Mechanical Ventilation in the Trauma Patient

*Jessica Lovich-Sapola, Jonathan A. Alter and Maureen Harders*

#### **Abstract**

In this chapter, we discuss the unique ventilatory strategies of the trauma patient. Injuries can be direct to the lung resulting from the trauma or indirect because of other injury to the body. We will discuss the airway and ventilation management and concerns in a patient with chest trauma, abdominal trauma, head trauma, orthopedic, and burn injury. The chapter will explain lung-protective strategies as well as innovative ventilation management techniques including extracorporeal membrane oxygenation.

**Keywords:** trauma, ventilation, burn, anesthesia, chest

#### **1. Introduction**

Trauma lung injury can result from a direct injury to the lung or secondary to injury elsewhere. The trauma and the associated aggressive resuscitation lead to bleeding, edema, and inflammation of the lungs. The trauma can result in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). The goal of the ventilation is to preserve the lung as well as the brain and other organs that are injured. Each form of traumatic injury results in an individualized approach to mechanical ventilation [1].

#### **1.1 Lung-protective ventilation strategies in the trauma patient**

The primary goal of the trauma patient is to avoid hypoxia and secondary tissue injury. Mechanical ventilation may be initiated for reasons other than respiratory compromise, such as brain injury, shock, intoxication, agitation, or combativeness. Lung-protective ventilation strategies aim to reduce the volume and pressure delivered to the lung. For example, the goal tidal volume is 6–8 mL/kg of predicted body weight regardless of the type of ventilation [1].

#### **1.2 Modes of ventilation in the trauma patient**

Volume-controlled ventilation (VCV) is the most used form of ventilation in the operating room. The tidal volume (Vt), respiratory rate, and FiO2 are set by the operator. This mode guarantees delivery of a set Vt and minute ventilation. The Vt is not reached if the peak inspiratory pressure (PIP) exceeds a set limit [1].

Pressure-controlled ventilation (PCV) can be used. In this type of ventilation, the Vt delivered is variable and depends on the airway resistance and the lung/chest wall compliance. This mode is recommended in the case of severe ARDS to promote better gas exchange [1].

Airway pressure release ventilation (APRV) is useful for the patient that has suffered a blunt trauma, with pulmonary contusions and severe atelectasis. APRV is also indicated for patients with morbid obesity and pregnancy. This mode of ventilation is a time-triggered, pressure-limited, and time-cycled mode of ventilation. The patient is able to breathe spontaneously. This mode is excellent for recruitment of the collapsed lung [1].

High-frequency oscillation ventilation (HFOV) results in the rapid delivery of very small tidal volumes with the application of high mean airway pressures. This type of ventilation results in active exhalation and therefore reduces air trapping. This type of ventilation is useful for patients with severe pulmonary contusion, ALI/ARDS, and smoke inhalation injury [1].

Noninvasive positive-pressure ventilation (NIPPV) including continuous positive airway pressure (CPAP) and bi-level airway pressure (BiPAP) can be used to treat acute respiratory failure. This mode of ventilation can be used in the trauma patient as well. This is not recommended for patients with brain injury, intoxication, or facial trauma. It is also not recommended for patients that are at increased risk of aspiration [1].

#### **2. Chest trauma**

Chest trauma, and the subsequent complications of chest injury, is significantly prevalent and the second most common cause of mortality in trauma. Injury sustained to the thorax can cause enormous damage to the heart, lungs, and major vasculature.

Any mechanism of injury to the chest wall or underlying organ systems has the potential to cause acute life-threatening issues with respiration. Mechanical ventilation, as it relates to the resulting complications of contusions, hypoxemia, and hemorrhage that occupy the spaces left behind by traumatic events, will be discussed throughout this chapter. Understanding the pernicious effects on respiratory mechanics and respiratory physiology helps the clinician to determine the timing of intubation and where the patient would most benefit on the spectrum of invasive ventilation.

#### **2.1 Respiratory physiology in chest trauma**

Injuries to the chest requiring mechanical ventilation may affect respirations in a variety of ways. Damage to the integument, musculoskeletal, nervous, or circulatory supply confined within and around the thoracic cavity can vastly change the physiology of respirations. Similarly, damage to the airways and lungs can significantly impede proper ventilation and oxygenation. As such, we can reduce respiratory compromise into two distinct circumstances: respirations compromised by altered mechanics of breathing, and respirations compromised by direct damage to the airway and lungs. Injuries to the respiratory system can also be categorized as being either penetrating or blunt in origin; however, the need for mechanical ventilation may exceed this distinction.

Integument provides a barrier from foreign organisms and elasticity, which is essential for expansion and contraction of the lungs; hindrance of integument

#### *Mechanical Ventilation in the Trauma Patient DOI: http://dx.doi.org/10.5772/intechopen.101578*

by injuries, such as in the case of burns or circumferential eschars, limits the compliance of the respiratory system and often necessitates positive pressure ventilation.

Skeletal trauma most commonly involves rib fractures. Splinting, caused by painful respirations and often associated with factures involving the ribs, sternum, vertebrae, clavicles, or scapulae as well as injuries to soft tissue or muscle, can lead to atelectasis, hypoxemia, and pneumonia. Disruption to breathing mechanics by a flail chest, when two or more ribs are fractured in two or more places, and by hemopneumothorax, whereby the thoracic cavity is occupied by blood or air, may impede lung expansion and limit tidal volumes as well as oxygenation. Massive thoracic trauma is often accompanied by significant abdominal trauma. Diaphragmatic injury inhibits the lungs' ability to expand and contract. Invasion of the lung cavity by penetrating wounds, bone spurs, and the like creates a discordance within the respiratory system, inhibiting lung expansion, and reversing physiology to an open cavity [2].

Damage to respiratory parenchyma, including alveoli, alveolar ducts, and bronchioles, will impede gas exchange. High kinetic energy to the chest wall commonly causes pulmonary contusions and is the most frequently diagnosed intrathoracic injury associated with blunt trauma.

Tracheobronchial wounds, and more rarely esophageal damage, can have profound consequences. Structural damage may result in tension pneumothorax, pneumomediastinum, and subcutaneous emphysema. Most importantly, damage to the tracheobronchial tree can create an immediate threat to oxygenation and perfusion, a situation requiring swift discovery, appropriate intubation technique in a patient with diminished respiratory reserve, and isolation of injury for surgical manipulation, exposure, and repair.

Vascular injury, cardiac injury, and cardiac tamponade may impair circulation *via* massive hemorrhage, diminished preload because of decreases in venous return, and impediments to cardiac ejection from impedance on myocardium [3, 4].

#### **2.2 Pulmonary contusion**

Blunt trauma often results in pulmonary contusion. The early signs of tachypnea, rhonchi, wheezing, or hemoptysis may indicate pulmonary contusion. Changes may not be visible on a chest X-ray for up to 4–6 hours. Pulmonary contusions usually resolve in 7 days, which are managed easily by treating with permissive hypercapnia, conservative fluids, routine lung recruitment, positive end-expiratory pressure (PEEP), and lung-protective ventilation [1].

#### **2.3 Hemothorax**

The most common cause of a hemothorax is the rupture of intercostal vessels. Chest tube placement is recommended to access the rate of blood loss. Massive hemothorax, >1500 ml or one third of a patient's blood volume, often requires emergent surgery [1].

#### **2.4 Bronchopleural fistulas**

Bronchopulmonary fistula is a communication between proximal and distal airways and the pleural space. Mechanical ventilation can be difficult. The mean airway pressure should be kept low. Some experts recommend PCV due to the ability to control the pressure gradient more precisely. Lung isolation may be required

if the leak is too large for proper ventilation. This can be achieved with main stem intubation, double-lumen tube, or bronchial blocker depending on the location of the fistula. The use of HFOV has been reported in some cases in addition to extracorporeal membrane oxygenation (ECMO) [1].

#### **2.5 Choosing the appropriate mechanical ventilation for a chest trauma patient**

#### *2.5.1 Non-invasive ventilation*

Provided the patient is hemodynamically stable without significant associated injury such as traumatic brain injury or severe abdominal trauma, non-invasive ventilation (NIV) techniques should be attempted. NIV has become common in acute chest trauma as it limits the hazard of further damaging the contused lung, which is at risk for diminished oxygenation and diffusion issues. Furthermore, NIV removes the risk of ventilator-induced lung injury, and many of the complications associated with endotracheal intubation should be considered prior to intubation attempts [5].

#### *2.5.2 Indications for intubation*

Respiratory compromise is depicted in many facets. Decreased tidal volume, increased respiratory rate, inadequate chest compliance, pleural compromise, failed lung mechanics, high oxygen requirements, and severe associated injuries (e.g., head trauma) are all situations that could require intubation. These indications are not absolute. These situations can quickly spiral out of ventilatory control. Surmounting a response prior to catastrophic failure and respiratory compromise is essential (**Table 1**) [6–8].

