Monitoring has been defined as “repeated or continuous observations or measurements of the patient, his or her physiologic function, and the function of life support equipment, for the purpose of guiding management decisions, including when to make therapeutic interventions, and assessment of those interventions.”1
Respiratory monitoring refers to the process of continuously evaluating the cardiopulmonary status of patients for the purpose of improving clinical outcomes. The goals of monitoring include alerting clinicians to changes in the patient’s condition and improving our understanding of pathophysiology, diagnosis, and cost-effective clinical management. These goals are accomplished through the use of physical examination, monitoring equipment, measurements, calculations, and alarms.
The goals of this chapter are to introduce the most common forms of respiratory monitoring in the intensive care unit (ICU), describe the information they provide, and discuss their application. Some of the information that normally would be included under respiratory monitoring, such as physical assessment, blood gas interpretation, and hemodynamic monitoring, is reviewed in other chapters of this book.
Arterial pressure of carbon dioxide (Paco2) is traditionally thought of as the standard for assessing ventilation (see Chapter 8). However, changes in the patient’s metabolism, lung mechanics, ventilatory efficiency, and equipment function will occur before changes are seen in the blood gases. It is therefore important to monitor the ventilatory parameters in addition to the blood gases. Table 14-1 provides a list of frequently used ventilatory parameters and their commonly cited reference ranges and critical values, with the critical value representing the threshold for insufficiency. In general, the respiratory therapist (RT) should not judge a patient’s status based on a single critical value, but instead should assess these parameters in combination with each other.
|Parameter||Common Reference Range||Critical Value|
|Tidal volume (VT)||5-8 mL/kg PBW||<4-5 mL/kg or <300 mL|
|Frequency (fb)||12-20 breaths/min||>30-35 breaths/min|
|Rapid shallow breathing index (RSBI)||>105 without PS or CPAP|
|Dead space–to–tidal volume ratio (VD/VT)||0.25-0.40||>0.60|
|Minute volume ()||5 to 6 L/min||>10 L/min|
|Vital capacity (VC)||65 to 75 mL/kg||<10-15 mL/kg|
|Maximum inspiratory pressure (PImax)||−80 to −100 cm H2O||0 to −20 cm H2O|
CPAP, continuous positive airway pressure; PBW, predicted body weight; PS, pressure control.
Ventilation is the process of moving gases between the atmosphere and the lung. These gases occupy spaces commonly called lung volumes. Although lung volumes have been described and their measurement discussed in Chapter 9, their importance to the critical care clinician is emphasized here.
Tidal volume (VT) is defined as the volume of air inspired or passively exhaled in a normal respiratory cycle. VT for a healthy person varies with each breath but usually ranges between 5 to 8 mL/kg of predicted body weight.2
VT has two components: alveolar volume (VA), or the portion of VT that effectively exchanges with alveolar-capillary blood, and dead space volume (VD), or the portion of VT that does not exchange with capillary blood. The common reference range cited for VD is 25% to 40% of the VT. The conductive airways and alveolar units that are ventilated but not perfused create the true or physiologic dead space. If the dead space exceeds 60% of the VT, the patient may need ventilator support to help with the associated increase in the work of breathing.2
In healthy, spontaneously breathing people, the VT occasionally increases to three or four times normal levels. These larger tidal breaths are known as sighs and normally occur about 6 to 10 times each hour. In acutely ill patients, there is often a loss of the sigh, and the size of the patient’s VT tends to diminish.3 A VT less than 5 mL/kg may indicate the onset of a respiratory problem.2 Impending respiratory failure causes VT to become more irregular.4 If shallow breathing without occasional sighing is maintained for prolonged periods, atelectasis and pneumonia may result, especially in patients breathing high oxygen concentrations or having compromised mucociliary clearance.
Conditions that may cause the VT to be reduced include pneumonia, atelectasis, chest or abdominal surgery, chest trauma, acute exacerbation of chronic obstructive pulmonary disease (COPD), congestive heart failure (CHF), pulmonary edema, acute restrictive diseases such as acute respiratory distress syndrome (ARDS), neuromuscular diseases, and CNS depression (especially of the respiratory centers). Larger than normal VT may be seen with metabolic acidosis, sepsis, or severe neurologic injury.
Critically ill patients without an artificial airway may not tolerate the measurement of VT. To accurately measure VT, a facemask or mouthpiece is required. Patients often change their breathing patterns when a mask or mouthpiece is applied, which alters their VT.
