First, it is essential to ensure an open and patent airway. A lack of oxygen is the most urgent threat to life. If the upper airway is obstructed, all further efforts to transport oxygen to the lungs will inevitably fail. Insufficient oxygenation of the blood will result in a critical undersupply to organs. The brain is most susceptible to permanent damage due to hypoxemia, and trauma patients are at risk for airway obstruction (Table 2.2). A patient who gives vocal responses will most probably have a patent airway up to that time point. If not, a simple chin lift or jaw thrust may quickly reopen the airway. The gentle insertion of nasopharyngeal or oropharyngeal airways into semiconscious patients may further secure the airway as bridging therapy. Patients with intact gag reflexes may not tolerate these devices. If they are tolerated, they may assist oxygen insufflation with non-rebreather masks in spontaneously breathing patients. Furthermore, they often facilitate bag-valve mask ventilation that may be indicated. If the patient is unconscious or has otherwise lost protective airway reflexes, a secure airway must be established immediately to prevent aspiration and ensure proper oxygenation. Whenever feasible, the patient’s airway should be assessed in advance for potential difficulties with airway maneuvers. The mnemonic LEMON (look, evaluate, mallampati, obstruction, neck) [3] may be helpful. Factors predictive of difficulties are listed in Table 2.3.

Endotracheal intubation is considered the gold standard but is also known to be potentially difficult, particularly in trauma patients. Furthermore, all trauma patients are non-fasting, and there is a high risk of aspiration. Orotracheal intubation should be performed using a standardized rapid sequence induction (RSI) technique. This includes preoxygenation [4–7] with 100 % oxygen to wash out nitrogen and maximize the oxygen pool and to delay arterial desaturation during successive apnea. All equipment required in the subsequent process must be at hand and tested for functionality. Next, medication to induce anesthesia is administered through a patent IV access. Bag-valve mask ventilation before intubation should be avoided unless the patient’s ventilation is inadequate. The vocal cords are visualized by direct laryngoscopy, and the endotracheal tube (ET) is gently passed through them. If the first attempt to correctly place the ET fails, a re-saturation of the patient by manual ventilation (100 % oxygen with a tight-fitting mask including reservoir) is required. If fluids such as blood or saliva occlude the visual field, cautious suctioning of the mouth and pharynx may improve conditions for the next attempt. Immediately after successful intubation, the correct endotracheal position of the tube must be verified by the use of a carbon dioxide detector, ideally by capnography. If capnography is not available, a colorimetric CO₂ monitoring device may indicate proper intubation of the airway or false esophageal intubation. Because neither device is capable of detecting main-stem bronchus intubation, a physical examination including a thorough auscultation in search of bilateral ventilation and thoracic excursion is required. Radiographic imaging can also identify an excessively deep intubation. Securely fixing the ET helps to prevent tube dislocation during later patient movement (e.g., transfer to computer tomography). During the entire airway maneuver, monitoring of oxygen saturation, cardiac rhythm, and blood pressure is mandatory. Common indications for endotracheal intubation are listed in Table 2.4
.

Additionally, trauma patients with suspected cervical spine injury require gapless immobilization of the cervical spine until a radiographic diagnosis can securely rule out an injury. Therefore, an additional assistant is required to properly provide manual inline immobilization (MILS) of the cervical spine during the entire airway maneuver [8]. The anterior portion of the cervical collar may be opened while strictly maintaining MILS, but conventional laryngoscopy may still be difficult.

