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Assessment of respiratory distress in the mechanically ventilated patient

Assessment of respiratory distress in the mechanically ventilated patient
Literature review current through: Jan 2024.
This topic last updated: Jun 15, 2022.

INTRODUCTION — Patients undergoing mechanical ventilation can develop respiratory distress, which is often referred to as "bucking" or "fighting" the ventilator (also known as patient-ventilator dyssynchrony) [1]. Detecting and effectively treating respiratory distress and improving patient-ventilator interaction is an important skill for clinicians who care for ventilated patients, since some of the associated causative conditions are immediately life threatening [2].

The differential diagnosis and evaluation of respiratory distress in a previously stable patient receiving mechanical ventilation will be reviewed here. The ventilator management of acute respiratory distress syndrome is discussed separately. (See "Acute respiratory distress syndrome: Ventilator management strategies for adults".)

ETIOLOGIES — The etiologies of respiratory distress in a mechanically ventilated patient are listed in the table (table 1). Common causes include errors in ventilator settings, endotracheal tube (ETT) obstruction, ETT or cuff leak, ETT displacement, mucus plugging, acute cardiogenic pulmonary edema, aspiration, pneumothorax, inadequate sedation, and compression of the lungs by pleural fluid or ascites.

In brief, etiologies are grouped as follows:

Ventilator equipment and settings – Errors in ventilator settings are common, especially when patients develop respiratory distress any time a ventilator setting is initiated or changed (eg, after the initiation of mechanical ventilation, following procedures or transport) [3]. Alternatively, the ventilator and ventilator circuit (including the heat moisture exchanger [HME]) may be a source of an airway leak or obstruction or be subject to a technical malfunction.

Airway issues – In a ventilated patient, the airway consists of the artificial airway, which is composed of the ETT, ventilator tubing, HME, and the native airways (ie, trachea and bronchi) [4-7]. Airway issues cause respiratory distress by increasing airway resistance.

Artificial airway issues:

-ETT obstruction – ETT obstruction (partial or complete) most commonly occurs due to inspissated secretions (picture 1) but can also be due to blood, torsion, ETT kinking (picture 2), or a foreign body [8]. Occasionally, the patient can bite on the ETT causing partial obstruction. Rarely, herniation of the ETT cuff over the end of the tube has been reported as a cause of respiratory distress and increased airway pressures [9].

-ETT or cuff leak – The balloon cuff at the end of the ETT can leak or rupture. Patients can also bite through the pilot balloon tube (ie, the tube that is used to inflate the cuff (picture 3)) or through the ETT itself [10].

-ETT displacement – The ETT can migrate out of position (figure 1A-B) superiorly (cephalad) above the vocal cords resulting in an air leak. Inferior (caudal) migration may result in mainstem intubation (typically right sided) [11]. Displacement can occur due to patient-related neck or other movements or to external factors such as turning, prone positioning, and transport.

-HME malfunction or ventilator tubing obstruction – Occasionally, respiratory distress occurs when the HME is obstructed or malfunctions or when ventilator tubing is kinked or obstructed with excess of secretions. (See "The ventilator circuit".)

Native airway issues:

-Mucus plugging with or without atelectasis – Abundant thick airway secretions, blood, or a foreign body may become impacted in a large- or medium-sized airway, causing distal obstruction and atelectasis. (See "Airway foreign bodies in adults".)

-Bronchospasm – Bronchospasm occurs most commonly in patients with obstructive lung disease or volume overload but may also be induced by bronchoscopy, airway suctioning, administration of beta-adrenergic receptor blockers, and allergic reactions to medications.

Pulmonary parenchyma (including dynamic hyperinflation [DHI]) and vasculature issues – Atelectasis, pneumonia, aspiration of oropharyngeal or gastroesophageal contents, pulmonary edema, pulmonary embolus (thrombo-, gas-, fat-, or amniotic fluid- embolism), and other rare conditions (eg, diffuse alveolar hemorrhage) can all cause respiratory distress in patients undergoing mechanical ventilation.

DHI (auto-PEEP) is another cause of respiratory distress. DHI is characterized by increased levels of intrinsic positive end-expiratory pressure (PEEPi or "auto-PEEP"). The hyperinflation is progressive (dynamic) because air accumulates in the lung with each breath as a result of a failure to achieve complete exhalation before the onset of the next breath (figure 2). Auto-PEEP usually occurs in the setting of acute or chronic airflow obstruction. It may also occur in patients with markedly increased minute ventilation (eg, acute respiratory distress syndrome) and may be precipitated by ventilator setting changes such as an increase in minute ventilation or a reduction in the peak inspiratory flow rate.

Acute pleural disorders – Acute pleural processes can cause respiratory distress by restricting inspiration. This includes pneumothorax and large pleural effusions. (See "Clinical presentation and diagnosis of pneumothorax" and "Treatment of secondary spontaneous pneumothorax in adults" and "Indications for bedside ultrasonography in the critically ill adult patient", section on 'Thoracic ultrasonography'.)

Extrapulmonary disorders – Extrapulmonary processes can cause respiratory distress by restricting inspiration (eg, ascites, ileus, or splinting from abdominal pain) or increasing respiratory drive (eg, fever, shock, pain, delirium, and anxiety).

CLINICAL FEATURES AND INITIAL RAPID BEDSIDE ASSESSMENT — Patients with respiratory distress on mechanical ventilation often appear anxious or agitated and are dyssynchronous with the ventilator (ie, a mismatch between the patient and ventilator-assisted breathing). Patients typically have tachypnea and tachycardia, use their accessory muscles of breathing, have uncoordinated thoracic wall or abdominal movement, or have evidence of deteriorating gas exchange [12]. Because respiratory distress may signify the onset of a life-threatening complication, an initial rapid, focused evaluation is required (algorithm 1 and figure 3). The purpose of the initial evaluation is to perform the following:

Perform a rapidly assessment of cardiopulmonary status

Rapidly assess the patient and the monitoring equipment (including ventilator mechanics and graphics, if time allows)

Identify the likely problem at hand

Perform initial maneuvers to treat the presumed cause

Put in place additional and follow-up testing and preventative measures, as needed

During the initial assessment, we keep in mind the common etiologies including endotracheal tube (ETT) obstruction, air leak or ETT displacement, acute cardiogenic pulmonary edema, aspiration, mucus plugging, inadequate sedation, large pleural effusion, or ascites. Other etiologies to keep in mind include those likely to occur in the setting of recent events such as tension pneumothorax following central catheter placement, acute cardiogenic pulmonary edema following the administration of fluid or blood products, or ventilator setting errors following transport (table 1). Although a comprehensive evaluation is ideal in all patients, those with cardiorespiratory instability require more urgent attention and the workflow is different. (See 'Cardiorespiratory instability' below and 'Cardiorespiratory stability' below.)

For the purposes of this topic, this assessment does not comprise patients who require advanced cardiac life support. (See "Advanced cardiac life support (ACLS) in adults".)

