Mechanical Ventilation
Author: Janet Poponick, MD, Assistant Professor, Case Western Reserve University, MetroHealth Medical Center, Cleveland, OH.
Peer Reviewers: Sandra M. Schneider, MD, FACEP, Professor and Chair, Department of Emergency Medicine, University of Rochester, NY; and Michael K. Shafé, MD, FACEP, FAAEM, Assistant Professor, Department of Emergency Medicine, Medical College of Georgia, Augusta.
Mechanical ventilation is known to be a life-saving tool in a variety of situations. Its importance became evident in support of patients with poliomyelitis in the 1950s.1 Since that time, mechanical ventilation has been delivered by a variety of different machines and techniques. Despite the mode of ventilation, the goal remains the same: provide rest to the respiratory muscles and reverse severe hypoxemia and acute respiratory acidosis.2,3
Patients who require mechanical ventilation will require admission to the intensive care unit (ICU) where they will receive treatment of the underlying disease and expert ventilator management by an intensivist. However, many patients spend several hours in the emergency department (ED) awaiting beds in the ICU. The ED physician will need to manage these very ill patients for several hours and, therefore, must be able to recognize and manage complications associated with mechanical ventilation.
This review will provide a guide to ventilator management to aid the ED physician. Pulmonary physiology and adverse effects of artificial ventilation on the pulmonary system will be discussed. Assist control ventilation is the most common mode of ventilation and should be used initially for patients in the ED. Pitfalls of therapy and troubleshooting the ventilator will be reviewed, recognizing that the respiratory therapist is a valuable reference and capable of handling the majority of mechanical ventilation issues. Finally, difficult cases will arise requiring early consultation with a critical care specialist to provide optimal ventilation while avoiding complications. — The Editor
Basic Physiology
Respiration involves ventilation and gas exchange between the atmosphere and the tissues of the body. Breathing is automatic, with air entering and leaving the lungs at a certain volume and rate that compensates for the body’s metabolic needs. (See Table 1.) Under normal circumstances, contraction of the respiratory muscles causes expansion of the chest wall, which leads to negative pressure in the trachea, alveoli, and intrapleural space. This negative pressure allows air to enter the lungs. The volume of air entering the lungs is dependent upon the intrapleural pressure, the resistance to flow in the airways, and the natural recoil of the lungs and chest wall. Negative intrapleural pressure also enhances venous return to the heart. Normally, expiration is a passive phenomenon dependent on elastic recoil properties of the lungs and chest wall.4
Table 1.
Normal Values in Spontaneous Respiration
Mechanical ventilation changes the mechanics of the cardiopulmonary system.4,5 Since the upper airway normally warms and humidifies the air entering the lungs, air delivered through the ventilator must be warmed and humidified artificially. The endotracheal tube (ETT) bypasses the upper airway, increases the resistance to airflow, and may increase bronchoconstriction by stimulating the irritant receptors in the trachea and larynx.
The mechanical ventilator delivers air into the pulmonary system, causing positive pressure to develop in the trachea, alveoli, and intrapleural space. Positive pressure places stress on the alveoli and airways; if too high, the alveoli may rupture leading to barotrauma and pneumothorax. The positive intrapleural pressure impedes venous return, leading to decreased right ventricular filling.5 Pulmonary vascular resistance also is increased, causing decreased left ventricular filling. The end result may be reduced cardiac output and hypotension, especially in a volume-depleted patient.
Indications/Contraindications
Mechanical ventilation is considered treatment for hypoxic and hypercapnic respiratory failure. When conventional methods of treatment have failed, intubation and mechanical ventilation will be necessary. In some cases, noninvasive treatment with BiPAP (bi-level positive airway pressure) may be appropriate for those who remain alert, appropriate, and capable of protecting their airway. BiPAP has been reviewed recently and will not be discussed in detail in this review.6
Indications for mechanical ventilation include acute respiratory failure (ARF), impending respiratory failure, and ventilatory support to rest the respiratory muscles and decrease the work of breathing. The goals are simple: reverse the process that caused respiratory decompensation. In other words, reverse the hypoxemia, reverse the progression of respiratory acidosis, and provide rest for the respiratory muscles. Other indications and objectives may include decreasing systemic or myocardial oxygen consumption (in acute myocardial infarction or sepsis), loss of ability to protect the airway (in overdose or stroke patients), allowing sedation or neuromuscular blockade (therefore allowing a test or procedure to be done safely), preventing or reversing atelectasis, stabilizing the chest wall, and as a temporizing measure to reduce intracranial pressure.1,7,8,9 (See Table 2.)
