Arterial Pulse Oximetry

The goal of breathing and circulation is adequate tissue oxygenation. All organs require O₂ delivery that meets O₂ use demands; the brain and kidneys have particularly high requirements. An important innovation in monitoring is the use of oximetry—a color spectrum measurement of pulsing arterial blood is used for continuous assessment of arterial oxygenation (SpO₂). The human eye is not good at detecting or quantifying arterial hypoxemia. Frank cyanosis does not develop until there is at least 5 g/dl of deoxyhemoglobin in the blood.³ The threshold at which cyanosis becomes apparent is affected by skin perfusion, skin pigmentation, and hemoglobin concentration. ABG analysis has been the accepted method of detecting hypoxemia in critically ill patients, but obtaining arterial blood can be painful and cause complications, and ABG analysis does not provide immediate or continuous data. For these reasons, SpO₂ has become the standard for a continuous, noninvasive assessment of SaO₂. SpO₂ does not measure PaCO₂, and patients breathing an elevated FiO₂ can build up CO₂ (increased PaCO₂), although SpO₂ values are acceptable. Ventilatory failure may go unnoticed unless ABGs are measured.

SpO₂ measurements are based on spectrophotometric principles, which are based on the law of Beer-Lambert. Lightweight probes direct filtered light of specific wavelengths (usually two) through a digit, the bridge of the nose, or an earlobe or reflected from a forehead sensor. The relative absorption of these spectrophotometric beams after passing through the tissue (which differs for O₂ saturated and desaturated blood) is converted into the appropriate saturation value with processor-stored algorithms.

Tissue O₂ sensors designed to measure SaO₂ of muscle or the brain were developed more recently.⁴ Brain oxygenation is crucial, and deep muscle tissue in compartment syndromes can become deoxygenated. This tissue oxygen sensing technique involves positioning of an emitter and detector (of usually four wavelengths) on the skin surface over the tissue or organ of interest. Light from the emitter reflects from tissue at a depth of one-third the distance between the emitter and detector. The light received by the detector is read, and algorithms determine tissue oxygenation, not SpO₂.

Although SpO₂ has been universally adopted, it does have limitations (Box 46-2).^5,6 Motion artifact is an important problem, resulting in inaccurate readings and false alarms. Motion artifacts are common because of shivering, seizure activity, pressure on the sensor, or transport of the patient. The choice of probe site may also affect accuracy. Finger probes appear to be more accurate than forehead, nose, or earlobe probes during low perfusion states. Intense daylight and fluorescent, incandescent, xenon, and infrared light sources have caused errors in SpO₂ readings. Anemia and deeply pigmented skin can affect the accuracy of SpO₂; however, the effect of anemia is not clinically significant until the hemoglobin level is markedly reduced. Carboxyhemoglobin and methemoglobin can produce falsely high SpO₂ values, and some colors of nail polish, particularly blue, green, and black, interfere with light transmission and absorbency, as do some blood-borne dyes, such as indocyanine green and methylene blue, which tend to produce falsely low SpO₂ values. Although rare, exposure to numerous toxins and drugs, including topical benzocaine, can elevate methemoglobin and produce falsely elevated SpO₂ values.

Oxygen Consumption

Oxygen consumption () is the volume of O₂ consumed by the body in milliliters per minute. Normal resting is approximately 250 ml/min, and increases with activity, stress, and temperature. The acquisition of O₂ from the lungs into the circulatory system is described by the Fick equations:

< ?xml:namespace prefix = "mml" />V˙O2=Q˙T(CaO2−Cv¯O2)orQ˙T=V˙O2/(CaO2−Cv¯O2)

in which is cardiac output (CO), and CaO₂ and are arterial and mixed venous oxygen contents. If the values for , CaO₂, and are normal, this becomes:

V˙O2in ml/min =Q˙T(CaO2−Cv¯O2)

=(5000 ml/min)(20 ml/100 ml−15 ml/100 ml)

=(5000 ml/min)(5 ml/100 ml)=250 ml/min

To an engineer or systems analyst, the function of the lungs is summarized by the Fick equation—O₂ in the alveoli diffuses into mixed venous blood flowing by at the pace of CO. This process converts deoxygenated venous blood to oxygenated arterial blood.

