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Hypoxemia whether critical or not is a complication associated with airway management. The abruptness with which the hypoxic events can occur during airway management in anticipated as well as unanticipated difficult airways provide very little time to the airway managers to avoid the whirlpool of complications that can ensue if hypoxia persists. An understanding of the etiology and mechanisms of hypoxemia and the techniques that can ensure oxygenation for a prolonged time provide a safe window to think and execute the airway management plans. Paraoxygenation is one such technique that ensures an uninterrupted oxygen supply to the patient after the onset of apnoea and prolongs the safe apnoea time significantly.
Department of Anaesthesiology and Critical Care, Pt. B.D. Sharma Post Graduate Institute of Medical Sciences, Rohtak, India
Manisha Manohar
Department of Anaesthesiology and Critical Care, Pt. B.D. Sharma Post Graduate Institute of Medical Sciences, Rohtak, India
*Address all correspondence to: ssinghal12@gmail.com
1. Introduction
Perioperative hypoxia occurs due to variety of causes. An anesthesiologist has to diagnose as well as treat the hypoxic events in a very short frame of time before the development of critical hypoxemia. An understanding of the causes and the pathophysiology of types of hypoxia is a prerequisite for successful management of hypoxic episodes. The technique of Paraoxygenation, also known as apneic oxygenation has found use in anaesthesia as well as critical care. This technique can be easily applied in patient population at risk of hypoxia with easily available equipments like nasal prongs, end bronchial catheters, RAE tube inside the operating theatres. Although associated with various complications, Paraoxygenation prolongs the duration of apnea without desaturation and buys time for the airway management before the development of critical hypoxemia.
1.1 Literature search
PubMed, Googlescholar, manual searches were used to find the relevant articles. The following key words were used for the search: apnoeicoxygenation, paraoxygenation, difficult intubation, hypoxia, hypoxemia, aventilatory mass flow.
1.2 Aim
This chapter focuses on understanding the pathophysiology of hypoxia and the role of paraoxygenation in various aspects of anaesthesiology and critical care.
Although used synonymously quite often, the term hypoxia and hypoxemia are different and should be used in appropriate clinical scenarios. Hypoxemia is the arterial PO2 below what is expected normal for a patient’s age while hypoxia is decreased level of tissue oxygenation. Hypoxia and Hypoxemia do not always coexist e.g., Hypoxia in cyanide poisoning is due to the defective utilisation of oxygen despite having normal oxygen levels in the blood.
2.2 Classification of hypoxia
1. Hypoxic hypoxia (Hypoxemia): is defined as arterial Pao2 less than 60 mmHg or SaO2 < 90%. Hypoxemia is one of the most feared and common complication related to tracheal intubation that can occur suddenly in the perioperative period. Hypoxemic episodes can occur during induction, maintenance, extubation and post extubation period (Figures 1 and 2).
Figure 1.
Classification of hypoxia.
Figure 2.
Common causes of perioperative hypoxemia.
2.2.1 Causes of hypoxemia
Hypoxemia due to the patient factors: Airway obstruction in unconscious patient is mostly due to tongue falling back against posterior pharynx and is commonly seen in patients with history of obstructive sleep apnea. Secretions/blood in the airway, laryngospasm, bronchospasm, glottic edema due to airway instrumentation, aspiration of vomitus, retained throat pack, external pressure on the trachea due to a neck hematoma can lead to critical hypoxemia.
