Scholarly article on topic 'Ventilatory strategies in trauma patients'

Ventilatory strategies in trauma patients Academic research paper on "Medical engineering"

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Academic research paper on topic "Ventilatory strategies in trauma patients"

Review Article

Ventilatory strategies in trauma patients

Shubhangi Arora, Preet Mohinder Singh1, Anjan Trikha

Departments of Anaesthesia, All India Institute of Medical Sciences, Delhi, 'Postgraduate Institute of Medical Education and Research, Chandigarh, India


Lung injury in trauma patients can occur because of direct injury to lung or due to secondary effects of injury elsewhere for example fat embolism from a long bone fracture, or due to response to a systemic insult such as; acute respiratory distress syndrome (ARDS) secondary to sepsis or transfusion related lung injury. There are certain special situations like head injury where the primary culprit is not the lung, but the brain and the ventilator strategy is aimed at preserving the brain tissue and the respiratory system takes a second place. The present article aims to delineate the strategies addressing practical problems and challenges faced by intensivists dealing with trauma patients with or without healthy lungs. The lung protective strategies along with newer trends in ventilation are discussed. Ventilatory management for specific organ system trauma are highlighted and their physiological base is presented.

Key Words: Modes of ventilation for trauma patients, recent trends in trauma ventilatory management, trauma ventilation

the end, special ventilator modes and newer strategies have also been reviewed.

Chest trauma

Trauma to the chest can lead to conditions like flail chest, pneumothorax, bronchopleural fistula, tracheobronchial rupture, and pulmonary contusion. Bony injury of chest wall may lead to respiratory failure due to malfunction of the respiratory muscles or inadequate voluntary breathing due to pain. In most cases of flail chest; adequate analgesia in the form of thoracic epidural, intercostal nerve blocks, paravertebral blocks, pleural catheter, and chest physiotherapy with regular clearance of secretions is sufficient. Mechanical ventilation is reserved for patients with pulmonary contusion and/or respiratory distress and blood gas abnormality (pO2 < 60 mmHg and pCO2 > 60 mmHg).[1,2]

Pneumothorax usually needs only chest tube drainage. In case mechanical ventilation is needed, a thoracostomy tube should be inserted to prevent the development of tension pneumothorax.[1]

In the presence of a bronchopleural fistula, thoracostomy tube closure during inspiration and release during expiration may be done to minimize air leak.[3,4] Another method can be the use of positive intrapleural pressure equal to the positive end expiratory pressure (PEEP) used.[5] In case of large bronchopleural fistula with massive air leaks, independent lung ventilation (ILV) may be required.[6] Other strategies include high frequency oscillatory ventilation (HFOV)[7] and ventilation of the healthy side while keeping the affected side open to the atmosphere or to a high oxygen tension source.[8]


With the increasing advances in technology and economical boost; the emergency physicians, surgeons, and anesthesiologists are likely to encounter more and more cases of severe trauma in the coming years. Lung injury in trauma patients can occur because of direct injury to lung or due to secondary effects of injury elsewhere, for example, fat embolism from a long bone fracture, or due to response to a systemic insult such as; acute respiratory distress syndrome (ARDS) secondary to sepsis or transfusion related lung injury. There are certain special situations like head injury where the primary culprit is not the lung, but the brain that necessitates mechanical ventilation. The ventilator strategy here is aimed at preserving the brain tissue and the respiratory system takes a second place. This article will familiarize the reader with the various ventilator strategies used in trauma victims depending upon the system compromised. Special situations like head injury and burns are discussed. In

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DOI: 10.4103/0974-2700.125635

Tracheobronchial rupture presents with dyspnea, pneumomediastinum, and pneumothorax which does not resolve with thoracostomy. Intubation for airway management should be done in awake state so as not to enlarge the ruptures by positive pressure. Rupture below the carina requires the use of a double lumen tube (DLT). Univent blockers and fogarty catheters have been used to isolate ruptures present further distally.[9] Surgery is the definitive treatment. ILV may be used in postoperative period to protect the bronchial anastamosis.[10]

Pulmonary contusion leads to breakdown of the fibroelastic skeleton of the lung.[11] Not only the affected side, but also the contralateral side has been shown to be affected.[12] Systemic inflammatory responses such as complement activation, increase in systemic inflammatory cytokines, and decrease in systemic cellular immunity have also been reported which are known to further increase during mechanical ventilation.[13]

All the above mechanisms lead to decrease in the compliance of the affected part of the lung. To counter this high pressures are needed. This high pressure gets preferentially distributed to the normal areas of the lung leading to volutrauma (injury due to overdistension of the alveoli) and barotrauma (injury due to high positive pressure) in this region. Atelectrauma (trauma due to repeated opening and closing of the alveoli) to the injured area occurs due to shear forces. All of these together are known as ventilator associated lung injury (VALI).