An alternative calculation for that does not require an arterial or mixed venous blood sample or measurement of cardiac output (CO) is:

V˙O2=[(FiO2)(V˙I)]−[(F E¯O2)(V˙E)]

where FiO₂ and are the mean inspired and expired fractional concentrations of oxygen, and and are the inspired and expired minute ventilations. If equals (normally is slightly greater than , but the difference is small), this becomes:

V˙O2=(FiO2−F E¯O2)V˙E

If the values for minute ventilation and inspired and expired gas concentrations are normal, this becomes:

V˙O2=(0.21−0.168)(6 L/min)=0.252 L/min,or approximately 250 ml/min

A normal resting of 250 ml/min represents approximately 25% of normal O₂ delivery (1000 ml/min). The blood carries a large reservoir of O₂ that can diffuse into deoxygenated tissues under high O₂ demand conditions.

may be useful in determining nutritional requirements and adequacy of O₂ delivery and may occasionally help determine the cause of a high ventilation requirement. If there is a stable tissue demand for O₂, measurements of may be used to follow the hemodynamic response to therapeutic interventions.

Alveolar-Arterial Oxygen Tension Difference

The alveolar and arterial oxygen tension difference (P(A − a)O₂) is a useful measurement of the efficiency of gas exchange. A healthy person breathing room air has P(A − a)O₂ of approximately 5 to 15 mm Hg. This value increases with age to approximately 10 to 20 mm Hg in elderly adults. P(A − a)O₂ also increases normally with an increase in FiO₂. A healthy person has P(A − a)O₂ of 5 to 15 mm Hg while breathing room air; however, P(A − a)O₂ increases to 100 to 150 mm Hg when the person is breathing 100% O₂.

Most importantly, an abnormal increase in P(A − a)O₂ is associated with gas exchange problems. If PaO₂ is 80 mm Hg while the patient is breathing 100% O₂, a significant gas exchange problem is present even though oxygenation seems acceptable.

If PaO₂ is 80 mm Hg, PaCO₂ is 40 mm, FiO₂ is 1, and barometric pressure (PB) is 760 mm Hg, then:

PAO2=PiO2−(PaCO2) (1.25)

PiO2=[(PB−PH2O) (FiO2)]=713

PAO2=[(760−47) (1)]−(40) (1.25)=663 mm Hg

P(A−a)O2=PAO2−PaO2=663−80

P(A−a)O2=583 mm Hg

where P_H2O is water vapor pressure. P(A − a)O₂ is markedly elevated considering that normal (A − a)O₂ is 100 to 150 mm Hg while the patient is breathing 100% O₂. (A − a)O₂ also can be used to give a rough estimate of percentage shunt, where:

Shunt≅(P(A−a)O2on 100% O2)20

In this example, percentage shunt would be approximately 29%: P(A − a)O₂/20 = 583/20 = 29.2%.

P(A − a)O₂ takes into account PaCO₂ and eliminates hypoventilation and hypercapnia from consideration as the sole cause of hypoxemia. Although P(A − a)O₂ is infrequently calculated, astute experienced clinicians consciously or subconsciously estimate P(A − a)O₂ of every blood gas value.

PaO₂/FiO₂ Ratio

The PaO₂/FiO₂ ratio has become important for the determination of the extent of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) in multicenter collaborative studies.7,8 A normal PaO₂/FiO₂ ratio while breathing room air is about 400 to 500 mm Hg. The PaO₂/FiO₂ ratio provides an index for the effect of O₂ on PaO₂ when a range of FiO₂ settings may be prescribed. The index allows comparisons of severity between patients or if FiO₂ is changed in the same patient. ARDS has been defined by a PaO₂/FiO₂ ratio less than 200 mm Hg. The PaO₂/FiO₂ ratio is easy to calculate and a reliable index of gas exchange when FiO₂ is greater than 0.5 and PaO₂ is less than 100 mm Hg—values often observed in critically ill patients. The level of applied mean airway pressure (MAP), which is strongly affected by PEEP, must also be considered as an independent factor that influences the PaO₂/FiO₂ ratio.

Oxygenation Index

Calculation of oxygenation index (OI) by the following equation provides an index that accounts for FiO₂ and MAP:

OI=FiO2*MAPPaO2

Quantification of Shunt

The most accurate and reliable measure of oxygenation efficiency is direct computation of the physiologic shunt (). The physiologic shunt is computed as follows:

Q˙S/Q˙T=(CcO2−CaO2)/(CcO2−Cv¯O2)

where CcO₂ is the oxygen content of alveolar capillary blood, CaO₂ is the oxygen content of arterial blood, and is the oxygen content of mixed venous blood, all expressed in milliliters of O₂ per 100 ml of blood. When the patient is breathing 100% O₂, can be estimated as follows:

Q˙S/Q˙T=[(P(A−a)O2)][0.003]/[(P(A−a)O2)][0.003]+[CaO2−Cv¯O2]

For measurement of physiologic shunt, both an arterial and a mixed venous blood sample must be obtained. A true mixed venous blood sample can be obtained only from the distal sample port of an indwelling pulmonary arterial catheter. The total O₂ content of the arterial, mixed venous blood, and pulmonary capillary blood (CaO₂, , CcO₂) is calculated in the same manner as any O₂ content calculations:

O2content=(1.34) (Hb) (SO2)+(0.003) (PO2)

where Hb is the hemoglobin concentration, SO₂ is the oxygen saturation, and PO₂ is the partial pressure of oxygen. If the patient is breathing 100% O₂, the capillary saturation is 100%, the PCO₂ (capillary PO₂) being the calculated PAO₂ value. Samples should be obtained and analyzed quickly to avoid error from continued metabolism. Similar to P(A − a)O₂, is influenced by mismatching and by fluctuations in mixed venous oxygen saturation () and FiO₂. A “shunt” calculation when FiO₂ is less than 1.0 is defined as venous admixture. If venous admixture is elevated but all alveoli are patent, venous admixture decreases toward the normal value (<5%) as FiO₂ is increased. Conversely, if increased venous admixture is caused by a true shunt such as an intracardiac defect, there would be no change in venous admixture as FiO₂ is increased.

Murray Lung Injury Score

ARDS is a syndrome of severe lung injury that was originally described by Ashbaugh and Petty in 1970.⁹ Evaluating and treating a patient with ARDS is a primary challenge for the ICU clinician. To monitor the severity of this disease, Murray and colleagues¹⁰ developed a lung injury score that is often calculated in studies of ALI/ARDS. The Murray lung injury score quantifies the injury level using the following four factors: chest radiographic findings, PaO₂/FiO₂ ratio, positive end expiratory pressure (PEEP) setting, and compliance. The Murray lung injury score is an example of a composite score that allows quantification of lung status according to different aspects of the injury—gas exchange, radiographic findings, and mechanics. This score is used as an index of the effectiveness of therapy or for interstudy comparisons. The method for calculating the Murray lung injury score is shown in Box 46-3. Other measures of lung injury are listed in Box 46-4.

Dead Space

The dead space/tidal volume (V_D/V_T) ratio is a measure of the efficiency of gas exchange. This ratio is an estimate of the proportion of ventilation participating in diffusion of CO₂. V_D/V_T can be calculated from the Enghoff modification of the Bohr equation as follows:

VD/VT=(PaCO2−P E¯CO2)/PaCO2

where is the CO₂ concentration in mixed expired gas. A rapid response capnometry or exhaled flow analysis provides a volumetric CO₂ method for attaining values.¹¹ When is determined, a specimen of arterial blood should be drawn for ABG analysis. When the gas and blood samples are analyzed, the preceding formula can be used to calculate V_D/V_T.

In healthy persons who are sitting, the V_D/V_T ratio is 0.20 to 0.40. This value varies little with age, position, exercise, V_T, or breath holding. In the setting of critical illness, however, the V_D/V_T ratio commonly exceeds 0.6. Frequently, the V_D/V_T ratio is increased in patients with congestive heart failure, pulmonary embolism, ALI, or pulmonary hypertension and in patients undergoing mechanical ventilation. The V_D/V_T ratio has been used to evaluate patients being considered for weaning from mechanical ventilation. A V_D/V_T ratio greater than 0.60 requires continuation of ventilatory support. Increased V_D/V_T in the early phase of ARDS has been associated with an increased risk of death.¹²

Monitoring of Inspired and Exhaled Gas Volumes

Although the best index of effective ventilation is measurement of PaCO₂, measurement of inspired and expired gas volumes is an important aspect of monitoring patients receiving mechanical ventilatory support. For patients receiving controlled mechanical ventilation, minute ventilation (), respiratory rate (f), and V_T are assessed by:

V˙E=(VT)(f) and VTaverage=V˙E/f

For patients receiving ventilation in the synchronized intermittent mandatory ventilation (SIMV) mode, total minute ventilation () is the sum of the patient’s spontaneous minute ventilation () and the machine minute ventilation () provided:

V˙ETOT=V˙Esp+V˙Emach andV˙ETOT=(VTmach)(fmach)+(VTpatient)(fpatient)

With an adequate V_T, increases in minute ventilation tend to increase alveolar ventilation and decrease PaCO₂, whereas decreases in minute ventilation tend to have the opposite effect. However, in the presence of rapid shallow breathing with normal or elevated minute ventilation, a decrease in effective ventilation can result in an increase in PaCO₂. This effect is caused by ineffective shallow tidal breaths that are at or below dead space volume. Spontaneous respiratory rate often is a sensitive indicator of the need for mechanical ventilation. Rates greater than 20 breaths/min may indicate distress, and a rate greater than 30 breaths/min with a spontaneous V_T of less than 300 ml often indicates the need for mechanical ventilatory support in adults because a large proportion of ventilatory effort is being expended to move dead space gases.