#### *2.5.3 Ventilator settings in chest trauma*

Initial ventilator settings in chest trauma are based on a lung-protective strategy. The Vt should be set between 4 and 8 mL/kg of ideal body weight with the plateau pressure < = 30 cm H20. While positive end-expiratory pressure (PEEP) has wellestablished benefits in ICU and ARDS patients, it is initially withheld to evaluate the level of pulmonary injury, barotrauma, air leaks, and pulmonary shunt. The FiO2 should be set = 1.0 and then titrated to an appropriate arterial oxygenation (PaO2). The respiratory rate should be set to 15–25 breaths per minute and then increased as need to achieve the desired PaCO2. Limiting plateau pressure to 30 cm H20 will help protect lung physiology (**Table 2**) [6–8].

#### **Indications for intubation in a chest trauma patient**


#### **Table 1.** *Indications for intubation in a chest trauma patient [6–8].*

*Mechanical Ventilation in the Trauma Patient DOI: http://dx.doi.org/10.5772/intechopen.101578*


#### **Table 2.**

*Initial ventilator settings in the chest trauma patient [6–8].*

#### **3. Abdominal trauma**

Abdominal trauma can result from compression of the organs, deceleration injury, or penetrating trauma such as a stab or gunshot. It is important to first determine whether the injury is superior (above the diaphragm), inferior (inguinal ligament and symphysis pubis), or lateral (anterior axillary lines). The location of the injury helps to determine the organs involved [9].

The pain from an abdominal trauma can lead to poor shallow respirations, increased respiratory rate, and a decreased ability to clear secretions. This can result in a secondary pneumonia. The use of early mechanical ventilation has been correlated with a decreased risk of pneumonia, but after 5 days of ventilation that risk of pneumonia begins to increase again [10].

A patient presenting to the operating room with an abdominal injury requires a rapid sequence induction with intubation secondary to the high risk of aspiration. Most trauma patients are considered a "full stomach" and have delayed gastric emptying secondary to the high catecholamine levels from the stress of the trauma [9].

#### **3.1 Abdominal compartment syndrome**

Abdominal compartment syndrome can result from increased intra-abdominal pressure secondary to massive fluid resuscitation (bowel edema) or continued bleeding. Intra-abdominal pressures exceeding 20–25 mmHg can result in poor circulation and tissue perfusion as well as decreased cardiac output. The abdominal compartment syndrome can lead to respiratory dysfunction that will present as high peak pressures, decreased tidal volume, worsening atelectasis, and hypercarbia. Emergent surgery is required to release the abdominal pressure [9].

#### **4. Head trauma**

Traumatic brain injury (TBI) resulting from a trauma has a primary and secondary injury component. The primary injury results from the initial trauma and resulting mechanical deformation of the skull and brain tissue. The secondary injury is a result of the progressive insult to the neurons (**Table 3**) [11].

#### **4.1 Brain injury and acute lung injury (ALI)**

Head injury can occur as an isolated trauma or along with other injuries to the trauma patient. Isolated head injuries have been shown in clinical and experimental studies to cause lung damage soon after the injury. Neurogenic pulmonary edema can occur due to the release of catecholamines. In addition, the injured brain can display a systemic inflammatory response, which can result in injury to the


#### **Table 3.** *Causes of brain injury [11].*

epithelial cells in the lungs. Subsequent mechanical ventilation (MV) can cause further pulmonary injury and strategies to minimize further damage to the lungs should be employed [12].

Mechanical ventilation in a patient with both a brain injury and ALI requires a balance between the principles that guide brain injury and the mechanical ventilation required to be protective of the lung. High PEEP can lead to elevated intrathoracic pressure, which results in decreased cerebral venous drainage and therefore poor cerebral perfusion. This effect is seen less in patients with ALI and ARDS; therefore, PEEP can often be safely applied in these patients. The key is to maintain the patient's volume status and mean arterial pressure. Also, the PEEP must be lower than the patient's intracranial pressure (ICP). The goal is to apply the lowest level of PEEP possible to still maintain oxygenation. Head elevation, avoiding tight endotracheal ties around the neck, and maintaining normocapnia are all important measures to monitor when ventilating a patient with head and lung injury [13].

Hypoxia, hypercarbia, and hypocarbia should be avoided in patients with a brain injury. Oxygenation should be monitored with a continuous pulse oximeter (goal >90%) and the PaO2 should be >60 mmHg. Hyperventilation can result in cerebral vasoconstriction and brain ischemia. Prolonged hyperventilation is not recommended and should be avoided in the first 24 hours after injury. Hyperventilation should only be used as a temporizing measure [11].

#### **4.2 Prolonged mechanical ventilation in the head injury patient**

Prolonged mechanical ventilation in the patient with a traumatic brain injury presents a unique set of goals, first, to avoid further increased ICP and to optimize cerebral blood flow (CBF). Maintaining adequate oxygenation is critical to ensuring adequate cerebral perfusion pressure (CPP). Another goal is to reduce the risk of ARDS. In a multicenter study of ventilated patients with severe brain injury, higher tidal volumes were associated with increased risk of ALI. Lower PaO2/FiO2 ratio and higher respiratory rate were also independent predictors of ALI in the same study [14]. Low tidal volumes and permissive hypercapnia are recommended. One systemic review of intubated patients showed a tidal volume range of 6–8 ml/kg may reduce the risk of ARDS [15].

When ARDS develops along with TBI, management can be more difficult. ARDS NET strategies to improve ventilation can conflict with the goal of maintaining CPP.

Increasing PEEP up to 15 cm H2O has a clinically insignificant effect on CPP; however, permissive hypoxia can lead to increased cerebral blood flow and increased CPP. ICP monitoring is suggested to monitor the effects of MV on CPP [12].

#### **4.3 High-frequency percussive ventilation (HFPV) in head injury**

Some studies show good results with HFPV in trauma patients with or without head injury. Using HFPV has resulted in improved oxygenation and reduced ICP [13].

#### **5. Orthopedic trauma**

Trauma management of a multiply-injured patient will require stabilization of pelvic and long bone fractures in as timely a manner that is safely possible. Research has shown that early stabilization of these fractures can reduce pain and improve patient outcomes. This includes a decrease in length of hospital stay and a reduction in pulmonary complications [16].

Patients with pre-existing pulmonary disease are at an even greater risk for significant pulmonary complications after a polytrauma. A chest X-ray or computed tomography (CT) scan is recommended on arrival to determine a baseline [16].

#### **5.1 Fat embolism**

Fat embolism syndrome (FES) is a result of the micro-embolism of fat and bone marrow from a patient's long bones [16]. Intraoperative transesophageal echocardiography performed on patients undergoing a long bone repair shows that most have some microembolization of fat and marrow [17]. This embolization can result in a varying degree of symptoms, including a significant acute inflammatory response [16, 17]. Most patients will not have a clinical impact. About 3–10% of patients will have clinically significant symptoms. The symptoms are usually progressive and develop over 12–72 hours. The most significant symptoms result in acute respiratory arrest and cardiac arrest [16].

The patient can present with hypoxia, tachycardia, mental status change, and a petechial rash. The rash is usually present on the upper body, including the conjunctiva, oral mucosa, neck, axilla, chest, and arms. Elevated pulmonary artery pressure and decreased cardiac output are seen with direct monitoring. When these symptoms arise, there are tests that can help confirm the diagnosis. These include testing for fat globules in the blood and urine, anemia, thrombocytopenia, and elevated ESR. A chest X-ray will often show bilateral alveolar infiltrates [16, 17].

The treatment for FES is supportive. The treatment for hypoxia requires early recognition and supplemental oxygenation, and may require ventilation management. Patients often require oxygen and PEEP. They may need long-term mechanical ventilation [16].

#### **6. Burn injury**

#### **6.1 Smoke inhalational injury**

Smoke inhalation is associated with increased mortality in a burn patient. Inhalational injury can be caused by the superheated air or the toxic compounds found in the smoke. These toxic compounds can include ammonia, sulfur, chlorine, and nitrogen dioxide [18].

There should be an increased suspicion of inhalational injury in any burn patient that presents with singed facial hair, carbonaceous deposits in the oropharynx, and blood carboxyhemoglobin levels greater than 10%. The chemical components of smoke can cause a significant inflammatory response that can lead to bronchospasm and impaired ciliary function. Lung necrosis and edema can lead to airway obstruction and atelectasis [19].

Signs and symptoms of inhalational injury include increased respiratory rate, increased secretions, stridor, dyspnea, use of accessory muscles, and facial burns. The first phase of inhalational injury includes asphyxia and acute toxicity. The second phase of inhalational injury begins at 24–96 hours after the injury and is the result of cellular level damage to the lungs. The treatment of inhalational injury includes ventilatory support, early pulmonary toilet, and nebulization therapy [18].

