Med Administration-Specialty Gases Flashcards
Nitric Oxide
A diatomic molecule
Colourlessgas at room temperature
Non-flammable but supports combustion
A free radical with a half-life of 3-50 s
Highly diffusible and lipid soluble
Nitric Oxide in the Body
- Produced endogenously in vascular endothelial cells
- Is an important mediator of physiologic function including:
- Vasodilation
- Neurotransmission
- Long-term memory
- Immunologic defense
NO and Smooth muscles
Physiologically causes relaxation of smooth muscle
Wheninhaledin small concentrations NO is 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 muscles of the capillaries supplying these alveoli
This vasodilation results in a decreased PVR-So we can get decreasing PVR without decreasing SVR!!
pulmonary vasodilation results in
Decreased intrapulmonary shunting
Improved oxygenation
Decreased PVR
Decreased pulmonary artery pressures
Inhaled NO effects are limited to
The effects are limited to the pulmonary circulation because after diffusing into the capillaries NO immediately binds to hemoglobin
This forms nitrosylhemoglobinwhich is rapidly oxidized to methemoglobin(metHb)
Nitric Oxide: The Indications
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
NO and methacholine challanges
Studies show NO reverses the bronchoconstriction resulting from histamine and methacholinechallenges.
Most Common Uses-Pulmonary Vasodilation
NO is primarily used for its selective pulmonary vasodilator effects!
PPHN
Congenital heart defects
ARDS
NO use for ARDS
No improvement in mortality is seen with the use of NO on ARDS (adult) patients
FDA has not approved NO for widespread use in the Tx of ARDS.
Most Common Uses-Bronchodilation
Usually to reverse methacholineor Common bronchoconstriction
NO Dose
Therapeutic dose range 2-80 ppm (Neo – 20 ppm)
Beneficial effects appear to peak at about 10 ppm in adult ARDS patients
NO Choosing the Dose
Will depend on hospital P&P
Start at 10 ppm and do an ABG after 5 min
Changing NO based on ABG results
If no response (PaO2increases <10 mmHg, SpO2increases <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
Patient’s should then be optimized to the lowest dose that shows a favorable response!
Weaning NO
Wean NO by 2-4 pm Q5 min while monitoring SpO2 and mean PAP.
If SpO2 falls by > 2% or mean PAP increases by > 5 mmHG return to last effective dose.
NO Toxcity
- 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
- Most toxic effects are due to its by-products:
- NO2
- Nitric Acid
- Methemoglobin
NO2
Nitrogen dioxide is produced when NO reacts with oxygen
Is a reddish-brown gas
More toxic than NO
The higher the FiO2 the more NO2 formed!
Clinically the goal is to keep NO2< 2 ppm!
Nitric Acid
Forms when NO reacts with H2O