Inspired versus Expired Tidal Volume

Normal inspired V_T and expired V_T should be nearly the same. However, in the presence of an air leak, inspired V_T may be larger than expired V_T, and measurement of delivered V_T versus exhaled V_T may be useful in detecting and quantifying the size of a leak—a situation that may require immediate attention.

Capnography

Capnometry is the measurement of CO₂ at the airway opening during the ventilatory cycle. Capnography refers to plotting CO₂ concentration against time or against exhaled volume. The normal CO₂ waveform is displayed in Figure 46-4. The height of the capnogram (the peak value) indicates the end-tidal CO₂ value. PetCO₂ normally is 1 to 5 mm Hg less than PaCO₂, ranging between 35 mm Hg and 43 mm Hg. Because PetCO₂ in healthy persons closely approximates PaCO₂, this measure is a potentially useful noninvasive index of the adequacy of ventilation. Abnormal waveform contours can indicate changes in the distribution of ventilation and perfusion, or airway obstruction. These changes typically are an irregular increase in CO₂ level and a lower than normal end-tidal CO₂ level. Positive pressure ventilation (especially with PEEP), pulmonary embolism, cardiac arrest, and pulmonary hypoperfusion also may cause an increase in PaCO₂ to PetCO₂ difference [P(a − et)CO₂]. Exercise and a large V_T can reverse the P(a − et)CO₂ difference, and PetCO₂ can exceed PaCO₂ temporarily.

Patients for whom capnometry may be a useful monitoring tool include patients with normal lungs but an unstable ventilatory drive who are breathing spontaneously or receiving low-level ventilatory support. In these patients, capnometry readings should initially be validated by comparison with PaCO₂. Changes in PetCO₂ can be used to alert the clinician to potential changes in patient ventilation. Thereafter, periodic reevaluation should be performed as the patient’s clinical state changes. Capnometry has been extremely useful in emergency situations, such as verification of endotracheal intubation and assessment of blood flow during or after cardiac arrest. Small in-line CO₂ monitors that employ colorimetry are now routinely used to verify endotracheal intubation.¹³

Although PetCO₂ and PaCO₂ values tend to correlate at a single point in time, correlation between changes in PetCO₂ and changes in PaCO₂ tend to be weaker.¹⁴ Decreases in ventilation are reflected by increases in PetCO₂ and PaCO₂. However, with very small V_T, PaCO₂ increases, whereas PetCO₂ may decrease. Although the appropriate role of capnometry in critical care may be unclear, integration of capnometry into modern ventilators is reasonable because the primary role of the ventilator is CO₂ extraction. As a guide for clinicians, the American Association for Respiratory Care (AARC) has created clinical practice guidelines for the use of capnometry in ventilated patients. Box 46-6 lists common causes of changes in monitored PetCO₂ values.

With improvements in infrared capnometry response time and a simultaneous measure of exhaled volume, volumetric CO₂ monitoring holds promise in the continuous monitoring of ventilation efficiency. VCO₂, or the net volume of CO₂ eliminated from the lungs, can be continuously monitored in a patient being weaned from mechanical ventilation as an indicator of adequate or improving ventilatory efficiency.¹⁵ The volumetric capnogram has been examined as a potential tool for detecting a pulmonary embolism¹⁶ and may be useful for tracking the efficiency of mechanical ventilation.¹⁷

Respiratory System Compliance

Respiratory system compliance during a tidal breath is an important measure of the stiffness of the lungs. Tidal compliance calculations should be routinely monitored in all ventilated patients. To attain an accurate assessment of compliance, two maneuvers must be performed because the alveolar pressures at end-inspiration and end-expiration are unavailable under dynamic conditions. An end inspiratory hold maneuver in a passive, ventilated patient allows equilibration of pressure across the lung and an estimation of peak alveolar pressure or the end inspiratory P_plat. Because compliance (C) is calculated as C = ΔV/ΔP, V_T (corrected for tubing compliance) is ΔV and (P_plat − PEEP_T) is ΔP. If auto-PEEP is present, it must be accounted for by adding the auto-PEEP level to the applied PEEP to attain a PEEP_T value.

Normal compliance ranges from 60 to 100 ml/cm H₂O. Diseases of the lung parenchyma, such as pneumonia, pulmonary edema, and any chronic disease causing fibrosis, cause decreased effective compliance. Acute changes, such as atelectasis, pulmonary edema, ARDS, and lung compression, caused by tension pneumothorax cause a rapid decrease in compliance. Compliance is often less than 25 to 30 ml/cm H₂O in patients with ARDS. Common causes of changes in respiratory system compliance are listed in Box 46-7. Several ventilators report breath-to-breath compliance and resistance values dynamically without the use of pause maneuvers. Monitoring these estimates can indicate impedance problems, but they should be verified by static maneuver calculations.