Table 2.
Indications and Contraindications
to Mechanical Ventilation
A recent, international one-day prevalence study evaluated various aspects of mechanical ventilation.10 The reasons to initiate mechanical ventilation included acute respiratory failure (66%), coma (10%), acute exacerbation of chronic obstructive pulmonary disease [COPD] (13%), and neuromuscular disorders (10%). Subgroups within the ARF group include acute respiratory distress syndrome (ARDS), heart failure, pneumonia, sepsis, complications of surgery, and trauma. The reasons for ventilatory support were similar among the different countries. In this study, 25% of ventilated patients were elderly. Age alone does not influence prognosis of elderly patients in the ICU; prognosis depends on severity of illness and functional status of the patient.
Contraindications to ventilator support are few. Pneumothorax that is untreated or unrecognized may lead to a tension pneumothorax and cardiac arrest. Other reasons to withhold mechanical ventilation are more ethical: patient or family refusal and medical futility.7 (See Table 2.)
Modes of Ventilation
The mode of ventilation refers to how the ventilator delivers a breath to the patient. The most common mode is assist control (AC), which accounted for 47% of ventilated patients in the recent international study.10 Other forms of ventilation used in the ICUs around the world include synchronized intermittent mandatory ventilation (SIMV), pressure support (PS), and a combination of the two.10,11
Ventilation can be done by setting the delivered amount of volume (AC and SIMV) or by setting the amount of pressure used to deliver a breath (PS).9,11 In the ED setting, AC is the preferred initial mode of ventilation. Generally ED patients are intubated using rapid sequence intubation (RSI) techniques and require a mode of ventilation that provides full support of the patient until paralytic agents are metabolized or until the underlying condition is stabilized.
AC ventilation delivers a set tidal volume (TV) and inspiratory flow for all breaths to be delivered. Between the set machine delivered breaths, the patient may initiate his or her own breath, and this breath will be supported at the same TV and flow as the full machine breaths. This mode is useful in patients who require full ventilatory support. It is the mode of choice after RSI, drug overdose, cerebral malfunction in which the patient makes no respiratory effort, or with inadequate respiratory effort. This mode provides complete rest for prolonged periods of time to recuperate from trauma or life-threatening medical illness. The advantages of the AC mode of ventilation are that it provides full support at a guaranteed TV and minute ventilation, and it minimizes the work of breathing while allowing some patient control of respiratory rate and minute ventilation. The disadvantages include the potential for barotrauma due to high pressures if the TV or flow rate is too high, it may be tolerated poorly in a fully awake non-sedated patient, may lead to respiratory alkalosis, may increase the work of breathing if the settings are not correct, and may lead to muscle atrophy if used for a prolonged period of time.
SIMV is a combination of spontaneous breathing and AC in which the ventilator will deliver a set number of mandatory breaths at the preset TV. The patient may breathe between the mandatory breaths at his or her own TV without support of the ventilator. Indications for SIMV ventilation include those patients that require full or partial support, and it commonly is used when the patient is ready to assume more of the work of breathing (weaning process). The advantages are the same as AC with the added advantages that spontaneous breathing may reduce respiratory alkalosis and may preserve respiratory muscle strength. The disadvantage is that work of breathing may be elevated if the ventilator valves do not open easily (patient effort opens the valve that allows air to flow). Also, fatigue and tachypnea may ensue if support is insufficient (SIMV respiratory rate too low).
Finally, pressure support (PS) delivers every breath at a preset pressure and inspiratory time. The major advantage is that the pressure is limited and, therefore, may avoid barotrauma. It also allows the patient to control the rate and minute ventilation, and may be more comfortable for the patient. The disadvantage is that there is no guaranteed TV. PS often is combined with SIMV to allow more patient control and to aid in the weaning process.
