Ventilator Management

Mariana Nunez, Roopa Kohli-Seth, Zinobia Khan, Moses Bachan, and Jennifer A. Frontera

Mechanical ventilation (also known as respiratory failure) is common in critically ill patients. Neurologic patients often require mechanical ventilation for failure to protect the airway due to poor mental status or neuromuscular disease, rather than for pulmonary insufficiency. Noninvasive positive pressure ventilation (NPPV) which is commonly used in COPD exacerbation, can be used in amyotrophic lateral sclerosis (ALS), Guillain-Barré, or myasthenia gravis patients when there is a minimal aspiration risk. Decreased mental status is a contraindication to NPPV. This chapter will focus on positive pressure ventilation in intubated patients. For details on intubation, see Chapter 16.

Case Example

You are called to the neuro-intensive care unit (NICU) to see a ventilated patient who recently underwent a laparotomy and who has a peak airway pressure of 55 cm H₂O on assist control/volume control (AC/VC) at a rate of 12 breathes per minute, fraction inspired oxygen (FIO₂) 40%, and positive end-expiratory pressure (PEEP) 5 cm H₂O.

Questions

What are the most recent arterial blood gas (ABG) and O₂ saturation?
Does the patient have a history of bronchospasm or mucous plugging?
What is the pulmonary history?
When was the patient intubated?
Is the patient biting the ETT? Is there any kinking of the ETT?

Urgent Orders

Remove the patient from the ventilator and manually bag on 100% O₂ to assess resistance. High resistance might be due to mucous plugging or to the patient biting the endotracheal tube (ETT).
Check the ventilator circuit for kinking or fluid pooling.
Check the ventilator settings: Excessively high tidal volume or flow rate could contribute to elevated peak airway pressure.
Auscultate the lungs: Wheezing indicates bronchospasm; decreased breath sounds may indicate intrinsic lung disease or the ETT in the right mainstem bronchus.
Check an inspiratory pause: If both peak and plateau pressures are high, there is an issue of poor compliance; if only peak airway pressures are high, the problem is high airway resistance.
Abdominal compartment syndrome can also lead to elevated peak inspiratory and mean airway pressures, hypotension, and oliguria. Abdominal compartment syndrome should be suspected in patients with recent abdominal surgery and can be assessed by checking a bladder pressure (a pressure >15 mm Hg is abnormal, and >25 to 35 mm Hg often requires surgical treatment).

History and Examination

History

Assess pulmonary and cardiac history (history of pneumonia, COPD, reactive airway disease, pulmonary emboli, congestive heart failure, myocardial infarction (MI), smoking history), details of intubation (including if it was a difficult, complicated intubation), duration of mechanical ventilation, and modes used. Look for a recent history of secretions (noting their color and character), mucous plugging, or atelectasis.

Physical Examination

Assess vital signs, oxygenation, and end-tidal CO₂; check ETT position (should be ~22 to 24 cm at the lips, depending on the patient’s size), assess for ETT air leak (listen at mouth for gurgling with inspiration), assess for signs of respiratory distress (tachypnea, diaphoresis, retraction, paradoxic abdominal breathing, cyanosis), and auscultate the lungs and heart. Assess for excessive secretions and sputum production.

Neurologic Examination

A full neurologic examination, including assessment of mental status, cranial nerves, motor skills, and reflexes, as well as a sensory and cerebellar exam, should be performed on all patients.
Particular attention should be given to mental status and the potential for ventilator liberation.

Differential Diagnosis

Indications for mechanical ventilation include

Airway protection
- Bulbar dysfunction, decreased consciousness, for example, head injury with Glasgow Coma Score (GCS) <8 (to prevent massive aspiration)
- Airway obstruction (e.g., acute laryngeal edema)
- Loss of airway (e.g., neck trauma)
Ventilation failure
- Neurologic disease
  - Loss of ventilatory drive due to sedation, narcosis, or brain injury
  - Spinal cord injury or lesions (e.g., high cord lesions)
  - Peripheral nerve injury (e.g., phrenic nerve in surgery), Guillain-Barré syndrome, poliomyelitis, motor neuron disease
- Muscular disease (e.g., myasthenia crises)
- Chest wall trauma (e.g., flail chest, pneumothorax)
Oxygenation failure
- Ventilation perfusion mismatch (e.g., pulmonary embolus)
- Diffusion abnormalities (e.g., pulmonary edema, pneumonia)
Need for moderate-profound sedation, for example, for surgery, status epilepticus treatment, or elevated intracranial pressure (ICP) management

