3. Case Study
• Dispatched to adult SZ patient
• 24 y/o male found in active SZ
• SZ activity for approx 4 hours.
o Hot to touch
o Tachycardic (Sinus) in 130’s
o SPO2 is in low 80’s
4. Case study continues
• Airway is dubious
o Jaw is clinched
o Secretions
o Family keeps trying to stick spoon in mouth
• Exam and history reveals:
o History of intractable SZ
o scaring to the neck from previous trachs
o Report of prior neck/throat surgery
5. Case study continues
TX:
o Fails to respond to IN versed nor IV valium.
o SPO2 is dropping (70’s)
o Airway remains dubious, and the jaw is still clinched.
• WHAT DO YOU DO?
8. Pre-oxygenation
• Proper Pre-oxygenation prolongs the period of “safe
apnea”, buying us time and space to solve problems
• Normally takes 2-3 min of full tidal Volume (Vt) breaths
or NIPPV
• 3 parts
o “Nitrogen Washout” of the aveolar space
o “Nitrogen Washout” of the blood Stream
o Improved PaO2/SPO2 as high as possible
9. So how have we
preoxygenated in the past?
http://omicsgroup.org/journals/2165-
7548/images/2165-7548-2-e116-g001.gif
10. Racine SX, et al (2010). Face mask ventilation in edentulous patients: a
comparison of mandibular groove and lower lip placement. Anesthesiology,
112 (5), 1190-3 PMID: 20395823
13. How quick can desaturation
occur?
Between IMMEDIATELY and 8 minutes.
14. KEY POINT
• “If patients have not achieved a saturation greater than
93% to 95% before tracheal intubation, they have a
higher likelihood of desaturation during their apneic and
tracheal intubation periods.”
• Weingart and Levitan conclude that it is “impossible to
predict the exact duration of safe apnea in a patient
[...] critically ill patients [...] are at high risk of
hypoxemia with prolonged tracheal intubation and
may desaturate immediately.”
o Weingart, S., & Levitan, R. (2011). Preoxygenation and Prevention of
Desaturation During Emergency Airway Management. Annals of
Emergency Medicine, 2012(59), 165-175. Retrieved November 20,
2014, from http://www.annemergmed.com/article/S0196-
0644(11)01667-2/fulltext
16. A game changer?
• Dr. Levitan is a world renown expert in emergency
airway management
• Dr. Levitan has coined a term NO DESAT
o Nasal
o Oxygenation
o During
o Efforts
o Securing
o A
o Tube
17. What is it?
• Simply put, it is a Nasal Cannula used in an atypical way
and role to improve oxygenation during airway
procedures.
19. Wait, what?
• Yep, 15 (or more) LPM
o Apniec Oxygenation
o The nasal pharynx is better suited for airflow than the oral pharynx
• Has been used across all age ranges
o Neonates 1-2 L/min (HFNC 3-6L/min)
o Infants and children <4-5 L/min (HFNC 5-20 L/min)
o Adults <15 L/min HFNC (>15-30 L/min)
20. Guess what?
• Several studies found High Flow NC in infants
comparable to CPAP, but far better than standard flow
NC
o Reduced HR, RR, WOB, increased SPO2
o Reduced % of intubation
o Primarily studied Broncheolitis (croup).
o DID NOT study asthma and pneumonia.
o Used specialized NC.
22. How long can this be
done?
• At least 100 min
o Nielsen ND, Kjaergaard B, Koefoed-Nielsen J, et al. Apneic oxygenation combined with
extracorporeal arteriovenous carbon dioxide removal provides sufficient gas exchange in
experimental lung injury. ASAIO J. 2008;54:401-405
o Enghoff H, Holmdahl MH, Risholm L. Oxygen uptake in human lungs without spontaneous or
artificial pulmonary ventilation. Acta Chir Scand. 1952;103:293-301.
o Holmdahl MH. Pulmonary uptake of oxygen, acid-base metabolism, and circulation during
prolonged apnoea. Acta Chir Scand Suppl. 1956;212:1-128..
23. Will it work every time?
• No. Those with “Shunt Physiology” will still require some
positive pressure. The exact type (C-PAP, Bi_PAP,
NIPPV) will depend on what you have available and
situation.