Initial Settings (Overview)
The initial settings for mechanical ventilation are just that, initial. (See Table 3.) Every patient on mechanical ventilation requires constant monitoring and changes until stabilized. The mode of ventilation in the ED is usually AC. It allows complete rest of respiratory muscles while aggressive therapy of the underlying process can be initiated. When choosing the initial settings, the physician and respiratory therapist must predict the ventilatory requirements of the patient. This prediction is based on age and size of the patient, as well as the underlying disease process.7,9
Table 3.
Initial Ventilator Settings (General)
An estimate of minute ventilation often is helpful. Normal healthy people have a minute ventilation of 5-7 L/minute. When exercising or stressed, the individual can double the minute ventilation to keep up with metabolic needs. Minute ventilation is a product of TV and respiratory rate. The initial starting point for TV is 8-10 mL/kg and for respiratory rate, 8-12 bpm. The initial settings usually will stabilize the pH and PaCO2. The other setting that the physician should choose is the fraction of inspired oxygen (Fi02). For those patients who are unconscious, known to be hypoxic, or trauma victims, 100% Fi02 usually is chosen. However, if mechanical ventilation is chosen for a patient who is tiring and has an elevated PaCO2 with adequate oxygenation on a 50% mask, it may be appropriate to start at 50% Fi02 and monitor the pulse oximeter.
The respiratory therapist then will set various alarms and pressure limits. The flow rate generally is 40 L/minute, and a normal inspiratory to expiratory (I:E) ratio of 1:3. The peak inspiratory pressure (PIP) alarm usually is set 10 cm of H20 above the pressure that is noted at the set tidal volume. The PIP should not be above 50 cm of H20 as the risk of barotrauma becomes high.
Positive end-expiratory pressure (PEEP) may be added to maintain pressure in the alveoli through the expiratory phase to prevent collapse of the small airways.7,9 (See Table 4.) PEEP is useful in cases of hypoxemia, enabling a reduction in the amount of oxygen required to maintain adequate oxygenation, therefore avoiding oxygen toxicity. By the addition of PEEP, the amount of lung injury may be reduced by preventing the shear forces associated with repeated opening and closing of small airways. In congestive heart failure (CHF), the addition of PEEP further reduces venous return even in those with healthy lungs. Many intensivists believe that 5 cm H20 of PEEP is physiologic and should be used as an initial setting. This amount of PEEP rarely causes problems; however, it is best to confirm endotracheal tube placement and exclude a pneumothorax before adding PEEP to the ventilator settings.
Table 4.
Indications and Contraindications to the Use of PEEP
PEEP also may cause problems in some cases. If too much PEEP is added, alveolar overdistention may occur, leading to pneumothorax. In those who are hypovolemic or have low cardiac output states, PEEP may contribute to further hemodynamic compromise with a decrease in venous return and cardiac output.12,13 In patients with an elevated ICP, PEEP may further increase the ICP by decreasing venous return.7,9
The initial setting should be chosen with the patient’s underlying disease in mind. If the ED physician knows that the cause of acute respiratory failure is ARDS or COPD, then this should be conveyed to the respiratory therapist, and ventilator settings should be chosen accordingly. What follows is a discussion of commonly seen diseases that require changes in ventilator management.
