Fig. 5
From: Kinematic signature of high risk labored breathing revealed by novel signal analysis
Respiratory muscle overload and imminent respiratory collapse. This figure shows the respiratory kinematic recordings of two female patients with elevated respiratory rates (90th and 99th percentiles for our dataset). They were both initially admitted to the acute care unit of the hospital for pneumonia and sepsis with acute respiratory failure. At admission, their supplemental oxygen needs were low (4 and 2 L per minute) and their blood gas studies were normal (pH of 7.43 and 7.44; pCO2 of 33 and 40 mmHg). Their Pneumonia Severity Index scores were also comparable at 127 and 125 [scores of 91–130 are Risk Class 4 (moderate risk) and are associated with a 30-day mortality of 9%]. Apart from tachypnea and hypoxemia, the drivers of risk were age, hyponatremia, and confusion in patient 1, and fevers, anemia, and neoplastic disease (acute myelogenous leukemia) in patient 2. Despite the similarities in these patients’ presentations and conventional risk levels, their clinically trajectories were dramatically different. Patient 1 remained stable on the acute care unit after her kinematic recording and was discharged home after a 7-day hospitalization. In contrast, Patient 2 developed a sudden respiratory collapse within 6 h of her kinematic recording (required emergent intubation), and died within 24 h of this recording. Severe hypoventilation from respiratory muscle overload was deemed to be the likely mechanism of the collapse; this conclusion was consistent with the rapidity of collapse, unresponsiveness to oxygen supplementation prior to intubation (low SpO2 despite 100% FiO2), and acute hypercapnia (pH 6.9 mm Hg; pCO2 103 mm Hg). A majority of both patients’ recordings were classified as labored breathing in the latent profile analysis (3 of 4 recordings in patient 1, and 3 of 3 recordings in patient 2). However, a comparison of the respiratory kinematic characteristics of these patients revealed an important difference. Patient 1 (the survivor) had lower grade derangements in all non-tachypnea physiomarkers than the deceased patient 2. The breath intervals were more regular in Panels B-D than in panels G-I (respiratory rate variability at 39th percentile in panel E vs. 99th percentile in panel J). The upper rib motion amplitude was much smaller than lower rib or abdominal motion amplitude in panels B-D than in panels G-I (recruitment of accessory muscles at 1st percentile in panel G vs. 81st percentile in panel J). And the breath phenotype was much more stable in patient 1 than in patient 2. Each breath had a same degree of lower rib dominance in panels C-D, whereas rib dominant breaths alternated with abdomen dominant ones in panels H-I (respiratory alternans at 11th percentile in panel E vs. 51st percentile in panel J). Consistent with the conventional wisdom in the field of bedside physical diagnosis, these findings suggest that respiratory kinematic characteristics contain signatures that are much more specific for respiratory muscle overload than just tachypnea.