• Pulmonary shunting is (in simple terms) impaired or
altered pulmonary blood flow causing impaired gas
exchange.
o Pulmonary Emboli
o Pulmonary Edema prohibiting gas exchange
24. What about CO2 build
up?
• CO2 rises 8-16 mm Hg in first minute of apnea
• THEN it slows to about 3 mm hg /minute AFTERWARD.
• This is important only in:
o prolonged apnea
o Increased ICP
25. Things that improve NO
DESAT
• At least 3 minutes
• At least 8 full breaths (not always practical)
o Even better if the patient breaths out fully before taking each breath…sill not
always practical
• Head Position
• Head/trunk elevated at least 20-30 degrees
• NPA’s
• Flow Rates above 15 LPM
• Combined with NIPPV
• Combined with NRB at 30-60 LPM
26. What does NOT work (or
work well)
• “Passive” BVM Use
• Supine Position (especially in the obese)
27. What uses for us in EMS?
• Possible tool to avoid the
CI/CV situation
• Buy time to better
manage the problem
• Pre-oxygenate during RSI
and avoid problems to
begin with!
o “PREOXYGENATION EXTENDS
THE SAFE APNEA PERIOD. IT
SHOULD BE DONE FOR EVERY
ED INTUBATION”
30. Final Key Points
• NO DESAT is just ONE method to provide better
oxygenation to the patient. It should be used with
multiple approaches
• NO DESAT effectiveness depends on multiple
physiologic factors
31. So, how did that case turn
out?
• SPO2 , now in the high 60’s/low 70’s,
• Anticipating RSI and difficult airway, a NC was applied at
15 LPM
• SPO2 immediately rose to mid 90’s
• HR dropped to the 110’s
• Airway remained dubious, but was managed with
recovery position and suctioning the buccal folds.
32. At the ER
• Based on radio report of possible difficult airway, the ER
MD had his team assembled.
• ETT was attempted with glidescope but only successful
on the third attempt, indicating the anticipation of a
difficult airway was logical and correct
• NO DESAT avoided a failed airway attempt, and bought
time to chose a more successful approach
33. Questions?
• Video: http://www.medscape.com/viewarticle/823961
o (free Registration required)
• http://www.epmonthly.com/archives/features/no-desat-/
• http://www.annemergmed.com/article/S0196-
0644(11)01667-2/fulltext
• Evidence Based Oxygenation :
http://vimeo.com/40307291
Editor's Notes
At the end of this presentation, you will become familiar with :
Become familier with the importance of preoxygenation
Discuss how to maximize pre-oxygenation
Discuss the use of “high flow” nasal cannula in the setting of respiratory and/or airway failure and in prexoygenation
from various levels of PaO2. Risk categories are
overlaid on the curve. Patients near an SpO2 of 90% are at
risk for precipitous desaturation, as demonstrated by the
shape of the curve.
Preoxygenation allows a safety buffer during
periods of hypoventilation and apnea.
Extends the period of safe apnea, defined as
the time until a patient reaches a saturation
level of 88% to 90%, to allow for placement of
a definitive airway.
Below this level, oxygen saturation can
decrease to critical levels <70% within
moments
Preoxygenation
Weingart SD and Levitan RM: Ann Emerg Med 2011
Another sizable study (250, 543 patients in the 6 OR) looked at the
incidence of adverse events associated with Cardiac Arrest during/following ETT , and found that Hypoxia,
Hypotension, and Hypovolemia were major predictors as well.
Olsson, G. L. and Hallén, B. (1988), Cardiac arrest during anaesthesia. A computeraided study in 250 543 anaesthetics. Acta
Anaesthesiologica Scandinavica, 32: 653–664. doi: 10.1111/j.13996576.1988.
tb02804.x
Standardly available nonrebreather masks can deliver FiO2
greater than or equal to 90% by increasing the flow rate to 30 to
60 L/minute.10 Such flow rates may be achievable on most flow
regulators in EDs by continuing to open the valve, though there
will be no calibrated markings beyond 15 L/minut
The first 2 goals are
imperative; denitrogenating and oxygenating the blood adds
little to the duration of safe apnea8 because oxygen is poorly
soluble in blood, and the bloodstream is a comparatively small
oxygen reservoir compared with the lungs (5
Can augment denitrogenatiton by asking patient
to take 8 large breaths (max inhalation and
exhalation)
Difficult for many patients in ED settings
including children to cooperate with 8 large
breaths% versus 95%).
