There are three general problems that may occur in patients who are mechanically ventilated:
1. Difficulty with oxygenation
2. Difficulty with ventilation
3. Difficulty with elevated peak airway pressures
In all three cases, a calm and cooperative patient is essential. Anxiolytics should be used if needed to support the patient and maximize patient synchrony with the mechanically delivered positive pressure breaths. If small doses of sedation are not effective, the use of neuromuscular blocking agents (paralytics) may be life-saving, provided that the airway is maintained.
II. Identify the Goal Behavior.
See Figure 1.
III. Describe a Step-by-Step approach/method to this problem.
Emergent respiratory decompensation, hypoxia, hypercapnia and high pressures
If the patient is hemodynamically stable, take the time to perform a focused history and physical examination with particular attention to wheezing (suggesting bronchospasm), decreased breath sounds (suggesting mucus plugging and lobar collapse, or pneumothorax) or abnormal chest wall motion. Verify the correct ventilator settings and proper ventilator circuitry. Measure the peak pressure and assess the plateau pressure by performing an end-inspiratory breath hold. An arterial blood gas can assess the adequacy of the patient’s oxygenation and ventilation. A chest radiograph may reveal a malpositioned endotracheal tube or confirm a pneumothorax or lobar collapse.
If the patient is hemodynamically unstable, disconnect the patient from the ventilator and manually ventilate by attaching a bag-valve-mask with 100% oxygen via the endotracheal tube. If this resolves the vital sign abnormality, the problem was likely related to the ventilator, and patient tolerance of mechanical ventilation. Consider switching to a new ventilator if adjusting the settings and/or sedating the patient do not lead to improvement.
If the patient continues to deteriorate despite manual ventilation with 100% fraction of inspired oxygen (FiO2), this is a medical emergency. Progressive hypotension and tachycardia may be related to increasing intra-thoracic pressure also known as intrinsic positive end expiratory pressure (intrinsic PEEP, or auto-PEEP). This leads to diminished systemic venous return and decreased cardiac output.
To treat intrinsic PEEP in a hemodynamically unstable patient, stop manual ventilations by disconnecting the endotracheal tube from the bag-valve-mask or ventilator circuit, and assist the patient in exhaling by gently pressing on the chest wall. Avoid manual or mechanical ventilations for 45 seconds to 1 minute; this should allow full exhalation and decreased positive pressure within the chest.
Suspect tension pneumothorax if the patient has respiratory decompensation as described above and progressive hypotension. The chest wall may appear hyper-expanded on one side with associated decreased breath sounds and a shift of the trachea to the opposite side. Do not wait for a chest radiograph to confirm a tension pneumothorax. Immediately place a large (fourteen gauge) angiocatheter into the chest just superior to the 2nd rib at the mid-clavicular line. A whoosh of air escaping through the catheter may be heard, and a rapid improvement of the patient’s blood pressure helps confirm the correct diagnosis. A chest tube should then be placed for more definitive management of the pneumothorax.
If the patient is hemodynamically stable but difficult to ventilate even with manual ventilations by bag-valve-mask, consider a problem with the endotracheal tube. Attempt to pass a suction catheter down the endotracheal tube to assess for obstruction from mucus plugging. If readily available, the integrity of the endotracheal tube and upper airway can also be assessed with flexible bronchoscopy. If mucus plugging of the endotracheal tube is suspected, the tube should be removed and the patient reintubated with a new endotracheal tube.
Obstruction of the endotracheal tube also may occur when a patient bites the tube and fails to relax. This can be life-threatening and can be reversed by a dose of an intravenous neuromuscular blocking agent.
If the patient is hemodynamically stable and not difficult to ventilate manually with 100% oxygen, but continues to have respiratory decompensation, consider the integrity of the endotracheal tube balloon. An air leak may be present. If there is damage to the endotracheal tube balloon at the distal end of the tube and it is not fully inflated, a portion of each breath will travel back up the trachea past the deflated balloon and out through the oropharynx. This can usually be heard as a loud low-pitched breath sound escaping through the mouth.
Another cause of an air leak may be endotracheal tube malposition. If the endotracheal tube has been displaced superiorly, the tip of the tube may be above the vocal cords and outside of the trachea. It may appear to be in the right place externally but does not ensure adequate delivery of each breath to the lungs. If a malpositioned tube is suspected, consider removing it and reintubating the patient with a new endotracheal tube. If readily available, flexible bronchoscopy can assess the integrity and placement of the endotracheal tube, and if superiorly displaced, the endotracheal tube can be advanced into the proper position under direct visualization.
The most straightforward approach to persistent hypoxemia is increasing the FiO2. If hypoxia remains, manipulation of airway pressures may improve the ventilation to perfusion ratio (V/Q ratio) and decrease dead space by recruiting and ventilating atelectatic lung. PEEP should be increased per the Acute Respiratory Distress Syndrome Network (ARDSNet) protocol commensurate with an increased FiO2. Be aware that increased PEEP will take minutes to hours before there is an increase in blood oxygenation (paO2) while an increased FiO2 should be reflected by an increase in paO2 within a minute.
Performing recruitment maneuvers may speed up improvements with increased PEEP, at the possible expense of temporarily decreasing cardiac output by decreasing venous return. Note that any increased pressure may lead to barotrauma and increased inflammation due to volutrauma, so adherence to low lung volume strategies as outlined by ARDSNET is advisable.
