

NO toxicity would be expected at 5000-20,000 ppm

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23
Q

What would the lower end of Nitric Oxide toxicity involve?

A

Possible direct cellular damage and impaired surfactant production

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24
Q

How is Nitrogen Dioxide [NO2] produced?

A

When NO reacts with oxygen

  • More toxic than NO
  • The higher the FiO2, the more NO2 formed
25
Q

How is Nitric Acid produced?

A

Forms when NO reacts with H2O

26
Q

What toxic effect do NO2 and Nitric have?

A

Both can cause the following (with increased dosage)

  • Cell damage
  • Chemical pneumonitis
  • Hemorrhage
  • Pulmonary edema
  • Death
27
Q

Clinically, what is the range should NO2 be kept?

A

The goal is to keep NO2<2ppm

28
Q

What treatment option is used for Nitric Oxide toxicity caused by Methemoglobin formation?

A

metHb > 30% can be treated with Methylene blue

  • cyanosis should resolve within the hour
29
Q

How does Methemoglobin form?

A

Any NO diffusing into the capillaries immediately binds to Hb resulting in MetHb (normal)

  • High levels of metHb reduce the oxygen carrying capacity of the blood
30
Q

What effect does Methemoglobin have physiologically?

A

MetHb reduces the oxygen carrying capacity of blood

  • Its a toxic effect from high concentrations of NO
31
Q

Normal metHb level?

A

Normal metHb < 2%

32
Q

Range for Methemoglobinemia?

A

when metHb > 2%

  • not commonly seen at the therapeutic dose of NO
33
Q

How often are metHb levels assessed?

A

q12h at the min

34
Q

How could Nitric Oxide result in worsening of hypoxemia (adverse effect lol)

A

Worsening hypoxemia thought to be due to worsened v/q when no shunt was initially present

35
Q

What is the rebound effect of Nitric Oxide?

A

Worsening of hypoxemia and pulmonary hypertension then before therapy

  • Seen during the withdrawal of NO therapy
36
Q

During anesthesia, why does FiO2 need to be closet to the patient?

A

Addition of NO during administration will reduce the FiO2

  • FiO2 needs to be distal to where NO is added
37
Q

Safety limit of NO during administration?

A

5 ppm

  • Safety limit is for workers
  • Extracted from the environment via scavenging system
38
Q

Where should an oxygen analyzer be placed during Nitric Oxide administration in a ventilated patient?

A

Oxygen analyzer must be downstream from the T in point bc NO reduces FiO2

  • NO/NO2 analyzer should accompany the O2 analyzer as well
39
Q

How is Nitric Oxide administered in spontaneously breathing patients?

A

Simple circuit of corrugated tubing with NO, air, and O2 blended to get desired FiO2 and ppm of NO

  • Requires prior analysis for baseline
40
Q

How can the rebound effect associated with withdrawal of Nitric Oxide therapy be prevented?

A

The following doesn’t apply if pt was a non responder to therapy

  • Reduce NO to lowest effective dose (ideally < 5ppm)
  • Maintain hemodynamic status w/adequate oxygenation on FiO2 <0.4 and low level of PEEP
  • Pt should be hyperoxygenated (FiO2 0.6-0.7) just prior to discontinuation
41
Q

FloLan (Caripul) function?

A

A prostaglandin (Epoprostenol) that:

  1. Inhibits natural platelet aggregation
  2. Reduces pulmonary hypertension (some systemic action as well) –> specfically Pulmonary artery hypertension
  • Sometimes refered to as Prostacyclin
42
Q

How is FloLan (Caripul) aka Epoprostenol sodium delivered?

A

Delivered via aerogen (vibrating mesh) nebulizer

  • “T” it in to a vent circuit or attach to a mask
43
Q

Difference between Epoprostenol and Trepostinil (glance)

A

Epoprostenol and treprostinil are both prostacyclin analogs used in the treatment of pulmonary arterial hypertension (PAH). Differ in route and kinetics

44
Q

Particle size deposited in the bronchi?

A

6-9 microns deposit in the bronchi

45
Q

Particle size deposited in the bronchiole?

A

3-6 microns deposit in the bronchioles

46
Q

Particle size deposited in the alveoli?

A

1-3 microns are deposited in the alveoli

47
Q

what device can deliver particle sizes smaller than 1 micron?

A

Vibrating screens/mesh

  • Any smaller, and must of the particles are exhaled
48
Q

What is the primary function Heliox gas?

A

Low density gas (light) used to decrease WOB

49
Q

What is a mandatory feature for Heliox gas administration?

A

Must be combined with oxygen

Common mixtures are the following:

  • 20% O2, 80% helium
  • 30% O2, 70% helium
50
Q

How does Heliox assist airflow in the upper airway?

A

Turbulent flow in large airways is more affected by gas density than viscosity

  • Breathing a low density gas improves flow through the airways
51
Q

Is Heliox effective in managing issues in the lower airways?

A

Not as much

  • Lower airways have laminar flow (smooth flow), flow is affected more by viscosity than density
52
Q

Clinical indications for Heliox use in the upper airways?

A

If upper airway obstruction is present, can help with:

  • Airway tumors
  • Post extubation stridor
  • Pediatric airway obstructions
53
Q

Clinical indications for Heliox use in the lower airways?

A
  • Severe COPD/Astha
  • Combined w/NIPPV and/or mech vent
  • Evidence not clear to effectiveness, but promising
54
Q

Delivery mechanisms intricacies for Heliox (4)

A
55
Q

If using a Heliox mixture (like 20% O2 + 80% He), what are some considerations that need to be met?

A

Use a tight fitting NRM or adequate seal for NP for peds/neos

56
Q

If using separate oxygen and helium tanks, what are some considerations that need to be met?

A

Monitor FiO2 and ensure adequate FiO2 delivered to patient

57
Q

If Helium is delivered by aerosolizing the gas, what are some considerations that need to be met?

A

Increase flow to ensure nebulizer power is adequate

  • May improve aerosol penetration
58
Q

If Helium is given on a mechanical vent, what are some considerations that need to be met?

A

He could alter Vt measurement and could lead to lung injury

  • some vents have heliox options
59
Q
A

Interventions 3 (19 decks)

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