Chapter 34 Respiratory monitoring
Clinical examination and the trend of vital signs such as respiratory rate (f), and quantity and nature of sputum are extremely important in managing patients with respiratory disease. In particular, clinical examination should look for evidence of excessive inspiratory and/or expiratory pleural pressure changes and effort such as accessory muscle use, tracheal tug, supraclavicular and intercostal indrawing, paradoxical abdominal movement (which is suggestive of diaphragmatic fatigue1) and pulsus paradoxus. During spontaneous ventilation an excessive fall in blood pressure during inspiration (> 10 mmHg) is found in a number of conditions such as cardiac tamponade, cardiogenic shock, pulmonary embolism, hypovolaemic shock and acute respiratory failure. A curvilinear relationship exists between the fall in blood pressure and the change in pleural pressure during inspiration; however, there is marked variation between individuals.2 Consequently, pulsus paradoxus is most useful in following trends; a reduction in the degree of paradox may be due to improvement and a fall in the negative pleural pressure needed for ventilation, or due to respiratory muscle insufficiency, and an inability to generate the same negative pleural pressure.
Additional information can be gained from blood gases and pulse oximetry (Chapter 14), and capnography, ventilatory pressures and waveform analysis in patients receiving respiratory assistance. This chapter will focus on tests of respiratory function that are directly relevant to critically ill patients.
Monitoring gas exchange
Oxygenation
This is reviewed in Chapter 14, and is only briefly discussed here. Hypoxaemia may be due to a low partial pressure of inspired O2 (rare), hypoventilation, diffusion impairment (rare), ventilation–perfusion mismatch and shunt. Inert gas analysis has been used to quantitate mismatch, and has demonstrated that hypoxaemia in acute respiratory distress syndrome (ARDS) is predominantly due to alveoli that are perfused but not ventilated (shunt),3 consistent with computed tomography (CT) scan evidence of increased dependent lung density. However, inert gas analysis remains a research tool, and less direct methods, such as the alveolar gas equation, are used to assess hypoxaemia:
where PAO2 is the alveolar PO2, and this is usually simplified to:
Carbon dioxide
PaCO2 is determined by alveolar ventilation , and CO2 production :
where is the minute ventilation minus the wasted or dead-space ventilation . The modified Bohr equation (assuming PACO2 = PaCO2) calculates the proportion of the VT which is wasted ventilation (i.e. physiological dead space: VDphys):
where is the mixed expired , and VDphys is composed of anatmical dead space (VDanat) and alveolar dead space (VDalv) – notionally due to alveoli that are ventilated but not perfused. Normally VDalv is minimal and VDanat comprises 30% of VT. Since the volume of an endotracheal tube is less than the mouth or nose, and pharynx, intubation may reduce VDanat; however, when the connection from the endotracheal tube is taken into account there is little change in dead space. Positive-pressure ventilation increases dead space by distension of the airways increasing VDanat, and through a tendency to increase alveoli that are ventilated but not perfused. In patients with ARDS, marked increases in VDalv lead to marked increases in the VDphys/VT ratio (exceeding 0.6), which is an independent prognostic factor.4
Capnography
Capnography measures and displays exhaled CO2 throughout the respiratory cycle, with sampling usually by a mainstream sensor since sidestream systems tend to become blocked by secretions. However, when capnography is used in non-intubated patients, sidestream sampling is commonly used (e.g. modified nasal cannulae). Infrared spectroscopy measures the fraction of energy absorbed and converts this to a percentage of CO2 exhaled. During expiration the capnogram initially reads no CO2, but as anatomical dead space is exhaled there is a rise in the exhaled CO2 to a plateau which falls to 0% CO2 with the onset of inspiration. In patients with significant respiratory disease a plateau may never be achieved. The end-tidal CO2 (PetCO2) is the value at the end of the plateau, and is normally only slightly less than the PaCO2. However, this gradient will increase when alveolar dead space (VDalv) increases, such as low cardiac output, pulmonary embolism and elevated alveolar pressure. Consequently the PetCO2 may not reflect PaCO2 in critically ill patients. Nevertheless, in a stable patient the gradient will be fairly constant, and can be used to guide during transport,5 and when other factors including the adequacy of minute ventilation are unchanged, sudden changes in the PetO2 may provide an early signal. Indeed, PetCO2 directly correlates with cardiac output, and PetCO2 monitoring has been used to assess adequacy of cardiopulmonary resuscitation, and its prognosis.6
The presence of exhaled CO2 is secondary confirmation of endotracheal tube placement, and is commonly recommended even when the tube is seen to pass through the vocal cords,7 since clinical assessment is not always reliable. Simple colorimetric devices may be used for this purpose. However, detection of expired CO2 is not infallible7 as false positives can rarely occur following ingestion of carbonated liquids, and false negatives may be due to extremely low pulmonary blood flow, or very large alveolar dead space such as pulmonary embolus or severe asthma. Monitoring with capnography has also been recommended for transport8 and respiratory monitoring9 in critically ill patients, and should be available for every anaesthetised patient.10
Lung volume and capacities (Figure 34.1)
The tidal volume (VT) is the volume of gas inspired and expired with each breath, with the volume at end-expiration termed the functional residual capacity (FRC). If a forced expiration is performed the expiratory reserve volume (ERV) is expired down to the residual volume (RV). If a maximum inspiratory effort is made from FRC, this is termed a vital capacity (VC) manoeuvre when the total lung capacity (TLC) is reached. Clinically, the most important of these are the FRC, VT and VC, and the latter two are easily measured using a spirometer or integrated from flow.
