Kerry Gomes

Inadequate alveolar oxygenation◦ Low environmental oxygen pressure

◦ Alveolar hypoventilation

Diffusion abnormalities

Dead space◦ High ventilation, low perfusion (V/Q)

Low V/Q mismatch

Shunt

Low venous blood saturation

Physiological shunt is the major cause of poor oxygenation in ill ED patients.

Areas of alveoli that are blocked from conducting oxygen, but still have intact blood vessels surrounding them.

Causes◦ Pneumonia

◦ Atelectasis

◦ Pulmonary oedema

◦ Mucus plugging

◦ ARDS

In normal patients, Hb reaching lungs has a saturation of 65-70%

Only small amount of exposure to O2 needed to rapidly bring saturation to 100%

In shocked state, venous blood with lower states reach the lungs, and will require more exposure to O2 to reach 100%◦ In injured lungs this may not occur

Always consider the circulatory system when evaluating respiratory status.

Preoxygenation allows a safety buffer during periods of hypoventilation and apnoea.

Extends the period of safe apnoea, defined as the time until a patient reaches a saturation level of 88% - 90%, to allow for the placement of a definitive airway.

Below this level, oxygen saturation can decrease to critical levels <70% within moments.

Weingart SD and Levitan RM: Ann Emerg Med 2011

Patients breathing room air before RSI, desaturation occurs in 45-60sec

Heller et al. showed marked time to desaturation if patients received preoxygenation with 100% oxygen.

Ideally preoxgenate for 3 minutes with high FiO2 source.◦ Can augment denitrogenation by asking patient to

take 8 large breathes

◦ Difficult in ED setting and paediatric patients

1. Achieve 100% oxygenation saturation prior to procedure

2. Denitrogenate the residual capacity of the lungs, maximizing oxygen storage

3. Denitrogenate and maximally oxygenate the bloodstream.

Weingart SD and Levitan RM: Ann Emerg Med 2011

If patients do not achieve a saturation >93%-95% pre intubation, they have a high likelihood of desaturation during the apnoeic and intubation periods.

If patients do not achieve this with a high flow source, it is likely they are exhibiting a physiological shunt.

In short term shunt can be partially overcome by augmenting mean airway pressures.

Study Patients Intervention Comparator Outcome

Delay et al RCT 28 obese, operative pts

NIV Spon vent at zero pressure

NIV pts achieved faster and more complete denitrogenation

Gander et al RCT 30 morbidly obese, operative pts

CPAP preO2 Spon vent at zero pressure

Time to reach a saturation of 90% after apnoea was extended by 1min

Herriger et al RCT 40 ASA I-II operative pts

CPAP preO2 Spon vent at zero pressure

Prolonged the non-hypoxic apnoea by > 2min

Critically ill pts requiring tracheal intubation in ICU.

At end of preoxygenation period:◦ Noninvasive positive pressure grp had 98% mean SpO2

◦ Std grp had 93% mean SpO2

During intubation procedure, oxygen saturation fell to:◦ 93% in Noninvasive positive pressure grp

◦ 81% in Std grp

12 of Std grp and 2 NIV grp had saturations below 80%

6 of 26 in NIV grp were unable to improve hypoxymicsaturation with high FiO2 until they received positive pressure.

Baillard et al. Am J Resp Crit Care Med. 2006

Study Intervention Method Outcome

Lane et al RCT pts preO2 in 20 degree head up

3min preO2

Sedation & mus. relax.Time to desat 100 – 95%

386 vs 283 sec

Ramkumaret al

RCT pts preO2 in 20 degree head up

3min preO2

Sedation & mus. relax.Time to desat 100 – 95%

452 vs 364 sec

Altermattet al

RCT in BMI >31, sitting position

RSIIntubated, left apneic and disconnectedTime to desat 100 – 90%

214 vs 162 sec

Reverse Trendelenburg position also improves preoxygenation and may be useful in patients who cant bend at shoulder or waist, i.e. possible spinal injury patients.

Lung O2

◦ 450ml in patient breathing room air◦ 3000ml in patient breathing 100% O2 for sufficient time

to replace alveolar nitrogen.

O2 reservoir in lungs and bloodstream◦ 1 -1.5L in patient breathing room air◦ 3.5 – 4L in patient optimally preoxygenated

Oxygen consumption during safe apnoea is 250ml/min in healthy patient.