### **6.2 Carbon monoxide toxicity**

Carbon monoxide is a byproduct of combustion. It is the cause of 80% of deaths associated with smoke inhalation from its ability to saturate hemoglobin at very low partial pressures. Burn patients with carbon monoxide toxicity may present with a normal pulse oximeter reading. It is important to always check arterial concentrations of oxy- and carboxy-hemoglobin. The treatment of carbon monoxide poisoning is oxygen therapy (**Table 4**) [18, 19].

#### **6.3 Airway injury**

Upper airway injury is often due to thermal heat injury. This leads to swelling and upper airway obstruction due to edema of the oropharynx (**Table 5**) [18].


#### **Table 4.**

*Carbon monoxide toxicity symptoms [18, 19].*


#### **Table 5.**

*Classic symptoms of impending airway obstruction in the burn patient [19].*

*Mechanical Ventilation in the Trauma Patient DOI: http://dx.doi.org/10.5772/intechopen.101578*


#### **Table 6.**

*Indications for immediate tracheal intubation in the burn patient [18, 19].*

#### **6.4 Ventilator strategies in the burn patient**

Patients with a large percentage of burn, burns to the head and neck, and inhalational injury will have an increased likelihood of need for mechanical ventilation. The large fluid load required to treat a burn can result in fluid overload to the lungs. Early bronchoscopy after intubation can help with the removal of secretions and burn-related debris and can help to reduce the length of time required for mechanical ventilation [10].

Non-invasive ventilation can be used for awake patients with minimal facial trauma that are stable hemodynamically. This can be started early upon arrival to the hospital (**Table 6**) [10].

Invasive mechanical ventilation can be lung-protective at low tidal volumes. Airway pressure release ventilation (APRV), high-frequency percussive ventilation (HFPV), and high-frequency oscillatory ventilation (HFOV) have been studied and shown useful in burn patients and to improve morbidity and mortality in comparison to VCV. These provide better oxygenation at lower FiO2 than conventional ventilation with minimal effects on hemodynamics. APRV can be used to improve lung recruitment and oxygenation. There is no marked improvement in mortality, but it has been shown to stabilize alveoli, reduce edema of the alveoli, and helps to prevent the development of ARDS [10, 13].

#### **6.5 Extubation of the burn patient**

Extubation of a burn patient should be based on the patient hemodynamics, fluid resuscitation, inhalational lung injury, and existing airway abnormalities. Burn patients often receive large volumes of fluid resuscitation, which can result in airway edema. Burn patients also require large amounts of opioids for pain control. This results in burn patients often requiring prolonged intubation and ventilation. The criteria for extubation should be similar to those of non-burn patients: resolution of intoxications, ability to follow commands, pain-controlled, gag reflex, and appropriate cough. Burn patients need to be able to protect their airway from aspiration. An early tracheostomy should be considered for patients with long-term respiratory failure. While early tracheostomy has the benefits of improved communication, oral and tracheal hygiene, and improved patient comfort, it has not been associated with improved outcome [18, 19].

#### **7. Extracorporeal membrane oxygenation (ECMO) in the trauma patient**

Polytrauma is the leading cause of death among adults. This is often secondary to hemorrhagic shock, hypoxia, acute respiratory distress syndrome (ARDS),

#### *Mechanical Ventilation*

hypothermia, coagulopathy, and brain injury. The lung is often the first organ to fail in a severe trauma. ECMO has been used for nearly two decades, and its use has been gradually expanded to treat severe trauma patients, but the indications are uncertain and clinical outcomes are variable. The mortality of a severe trauma patient on ECMO is still high. There is much research needed on the proper initiation time for ECMO in the trauma patient and which patients will have the most benefit from ECMO. The safety and efficacy of ECMO still needs to be studied [20].

#### **7.1 What is ECMO?**

ECMO is a simplified version of the heart-lung machine used in open heart surgery. It is a method of gas exchange outside the body, so the lungs are exposed to minimal volume, pressure, rate, Fio2, and they potentially have some time to recover [10]. ECMO can provide adequate tissue oxygenation, help in rewarming, and infuse large amounts of blood products quickly [20].

#### **7.2 Complications of the trauma patient on ECMO**

Complications associated with a trauma patient on ECMO include bleeding and thrombotic complications. Patients also presented with abdominal compartment syndrome, lung and brain edema, and pancreatitis [20].

### **8. Conclusion**

As cases of severe trauma continue to increase, more and more trauma patients will be arriving in the operating rooms and intensive care units. It is important to understand how the mechanism of injury in a trauma affects the goals and types of mechanical ventilation required. The understanding of these individual cases will lead to improved patient outcomes.

### **Conflict of interest**

The authors declare no conflict of interest.

*Mechanical Ventilation in the Trauma Patient DOI: http://dx.doi.org/10.5772/intechopen.101578*

#### **Author details**

Jessica Lovich-Sapola\*, Jonathan A. Alter and Maureen Harders MetroHealth Medical Center, Cleveland, Ohio, USA

\*Address all correspondence to: jlsapola@gmail.com

© 2021 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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[5] Chiumello D, Coppola S, Froio S, et al. Noninvasive ventilation in chest trauma: Systematic review and metaanalysis. Intensive Care Medicine. 2013;**70**:1171-1180. DOI: 10.1007/ s00134-013-2901-4

[6] Richter T, Ragaller M. Ventilation in chest trauma. Journal of Emergencies, Trauma, and Shock. 2012;**4**(2):251-259. DOI: 10.4103/0974-2700.82215

[7] Prunet B, Bourenne J, David J-S, et al. Patters of invasive mechanical ventilation in patients with severe blunt chest trauma and lung contusion: A French multicentric evaluation of practices. Journal of Intensive Care Society. 2019;**20**(1):46-52. DOI: 10.1177/1751143718767060

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[15] Fuller BM, Mohr NM, Drewry AM, et al. Lower tidal volume at initiation of *Mechanical Ventilation in the Trauma Patient DOI: http://dx.doi.org/10.5772/intechopen.101578*

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#### **Chapter 4**

## Ventilation Strategies in Obese Patients

*Pavol Pobeha*

#### **Abstract**

Obesity is an increasingly prevalent disease and is a root and complication of conditions necessitating mechanical ventilation. Obese patients require a careful approach due to the particular manner of how ventilatory mechanics is affected, if obstructive sleep apnea (OSA) is present. The two main diagnoses we may encounter while ventilating these patients are obesity hypoventilation syndrome (OHS) and chronic obstructive pulmonary disease (COPD) in an obese patient, which has been recently proposed as a novel phenotype of COPD. The excessive amount of fat in the abdomen, chest wall, and around upper airways warrants the use of special ventilation modes and settings. This chapter provides insight into which issues should be considered when ventilating an obese patient, either in acute or chronic conditions. We stress the importance of acknowledging the high risk of OSA and how OSA affects the ventilation algorithms.

**Keywords:** non-invasive ventilation, obesity hypoventilation syndrome, COPD, overlap syndrome, sleep-disordered breathing, ventilation strategies

#### **1. Introduction**

Obesity is a disease with prevalence increasing significantly; about a third of the world's population is overweight or obese. The number of obese people has doubled in the last 20–30 years, and this trend continues [1]. This is closely related to the increase in the number of obese patients admitted to the intensive care units (ICU) as well as those requiring mechanical ventilation. The specificity of obesity in critically ill patients lies in the increased risk of infections, impaired respiratory drive, respiratory mechanics as well as the presence of sleep-disordered breathing [2]. A frequently mentioned diagnosis linking respiratory failure and obesity is obesity hypoventilation syndrome (OHS), but obesity also affects patients with other diseases, including respiratory and lung diseases. It is necessary to mention patients with chronic obstructive pulmonary disease (COPD), where a subset of obese patients benefits from a different approach to diagnosis and treatment compared to low-weight patients. This chapter aims to clarify the issue of respiratory failure in obesity and its treatment using mechanical ventilation in both acute and chronic conditions.

#### **2. Mechanisms of respiratory failure development in obesity**

The development of respiratory failure in obesity is a gradual and often longterm process. Although the proportion of individual factors may vary from patient to patient, the disease results from a complex of the following mechanisms [3–6]:


All these pathomechanisms affect the development and course of the disease in individual patients and should be considered in the diagnosis and treatment of respiratory failure and the setting of ventilation strategies. Guideline for mechanical ventilation generally distinguishes recommendations for the treatment of patients with obstructive pulmonary disease and restrictive diseases and separately for the diagnosis of obesity hypoventilation syndrome [7–9]. However, as obesity is present in various diseases and the above-mentioned pathomechanisms contribute to the clinical picture, in the following, we will mention the specifics of the treatment of respiratory failure in multiple diseases.