Intermittent positive pressure ventilation (IPPV) usually forms the cornerstone of management of pulmonary contusion. There is no evidence to suggest if volume based or pressure based mode is preferable in these patients.[14] The ventilatory goal in this situation is protective lung ventilation with low FiO2, plateau pressure (Pplat), and tidal volumes so as to prevent VALI even if the physiological parameters (SpO2, CO2, and pH) do not get fully corrected.[15] The tidal volume should be limited to <6 ml/kg ideal body weight and Pplat to below 30 cmH2O. If possible a Pplat of < 28 cmH2O is preferable.[16] FiO2 (preferably less than 0.6) should be kept as low as possible so as to obtain a PaO2 of 60-80 mmHg or a saturation of 3 90%. The PEEP should be optimal, that is, up to 14-16 cmH2O in severely compromised patients, provided, hemodynamic stability is maintained. Hypercapnia can be tolerated as long as blood pH is above 7.2.[8]

Noninvasive positive pressure ventilation (NIV) may be used in suitable patients in the form of continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP) titrated to provide optimal oxygenation and CO2 removal at lowest possible inspiratory pressures so as to avoid hypotension.[17] However, if PEEP or expiratory positive airway pressure (EPAP) of >12 cmH2O is required, IPPV should be considered.[1]

Abdominal trauma

Abdominal trauma can cause severe pain and lead to shallow breathing and nonclearance of secretions and hence increased

risk of pneumonia. Use of mechanical ventilation early on in these patients has been shown to decrease the incidence of pneumonia. However, mechanical ventilation for longer than 5 days increases the risk of the late onset pneumonia.[18] Epidural analgesia helps to reduce these complications both by providing pain relief as well as by decreasing proinflammatory cytokines. Adequate suctioning and clearance of secretions is mandatory.

Head trauma

Head trauma patients usually require ventilator support due to respiratory failure secondary to impaired consciousness, decreased respiratory drive, chest injury, or ARDS. In case of isolated brain injury a degree of vulnerability is present in the lung tissue secondary to the proinflammatory state.[19-21] This is aggravated by the use of high tidal volumes.[22]

The main goal of ventilation in head injury patients has been to keep a low PaCO2 so as to prevent an increase in intracranial pressure (ICP) secondary to cerebral vasodilation. However, this can lead to reduced cerebral blood flow which can lead to cerebral ischemia.[23,24] Guidelines stated by Brain Trauma Foundation (BTF) suggest that:[16

1. Prophylactic hyperventilation to a PaCO2 £ 25 mmHg (in the absence of intracranial hypertension) is not recommended (level II evidence).

2. Hyperventilation is only recommended as a temporizing measure for the reduction of elevated ICP (level III evidence).

3. Hyperventilation should be avoided during the first 24 h after injury when cerebral blood flow is often critically reduced.

4. If hyperventilation is used, cerebral oxygen delivery should be monitored by jugular oxygen saturation (SjO2) or brain oxygen tension (PbrO2).

They recommend that oxygenation should be monitored and hypoxia (PaO2 < 60 mmHg or O2 saturation <90%) avoided. Mascia et aL, report that for isolated head injury an average minute ventilation of 7.6 l/min in order to maintain a PaCO2 of 35 cmH2O should suffice.[22]

In case traumatic brain injury and acute lung injury are present together the control of PaCO2 takes the priority/20 even if higher tidal volumes, which lead to pulmonary injury are required.