CARDIORESPIRATORY INSTABILITY — If respiratory distress is severe or the patient is hemodynamically unstable, stabilization must take precedence over a detailed evaluation or diagnostic procedures (algorithm 1). The evaluation and management are team focused, such that the clinician, respiratory therapist, and nursing staff work together to avoid further deterioration. If adequate staff is available, assigning key roles may be helpful (eg, one is assigned to examine the ventilator and circuitry while another assesses the patient).

Disconnection, bag ventilation, and capnography — For patients with respiratory distress who are unstable, we typically disconnect the endotracheal tube (ETT) from the ventilator and perform manual bag ventilation through the ETT with 100 percent oxygen. Manual bag ventilation should not be overly aggressive and should target approximately 10 breaths per minute at 300 to 400 mL per breath. Overventilation may cause or lead to worsening dynamic hyperinflation (DHI), precipitating tension pneumothorax, or cardiac arrest.

We concurrently use capnography to evaluate airway placement of the ETT and are careful not to overventilate patients manually. (See "Carbon dioxide monitoring (capnography)".)

Ventilator disconnection may be lifesaving when the issue is ventilator related. This maneuver also allows the clinician to manually assess resistance to ventilating the patient during manual bag ventilation, which may indicate a problem with the ETT or lung parenchyma. Occasionally, air may escape from the ETT after disconnection, which may suggest DHI.

Patients who improve (likely ventilator-related issue) — If the patient's status improves immediately after disconnection, the ventilator (settings or machine) or the ventilator circuit is the likely source of the problem.

The ventilator settings and the machine and circuitry should be examined, and the culprit etiology identified. Any identified problem should be corrected before resuming mechanical ventilation, typically on the original or corrected ventilator settings. If the problem recurs, components of the ventilator or, rarely, the ventilator itself may need to be replaced. Further details are provided separately. (See 'Ventilator and equipment' below and "The ventilator circuit" and "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit".)

Patients who do not improve — If the patient's condition does not improve or deteriorates despite disconnection from the ventilator, we continue manual ventilation with capnography and simultaneously evaluate resistance to bag ventilation while also considering the empiric treatment of life-threatening conditions when they are strongly suspected (algorithm 1). For the latter, we take a brief history and perform a rapid chest, cardiovascular, abdominal, and neurologic examination. We also perform focused bedside ultrasound examination, although that expertise is not universally available. (See 'Focused history and examination' below.)

Evaluate difficulty of bag ventilation — The difficulty of bag ventilation can help narrow the differential diagnosis of respiratory distress in the ventilated patient.

Difficult manual ventilation – Difficulty in manual ventilations may suggest an obstruction in the ETT or major airway or an intrinsic pulmonary problem (eg, poor lung compliance, DHI, or increased respiratory effort). The passage of a suction catheter through the ETT into the trachea helps differentiate these options.

Catheter resistance – If the catheter meets resistance, this suggests ETT or major airway obstruction. Efforts should be made to remove the obstruction. Further details regarding clinical assessment and management of suspected ETT or airway obstruction are provided below. (See 'Obstruction' below.)

Minimal catheter resistance – If the suction catheter passes easily, a trial of increased sedation, with or without short-term neuromuscular paralysis, may help determine whether respiratory distress is the result of an intrinsic respiratory compliance problem, or the consequence of an increase in the patient's respiratory efforts.

-If the distress resolves with sedation or neuromuscular blockade, active respiratory effort is the likely part of the cause and the underlying etiology must be sought. Possibilities include hypercapnia or hypoxemia, delirium, pain, fever, shock, or a structural central nervous system lesion. (See 'Extrapulmonary disorders' below and "Neuromuscular blocking agents in critically ill patients: Use, agent selection, administration, and adverse effects" and "Sedative-analgesia in ventilated adults: Management strategies, agent selection, monitoring, and withdrawal".)

-Persistent difficulty with manual ventilations despite sedation or paralysis suggests the presence of a new lower airway, parenchymal, or thoracic wall problem. A rapid history, focused physical examination, measurement of respiratory mechanics, bedside ultrasonography, and chest radiograph will often lead to the correct diagnosis. For proper assessment of respiratory mechanics, the patient should be placed back on the ventilator. (See 'Native airway issues' below and 'Pulmonary parenchyma and vasculature' below and 'Extrapulmonary disorders' below.)

No difficulty with manual ventilation – When manual ventilations meet with minimal resistance, an air leak should be suspected; we examine the patient for cephalad displacement of the ETT and the cuff for an air leak by measuring cuff pressure. Further details regarding clinical assessment and management of a suspected air leak are provided below. (See 'Cuff leak' below and "Complications of the endotracheal tube following initial placement: Prevention and management in adult intensive care unit patients", section on 'Displacement and unplanned extubation' and "Complications of the endotracheal tube following initial placement: Prevention and management in adult intensive care unit patients", section on 'Endotracheal cuff leaks'.)

Empiric treatment of immediately life-threatening conditions — Empiric treatment of immediately life-threatening conditions may be required before a definitive diagnosis is made. As examples:

Respiratory distress accompanied by hypotension and unilateral decreased breath sounds may require presumptive treatment of a tension pneumothorax with needle decompression followed by placement of a thoracostomy tube. (See "Thoracostomy tubes and catheters: Indications and tube selection in adults and children" and "Treatment of secondary spontaneous pneumothorax in adults".)

Respiratory distress associated with hypotension in a patient with metastatic cancer whose bedside echocardiography shows right ventricle strain or obvious thrombus may prompt the administration of thrombolysis for presumed pulmonary embolism. (See "Approach to thrombolytic (fibrinolytic) therapy in acute pulmonary embolism: Patient selection and administration", section on 'Hemodynamically unstable patients (high-risk pulmonary embolism)'.)

When venous air embolism is suspected, the patient should be positioned left lateral side and head down. (See "Air embolism", section on 'Treatment'.)

Patients with life-threatening shock should also be treated accordingly. (See "Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock", section on 'Common conditions needing lifesaving interventions'.)

CARDIORESPIRATORY STABILITY — If respiratory distress is present but not severe and the patient is hemodynamically stable, we typically perform a complete evaluation to diagnose and manage the underlying cause of respiratory distress and if necessary, increase the fraction of inspired oxygen during the evaluation.

Detailed evaluation includes the following:

A focused history and physical examination. (See 'Focused history and examination' below.)

Assessment of ventilator and graphics. (See 'Ventilator settings and equipment' below and 'Ventilator mechanics' below.)

Assessment of gas exchange and capnography. (See 'Arterial blood gas analysis and capnography' below.)

Bedside imaging (eg, ultrasound and chest radiography). (See 'Bedside imaging' below.)

Additional tests may be needed depending on the suspected etiology. (See 'Other tests' below.)

Focused history and examination — We simultaneously perform the following:

We obtain information regarding any recent events that may have led up to the onset of respiratory distress that helps provide clues for potential specific etiologies. This includes recent transport, change in ventilator settings, change in quality or quantity of secretions, hemoptysis, vomiting, trauma, recent central intravenous catheter insertion or other procedure, chest pain, and medication administration.