#### **3. Obesity hypoventilation syndrome**

Obesity hypoventilation syndrome is standardly defined by the combination of:


As the development of hypoventilation in OHS is gradual, the diagnosis is in most cases made at a stable stage, when the patient is examined in a sleep laboratory for symptoms of sleep-disordered breathing [10]. Approximately one-third of patients are diagnosed at the point of acute-on-chronic hypercapnic respiratory *Ventilation Strategies in Obese Patients DOI: http://dx.doi.org/10.5772/intechopen.101246*

failure [11], and these patients often require critical care. Comorbidities such as heart failure (usually with preserved ejection fraction), pneumonia, and sepsis contribute to the acute condition. A major problem in the acute and long-term management of these patients is that instead of making a correct diagnosis of OHS, other diseases such as COPD or asthma are misdiagnosed [12, 13]. The misdiagnosis of obstructive pulmonary disease without adequate lung function examination incorrectly directs treatment to the application of bronchodilators instead of adequate respiratory support.

#### **3.1 Classification of OHS patients**

Based on the presence of OSA and hypoventilation, three phenotypes of patients with OHS were observed [14, 15]:


#### • **Combined OHS and OSA**.

Polysomnographic (PSG) findings for individual phenotypes are shown in **Figure 1**.

**Figure 1** describes the excerpts of polygraphic recordings displaying from the top oxygen saturation, thoracic respiratory effort, airflow, and snoring. The first excerpt of severe OSA is exhibiting short interapneic intervals with oxygen saturation rising above 90%. The second excerpt illustrates low baseline oxygen saturation with further desaturations after apneic events. The third excerpt shows low baseline saturation with no desaturations reflecting isolated hypoventilation.

The classification is based on observations and medical evidence. It is a fact that a significant proportion of patients with OHS have concomitant OSA (near 70%

**Figure 1.** *Phenotypes of OHS.*

of patients have severe OSA), and its presence should be presumed in treatment, especially in acute situations [14]. In a stable state, it is appropriate to devote time to the precise diagnosis, differential diagnosis, and titration of treatment.

#### **3.2 Ventilation strategies in acute hypercapnic respiratory failure and OHS**

While continuous positive airway pressure (CPAP) treatment may be appropriate for OHS and chronic hypercapnic respiratory failure, noninvasive ventilation (NIV) is the method of choice for acute or acute-on-chronic respiratory failure. It is a better alternative to invasive ventilation because it significantly reduces patient morbidity and mortality and reduces the risk of reintubation [7, 15].

#### *3.2.1 Indications for NIV in acute hypercapnic respiratory failure in OHS*

In an obese patient with a known or suspected diagnosis of OHS who meets the criteria for initiating ventilation support, noninvasive ventilation should be considered the first treatment modality.

Acute ventilatory support in OHS patients is indicated if the following criteria are met [16]:


#### *3.2.1.1 Notes*


#### *3.2.2 Examinations and procedures before the start of the NIV*

Before starting treatment with NIV, it is necessary (assuming patient safety—no delay of NIV) to perform the following procedures:


#### *3.2.3 Management of NIV in acute OHS patient*

In the case of acute OHS, the NIV should be started immediately. OHS patients with severe daily sleepiness may be so somnolent that they cannot participate in placing their face masks. Treatment should be provided by staff experienced in NIV, and the patient should be placed in a high dependency unit (HDU) or intensive care unit (ICU) for close monitoring [17].

#### *3.2.3.1 Important notes on the management of acute NIV in OHS*


minimum-maximum) should be in an acceptable range (starting 4 cm H2O above EPAP) to allow the device to reach the desired tidal volume. The rate of pressure change (to adjust tidal volume) is suitable to choose medium to fast. Volume-targeted ventilation modes are accompanied by higher mask air leaks but can (assuming good mask fitting) improve breathing synchronization instead of changing to other modes.


#### *3.2.3.2 Contraindications to the use of NIV*

Absolute:


Relative:


#### *3.2.3.3 Monitoring in acute NIV*

Patients treated with NIV require intensive care and careful monitoring, including:


#### *3.2.3.4 Failure of acute NIV and indication of endotracheal intubation in OHS*

Despite careful monitoring and proper ventilation, NIV failure may occur in some cases. There is no exact algorithm to determine when to indicate intubation, but it is necessary to know the most common predictors of NIV failure [23–25]:


#### *3.2.3.5 Further recommendations after successful acute ventilation in OHS*

Data show that patients with a diagnosed or suspected diagnosis of OHS have a higher risk of death if they are discharged from the hospital without home positive airway pressure (PAP) treatment. Therefore, it is appropriate to set these patients for NIV treatment (ideally with pressure settings as in

hospitalization or with auto-PAP settings) and to schedule an early examination in the sleep laboratory and titration of PAP treatment (within 3 months) [26]. In patients acutely ventilated invasively, the use of NIV is an appropriate weaning strategy, as it effectively prevents respiratory failure in the first 48 h after extubation [24]. In patients requiring tracheostomy for prolonged invasive ventilation, it is advisable to perform decannulation and adjustment to home NIV after successful weaning instead of indicating long-term mechanical ventilation via tracheostomy.

#### **3.3 Ventilation strategies in chronic hypercapnic respiratory failure and OHS**

Initiating treatment of OHS patients in a stable stage allows assessing the ventilation strategy carefully. The choice of appropriate treatment should be based upon the severity of clinical state, the laboratory, functional and polysomnographic findings, reasonable cost-effectiveness, and the physician's experience. Clinical practice and literature data do not favor treatment by either CPAP or NIV as they are comparable, though some studies acknowledge certain benefits of NIV over CPAP.

#### *3.3.1 Comparison of effectivity of CPAP and NIV*

In the medium-term treatment, both CPAP and NIV have improved:


NIV was superior to CPAP in terms of:


In the long-term treatment, both CPAP and NIV have improved:


The concerns about the potentially harmful effect of NIV of hemodynamics due to the application of unphysiological positive pressure have been addressed by utilizing impedance cardiography, but it has not shown any deleterious impact on ventricular function [33].

The one undeniable benefit of CPAP over NIV is its lower cost [34]. The novel guidelines for the management of OHS by the American Thoracic Society [26] propose a switch of treatment from NIV to CPAP once the patient has achieved significant clinical improvement. This switch has been shown to be feasible and even favored by patients [35].

#### *3.3.2 Obstructive sleep apnea*

The one defining feature of OHS is its high prevalence of OSA, mainly of severe degree (estimated in around 70% of OHS patients). Thus, in patients with an apneahypopnea index (AHI) cut-off ≥30 episodes/h, it is reasonable to start with CPAP, as the primary aim is to alleviate obstruction in the upper airways, which might lead to the eventual resolution of chronic hypercapnia. For the patients without severe OSA, we should aim to improve the mechanics in the respiratory system and depression of the respiratory center; that is why NIV is used as an initial treatment.

#### *3.3.3 Failure of CPAP*

The patients initially set on CPAP should be monitored for signs of CPAP failure. In that case, a switch to NIV is warranted. The definition of CPAP failure is inconsistent among different researchers. Some of the criteria used for CPAP failure in OHS patients were:

	- Oxygen saturation below 90% for more than 20% of total sleep despite adequate abolition of apneas and hypopneas [36]
	- Oxygen saturation < 85% or hypercapnia despite maximal CPAP [37]
	- Oxygen saturation below 90% for more than 30% of titration night [38]
	- Oxygen desaturation < 80% over 10 min [9]
	- ≥5 min-long increase in nocturnal PTcCO2 > 55 mm Hg and in PaCO2 ≥ 10 mm Hg compared to the awake state [9]
	- Daytime PaCO2 > 45 mm Hg [38]

The choice of criteria for CPAP failure should be suited for the practice of a particular sleep laboratory, and it should be consistent over time.

Careful evaluation is necessary to avoid deeming inadequate patient compliance as CPAP failure.

It is important to note that a failure of CPAP during titration does not necessarily lead to failure of the CPAP treatment [36]. A single or few titration nights of CPAP may falsely display a failure, when in fact, a more extended period of treatment (2–3 months) might be necessary for CPAP to be effective. The length of a trial should be adapted according to the convenience of a sleep laboratory.

#### *3.3.3.1 Predictors of CPAP failure*

The high proportion of CPAP failure in OHS patients has led to identifying certain predictors when CPAP should be tried with a reasonable expectation of success and when to proceed straight to NIV.

Recognized CPAP failure predictors were:


Generally, worse blood gases [38], higher obesity, significant comorbidities, and clinician's preference warrant the trial of NIV in the first step.