Acute Respiratory Distress Syndrome (ARDS)
Severe injury to the pulmonary parenchyma may result from infection, gastric aspiration, severe trauma, multiple transfusions, fat emboli, or pancreatitis. Sepsis remains the most common precipitating factor of ARDS. The lung injury of ARDS is defined as acute in onset with a Pa02/Fi02 ratio less than 200 mmHg, bilateral pulmonary infiltrates, and the absence of left ventricular failure. Acute lung injury similarly is defined but with a lesser degree of oxygen impairment (Pa02/Fi02 < 300 mmHg).14,15 The prognosis of ARDS generally is poor, with prolonged hospitalizations and a mortality rate of 35-50%.14-16
In ARDS, lung compliance is decreased, making the lungs stiff and difficult to ventilate, resulting in hypoxemic respiratory failure. Lung injury develops from the damaging effects of inflammatory mediators, leading to injury to the vascular and epithelial lining resulting in capillary leak.16 Such patients are difficult to oxygenate and ventilate. Recent animal studies and in vitro studies raise concern of microvascular injury as a direct effect of mechanical ventilation.17 This injury usually is in the context of high volume or pressure, and has been termed ventilator-induced lung injury (VILI).18 High volume and pressure have been associated with overdistention of alveoli and fracture of the capillary-endothelial membrane, leading to leakage of proteins and fluid into the alveoli. An influx of leukocytes and cytokines causes further damage to the pulmonary parenchyma. Standard ventilator settings (the old 10-15 mL/kg tidal volume) have been shown to cause further damage to the lungs, overdistention of alveoli, and barotrauma.19 Because of this concept of VILI, lung protective strategies have been adopted by many intensivists.9,16 The ARDS Network study20 has demonstrated that low tidal volume ventilation is associated with lower mortality and increased days without mechanical ventilation.
The goal tidal volume in protective lung strategies is 4-6 mL/kg with a respiratory rate high enough to maintain an appropriate minute ventilation.20 A Pa02 of 55-80 mmHg with a saturation of 88-95% is acceptable. Initially the patient is placed on the ventilator with a tidal volume of 8-10 mL/kg ideal (or predicted) body weight (see Table 5), then over the course of the next four hours, tidal volume is reduced to 6 mL/kg with minute ventilation maintained by increasing the respiratory rate (no more than 35 breaths/minute).
Table 5.
Body Weight Prediction Rules
The I:E ratio is set between 1:3 and 1:1. Mild hypoxemia is accepted, as high Fi02 may lead to oxygen toxicity. PEEP is added to improve oxygenation as the Fi02 is reduced below 60%. The overall goal is to limit stress on the lungs by maintaining plateau pressure below 30 cm of H20. (See Table 6.) (In the ED setting, it sometimes is easier to follow peak inspiratory pressure and maintain it at a level below 30 cm of H20.)21
Table 6.
Ventilator Settings in ARDS
When following this protocol, the patient may develop respiratory acidosis known as permissive hypercapnea.22 Most patients in the ARDS Network study tolerated the acidosis well, but attention to the patient is important.20,23 The acidosis may lead to arrhythmias and hypotension. In some patients, following the stringent guidelines may not be possible. A more generous plateau pressure of 30-35 cm of H20 may be more appropriate to maintain hemodynamic stability.21 Other maneuvers, such as prone positioning and elevated PEEP trials may be used to recruit lung zones that are not fully functioning.24,25 These primarily are used in the ICU setting and are beyond the scope of ED practice.16,21,24
Despite data supporting the use of low tidal volumes in ARDS being available for 4-6 years, many centers have not adopted the practice.26,27 Some studies have not arrived at the same conclusion as the ARDS Network. One study using low tidal volumes to achieve a peak inspiratory pressure less than 30 cm of H20 concluded that this practice did not reduce mortality and may have increased morbidity in patients deemed to be at high risk for ARDS.21 At this time, however, the ARDS Network protocol20 is the best available large study suggesting that mortality and complications may be reduced by lower tidal volume ventilation.
