A key component in the planning of intubation is pre-oxygenation. Recently apnoeic oxygenation during laryngoscopy has been adopted too. These are just two components of an overall oxygenation strategy to consider when intubating the critically ill. Some patients will require proactive preparation of the components of successful post-intubation oxygenation, especially those with severe lung pathology like ARDS.
Here’s a handy list of things to consider when planning a peri-intubation oxygenation strategy. Some people like their airway stuff to begin with ‘P’, so I’ve obliged:
High Flow Nasal Cannulae (HFNC) oxygen therapy was introduced in paediatric interfacility retrievals undertaken by the Mater Children’s PICU Retrieval Team in Queensland, Australia. In 793 under 2 year olds, HFNC was associated with a reduction in infants receiving invasive or non-invasive ventilation. 77% of the patients had bronchiolitis.
The rationale for this treatment is explained as:
Owing to the inherent properties of the infant respiratory system with small airways and high chest compliance, the risk of developing atelectasis is high in bronchiolitis. HFNC therapy applied early in the disease process may prevent progression of the disease and maintain normal lung volumes, thereby preventing atelectasis. As a result, the functional residual capacity can be maintained and work of breathing reduced, which may stabilize the patient sufﬁciently to avoid the need for intubation. For this purpose we used ﬂow rates of 2 L/kg/min which have been shown to result in a positive end-expiratory pressure of 4–5 cmH2O
Read more on high-ﬂow nasal cannula oxygen therapy.
High-ﬂow nasal cannula (HFNC) support in interhospital transport of critically ill children
Intensive Care Med. 2014 Feb 15. [Epub ahead of print]
BACKGROUND: Optimal respiratory support for interhospital transport of critically ill children is challenging and has been scarcely investigated. High-flow nasal cannula (HFNC) therapy has emerged as a promising support mode in the paediatric intensive care unit (PICU), but no data are available on HFNC used during interhospital transport. We aimed to assess the safety of HFNC during retrievals of critically ill children and its impact on the need for invasive ventilation (IV).
METHODS: This was a retrospective, single-centre study of children under 2 years old transported by a specialized paediatric retrieval team to PICU. We compared IV rates before (2005-2008) and after introduction of HFNC therapy (2009-2012).
RESULTS: A total of 793 infants were transported. The mean transport duration was 1.4 h (range 0.25-8), with a mean distance of 205 km (2-2,856). Before introduction of HFNC, 7 % (n = 23) were retrieved on non-invasive ventilation (NIV) and 49 % (n = 163) on IV. After introduction of HFNC, 33 % (n = 150) were retrieved on HFNC, 2 % (n = 10) on NIV, whereas IV decreased to 35 % (n = 162, p < 0.001). No patients retrieved on HFNC required intubation during retrieval, or developed pneumothorax or cardiac arrest. Using HFNC was associated with a significant reduction in IV initiated by the retrieval team (multivariate OR 0.51; 95 % CI 0.27-0.95; p = 0.032).
CONCLUSIONS: We report on a major change of practice in transport of critically ill children in our retrieval system. HFNC therapy was increasingly used and was not inferior to low-flow oxygen or NIV. Randomized trials are needed to assess whether HFNC can reduce the need for IV in interhospital transport of critically ill children.
This paper is an excellent review article citing the cogent relevant evidence for optimal preoxygenation prior to RSI in the critically ill patient. The evidence has been interpreted with pertinent recommendations by two of the world’s heavy hitters in emergency medicine – Scott Weingart and Rich Levitan. If you can get a full text copy of the paper, laminate Figure 3 (‘Sequence of Preoxygenation and Prevention of Desaturation‘) and stick it to the wall in your resus bay!
The points covered include:
- Why preoxygenate? Preoxygenation extends the duration of safe apnoea and should be considered mandatory, even in the crashing patient.
- Standard non-rebreather facemasks set to the highest flow rate of oxygen possible should be used.