Maintenance of oxygenation may require high levels of PEEP which may compromise the cerebral circulation by a number of mechanisms. In some patients PEEP may lead to overdistension of the normal alveoli leading to an increase in dead space rather than recruitment of the atelectatic alveoli.[25] This will lead to an increase in PaCO2 leading to cerebral vasodilation and a potentially harmful rise in ICP. PEEP may get passively transmitted to the right atrium, increasing its pressure, and thus that of the internal jugular vein (IJV) and impair the cerebral venous drainage.[26] This would in turn lead to a rise in ICP. Also, PEEP may reduce the cerebral blood flow by decreasing the systemic arterial pressure due to decrease in venous return to

the heart. This may lead to vasodilation in the areas of the brain where autoregulation is preserved. This would in turn lead to a rise in ICP due to already compromised compliance.[27]

To maintain cerebral venous drainage a head up position of 30 degrees may be used, which allows some blood flow to occur through the vertebral veins which are not affected by the PEEP.[28] Also, keeping a PEEP lower than the initial ICP of the patient has been found to be useful.[29,30] Euvolemia will prevent the effect of PEEP on cerebral arterial blood pressure.[31]

In cases where very high levels of PEEP are necessary to maintain cerebral oxygenation, new alternative strategies may be used. High frequency percussive ventilation (HFPV) has not only been shown to improve oxygenation and decrease airway pressures, but also to decrease ICP in head injury patients with ARDS.[32,33] Tracheal gas insufflations (TGI) is a form of ventilation in which insufflations of gas in the trachea in the middle of or at the end of expiration clears CO2 while maintaining lung protective ventilation.[34] Low frequency positive pressure ventilation with extracorporeal removal of CO2 (LFPPV-ECCO2R) maintains the lungs at the functional residual capacity (FRC) to prevent lung injury and ensures oxygenation, while the CO2 is removed through a bypass circuit.[35] More recently, pumpless assist systems which do not require heparinization have also come up.[36,37] Extracorporeal membrane oxygenation (ECMO) and HFOV[38] are other useful techniques. Prone positioning may be useful.[39] However, a recent study reports an increase in ICP in prone position.[40]

Tracheostomy is necessary in all those cases where an oral or nasal intubation is contraindicated such as maxillofacial trauma. Also in cases of upper airway obstruction such as neck hematoma, or damage to vocal cords, vocal cord palsy it may be the only way to secure the airway. In other cases if more than 2 weeks of ventilator support is anticipated, a tracheostomy should be considered.[41]


Patients suffering from burns may require mechanical ventilation for two reasons:

1. Compromise of the upper airway: Not only can burn injury to the face, mouth, and neck compromise the airway; heat may cause edema of the lips tongue, epiglottis, and aryepiglottic folds. Due to spasm of the vocal cords the lower part of the airway is spared from this damage.

2. Another reason can be toxic injury to the capillary endothelium, the epithelium of the airway, the bronchi, and the mucuciliary apparatus; leading to pulmonary edema and bronchospasm.

Since 1997 there has been an increase in the use of mechanical ventilation in burn patients. This has been attributed to change in emergency trauma management strategies.[42] Mechanical

ventilation also increases fluid retention in burn patients regardless of inhalational injury.[43] High percentage of burns, head and neck burns, flame injury, and inhalational injury increase the risk of mechanical ventilation.[44] Presence of cutaneous burn increases the risk of pulmonary edema due to administration of large fluid load to the injured lungs.[45] Use of bronchoscopy to remove secretions and debris significantly reduces the duration of mechanical ventilation patients with burns and inhalational injury.[46]

Ventilator strategies

Hemodynamically stable conscious patients without any significant facial trauma are the primary candidates for the use of NIV NIV should be initiated early on in burn patients, at the time of aggressive fluid resuscitation before the signs of upper airway compromise occur.

Invasive ventilation

Lung protective ventilation with low tidal volumes, limited Pplat (<30 cmH2O), and permissive hypercapnia should be used, as detailed above for pulmonary contusion. Airway pressure release ventilation (APRV), HFOV, and ECMO[47] have also found to be useful in these patients. A number of studies have recently come up for the use of HFPV in patients of inhalational injuries. It has been shown to improve the morbidity and mortality in patients with <40% burns.[48] It provides better oxygenation at lower FiO2 levels than conventional ventilation[49] without compromising the hemodynamics.[50,51]

ARDS (Acute Repiratory Distress Syndrome)

Severe trauma patients, without any direct injury to the lung (e.g., chest trauma or inhalational injury) may develop ARDS secondary to multiple factors such as sepsis, fat embolism, chest infection, blood transfusion, etc. The management of ARDS in trauma is same as in other patients of ARDS, the key point being lung protective ventilation. Newer complex modes of ventilation such as APRV, HFOV, HFPV, and ECMO are also being used in these patients.