We examine the patient's appearance (eg, cyanosis, facial swelling, subcutaneous air, agitation, biting), trends in vital signs (including pulse oximetry), cardiac rate and rhythm, and other available hemodynamic data (eg, pulmonary artery catheter readings). Tachypnea is almost universal in this setting. We also examine the patient for unequal air entry, obvious wheezes, rhonchi, crackles, new cardiac murmurs, signs of volume overload, new abdominal tenderness and swelling, or an audible air leak from the nose or mouth. We also look for the presence of any nonpulmonary abnormalities, including abdominal distension, gross neurologic abnormality, and signs of deep venous thrombosis.

We assess the position and condition of the endotracheal tube (ETT; eg, original and current position at the lip) and measure capnography, the value of which is discussed below. (See 'Arterial blood gas analysis and capnography' below.)

The history and examination often provide the basis for narrowing the differential diagnosis. As examples:

Respiratory distress that occurs soon after the initiation (or re-establishment) of mechanical ventilation is often the result of inadequate ventilator support, insufficient sedation, or errors in ventilator settings [3]. (See 'Ventilator and equipment' below.)

An audible air leak from the nose or mouth may suggest a cuff or ETT leak or superior (cephalad) migration of the ETT. (See 'Displacement' below and 'Cuff leak' below.)

Hypotension in combination with an increase in central venous pressure may accompany excessive auto-positive end-expiratory pressure (PEEP), tension pneumothorax, or massive pulmonary embolism. Fever may complicate infection, PE, or allergic reaction. Respiratory distress following vomiting should prompt evaluation for aspiration. Unequal breath sounds suggest unilateral mainstem bronchus intubation, pneumothorax, or pleural effusion. Respiratory distress following the administration of blood products should prompt evaluation for pulmonary edema. Crackles, wheezing, or rhonchi may also reflect pulmonary edema. The recent placement of a central venous catheter may prompt evaluation for a pneumothorax or displacement. (See 'Pulmonary parenchyma and vasculature' below and 'Acute pleural disorders' below.)

Bronchospasm from drugs or allergies usually presents with wheezing or rhonchi. A history of thick tenacious secretions should prompt evaluation for obstruction. (See 'Native airway issues' below.)

Hypertension and tachycardia may signify pain, delirium, or anxiety. Unequal pupils or hemiplegia may suggest an acute central lesion such as an intracerebral bleed. (See 'Extrapulmonary disorders' below.)

Assessment of ventilator, alarms, graphics, pressures — Simultaneous with the history and physical examination, we assess the ventilator settings, equipment, and mechanics; assess gas exchange; and perform bedside imaging.

Ventilator settings and equipment — This assessment may reveal a potential reason for respiratory distress including incorrect settings, excess secretions in the ventilator circuit, or a blocked heat moisture exchanger. Details of the assessment are provided below. (See 'Ventilator and equipment' below.)

Ventilator mechanics — We also examine ventilator graphics (eg, shape of the pressure/flow volume curves), compare the set and delivered tidal volume, and pay attention to ventilator alarms (eg, high peak pressure [Ppeak], low tidal volume). Recognizing trends and acute changes in respiratory mechanics can narrow the differential for respiratory distress. Importantly, ventilator graphics are different for patients on volume-controlled and pressure-controlled ventilation. Accordingly, clinicians should familiarize themselves with these differences so that the differential can be narrowed appropriately.

Volume-controlled ventilation — When on volume-controlled ventilation, we examine the Ppeak and tidal volume changes. We additionally manually measure the plateau pressure (Pplat) by applying an inspiratory pause, so that the delta Ppeak – Pplat (figure 4) can be assessed. Pplat should be measured with a constant flow (ie, square wave) pattern [13] and may require additional sedation for accurate assessment.

The Ppeak is the highest pressure measured during the respiratory cycle and is a function of both the resistance of the airways plus respiratory system compliance. Pplat is the pressure recorded during a pause at end-inspiration and reflects the static compliance of the respiratory system [14,15]. The difference between the two (ie, delta Ppeak – Pplat) can help classify whether the cause of respiratory distress lies in the artificial or native airways (ie, airways resistance issue) or is due to reduced respiratory system compliance (ie, the lung parenchyma, chest wall, and abdomen) [16,17].

Although there is no "normal" value for Ppeak or Pplat, the delta Ppeak – Pplat is generally 3 to 10 cmH2O, although the difference is generally a product of airway resistance and inspiratory flow rate. Thus, assuming normal airways resistance, the expected delta Ppeak – Pplat is 7 to 10 cm H2O at a flow rate of 60 L/minute or 3.5 to 5 cmH2O at a flow rate of 30 L/minute. Most flow rates are set at approximately 60 L/minute; thus, a delta Pplat – Ppeak greater than 10 cmH2O often indicates an airways resistance problem.

The sections below are interpretations of ventilator mechanics that can occur in patients with respiratory distress on volume-controlled ventilation that help narrow the differential for respiratory distress.

Reduced Ppeak and tidal volume — A sudden decrease in tidal volume and peak pressure (Ppeak) suggest an air leak from cephalad ETT displacement above the vocal cords or a ruptured cuff. It is rarely due to a leak from the ETT itself, ventilator tubing, or disconnections within the system. (See 'Cuff leak' below and 'Displacement' below and 'Ventilator and equipment' below.)

An increase in the Ppeak with a widening of the delta Ppeak – Pplat — This pattern suggests that an increase in airway resistance is the cause of respiratory distress [18]. Obstruction of the ETT or major airway (eg, by inspissated secretions, a kinked ETT, or the patient biting the tube), ventilator tubing, airway edema (eg, anaphylaxis), and bronchospasm can cause this change in respiratory mechanics.

An increase in both the Ppeak and Pplat with a delta Ppeak – Pplat that is unchanged or reduced — This pattern suggests a decrease in respiratory system compliance. Abrupt decreases in the respiratory compliance can be due to unilateral mainstem bronchus intubation, pneumothorax, severe atelectasis, pneumonia, pulmonary edema, dynamic hyperinflation (ie, elevated intrinsic PEEP [auto-PEEP]), large pleural effusion with compressive atelectasis, acute aspiration, or abdominal distension (eg, abdominal ascites, gas, adipose tissue, and pregnancy).

Pressure-controlled ventilation — During pressure-controlled ventilation, the interpretation of ventilator mechanics is different. Because pressure is maintained during pressure-controlled ventilation, altered mechanics are reflected in changes in tidal volume and expiratory flow.

Maintenance of airway pressure, increase in tidal volume, and expiratory flow that does not return to baseline — Maintenance of airway pressure associated with an increase in tidal volume and expiratory flow that does not return to baseline before the next ventilator-delivered breath is a pattern seen in patients with an air leak. (See 'Reduced Ppeak and tidal volume' above.)

Maintenance of airway pressure, reduction in tidal volume, and delayed return of expiratory flow — Maintenance of airway pressure, reduction in tidal volume, and slow return of expiratory flow toward the baseline is a pattern seen in patients who have increased airway resistance similar to those in whom a widened Ppeak – Pplat is seen when on volume-controlled ventilation. (See 'An increase in the Ppeak with a widening of the delta Ppeak – Pplat' above.)