PEEP is used in patients with ARDS to maintain oxygenation and prevent collapse of alveoli. Since high oxygen concentrations may lead to oxygen toxicity and further pulmonary damage, PEEP is added to lower the Fi02 to maintain saturation of 88-95%.7,9 However, how much PEEP is too much? If distention of alveoli by tidal volumes causes VILI, does PEEP also contribute to this entity? In a recent trial from the ARDS Network group, no difference was demonstrated with low vs. high PEEP.28
Obstructive Pulmonary Diseases
Asthma and COPD are common problems seen in the ED. Aggressive treatment with bronchodilators and steroids will treat an exacerbation successfully in most cases. However, approximately 1-3% of such patients will require artificial ventilation to support oxygenation and rest the fatigued respiratory muscles.29 Noninvasive ventilation with BiPAP has been shown to be effective in carefully chosen cases as bridge therapy until bronchodilators and steroids provide relief.6,30-32 Those that require conventional mechanical ventilation present a challenge. Complications such as profound hypotension and barotrauma are frequent. The mortality rate for patients with asthma who require mechanical ventilation may approach 38%; COPD mortality is also high at 14.4%.29,33
With airway obstruction, expiratory flow is too slow to empty the lungs before the next breath. The result is a higher functional residual capacity (air that remains in the lungs after expiration), leading to gas trapping and dynamic hyperinflation. When these patients are on a ventilator, the higher alveolar pressure needs to be overcome prior to receiving the next breath. Gas trapping and dynamic hyperinflation leads to a higher end-expiratory pressure known as auto-PEEP or intrinsic PEEP. Most ventilators are capable of displaying this value with help from the respiratory therapist. High peak airway pressures are common in obstructive diseases. An elevated airway pressure is a guide to dynamic hyperinflation, and when the plateau pressure is greater than 30 cm of H20, complications such as barotrauma and hypotension ensue.34,35
The key strategy for providing mechanical ventilation to patients with COPD or asthma is to avoid overdistention and keep dynamic hyperinflation to a minimum. Components of dynamic hyperinflation include tidal volume, minute ventilation, and inspiratory time.34 Therefore, tidal volume recommendations remain at 8-10 mL/kg, but should be kept at the low side to reduce overdistention.9 A respiratory rate is chosen to provide adequate ventilation, but should be guided by a need for longer expiratory time: The higher the respiratory rate, the more likely the expiratory phase has not been completed, leading to auto-PEEP and dynamic hyperinflation (sometimes referred to as stacking breaths). Finally, the inspiratory flow rate may be increased to allow a prolonged expiratory phase for those with obstructive lung disease.36,37
In COPD patients, this strategy has been shown to improve gas exchange and pulmonary mechanics.37 However, the patient may require heavy sedation to adequately control the above variables. When setting the ventilator, it also is important to ventilate the patient to his or her baseline arterial blood gas (ABG). Many patients with COPD have a compensated respiratory acidosis. Care must be taken to avoid overventilation and iatrogenic respiratory alkalosis.36
Finally, some patients will have considerable dynamic hyperinflation and auto-PEEP despite the above maneuvers. In some patients with severe obstruction, expiration may be a more active phase of respiration, causing positive pleural pressure and collapse of airways. Low levels of PEEP may be added to counterbalance the collapse of airways allowing more complete expiratory phase. Adding small levels of PEEP does not increase alveolar pressure and may decrease the work of breathing.39
Miscellaneous Conditions
Blunt chest trauma victims may require intubation and mechanical ventilation. It is important to note that some cases of isolated chest trauma may be managed appropriately early with noninvasive ventilation. However, a significant pulmonary contusion may progress to an ARDS-like picture. Initial tidal volume should be 8 mL/kg and lowered if ARDS develops. It is important to ventilate these patients at the lowest airway pressures while maintaining stable hemodynamics.9,25 The addition of PEEP may be necessary to maintain adequate oxygenation; however, it should be added cautiously until pneumothorax has been excluded. Fluid resuscitation is necessary in all trauma victims. Adding PEEP early may cause worsening hypotension if adequate fluid resuscitation has not been initiated.12,13
The burn victim always has a component of smoke inhalation that mimics ARDS. Therefore, low tidal volume ventilation is used to keep airway pressures as low as possible to avoid further lung injury. Burn victims usually are hypermetabolic and will require higher minute ventilation to maintain a normal pH. Carbon monoxide levels also are high, and the Fi02 will need to be maintained at 100% until the carboxyhemoglobin is less than 10%.7