So how have we preoxygenated in the past?
NRB at the traditional 15-20 LPM only delivers 60-80% FIO2 at best
HOW MUCH TIME DO I HAVE?
The answer to this question is multifactorial. The primary benefit of preoxygenation is to denitrogenate the lungs and create an oxygen reservoir in the alveoli, as opposed to increase the PaO2 in the bloodstream. As classically described by Benumof et al (see curve below), time to desaturation ranges from ~3 - 8 minutes. However, this does not take into account critical pathophysiology such as poor CO, sepsis, anemia, and volume depletion. Studies in the ICU setting have proposed safe apnea times of only 23 seconds (Mort 2005).
Thus, Weingart and Levitan conclude that it is “impossible to predict the exact duration of safe apnea in a patient [...] critically ill patients [...] are at high risk of hypoxemia with prolonged tracheal intubation and may desaturate immediately.”
Also, as borne out in the discussion, data has suggested that succinylcholine may increase O2 consumption and shorten the safe apnea time.
Weingart, S., & Levitan, R. (2011). Preoxygenation and Prevention of Desaturation During Emergency Airway Management. Annals of Emergency Medicine, 2012(59), 165-175. Retrieved November 20, 2014, from http://www.annemergmed.com/article/S0196-0644(11)01667-2/fulltext
After the induction of apnea, nasal cannula diffuses oxygen down the trachea to the alveolus. It is
absorbed across the alveolar capillary membrane, despite the absence of respiratory movements, even as
laryngoscopy is being performed. This occurs because of the difference in gas production and uptake in
the alveolus, and the differences in the solubility of oxygen and carbon dioxide in the blood. Carbon
dioxide excretion into the alveolus diminishes during apnea because carbon dioxide is approximately 25
times more soluble than oxygen in blood. It is estimated that during apnea CO2 is excreted into the
alveolus at only 10 ml/min. Conversely, oxygen is absorbed at 250 ml/min. The resultant negative
pressure gradient (-240 ml/min) creates a sub-atmospheric pressure in the alveolus. The net result is that
during apnea, oxygen insufflated into the upper airway will be “drawn” down the trachea and into the
alveolus. Oxygenation can be maintained in non-breathing humans for 100 minutes through apneic
diffusion, even as carbon dioxide builds up in the blood.
Some investigators simply define HFNC as flow
rates simply exceeding standard norms
Neonates 1-2 L/min (HFNC 3-6L/min)
Infants and children <4-5 L/min (HFNC 5-20 L/min)
Adults <15 L/min HFNC (>15-30 L/min)
McKiernan et al. J Pediatr 2010
Studied respiratory support received by 115 infants with bronchiolitis over two time periods—before and after HFNC was introduced in their pediatric ICU. The authors showed that HFNC resulted in an absolute risk reduction of intubation of 14 % (p < 0.05).
Schibler et al. Intensive Care Med 2011
167 infants with bronchiolitis supported with HFNC and showed that <5 % of infants required intubation. Outcomes – assessed at 60-90 min – 20% reduction
in respiratory rate and heart rate.
HFNC appears to be feasible in infants with bronchiolitis and may decrease the need for intubation when compared to standard nasal cannula. HFNC in children has not been demonstrated in other common respiratory conditions such as asthma and pneumonia.
After the induction of apnea, nasal cannula diffuses oxygen down the trachea to the alveolus. It is
absorbed across the alveolar capillary membrane, despite the absence of respiratory movements, even as
laryngoscopy is being performed.