Chest Wall Compliance

In a significant proportion of patients, chest wall or abdominal pathology can influence the P-V relationship during ventilation. The external effect on the lungs of a pleural effusion or abdominal fluid (ascites) can increase airway pressure in a ventilated patient. Although this elevated pressure might be considered detrimental, it may buffer the lung-damaging effect of elevated airway pressure by reducing transpulmonary pressure (Ptp). In a passively ventilated patient who may be vulnerable to lung damage from elevated airway pressure, measurement of the chest wall effect can be made by esophageal or bladder pressure determinations. If the bladder pressure is elevated, Ptp is reduced but usually at the expense of effective ventilation.

End inspiratory Ptp can be monitored to evaluate the potential for overdistention—usually allowing some liberty in accepting higher P_plat to deliver adequate ventilation. The monitoring of end expiratory Ptp has been used more recently as a rationale for setting PEEP. A negative Ptp probably indicates lung closure (dependent lobe) during expiration that can result in lung opening and closing during the ventilatory cycle. Adequate PEEP is the PEEP level that establishes a positive Ptp or dependent lobe recruitment. (See Chapter 44 for details.)

Resistance

Depending on the driving pressure measured, various resistances can be calculated, including airway, pulmonary, chest wall, and total respiratory system resistance. An airway resistance (Raw) can be determined dynamically from simultaneous measurements of airflow and the pressure difference between the airway opening (P_ao) and the alveoli (P_alv) by Raw = (P_ao − P_alv)/flow. Because resistance changes throughout inspiration and expiration, and expiratory resistance generally is greater than inspiratory resistance, instantaneous measures of resistance are not performed clinically. Inspiratory resistance can be calculated simply during constant flow, volume ventilation. This allows monitoring of airway status over time or after the effects of bronchodilator therapy and is determined by dividing the pressure change by the flow rate (see previous equation).

Raw=ΔP/ΔF=(Ppeak−Pplat)/flow

where P_peak is peak airway pressure and P_plat is plateau pressure. Automated methods of measuring expiratory resistance have been integrated into some ventilators.

In ventilated patients, a significant component of the total flow resistance is from endotracheal tubes, which have highly curvilinear flow-resistive properties.²² In healthy persons, flow is relatively laminar during tidal ventilation and becomes turbulent only with increasing ventilatory demands. The flow resistance offered by the endotracheal tube increases markedly with increasing flow and varies with the size of the tube. Normal airway resistance is approximately 1 to 2 cm H₂O/L per second; however, intubated patients receiving mechanical ventilatory support typically have an airway resistance of 5 to 10 cm H₂O/L per second or more. Automated tube compensation modes have been added to mechanical ventilators to deliver flow that accounts for the added resistance of the endotracheal tube. Common causes of changes in airway resistance in mechanically ventilated patients are listed in Box 46-7.

Peak and Plateau Pressures

The maximum value of airway pressure at the airway opening during a ventilatory cycle is routinely monitored in the ICU. Peak airway pressure greater than 50 to 60 cm H₂O is generally discouraged because high values of peak pressure carry increased risk of barotrauma and hypotension.²³ An increase in peak pressure results from increased resistive pressure or increased elastic pressure from decreased lung or chest wall compliance. Measurement of end inspiratory P_plat helps to differentiate between the resistive and elastic components. The P_plat level should be monitored for all ventilated patients. P_plat ideally should not exceed 30 cm H₂O because elevated P_plat increases the likelihood of developing ventilator-induced lung injury.

Auto–Positive End Expiratory Pressure (Intrinsic Positive End Expiratory Pressure)

PEEP is the pressure maintained in the airway by the ventilator at end-exhalation. An alveolar pressure that exists above the applied or extrinsic PEEP level at end-exhalation is termed intrinsic PEEP or auto-PEEP. At the bedside, total PEEP is the sum of extrinsic PEEP and intrinsic PEEP. Confusion exists when total PEEP is designated as intrinsic PEEP; however, when PEEP is increased to counterbalance intrinsic PEEP, they approach equivalency.