The quality as well as the quantity of breathing and ventilation are essential parts of the initial assessment. In spontaneously breathing patients, the evaluation of the respiratory rate, rhythm, and effort to breathe provides a quick overview of the patient’s condition. While approaching the patient, the examination should note signs such as nose flaring, agitation, labored respiration, or the inability to speak several words coherently. Any abnormalities may indicate respiratory distress and compromised air exchange. In addition, the respiratory rate should be counted or at least assessed. A slow (<10) or high (>20) respiratory rate urgently needs attention. Changes in the respiratory rate require immediate treatment, as they are reliable markers for insufficient ventilation. The supply of oxygen by a non-rebreather face mask with a reservoir may not be enough to compensate for insufficient ventilation. In these cases, assisted bag-valve mask ventilation facilitates ventilation, optimizes oxygenation, and may avert further deterioration of the patient’s respiratory condition. A respiratory rate within the normal range combined with a shallow depth of breathing also indicates that assistance is needed. This type of breathing is considered to be hypoventilation causing respiratory hypercarbia/hypercapnia, and it has the potential to influence mental status (e.g., somnolent or very fatigued patients). The responsible physician should look for symmetry of chest raises (e.g., flail chest) and thoroughly auscultate for bilateral lung sounds in patients that are spontaneously breathing or on mechanical ventilation (if not performed during airway management). Audible respiratory sounds indicate upper airway obstruction, whereas decreased or absent lung sounds are highly suspicious of a pneumothorax or hemothorax. The suspicion should be ruled out or confirmed and diagnosed more precisely with a chest x-ray [27]. Painful or irregular breaths may be trauma-related and should be monitored to identify any thoracic injuries. Severe impairment of breathing and ventilation is suspected in the presence of a tension pneumothorax, injuries to the spinal cord, or traumatic brain injury with alterations to the regulatory respiration center. Clinical signs of a pneumothorax include rather unspecific findings such as tachypnea and tachycardia but also more specific findings as pulsus paradoxus, decreased breath sounds, and hyperresonance on percussion on the affected side. In addition to these signs and symptoms, some patients present with diminished mental status caused by hypoxia. Audible breath sounds do not rule out a pneumothorax. A hypoxic, cyanotic patient with increased jugular venous distention is highly susceptible to a tension pneumothorax and needs urgent treatment. A tension pneumothorax increases the intrathoracic pressure. Therefore, the need for unusually high airway pressure in patients on mechanical ventilation is another sign of a life-threatening tension pneumothorax. Lifesaving decompression of the chest should be initiated immediately in hemodynamically instable patients (obstructive shock). Rapidly performed needle decompression can bridge therapy until a chest tube can be inserted to restore an air-free pleural space. Whereas radiographic imaging corroborates the diagnosis of a pneumothorax and allows for differentiation of a hemothorax, a tension pneumothorax must be treated without delay, i.e., without waiting for radiologic confirmation. The diagnosis can be made mainly on the basis of clinical examination findings and attentive observance of the patient.

Inadequate ventilation may also be caused by the other factors listed in Table 2.5. It is important to note that a patient may suffer from various conditions in parallel that interfere with ventilation. Therefore, all possible reasons for inadequate ventilation must be assessed if the patient is in respiratory distress. An intubated patient may also rapidly deteriorate. As a first step, the patient is taken off the ventilator, and manual ventilation is performed. This change adds the sense-based information derived from the use of the bag. At the same time, the use of the mnemonic DOPE [26] to quickly assess the most common causes of an acute decline in patients on mechanical ventilation may be helpful:

D. Displaced tube? Bilateral breath sounds still present? Positive capnography?

O. Obstructed tube? Does thick mucus obstruct the tube? If so, perform suctioning. Does the patient bite on the tube? Ensure adequate anesthesia depth.

P. Pneumothorax? Positive pressure ventilation may exacerbate the valve effect of an existing pneumothorax and progressively build up further pressure in the pleural space. Auscultate and check for elevated airway pressure.

E. Equipment failure? Check for oxygen supply. Does the ventilator function correctly? If in doubt, replace any questionable equipment.

Once a patent or secured airway and optimized conditions for breathing and ventilation are established, gas exchange and oxygenation of the blood can take place. Subsequently, sufficient circulation is a mandatory precondition to transport oxygen to the tissues on demand. Although initial monitoring of a trauma patient includes standard monitoring (i.e., ECG, pulse oximetry, and noninvasive blood pressure measurement), a brief, easy-to-perform, and focused clinical examination will provide valuable information on the patient’s perfusion and circulatory condition. This includes pulse palpation and an assessment of cardiac rhythm. The absence of a palpable pulse on an uninjured extremity may indicate the decompensated phase of shock. Pale, cold, and damp skin is also associated with shock and severely diminished perfusion and can be evaluated within seconds. Furthermore, a prolonged capillary refill time (>2 s) is suggestive of affected perfusion. However, trauma patients are disproportionately young and without limiting comorbidities [28]. Therefore, they can often compensate severe blood loss for a certain period of time without being hemodynamically compromised. Once the blood loss overcomes the compensatory capacities, a rapid and potentially fatal breakdown of circulation occurs. To assess the severity of insufficient circulation and shock, lactate and/or base excess measurement is recommended [29]. To prevent circulatory collapse and avoid secondary damage to the patient, bleeding control at the earliest possible moment is crucial.