Hypoxemia due to the equipment factors: Delivery and monitoring of the anaesthetic gases to the patient is done through a series of equipment. Any fault with the functioning of the equipment e.g.: pipeline, oxygen cylinder, anaesthesia machine, anaesthesia circuit, pulse oximetry can lead to the development of hypoxemia
2.3 Clinical effects of hypoxemia
The cardiovascular response to hypoxemia is a product of neural, humoral and direct effects. The neural reflex which is excitatory is mediated by aortic, carotid chemoreceptors, baroreceptors and central cerebral stimulation while the humoral reflex which is vasoconstrictive is mediated by release of catecholamines and renin angiotensin release. The direct local vascular effect of hypoxia is seen late and is manifested as inhibitory and vasodilatory effect. Mild arterial hypoxemia causes generalised activation of the sympathetic nervous system and release of catecholamines leading to an increase in heart rate, stroke volume and myocardial contractility. With the onset of moderate hypoxemia local vasodilation begins to predominate and systemic vascular resistance and blood pressure begin to decrease, however heart rate increases due to the hypotension induced stimulation of baroreceptors. With severe hypoxemia the local depressant effect dominates and blood pressure falls rapidly, pulse slows down, shock develops and heart either fibrillates or becomes asystolic [1] (Figure 3).
V/Q mismatch/Q mismatch is the most common underlying mechanism for hypoxemia. Ventilation and perfusion should match each other in all lung regions for optimal gas exchange. If ventilation and perfusion are not matched gas exchange is affected. Low V/Q will impair oxygenation since ventilation is insufficient to fully oxygenate the blood. The degree of impairment will depend on the degree of V/Q mismatch. Alveolar arterial oxygen difference is increased with impairment of v/q ratio. Hypoxemia seen in chronic obstructive pulmonary disease, emphysema, pulmonaryembolism, asthma is mostly due to underlying V/Q mismatch
Right to left shunt: when the blood passes through the lungs without coming in contact with the ventilated alveoli neither oxygen nor the carbon dioxide is released from the blood. This leads to a decrease in Pao2 and an increase in Paco2 and the condition is called SHUNT. Hypoxemia seen in pulmonary carbon dioxide is largely due to the right to left shunting of the blood
Diffusion impairment: impaired diffusion across the alveolar capillary membrane either due to fibrosis or vascular abnormality leads to slow diffusion of gases across the membrane. Hypoxemia seen in pulmonary fibrosis or in pulmonary edema is due to undergoing diffusion impairment
Hypoventilation: Paco2 more than 45 mmHg is the hallmark of hypoventilation. Adequate ventilation is required both for oxygenation as well as removal of carbon dioxide. Hypoventilation leads to a low PAO2 which subsequently leads to low Pao2.One of the characteristic features of hypoxemia cause due to hypoventilation is that it is corrected by administration of oxygen even if hypoventilation and hypercapnia persists.
2. Anaemic hypoxia: Anaemic hypoxia is characterised by decreased oxygen carrying capacity of the blood either due to low haemoglobin or due to presence of abnormal haemoglobin (carboxyhaemoglobin, methaemoglobin). A reduction in the haemoglobin concentration of the blood is accompanied by a corresponding decline in the oxygen carrying capacity of the blood. Although Pao2 is normal in anaemic hypoxia, the absolute quantity of the oxygen transported per unit volume of the blood is diminished. As the anaemic blood passes through the capillaries the usual quantity of oxygen is removed from it and Pao2 and saturation in the venous blood decline to a greater extent than normal. Presence of carbon monoxide in the blood leads to the formation of carboxyhaemoglobin there by reducing the amount of oxyhaemoglobin. The arterial oxygen decreases in proportion to the increase in carboxyhaemoglobin reflecting the ability of Carbon monoxide to block oxygen binding to haemoglobin.
3. Ischemic or stagnant hypoxia or Hypokinetic hypoxia: Decreased cardiac output or sluggish blood flow either due to heart failure, shock, or haemorrhage leads to stagnant hypoxia. The blood remains in the tissues for a greater period of time leading to increased extraction of oxygen. The Pao2 is usually normal but the venous and the tissue po2 values are reduced as a consequence of reduced tissue perfusion and greater tissue extraction.
4. Histotoxic hypoxia: is due to the inability of the tissue to utilise oxygen despite adequate availability of oxygen in the blood. Cyanide induced inhibition of cytochrome oxidase halts the process of oxidative metabolism in mitochondria leading to an increased uptake of pyruvate by mitochondria resulting in excess production of lacticacid.
