**2. Pathophysiology of oxygen delivery**

Oxygenation during anesthesia mostly depends on three parameters: alveolar ventilation (VA), ventilation-perfusion distribution and VO2.

#### **2.1. Oxygen reserves**

Tissue oxygenation during apnea is usually sustained at the expense of body O<sup>2</sup> reserves that are present in the lungs, plasma, and hemoglobin [2]. When the ambient air is breathing, the lung O2 reserve is calculated as: 0.21 × 3000 = 630 mL for 3000 mL functional residual capacity (FRC). After full preoxygenation, FAO<sup>2</sup> is close to 0.95 and the reserve increases as follows: 0.95 × 3000 mL = 2850 mL. These theoretical figures are the maximum values; in practice, the rate of ventilation-perfusion is lower than that of FAO<sup>2</sup> because of the heterogeneity. In a subject inhaling ambient air (PaO<sup>2</sup> = 80 mmHg) and a plasma volume of 3 liters, plasma oxygen reserve is calculated as 0.003 × 80 × 3 × 10 = 7 mL. At 500 mmHg PaO<sup>2</sup> , this plasma reserve reaches 45 mL. The hemoglobin O<sup>2</sup> reserve is calculated in the ambient air (SpO2 = 98%) for a hemoglobin concentration of 12 g/100 mL and a total blood volume of 5 L as follows: 1.34 × 0.98 × 12 × 10 × 5 = 788 mL. This value increases to 804 mL for 1 FiO<sup>2</sup> (SpO2 = 100%). In cases of anemia, hyperoxic ventilation increases the availability of O<sup>2</sup> by replicating solute O2 [3]. Considering the basic physiological O<sup>2</sup> reserves, while the ambient air is inhaled, the total O2 reserve is approximately 1450 mL and reaches approximately 3700 mL in the pure O<sup>2</sup> solution. This increase (approximately 2250 mL) is mainly due to the rice FAO<sup>2</sup> in FRC. Several factors influence O<sup>2</sup> availability: the initial rise in PaCO<sup>2</sup> (Haldane effect), FRC, FAO<sup>2</sup> , fraction of shunt, VO2 , hemoglobin concentration, and cardiac output. Replacement of nitrogen by O<sup>2</sup> in the lung reservoir during preoxygenation obeys an exponential law [2]. The change in O2 reserve over time is linear in both blood and tissue compartments.

#### **2.2. O2 consumption**

In an anesthetized patient, oxygen consumption (VO2

) drops directly to PAO<sup>2</sup>

partial oxygen pressure (PAO<sup>2</sup>

Since oxymetry detects the fall in SpO<sup>2</sup>

**2. Pathophysiology of oxygen delivery**

(VA), ventilation-perfusion distribution and VO2.

rate of ventilation-perfusion is lower than that of FAO<sup>2</sup>

(FRC). After full preoxygenation, FAO<sup>2</sup>

reaches 45 mL. The hemoglobin O<sup>2</sup>

Considering the basic physiological O<sup>2</sup>

oxygen (PaO2

24 Tracheal Intubation

decline, SpO2

**2.1. Oxygen reserves**

lung O2

This is delivered to the tissues by hemoglobin whose oxygen is then replenished, on return to the pulmonary circulation, by the diminishing store of oxygen within the lungs. Alveolar

lungs but also due to the severe negative intrathoracic pressure produced by this oxygen uptake, if the airway is occluded at the same time. However, the arterial partial pressure of

quent declines are constant and fast at around 30% per minute. At the beginning of this rapid

cause life-threatening complications. Anesthesia induction usually leads to apnea. In this case,

In some cases, adequate oxygenation cannot be achieved due to pulmonary disease, inadequate mask ventilation or difficulties in intubation. These critical situations are often predictable and

Oxygenation during anesthesia mostly depends on three parameters: alveolar ventilation

are present in the lungs, plasma, and hemoglobin [2]. When the ambient air is breathing, the

0.95 × 3000 mL = 2850 mL. These theoretical figures are the maximum values; in practice, the

ject inhaling ambient air (PaO<sup>2</sup> = 80 mmHg) and a plasma volume of 3 liters, plasma oxygen

hemoglobin concentration of 12 g/100 mL and a total blood volume of 5 L as follows: 1.34 ×

reserve is approximately 1450 mL and reaches approximately 3700 mL in the pure O<sup>2</sup>

reserve is calculated as: 0.21 × 3000 = 630 mL for 3000 mL functional residual capacity

is still around 90–95%. This bending point can be defined as "critical hypoxia."

remains above 90% as long as hemoglobin can be oxygenated again in the lungs. SpO<sup>2</sup>

to fall only when the oxygen stores in the lungs are empty and PaO<sup>2</sup>

place in helping clinical applications to detect and avoid critical situations.

tissue oxygenation is maintained by the use of oxygen reserve and continuous O<sup>2</sup>

Preservation of oxygenation during intubation is essential because lack of control of O<sup>2</sup>

can be avoided by alternative oxygenation methods by following a valid algorithm [1].