- Allow 8 vital capacity breaths for co-operative patients or 3 minutes for everyone else.
- Increasing mean airway pressure by CPAP/NIV or PEEP valves improves preoxygenation. However caution should be used in hypovolaemic shocked patients (decreased venous return) and should be reserved for patients who cannot preoxygenate >93-95% with high FiO2.
- 20-degree head up or reverse Trendelenburg (in suspected trauma) improves pre oxygenation.
- Apnoeic diffusion oxygenation can extend safe duration of apnoea after the RSI. Set nasal cannulae at 15L/min and leave on during intubation attempts. Ensure upper airway patency (ear to sternal notch and jaw thrust).
- Active ventilation during onset of muscle relaxation should be assessed on a case by case basis and reserved for patients at high risk of desaturation (6-8 breaths per minute slowly, TV 6-7ml/kg).
- If there is a high risk of desaturation rocuronium (1.2 mg/kg) may provide a longer duration of safe apnoea than suxamethonium with similar onset time.
Preoxygenation and Prevention of Desaturation During Emergency Airway Management
Ann Emerg Med. 2011 Nov 1. [Epub ahead of print]
Patients requiring emergency airway management are at great risk of hypoxemic hypoxia because of primary lung pathology, high metabolic demands, anemia, insufficient respiratory drive, and inability to protect their airway against aspiration. Tracheal intubation is often required before the complete information needed to assess the risk of periprocedural hypoxia is acquired, such as an arterial blood gas level, hemoglobin value, or even a chest radiograph. This article reviews preoxygenation and peri-intubation oxygenation techniques to minimize the risk of critical hypoxia and introduces a risk-stratification approach to emergency tracheal intubation. Techniques reviewed include positioning, preoxygenation and denitrogenation, positive end expiratory pressure devices, and passive apneic oxygenation.
Patients with acute exacerbations of asthma randomised to receive high concentration oxygen therapy showed a greater rise in CO2 than those who received titrated oxygen to keep SpO2 > 93%.
This study has a few weaknesses but raises an interesting challenge to the dogma of high flow oxygen (and oxygen driven nebulisers) for all acute asthma exacerbations.
The suggested main mechanism for the elevation in CO2 is worsening ventilation/perfusion mismatching as a result of the release of hypoxic pulmonary vasoconstriction and a consequent increase in physiological dead space. The authors remind us that this has been demonstrated in other studies on asthma and acute COPD exacerbations. The authors infer that high concentration oxygen therapy may therefore potentially increase the PaCO2 across a range of respiratory conditions with abnormal gas exchange due to ventilation/perfusion mismatching
Some of the weaknesses include lack of blinding, recruiting fewer patients than planned, and changing their primary outcome variable after commencing the study (which the authors are honest about) from absolute CO2 to increase in CO2 (since it was apparent on preliminary analysis of the first few patients that presenting CO2 was the primary determinant of subsequent CO2). Furthermore, the CO2 was measured from a transcutaneous device as opposed to the true ‘gold standard’ of arterial blood gas analysis, although good reasons are given for this.
Despite some of these drawbacks this study provides us with a further reminder that oxygen is a drug with some unwanted effects and therefore its dose needs to be individualised for the patient.
Background The effect on Paco(2) of high concentration oxygen therapy when administered to patients with severe exacerbations of asthma is uncertain.
Methods 106 patients with severe exacerbations of asthma presenting to the Emergency Department were randomised to high concentration oxygen (8 l/min via medium concentration mask) or titrated oxygen (to achieve oxygen saturations between 93% and 95%) for 60 min. Patients with chronic obstructive pulmonary disease or disorders associated with hypercapnic respiratory failure were excluded. The transcutaneous partial pressure of carbon dioxide (Ptco(2)) was measured at 0, 20, 40 and 60 min. The primary outcome variable was the proportion of patients with a rise in Ptco(2) ≥4 mm Hg at 60 min.