Maintenance of airway pressure, reduction in tidal volume, and rapid return of expiratory flow — Maintenance of airway pressure, reduction in tidal volume, and rapid return of expiratory flow toward the baseline is a pattern that typically represents conditions with reduced lung compliance (ie, conditions similar to those in whom the delta Ppeak – Pplat is narrow or unchanged). (See 'An increase in both the Ppeak and Pplat with a delta Ppeak – Pplat that is unchanged or reduced' above.)

Arterial blood gas analysis and capnography — We typically obtain an arterial blood gas, especially if the cause of respiratory distress is not immediately apparent, pulse oximetry demonstrates desaturation, or the pulse oximetry waveform is unreliable (eg, poor peripheral perfusion, excessive patient movement, abnormal hemoglobin, very low oxygen saturation, and certain dyes). The presence of worsening hypoxemia or hypercapnia on blood gas analysis supports diagnostic possibilities such as a new-onset pulmonary vascular or parenchymal condition (eg, pulmonary embolus, aspiration, or edema) or acute bronchospasm from chronic obstructive pulmonary disease [19]. (See "Measures of oxygenation and mechanisms of hypoxemia".)

We also perform capnography to determine airway placement of the ETT. This evaluation can help distinguish ETT displacement from other issues. (See "Carbon dioxide monitoring (capnography)".)

Bedside imaging — While in the past chest radiography was the only bedside imaging tool used to evaluate respiratory distress in mechanically ventilated patients, we now often use point-of-care ultrasonography, which in many cases is more readily obtainable.

Together, these imaging modalities can reveal potential etiologies for respiratory distress, including ETT displacement, pulmonary edema, pneumothorax, pleural effusion, atelectasis, or consolidation. Bedside ultrasonography of other organs (eg, heart, abdomen, legs) may also provide a clue to an extrapulmonary etiology (eg, ruptured mitral valve or septal defect, pericardial tamponade, pneumoperitoneum, ruptured aortic aneurysm). The value of critical care ultrasonography is discussed separately. (See "Indications for bedside ultrasonography in the critically ill adult patient".)

Other tests — We generally obtain routine laboratory studies, although they are often not specific for select etiologies, (eg, complete blood count, chemistries, coagulation studies, lactate, brain natriuretic peptide, D-dimer, troponin) and are not necessary if the etiology is evident and easily remediable (eg, airway obstruction from secretions).

Direct laryngoscopy may be needed to determine cephalad ETT displacement. (See 'Displacement' below and "Direct laryngoscopy and endotracheal intubation in adults".)

Other tests may be guided by clinical suspicion (eg, an electrocardiography, formal echocardiography, computed tomographic pulmonary angiography, lower extremity dopplers).

Follow-up — Once a specific etiology is identified, it should be treated accordingly and plans put in place to avoid recurrence. (See 'Evaluation and management of specific etiologies' below.)

EVALUATION AND MANAGEMENT OF SPECIFIC ETIOLOGIES — An overview of common problems that cause respiratory distress in the mechanically ventilated patient can be found in the table (table 1).

Ventilator and equipment — In all cases of respiratory distress, the ventilator, the ventilator circuit, and all connections should be examined carefully to identify the culprit etiology. These include incorrect or inadequate settings (eg, erroneously low fraction of inspired oxygen or tidal volume), excess secretions in the ventilator tubing, leak in the ventilator circuit, blocked heat moisture exchanger, or ventilator malfunction. Each ventilator should also undergo individual standard ventilator checks to help identify problems with issues such as valves, compressors, or gas mixtures.

Presentation – Ventilator-related issues should be suspected in patients with the following scenarios (see "Overview of initiating invasive mechanical ventilation in adults in the intensive care unit", section on 'Settings' and "The ventilator circuit"):

Patients who develop respiratory distress after the initiation of mechanical ventilation, following procedures or transport, or when ventilator settings are temporarily changed [3].

Patients with a sawtooth pattern on the expiratory curve of ventilator graphics; this appearance represents partial obstruction of the ventilator tubing by secretions or condensate and can also be seen when patients have significant endobronchial secretions.

Patients in whom disconnection from the ventilator resolves respiratory distress.

Ventilator mechanics and graphics – Ventilator mechanics may show the following:

Obstruction – Obstruction in the ventilator tubing or heat moisture exchange system on volume-controlled ventilation may reveal an elevated peak pressure (Ppeak) with widened delta Ppeak and plateau pressure (ie, delta Ppeak – Pplat); on pressure-controlled ventilation airway pressure is maintained, tidal volume decreases, and the expiratory flow is slow to return to baseline. (See 'An increase in the Ppeak with a widening of the delta Ppeak – Pplat' above and 'Maintenance of airway pressure, reduction in tidal volume, and delayed return of expiratory flow' above.)

Leak – On volume-controlled ventilation, a decrease in Ppeak and tidal volume is consistent with an air leak, while on pressure-controlled ventilation, an airway leak is suggested by an airway pressure that is unchanged, an increase in tidal volume, and an expiratory flow curve that does not return to baseline. (See 'Reduced Ppeak and tidal volume' above and 'Maintenance of airway pressure, increase in tidal volume, and expiratory flow that does not return to baseline' above.)

Treatment – The problem should be corrected before resuming mechanical ventilation, usually at the previous settings. Sometimes, if distress recurs when reconnected to the ventilator and no apparent error in settings or mechanical or technical problem is found, we may alter ventilator settings to "match" patient effort (eg, increase the tidal volume or respiratory rate, change the inspiratory flow, or switch to pressure support or pressure-controlled mode); changes should be incremental and ensure that new settings do not place the patient at risk of volutrauma or barotrauma. Occasionally, if the problem recurs despite these maneuvers, components of the ventilator, or rarely, the ventilator itself, may need to be replaced. (See "Diagnosis, management, and prevention of pulmonary barotrauma during invasive mechanical ventilation in adults", section on 'Pathogenesis and risk factors' and "Acute respiratory distress syndrome: Ventilator management strategies for adults", section on 'Low tidal volume ventilation: Initial settings'.)

Endotracheal tube issues — Several issues including endotracheal tube (ETT) obstruction, displacement, and cuff leak can result in respiratory distress, some of which require ETT replacement. ETT replacement should always take into consideration whether or not the airway might be lost if the patient has a "difficult" airway; in such cases, consulting a clinician with expertise in difficult airway management is appropriate. (See "Complications of the endotracheal tube following initial placement: Prevention and management in adult intensive care unit patients", section on 'Exchanging the endotracheal tube'.)

Obstruction

Presentation – ETT (or tracheostomy) obstruction should be suspected in patients with acute respiratory distress who have thick, inspissated secretions. It should also be suspected in those with hemoptysis, and those with agitation who are biting down on the ETT (table 1). Occasionally, an inhaled foreign body such as a dislodged tooth (eg, patient with poor dentition) or airway edema from anaphylaxis is the culprit (eg, patient with recently administered antibiotic).

Ventilator graphics and mechanics – Ventilator graphics and mechanics show an elevated Ppeak with an increased delta Ppeak – Pplat (on volume-controlled ventilation) or unchanged airway pressure, decreased tidal volume, with prolonged expiratory flow (on pressure-controlled ventilation). Patients with partial obstruction may maintain the delivered tidal volume (particularly if the Ppeak is below the upper limit set in the alarms), while those with complete obstruction may experience a significant drop in tidal volume. (See 'An increase in the Ppeak with a widening of the delta Ppeak – Pplat' above and 'Maintenance of airway pressure, reduction in tidal volume, and delayed return of expiratory flow' above.)