Patients receiving continuous mechanical ventilation (CMV) are routinely ventilated with VT of 8 to 10 mL/kg, approximately two times the normal spontaneous VT. When normal spontaneous VT is used during CMV without positive end-expiratory pressure (PEEP), there is a reduction in functional residual capacity (FRC), an increase in intrapulmonary shunt, and a fall in partial pressure of arterial oxygen (Pao2). These potentially harmful conditions can be reversed in part or totally by increasing the VT or by applying PEEP.5
The use of higher VT ventilation can cause complications, particularly in patients with severe respiratory failure.6–9 Evidence exists that lung injury may occur with a high VT that increases alveolar pressures (plateau pressure) beyond 30 cm H2O.6,9 The use of high-VT ventilation may predispose patients to volutrauma, a lung injury that occurs from overdistention of the terminal respiratory units. Volutrauma often develops in nondependent lung regions and is a main reason why lung damage persists after recovery from severe protracted ARDS.10 To avoid this lung injury, patients at risk for developing ARDS should be ventilated with mechanical VT of 6 mL/kg or less at a higher frequency (breaths per minute) to maintain an acceptable acid-base balance (pH > 7.30).9 Unfortunately, patients receiving low VT (4 mL/kg) who have a strong respiratory drive may experience breath “stacking.”11 The stacking results from a patient trying to inhale a VT greater than set, decreasing their airway pressure and triggering an additional breath on top of the previous VT.
When using a smaller VT, the application of PEEP maintains FRC and prevents the fall in Pao2. Although no single approach to setting PEEP has been adopted, a recent review recommends setting the PEEP level to that resulting in the best compliance and lowest driving pressure.6
Monitoring VT during mechanical ventilation of a critical ill patient is crucial. Discrepancies between set and measured VT are often seen in these patients. Most of the time, the differences are not clinically significant, and the clinician can make small adjustments in the VT settings to meet the patient’s delivered VT needs. The differences are often caused by the compressible volume of the ventilator circuit or environmental factors at the different locations of the inspiratory and expiratory flow sensors (i.e., heated, humidified gases or differing flow profiles). Compressible volume is an important consideration in neonatal and pediatric patients and in patients with higher peak airway pressures and lower VT. Most of today’s ventilators will correct for volume loss to the ventilator circuit and humidifier if circuit compliance correction is selected and performed before the ventilator and circuitry are connected to the patient. Other sources that may cause a difference between set and measured VT include leaks in the ventilator circuit, a leaky endotracheal (ET) tube cuff, and bronchopleural fistula.
A low measured VT also can be caused by severe air trapping or dynamic hyperinflation, which is a problem seen with severe airway obstruction. If not enough time is allowed for exhalation before the next breath is initiated by the ventilator, the subsequent VT will stack on top of the previous breath. This problem creates higher peak airway pressure, and pressure injury to the lung or barotrauma may result. Increasing expiratory time, administering bronchodilators, or decreasing the VT may help resolve the problem. Expiratory time is increased by reducing ventilator rate (if inspiratory time remains constant), increasing inspiratory flow rate, or decreasing inspiratory time.
If the circuit compliance feature is not used, then corrected tidal volume will need to be calculated. The corrected or delivered VT is determined by calculating the compressible volume of the ventilator circuit and subtracting it from the exhaled VT. To calculate the compressible volume of the ventilator circuit, the clinician needs to know the compliance of the ventilator circuit being used. If the circuit’s compliance is unknown, then it can be determined by increasing the high pressure limit to 120 cm H2O, setting PEEP to 0 cm H2O, and setting a VT of 100 mL. Then divide the 100 mL by the resulting peak inspiratory pressure to obtain circuit compliance. The compliance of the adult ventilator circuit varies with the structure and diameter of the tubing but is generally 1 to 3 mL/cm H2O. If the patient is being ventilated with high airway pressures, a significant portion of the VT is lost to tubing expansion, and erroneous respiratory system compliance measurements would be computed if this loss were not considered.
Where VT is monitored often plays an important role in data interpretation. Proximal volume monitoring eliminates the loss of compressible volume to the circuit and may reflect a more accurately delivered VT than does expiratory limb monitoring. This is particularly true during conditions of low VT, low lung compliance, and high airway resistance (Raw). Proximal monitoring is not without drawbacks. Proximal sensing makes the measuring device more susceptible to condensate and secretions, potentially reducing reliability and accuracy. It also may increase circuit resistance and dead space, increasing the patient’s imposed work of breathing.