Numerous factors, both internal and external to the patient, contribute to the development of auto-PEEP. Expiratory muscle activity can increase auto-PEEP and may interfere with attempts at assessment of auto-PEEP based solely on dynamic hyperinflation. Patients receiving mechanical ventilation for obstructive airways disease have a large degree of inhomogeneity in the emptying of lung units, and auto-PEEP can develop even at relatively low minute ventilation. Auto-PEEP is common in mechanically ventilated patients receiving high minute ventilation and occurs in patients with ARDS.²⁴ The presence of auto-PEEP can underestimate the effect of mean alveolar pressure when MAP is being monitored to reflect mean alveolar pressure. An increase in mean alveolar pressure owing to auto-PEEP may exacerbate the hemodynamic effects of positive pressure ventilation and increase the likelihood of barotrauma in a manner similar to the application of PEEP. In addition, auto-PEEP alters the effective trigger sensitivity of the ventilator, making it more difficult for the patient to trigger a ventilator-assisted inspiration.

Finally, if unrecognized, auto-PEEP leads to erroneous calculation of static lung compliance by underestimation of total PEEP. Decreasing minute volume can reduce or eliminate auto-PEEP; however, minimal auto-PEEP can be benign. In addition, increasing expiratory time allows more time for airways to empty normally, decreasing auto-PEEP. The use of extrinsic PEEP can partially overcome the trigger sensitivity problem seen with auto-PEEP and may provide a “stent” to allow more complete lung emptying.²⁵

Mean Airway Pressure

MAP represents the average airway pressure over the total ventilatory cycle. Correct measurement of this value requires continuous sampling of airway pressure at the airway opening—this is an automated feature of modern ventilators. MAP is related to mean lung volume, which correlates with oxygenation if perfusion is adequate. When MAP is increased, arterial O₂ levels often improve, but venous return and subsequently arterial pressure can be adversely affected.

In an effort to increase oxygenation while monitoring arterial pressure, the clinician can manage MAP by several means, including V_T, frequency, inspiratory-to-expiratory (I : E) ratio, and PEEP. The management of MAP relates to a concern for improving oxygenation balanced against its detrimental influence on venous return to the chest. Normally, expiratory resistance is greater than (twice) inspiratory resistance, and mean alveolar pressure normally is greater than MAP. For patients with COPD and elevated expiratory resistance, high mean alveolar volume can be significant during mechanical ventilation. For patients with ALI/ARDS, airway resistance is more typically low, so MAP and mean alveolar pressures may be similar. Mean alveolar volume is related to gas exchange, in particular, oxygenation, depending on regional lung perfusion. Mean alveolar pressure or mean alveolar volume cannot be easily measured, but with some reasonable assumptions about their relationships, MAP directly affects arterial oxygenation.

There is an understandable caution while increasing MAP, usually by increasing PEEP, yet two ventilator modes apply dramatic increases in MAP—high-frequency oscillation and airway pressure release ventilation. The marked improvements in oxygenation seen with these modes can be attributed to high MAP. In the case of high-frequency oscillation, the lungs are never allowed to derecruit between breaths. Airway pressure release ventilation is more complicated because the lung deflates to varying unknown alveolar volumes on exhalation. In the use of either mode, end expiratory alveolar lung volume status cannot be easily determined, but oxygenation is often improved.

Driving Pressure

Driving pressure is a measure of the pressure difference between P_plat and total PEEP (PEEP plus auto-PEEP). The swing in pressure from end-inspiration to end-expiration may be an independent stress factor on the lungs. Driving pressure monitors the roles of reducing P_plat and increasing PEEP.

Esophageal Pressure Monitoring

Esophageal pressure monitoring is used to reflect clinically intrapleural pressure change, or the distending pressure of the lungs and chest wall. Esophageal pressure monitoring allows calculation of WOB and measurement of Ptp. The thin esophageal catheter (approximately 2-mm diameter) used for monitoring esophageal pressure is not as uncomfortable as a nasogastric tube, is simple to insert, and poses little risk of esophageal perforation. Appropriate placement is achieved by first inflating the 10-cm long balloon with approximately 0.5 to 1.0 ml of air and passing it into the stomach. The catheter is carefully withdrawn until the final position of the balloon is within the lower third of the esophagus, as verified by the presence of cardiac oscillations within the pressure tracing. Proper placement can also be confirmed by occluding the airway and measuring the simultaneous deflections in pressure at the airway opening and esophageal pressure.

Oxygen Cost of Breathing

The amount of O₂ consumed by the ventilatory muscles () is an estimate of respiratory effort at its most basic level. can be estimated by measurement of O₂ consumption during active breathing compared with the patient being fully supported in the control mode:

V˙O2R=V˙O2 active breathing−V˙O2apnea

Normal is approximately 2% to 5% of total O₂ consumption; however, can be 30% of total O₂ consumption during hyperventilation owing to severe dyspnea. Theoretically, accounts for all factors that tax the respiratory muscles—that is, the external workload and the efficiency of the conversion between cellular energy and useful work. is difficult to measure if the patient’s condition is unstable. Other measures of respiratory muscle function are sought to assess the cost of breathing.