The process of intubation inherently makes the patient prone to hypoxemia due to the reduced functional residual capacity (FRC) insupine position, hypoventilationdue to anaesthetic agents and deliberately induced apnoeawith musclerelaxants. Hypoxemia can develop with startling abruptness during the perioperative period without giving much time for the patient rescue. Oxygenating a patient prior to the induction of anaesthesia is called Preoxygenation. Adequate preoxygenation prolongs the duration of apnoea without desaturation (DAWD) by building up the oxygen reserve in the functional residual capacity which acts like a reservoir from where the oxygen can be extracted and delivered to blood thereby avoiding the desaturation to critical levels. Preoxygenation is currently the standard of care in all patients undergoing general anaesthesia. However, conventional preoxygenation techniques may be inadequate in providing a safe apnoeic period (time from apnoea onset to spo2 90%) in all patient’s population especially the one with high oxygen requirements (paediatric, obstetric, obese) or those with difficult airways. In order to supplement preoxygenation and to prolong the safe apnoea time further Para oxygenation or apnoeic oxygenation can be used as a useful adjunct to preoxygenation.
Para oxygenation is the technique of providing uninterrupted oxygen supply to the patient after the onset of apnoea in order to prolong the safe apnoea time especially in patients with difficult airways to provide adequate time to the anaesthesiologist for uninterrupted execution of the attempts to secure the airway. Paraoxygenation is also known as apnoeic oxygenation.
3.1 Physiologic basis of para oxygenation:
Aventilatory mass flow [3]/diffusion respiratio [4]/apnoeic diffusion of oxygen [5]: The oxygen consumption of a health adult is 250 ml/min while the carbon dioxide production is 200 ml/min. Inapnoeic patients the extraction of oxygen from the alveoli continues at the rate of 250 ml/min while carbon dioxide delivery to the alveoli is 21 ml/min thereby causing the alveolar pressure to become sub atmospheric leading to a generation of pressure gradient which enables the movement of additional administered oxygen provided the airway is patent. Preoxygenation facilitates the process of apnoeic oxygenation by denitrogenating the alveoli. In the absence of adequate preoxygenation, the persistence of nitrogen in the lungs along with the accumulating carbon dioxide will diminish the pressure gradient available for the mass flow of oxygen into the alveoli thereby hastening the onset of hypoxemia. The persistent delivery of 100 percent oxygen prevents the renitrogenation of the alveoli during the apnoea. The sub atmospheric pressure also promotes carbon dioxide transfer from blood to the alveoli. The degree of oxygen extraction from the alveoli exceeds the degree of carbon dioxide return to the alveoli since carbon dioxide is buffered in the body but with time the alveolar accumulation of carbon dioxide reaches a critical level beyond which the pressure gradient is reduced thereby reducing the aventilatory mass flow of oxygen.
3.2 Prerequisite for para oxygenation
Patent upper airway: A patent airway is an absolute prerequisite for successful paraoxygenation. This allows the oxygen to be delivered to the hypopharynx and be entrained into the trachea Patient should be positioned to maximise upper airway patency using ear to sternal notch positioning. During the apnoeic period, upper airway obstruction should be prevented by using the airway manoeuvres like head tilt, chin lift, jaw thrust or by using the oropharyngeal airway/nasopharyngeal airway.
Adequate preoxygenation: The benefit of apnoeic diffusion oxygenation is dependent on achieving maximal preoxygenation before apnoea.
Placement of a device to deliver oxygen: Para oxygenation can be achieved by using any device that administers oxygen into the respiratory tract including, nasal cannula, nasopharyngeal catheter, rigid bronchoscope, catheter placed in trachea, endobronchial catheters, front of neck catheter, channels located in direct and video laryngoscopes.
Oxygen source: Auxiliary port in the anaesthesia machine or an oxygen cylinder in case of intubations done in out of operating room settings can be used for the oxygen denitrogenating supply.
