To calculate the respiratory variations in the PLET waveform, I have used the 2 methods that are described for their quantification during mechanical ventilation.2 The first method, termed ΔPOP, is calculated as the difference between the maximal and minimal PLET amplitudes (POP) divided by their mean, namely, (POPmax − POPmin)/[(POPmax + POPmin) × 0.5].2 The second method, termed PVI, is a measure of the variation of the PLET perfusion index (PI) over 1 mechanical breath. The PI is the ratio between the pulsatile and nonpulsatile infrared light absorption from the pulse oximeter and is physiologically equivalent to the PLET amplitude. The PVI is calculated as the difference between the maximal and minimal PI divided by the maximal PI, namely, [(PImax − PImin)/PImax] × 100, where PImax and PImin represent the maximal and the minimal values of the PI, respectively.2 The PVI is automatically calculated by a commercial pulse oximeter (Masimo Radical 7®; Masimo Corp, Irvine, CA)7 and may soon be available in other monitors as well. I have, therefore, adopted this latter method for the measurement of the sPVI, which is the term chosen to describe the PVI during spontaneous ventilation.
Whenever the AP waveform was available, I also calculated the pulsus paradoxus, which is the difference between the maximal and the minimal systolic AP values during 1 respiratory cycle,8 and the pulse pressure (PP) variation (PPV), calculated as (PPmax − PPmin)/[(PPmax + PPmin) × 0.5].9
The first case demonstrates the appearance of UAO in a sedated patient during regional anesthesia, where the sPVI increased from 9% during normal breathing (Fig. 1A) to 25% after the appearance of UAO (Fig. 1B). All other cases also demonstrate very prominent sPVI values during clinically diagnosed significant UAO, and 2 of them include significant variations of the AP waveform as well (Figs. 2 and 4). The ranges of the ΔPOP and sPVI values in the 4 cases were 28% to 42% and 25% to 39%, the values of the pulsus paradoxus were 28 and 40 mm Hg, and those of the PPV were 19% and 34%, respectively (Table 1 and Figs. 1–4).
The analog signals of impedance plethysmography (as measured by the electrocardiograph electrodes) and capnography were included when available (Figs. 1, 2, and 4). A seemingly complete UAO was associated with the disappearance of the capnographic waveform (Fig. 1). However, in 2 other cases, the signals of impedance plethysmography and capnography persisted in spite of the significant UAO (Figs. 2 and 4).
These observations show that clinically significant UAO results in excessively high values of sPVI, which correspond to the marked variations seen in the analog waveforms of the PLET signal. These sPVI values are 2 to 3 times higher than the range of 9.5% to 15% that was repeatedly found as the best threshold for the identification of fluid responsiveness in mechanically ventilated patients.2
The inspiratory efforts against an obstructed upper airway cause negative swings in the pleural pressure, the magnitude of which is determined by the degree of obstruction and by the inspiratory effort. The excessive negative pleural pressure is transmitted to the LV, causing a sudden increase in the pressure gradient for LV ejection, which may cause a significant and abrupt decrease in LV stroke volume.8,10,11 In addition, changes in myocardial mechanics have been described during the Mueller maneuver, which is a voluntary sustained inspiration against an occluded airway, mimicking severe UAO.12
The observed inspiratory decrease in the systolic AP of >10 mm Hg during UAO can be considered as pulsus paradoxus.8 However, pulsus paradoxus is usually mentioned in association with asthma, cardiac tamponade, and exacerbations of chronic obstructive pulmonary disease, and its physiological origins may be quite variable and complex.8 Pulsus paradoxus has also been shown to correlate with the respiratory fluctuations of the PLET waveform in asthmatic children.13,14 However, in the appropriate clinical settings, excessive variations in the PLET and AP waveforms during spontaneous ventilation should be regarded, first and foremost, as an important warning sign of UAO.15,16 Furthermore, the magnitude of changes in the height and area under the curve of the PLET waveform were shown to correlate with the severity of simulated airway obstruction in healthy volunteers.17
These observations may have important clinical implications as they may contribute to an earlier diagnosis of UAO. UAO is a life-threatening acute disorder that may appear in a variety of clinical conditions.18 Its clinical picture may include obtunded consciousness, dyspnea, stridor, use of accessory muscles, intercostal and suprasternal retractions, paradoxical chest/abdominal movements, and inspiratory stridor that may disappear when the obstruction becomes complete.19 When prolonged or very significant, UAO may result in hypoxemia, cyanosis, negative pressure pulmonary edema, and cardiac arrest. UAO needs to be recognized promptly and managed effectively to prevent morbidity and mortality.18 Although visual assessment and auscultation may provide an immediate diagnosis, they do require significant expertise, which is not always available in a timely manner.