Tidal volume
Minute volume is composed of f and VT – normally ∼17 breaths/min and ∼400 ml respectively in adults.11 Rapid shallow breathing is common in patients with respiratory distress, and in those failing weaning. Although a proposed index, an f/VT ratio > 100 was initially shown to be highly predictive of weaning failure;12 subsequent studies have reported varying results.
Vital capacity
At TLC the forces due to the inspiratory muscles are counterbalanced by elastic recoil of the lung and chest wall. Consequently, the TLC is determined by the strength of the inspiratory muscles, the mechanics of the lung and chest wall and the size of the lung, which varies with body size and gender (Table 34.1). Since the VC is the difference between TLC and FRC, factors that reduce FRC, such as increased abdominal chest wall elastance and premature airway closure in chronic obstructive pulmonary disease (COPD), will also reduce it. The normal VC is ∼70 ml/kg and reduction to 12–15 ml/kg has previously indicated a probable need for mechanical ventilation. However, many other factors need to be considered, including the patient’s general condition, the strength of the patient’s expiratory muscles, glottic function and the use of non-invasive ventilation. Indeed, many chronically weak patients are able to manage at home with extremely low VC with the assistance of non-invasive ventilation.
Decreased muscle strength |
Increased lung elastance |
Increased chest wall elastance |
Reduced functional residual capacity |
Functional residual capacity
Direct measurement of FRC is rarely measured in ICU; however, techniques such as nitrogen wash-in and wash-out13 to estimate FRC are becoming available on modern ventilators. When FRC is less than the closing volume, the lung volume at which airway closure collapse is present during expiration, there is a marked increase in mismatch. Consequently, positive end-expiratory pressure (PEEP) is commonly used to elevate FRC. Increases in lung volume above resting lung volume can be directly measured from a prolonged expiration to atmospheric pressure using either a spirometer or integration of flow,14 or by repeated FRC measurements. FRC is decreased in ARDS and pulmonary oedema, in patients with abdominal distension and following abdominal and thoracic surgery. An increase in FRC places the diaphragm at a mechanical disadvantage, and is seen with severe airflow limitation and dynamic overinflation, and when there is loss of elastic recoil (e.g. emphysema).
Measurement of lung mechanics
Elastic properties of lung and chest wall
The respiratory system (RS) is composed of the lung (L) and chest wall (CW), which is comprised of the ribcage and abdomen. Although it is often convenient to consider respiratory system mechanics as implying information about the lung, abnormal chest wall compliance can markedly influence these measurements.15–18
Although the Pes is not always an accurate measure of the absolute Ppl, the change in Pes reflects the change in Ppl. However, this requires an appropriately positioned and functioning oesophageal balloon. In spontaneously breathing subjects a thin latex balloon sealed over a catheter is introduced into the lower third of the esophagus and Pes and Pao are measured simultaneously during an end-expiratory airway occlusion. A well-positioned oesophageal balloon will have a ratio of ΔPes/ΔPao of ∼1.19 This technique is reliable in supine, intubated spontaneously breathing patients,20 and in paralysed subjects it appears that a similar pressure change, induced by manual ribcage pressure,21 can be used to verify oesophageal balloon function.
Measurement of elastance
Elastance and resistance are frequency-dependent, and respiratory mechanics depend upon the volume and volume history of the lung.22 With increasing frequency of breathing, total respiratory system resistance falls and elastance increases, and this is particularly obvious in patients with airflow obstruction.23,24 Consequently these factors must be taken into account when interpreting respiratory mechanics. In a passively ventilated subject Pao is the sum of: (1) the pressure required to overcome airway, endotracheal tube and circuit resistance (Pres); (2) the elastic pressure required to expand the lung and chest wall (Pel); (3) the elastic recoil pressure at end-expiration or total PEEP (Po); and (4) the inertial pressure required to generate gas flow (Pinert):
Since the elastance (E) is equal to ΔP/ΔV, with the resistance (R) equal to ΔP/Δ, and ignoring the inertance,25 this can be rewritten as the single-compartment equation of motion:
END-INSPIRATORY OCCLUSION METHOD
The simplest estimate of ERS can be made using a rapid end-inspiratory airway occlusion during a constant-flow breath, provided that the respiratory muscles are relaxed (Figure 34.2). If a plateau is introduced at end-inspiration there is a sudden initial pressure drop due to dissipation of flow resistance (Ppk – P1) followed by a slower, secondary pressure drop to a plateau (Pdif = P1 – P2) due to stress relaxation. At least 1–2 seconds are taken for this plateau to be achieved, and P2 is often called the plateau pressure; however, if Pplat is measured too soon it will lie somewhere between P1 and P2.
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