Management – When ETT or major airway obstruction is suspected, we typically assess the difficulty associated with passing a suction catheter through the ETT into the trachea.

If the catheter meets resistance, this suggests ETT or major airway obstruction. Suctioning may help remove thick secretions, blood, small foreign body, or debris, thereby alleviating the problem. Occasionally, repeated attempts with small amounts of saline lavage may be needed to dislodge mucus (eg, up to three attempts). Because most cases are due to mucus or blood, suctioning is often sufficient unless secretions are more concrete and impacted.

If there are no or minimal secretions, kinking or biting of the ETT or tracheal obstruction are possibilities such that empirically repositioning the patient's head or tubing (to alleviate kinking) or inserting a bite block and increasing sedation may help.

If these maneuvers fail and the obstruction persists, the ETT should be replaced, preferably using a flexible exchange catheter and a larger ETT.

Bronchoscopy should be performed if obstruction is expected to be in the trachea or the problem persists following ETT replacement. (See "Flexible bronchoscopy in adults: Indications and contraindications".)

Displacement

Presentation – ETT displacement should be suspected when respiratory distress occurs immediately following endotracheal intubation or tracheostomy placement or patient repositioning or transport. It is also seen in patients a strong gag or cough reflex or patients with agitation who may cough up or manually displace the ETT or tracheostomy. ETT displacement may cause respiratory distress by migrating out of position superiorly (cephalad), resulting in an air leak, and inferiorly (caudal), resulting in mainstem intubation (figure 1A-B) [11].

To assess ETT displacement, we examine the position of the ETT at the lips, listen for an audible air leak, test the cuff pressure with cuff manometry, measure capnography (to confirm or refute airway placement (see "Carbon dioxide monitoring (capnography)")), and examine bedside ventilator graphics. An air leak is usually associated with generalized poor air entry on chest auscultation, while caudal displacement is associated with reduced air entry unilaterally (usually left sided). If the ETT is suspected to be in the oropharynx, we additionally perform direct visualization with laryngoscopy.

Ventilator graphics and mechanics – On volume-controlled ventilation, a decrease in Ppeak and tidal volume is consistent with superior migration above the vocal cords, while an increase in Ppeak and maintenance of tidal volume with reduced air entry on one side is consistent with mainstem intubation. On pressure-controlled ventilation, an airway leak is suggested by an airway pressure that is unchanged, an increase in tidal volume, and an expiratory flow curve that does not return to baseline, while mainstem intubation should reveal an airway pressure that is unchanged, a decrease in tidal volume, and rapid return of the expiratory flow to baseline. (See 'Reduced Ppeak and tidal volume' above and 'An increase in both the Ppeak and Pplat with a delta Ppeak – Pplat that is unchanged or reduced' above and 'Maintenance of airway pressure, increase in tidal volume, and expiratory flow that does not return to baseline' above and 'Maintenance of airway pressure, reduction in tidal volume, and rapid return of expiratory flow' above.)

Capnography – Capnography helps distinguish whether a suspected leak is due to ETT displacement or to a leak at any other point in the artificial airway, such as the ETT cuff or ventilator tubing. In most cases, capnography should confirm or refute that the ETT is in the airway (unless the ETT cuff is at the level of the vocal cords). Airway leak from ETT displacement is frequently misinterpreted as cuff rupture, leading to unnecessary ETT replacement. In a series of 18 patients whose ETT was replaced due to a large airway leak, only 38 percent actually had a mechanical fault in the cuff [20].

Chest radiography and management – Chest radiography is also useful in the evaluation of displacement:

When cephalad migration is suspected and the balloon of the ETT is estimated to be located below the vocal cords and intact, a chest radiograph should be performed. Once confirmed, the ETT can be moved distally.

When cephalad migration is suspected and the tip or balloon of the ETT is suspected or confirmed to be in the oropharynx (eg, by capnography or direct visualization of the ETT), then prompt reintubation with direct laryngoscopy should be performed without performing a chest radiograph. Although not always necessary, a new ETT is typically placed under these circumstances; the rationale for this approach is based upon the avoidance of a third attempt at reintubation if the displacement was originally due to a significant cuff leak/rupture. (See "Direct laryngoscopy and endotracheal intubation in adults".)

When caudal displacement is confirmed by chest imaging, the cuff should be deflated, the ETT be pulled back by a predetermined distance, the cuff reinflated, and another radiograph obtained.

Cuff leak — The incidence of endotracheal cuff leaks in patients admitted to the intensive care unit is 6 to 11 percent [21,22]. The causes of endotracheal cuff leaks can be classified as leaks due to a defective cuff/inflation system (eg, leaks due to a punctured pilot balloon, inflation line, or cuff) or leaks around an intact cuff/inflation system (eg, cuff underinflation, cephalad migration of the ETT, tracheal misplacement of oro/nasogastric tubes, discrepancy between ETT and tracheal diameter [eg, occasionally the balloon will "soften" over time, or some patients have tracheomalacia], and high peak airway pressures) [23].

Presentation – A cuff leak is generally suspected by hearing an audible leak (often a bubbling sound due to air escaping through the glottis).

The clinical consequences of an air leak vary from trivial to emergent respiratory compromise depending upon patient characteristics and the degree of leak. For example, a small leak (eg, 25 mL) may not be tolerated well in a patient with severe acute respiratory distress syndrome on high ventilatory pressures and high fraction of inspired oxygen, while larger volumes may be tolerated in patients with normal underlying lung function who are intubated for airway protection.

Ventilator mechanics and graphics – Ventilator mechanics show a reduction in the delivered tidal volume and Ppeak during volume-controlled ventilation or an increase in tidal volume and an expiratory flow curve that does not return to baseline when receiving pressure-controlled ventilation. (See 'Reduced Ppeak and tidal volume' above and 'Maintenance of airway pressure, increase in tidal volume, and expiratory flow that does not return to baseline' above.)

Management – When an air leak is suspected, we examine the cuff inflation volume and pressure with a manual syringe and manometer, respectively. If either the volume or pressure are low, this suggests a cuff leak. In addition, we perform capnography; confirmation that the ETT is in the airway by capnography also supports the presence of a cuff leak (although a leak elsewhere in the artificial airway system is still a possibility).

If the cuff leak is minor, some patients can be treated by manually reinflating the pilot balloon. However, when large leaks are suspected and this maneuver fails, prompt reintubation with a new ETT is needed.

Occasionally, when a cause for a substantial air leak cannot be determined, many clinicians opt to replace the ETT. (See "Complications of the endotracheal tube following initial placement: Prevention and management in adult intensive care unit patients", section on 'Exchanging the endotracheal tube'.)

Suggested management of an air leak due to suspected cephalad displacement of the ETT is provided separately. (See 'Displacement' above.)

Native airway issues

Lower airway obstruction (eg, mucus plug, airway mass, or foreign body) — Mucus plugs can block airways at any level, from the major airways (eg, trachea and mainstem bronchi) to smaller airways where they cause atelectasis (table 1).