Pulse oximetry, though widely used, may be relatively insensitive to the development of UAO because significant changes in the arterial partial pressure of oxygen may occur with little alteration in oxygen saturation, especially when supplemental oxygen is being administered. Monitoring respiratory rate by impedance plethysmography may also be misleading, as clearly shown in Figures 2 and 4, since chest movement may continue, sometimes even more forcefully, without effective ventilation.20 The disappearance of the exhaled CO2 signal may be an early sign of UAO, as seen in Figure 1. However, the capnographic signal may not disappear completely during partial UAO, as shown in Figures 2 and 4. An attempt to automatically integrate exhaled CO2, respiration rate, pulse rate, and SpO2 for respiratory monitoring has been shown to miss many respiratory events that require attention during procedural sedation.21 It is clear, therefore, that the timely diagnosis of UAO may present a significant challenge.
There are a few medical fields and conditions in which an earlier and a better diagnosis of UAO may be of utmost importance. For example, the primary causes of morbidity during procedural sedation are drug-induced respiratory depression and UAO.20 Sedation has been shown to be associated with increased collapsibility of the upper airway due to depression of central respiratory output to upper airway dilator muscles and of upper airway reflexes.22 The danger of developing UAO during sedation is clinically significant because it is not always possible to predict how an individual patient will respond.20 Deep sedation may occur even during elective endoscopy,23 requiring frequent airway modifications.24 Routinely measured respiratory variables may often fail to detect the development of UAO during procedural sedation,20 and better monitoring may prevent adverse respiratory events, leading to severe morbidity and mortality.25 Since pulse oximetry is routinely used in all patients undergoing sedation/analgesia, the sPVI should be closely monitored under these conditions.
Another condition in which the monitoring of sPVI may be of value is that of laryngospasm, which is usually defined as partial or complete airway obstruction associated with increasing abdominal and chest wall efforts to breathe against a closed glottis.18,26 The clinical picture of laryngospasm includes suprasternal and supraclavicular retractions, tracheal tug, paradoxical chest, and abdominal movements. Laryngospasm may also present atypically and, if not promptly managed effectively, may lead to morbidity and mortality.26 Since exaggerated sPVI reflect the presence and severity of laryngospasm (Fig. 4), it should be added to its formal clinical description.18,26
Obstructive sleep apnea (OSA) is another prevalent disorder in which UAO occurs due to anatomical compromise and loss of protective reflexes during sleep.27 The formal diagnosis of OSA is based on the identification of respiratory events (either apnea or UAO) by a variety of physiologic variables during polysomnography.28 Home diagnosis using pulse oximetry is also being used as a less expensive and more comfortable option.29,30 The sPVI could add significantly to the diagnosis of OSA, which currently does not consider the amount of effort that is created against the obstructed airway. In addition, monitoring the sPVI may prove beneficial in patients with OSA who undergo procedural sedation, general anesthesia, and/or receive patient-controlled analgesia or neuraxial opioids in the postoperative period, since these patients are at increased risk of developing UAO.31
Name: Azriel Perel, MD.
Contribution: This author wrote the manuscript.
Attestation: Azriel Perel attests to the integrity of the original data and the analysis and to having approved the final manuscript and is also the archival author who is responsible for maintaining the study records.
Conflicts of Interest: Azriel Perel is a member of the Medical Advisory Board of Pulsion Medical Systems, Munich, Germany, and received a 1-time honorarium for an in-house lecture from Masimo, Irvine, CA.
This manuscript was handled by: Maxime Cannesson, MD, PhD.
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© 2014 International Anesthesia Research Society
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