Speciatly Gases Flashcards
1
Q
Nitric Oxide Properties
A
- Colorless gas at room temperature
- Non-flammable but supports combustion
- A free radical with a half life of 3-5 sec
- Highly diffusible and lipid soluble
2
Q
NO effects in the body
A
- Will be produce endogenously in vascular endothelial cells
- Is important mediator of physiologic functions
- Vasodilation
- Neurotransmission
- Long term memory
- immunologic defense
3
Q
Effects of NO
A
- When inhaled in small concentration NO is a potent pulmonary vasodilator
- Considered to be a selective pulmonary vasodilator as it only affects ventilated alveoli
- Thus NO increases blood flow only to ventilated alveoli by relaxing the smooth muscle of the capillaries supplying these alveoli
- This vasodilation results in a decrease PVR, so that we can get a decrease PVR without a decrease SVR
4
Q
Pulmonary Vasodilation of NO
A
- The pulmonary vasodilation results in
- Decreased intrapulmonary shunting
- Improved oxygenation
- Decreased PVR
- Decreased pulmonary artery pressure
- The effects are limited to the pulmonary circulation because after diffusing into the capillaries NO immediately binds to hemoglobin
- This forms nitrosylhemoglobin which is rapidly oxidized to methemoglobin (metHb)
5
Q
NO Potential Uses
A
ARDS
Pulmonary Hypertension
Heart Transplantation
Acute pulmonary embolism
COPD
Bronchodilation
Congenital diaphragmatic hernia
Congenital heart disease
Testing pulmonary vascular responsiveness
6
Q
Most Common Uses of NO
A
-
Pulmonary Vasodilation
- PPHN
- Congenital heart defects
- ARDS
-
For Bronchodilation
- Usually to reverse methacholine or histamine induced bronchoconstriction
NO is primarily used for its selective pulmonary vasodilatory effects
7
Q
NO Dosing
A
- Therapeutic dose range 2-80 ppm (Neo – 20 ppm)
- Beneficial effects appear to peak at about 10 ppm in adult ARDS patients
8
Q
Calgary Health Region Adult NO Dose
A
- Start at 10 ppm and do an ABG 5 min after initiation
- 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
- If still no response:
- For ARDS—discontinue NO (treatment failure!)
- For pulm. HTN—increase to 40 ppm and assess response
9
Q
Optimizing NO
A
- Wean NO by 2-4 pm Q5min while monitoring SpO2 and mean PAP
- If SpO2 falls by >2% or mean PAP increase by >5 mmHg return to last effective dose
10
Q
NO Toxicity
A
- In high concentration (5000-20,000 ppm) NO causes acute pulmonary edema and can lead to death
- Lower concentrations are associated with direct cellular damage and impaired surfactant production
11
Q
NO by products
A
- Most toxic effects are due to its by-products:
- NO2
- Nitric Acid
- Methemoglobin
12
Q
NO2 and Nitric Acid
A
- NO2
- (Nitrogen dioxide) is produced when NO reacts with oxygen
- Is a reddish-brown gas
- More toxic than NO
- Nitric Acid
- Forms when NO reacts with H2O
The higher the FiO2 the more NO2 formed!
13
Q
NO Can Cause
A
- Cell damage
- Chemical pneumonitis
- Hemorrhage
- Pulmonary edema
- Death
14
Q
Want to keep NO2 below
A
Clinically the goal is to keep NO2 < 2 ppm!
15
Q
Methemoglobin
A
- Any NO diffusing into the capillaries immediately binds to Hb resulting in metHb
- High levels of metHb reduce the oxygen carrying capacity of the blood
- Normal metHb is < 2%
- Methemoglobinemia is defined as metHb > 2%
- In the CHR metHb levels are assessed at least Q12h.
- Methemoglobinemia is not commonly seen at the therapeutic dose of NO
- Causes blood to appear rusty brown in colour
- MetHg >30% can be treated with methylene blue
- Oximetry readings may be erroneously high.