This occurs because of the difference in gas production and uptake in the alveolus, and the differences in the solubility of oxygen and carbon dioxide in the blood. Carbon dioxide excretion into the alveolus diminishes during apnea because carbon dioxide is approximately 25
times more soluble than oxygen in blood. It is estimated that during apnea CO2 is excreted into the
alveolus at only 10 ml/min. Conversely, oxygen is absorbed at 250 ml/min. The resultant negative
pressure gradient (-240 ml/min) creates a sub-atmospheric pressure in the alveolus. The net result is that
during apnea, oxygen insufflated into the upper airway will be “drawn” down the trachea and into the
alveolus. Oxygenation can be maintained in non-breathing humans for 100 minutes through apneic
diffusion, even as carbon dioxide builds up in the blood.
The difference in oxygen and carbon dioxide movement across
the alveolar membrane is due to the significant differences in gas
solubility in the blood, as well as the affinity of hemoglobin for
oxygen. This causes the net pressure in the alveoli to become
slightly subatmospheric, generating a mass flow of gas from
pharynx to alveoli. This phenomenon, called apneic
oxygenation, permits maintenance of oxygenation without
spontaneous or administered ventilations. Under optimal
circumstances, a PaO2 can be maintained at greater than 100
mm Hg for up to 100 minutes without a single breath, although
the lack of ventilation will eventually cause marked hypercapnia
and significant acidosis.54
Shunt refers to perfusion without ventilation. More specifically, intrapulmonary shunt refers to areas in the lung where perfusion exceeds ventilation.
Pulmonary shunting is minimized by the normal reflex constriction of pulmonary vasculature to hypoxia. Without this hypoxic pulmonary vasoconstriction, shunt and its hypoxic effects would worsen. For example, when alveoli fill with fluid, they are unable to participate in gas exchange with blood, causing local or regional hypoxia, thus triggering vasoconstriction. Blood is then redirected away from this area, which poorly matches ventilation and perfusion, to areas which are being ventilated.
Because shunt represents areas where gas exchange does not occur, 100% inspired oxygen is unable to overcome the hypoxia caused by shunting.
A decrease in perfusion relative to ventilation (as occurs in pulmonary embolism, for example) is an example of increased dead space.[3] Dead space is a space at which gas exchange does not take place, such as the trachea. It is ventilation without perfusion.
Pulmonary shunting causes the blood supply leaving a shunted area of the lung to have lower levels of oxygen and higher levels of carbon dioxide (i.e., the normal gas exchange does not occur).
A pulmonary shunt occurs as a result of blood flowing right-to-left through cardiac openings or in pulmonary arteriovenous malformations. The shunt which means V/Q = 0 for that particular part of the lung field under consideration results in a de-oxygenated blood going to the heart from the lungs via the pulmonary veins. If giving pure oxygen at 100% for five-ten minutes doesn't raise the arterial pressure of O2 more than it does the alveolar pressure of O2 then the defect in the lung is because of a pulmonary shunt. This is because although the PO2 of alveolar gas has been changed by giving pure supplemental O2, the PaO2 ( Arterial gas pressure ) will not increase that much because the V/Q mismatch still exists and it will still add some de-oxygenated blood to the arterial system via the shunt.[4]
Pre-oxygenation combining high flow nasal cannula and a non-rebreather mask
http://www.epmonthly.com/archives/features/no-desat-/
While the common perception is that a non-rebreather mask is the pinnacle of oxygen adminstration, effective FiO2 from these masks may not create optimal pre-oxygenation at flow rates of 15 lpm. This is because the measured inspired oxygen in the hyopharynx with a non-rebreather at 15 lpm is only 60-70%. The reason for this is the patients expired gasses are mixing with the applied oxygen, and also because expired gasses accumulate in the nasopharynx. Quiet breathing involves flow rates as high as 30 lpm; maximal pre-oxygenation with a loose-fitting non-rebreather may require a flow rate as high as 48 lpm. High flow nasal oxygen has been shown to flush the nasopharynx with oxygen, and then when patients inspire they inhale a higher percentage of inspired oxygen. Small changes in FiO2 create dramatic changes in the availability of oxygen at the alveolus, and these increases result in marked expansion of the oxygen reservoir in the lungs prior to the induction of apnea.
Oral intuabtion with nasal cannula running high flow oxygen
http://www.epmonthly.com/archives/features/no-desat-/