Diagnostic Evaluation

The following suggest the need for mechanical ventilation:

Vital capacity (VC): <10–15 mL/kg
Negative inspiratory force (NIF): Weaker than -20 cm H₂O
Tidal volume (TV): <5 mL/kg
Respiratory rate (RR): >35 breaths/minute
Minute ventilation (TV xRR): <10 L/minute
Rise in pCO₂: >10 mm Hg
Alveolar-arterial gradient (FiO₂ = 1.0): >450
PaO₂ with supplemental O₂: <55 mm Hg
PaO₂/FiO₂ (P/F): <150
Physical appearance: Labored breathing, retracting, nasal flaring, paradoxic abdominal breathing
Mental status: Comatose or not protecting the airway

Life-Threatening Diagnoses Not to Miss

Respiratory failure due to massive pulmonary embolism or pneu-mothorax (both require emergent treatment)
Respiratory failure due to insecure airway (accidental extubation, esophageal intubation, or obstructed airway)

Treatment

Basic Ventilator Settings

Tidal volume (TV): A typical initial TV is 8 to 10 mL/kg. Higher TV (10 to 15 mL/kg) is associated with barotrauma. In patients with acute lung injury (ALI) or acute respiratory distress syndrome (ARDS), lung protective ventilation with 6 mL/kg of predicted body weight is recommended. There are some data that TV of 6 mL/kg might be protective in other disease processes as well. ↑TV = ↓PaCO₂ and ↑pH.

The pressure volume curves in Fig. 17.1 demonstrate both patient triggered breaths and if the patient is receiving too much tidal volume.
Respiratory rate (RR): Initial RR is often set at 12 breaths per minute. In patients with ALI/ARDS, low-volume, high-frequency respiration is sometimes used. ↑RR = ↓PaCO₂ and ↑pH.
Fraction of inspired oxygen (FiO₂): Oxygenation goals are to maintain an O₂ saturation >90% and a PaO₂ >60 mm Hg utilizing the lowest FiO₂ possible to avoid oxygen toxicity and free radical injury. Typical initial setting is FiO₂ of 40%. A PaO₂ slightly <60 mm Hg can be accepted in the setting of ARDS if the tradeoff is higher plateau pressures and greater volutrauma. Causes of hypoxia include endobronchial intubation, accidental extubation, ventilator dysfunction, pneumothorax, pulmonary embolus, and primary pulmonary pathology (pneumonia, reactive airway disease, ARDS, pulmonary contusion, etc.). In patients with methemoglobinemia, ABGs will reveal normal PaO₂ in the context of cyanosis. The oxygen saturation on the ABG will be abnormally low. Pulse oximetry is unreliable in methemoglobinemia and tends to 85% regardless of the true oxygenation status or changes in FiO₂. In carbon monoxide poisoning, the pulse oximetry reveals a summation of oxyhemoglobin and carboxyhemoglobin and may give a falsely reassuring value in the face of arterial oxygen desaturation. Screening for either carboxyhemoglobin or methemoglobin can be done with co-oximetry. To troubleshoot hypoxia, increase the FiO₂ to 100%, auscultate the chest, check the ETT position, suction the patient and manually bag with 100% O₂, check the ventilator circuitry, check a chest x-ray (CXR), adjust FiO₂ and PEEP as needed, and treat the underlying pathology.
Positive end-expiratory pressure (PEEP): PEEP prevents alveoli from collapsing on expiration and facilitates alveoli expansion with subsequent breaths. Increases in PEEP (which affects mean alveolar pressure) and mean airway pressure can improve oxygenation and lung recruitment. PEEP may improve secretion drainage from otherwise closed alveoli and can reduce right ventricular venous return and also lower left ventricular afterload. The disadvantages of PEEP include risk of barotrauma and worsening hypoxemia in patients with localized lung disease such as pneumonia (lung heterogeneity). Because increasing PEEP will increase mean intrathoracic pressure as well, elevated PEEP can lead to decreased preload and hypotension. PEEP that exceeds central venous pressure can theoretically lead to elevations in ICP, though studies with PEEP up to 15 cm H2O do not show a significant effect on ICP or cerebral perfusion pressure (CPP).1 Other disadvantages include the risk of increased cardiac shunt, especially in patent foramen ovale, hepatic congestion, and decreased renal perfusion. PEEP over 20 cm H₂O is rarely beneficial and results in additional pressure-induced lung injury.