Air trapping and dynamic hyperinflation often occur in mechanically ventilated patients with severe airway obstruction. One technique that can measure the degree of dynamic hyperinflation is to measure the volume of gas exhaled during an expiratory hold on a ventilator. This maneuver measures the additional trapped gas above the patient’s normal FRC. Ventilatory adjustments that reduce minute ventilation (), VT, and lengthen expiratory time should reduce the degree of air trapping.
Patients receiving synchronous intermittent mandatory ventilation (SIMV) are allowed to breathe spontaneously through the ventilator circuit between mechanical breaths. As a result, their spontaneous VT may differ in size from the mechanical VT being delivered by the ventilator. It is important for the clinician to distinguish between spontaneous and mechanical VT during weaning so that a true assessment of the patient’s ventilatory status can be made.
When a patient is ready to be weaned from mechanical ventilation, a spontaneous breathing trial (SBT) should be attempted. The patient should be monitored for gas exchange, respiratory distress, and hemodynamic stability during this trial. Box 14-1 outlines the criteria used to define SBT failure.12 VT also may decrease if the patient fatigues during the SBT, as indicated by breath volumes below 300 mL or less than 4 mL/kg.12 Usually more than one of these signs is present when a patient fails an SBT.
RSBI values greater than 105 have been reported to be strong prognostic indicators of weaning failure.13 More predictive than a single measurement is the progressive change in RSBI. Patients who demonstrate a significant increase in their RSBI on ventilator removal are very likely to fail weaning.14,15 Serial measurements of the RSBI during a period of spontaneous breathing may more accurately predict the ability to be successfully weaned from mechanical ventilator support.15 However, early measures of RSBI during a spontaneous breathing trial appear to be of little value in predicting weaning outcomes in COPD patients.16
is the product of VT and respiratory rate or frequency and represents the total volume of gas inspired or exhaled by the patient in 1 minute. The average for a normal healthy adult is 5 to 6 L/minute.2 As with VT, approximately 25% to 40% of is dead space ventilation. is often increased in the early stages of respiratory failure; it is not until later stages of failure that begins to fall.
Paco2 is considered an indicator of the adequacy of ventilation. The relationship of to Paco2 indicates the efficiency of ventilation. A of 6 L/minute is usually associated with a Paco2 of approximately 40 mm Hg in a healthy person with a normal metabolic rate. If a higher than normal occurs with a normal Paco2 in a patient with a normal metabolic rate, there must be an increase in dead space ventilation. This is usually associated with hypovolemia, pulmonary embolism, or obstructive disease.
An increase in carbon dioxide production caused by an increased metabolism (as occurs with trauma or fever) or high carbohydrate loading accompanying parenteral feedings may result in an increased in with a normal Paco2 (see Chapter 18). The elevated production of CO2 requires an increase in ventilation to maintain the Paco2 in normal range. Patients with varying metabolic rates should be ventilated with modes that allow them to set their own frequency of breathing and thereby vary as needed to maintain a normal Paco2.
A resting spontaneous of 10 L/minute or less during an SBT is often considered an acceptable weaning criterion. may fluctuate widely both during traditional T-piece weaning and during low-rate SIMV. Many therapeutic activities also can alter . A good example is the postoperative administration of opiates to control pain. Opiates like morphine can blunt the respiratory drive sufficiently to cause a sudden onset of hypoventilation.
For these reasons, should be monitored frequently before and during weaning. A sudden rise or drop in should be investigated because both may signal ventilatory failure. If a greater than 10 L/minute is needed for a mechanically ventilated patient to maintain a normal Paco2, weaning is not likely to be successful. The elevated indicates that the patient’s respiratory muscles will probably fatigue when the mechanical ventilation is discontinued. Compared with the RSBI, however, a patient’s spontaneous is a much less reliable predictor of weaning success.12,13
Vital capacity (VC) is the maximum volume of gas that can be expired from the lungs following a maximal inspiration. The typical reference range for healthy subjects is 65 to 75 mL/kg of predicted body weight.2 The VC maneuver depends on the patient’s effort and position; the largest values usually are recorded with the patient in the upright position.
The VC is an excellent measurement of ventilatory reserve in the cooperative patient. It reflects the respiratory muscle strength and volume capacity of the lung while the patient is performing a maximal inspiratory and expiratory maneuver. These are of paramount importance in maintaining an adequate cough to clear secretions and in guaranteeing periodic inflation of alveoli that may be prone to collapse.
As described in Chapter 9, VC can be measured as either a forced maneuver (FVC) or a slow maneuver (SVC). The SVC maneuver may be much easier for the patient to perform, especially if the patient is lethargic, medicated, or experiencing pain or has obstructive airway disease.