The patient with brain injury as a result of stroke, hepatic failure, post-resuscitation hypoxia, or trauma may require intubation and mechanical ventilation to protect the airway from aspiration.7-9 If the patient has no C-spine issues, the head of the bed should be elevated to 30°. Hyperventilation to treat an elevated ICP no longer is appropriate.9 The key is to maintain an adequate minute ventilation to provide adequate oxygenation, normal pH, and hemodynamic stability. Application of PEEP usually is not necessary; however, low levels of PEEP (5 cm of H20) rarely have an affect on ICP.7
The cardiac patient who presents with pulmonary edema/CHF often is managed best with noninvasive methods of ventilation while diuretic and vasodilator therapy provides reduction of preload and afterload.31,32 However, patients may become more anxious with the tight-fitting mask. Patients who become anxious on noninvasive ventilation, desaturate, or develop chest pain should be intubated promptly and provided full support with mechanical ventilation to decrease the work of breathing and provide adequate oxygen to the myocardium. Ventilator settings are standard initial settings with PEEP.7,9 Frequent monitoring of oxygenation and hemodynamic status is necessary. Positive pressure ventilation and PEEP may adversely affect the compromised myocardium. In some cases, invasive hemodynamic monitoring may be required.12,13
Finally, drug overdose patients may require mechanical ventilation. The usual indications include the obtunded patients, those with signs of ARF, or impending respiratory failure. Those who are out of control despite large doses of sedatives also may require intubation. These patients are the ones that cause the most debate among ED physicians and ICU physicians. Safety of the patient and staff enter into the decision in a busy ED. Most drug overdose patients are young, healthy, and should be ventilated to normal pH.7
Monitoring Mechanical Ventilation
After choosing the initial settings, every patient should be monitored with continuous pulse oximetry and cardiac monitoring, and frequent blood pressures. Initially, a chest x-ray will be required to assess ETT placement, being certain that it is located 3-4 cm above the carina. The chest x-ray will exclude a pneumothorax and potentially confirm the working diagnosis of pneumonia or CHF. An electrocardiogram (ECG) should be performed to exclude cardiac ischemia or infarction. Finally, an ABG should be obtained 15-20 minutes after being placed on mechanical ventilation. Changes in ventilator settings should be done with the respiratory therapist as alarms and pressure limits must be reset for the new settings. Any change in the patient’s hemodynamic status should be followed by a re-evaluation of the patient and the ventilator. (See Table 7.)
Table 7.
Evaluation After Initiation
of Mechanical Ventilator
Complications/Pitfalls
Intubation and mechanical ventilation are not without complications. (See Table 8.) Problems may arise at any time after intubation and throughout the course of mechanical ventilation.39,40 The complications that the ED physician may encounter include hypoxemia, acid-base disturbances (especially respiratory alkalosis), dysrhythmia, and hypotension. Such complications indicate a change in the patient’s status and require prompt assessment, with physical examination, ECG, ABG, and chest x-ray.
Table 8.
Complications of Mechanical Ventilation
Other complications may occur throughout the patient’s course on mechanical ventilation: ventilator malfunction, self-extubation or dislodgement of the ETT, anxiety, nosocomial pneumonia, and VILI. Additional problems may arise while the patient is in the ED, including aspiration, mucous plugging, pneumothorax, and pulmonary edema. Prompt attention with suctioning, chest tube insertion, or diuresis quickly will improve oxygenation. All patients who require mechanical ventilation are at risk for pulmonary embolism; therefore, prophylaxis should be initiated as early in the course of illness as possible.
The use of low tidal volumes may not be appropriate for all patient groups. Low tidal volumes have been shown to be a benefit to patients with ARDS and obstructive lung diseases. A recent retrospective study has documented that the practice of low tidal volume ventilation has become more widespread even in those with no significant lung damage, such as post-operative patients and cardiac patients.41 The use of lower tidal volumes in other populations has been shown to increase the incidence of atelectasis. Therefore, low tidal volumes may not be for everyone. All patients should be monitored carefully when mechanical ventilation is initiated.
Hypoxemia
Hypoxemia in a patient on mechanical ventilation generally is multifactoral.39,42 The most common reason is progression of the underlying disease process such as worsening pneumonia or pulmonary edema, increased bronchospasm, or progression to ARDS. Treatment is directed at the underlying disease process. Procedures commonly done in the ED/ICU, such as central line placement or suctioning, may cause hypoxemia.
Ventilator-related problems also may account for worsening oxygenation.39,42,43 Ventilator settings may have been changed or the ventilator may have an internal problem or have been disconnected. Alarms usually sound, alerting staff to a problem. While the respiratory therapist troubleshoots the ventilator, the patient should be removed from the ventilator and ventilated by bag-valve-ETT on 100% oxygen. The oxygen also may become disconnected from the source, so be certain the tubing is connected to the wall outlet.