3.3 Techniques
Various techniques for administration of paraoxygenation have been described. Oxygen can be delivered at different locations in the upper and lower airway during apnoea: Devices can be placed at following sites: Nares, nasopharynx, oropharynx, oral cavity, trachea, Primarybronchi (Figure 4).
NODESAT: Nasal oxygenation during efforts securing a tube
Direct pharyngeal insufflation
THRIVE: Trans nasal humidified rapid insufflation ventilatory exchange
Other techniques: Apnoeic oxygenation with nasopharyngeal catheters, intratracheal catheters, Bilateral or unilateral endobronchial catheters, buccal oxygen delivery with modified RAE tube, channels located in direct and videolaryngoscopes,
Figure 4.
Techniques of paraoxygenation.
3.3.1 NODESAT: Nasal oxygenation during efforts securing a tube.
NODESAT was first described by Levitan [6], as a method to extend the safe apnea time during rapid sequence anaesthesia in the emergency department. Inappropriately sized nasal cannula is used to administer the standard unwarmed and dry oxygen at the rate of 15 litres/min while attempts for intubating the trachea by conventional laryngoscopy or video laryngoscopy or flexible fibreoptic bronchoscope are being made. Unlike other techniques, this technique does not require any special equipment and can be easily done in the operating theatre with nasal prongs and auxiliary oxygen port. However, they can impair the face mask seal during bag mask ventilation. The administration of dry, cold oxygen at high flows can lead to mucosal injury and mucociliary dysfunction (Figure 5).
Figure 5.
(a) NODESAT during preoxygenation; (b) NODESAT during intubation.
3.3.2 Direct pharyngeal oxygen insufflation:
Para oxygenation can be achieved by using any device that administers oxygen to the pharynx (Figure 6).
Figure 6.
Naso-Flo (Medis medical CO Ltd).
Nasopharyngeal catheter: A nasopharyngeal catheter advanced into the nasopharynx can be used to deliver oxygen during apnoea. The distance from the nares to the tragus of the ear is measured as taken as depth of the catheter insertion. Achar et al [7] found nasopharyngeal catheters to be more effective than nasal prongs in delivering oxygen during apnoea. The Naso-Flo®(Medis medical CO Ltd) is soft silicone nasopharyngeal airway device that allows for direct oxygen delivery into the pharynx, while humidification vents positioned towards the distal tip facilitate heat and moisture transfer.
Buccal oxygen delivery: An inexpensive, readily available method of apneic oxygenation was described by Andrew Heard et al. [8]. A 3.5 mm south facing Ring Adair and Elwin (RAE) tube was cut above the murphy’s eye. Standard oxygen tubing was connected from the cut end to the auxiliary oxygen outlet on the anaesthesia machine. The blunt proximal end was placed in the buccal space with the tube angle opposed to the left side of the mouth. The tube was fixed to the external cheek to maintained the position. This method of buccal oxygen delivery provided a viable alternative to the nasal route (Figure 7).
Figure 7.
Buccal oxygen delivery device. As described by Andrew Heard et al. [8] (a) RAE tube (b) RAE tube cut above murphy’s eye (c) Standard oxygen tubing connected from the cut end to the oxygen source. The Blunt proximal end (connector detached) is placed in the buccal space with the tube angle apposed to the side of the mouth.
3.3.3 THRIVE: Trans nasal humidified rapid insufflation ventilatory exchange:
Patel and Nourae, in 2013, introduced the delivery of warm and humidified high flow nasal oxygen using OPTIFLOW™ system (Fischer and Paykellhealth care LTD Auckland, newzealand). Not only the apnea time were prolonged but the rate of rise of carbondixoide was found to be one third of what was expected [9]. This suggested a physiology supplementing classic apneic oxygenation. The clearance of carbondioxide can be explained by the interaction of cardiogenic oscillations and turbulent primary supraglottic vortex [10].