Tissue oxygenation during apnea is usually sustained at the expense of body O<sup>2</sup>

reserve is calculated as 0.003 × 80 × 3 × 10 = 7 mL. At 500 mmHg PaO<sup>2</sup>

0.98 × 12 × 10 × 5 = 788 mL. This value increases to 804 mL for 1 FiO<sup>2</sup>

of anemia, hyperoxic ventilation increases the availability of O<sup>2</sup>

) remains fairly constant at 250 mL/min.

)

begins

intake can

administration.

reserves that

, this plasma reserve

(SpO2 = 100%). In cases

[3].

solution.

by replicating solute O2

is 6–7 kPa. Their subse-

) is constantly reduced not only due to oxygen uptake by the

, while arterial hemoglobin oxygen saturation (SpO2

before any obvious clinical sign, it has an important

is close to 0.95 and the reserve increases as follows:

reserve is calculated in the ambient air (SpO2 = 98%) for a

reserves, while the ambient air is inhaled, the total O2

because of the heterogeneity. In a sub-

The VO2 value of an awake person is about 300 mL/min and falls about 15% in old aged people. After ventilation in ambient air, O<sup>2</sup> reserves allow apnea for up to 3 minutes without serious eff on O2 transport. This time can be doubled with the correct applied preoxygenation. The duration of apnea tolerated is additionally decreased if O<sup>2</sup> reserves are low due to decreased FRC, low PAO<sup>2</sup> and/or high VO<sup>2</sup> and the O2 reserves are reduced due to low FRC, PaO<sup>2</sup> and/or high VO2.

#### *2.2.1. Ventilation/perfusion incompatibility*

Preoxygenation leads to an increase in shunt and microatelectasis after induction of anesthesia [4]. The inspired high O2 fraction (FiO<sup>2</sup> ) is not the only responsible mechanism; atelectasis was also observed when FiO<sup>2</sup> was used as 0.4 [5]. The use of 0.8 FiO<sup>2</sup> does not inhibit the emergence of microatelectasis and results in a considerable shortening of the time limit before critical desaturation compared to the use of 100% oxygen [6]. Microatelectasis are reversible with alveolar engraftment (>30 cmH<sup>2</sup> O tracheal pressure for 15 seconds) and can be prevented by the addition of 10 cmH<sup>2</sup> O positive end expiratory pressure (PEEP) [7]. In morbidly obese patients and in parturients, shunt can exceed 20% and even increasing FiO<sup>2</sup> to 1 does not provide correction of the hypoxemia. Implementation of a microatelectasis prevention strategy of alveolar recruitment maneuvers and PEEP limits the extent in elderly and obese patients [8, 9].

#### **2.3. Epidemiology of arterial desaturation during anesthesia induction and intubation**

Arterial O<sup>2</sup> desaturation occurs if O<sup>2</sup> reserves are insufficient to support O<sup>2</sup> consumption during apnea. There are three responsible mechanisms: quantitative reduction in the reserve (decline in FRC, deterioration in gas exchange), VO<sup>2</sup> increase (birth, fever), and prolonged apnea.

It is especially important to mention the four high-risk situations:


After rapid sequence induction, spontaneous ventilation reinitiation does not occur rapidly after an unsuccessful intubation procedure and saturation falls below 90% in 11% of patients [10]. Administration of succinylcholine (0.56 and 1 mg/kg) after induction with propofol (2 mg/kg) and fentanyl (μg/kg) has increased desaturation risk and apnea duration compared to placebo [11]. In a pharmacodynamic study with succinylcholine (0.3–1 mg/kg), it found that the intubation conditions were excellent at doses above 0.5 mg/kg, but the delay in resumption of spontaneous breathing rose from 4.0 to 6.16 minutes after administration of 0.6 and 1 mg.kg−1, respectively [12]. Reversal of deep neuromuscular block (induced by high-dose rocuronium) with sugammadex (16 mg/kg) used for rapid sequence induction is significantly faster than spontaneous recovery of succinylcholine (6.2 ± 1.8 versus 10.9 ± 2.4 minutes) [13]. Reversal with sugammadex following rapid sequence induction with rocuronium allows earlier restoration of spontaneous respiration compared to succinylcholine (216 versus 406 seconds) [14]. Thus, the choice of the rocuronium would increase the margin of safety for a resumption of spontaneous ventilation after a rapid sequence induction.

an integral component during rapid sequence induction/intubation [22–25]. It is also important when difficulties associated with preoxygenation, ventilation, or tracheal intubation are

Guidelines developed by the Difficult Airway Society in the United Kingdom for unforeseen difficult intubation management in 2015 suggest that all patients must undergo preoxygenation prior to induction of general anesthesia [28]. Residual effects of anesthetics or inadequate reversal of muscle relaxants can complicate emergence from anesthesia. These effects may result in decreased functional activity of the pharyngeal muscles, upper airway obstruction, effective cough insufficiency, a fivefold increase in aspiration risk, and hypoxic weakness controlled by peripheral chemoreceptors [29, 30]. Hypoventilation, hypoxemia and loss of airway may follow these changes. Preoxygenation can also minimize neostigmine-induced cardiac arrhythmias [31]. Considering the potential for airway and ventilation problems, "routine" preoxygenation is recommended before reversing neuromuscular blockage and before tracheal extubation [32]. The recommended guidelines for the management of tracheal extubation in 2012 by the Difficult Airway Society in the United Kingdom state that preoxygenation must be performed before extubation due to various perioperative anatomical and physiological changes that may put gas exchange in jeopardy [33]. Preoxygenation is also recommended before any ventilation interruption, such as open tracheobronchial aspiration.