Extrinsic PEEP is the PEEP set on the ventilator (typically beginning at 5 cm H₂O). Intrinsic PEEP is also known as stacking or auto-PEEP and occurs when there is insufficient time for complete expiration of a tidal volume. On ventilator flow curves (see below), the expiratory phase fails to return to baseline when the inspiratory phase starts. An expiratory pause maneuver allows quantification of auto-PEEP (normal auto-PEEP should be zero). With auto-PEEP there is increase work of breathing because the patient must generate enough pressure to overcome this intrinsic PEEP and trigger the ventilator. The easiest way to treat auto-PEEP is to slow the RR and allow for additional expiratory time (this may require sedation). Other options include increasing flow rates to allow for a longer expiratory phase and applying extrinsic PEEP (<80% of auto-PEEP) to ease the work of breathing. Lower TV can limit the risk of hyperinflation as well. COPD patients are particularly susceptible to auto-PEEP. Excessive auto-PEEP, just like extrinsic PEEP, can lead to hypotension due to elevated intrathoracic pressures and decreased venous return (Fig. 17.2).
Flow rate and inspiratory:expiratory (I:E): The peak flow rate determines the maximal inspiratory flow. A normal flow rate is 60 L/minute. Increasing the flow rate will shorten the inspiratory time and prolong the expiratory time. This may be useful in patients with reactive airway disease. Conversely, slowing the flow rate will inverse the normal I:E (1:2) and can be employed to improve oxygenation in cases of ALI/ARDS, but at the expense of potential auto-PEEP.

Fig. 17.1 Tidal volume: Pressure volume curves demonstrating both patient triggered breaths and if patient is receiving too much tidal volume.

Fig. 17.2 Intrinsic positive end-expiratory pressure (PEEP): On ventilator flow curves the expiratory phase fails to return to baseline when the inspiratory phase starts.

Ventilator Modes

Volume Cycled Ventilation

In this mode, inspiration is terminated after a present TV is delivered a set number of times per minute. The pressure delivered depends on the lung mechanics (resistance and compliance). Advantages of this mode are that TV and minute ventilation are guaranteed, but disadvantages are that the airway pressure is not controlled, and this mode is somewhat less comfortable than other modes. Troubleshoot peak and plateau airway pressures. Examples of volume cycled ventilation include:

Controlled mechanical ventilation (CMV): The ventilator is preset to give only a certain number of breaths per minute of a set volume. The patient is not able to trigger any additional breaths. This mode is uncomfortable and requires sedation or paralysis and is infrequently used. CMV can lead to diaphragm dysfunction (Fig. 17.3).
Assist control/volume control (AC/VC): In this mode, the ventilator provides full tidal volume at a minimum preset rate with additional full tidal volumes given if the patient initiates extra breaths. The pressure varies with each breath. It provides near complete resting of ventilatory muscles and can be effectively used in awake, sedated, or paralyzed patients. However, patients can hyperventilate and become alkalotic or can “stack” breaths and develop barotrauma, making this a less appealing mode in patients with obstructive lung disease. This is one of the most widely used basic modes of ventilation. Note in Fig. 17.4 that the dip before the assisted breath indicates patient initiation.
Synchronized intermittent mandatory ventilation (SIMV): The ventilator provides set TV at a preset rate. When a ventilator breath is programmed to occur, the ventilator waits a predetermined trigger period. The patient can take additional breaths, but the TV of these extra breaths is dependent on the patient’s inspiratory effort. SIMV can be combined with pressure support to augment spontaneous breaths with a prespecified pressure (pressure support). SIMV can cause chronic respiratory fatigue if the set ventilatory rate is too low, resulting in high respiratory rate, rising pCO₂, increased work of breathing, greater oxygen consumption, and elevated blood pressure. SIMV is not a favored mode of ventilation because of increased work of breathing (Fig. 17.5).