Primary supraglottic vortex: High-flow nasal oxygen enters the nose at 70-90 L/min, loops around the soft palate, and exits through the mouth. This creates a highly turbulent ‘primary supraglottic vortex” which has the following effects:
It replenishes the pharynx with oxygen and prevents entrainment of room air.
It effectively bypasses the upper airways which ordinarily account for approximately 50% of the resistance of the entire respiratory system to airflow [11]. By effectively breathing ‘directly from the glottis’, work of breathing is reduced by approximately 50% [12].
It also generates a positive airway pressure which in turn reduces upper airway collapsibility and distal airway atelectasis [13].
The primary vortex does not, however, extend deep into the trachea and cannot by itself account for the observed level of gaseous exchange.
Cardiogenic oscillations: The compression and expansion of the small airways is brought about by the blood leaving and entering the thoracic cavity with each heartbeat [14]. The typical amplitude of a ‘cardiogenic breath’ is around 7-15 ml per heartbeat [10]. Ordinarily, cardiogenic oscillations result in small-volume mass movement of gases within the trachea.
During THRIVE, this small volume is flushed into the supraglottic vortex during cardiogenic ‘expiration’, is removed, and replaced by 100% oxygen. Cardiogenic ‘inspiration’ moves this oxygen towards the distal airways and also entrains turbulence, which enhances intratracheal mixing. e.g.
Volume of a ‘cardiogenic breath’ to be 12 ml per heartbeat,
Heart rate:70 beats per minute.
840 ml of gas which contains CO2 is removed, and is replaced with 100% oxygen. This is not enough to achieve full CO2 clearance. That is why carbondioxide still accumulates during THRIVE, but at a slower rate than with classical apnoeic oxygenation.
THRIVE is administered through a standard commercially available high flow oxygen delivery system e.g. Optiflow (Fischer and Paykel health care), Airvo, Airvo2 (Fischer and Paykel health care). It consists of a flowmeter, humidifier, heating system, heated non condensing circuit, and an oxygen connector for gas supply. Some of the ventilators. e.g Bellavista ventilators, IMT medical, Switzerland available in the market have an inbuilt system that provides the high flow oxygen therapy as well as invasive ventilation modes (Figures 8–10).
Figure 8.
Nasal prongs for high flow nasal oxygenation.
Figure 9.
Equipment for high flow nasal oxygenation (Fischer & Paykel health care) AIRVO2.
Endobronchial catheters: Endobronchial catheters are placed in the main stem bronchi. The catheter placedeither in right or left main stem bronchi or in both the bronchi can be used for apnoeic oxygenation. Babinski et al. used two polyethylene catheters (2.5 mm OD) with angulation of 20 degree for the right side and 30 degree for the left were placed in the bronchi under fibreoptic guidance for endobronchial apnoeic oxygenation. Humidified oxygen was delivered at 0.6 to0.7 L/min. The authors found the adequate oxygenation was maintained till 30 minutes with a mean co2 rise at rate 0.6mmhg/min [15] (Figure 11).
Figure 11.
ShileyEndobronchial suction catheters( COVIDIEN, MEDTRONIC) with color coded connectors.
Dual use laryngoscopes: Dual use laryngoscopes are specifically designed to allow for the insufflation of oxygen during laryngoscopy. The miller port American profile conventional blade (Sun Med LLC) is commercially available laryngoscope that has an integrated tube that permits the delivery of oxygen and other gas mixtures during laryngoscopy (Figure 12).
Figure 12.
Miller port American profile blade (Sun MED LLC).
Tracheal tube introducer: An Eschmann tracheal tube introducer was used by Millar et al. for administering apnoeic oxygenation. Two holes were drilled at both the end of the Eschmann gum elastic bougie (SIMSportex, Hythe Kent, UK) and apnoeic oxygenation was tested on an anaesthetic simulator model. The modified bougie was positioned 2–3 cm beyond the vocal cords with 8 l/min of oxygen flowing through it. The time taken for the oxygen saturation to fall was significantly prolonged when modified gum elastic bougie was used for apnoeic oxygenation [16]. COOKS airway exchange catheter (AEC) has a blunt tip which is a traumatic to internal structures. The lumen and distal side ports are designed to deliver oxygen. The removable Rapi-Fit Adapter permits oxygen delivery during an airway exchange procedure. Although cook’s airway is intended for tracheal tube exchange, it can also be used to paraoxygenate the airways (Figure 13a–c).