tissues is difficult, but the estimated increases are notable when assuming that the partition

The effectivity of preoxygenation is assessed by efficacy and efficiency. Efficacy indices include

efficiency of preoxygenation is assessed by the decrease in oxyhemoglobin desaturation (SpO<sup>2</sup>

terms preoxygenation and denitrogenation have been used synonymously to describe the

breathing [34].

The key to achieve maximum preoxygenation is the excretion of alveolar nitrogen (N<sup>2</sup>

**Body store Room air 100% O2** Lungs 450 3000 Blood 850 950 Dissolved in tissue fluids 50 100 Combined with myoglobin 200 200 Total 1550 4250

coefficient for gases approximates the gas-water coefficients (**Table 1**, **Figure 1**) [2, 34].

stores, the main increase occurring in the functional

and decreases FAN<sup>2</sup>

), and increase in PaO2

Pathophysiology of Apnea, Hypoxia, and Preoxygenation

http://dx.doi.org/10.5772/intechopen.76851

27

volume in various body

[35–42]. The

(**Figure 2**) [45].

)

). The

reserves are limited [26, 27].

**3. Physiological basis, efficiency, and productivity**

residual capacity. Accurate quantification of the increases in the O<sup>2</sup>

increase, decreases in alveolar nitrogen fraction (FAN<sup>2</sup>

during apnea [10, 43, 44]. Preoxygenation increases FAO<sup>2</sup>

stores (in mL) during room air and 100% O<sup>2</sup>

Preoxygenation increases the body O2

FAO<sup>2</sup>

**Table 1.** Body O2

predicted and the patient's O2

#### *2.3.1. Desaturation in pediatrics*

Desaturation attacks occur frequently in children, with 4–10% during induction and 20% during tracheal intubation [15]. Desaturation occurs faster if the child is younger [16, 17] and apnea duration in predesaturation has a linear relationship with the age of the patient. The low weight of the child increases the frequency of severe arterial desaturation. It is suggested that 95% SpO<sup>2</sup> may be the safe apnea limit during induction of pediatric anesthesia [18]. It was noted that upper respiratory tract infection increased desaturation risk during induction [15]. The number of important factors effect the time from the onset of apnea to the development of critical hypoxemia.

#### *2.3.1.1. Functional residual capacity (FRC)*

FRC is the most important oxygen storage in the body. The larger the FRC, the longer apnea times can be preceded before the critical hypoxia develops. Alveolar oxygen fraction (FAO<sup>2</sup> ) is around 13% in air breathing. For an adult with normal FRC and VO<sup>2</sup> , the oxygen content of the lungs (290 mL) will be consumed within 1 minute. This explains why you can expect a critical hypoxia after 1-minute apnea. Reduced FRC patients (lung disease, kyphoscoliosis, pregnancy, and obesity) reach critical hypoxia much faster.

#### *2.3.1.2. Preoxygenation*

Preoxygenation using a high FiO<sup>2</sup> before anesthesia induction and tracheal intubation is particularly recommended in patients at risk for apneic arterial oxyhemoglobin desaturation. The success of preoxygenation to delay the onset of desaturation has been known for many years [19–21]. Preoxygenation during anesthesia induction is highly recommended in cases of desaturation prior to airway safety with endotracheal intubation. In situations where manual ventilation is not desired, such as patients with aspiration risk, preoxygenation has become an integral component during rapid sequence induction/intubation [22–25]. It is also important when difficulties associated with preoxygenation, ventilation, or tracheal intubation are predicted and the patient's O2 reserves are limited [26, 27].

Guidelines developed by the Difficult Airway Society in the United Kingdom for unforeseen difficult intubation management in 2015 suggest that all patients must undergo preoxygenation prior to induction of general anesthesia [28]. Residual effects of anesthetics or inadequate reversal of muscle relaxants can complicate emergence from anesthesia. These effects may result in decreased functional activity of the pharyngeal muscles, upper airway obstruction, effective cough insufficiency, a fivefold increase in aspiration risk, and hypoxic weakness controlled by peripheral chemoreceptors [29, 30]. Hypoventilation, hypoxemia and loss of airway may follow these changes. Preoxygenation can also minimize neostigmine-induced cardiac arrhythmias [31]. Considering the potential for airway and ventilation problems, "routine" preoxygenation is recommended before reversing neuromuscular blockage and before tracheal extubation [32]. The recommended guidelines for the management of tracheal extubation in 2012 by the Difficult Airway Society in the United Kingdom state that preoxygenation must be performed before extubation due to various perioperative anatomical and physiological changes that may put gas exchange in jeopardy [33]. Preoxygenation is also recommended before any ventilation interruption, such as open tracheobronchial aspiration.
