“[A] multicomponent assessment of dyspnea is important in awake venoarterial ECMO patients.”
Dyspnea, like pain, is a complex and multidimensional symptom. Clinical signs include rapid, shallow breathing; use of accessory muscles of inspiration; and activation of expiratory muscles and are often accompanied by tachycardia, hypertension, and diaphoresis. At the same time, a patient’s perceptions of breathing discomfort are at least as important as clinical signs and physician’s observations. There is increased emphasis on treating dyspnea, as it is recognized as a significant burden to the patient and related to negative outcomes in mechanically and in noninvasively ventilated patients.
Dyspnea can be rated using simple, unidimensional scales, as with pain; on a numeric scale of 0 to 100, a rating greater than 40 is considered an important discomfort for patients. Such scales provide reproducible results but no detailed information about the quality of breathing discomfort. Perceptions of dyspnea differ; it can be unacceptable even if rated less than 20 for some or acceptable even if greater than 60 for others. One patient’s “difficult breathing” may differ from another’s “breathing discomfort.” In hospitalized patients, “air hunger” is a marked sensation, and anxiety and frustration are dominant emotions associated with dyspnea. Bureau et al. used the Multidimensional Dyspnea Profile to explore such properties of dyspnea, i.e., the quality of breathing discomfort, how unpleasant it is, and the associated emotional responses. The three primary Multidimensional Dyspnea Profile components are as follows: (1) sensory, which quantitates the intensity of (i) physical effort required for breathing, (ii) air hunger, (iii) chest tightness, (iv) mental effort needed, and (v) degree of breathing difficulty; (2) affective, which quantitates breathing discomfort; and (3) emotional, which quantitates the emotional response to dyspnea by grading intensity of feeling depressed, anxious, angry, frustrated, and afraid. All components are answers on specific questionnaires and ranked from 0 to 10.
Venoarterial ECMO is increasingly used to treat cardiogenic shock (with or without unloading of the left ventricle) with better outcomes for reversible causes. A venoarterial ECMO circuit is similar to cardiac surgery bypass, i.e., connects the venous to the arterial circulation via a pump, which has a gas exchange unit (membrane oxygenator) to normalize Paco2, Pao2, and pH. The fraction of O2 in the “inspired” gas is adjustable, and the gas flow is “swept” (mixed) with the venous blood flow that is removed from the patient. The oxygenated blood is returned centrally (mostly used in postcardiotomy cardiogenic shock) or, most often, peripherally (femoral artery). Patients are usually intubated and mechanically ventilated. However, spontaneous ventilation may have benefits. In respiratory failure, “awake” venovenous ECMO is an alternative to invasive mechanical ventilation in nonintubated, spontaneously breathing patients to avoid several side effects related to sedation, intubation, and mechanical ventilation. In the current study by Bureau et al., patients in cardiogenic shock were managed with “awake venoarterial ECMO,” a rather nontypical practice—at least for North America—which reportedly decreases respiratory complications.
Bureau et al. prospectively collected dyspnea parameters and clinical data at baseline and after three stepwise increases in venoarterial ECMO sweep gas flow, at constant fractional inspired oxygen tension. Increasing sweep gas flow resulted in a significant decrease in dyspnea, without clinically important changes in arterial blood gases, heart rate, or blood pressure. Similarly, respiratory drive was also decreased, as indicated by decreased electromyographic activity of intercostal and alae nasi muscles. Patients reported a larger decrease in the unpleasantness than in the intensity and emotional perceptions of dyspnea. There were negative correlations (1) between venoarterial ECMO sweep gas flow with severity of dyspnea and respiratory drive but not with Paco2 and (2) between respiratory drive and unpleasantness and intensity of dyspnea. The authors suggest a mechanism linking decreased respiratory drive with an improvement of dyspnea. The take-home messages are that (1) dyspnea is an important and complex symptom, (2) there may be an easy way to treat dyspnea in this setting, and (3) a decrease in respiratory drive is a plausible reason for symptomatic relief.
The results of this study link dyspnea to a respiratory center being in “overdrive” mode. The respiratory center receives and processes cortical, metabolic, and chemical input (pH, Paco2, Pao2) and sends output signals to inspiratory and expiratory muscles. Respiratory drive is the intensity of the respiratory center’s output. The difference between the ventilation “desired by the brain” (as determined by afferent input) and actual ventilation contributes to dyspnea, i.e., dyspnea increases when ventilatory demands are not met. In critically ill patients, aside from chemical inputs (pH and Paco2), sensory (pain) and emotional (anxiety) inputs also affect respiratory drive. Respiratory drive cannot be directly measured. Instead, it can be quantified by its output, i.e., changes in inspiratory flow and/or the electrical activity of the phrenic nerve (during quiet breathing) and diaphragm and inspiratory muscles (during active breathing). Electromyographic activity can be recorded with surface electrodes and/or invasive instrumentation (such as via an esophageal catheter). In mechanically ventilated patients undergoing a spontaneous breathing trial, dyspnea increased significantly in those who failed the weaning trial, and the increase was significantly correlated with the electromyographic activity of the alae nasi.
This study provides a potential mechanism to explain the decrease in dyspnea with increased sweep speed. In patients with acute respiratory syndrome supported by venovenous ECMO, a decrease in Paco2 reduced respiratory drive. In this study, the increased sweep gas flow was correlated with a small decrease in Paco2, along with a more significant correlation with decreased dyspnea, breathing discomfort, and decreased respiratory drive. Based on physiology, it is plausible that the decreased respiratory drive led to a decrease in dyspnea, and breathing discomfort, considering the change in Paco2, was, although statistically significant, otherwise clinically imperceptible. Therefore, we are provided with a simple intervention to potentially alleviate a patient’s dyspnea in this setting.
These pilot findings should be replicated in additional studies, more so because the projected sample size was not met in the current study due to the problems with enrollment during the COVID pandemic. The authors provide us with a detailed list of limitations, which should be considered in future studies: a cohort of relatively younger patients with predominately nonischemic cardiac diseases, which on their own contribute to dyspnea perception, neither patients nor researchers blinded to interventions, a nonrandomized change in pump sweep gas flow, as well as not measuring minute ventilation to explore its dependency on sweep gas flow and the long-term effects on dyspnea.
This study emphasizes the importance of systematically assessing an individual patient’s discomfort and symptoms. Similar to delirium screening using the Confusion Assessment Method a multicomponent assessment of dyspnea is important in awake venoarterial ECMO patients. Simply assessing respiratory rate and Paco2 and other clinical signs may not be enough to optimally guide clinical interventions.
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