Figure 13.
Cooks airway exchange catheter (cook medical). (a) Cook’s Airway exchange catheter; (b) Distal end of Cook’s AEC Designed to deliver oxygen; and (c) distal lumen of the cooks airway exchange catheter.
Intratracheal catheters: A retrospective study was conducted by Rudlof and Hohenhorst [17] analysing 47 patients who underwent apnoeic oxygenation at 0.5 l/min using a catheter inserted into the trachea. The median Spo2 at the end of the apnoeic period was found to be 100 percent. The mean apnoea time was found to be 24.7 min with no adverse effects.
3.4 Clinical applications of paraoxygenation/apnoeic oxygenation
Para oxygenation through nasal or nasopharyngeal catheter prolongs the safeapnoea time and also decreases the degree of desaturation during induction of anaesthesia and endotracheal intubation in adult ASA 1–2 patients undergoing anaesthesia for elective surgery [18]. Apnoeic oxygenation has been shown to be associated with increased per intubation oxygen saturation, decreased rate of hypoxemia and first pass intubation success [19]. During one lung ventilation, apneic oxygenation of the deflated lung through a suction catheter can reduces the likelihood of hypoxemia and need for resumption of double lung ventilation [20, 21].
3.4.2 Difficult airway management
Awake intubation: Awake fibreoptic intubation is indicated in cases with anticipated difficult airways. Even though the procedure can be done with local anaesthesia, sedation is often required to improve the patient tolerance and cooperation. Sedative induced apnea, can lead to hypoventilation, and upper airway obstruction during awake fibreoptic intubation in difficult airway resulting in critical oxygen desaturation. Paraoxyygention can be used as an effective tool to ensure adequate oxygenation while the airway is being navigated by the scope. Schroeder et alevaluated a special oropharyngeal oxygenation device (OOD), allowing a continuous laryngeal oxygen insufflation during and parallel with bronchoscopy [22]. Apnoeic laryngeal oxygenation in a preoxygenated manikin with both oxygen insufflation via the OOD and the bronchoscope kept oxygen saturation in the test lung at 95% over 20 min. Oxygen insufflation via OOD or bronchoscope was found to be more effective than nasal oxygen insufflation.
Physiologically difficult airway: Peri intubation hypoxia is more common in physiologically difficult airways e.g., paediatric, obstetric and obese patient population. Obesity leads to decreased in function residual capacity, increases atelectasis and shunting in the dependent region of the lung. Resting metabolic rate, work of breathing and minute oxygen demand however are increased. This combination of the factors makes the obese patient prone to hypoxemia during the induction of the induction of anaesthesia. Oxygen insufflation at 15 l/min through nasopharyngeal airway and standard nasal cannula can significantly increase the safe apnea time during induction of anaesthesia in obese patients [23].
Although apnoeic oxygenation is extensively studied in the adult population, very few studies have been conducted on the paediatric population, there is evidence that apnoeic oxygenation is a simple easy to apply intervention that can decrease hypoxemia during paediatric endotracheal intubation. Not only it increases the time until desaturation but also reduced the overall incidence of hypoxia during laryngoscopy in paediatric population [24].
Difficult airway society and obstetric anaesthetist association guidelines issued in 2015 for the management of difficult tracheal in obstetric patients emphasised on the role of apnoeic oxygenation via nasal cannula, nasopharyngeal catheter or mask [25]. AIDA Arecommends the universal use of 15 L/min oxygen insufflation via nasal cannula for obstetric general anaesthesia they recommend the use of nasal prongs to insufflate oxygen during the apnoeic period in patients with difficult airway [26].