#### *3.3.4 Setup strategies of NIV*

Novel increasingly intelligent auto-titrating devices are able to adjust to a patient's ventilatory need depending on his/her body position or the sleep stage.


Similarly, as the OHS patients are monitored for signs of CPAP failure, patients with NIV should be checked frequently, as there is a possibility of improvement of the respiratory center sensitivity, and a switch from NIV to CPAP might be considered.

#### **4. Chronic obstructive pulmonary disease (COPD)**

COPD is a serious disease with an increasing prevalence, accompanied by a high risk of respiratory failure [41]. Unlike OHS, COPD is a disease where, in addition to the failure of the ventilatory pump (muscle weakness, shortening of the diaphragm), lung disease (obstructive airway disorder) is added [42]. The severity of the situation and the fact that it is a progressive disease also affect the management of respiratory failure. The use of NIV in COPD is common practice today. This treatment has clearly been shown to be effective in acute exacerbations of COPD (AECOPD) [43] and has long been a controversial topic in chronic indications [44]. However, recent studies have provided clear evidence in favor of treatment (including the effect on survival), and the greatest benefit of NIV has been present with higher pressures in NIV settings for maximum CO2 reduction, in patients with higher basal PaCO2 values, and in those who achieve high treatment compliance [45–47]. In the management of hypercapnic respiratory failure in COPD, there is growing evidence of the effectiveness of so-called high-intensity NIV (HI-NIV) [48]. However, many studies and guidelines perceive COPD as a single disease and do not reflect the existence of different phenotypes, comorbidities, and the need for a unique approach to them. One of them is an obese patient with COPD.

#### **4.1 Obese patient with COPD**

Several respiratory societies perceive COPD, not as a single homogeneous airway disease but also distinguishes between several phenotypes characterizing differences between patients [49, 50]. In intensive care units, patients with COPD often appear to be classified as a classic "Blue bloater." These patients are generally classified as chronic bronchitis phenotype, but its definition does not fully describe such a complex clinical trait. On the contrary, there is increasing evidence that this trait of COPD patients is characterized by different radiological findings than those seen in emphysema, and it is associated strongly with obesity and frequently also with OSA [51]. The prevalence of obesity among COPD patients is also very high and variable (18–54%) [51, 52]. Obesity is strongly linked with the presence of OSA, and in COPD patients requiring inpatient pulmonary rehabilitation, the number of obese patients with OSA increases significantly [53]. The presence of obesity and the COPD-OSA overlap syndrome appears to be a key factor in the pathogenesis and development of clinical signs of the blue bloater trait. This statement is underlined with evidence that the severity of static hyperinflation is negatively associated with the apnea-hypopnea index in both COPD and non-COPD patients surviving acute hypercapnic respiratory failure [54]. This evidence is following data showing that overlap syndrome increases the risk of respiratory failure, pulmonary hypertension, and COPD exacerbations [55]. In line with the above literary data [56], a new "obese patient with COPD" phenotype (characterized by predominantly chronic bronchitis, less hyperinflation, metabolic and cardiovascular comorbidity, sleep apnea symptoms, that is, daytime sleepiness, snoring, nonrefreshing sleep, and/or hypercapnic respiratory failure) was proposed [57] with a recommendation of screening for sleep-disordered breathing in this group of patients [50].

#### **4.2 Ventilation strategies in acute exacerbation of COPD in obese patients**

Acute exacerbation of COPD (AECOPD) is a severe condition that requires urgent intervention, and recommendations for its treatment are well known [41]. NIV has an irreplaceable place in the management of AECOPD in the event of acute or acute-on-chronic respiratory failure [17, 43]. In a patient with COPD who is obese, it should be borne in mind that obesity is probably one of the predominant factors predisposing to respiratory failure. Other possible factors such as cardiogenic edema, infection, uncontrolled excessive oxygen therapy, or pneumothorax should not be forgotten [17]. Because NIV effectively prevents endotracheal intubation and survival in patients with AECOPD [23, 58], it should be indicated whenever a patient meets the criteria for initiation.

#### *4.2.1 Indications for NIV in acute hypercapnic respiratory failure in COPD*

Acute ventilatory support in AECOPD is indicated in the same criteria as in OHS patients:


#### *4.2.1.1 Notes*

It should be emphasized that controlled low-flow oxygen therapy (to achieve a saturation of 88–92%) is the basis for treating respiratory insufficiency in COPD. However, if respiratory acidosis develops or progresses (pH < 7.35) during careful monitoring of this treatment, NIV is recommended [7, 23].

#### *4.2.2 Examinations and procedures before the start of the NIV*

Examinations before the start of NIV are recommended the same as in Section 3.2.2. A chest radiograph is necessary to determine whether the deterioration of the patient's condition is caused by pneumothorax or pulmonary edema.

#### *4.2.3 Management of NIV in an obese patient with AECOPD*

A patient with AECOPD with respiratory acidosis is at extreme risk of early death, and early intervention is necessary [59]. NIV is highly effective in this indication but does not replace the standard treatment of AECOPD, which must be given in each case. NIV should be started as soon as it is confirmed that regulated oxygen therapy is failing. In the case of AECOPD, as in the case of OHS, CPAP is not an appropriate treatment (as respiratory support). The method of choice is bilevel ventilation [7, 17, 23]. In treating obese patients with COPD, we can generally proceed from the procedures in OHS, with certain specifics for airway disorder.

#### *4.2.3.1 Important notations on the management of NIV in obese patients with AECOPD*


#### *4.2.3.2 Failure of acute NIV and indication of endotracheal intubation in AECOPD*

Predictors of NIV failure have already been mentioned in Section 3.2.3. The documented percentage of NIV failure ranges widely from 5 to 40% (depending on the predictors of failure, patient selection, and staff experience with NIV). Analysis of several studies has shown that the most significant predictor of NIV failure is pH 1 h after the onset of NIV, followed by the severity of the underlying disease and patient compliance [61]. If the pH after 1–2 h of NIV is below 7.25, respiratory rate > 25/min, or new confusion or distress appears, consider intubation [17]. Nevertheless, if NIV adds to patient distress and intubation has been inappropriate, NIV should be discontinued, and palliative care measures adopted [17].

In case of NIV failure and planning for escalation of treatment to invasive mechanical ventilation (IMV), it is necessary to [23, 60]:


#### *4.2.4 Further recommendations after successful acute ventilation in COPD*

NIV may be an appropriate option in patients who have survived intubation and invasive mechanical ventilation and require continued treatment for chronic respiratory failure. However, in ventilator-dependent patients requiring ventilation for 12 h or more, tracheostomy may be considered and is highly recommended if

the ventilation time exceeds 16 h per day. In this case, it is necessary to provide a ventilation device with an integrated battery [17, 40]. There are at least two reasons why we can assume that patients who have survived AECOPD with a need for NIV or IMV will be candidates for long-term home ventilation. The first is that obese patients with COPD have probable or known sleep-disordered breathing and will require some form of PAP treatment [53, 56]. Secondly, an episode of acute hypercapnic respiratory failure (AHRF) is a milestone in the course of the disease that predicts adverse development and prognosis [17]. In contrast to OHS (where weight reduction can reverse the course of the disease), this fact supports the planning of long-term ventilation treatment in obese patients with COPD. Therefore, clinicians should discuss the management of possible future episodes of AHRF with patients following an episode requiring ventilatory support because there is a high risk of recurrence [17]. Timing of indications for home mechanical ventilation (HMV) in COPD is a debated topic and ultimately depends on the decision of the patient and the physician. If the patient's condition after AHRF is stable, does not require continued ventilation, he/she may be discharged from the hospital with a scheduled early follow-up. It is recommended to reassess postacute NIV COPD patients 2–4 weeks after clinical recovery. NIV should be considered if the pCO2 remains >7 kPa (53 mm Hg) [47] or if sleep-disordered breathing is detected in a sleep study.

#### **4.3 Ventilation strategies in stable obese COPD patients**

COPD is a disease associated with a high risk of developing chronic respiratory insufficiency [41]. Despite long-standing discussions about whether long-term NIV can affect the course and prognosis of the disease, the reality is that more than a third of patients treated are patients with lung and airways diseases [62]. Moreover, we now know that long-term NIV positively affects the quality of life and symptoms and improves survival [46, 47]. Thus, the question is not whether to ventilate COPD patients, but which COPD patients benefit from NIV and when it should be initiated.