Assessing Ventilatory Drive

Until more recently, little attention was paid to measurement of respiratory drive during critical illness. During machine-assisted breathing, ventilatory drive can play an important role in determining the energy expenditure of the patient. One study showed that patients not being weaned from mechanical ventilation often have an elevated drive to breathe and a limited ability to respond to increases in ventilatory load (e.g., increased PaCO₂).²⁸

A measure that has been used to index drive is P_0.1. P_0.1 is the pressure recorded 100 msec after initiation of an inspiratory effort against an occluded airway. P_0.1 is influenced by muscle strength and lung volume but does not depend on respiratory mechanics. Elevated P_0.1 (>6 cm H₂O) indicates a continuing need for mechanical ventilation.

In a sophisticated, commercially available system, a direct measure of the neural drive to breathe from the phrenic nerve can be measured by a catheter positioned within the esophagus. This signal is integrated into a feedback circuit in a modern ventilator. As a mode within the ventilator, flow delivery is coordinated and augmented in response to the neural drive to breathe; this is known as neurally adjusted ventilatory assist. (See Chapters 42 and 44 for details.)

Rapid Shallow Breathing Index

When muscular strength is limited, patients tend to meet minute ventilation () requirements by increasing frequency (f) while decreasing V_T. Although smaller breaths require less effort, rapid shallow breathing increases dead space ventilation causing a need for higher minute ventilation to eliminate CO₂. A very high and continuously increasing frequency (>30 breaths/min) is a sign of ventilatory muscle decompensation and, potentially, impending fatigue.

Considerable attention has been focused on the rapid shallow breathing index (f/V_T ratio), a simple bedside index that indicates whether mechanically ventilated patients can breathe without mechanical assistance.²⁹ The f/V_T ratio is easy to measure and is independent of the patient’s effort and cooperation. Discontinuation of ventilator support is likely to prove successful if f/V_T ratio is less than 105 breaths/min per L within the first minute of a brief trial of fully spontaneous breathing.²⁹

Respiratory Inductive Plethysmography

Respiratory inductive plethysmography is a noninvasive means of monitoring frequency, V_T, fractional duration of inspiration (T_i/T_tot), and respiratory muscle coordination. With this technique, loose elastic bands encircle the chest and abdomen. Band expansion and contraction during ventilation (spontaneous or supported) provides a volume-time plot that can also reflect short-term shifts in actual lung volume.

Endurance: Maximum Voluntary Ventilation

Respiratory muscle fatigue (lack of endurance) may be a cause of respiratory failure. Maximum voluntary ventilation (MVV) is a measure used to assess respiratory muscle reserve, endurance, or fatigue. VC is measured to assess the patient’s coordinated muscle function from a single breath; MVV is measured to determine the ability of a patient to sustain ventilation over time. Similar to the VC maneuver, the MVV procedure can be performed with a respirometer attached to the patient’s airway as the patient is encouraged to breathe as deeply and as fast as possible over a predefined time interval (10 or 15 seconds). The value is extrapolated to a full minute.

Normal MVV values for adults range from 120 to 180 L/min. Values less than twice the spontaneous minute ventilation are associated with difficulty in maintaining spontaneous ventilation without mechanical assistance.³¹

Lung Stress and Strain

During mechanical ventilation, the lungs are exposed to positive pressure that exerts more stress and strain on the lungs than experienced during spontaneous ventilation. This lung stress and strain may cause injury or extend existing lung injury along the injury/normal tissue border. When positive pressure becomes injurious, it is referred to as ventilator-induced lung injury. However, the concepts of stress and strain as applied to the lungs are not clearly defined. The physical definition of stress is a force per unit area. Strain is the deformation of a structure compared with its overall size. Hooke’s law associates the two factors by the following relationship: stress = k * strain.

Working definitions for stress and strain applied to the lungs have been studied.³² Stress is simply defined as Ptp (P_airway − P_esophageal). Driving pressure, as previously discussed, may be an alternative measure of stress. Strain has been defined as V_T (the deformation) divided by FRC (the resting size of the lungs). These definitions have been associated as stress = 13.5 * strain, predicting that a stress of 27 cm H₂O (Ptp of 27 cm H₂O) and a strain of 2 (V_T of twice the FRC) approach the limits of safe ventilation.³² As previously discussed, Ptp requires placement of an esophageal catheter. To measure strain, automated FRC determinations have become available on some modern ventilators.³³ Stress can also occur at lower pressures if lung units are opening and closing during the ventilator cycle.