Presentation – Mucus plugging of the airways should be suspected in patients with respiratory distress who have a large volume of tenacious secretions. Occasionally, mucus plugging may be asymptomatic and seen on routine chest radiography. When airway tumor, airway hemorrhage, or foreign body is suspected, we perform diagnostic bronchoscopy.

Ventilator mechanics and graphics – Excessive airway secretions can sometimes be suspected when a sawtooth pattern is seen on ventilator graphics; the sawtooth pattern represents intermittent changes in airway resistance [24]. Ventilator mechanics are similar to that seen in patients with an ETT obstruction. (See 'Obstruction' above and 'An increase in the Ppeak with a widening of the delta Ppeak – Pplat' above and 'Maintenance of airway pressure, reduction in tidal volume, and delayed return of expiratory flow' above.)

Management – Frequent airway suctioning and pulmonary toilet are typically used to facilitate clearance of secretions with prompt resolution of distress [25]. When these measures fail, bronchoscopy is generally needed to remove secretions. In some cases, when complete lung collapse is noted, we ventilate patients with the "nonobstructed" side down.

Following secretion removal, ensuring adequate humidification of the inspired gases may diminish inspissation of secretions. Rarely, saline or n-acetyl cysteine nebulizations may help reduce recurrence.

When obstruction is due to blood in the airway, a cancerous mass, or a foreign body, therapeutic bronchoscopy may be of value. Evaluation and treatment of these entities are provided separately. (See "Clinical presentation, diagnostic evaluation, and management of malignant central airway obstruction in adults" and "Airway foreign bodies in adults" and "Evaluation and management of life-threatening hemoptysis".)

In severe cases of upper airway edema caused by ETT trauma, we may treat bronchospasm with corticosteroids. (See "Extubation management in the adult intensive care unit", section on 'Glucocorticoids'.)

Bronchospasm

Presentation – Bronchospasm should be suspected in patients with underlying obstructive lung disease or volume overload (table 1). It should also be suspected when respiratory distress follows bronchoscopy, airway suctioning, or administration of medications including beta-adrenergic receptor blockers or select medication to which the patient may be allergic. Wheeze or rhonchi are typically heard on chest examination. Accompanying signs of allergy or anaphylaxis may be present (eg, hypotension, lip and tongue swelling, rash). (See "Anaphylaxis: Confirming the diagnosis and determining the cause(s)" and "Anaphylaxis: Acute diagnosis" and "Differential diagnosis of anaphylaxis in adults and children".)

Ventilator mechanics and graphics – Ventilator mechanics and graphics are similar to that seen in patients with an ETT obstruction. (See 'Obstruction' above and 'An increase in the Ppeak with a widening of the delta Ppeak – Pplat' above and 'Maintenance of airway pressure, reduction in tidal volume, and delayed return of expiratory flow' above.)

Management – Conventional treatment of bronchospasm with inhaled bronchodilators (typically beta-2 agonists) is usually sufficient. In cases due to allergy or anaphylaxis, additional therapies may be needed (eg, epinephrine, antihistamine, histamine receptor blockade). Treatment of allergies and anaphylaxis are discussed separately. (See "Invasive mechanical ventilation in adults with acute exacerbations of asthma" and "Anaphylaxis: Emergency treatment".)

Bronchospasm may also be complicated by dynamic hyperinflation (DHI; also called auto-PEEP), which is discussed below. (See 'Dynamic hyperinflation (auto-PEEP)' below.)

Pulmonary parenchyma and vasculature — Several disorders of the pulmonary parenchyma and vasculature can present with respiratory distress.

Dynamic hyperinflation (auto-PEEP) — DHI is characterized by increased levels of intrinsic positive end-expiratory pressure (auto-PEEP). The hyperinflation is progressive (dynamic) because air accumulates in the lung with each breath as a result of a failure to achieve complete exhalation before the onset of the next breath (figure 2 and table 1).

Presentation – DHI should be suspected in patients with respiratory distress who have acute or chronic airflow obstruction, patients with markedly increased minute ventilatory requirements (eg, acute respiratory distress syndrome), and patients in whom the tidal volume and/or respiratory rate (ie, minute ventilation increase) was recently increased or peak inspiratory flow setting was reduced on the ventilator.

Ventilator graphics and mechanics – DHI may be confirmed by review of the flow-time waveforms (figure 5) as inadequate return of expiratory flow to baseline before the next ventilator-delivered breath. Although auto-PEEP can be quantified by execution of an expiratory hold maneuver during mechanical ventilation (figure 6), this method may be inaccurate. On volume-controlled ventilation, ventilator graphics may reveal an elevated Ppeak with a narrow or unchanged delta Ppeak – Pplat, while on pressure-controlled ventilation, airway pressure is maintained, tidal volume decreases, and the expiratory flow rapidly returns to baseline. (See 'Maintenance of airway pressure, reduction in tidal volume, and rapid return of expiratory flow' above.)

Management – Management involves treatment of the underlying cause, reducing respiratory rate and/or tidal volume (with the goal of reducing minute ventilation), and reducing inspiratory time by increasing inspiratory flow. The diagnosis and management of DHI are discussed in further detail separately. (See "Invasive mechanical ventilation in adults with acute exacerbations of asthma", section on 'Dynamic hyperinflation' and "Invasive mechanical ventilation in acute respiratory failure complicating chronic obstructive pulmonary disease", section on 'Dynamic hyperinflation' and "Clinical and physiologic complications of mechanical ventilation: Overview", section on 'Auto-PEEP'.)

Others — Atelectasis, pneumonia, aspiration of oropharyngeal or gastroesophageal contents, pulmonary edema, and pulmonary embolism (PE) can all cause acute respiratory distress in patients undergoing mechanical ventilation (table 1). Other embolism syndromes are rare.

In most cases, while on volume-controlled ventilation, ventilator graphics reveal similar elevations in both the Ppeak and Pplat with an unchanged delta Ppeak – Pplat. By contrast, on pressure-controlled ventilation, the airway pressure remains unchanged while the tidal volume decreases. (See 'An increase in both the Ppeak and Pplat with a delta Ppeak – Pplat that is unchanged or reduced' above and 'Maintenance of airway pressure, reduction in tidal volume, and rapid return of expiratory flow' above.)

These conditions can usually be differentiated by physical examination together with bedside ultrasonography, echocardiography, and plain chest radiography. Bedside ultrasonography including echocardiography may also help in the rapid assessment of suspected pneumothorax, pleural effusion, and abdominal ascites. (See "Indications for bedside ultrasonography in the critically ill adult patient" and 'Extrapulmonary disorders' below.)

A brief synopsis of the diagnostic evaluation and initial management of select pulmonary parenchymal and vascular conditions are provided below, while detailed information is in the linked topics:

Aspiration with or without atelectasis – Aspiration with or without atelectasis may be suspected in a ventilated patient who has been vomiting or is intolerant of tube feeds. However, atelectasis may occur in the absence of aspiration (eg, high volume of endotracheal secretions), and aspiration may be silent. Management involves endotracheal and oropharyngeal suctioning. Antibiotics are not necessary unless bacterial infection is suspected. (See "Aspiration pneumonia in adults".)