#### *4.3.1 Overlap syndrome COPD-OSA*

Obese patients with COPD are very likely to have OSA simultaneously, commonly referred to as overlap syndrome [63]. The prevalence of these diseases in the general population is up to 10%, but in severely ill patients with COPD, the prevalence of OSA may be much higher, especially in the obese [53]. The coexistence of both diseases leads to a combination of continuous hypoxia (due to COPD) and chronic intermittent hypoxia (during sleep in apnea episodes due to OSA) in patients, which contributes to the development of the described clinical phenotype (Section 4.1) [57]. CPAP is the standard treatment for OSA and overlap syndrome [64]. However, CPAP treatment alone is more suitable for normocapnic patients with COPD, as it may not be effective in reversing hypoventilation and hypoxemia. Options should be carefully considered, and if nocturnal hypoxemia persists despite CPAP treatment, NIV may be an appropriate treatment instead of adding oxygen therapy to CPAP. In COPD patients diagnosed with OSA in the sleep laboratory, CPAP has been shown to fail in more than one-fifth. Although there are no clear limits to the efficacy of CPAP, treatment failure and NIV indication are more common in patients who are more obese, have worse lung function, hypercapnia, and more severe hypoxemia (with a longer desaturation time below 90% during nocturnal PSG) [65].

#### *4.3.2 Indications for NIV in chronic hypercapnic respiratory failure in COPD*

There is not only one criterion for indicating long-term NIV in COPD, which is confirmed by common practice that patients need to be approached individually [7, 9, 44, 66]. Long-term NIV may be indicated at a stable stage of COPD or after overcoming an acute exacerbation, meeting specific criteria, and considering the patient's needs. An important factor influencing the decision on the need for NIV is the presence of OSA. Contrary to the diagnosis of OHS with severe OSA, in the case of COPD-OSA overlap and hypercapnia, CPAP is not an appropriate option. CPAP may be effective in normocapnia in this case, but in hypercapnic COPD and the likelihood of progression of the underlying lung disease, NIV is the treatment of choice.

**Long-term NIV may be indicated in well-established COPD** (treated according to guidelines) in which there are persistent symptoms of chronic hypoventilation (hypercapnia), **and at least one of the following criteria is met:**


#### *4.3.3 Examinations before the start of long-term NIV*

Blood gas collection and chest X-ray are recommended as standard. If possible, it is advisable to carry out a sleep study, preferably with the measurement of transcutaneous capnometry. Finally, the examination of lung functions is critical. Although this is not indicated directly in COPD exacerbation, in patients with a controversial diagnosis (especially in an obese patient), a misdiagnosis of COPD is common. Planning spirometry and possible body plethysmography with a distance from exacerbation before setting for long-term NIV will make it possible to clarify the diagnosis and set up treatment effectively.

#### *4.3.4 Management of long-term NIV*

Because patients with COPD form a wide range of different phenotypes, making precise recommendations on setting long-term NIV is not easy. In recent years, various approaches have been used, including the so-called low-intensity NIV (LI-NIV) and high-intensity NIV (HI-NIV) [44, 66]. The main difference is that HI-NIV uses higher values of IPAP and backup frequency to achieve normocapnia [48]. This approach has been shown in clinical trials to be effective in improving symptoms and quality of life and even in improving survival [45–47]. NIV was most effective

in those COPD patients where IPAP over 18 cm H2O was used, baseline paCO2 was over 55 mm Hg, and NIV was used overnight for more than 5 h [44]. Another option is to use volume-targeted ventilation modes. In COPD, their use is equally effective compared to HI-NIV [67]. It can make sense to obese patients with COPD because they allow them to better adapt to current and later patient needs when set up correctly.

#### *4.3.4.1 Important notes on the management of long-term NIV in obese patients with COPD*


### **5. Conclusion**

This chapter aimed to discuss different approaches to the treatment of respiratory failure depending on the situation and diagnosis in obese patients. Up-to-date information from evidence-based medicine and international guidelines was used in the preparation of the chapter. Although COPD and OHS are different diagnoses with different prognoses, in obese patients, they are associated with the presence of sleep-disordered breathing. It is obstructive sleep apnea that seems to be a key factor contributing to the clinical picture of the so-called obese patient with COPD, and early diagnosis and treatment can reverse the negative impact of the disease on patients' health.

*Ventilation Strategies in Obese Patients DOI: http://dx.doi.org/10.5772/intechopen.101246*

### **Author details**

Pavol Pobeha

Department of Respiratory Medicine and Tuberculosis, Faculty of Medicine, P.J. Safarik University and L. Pasteur University Hospital, Kosice, Slovakia

\*Address all correspondence to: pavol.pobeha@upjs.sk

© 2021 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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[35] Orfanos S, Jaffuel D, Perrin C, Molinari N, Chanez P, Palot A. Switch of non-invasive ventilation (NIV) to continuous positive airway pressure (CPAP) in patients with obesity hypoventilation syndrome: A pilot study. BMC Pulmonary Medicine. 2017;**17**(1):50. DOI: 10.1186/s12890- 017-0391-9

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#### **Chapter 5**

## Mechanical Ventilation in Neurocritical Patients

*Thierry Hernández-Gilsoul, Jose de Jesús Vidal-Mayo and Alan Alexis Chacon-Corral*

#### **Abstract**

Patients under neurocritical care may require mechanical ventilation for airway protection; respiratory failure can occur simultaneously or be acquired during the ICU stay. In this chapter, we will address the ventilatory strategies, in particular the role of protective lung ventilation, and the potential increase in intracranial pressure as a result of permissive hypercapnia, high airway pressures during recruitment maneuvers, and/or prone position. We will also describe some strategies to achieve mechanical ventilation liberation, including evaluation for tracheostomy, timing of tracheostomy, mechanical ventilation modalities for weaning and extubation, or tracheostomy weaning for mechanical ventilation.

**Keywords:** mechanical ventilation, neurocritical

#### **1. Introduction**

Neurological critically ill patients represent an important group in the intensive care unit (ICU) worldwide. About 20% of these patients require mechanical ventilation (MV) of which 20–25% will develop acute respiratory distress syndrome (ARDS) [1, 2]. Ventilatory management is controversial in this kind of population due to the complexity of the event and singularity of each case with acute brain injury (ABI). This includes traumatic brain injury (TBI), intracerebral hemorrhage (ICH), aneurysmatic subarachnoid hemorrhage (aSH), acute ischemic stroke (AIS), and other entities associated with high intracranial pressure (ICP). Additionally, brain damage may be prevented by avoiding pulmonary and systemic injury associated with mechanical ventilation. Thus, this topic is particularly important, since respiratory failure is the most frequent extracerebral organic failure in patients with ABI [3].

Recently, the VENTILA group reported some interesting characteristics, in the evolution of the ventilatory management in neurological critically ill patients, in three cohorts of patients with mechanical ventilation (2004, 2010, and 2016) [4]. In this multicentric international report of 4152 patients, the main pathologies were intracerebral hemorrhage and traumatic brain injury. One of the main results was an increment in the use of lung protective ventilation through time (47% in 2004, 63% in 2010 vs 65% in 2016; p<0.001). However, there were no differences in other outcomes such as length of stay in ICU, length of stay in hospital, mortality in the ICU, and mortality in the hospital. Some variables were associated with mortality in multivariate analyses such as age > 75 years old (OR 1.80, CI 95% 1.40–2.30),

SAPS II (Simplified Acute Physiology Score II) > 50 points (OR 2.31, CI 95% 1.87–2.86), occurrence of organic failure within the first 48 h after ABI (OR 1.79, IC 95% 1.59–2.0), and etiology of ABI, specifically TBI (OR 1.8, CI 95% 1.4–2.3), ischemic stroke (OR 3.94, CI 95% 2.47–6.31), and cerebral hemorrhage (OR 3.96, CI 95% 2.59–6.06).

#### **2. Brain-lung cross talking**

Acute brain injury can create issues in lung function and vice versa. This bidirectional brain-lung interaction is supported in experimental models and basic studies in humans, which have shown several neuroinflammatory, autonomic, immunologic, and endocrine pathways [5]. According to the so-called two-stroke model, when ACL occurs, a lung injury associated with systemic inflammation due to a "catecholamine storm" appears, first hit; subsequently these events can trigger an increase in permeability into the pulomnary capillaries, vasoconstriction in the pulmonary arterioles and recruitment of inflammatory cells in the alveoli, second hit [6].

Hypoxemia and hypercapnia are associated with lung injury and amplify acute brain injury. Both situations reduce cerebral vascular resistance, which consequently raises cerebral blood flow and increases ICP. Also, they can increase the systemic inflammatory response and produce extracerebral organic failures. In the literature, this chain of events had been denominated *dangerous cross talk* [7, 8]. Thus, ventilatory management has been considered a strategy to avoid ventilatorinduced lung injury (VILI) through the use of lung-protective ventilation.

#### **3. Ventilatory management**

The most recent guidelines related to this topic are provided by the European Society of Intensive Care Medicine [9]. Evidence about most of these recommendations remains at a low level; for this reason, we present the most general suggestions in order to give a safety and efficient ventilatory management to these patients.