Duration of safe apnoea◦ 1 min in room air◦ 8 min breathing high FiO2

Benumof JL et al. Anesthesiology. 1997

Benumof curves ◦ Assume preO2 with device generating ~90% FiO2

and optimal time

◦ Assume complete denitrogenation

◦ Ignore pulse oximeter lag time

Times depicted not applicable to critically ill ED pts, or pts poor cardiac output.

Farmery and Roe, desaturation to 85% may be as short as 23 sec in critically ill vs 502 sec in healthy adult.

During apnoea◦ 250ml/min O2 will move from alveoli to bloodstream

◦ 8-20ml/min CO2 moves into alveoli

◦ Net pressure in alveoli - slightly sub-atmospheric, generating a mass flow of O2 form pharynx to alveoli.

Apnoeic oxygenation◦ Under optimal conditions PaO2 can be maintained for

>100mmHg for up to 100min without a breath.

◦ Lack of ventilation will eventually cause marked hypercapnia and significant acidosis.

Nielsen et al. ASAIO j. 2008

Study Patients Intervention Outcome

Teller et al 1998

RCT 12 pts,blind crossover

Nasopharyngeal cathethers 100% FiO2 at 3L/min vs room air

Sat ≤92 or 10minNo desat <98% in 10min

Taha et al 2006

RCT 30 pts Nasal catheters 5L/min of 100% vs room air

No desat in O2

armControl desat<95%in average 3.65 min

Ramachandran2010

RCT 30 obese pts

Nasal catheters5L/min of 100% vs room air

O2 grp had longer duration of SpO2 ≥ 95%5.29 vs 3.49min

Nasal cannula provide limited FiO2 to spontaneously breathing patient.

Decreased oxygen demand during apnoea allow nasal cannula to fill pharynx with high level FiO2 gas.

Increasing rate to 15L/min, near FiO2 can be obtained.

Nasal cannula can be left on during intubation

High-flow nasal cannula also available, can humidify O2 and allow rates <40L/min.

Ventilation provides 2 potential benefits◦ Ventilation

Minimal, exception in profound met. Acidosis and raised ICP

◦ Increased oxygenation through alveolar distension and reduction in shunting lengthening duration of safe apnoea

But, pressures > 25mmHg H2O can overwhelm oesophageal sphincter – risk regurg and aspiration

Keep bagging pressures < 25mmHg H2O Slow breathes over 1-2 sec at low vol 6ml/kg

and at a low rate 6-8breaths/min

Operative pts receiving succinylcholine desat. faster than those receiving rocurononium.◦ Adult pt: Succ 242s vs Roc 378s to desat (Taha SK et al. 2010)

◦ Obese pt: Succ 283 sec vs Roc 329s to desat (Tang et al.

2011)

When doses >1.2mg/kg used, intubating conditions identical.

? Fasciculation's induced by succinylcholine may cause increased oxygen use.

Breaking sequence of sedative and paralytic agent to allow adequate preoxygenation.

Administration of specific sedative agents, which do not blunt spontaneous ventilations or airway reflexes.

Ketamine◦ 0.3mg/kg titrated up to 1.5 mg/kg by slow iv push

Advantage of DSI is that frequently patients on NIV improve their respiratory parameters and intubation can be avoided.

Risk category PreO2 period Onset of muscle relaxation

Apnoeic period during intubation

Low riskSpO2 96-100%

NRB mask with max O2 flow rate

NRB mask and nasal O2 at 15L/min

Nasal O2 at 15L/min

High riskSpO2 91-95%

NRB mask or CPAP or BVM with PEEP valve

NRB mask, CPAP, or BVM with PEEP and nasal O2 at 15L/min

Nasal O2 at 15L/min

HypoxemicSpO2 <90%

CPAP or BVM with PEEP

CPAP or BVM with PEEP and nasal O2 at 15L/min

Nasal O2 at 15L/min

Weingart SD and Levitan RM: Ann Emerg Med 2011

Conventional preoxygenation techniques provide safe intubation techniques for majority of ED patients.

Subset of patients, will desaturate. Optimising preoxygenation and preventing

deoxygenation is needed to safely intubate this group.

NIV as preoxygenation technique, apnoeic oxygenation, head-up and breaking the sequence of RSI may make the prei-intubation period safer.