Pneumonia – Ventilator-associated pneumonia should be suspected in patients who have a fever and elevated white blood cell count together with radiographic or ultrasonography findings of consolidation. Antibiotics targeted at specific micro-organisms is the mainstay of therapy. (See "Clinical presentation and diagnostic evaluation of ventilator-associated pneumonia" and "Treatment of hospital-acquired and ventilator-associated pneumonia in adults".)

Acute pulmonary edema – Acute cardiogenic pulmonary edema may be suspected in patients with underlying cardiac disease in association with ultrasonographic, echocardiographic, and radiographic features of pulmonary vascular congestion, and an elevated brain natriuretic peptide. It is largely managed with diuresis and, occasionally, heart rate control and afterload reduction. The underlying cause should be addressed and the head of the bed should be kept elevated at 45 degrees. (See "Approach to diagnosis and evaluation of acute decompensated heart failure in adults" and "Treatment of acute decompensated heart failure: General considerations" and "Treatment of acute decompensated heart failure: Specific therapies".)

Acute noncardiogenic pulmonary edema (eg, neurogenic, transfusion-related reactions) may also mimic cardiogenic pulmonary edema but is more likely to present in the setting of a known risk factor. Management is generally supportive. (See "Noncardiogenic pulmonary edema" and "Transfusion-related acute lung injury (TRALI)" and "Transfusion-associated circulatory overload (TACO)".)

Acute pulmonary embolism – Acute PE is difficult to diagnose in the mechanically ventilated patient. Although echocardiography can be done emergently at the bedside with a high degree of diagnostic sensitivity in hemodynamically compromised patients, it is not specific. Ventilation scans are difficult to perform and interpret in mechanically ventilated patients, although mobile units are available in some institutions [26]. Computed tomographic pulmonary angiography is diagnostic but requires patient transport, which may be unsafe in a patient with acute respiratory distress and may be challenging to perform in patients with renal insufficiency (due to contrast administration).

When the suspicion for PE is high, we sometimes empirically treat with anticoagulant therapy and, rarely, with thrombolytic therapy, generally with a view to obtaining the diagnosis when the patients stabilizes. Further details are provided separately. (See "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism" and "Treatment, prognosis, and follow-up of acute pulmonary embolism in adults" and "Approach to thrombolytic (fibrinolytic) therapy in acute pulmonary embolism: Patient selection and administration".)

Other embolic syndromes:

Air embolism – Air embolism should be suspected when patients experience sudden-onset respiratory distress (venous air embolism) or experience a neurologic event (arterial embolism) in the setting of a known risk factor (eg, intravenous catheter insertion, trauma (table 2 and table 3 and table 4)). When suspected, a high fraction of inspired oxygen should be administered and the patient should be positioned to avoid further embolization (ie, the left lateral decubitus with or without head down, for patients with suspected venous air embolism, or the supine position when arterial embolism is suspected). Bedside echocardiography may demonstrate air in the intravascular space or organs. However, because air may be rapidly absorbed from the circulation, it is often missed. Some patients require hyperbaric oxygen. (See "Air embolism".)

Fat embolism syndrome (FES) - FES is rare but should be suspected in patients who develop respiratory distress in the setting of traumatic fractures or other risk factors (table 5). FES typically manifests 24 to 72 hours after the initial insult, and patients classically develop respiratory distress in association with acute hypoxemia, neurologic abnormalities, and a petechial rash. It is a diagnosis of exclusion and management is supportive. (See "Fat embolism syndrome".)

Amniotic fluid embolism (AFES) – AFES most commonly occurs during labor and delivery, or immediately postpartum or following a first or second trimester abortion, amniocentesis, or abdominal/uterine trauma; rare cases present 48 hours later. Patients typically present with respiratory distress, cardiovascular collapse, and seizures. Management is supportive and also involves rapid delivery of the fetus. (See "Amniotic fluid embolism".)

Acute alveolar hemorrhage – Rare conditions such as diffuse alveolar hemorrhage (DAH) may cause acute respiratory distress in a ventilated patient (table 6 and table 7). DAH is generally suspected in patients with hemoptysis, diffuse radiographic opacities, and severe gas transfer abnormalities. Sequential bronchoalveolar lavage showing progressively more hemorrhagic effluent is the usual method for diagnosis of DAH. Management is largely supportive and involves treatment of the underlying disorder. (See "The diffuse alveolar hemorrhage syndromes".)

Acute pleural disorders — Acute pleural processes can cause respiratory distress by restricting inspiration. This includes pneumothorax and large pleural effusions.

Ventilator graphics and mechanics demonstrate signs consistent with reduced respiratory system compliance. (See 'An increase in both the Ppeak and Pplat with a delta Ppeak – Pplat that is unchanged or reduced' above and 'Maintenance of airway pressure, reduction in tidal volume, and rapid return of expiratory flow' above.)

Acute pleural disorders can by identified during bedside ultrasonography and/or chest radiography and are managed by drainage of air or fluid, respectively. For unusual causes of pleural fluid accumulation, additional therapy may be needed such as surgical exploration for large-volume chylothorax or hemothorax.

Details regarding the presentation and management of pneumothorax and pleural effusions are provided separately. (See "Clinical presentation and diagnosis of pneumothorax" and "Treatment of secondary spontaneous pneumothorax in adults" and "Indications for bedside ultrasonography in the critically ill adult patient", section on 'Thoracic ultrasonography'.)

Extrapulmonary disorders — Extrapulmonary processes can cause respiratory distress by restricting inspiration or increasing respiratory drive. Ventilator mechanics are similar to those seen in patients whose compliance is reduced. (See 'Pulmonary parenchyma and vasculature' above and 'An increase in both the Ppeak and Pplat with a delta Ppeak – Pplat that is unchanged or reduced' above and 'Maintenance of airway pressure, reduction in tidal volume, and rapid return of expiratory flow' above.)

As examples:

Abdominal problems, such as ascites, ileus, or splinting from abdominal pain, may limit chest wall expansion and lower the compliance of the respiratory system [27]. These conditions can be diagnosed using bedside plain radiography and/or ultrasonography. The mainstay of therapy is treatment of the underlying cause (eg, large-volume thoracentesis for massive ascites, pain control). (See "Abdominal compartment syndrome in adults".)

Fever, shock, pain, delirium, and anxiety can increase respiratory drive and cause apparent respiratory distress and agitation without a change in respiratory mechanics or gas exchange. These are diagnoses of exclusion, however, and life-threatening disorders must always be considered before administering sedatives, analgesics, or neuroleptics. The source of the patient's pain or discomfort should be sought and specifically treated [28]. Primary measures to prevent and treat delirium (such as minimizing sleep deprivation, reassurance, and providing orientation to time, place, and situation) may be effective. (See "Acute toxic-metabolic encephalopathy in adults" and "Pain control in the critically ill adult patient" and "Sedative-analgesia in ventilated adults: Management strategies, agent selection, monitoring, and withdrawal".)

SUMMARY AND RECOMMENDATIONS

Etiologies and clinical features – Patients receiving mechanical ventilation can develop respiratory distress, often referred to as "bucking" or "fighting" the ventilator or patient-ventilator dyssynchrony.