Tubeless anaesthesia: Managing the shared airway in the glottic and subglottic pathologies presents a challenge to the anaesthesiologist as well as the surgeon. Tubeless anaesthesia with apnoeic oxygenation allows a good access and visualisation of the glottis without oxygen desaturation. Apneic oxygenation enables tubeless anaesthesia for extended period of time. Vocalcordbiopsy, balloon dilation of subglottic stenosis has been done using this technique. Apnoeic oxygenation with nasal cannula and THRIVE has been found to be safe and feasible for the endoscopic management of subglottic stenosis in short glottic surgical procedures [27].
Bronchoscopy: Apnoeic oxygenation can be done in patient undergoing rigid bronchoscopy with passive oxygen insufflation through the side port of the bronchoscope or a tracheal catheter [28, 29]. High flow administration of oxygen via side sport of bronchoscope risk barotrauma if the path for gas egress becomes obstructed even for brief period.
Critical care: Recent guidelines for the management of airway in critical care patients have recommended that nasal oxygen should be applied throughout the airway management. If the standard nasal cannula is used it should be applied during preoxygenation with a flow of 5 L/min while awake and increased to 15 L/min when the patient loses conscious. A high flow nasal cannula can also be used if already in place [30].
Diagnosis of brain death: Apnoea test done in diagnosis of brain death involves the temporary suspension of mechanical ventilation. During this time oxygen is insufflate through the tracheal tube via a catheter to prevent hypoxemia.
3.4.3 Emergency intubation
Patients requiring emergency airway management are at a greater risk of hypoxemia due to underlying lung pathology, high metabolic requirements, high respiratory drive or inability to protect the airway. Rapid sequence intubation in critically ill patients is associated with episodes of hypoxia. Apneic oxygenation has been shown to reduce the incidence of desaturation in patient undergoing rapid sequence intubation in emergency [31]. A systematic review to investigate the effect of apnoeic oxygenation on incidence of clinically significant hypoxemia during emergency endotracheal intubation concluded that paraoxygentaion reduces the incidence of hypoxemia in emergency endotracheal intubation and supported the inclusion of apnoeic oxygenation in everyday practice (Figure 15) [32].
Figure 15.
Complications of paraoxygenation.
3.5 Complications of paraoxygenation
Hypercarbia: During Para oxygenation carbon dioxide cannot be vented out. Co2 levels continue to rise leading to an increase in PH and development of respiratory acidosis [15, 33, 34]. Paco2 levels increase with a speed of 1.1–3.4 mmHg. Mean CO2 levels can reach as high as 160 mmHg [33]. However, with THRIVE the rate of carbon dioxide accumulation is less than that seen in classic apnoeicoxygenation [9]. The effects of hypercarbia are versatile ranging from tachycardia, increased cardiac output, increased cerebral blood flow. Prolonged apnoeic oxygenation should be avoided in patients with contraindication to hypercapnia e.g., cardiac arrythmia, hemodynamicinstability, raised intracranial pressure. Para oxygenation interrupts the early detection of rise of carbon dioxide. Since the end-tidal carbon dioxide monitoring cannot be done during apnea, transcutaneous carbon dioxide measurements may help in minimizing the risk and optimal utilization of Para oxygenation [35].
Acidosis: Gradual increase in the carbon dioxide levels leads to respiratory acidosis however, during testing for brain death in addition to respiratory acidosis, a mild metabolic acidosis of unknown cause also develops during apnoeic oxygenation [36].
Accidental awareness: Apnoeicoxygenation does not deliver volatile agents to the lung. Hence adequate anaesthesia during the airway management should be ensured to avoid accidental awareness [37]. Total intravenous anaesthesia {TIVA} can be used during paraoxygenation to avoid the accidental awareness during this procedure. Tubeless anaesthesia with apnoeic oxygenation for the short glottic procedures also requires the administration of intravenous anaesthesia to ensure adequate depth during the procedure.