Special ventilation strategies

Special ventilation strategies may be required in cases of ARDS or chest trauma when adequate oxygenation is not achieved in spite of maximum allowable support with conventional ventilation. ILV also finds use in cases of massive chest trauma where lung isolation may be necessary due to bleeding or infection.

ILV: One lung ILV (OL-LIV) is primarily used for containment of harmful fluids, secretions, and blood. It can be achieved by a DLT, or a bronchial blocker which is placed with the help of a flexible bronchoscope. Although the DLT can be blindly inserted, it is preferable to use a flexible bronchoscope, since it allows exact delineation of the bleeding area. However, when the site of bleeding is unknown it is necessary to use a DLT to ensure lung isolation. Two lung ILV (TL-ILV) may be synchronous when the two lungs are ventilated at the same rate

or asynchronous when the rates are different. TL-ILV can be used to ventilate each lung with a different level of PEEP or even with a different mode of ventilation tailored to the specific requirement of each lung.[6]


The open lung concept was first introduced by Lachman in 1992.[52] It focuses on keeping the alveoli open both during inspiration and expiration. This helps to avoid volutrauma in the normal alveoli with normal compliance, while at the same time preventing collapse in the injured alveoli, thus preventing atetlectrauma. While HFOV achieves this by maintaining a constant airway pressure and delivering low tidal volume at a high frequency around it, APRV achieves this by keeping the lung in the inspiratory state and allowing expiration only at the time of release. Hence, while HFOV keeps the lung open at the deflation limb of the pressure volume curve, APRV does the same at the inflation limb.[53] Thus in contrast to HFOV, APRV not only allows spontaneous ventilation, it also decreases the work of breathing associated with it. By allowing spontaneous ventilation it decreases the shunt fraction as well.[54]


It is a relatively newer mode of ventilation first described by Stock et aL, in 1987.[55] This mode can be defined as CPAP with intermittent, brief release of pressure at regular intervals when the pressure falls to a baseline pressure and expiration takes place. The tidal volume depends upon the difference in these two pressure levels. Since it allows spontaneous breathing in any phase of the respiratory cycle it precludes the need for heavy sedation. This is a pressure limited time cycled mode.[55] The ventilatory support of APRV depends upon the difference in the two pressure levels and their duration. The oxygenation is determined by the FiO2, the CPAP, and the duration for which the CPAP is given; while the ventilation is determined by the difference between the two pressures (which determines the tidal volume), duration of release, and the spontaneous breathing of the patient. Over the first 24 h of APRV alveoli get recruited, hence there is an initial improvement in oxygenation.!56! The gas exchange takes place by convection, diffusion, cardiogenic mixing,[57] and spontaneous ventilation. When initiated for the first time, CPAP should be equal to the Pplat of the patient when on conventional ventilator and its duration should be kept as high as possible to prevent alveolar derecruitment. To wean the patient from APRV, the level of CPAP is decreased and its duration increased so that the number of releases decreases. Shift to conventional ventilation can be done once the CPAP has been reduced to 20 cmH2O, its duration increased to 6 s at FiO2 of 0.4.[53] APRV may lead to hemodynamic instability. It is contraindicated in nonspontaneously breathing patients. It is also contraindicated in severe obstructive disease.


The basic principle of HFOV is maintaining a constant mean airway pressure (mP) that keeps the alveoli open while delivering a very low tidal volume at a very high rate.

In a consensus article, Fessler et al.,[58] suggested that HFOV should be used:

1. If the FiO2 requirement is >70% with a PEEP of >14 cmH2O to maintain adequate gas exchange.

2. If the pH < 7.25 with a tidal volume of >6 ml/kg and Pplat > 30 cmH2O.

It is important to open up the lung before the start of HFOV, for it to have any beneficial effect. Recruitment may be required for the first few days of HFOV[58] HFOV uses a piston attached to a diaphragm and oscillates it to deliver a fixed small tidal volume (1-2 ml/kg) at 3-10 Hz (or 180-600/min). The amplitude of oscillation is usually 60-90 cmH2O at the upper airways. As we go down the respiratory tract, the oscillations dampen and at the level of alveoli a constant mP is present, which is usually 3-5 cmH2O above the mP required prior to HFOV This pressure can be altered by changing the inspiratory flow. The ventilation and oxygenation are decoupled in HFOV Ventilation depends upon the pressure gradient (dP) in the upper airways, while the oxygenation depends on the mP in the lower airways and FiO2.[53] Since the expiration is also active, there is reduced chance of air trapping and hyperinflation.[59]