The accuracy and repeatability of the values depend on the patient’s effort and the coaching skills of the therapist. It is important that the patient understand how to perform the maneuver correctly. A tight seal around the mouthpiece or mask is crucial. The patient may perform better if able to observe the tracing generated by the effort or to receive some similar visual feedback.
During preoperative evaluation of a patient’s lung function, an FEV1% (ratio of FEV in 1 second to the FVC) less than 50% of normal or an FVC of less than 20 mL/kg indicates that the patient may be at high risk for developing pulmonary complications in the postoperative period. Factors that influence the degree of decrease in VC during the postoperative period and the incidence of postoperative pulmonary complications include the surgical site, smoking history, age, nutritional status, obesity, pain, type of anesthesia, and type of narcotics used for pain control.
Although many factors can contribute to a reduction in VC postoperatively, one of the most important is the incision site. Thoracic and abdominal surgeries produce a significant fall in VC postoperatively, and this reduction may persist for a week or more.17,18 Operative procedures below the umbilicus are associated with fewer pulmonary complications.
A VC of 10 to 15 mL/kg is usually needed for effective deep breathing and coughing. Values below this range are usually associated with impending respiratory failure.2 Values greater than 15 mL/kg usually indicate adequate ventilatory reserve and the possibility of discontinuing CMV and extubation.
VC also is measured to follow the responsiveness of the patient to various respiratory therapies such as incentive spirometry or intermittent positive-pressure breathing (IPPB). A common goal of both these maneuvers is to promote lung expansion.
FRC is the volume of gas remaining in the lungs at the end of a normal passive exhalation. It is rarely measured in the ICU. The FRC is continuously in contact with pulmonary capillary blood and undergoing gas exchange. It is composed of a combination of residual volume (RV) and expiratory reserve volume (ERV). Normally, FRC is about 40 mL/kg of predicted body weight, or about 35% to 40% of total lung capacity (TLC). FRC can vary from breath to breath by as much as 300 mL in healthy people.19 Changes in body position affect FRC, with the greatest values being recorded in the upright position.20 These changes in FRC between 30-degree Fowler and supine positions may not occur in overweight or obese patients.21 When alveolar volume falls, as with atelectasis, FRC is reduced, and there are regional changes in alveolar pressure-volume curves. Initially, as FRC decreases, dependent alveoli collapse and require higher distending pressures to inflate. Because the apical alveoli remain at least partially open, they are more compliant and require less pressure to inflate. Subsequently, during mechanical ventilation, the inspired volumes are preferentially distributed to the apices. This distribution of inspired volumes to nondependent, poorly perfused alveoli contributes to the abnormal gas exchange seen in patients with decreased FRC. Dependent atelectatic alveoli open throughout inspiration as alveolar pressure increases and collapse during expiration. Experimental evidence now demonstrates that repeated collapse and reinflation of alveoli leads to alveolar damage, capillary rupture, and considerable lung injury. The application of PEEP prevents alveolar collapse and may reduce the extent of acute lung injury.22–24 Therapeutic modalities, such as PEEP or continuous positive airway pressure (CPAP), increase FRC. This is the primary benefit to patients with atelectasis and refractory hypoxemia.
Airway pressures should be measured as closely as possible to the ET tube. This prevents resistance caused by the ventilator circuit from influencing the peak pressure measurement. On certain occasions, as when using high-frequency ventilation or tracheal gas insufflation (TGI), the pressure should be measured at the distal tip of the ET tube.
Peak inspiratory pressure (PIP) is the maximum pressure attained during the inspiratory phase of mechanical ventilation (Fig. 14-1). It reflects the amount of force needed to overcome opposition to airflow into the lungs. Causes of this opposition to flow include resistance generated by the ventilator circuit, the artificial airway (ET tube), and the patient’s airways and elastic recoil of the thoracic cage and the lungs. Sudden increases in PIP or peak airway pressure should alert the clinician to the possible presence of a patient-ventilator interface problem. Potential causes of an increase in peak pressure are listed in Box 14-2.
An increase in PIP while the plateau pressure (explained later) remains unchanged suggests an increase in Raw. Common causes include bronchospasm, airway secretions, and mucous plugging. As a result of the relationship between PIP and Raw, monitoring the PIP provides valuable information about the bronchodilator-induced changes in lung function of the mechanically ventilated patient.25,26 It is important to note that whenever changes in the PIP are used for evaluating Raw, no changes in the inspiratory flow, flow pattern, or VT should be made.
High PIP may cause barotrauma.23,27 However, evidence suggests that high peak alveolar pressures from overdistention lead to alveolar rupture, or volutrauma.23,28