It is critical to assess the ETT as part of the evaluation of the hypoxic ventilator patient.7 After intubation, the ETT position generally is noted at centimeters at the lips (or teeth) and confirmed with a chest x-ray. Any change in position can be assessed quickly by noting the position. End-tidal CO2 also will be helpful to confirm ETT placement in the trachea. A repeat chest x-ray may show a new process such as a pneumothorax or the ETT in the right mainstem bronchus.
Hypotension
Hypotension is a common complication of intubation and mechanical ventilation.42,43 The causes include hypoxemia, ETT dislodgement, respiratory alkalosis, cardiac dysrhythmia, ischemia or myocardial infarction, low intravascular volume, positive pressure ventilation, tension pneumothorax, intrinsic PEEP, and sedation. Usually hypotension is multifactoral. The effects of sedation and paralytic agents alone rarely are the only cause of the hypotensive episode.
The most common cause of hypotension is the combination of low intravascular volume with the addition of positive pressure ventilation. The intrathoracic pressure during the inspiratory phase of mechanical ventilation is positive, causing two adverse effects on the heart: it decreases right ventricular filling by decreasing venous return, and it increases pulmonary vascular resistance, causing a decrease in left ventricular filling. This leads to a reduced cardiac output, which causes hypotension. The decreased venous return and cardiac output mimic a low intravascular volume and further adds to the effects of dehydration. The hypotensive episode can be quite profound, giving a picture of hypovolemic shock. Even the patient with COPD may be dehydrated because of fever or insensible losses from hyperventilation. It is not unusual to infuse more than one liter of crystalloid solution during such an episode.
Barotrauma caused by positive pressure ventilation may cause hypotension. Tension pneumothorax, simple pneumothorax, and pneumomediastinum all may develop in the course of mechanical ventilation. An unrecognized simple pneumothorax may be converted to a life-threatening tension pneumothorax when mechanical ventilation is instituted. Recognition and treatment of pneumothorax are life-saving in the hypotension associated with mechanical ventilation.
Hypotension may be the result of intrinsic PEEP, or unintentional end-expiratory pressure, or auto-PEEP.9 Patients with severe bronchospasm or emphysema are most likely to develop this complication. Prior to intubation, such patients have a prolonged inspiratory to expiratory phase ratio; if not given enough time to exhale, air becomes trapped in the alveoli at end expiration. This increases intrathoracic pressure, leading to barotrauma and hypotension. The respiratory therapist can measure auto-PEEP and increase the inspiratory flow rate to allow for more time in the expiratory phase.37 PEEP may also be added to counteract the auto-PEEP.38 If these maneuvers fail, the patient may require sedation until the bronchospasm is treated effectively.
Acute myocardial infarction or ischemia also may occur due to the stress of illness in those with risk factors. Dysrhythmias also may develop secondary to hypoxemia, electrolyte abnormalities, especially potassium and magnesium. A post-intubation ECG is recommended.
Respiratory Alkalosis
This acid-base abnormality is quite common, especially in the patient with COPD who has known hypercapnea.36 Often the initial settings cause normalization of the PaCO2. The patient may have had a compensated respiratory acidosis prior to starting mechanical ventilation. If ventilated to a normal PaCO2, alkalosis ensues and may precipitate hypotension, cardiac dysrhythmias, and cardiac arrest. To avoid this common problem in the COPD patient, the ventilator should be set to achieve a PaC02 at the patient’s baseline, or to a low normal pH. The goal of mechanical ventilation is to achieve adequate oxygenation and a pH within the normal range.
Anxiety
Agitation and anxiety may be the result of hypoxia, medications, drugs of abuse or withdrawal, metabolic disorders, or infections.42 Hypoxia is probably the most important cause of anxiety.39 The ETT may have changed positions or is at the carina causing bronchospasm and the feeling of dyspnea that leads to anxiety.
Sudden onset of anxiety in a previously calm patient should alert the staff. The differential diagnosis includes hypoxia, ETT dislodgement, or pneumothorax. The patient should be removed from the ventilator, bagged with 100% oxygen, and suctioned while the respiratory therapist checks the ventilator. An ECG and chest x-ray should be obtained. Benzodiazepines are an ideal treatment in this situation, allowing rest and relief of anxiety.