The etiologies of respiratory distress in a mechanically ventilated patient are listed in the table (table 1). Common causes include errors in ventilator settings, endotracheal tube (ETT) obstruction, ETT or cuff leak, ETT displacement, mucus plugging, acute cardiogenic pulmonary edema, aspiration, pneumothorax, inadequate sedation, and compression of the lungs by pleural fluid or ascites. (See 'Etiologies' above.)

Signs of respiratory distress include agitation, tachypnea, tachycardia, use of accessory muscles of breathing, uncoordinated thoracic wall or abdominal movement, dyssynchrony with the ventilator, and deterioration in gas exchange. Although a comprehensive evaluation is ideal in all patients, those with cardiopulmonary instability require more urgent attention and the workflow is different. (See 'Clinical features and initial rapid bedside assessment' above.)

Patients with unstable cardiorespiratory status – For patients with severe respiratory distress or hemodynamic instability, we recommend simultaneously doing the following (algorithm 1) (see 'Cardiorespiratory instability' above and 'Disconnection, bag ventilation, and capnography' above):

-Disconnect the ETT from the ventilator

-Perform manual bag ventilation through the ETT with 100 percent oxygen, ensuring that ventilations are not overly aggressive

-Perform capnography or examine existing capnographic tracing to confirm ETT placement in the airway

Improvement – If the patient's status improves immediately, the ventilator settings, machine, or circuit is the likely source of the problem. The ventilator should be examined, and the culprit etiology identified and corrected before resuming mechanical ventilation. (See 'Patients who improve (likely ventilator-related issue)' above and 'Ventilator and equipment' above.)

No improvement – If the patient's condition does not improve or deteriorates despite disconnection from the ventilator, we assess resistance to manual ventilation and simultaneously consider empiric treatment of suspected life-threatening conditions. (See 'Patients who do not improve' above.)

-Resistance to bag ventilation – When bag ventilation is met with resistance, this suggests obstruction (eg, ETT or major airway) or an intrinsic pulmonary problem (eg, poor lung compliance or increased respiratory effort). To distinguish these, we pass a suction catheter through the ETT into the trachea. (See 'Evaluate difficulty of bag ventilation' above.)

-If the suction catheter is met with resistance, this suggests obstruction and efforts should be made to resolve it. In most cases, the obstruction is due to mucus impaction and suctioning is sufficient to remove it. In cases where ETT kinking or biting is suspected, then repositioning the head or inserting a bite block may be helpful. In patients with airway mass or hemorrhage or foreign body, bronchoscopy may be needed to identify and relieve the obstruction. If these maneuvers fail, then the ETT should be replaced. (See 'Obstruction' above.)

-If the suction catheter passes easily, we administer a trial of increased sedation, with or without short-term neuromuscular paralysis. If the distress resolves with sedation/paralysis, active respiratory effort is the likely cause, and the underlying etiology must be sought. Possibilities include hypercapnia or hypoxemia, delirium, pain, fever, shock, or a structural central nervous system lesion. (See 'Extrapulmonary disorders' above.)

-Persistent difficulty with manual ventilations despite sedation or paralysis suggests the presence of a new lower airway, parenchymal, or thoracic wall problem. A rapid history, focused physical examination, measurement of respiratory mechanics, bedside ultrasonography, and chest radiograph and/or ultrasonography will often lead to the correct diagnosis. For proper assessment of respiratory mechanics, the patient will need to be placed back on the ventilator. (See 'Cardiorespiratory stability' above and 'Native airway issues' above and 'Pulmonary parenchyma and vasculature' above and 'Extrapulmonary disorders' above.)

-Minimal resistance to bag ventilation – When manual ventilations meet with minimal resistance, an air leak should be suspected, especially when cephalad displacement of the ETT is obvious or the ETT cuff pressure is low. When cephalad displacement of the ETT is confirmed (by capnography and/or direct visualization of the ETT in the oropharynx), or when a cuff leak is suspected (eg, cuff pressure is low and ETT is in the correct position), we suggest that a new ETT be placed. (See 'Displacement' above and 'Cuff leak' above and "Complications of the endotracheal tube following initial placement: Prevention and management in adult intensive care unit patients", section on 'Displacement and unplanned extubation' and "Complications of the endotracheal tube following initial placement: Prevention and management in adult intensive care unit patients", section on 'Endotracheal cuff leaks'.)

-Concurrent assessment of life-threatening conditions that may need immediate treatment – This assessment includes, but is not limited to, anticoagulation or thrombolysis for presumed pulmonary embolism, the placement of a thoracostomy tube for tension pneumothorax, positioning the patient left lateral side and head down for venous air embolism, and treatment of life-threatening causes of shock (eg, anaphylaxis). In such situations, rapid bedside ultrasonography or echocardiography may be helpful in the provision of preliminary data to support empiric therapy. (See 'Empiric treatment of immediately life-threatening conditions' above.)

Patients with cardiopulmonary stability – When respiratory distress is not severe and the patient is hemodynamically stable, we perform a comprehensive diagnostic evaluation that involves the following (see 'Cardiorespiratory stability' above):

Clinical assessment – A focused history and physical examination that centers on clinical features that provide clues to potential etiologies, and an assessment of the position and condition of the artificial airway including capnography (table 1). (See 'Focused history and examination' above.)

Ventilator mechanics and graphics – Assessment of the ventilator, machine, settings and circuit (including the heat moisture exchanger), ventilator graphics (eg, shape of pressure/flow volume curve), ventilator alarms (eg, a change in tidal volume or peak pressure [Ppeak]), and measurement of the plateau pressure (Pplat) so that the delta Ppeak – Pplat can be measured (figure 4). Importantly, ventilator graphics are different for patients on volume-controlled and pressure-controlled ventilation such that clinicians should familiarize themselves with these differences so that the differential can be narrowed appropriately (figure 3). (See 'Assessment of ventilator, alarms, graphics, pressures' above.)

Arterial blood gas analysis and capnography – Arterial blood gas analysis may support diagnostic possibilities such as new-onset pulmonary vascular or parenchymal conditions (eg, pulmonary embolus, aspiration, or edema) or acute bronchospasm from chronic obstructive pulmonary disease. We also perform capnography to determine airway placement of the ETT. (See 'Arterial blood gas analysis and capnography' above.)

Bedside imaging – Bedside imaging including point-of-care ultrasonography and chest radiography may identify ETT displacement, pulmonary edema, pneumothorax, pleural effusion, atelectasis, or consolidation. Bedside ultrasonography of other organs (eg, heart, abdomen, legs) may also provide a clue to an extrapulmonary etiology (eg, ruptured mitral valve or septal defect, pericardial tamponade, pneumoperitoneum, ruptured aortic aneurysm). Critical care ultrasonography is discussed separately. (See "Indications for bedside ultrasonography in the critically ill adult patient".)

Management – Once a specific etiology is suspected, it should be treated accordingly (table 1) and plans put in place to avoid further recurrence of respiratory distress. (See 'Follow-up' above and 'Evaluation and management of specific etiologies' above.)

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Topic 1633 Version 18.0

References

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