Results The proportion of patients with a rise in Ptco(2) ≥4 mm Hg at 60 min was significantly higher in the high concentration oxygen group, 22/50 (44%) vs 10/53 (19%), RR 2.3 (95% CI 1.2 to 4.4, p<0.006). The high concentration group had a higher proportion of patients with a rise in Ptco(2) ≥8 mm Hg, 11/50 (22%) vs 3/53 (6%), RR 3.9 (95% CI 1.2 to 13.1, p=0.016). All 10 patients with a final Ptco(2) ≥45 mm Hg received high concentration oxygen therapy, and in five there was an increase in Ptco(2) ≥10 mm Hg.
Conclusion High concentration oxygen therapy causes a clinically significant increase in Ptco(2) in patients presenting with severe exacerbations of asthma. A titrated oxygen regime is recommended in the treatment of severe asthma, in which oxygen is administered only to patients with hypoxaemia, in a dose that relieves hypoxaemia without causing hyperoxaemia.
Randomised controlled trial of high concentration versus titrated oxygen therapy in severe exacerbations of asthma
Thorax. 2011 Nov;66(11):937-41
Suxamethonium increases muscle oxygen consumption as a result of skeletal muscle fasciculation. In a comparison between sux and rocuronium in rapid sequence intubation, this resulted in faster desaturation in the sux group. A further study demonstrates a similar finding in obese patients.
BACKGROUND: Rapid sequence induction may be associated with hypoxemia. The purpose of this study was to investigate the possible difference in desaturation during rapid sequence induction in overweight patients using either succinylcholine or rocuronium.
METHODS: Sixty patients with a body mass index (BMI) between 25 and 30 kg/m², American Society of Anesthesiologists class I or II, undergoing general anesthesia were randomly divided into a succinylcholine group and a rocuronium group. After a 3-min preoxygenation, patients received rapid sequence induction of general anesthesia with midazolum-fentanyl-propofol and succinylcholine (1.5 mg/kg) or rocuronium (0.9 mg/kg). Ventilation was not initiated until oxygen saturation declined to 92%. We measured the times when oxygen saturation reached 98%, 96%, 94% and 92%. Safe Apnea Time was defined as the time from administration of neuromuscular blocking drugs to oxygen saturation fell to 92%. The recovery period was defined as the time from initiation of ventilation until oxygen saturation was 97%. Arterial blood gases were taken at baseline, after preoxygenation and at 92% oxygen saturation.
RESULTS: The mean Safe Apnea Time (95% CI) was 283 (257-309) s in succinylcholine vs. 329 (303-356) s in rocuronium (P=0.01). The mean recovery period (95% CI) was 43 (39-48) s in succinylcholine vs. 36 (33-38) s in rocuronium (P=0.002). Blood gas analysis showed no difference between the two groups.
CONCLUSIONS: Succinylcholine was associated with a significantly more rapid desaturation and longer recovery of oxygen saturation than rocuronium during rapid sequence induction in overweight patients.
Desaturation following rapid sequence induction using succinylcholine vs. rocuronium in overweight patients
Acta Anaesthesiol Scand. 2011 Feb;55(2):203-8
A Cochrane review examined the evidence from randomised controlled trials to establish whether routine use of inhaled oxygen in acute myocardial infarction (AMI) improves patient-centred outcomes, the primary outcomes being death, pain and complications.
Three trials involving 387 patients were included and 14 deaths occurred. The pooled relative risk (RR) of death was 2.88 (95% CI 0.88 to 9.39) in an intention-to-treat analysis and 3.03 (95% CI 0.93 to 9.83) in patients with confirmed AMI. While suggestive of harm, the small number of deaths recorded meant that this could be a chance occurrence. Pain was measured by analgesic use. The pooled RR for the use of analgesics was 0.97 (95% CI 0.78 to 1.20).
There is therefore no conclusive evidence from randomised controlled trials to support the routine use of inhaled oxygen in patients with acute AMI. A definitive randomised controlled trial is required.
Oxygen therapy for acute myocardial infarction