Pneumonia
Nosocomial pneumonia is a leading cause of death in hospitalized patients.44 Pneumonia increases when a patient is on mechanical ventilation and is referred to as ventilator-associated pneumonia (VAP).45 When VAP occurs early (within 48-72 hours) antibiotic-sensitive bacteria usually are the cause. VAP that occurs after this period frequently is due to antibiotic-resistant organisms such as Pseudomonas aeruginosa, Staphylococcus aureus, and Enterobacter species. Mortality may be as high as 10%, especially in the cases of late-onset VAP.
Respiratory Distress While on Mechanical Ventilation
More often, patients who are critically ill spend several hours in the ED awaiting an ICU bed. Complex patients who are on mechanical ventilators require close monitoring, frequent suctioning, ABGs, and frequent changes in therapy. The respiratory therapist plays a vital role in maintaining the ventilator and monitoring the patient. Some difficult cases, such as ARDS or severe asthma, may benefit from early consultation with the intensivist.
At some point during the patient’s stay, the ED physician may be notified of a sudden change in status. This may be defined as an increase in heart rate or respiratory rate, a desaturation, or if awake, a complaint of shortness of breath, air hunger, or anxiety. While it is easy to assume that the patient is awakening from paralysis and may require sedation, a systematic approach should be used to exclude complications. (See Figure 1.) Complications such a pneumothorax, hypoxia, myocardial infarction, or loss of airway can occur at any point during mechanical ventilation.
When confronted with the patient with sudden respiratory distress or change in status, the problem may be a patient-centered problem or a ventilator problem. Assessment for either source of the problem should be performed simultaneously with the help of the respiratory therapist. The first step always should be removing the patient from the ventilator and providing ventilation by bag-valve-ETT with 100% Fi02. While the patient is being ventilated manually, assess the vital signs and pulse oximetry, auscultate the chest, and note symmetry of chest rise with ventilation. If the patient improves with manual ventilation, then the problem is in the ventilator or the patient is fighting the ventilator. While the physician evaluates the patient, the respiratory therapist will perform a detailed check on the ventilator, looking for air leaks, appropriate oxygen levels and settings, and overall performance of the machine.
If there is no improvement with manual ventilation, then assess the airway. If it is difficult to bag or ventilate the patient, there is increased resistance to airflow. There may be an obstruction to the airway or a pneumothorax. The patient should be suctioned to relieve the obstruction by secretions, or if unable to pass the catheter, consider an actual ETT problem. If it is easy to ventilate the patient and there seems to be no resistance to airflow, the ETT may have been dislodged or there is a cuff leak. If manual ventilation is normal, the airway is not the problem; therefore, other reasons for the patient’s distress should be assessed. (See Table 8.)
For the patient who remains in distress and may be fighting the ventilator, sedation may be the appropriate option. However, it is important to evaluate the chosen ventilator settings closely with the respiratory therapists or consultant. The settings may not be appropriate. For example, the patient may require a longer time to exhale, or may require smaller tidal volume and a higher respiratory rate to feel comfortable.
Conclusion
The ED physician will treat many patients with ARF who may require mechanical ventilation. It is important to determine the cause of ARF and choose ventilator settings based on the underlying pathology (or potential pathology). Recent data support ventilating patients with lower tidal volumes for those with ARDS or obstructive lung diseases to avoid parenchymal lung injury and pneumothorax. Consulting the respiratory therapist or intensivist is a valuable step in managing the difficult cases.
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This review will provide a guide to ventilator management to aid the ED physician. Pulmonary physiology and adverse effects of artificial ventilation on the pulmonary system will be discussed. Assist control ventilation is the most common mode of ventilation and should be used initially for patients in the ED. Pitfalls of therapy and troubleshooting the ventilator will be reviewed, recognizing that the respiratory therapist is a valuable reference and capable of handling the majority of mechanical ventilation issues. Finally, difficult cases will arise requiring early consultation with a critical care specialist to provide optimal ventilation while avoiding complications.
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