The mechanism of gas exchange changes from convection to diffusion. The main mechanisms of gas exchange suggested are[60] direct bulk flow to alveoli close to proximal airways, lateral convective mixing, pendelluft phenomenon (asynchronous flow among alveoli due to asymmetries in gas impedance), Taylor dispersion (radial diffusion due to concentration differences), collateral ventilation through nonairway connections, and cardiogenic oscillations.

HFOV can lead to atelectasis if the lung is not recruited prior to initiation. Other adverse effects include hemodynamic instability especially in hypovolemic patients, volutrauma and barotrauma, and a risk of pneumothorax.[53]

Weaning from HFOV should be attempted only once the Paw has been reduced to 20-25 cmH2O and the FiO2 to less than 40% and the patient is able to maintain a saturation of 88% or greater.[53]


HFPV has been described as a "hybrid" of conventional pressure control ventilation (PCV) and HFOV[61] A special valve called phasitron is used to deliver low tidal volumes at a high frequency of 200-900/min (just like HFOV) at two different steady baseline pressure levels (the inspiratory and expiratory

pressure levels of PCV). The frequency of switch between these two pressure levels is 12-15/min, that is, the typical respiratory rate set in conventional PCV[62] HFPV allows use of low FiO2, clears secretions, and is associated with a steady improvement in PaO2/FiO2 ratio without any adverse effects on hemodynamics.[48,63,64]


ECMO was first described by Hill et a/.,[65] It is a method of gas exchange outside the body so as to expose the lungs to minimal volume, pressure, rate, and FiO2 and thus allow them to recover. Anticoagulation may pose a problem in severe trauma patients. Cost is another issue. As of now it is reserved for patients with isolated lung injuries^6


Closed loop ventilation is a newer technology in which a computer changes the FiO2 and other ventilator parameters based on the patient's response, for example, SpO2. This mode thus aids in weaning the patient. Another mode is adaptive support ventilation (ASV) which uses a target expired volume based on the patient's body weight to adjust the ventilator parameters in order to achieve the same.[66]

Partial liquid ventilation was first described by Clark and Gollan.[67] This method uses perflourocarbons instead of gaseous mixture to ventilate the lungs. They are theorized to allow free diffusion of O2 and CO2 across the alveolocapillary membrane, provide a PEEP to prevent atelectasis, and have surfactant properties. However as of now, none of the clinical studies have proven the benefit of this technique.[6]


Prone position leads to a change in the shape and mechanical properties of the chest wall. It also leads to change in alveolar ventilation and distribution, as well as perfusion. This leads to more homogenous ventilation and perfusion and hence improves oxygenation.[68]

Johannigman et a/., reported that administration of nitric oxide to either the normal lung or both the lungs resulted in improvement of oxygenation along with differential ventilation. They attributed this to vasodilation in the normal lung leading to a decrease in ventilation/perfusion (V/Q) mismatch.[69]


As the cases of severe trauma are on the rise, it is important to familiarize the physicians attending to trauma emergencies to the various aspects of respiratory support in cases of trauma.

Protective lung ventilation forms the basis of respiratory support in most cases of chest trauma and toxic injury to the lung. Isolation of the lungs becomes important when one lung is severely injured and needs rest, while the other is imperative to maintain oxygenation of the body. The brain takes the upper hand when both pulmonary and head injury are concomitantly present. Several newer modes of ventilation have come up which are based on "open lung" concept and aim at putting the lung through minimum possible stress while still continuing to use them of oxygenation. ECMO is the last resort, where, the job of ventilation is completely or partially taken over by the machine.


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How to cite this article: Arora S, Singh PM, Trikha A. Ventilatory strategies in trauma patients. J Emerg Trauma Shock 2014;7:25-31. Received: 09.07.13. Accepted: 02.09.13. Source of Support: Nil. Conflict of Interest: None declared.

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