#### **3.1 Oxygenation and carbon dioxide (CO2) targets**

In patients with ABI, it is fundamental to guarantee an optimal oxygenation to avoid secondary brain injury [10]. It is recommended to target "normoxia" with a partial arterial pressure of oxygen (PaO2) between 80-120 mmHg and or a peripheral oxygen saturation (SpO2) of ≥95% in patients with or without intracranial hypertension [9, 11].

In addition, some evidence suggests that hyperoxia is an independent factor associated to greater mortality and outcomes driven by several mechanisms: vasoconstriction of brain arteries, synthesis of reactive oxygen species (ROS) and damage associated molecular patterns (DAMPs) [10]. In a clinical trial of patients with traumatic brain injury (TBI), which evaluated two oxygenation strategies (normobaric hyperoxia and normoxia), there were no differences in the hospital length of stay, but the modified Rankin scale at discharge and at 6 month followup was better in the normoxia group [12].

In relation to the minute ventilation settings (respiratory rate times tidal volume) to modify the CO2 content of the blood, it is recommended to adjust the ventilation to maintain normal levels of arterial pressure of carbon dioxide (PaCO2) between 35 and 45 mmHg. Traditionally, it was considered that patients with ABI (specially population with TBI) should be maintained with hyperventilation;

*Mechanical Ventilation in Neurocritical Patients DOI: http://dx.doi.org/10.5772/intechopen.101029*

however, this situation can lead to cerebral vasoconstriction that can worsen cerebral tissue hypoxia and ischemia [13]. In a randomized clinical trial conducted by Muizelaar et al., it found that patients with TBI undergoing systematic hyperventilation (PaCO2 25 ± 2 mmHg) had poorer outcomes at 3 and 6 months' follow-up compared with the normocapnia group (PaCO2 35 ± 2 mmHg). Deleterious findings were also documented in head injury patients who were managed with hyperventilation plus tromethamine addition as buffer [14]. Transient hyperventilation (PaCO2 30–35 mmHg) is only recommended as a rescue maneuver in cases of brain herniation [9].

#### **3.2 Tidal volume (Vt)**

Ventilation with Vt between 6 and 8 ml/kg of predicted body weight is considered a standard of ventilatory treatment in patients with ARDS and its application in general in patients under invasive ventilatory support. However, historically, neurocritical patients have been excluded from clinical trials that have evaluated this ventilatory therapeutic strategy due to the potential increase in intracranial pressure caused by hypercapnia and increased intrathoracic pressures [15].

In a multicenter cohort study, it was found that an average Vt of 9 ml/kg of predicted weight was used in this group of patients [15]. Additionally, it has been described that the use of high Vt has been associated with the development of ARDS in these patients [16] while other observational studies have found no evidence of this association; instead, driving pressure was the only ventilatory variable associated with the development of ARDS [17]. Likewise, there is no consistent evidence that the use of a Vt by itself increases intracranial pressure [15, 18].

A recent multicenter prospective study that used a strategy of low Vt (less than 7 ml/kg), moderate PEEP (6–8 cmH2O), and a protocol for early extubation was associated with more days free of mechanical ventilation and lower mortality at 90 days, with no serious adverse events associated with this intervention [19]. Condensing this information, the administration of Vt of 6–8 ml/kg is suggested to maintain a plateau pressure of less than 25 cmH2O and a driving pressure of less than 15 cmH2O [8, 11, 13].

#### **3.3 Positive end expiratory pressure (PEEP)**

Implementation of PEEP associated with low Vt in the pulmonary protective ventilation strategy has been associated with better clinical outcomes, even in patients without ARDS [20]. Its use has been a useful strategy in neurocritical patients where oxygenation and ventilation are essential. The PEEP level has been considered a potential indirect maneuver that increases ICP in a directly proportional way. This led Asehnoune et al. to study the use of PEEP and its effect on intracranial pressure, comparing PEEP levels less than or greater than 5 cmH2O; no clinically significant differences of episodes of intracranial hypertension were seen [19]. Boone et al. analyzed 341 patients with ABI, in which nonsignificant effects of PEEP on ICP or cerebral perfusion pressure (CPP) were documented [21]. Furthermore, in a study of patients with aSH divided into groups according to respiratory compliance, those with decreased respiratory compliance (<45 ml/cmH2O) did not show changes in the hemodynamic variables, including CPP at diverse levels of PEEP [22].

In another prospective study of 20 patients with TBI with brain-tissue oxygenation (PbtO2) monitorization, an increase in the level of PEEP from 5 to 10 cmH2O (24.60 ± 6.84 to 26.55 ± 7.09; *p* = 0.0001) and from 10 to 15 cmH2O (26.55 ± 7.09 to 29.05 ± 7.07; *p* = 0.0001) significantly increased PbtO2 in these patients, without significant changes in ICP or CPP [23].

Therefore, it is recommended to administer a sufficient PEEP (5–8 cmH2O) to maintain adequate oxygenation. In cases where PEEP is greater than 10–15 cmH2O, it is suggested that advanced neuromonitoring be used to adjust this variable optimally [11, 13, 24].

#### **3.4 Prone positioning**

Mechanical ventilation in the prone position is also a standard of treatment for patients with moderate-severe ARDS, since it reduces mortality in addition to improving oxygenation, respiratory mechanics, and ventilation-perfusion imbalance. However, due to the potential increase in ICP and reduction in CCP, these patients have also been excluded from clinical studies to evaluate this intervention [13].

In an observational study of patients with aSH, who fulfilled criteria for ARDS within the first 2 weeks, a significant increase in oxygenation was found (97.3 ± 20.7 mmHg in the supine position to 126.6 ± 31.7 mmHg in the prone position) as well as an increase in PbtO2 (26.8 ± 10.9 mmHg to 31.6 ± 12.2 mmHg; *p* < 0.0001) with a good tolerance of the intervention (prone position for 14 hours). In contrast to a concomitant increase in ICP and a decrease in CPP, however, overall, the benefit in systemic oxygenation was greater than the effects on cerebral perfusion and intracranial pressure [25].

In the same way, other observational studies have reported that this maneuver improves patient oxygenation and PbtO2 with a tendency to increase ICP but without reducing CPP. One report with 8 patients showed a significant increase in oxygenation with an increase in ICP and CPP as well as an improvement in PbtO2 [26]. Roth et al. found in a retrospective study that patients had a significant increase in oxygenation with an increase in ICP without significant changes in CPP [27].

Recommendations in this group of patients suggest ventilation in the prone position. In patients with moderate-severe ARDS without evidence of intracranial hypertension, it is a safe and effective strategy. However, the risks and benefits of the intervention should be considered, and the patient must have multimodal monitoring to determine the effects on both systemic and cerebral hemodynamics and oxygenation [9, 11].

#### **3.5 Alveolar recruitment maneuvers**

Another controversial aspect is the use of alveolar recruitment maneuvers, due to the potential risk of increasing intracranial pressure with reduction of CPP [13]. In systematic reviews and meta-analysis of ARDS studies, it was found that this intervention is associated with an improvement in the oxygenation of patients but without effects in other outcomes such as mortality or duration of mechanical ventilation [28, 29].

In studies carried out in this population, conflicting results have been found regarding the efficacy of this intervention to improve oxygenation; however, regarding neurological variables, some studies described an increase in ICP associated with a decrease in CPP without improvement in oxygenation [30, 31]; another study found that recruitment maneuvers significantly affected cerebral hemodynamics [32].

Although the most recent guidelines for ventilatory management of these patients do not issue any recommendation due to limited evidence [9], expert recommendations suggest that this intervention can be considered individually in patients with acute brain injury and concomitant ARDS with an invasive neuromonitoring for the potential risks and benefits of these maneuvers [8, 13].

#### **4. Extracorporeal life support (ECLS)**

Extracorporeal membrane oxygenation ventilation (ECMO) and extracorporeal CO2 removal (ECCO2R) have gained popularity for patients with hypoxemic respiratory failure refractory to conventional ventilation strategies; however, because the evidence for this intervention is anecdotal in this patient population [33, 34] and there is a risk of catastrophic complications in patients with ABI (especially intracranial hemorrhage due to the need for routine anticoagulation), there is no consensus to carry out this intervention in neurocritical patients [9, 11, 13]. Heparin-free regional citrate anticoagulation, like in renal replacement circuits, may offer an alternative to this problem [35]. The use of regional citrate anticoagulation continuous veno-venous hemofiltration (RCA-CVVH) connected to an ECMO circuit, with low heparin or heparin-free ECMO, has been reported [36].

In an experimental model of severe hypercapnic acidosis, regional anticoagulation with citrate solution achieved the anticoagulation goal as well as standard heparin anticoagulation but did not improve CO2 removal and led to more hypocalcemia and hypotension [37].