NODESAT, direct pharyngeal insufflation delivers dry and cold oxygen to the respiratory tree. Administration of dry and cold gases can induce bronchoconstriction in patients with asthma [38]. Airway resistance is increased to reduce the airflow in the upper and trachea to protect the lungs from the challenge of dry and cold gases [39, 40]. Dry gases cause excessive water loss by the nasal mucosa [41]. This may reduce the nasal mucociliary clearance rate due to the changes in the rheological properties or adhesiveness of the nasal mucus and slowing of ciliary pulses [42]. High flow dry gases result in inspissated secretions that can cause life threatening airway obstruction [43].
Barotrauma: Apnoeic oxygenation is a widely accepted method for apnea testing in brain death. During the apnea testing, ventilator assistance is discontinued and oxygen is delivered into the trachea via an oxygen catheter placed at the level of carina while waiting for the spontaneous respiratory movements. Apnea testing related pneumothorax was first reported by Bar joseph et al. [44]. In order to avoid pneumothorax authors proposed that the oxygen flow rates should not exceed 6 l/min, oxygen catheter diameter should be narrower than the diameter of the endotracheal tube and the tip of the oxygen catheter should not exceed the tip of the endotracheal tube to avoid wedge position in the trachea. A case of pneumothorax and pneumomediatinum was reported by saposnik et al. [45] during apnea testing. Vivien et al. [46] proposed that a 12 french catheter should be advanced only 5 cm into the endotracheal tube and oxygen flow rates should not exceed 8 l/min to avoid pneumothorax during apnea testing. Barotraumacan occur if there is no clear route for egress of gases during apnoeicoxygenation.AT- piece or a self-inflating bag valve system can be used as an alternative technique to conductapnoeatest. Serious air leak syndromes have been reported with the use of high flow especially in paediatric age group. HFNC is being used as a respiratory support for preterm infants. HFNC is being used as an alternative to nasal continuous positive airway pressure (CPAP) and in particular to prevent postextubation failures. A case of tension pneumocephalus in a preterm infant was reported by Iglesias et al. [47] as a complication during HFNC ventilation. Significant neurological impairment was detected and support was eventually withdrawn. Clinicians need to be aware of this rare but possible complication during HFNC therapy, as timely diagnosis and treatment can prevent neurological sequelae. Paying close attention to flow rate, nasal cannula size and insertion, regularly checking insertion depth can help to avoid these complications. Cases of pneumo-orbitus [48], epistaxis, subcutaneous emphysema, oesophageal rupture, gastric rupture [49, 50] have all been reported with use of apneic oxygenation.
Perioperative critical hypoxia is one of the most feared complication an anesthesiolgist may come across. These episodes often occur abruptly and demand prompt intervention to avoid irreversible damage. Management of these life-threatening situations requires simultaneous diagnosis and treatment of hypoxia. Differentiating between the patient factors and the machine factors leading to hypoxic event is imperative. Paraoxygenationor apneic oxygenation techniques can help to buy time, avoid panic and execute airway securing strategies by delaying the development of critical hypoxemia. Routine application of paraoxygenation techniques in everyday clinical practice and a knowledge of various equipments that can be used to administer paraoxygenation to the patient can help prevent the nightmare of critical hypoxic perioperative events (Figure 16 and Table 1).
Figure 16.
Paraoxygenation: Preparation to execution.
Technique
Device used
Advantages
Disadvantages
NODESAT
Nasal prongs
1.No special equipment required 2.Easily done in emergency and elective settings
Dry and cold oxygen delivery leading to mucosal injury
Trans nasal humidified rapid insufflation ventilatory exchange.
V/Q ratio
ventilation/perfusion ratio.
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Written By
Suresh Kumar Singhal and Manisha Manohar
Submitted: 08 February 2022Reviewed: 28 July 2022Published: 02 December 2022
Open access peer-reviewed chapter
