Breathing Pattern

Abnormalities in respiratory frequency (fr) and tidal volume (Vt) are extremely common in critically ill patients and, among other causes, can reflect respiratory muscle dysfunction. In several studies, an elevated fr has been shown to predict an adverse outcome in general populations of critically ill patients. In a case-controlled study of patients discharged from an ICU, fr (p < 0.0002) and hematocrit (p = 0.01) were the only continuous variables that predicted readmission to the ICU (4). Patients readmitted to the ICU had a much higher mortality than the control patients (42 and 7%, respectively). In a study of patients who had undergone a cardiopulmonary arrest, 53% had a documented deterioration in respiratory function in the 8 hours preceding the arrest (5). Respiratory frequency was elevated in the majority of these patients (mean ± SE, 29 ± 1 breaths/minute), while other routine laboratory tests, including electrocardiograms, showed no consistent abnormalities. These and other studies (6, 7) demonstrate that tachypnea is an extremely sensitive marker of a worsening clinical status. However, it is also extremely nonspecific, and a physician needs to undertake additional diagnostic testing to elucidate the nature of the underlying disorder.

Tidal volume (Vt), breathing frequency (fr), and minute ventilation are easy to measure in intubated patients, and the values are continuously displayed on virtually all modern mechanical ventilators. However, the accuracy and reliability of the instrumentation used for volume measurements have undergone remarkably little evaluation (8). To ensure reliability of volume measurements, a simple handheld spirometer is preferred. Tidal volume is rarely measured in the nonintu-bated patient, because these patients have a poor tolerance of mouthpieces. Moreover, such instrumentation usually causes a spurious increase in Vt and decrease in frequency (9, 10).

Systematic studies have not been undertaken in large populations of healthy subjects to define the normal range for breath components. Moreover, the values depend on whether recordings are made nonobtrusively or with instrumentation requiring the use of a mouthpiece (9, 10). The largest study using nonobtrusive methodology in healthy subjects (n = 65) revealed a mean ± SD Vt of 383 ± 91 ml, fr of 16 ± 2.8 breaths/ minute;, and minute ventilation of 6.01 ± 1.39 L/minute (11).

Additional data in smaller study populations are consistent with these values. Breath components display considerable breath-to-breath variability, and thus it is important to base the measurement on an adequate sampling period; unfortunately, investigations have not been conducted to define the optimal sampling duration. Calculations of breath components based on the mean of approximately 250 breaths revealed good reproducibility on a day-to-day basis in healthy subjects (coefficient of variation less than 9%) (12).

Rapid shallow breathing is particularly common in critically ill patients (Figure 1) (13), and some (14-16), but not all (17, 18), investigators have related its development to respiratory muscle fatigue. Even when rapid shallow breathing has been demonstrated following the induction of fatigue in healthy volunteers (16), it occurred when the subjects were employing only a small fraction of the pressure-generating capacity of the inspiratory muscles, making it unlikely that this alteration in breathing is a manifestation of fatigue per se. Critically ill patients are susceptible to many simultaneous challenges, and rapid shallow breathing in these patients may be the result of several mechanisms, including increased mechanical load, chemoreceptor stimulation, operating lung volume, reflexes originating in the lungs and respiratory muscles, altered respiratory motoneuron discharge patterns, sense of effort, and cortical influence. If rapid shallow breathing were an effective strategy for avoiding respiratory muscle fatigue in critically ill patients, one would expect a negative correlation between the degree of rapid shallow breathing and a measure of respiratory muscle fatigue. In 17 patients who failed a trial of weaning from mechanical ventilation, Jubran and Tobin (18) found no relationship (r = 0.08) between frequency-to-tidal volume ratio (fr/Vt) and tension-time index. Vassilako-poulos and coworkers (19) have confirmed the lack of a relationship between fr/Vt and tension-time index (r = 0.16) in 30 patients who failed a weaning trial. In the latter study (19), tension-time index decreased from a value of 0.162 ± 0.032 (SD) in patients who could not be weaned to 0.102 ± 0.023 at the time of weaning success. When a large number of variables reflecting respiratory muscle function, lung volumes, and mechanics were entered into a logistic regression model, fr/Vt and tension-time were the only variables that were significantly related to weaning outcome.

While the pathophysiological mechanism(s) responsible for rapid shallow breathing is unknown, this does not detract from its use in clinical decision-making, especially with regard to the timing and pace of the weaning process (see subsequent text). Moreover, initial studies of computerized closed-loop adjustments of ventilator settings, based on Vt and fr, with or without end-tidal Pco2 and pulse oximetry, provide encouraging data suggesting that ventilator adjustments based on changes in breathing pattern might help in expediting the weaning process (20-22).

Asynchronous and paradoxic motion of the rib cage and abdomen is commonly detectable by inspection and palpation in critically ill patients. The magnitude of abnormal motion can be quantified with magnetometers or inductive plethysmography combined with the Konno-Mead method of analysis (23) (see Estimation of Ventilation Based on Chest Wall Motion: Konno-Mead Diagram in Section 6 of this Statement). Ashu-tosh, Gilbert, and coworkers (24, 25) showed that patients dis playing asynchronous rib cage-abdominal motion had an increased risk of ventilatory failure necessitating mechanical ventilation (24) and a poor prognosis (24). Subsequently, abdominal paradox and respiratory alternans, i.e., cyclic alteration in the relative contribution of the rib cage and diaphragmatic muscle groups, were thought to reflect respiratory muscle fatigue (14, 26, 27). Such an interpretation has major implications for the critically ill patient being weaned from mechanical ventilation. Because muscle rest with mechanical ventilation is the main means of reversing fatigue, the presence of paradox would prohibit the discontinuation of mechanical ventilation. Patients who fail a weaning trial, as a group, exhibit greater abdominal paradox than successfully weaned patients (28, 29), but there is considerable overlap among individual patients of the two groups. This lack of discrimination between the two groups of patients partly stems from the fact that the more seriously ill patients also switch between predominant use of the rib cage and diaphragmatic muscles (14, 28, 29). Moreover, in systematic experimental studies, respiratory muscle fatigue was shown to be neither necessary nor sufficient for the development of abnormal rib cage-abdominal motion (30, 31). Thus, quantification of abdominal paradox alone is not helpful in detecting respiratory muscle fatigue or predicting the development of respiratory failure. However, studies in small numbers of patients suggest that a global measure of overall asynchronous and paradoxic motion of both the rib cage and abdomen might be useful in predicting ventila-tory failure (14, 24, 25, 28-30). Because quantification of abnormal rib cage-abdominal motion is relatively complex, such an index cannot be recommended for general clinical use without undertaking controlled prospective trials to determine if such a measurement is superior to simpler tests that are more easily performed (32).

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