#### **5. Weaning from mechanical ventilation**

Historically, the population of neurocritical patients has been considered at high risk of failure to extubation (from 10 to 38% failure), and hence there is delayed withdrawal of mechanical ventilation which is associated with higher rates of ventilator associated pneumonia (VAP) and airway injury; longer mechanical ventilation and ICU length stay, and higher mortality [15, 38, 39].

The recommendations of the international guidelines for the withdrawal of mechanical ventilation do not contemplate specific aspects for this population [40, 41], in addition to the fact that certain general aspects of these consensuses are not applicable for neurocritical patients:


There is evidence that multidisciplinary and standardized protocols in these patients are associated with better outcomes and a higher rate of successful withdrawal from mechanical ventilation [46, 47]. One tool designed for this population is the VISAGE score by Asehnoune et al [44]. This score was derived from a multicenter prospective cohort that included a heterogeneous population of patients with ABI (*n* = 437), of which 77.3% had a successful extubation. From the multivariate analysis of the factors associated with successful extubation, 4 variables with significant association were found that made up the VISAGE score: visual pursuit, swallowing attempts, age under 40 years, and GCS greater than 10 points (**Table 1**). According to the original validation study, a score on this scale greater than or equal to 3 points

```
A score ≥ 3 is associated with 90% extubation success; each variable has a value of 1 point
```

```
• Age < 40 years
```

```
• Visual pursuit
```

```
• Swallowing attempts
```
#### • Glasgow coma score > 10 points

#### *[44].*

**Table 1.** *VISAGE score.*

has a sensitivity of 62%, specificity of 79%, positive predictive value of 90%, negative predictive value of 39%, positive likelihood ratio of 2.9, and negative likelihood ratio of 0.5 to predict extubation success. This scale represents a practical tool for use in the patient's bed, for which several experts have recommended its clinical use; however, external validation in other patient cohorts is still pending [48, 49].

In a systematic review with meta-analysis, Wang et al. found that other variables associated with extubation failure in neurocritical patients are the presence of pneumonia, atelectasis, mechanical ventilation for more than 24 h, a score of GCS lower than 8 (OR = 4.96.95% CI = 1.61–15.26, *p* = 0.005), the inability to follow orders (OR = 2.07.95% CI = 1.15–3.71, *p* = 0.02), thick secretions, and alteration in cough reflex [50]. Another score that evaluates the ability to protect the airway has been proposed (the Airway score), which takes into consideration variables such as the amount and quality of respiratory secretions, gag and cough reflex, and patients with a score of less than 6 who are candidates for IMV withdrawal. Nevertheless, it should be considered that there is a wide variability in the qualitative assessment of respiratory secretions and that there is no extensive external validation of this tool [51].

Regarding the actual evidence of tracheostomy performance, it has been observed that intensivist achieves more frequently tracheostomies in neurocritical patients (up to 45%) compared to general patients in the ICU [52]. The theorical benefits of tracheostomy are that it decreases the work of breathing and improves patient comfort when compared to an endotracheal tube. Tracheal stoma that does not generate pain after 48–72 h of tracheostomy placement. Reduction or suspension of sedation and opioid analgesia, as well as less work of breathing are the theorical benefits that generate greater patient comfort. Contrary to general belief, there is no evidence that it decreases the frequency of tracheal stenosis associated with prolonged ventilation. Even more, an endotracheal cannula also requires the inflation of a balloon to isolate and protect the airway from bronchoaspiration; thus, tracheal stenosis is also a complication, which according to a case study is more complicated (infraglottic stenosis) and may not resolve more frequently compared to tracheal stenosis acquired with an orotracheal tube [53].

According to this information and consensus, it is recommended to consider to facilitate the withdrawal of mechanical ventilation in the following cases: infratentorial lesions, inability to protect the airway (inadequate management of respiratory secretions), altered central respiratory drive, slow or unfavorable neurological recovery, and patients with recurrent extubation failure.

However, the precise indications for its performance and the timing of the intervention remain poorly defined in the literature [38, 48, 54].

A highly controversial aspect is the performance of "early tracheostomy," which has been defined as placing it within the first 7 days [55] (there are reports that define it from day 5 to day 10) of mechanical ventilation [56, 57].

Large series of patients that have compared early versus late tracheostomy have not found a benefit in terms of mortality, although there is a trend of better *Mechanical Ventilation in Neurocritical Patients DOI: http://dx.doi.org/10.5772/intechopen.101029*

outcomes in the early tracheostomy group, such as reduction in the frequency of ventilator-associated pneumonia, fewer days of mechanical ventilation, and a shorter length of stay in intensive care [58, 59]. In the SETPOINT study (Strokerelated Early Tracheostomy vs. Prolonged Orotracheal Intubation in Neurocritical care Trial) that randomized 60 patients with stroke or cerebral hemorrhage to early tracheostomy (day 1–3 of mechanical ventilation) versus standard tracheostomy (between 7 and 14 days), no difference was found in the primary endpoint, which was the length of stay in the ICU (median, interquartile range [IQR] 8, 16–28 days versus 17 [13–22] days, median difference: 1 [−2 to 6]; *p* = 0.38) although in the intervention group, mortality in the ICU and at 6 months was significantly lower (10 versus 14%; *p* < 0.01 and 27% versus 60% *p* = 0.02), without finding other differences in other secondary outcomes [60].

The CENTER-TBI study that was a prospective European multicenter cohort of adult patients with head trauma found that the factors associated with the decision to perform a tracheostomy were older age (HR = 1.04, 95% CI 1.01–1.07; *p* = 0.003), GCS less than or equal to 8 (HR = 1.70, 95% CI = 1.22–2.36 at 7; *p* < 0.001), thoracic trauma (HR = 1.24, 95% CI = 1.01–1.52, *p* = 0.020), hypoxemia (HR = 1.37, 95% CI = 1.05–1.79, *p* = 0.048), and absence of pupillary reactivity (HR = 1.76, 95% CI = 1.27–2.45 at 7; *p* < 0.001). Additionally, a wide heterogeneity was identified in the frequency (7.9–50.2%) and timing of early tracheostomy practice (0–17.6%) in


*A score > 8 in combination with an estimate of an experienced neurointensivist suggests prolonged ventilation and need of tracheostomy.*

*GCS = glasgow coma scale. ICH = intracerebral hemorrhage. PaO2 = partial arterial pressure of oxygen. APACHE II = acute physiology and chronic health evaluation II. LIS = lung injury score. [62, 63].*

#### **Table 2.**

*SET score to estimate tracheostomy need after severe stroke.*

this cohort. Late tracheostomy (after 7 days) was associated with worse neurological outcomes and a longer stay in the intensive care unit [61].

In acute cerebrovascular events (ischemic stroke, cerebral hemorrhage, and aSH), a specific score for predicting tracheostomy has been designed and tested in these patients. The SET score (**Table 2**) that combines various variables from 3 items (neurological evaluation, characteristics of the injury, and extracerebral organic procedure/function) is the one with the greatest external validation for use in this population. A SET score of >10 points has a sensitivity of 64–81%, a specificity of 57–86%, and an area under the curve of 0.74 (95% CI 0.68–0.81) [62, 63].

In terms of an invasive procedure without complications, percutaneous tracheostomy is practically equivalent to surgical tracheostomy. Some systematic reviews with meta-analyses have found that the former has fewer stoma infections, with similar rates of bleeding and other procedural complications [64–66].

#### **6. Conclusion**

Neurocritical patients represent a particularly challenging subgroup for ventilatory management due to coexistence of acute brain injury associated with other organ failure, the most frequent being respiratory failure. Management of mechanical ventilation should prevent secondary brain injury by ensuring optimal ventilation and oxygenation. The use of additional strategies to standard management of pulmonary protective ventilation (high PEEP, recruitment maneuvers, and extracorporeal circulatory support) in patients with refractory respiratory failure should be individualized and be accompanied by advanced neuromonitoring (invasive measurement of intracranial pressure and cerebral tissue pressure oxygen). It is important to avoid a late withdrawal of mechanical ventilation using adjuvant scales such as the VISAGE score; theorical benefits from tracheostomy include reduction and suspension of sedation and opioid analgesia as well as patient comfort due to lower work of breathing and may be considered in patients with slow neurological recovery, failure to extubation, and those patients with dysphagia or altered state of consciousness resulting from a primary injury to the central nervous system.

#### **Author details**

Thierry Hernández-Gilsoul\*, Jose de Jesús Vidal-Mayo and Alan Alexis Chacon-Corral Emergency Department, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubrian (INCMNSZ), Mexico City, Mexico

\*Address all correspondence to: thierry.hernandezg@incmnsz.mx

© 2021 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

*Mechanical Ventilation in Neurocritical Patients DOI: http://dx.doi.org/10.5772/intechopen.101029*

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### Section 3