Stress Index

Another index involving the dynamic measurement of stress has been reported.³⁴ The stress index is a value derived from the airway pressure-time curve during constant flow delivery of a tidal breath. During constant flow (when resistance is constant), the slope of the pressure-time tracing is analyzed to evaluate the elastic properties of the lungs. The index is calculated by performing a curve fit of the slope of the pressure-time tracing, where pressure = a * time^b + c. Ideally, a slope (b) of 1 indicates normal filling during lung expansion, whereas a slope greater than 1 indicates overdistention, and a slope less than 1 indicates lung recruitment (Figure 46-8). This measure can be calculated for each delivered tidal breath, although an acceptance criterion should be used to exclude analysis of artifacts and factitious breaths. Although the index may not determine a threshold for excessive stress or strain, it may be a useful indicator of lung response to positive pressure. If the chest wall contributes variably to airway pressure, the calculated index can be altered and deceptive.³⁵

Lung Mapping

The extent of gas exchange abnormalities is revealed by ABG values and SpO₂, but the location or source of the disorder remains unknown. The source, but not the extent or type of the pathologic process, can be assessed by auscultation. Localization of the disorder within the lungs is more precisely evaluated by static images obtained by radiographic techniques, such as chest x-ray or computed tomography (CT). These assessments are key to directing therapeutic approaches and for tracking changes in pathology. However, thorough imaging studies frequently require transportation of the patient to a radiology suite, and transport presents risks to the patient.³⁶ Also, the imaging is often static, not dynamically obtained throughout the ventilator cycle.

Mapping techniques that can actively locate regions of interest have been developed more recently. Two techniques are available that allow mapping of the lungs during ventilation: electrical impedance tomography (EIT) and acoustic respiratory monitoring (ARM). Each technique provides imaging of ventilation that allows localization of the injury and an assessment of the extent of injury. Each technique produces a two-dimensional video or graphic representation of ventilation; quiet regions without ventilation are not “seen.” With EIT and ARM, there is an opportunity to perform at the bedside a real-time evaluation of the effects of PEEP, recruitment maneuvers, or other changes in ventilatory support.

The application of EIT or ARM is simple, and systems are becoming available for clinical use. Both are stand-alone devices that are not, as yet, integrated with ventilators. EIT requires placement around the chest of either 16 or 32 electrodes. Impedance measures between electrodes are rapidly completed, and a video reconstruction of ventilation is created (Figure 46-9). Completion of regional ventilation studies with the use of EIT has been reported more recently.^37,38 ARM involves placement of a series of stethoscopes around the chest. The sounds during ventilation are localized, and, similarly, a map of sounds (ventilation) is reconstructed. Specific characteristics of crackles from interstitial pulmonary fibrosis compared with congestive heart failure have been differentiated by ARM.³⁹

Lung Ultrasonography

Bedside echocardiography has become routine within ICUs. An echocardiograph is obtained by skilled technicians interrogating the heart with an external ultrasound probe on the chest surface. The images obtained are two-dimensional dynamic videos that clearly display the chamber sizes, wall thicknesses, and cardiac performance. Ultrasound technology is not as helpful for imaging the lungs because air-filled lung tissue is not penetrated by ultrasound. However, pathologic processes outside the lungs can be seen by ultrasound, such as pleural fluids, air, or lesions. Pneumothorax, empyema, and pleural effusions are most frequently located by lung ultrasonography; their extent can be defined and treated with the use of ultrasound. As a diagnostic tool, lung ultrasonography is relatively inexpensive, can be performed in 15 minutes, and does not emit ionizing radiation. There is potential for ultrasonography to evaluate the lung expansion effects of recruitment maneuvers or high-frequency oscillation.

Graphics Monitoring

Monitoring of graphic tracings generated during mechanical ventilation has become widely available and accepted in the ICU. A visual display of pressure, flow, and volume tracings is available on all modern ventilators. Graphic displays are possible through the development of improvements in sensing technology, integrated circuitry, and graphic-user interface. Ventilators measure inspiratory and expiratory flow and circuit pressure with pneumotachometers and transducers. The volume displays are generated through calculation of an integral of the flow tracings. All three values (flow, pressure, and volume) can be displayed and plotted against time or each other (Figure 46-11).

Ventilator manufacturers have developed the graphic displays that allow astute clinicians to base decisions on many more factors than gas exchange values (Box 46-8). However, the study and verification of features observed in ventilator graphics have not developed at the pace of the technology. Ventilator graphics show many important patient-ventilator interactions, such as presence of auto-PEEP, elevated airway pressure, presence of secretions, and general pattern and dependability of supported ventilation (Figure 46-12). The potential for expanded use of ventilator graphics awaits further investigation of the clinical importance of the graphic displays. For more details, see Chapter 44.