Manipulating the inspiratory to expiratory ratio (I:E ratio) can also improve oxygenation, but is uncomfortable for the patient and can lead to a decreased minute ventilation and higher levels of carbon dioxide. In patients with severe obstructive lung disease (chronic obstructive pulmonary disease, asthma, etc.) this strategy can adversely affect intrathoracic pressure by creating auto-PEEP with the potential for respiratory decompensation and hemodynamic collapse.
Alternate ventilator modes can increase patient oxygenation. Airway pressure release ventilation (APRV) delivers a mechanical breath to the patient by providing a prolonged inspiratory time at a high pressure with the tidal volume determined by the compliance of the patient’s lung. Ventilation occurs for a brief 0.6 seconds at no pressure allowing a quick exhalation. BiLevel ventilation is similar to APRV, however both a high and low pressure are set, as well as a cycle rate.
High frequency oscillating ventilation is another mode of mechanical ventilation used more frequently in infants. It maintains a set mean airway pressure to keep the lungs open while oscillating air at a high frequency allowing for movement of oxygen and carbon dioxide down their respective diffusion gradients. High frequency oscillating ventilation has fallen out of favor after a series of trials demonstrated equivocal or worsened outcomes with their use. All of these advanced modes of ventilation should be used with the assistance of an expert.
Prone positioning – placing the patient in the “swimmer’s position” or in a specialized proning bed – improves oxygenation and increases survival in patients when used early in the treatment of patients with hypoxic respiratory failure. Nursing protocols are required to ensure patient safety with positioning. Inhaled nitric oxide can promote V/Q matching by dilating capillaries that perfuse ventilated alveoli. Despite consistently improving oxygenation, no studies have demonstrated an increased in survival with the use of inhaled nitric oxide.
Difficulties with ventilation are often better tolerated than profound hypoxemia. In ARDSNET studies, the average pH was lower in the low lung volume group without an adverse effect on mortality. Although uncomfortable for the patient, it is acceptable to tolerate an elevated partial pressure carbon dioxide (pCO2) provided the pH remains above 7.2, except in patients with increased intracranial pressure.
When presented with a patient with a low pH and high pCO2, the first step is to verify that the ventilator circuit and endotracheal tube are intact. One can use minute ventilation as a surrogate marker for ventilation and pCO2. The higher the minute ventilation, the lower the pCO2. Exhaled end-tidal carbon dioxide (etCO2) can also be used to estimate pCO2. Unfortunately, this is not an accurate measure when there is increased dead space or very low blood pressure.
Ways to increase the minute ventilation, and thus decrease the pCO2, include increasing the tidal volume (or driving/inspiratory pressure in pressure control ventilation), increasing the rate, and decreasing the I:E ratio. Keep in mind that these ventilator manipulations can adversely affect oxygenation and intrathoracic pressure.
A common problem in mechanical ventilation is related to increases in pressure within the chest cavity. This can manifest in volume control ventilation as elevated peak pressures, or in pressure control ventilation as decreasing tidal volumes.
The highest pressure during the respiratory cycle is a function of the resistance to flow within the airways and the compliance or stiffness of the lungs and chest wall, and is known as the peak pressure. By measuring the pressure within the lungs at the end of an inspiratory breath (the plateau pressure), we can remove the contribution to pressure from flow-related resistance. The plateau pressure reflects the pressure seen by the alveoli and elevated plateau pressures are worrisome for barotrauma. A large difference between peak and plateau pressure indicates increased resistance within the airways. This can be related to bronchospasm or mucus plugging.
Intrinsic PEEP is a condition where the alveoli are still attempting to expel air at the end of the mechanical exhalation leading to a positive pressure gradient from the alveoli to the bronchi, and out to the ventilator. Clinically this occurs in patients with obstructive lung diseases. This pressure gradient can accumulate and increase peak pressures. It increases the work of breathing because more effort must be expended by the diaphragm to reach the negative pressure threshold required to trigger a mechanical breath. It should be suspected in the right clinical setting, when the pressure-time loop displayed on the ventilator does not reach baseline on exhalation, and confirmed by measuring the pressure remaining in the lungs at the end of exhalation (end-expiratory breath hold).
Emergent treatment involves removing the patient from the ventilator to allow for complete exhalation. Semi-emergent treatment involves decreasing the I:E ratio, and decreasing the minute ventilation. One can also attempt to match the PEEP given by the ventilator to the intrinsic PEEP measured, decreasing the work required to trigger mechanical breaths.
IV. Common Pitfalls.
Although uncomfortable, patients tolerate a high pCO2 better than might be expected. By trying to “blow down” the pCO2 to normal with an increased respiratory rate or larger tidal volumes, one can increase the intrathoracic pressure to a point of compromised cardiac function and hemodynamic instability.
Increasing PEEP should improve oxygenation, but will take minutes to hours to recruit atelectatic lung. Increase the FiO2 at the same time to allow time for PEEP to work.
In an emergency, take the patient’s contribution out of the equation. Appropriate sedation is a good thing when mechanically ventilated and unstable.
V. National Standards, Core Indicators and Quality Measures.
No national standards established yet.
VI. What's the Evidence?
Guerin, C. “Prone positioning in severe Acute Respiratory Distress Syndrome”. NEJM. vol. 368. 2013. pp. 2159-2168.
Ferguson, ND. “High-frequency oscillation in early acute respiratory distress syndrome”. NEJM. vol. 368. 2013. pp. 795-805.
Young, D. “High-frequency oscillation for acute respiratory distress syndrome”. NEJM. vol. 368. 2013. pp. 806-813.
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- I. Problem/Challenge.
- II. Identify the Goal Behavior.
- III. Describe a Step-by-Step approach/method to this problem.
- IV. Common Pitfalls.
- V. National Standards, Core Indicators and Quality Measures.