Critical Care Medicine
Respiratory Distress on the Ventilator
Respiratory Distress on the Ventilator
Fighting the ventilator, air hunger, dyspnea, hypoxemia, diaphoresis, tension pneumothorax, airway obstruction
1. Description of the problem
Respiratory distress on the ventilator is a common problem in the ICU and can be life-threatening. The etiology of respiratory distress is often multifactorial and ranges from equipment failure to physiologic disturbances.
Commonly known as "fighting the ventilator," respiratory distress on the ventilator conjures a physical image of the patient. The eyes are wide open, nasal flaring occurs despite the presence of an artificial airway, the forehead beads with sweat, accessory muscle use in the neck and chest is pronounced, the skin becomes mottled or cyanotic, there is often a see-saw motion of the chest and abdomen, airway pressures are elevated and visual and aural alarms fill the environment.
IMPORTANT: Respiratory distress on the ventilator requires immediate treatment. If the cause isn't immediately obvious, treatment is far more important than the diagnosis.
The clinical presentation of patients experiencing respiratory distress on the ventilator portends a uniform appearance. This includes tachypnea, diaphoresis, accessory muscle use, nasal flaring, agitation and thoracoabdominal paradox. Hypoxemia (low SpO2) and cyanosis are common but not always seen.
2. Emergency Management
Upon arrival the clinician should look for obvious causes (kinked endotracheal tube, biting of the tube, ventilator disconnect) and remedy the problem.
In the absence of obvious causes, remove the patient from the ventilator and manually ventilate the patient with 100% oxygen and the appropriate positive end expiratory pressure (PEEP).
Manual resuscitators were not designed for spontaneous breathing. When manually ventilating the patient, provide the power for ventilation.
If manual ventilation solves the problem, the ventilator or ventilator settings are probably the cause. Increase inspired oxygen (FIO2) or PEEP and adjust ventilation settings as required.
If manual ventilation fails to resolve the problem, diagnosis and treatment options are dictated by patient condition.
If ventilation is accompanied by an audible air leak (usually with easy bagging) a cuff leak or proximal tube migration should be suspected.
If the patient is in life-threatening extremis WITH SHOCK and is difficult to bag:
Pass a suction catheter down the airway to confirm an unobstructed tube.
Auscultate the lungs and if sounds are absent unilaterally, perform needle thoracentesis to relieve pneumothorax. Unilateral sounds without hemodynamic compromise may also suggest migration of the tube into the right mainstem or proximal airway obstruction from secretions.
Confirm airway position via auscultation, visual inspection or presence of airway carbon dioxide.
If respiratory distress is non-life-threatening, a more measured approach is warranted:
Perform a physical exam looking for changes in respiratory and hemodynamic status.
Evaluate monitoring devices. SpO2 for hypoxemia, airway pressure for signs of partial airway obstruction or worsening compliance or resistance. If end tidal carbon dioxide (ETCO2) is available, elevation in ETCO2 suggests worsening lung function or sepsis, and a fall in ETCO2 suggests airway dislodgement, ventilator malfunction, pulmonary embolus or cardiovascular collapse.
Obtain a chest radiograph to evaluate endotracheal tube position, worsening atelectasis or pulmonary edema.
Evaluate airway pressure. Increasing WITH SIMILAR RISES in peak pressure and plateau pressure suggest a decrease in compliance caused by pneumothorax, migration of the tube into one lung, dynamic hyperinflation or worsening of lung dysfunction. Increased peak airway pressure with no increase, or out of proportion to the rise in, plateau pressure, suggests an increase in airway resistance. This may be the result of bronchospasm, secretions, partially occluded or kinked tracheal tube, or airway malfunction - see flow diagram in
Drugs and dosages
Pharmacologic treatment of respiratory distress is typically successful only when agitation is the cause. Benzodiazepines, opioids, and finally neuromuscular blockade may be used.
Once the patient is stabilized using manual ventilation, the etiology of respiratory distress can be elucidated. Determining the cause of distress requires a uniform approach, careful observation and a suspicious nature.
Disconnect the patient from the ventilator and manually ventilate the patient. If this solves the problem, the problem likely resides with the ventilator. If the problem persists, look toward the patient.
Pass a suction catheter down the tube to ensure patency. Caution: on rare occasions a mucus plug will stick to the end of the ET tube. Passing the catheter will push it out of the way, but it will migrate back into the tube after several breaths. After repeated attempts, look with the bronchoscope!
Listen to breath sounds. Unilateral absence of sounds with life-threatening hypotension suggests pneumothorax.
Evaluate airway pressures for evidence of increased resistance or decreased compliance.
A Chest radiograph can be helpful in non-life-threatening conditions.
A careful history from the bedside caregivers may be helpful to determine recent procedures or changes.
If the patient is able to communicate, interview the patient.
Evaluate non-pulmonary issues including pain, anxiety or substance withdrawal. Unilateral chest pain may suggest pulmonary embolus.
Evaluate cardiac rhythm for signs of ischemia or arrhythmia.
Blood gas and pH measurement are helpful but not always immediately available.
Evaluate the ventilator graphics - pressure, flow and volume for signs of asynchrony.
Respiratory distress during ventilatory support arises from a number of mechanisms:
The artificial airway
Changes in airway resistance
Changes in lung and chest wall compliance
Excessive secretions (see
Saw tooth pattern in the expiratory flow waveform suggesting the need for suctioning or condensate in the ventilator circuit.
The artificial airway:
Migration down the right mainstem
Migration above the vocal cords
Dislodgement of the tube into the esophagus
Migration of a tracheostomy tube into the subcutaneous tissue (rare but life-threatening)
Herniation of the cuff over the tip of the tube, obstructing flow (rare)
Kinking of the tube outside the lips or in the oropharynx
Wire-reinforced tubes kinked by biting or external compression
Changes in airway resistance:
Retained airway secretions
Dried secretions in artificial airway lumen
Patient biting the tube
Changes in lung/chest wall compliance:
Worsening ARDS, atelectasis, pneumothorax, pneumonia
Position changes - particularly semi-Fowler's to supine
Dynamic hyperinflation causing air trapping and PEEPi.
Missed triggers (see
Insufficient ventilatory support - wrong mode
Excessive or thick/dried secretions:
Pneumonia, pulmonary edema
Pulmonary edema, pulmonary hemorrhage
Heat and moisture exchanger occluded by secretions (
Circuit failure, disconnection or leaks
Condensation in the ventilator circuit can result in auto-triggering.
Up-draft nebulizers using a continuous flow source can complicate triggering and volume monitoring.
In the presence of COPD, missed triggers can be seen in the expiratory flow signal. These represent patient effort without ventilator response, which may result in respiratory distress.
HME occluded with secretions causing elevated resistance, high PIP, air-trapping and respiratory distress.
There are no data on the incidence of respiratory distress during mechanical ventilation requiring treatment.
The incidence of barotrauma during mechanical ventilation has fallen significantly since introduction of low tidal volumes and lung protection. In most studies, the incidence is < 3%.
Patient/ventilator asynchrony is a common finding in patients with COPD, with an asynchrony index of >10% in about one third to half of patients.
Migration of the ET tube into the right mainstem has been reported to occur as frequently as in 10% of patients.
Special considerations for nursing and allied health professionals.
What's the evidence?
Tobin, MJ. "What should the clinician do when the patient fights the ventilator?". Respir Care. vol. 36. 1991. pp. 395-406.(Excellent early review of identifying and treating respiratory distress in the ventilated patient.)
Jubran, A, Tobin, MJ. "Use of flow volume curves in detecting secretions in ventilator-dependent patients". Am J Respir Crit Care Med. vol. 150. 1994. pp. 766-769.(Describes the use of ventilator waveforms to determine when patients require suctioning.)
Thille, AW, Rodriguez, P, Cabello, B, Lellouche, F, Brochard, L. "Patient ventilator asynchrony during assisted mechanical ventilation". Intensive Care Med. vol. 32. 2006. pp. 1515-1522.(Describes the most common causes of asynchrony and defines the asynchrony index.)
Thille, AW, Cabello, B, Galia, F, Lyazidi, A, Brochard, L. "Reduction of patient ventilator asynchrony by reducing tidal volume during pressure support ventilation". Intensive Care Med. vol. 34. 2008. pp. 1477-1486.(Describes reducing missed triggers by reducing pressure support and shortening inspiratory time.)
Marcy, TW, Marini, JJ. "Respiratory distress in the ventilated patient". Clin Chest Med. vol. 15. 1994. pp. 55-73.(Excellent review of the process for identifying the cause of respiratory distress in the mechanically ventilated patient.)
Kondili, E, Akoumianaki, E, Alexopoulou, C, Georgopoulous, D. "Identifying and relieving asynchrony during mechanical ventilation". Expert Rev Respir Med. vol. 3. 2009. pp. 231-243.(Excellent review of asynchrony with many graphic examples.)
Copyright © 2017, 2013 Decision Support in Medicine, LLC. All rights reserved.
No sponsor or advertiser has participated in, approved or paid for the content provided by Decision Support in Medicine LLC. The Licensed Content is the property of and copyrighted by DSM.
Renal and Urology News Articles
Sign Up for Free e-newsletters
NEPHROLOGY & UROLOGY NEWS
- Acute Kidney Injury (AKI)
- Chronic Kidney Disease (CKD)
- Contrast Nephropathy
- Cardiovascular Disease (CVD)
- Diabetic Nephropathy
- End-stage Renal Disease (ESRD)
- Lupus Nephritis
- Peritoneal Dialysis
- Secondary Hyperparathyroidism (SHPT)