Automatic Selector Between Cardiogenic Oscillation and Airway Secretion in Mechanical Ventilation Flow Signals Using Artificial Immune System

The accumulation of secretions in the airways of ventilator-dependent patients is a common problem, and if not detected and treated in due time, it greatly increases the risk of infections and asynchrony. Unfortunately, cardiogenic oscillation modifies the flow signal shape that can confuse clinical staff and modern lung ventilators. In this article, the authors use an artificial immune system algorithm in a pre-processed flow signal. The authors' approach was able to automatically detect the presence or absence of airway secretions, even if the sample contains the influence of cardiogenic oscillation. The training and validation of the algorithm was carried out using a database containing flow signals of 457 respiratory cycles, obtained from three patients in different ventilation modes. The algorithm trained with 60% of the base cycles, was able to achieve specificity and sensitivity above 0.96 in the classification of the remaining cycles of the base.

Cardiogenic oscillation induced ventilator autotriggering

Cardiogenic oscillation during mechanical ventilation can auto-trigger the ventilator resembling patient initiated breadth. This gives a false sense of intact respiratory drive and determination brain death, even if other tests are positive, is not appropriate in such a situation. It will prolong the ICU stay and confound the brain-death determination. In this case report, we describe a 35 year old man who was brought to the hospital after many hours of critical delay following multiple gun shot injuries. The patient suffered a cardiac arrest while on the way from another hospital. After an emergency laparotomy, patient was shifted to Intensive Care Unit (ICU) with Glasgow Coma Scale (GCS) score of E1VTM1 and was mechanically ventilated. Despite absence of brainstem reflexes, the ventilator continued to be triggered on continuous positive airway pressure (CPAP) mode and the patient maintained normal oxygen saturation and acceptable levels of carbon dioxide. An apnoea test confirmed absent respiratory drive. Ventilatory waveform graph analysis, revealed cardiogenic oscillation as the cause for autotrigerring.

Cardiogenic Oscillation and Ventilator Autotriggering in Brain-Dead Patients: A Case Series

Brain death is manifested by a flaccid, areflexic patient on assessment of brain function with fixed and dilated pupils at midpoint, loss of consciousness, no response to stimulation, loss of brainstem reflexes, and apnea. A lesion or clinical state responsible for the loss of consciousness must be found. An integral part of clinical evaluation of brain death is apnea testing, which indicates complete loss of brainstem function and respiratory drive. Ventilator triggering or overbreathing the ventilator’s set rate may be considered consistent with intrinsic respiratory drive consequent to residual brainstem function. Ventilator autotriggering, however, may potentially occur in a brain-dead patient as a result of interaction between the hyperdynamic cardiovascular system and compliant lung tissue altering airway pressure and flow patterns. Also, chest wall and pre-cordial movements may mimic intrinsic respiratory drive. Ventilator autotriggering may delay determination of brain death, prolong the intensive care unit experience for patients and their families, increase costs, risk loss of donor organs, and confuse staff and family members. A detailed literature review and 3 cases of cardiogenic ventilator autotriggering are presented as examples of this phenomenon and highlight the value of close multidisciplinary clinical evaluation and examination of ventilator pressure and flow waveforms.

Cardiogenic oscillation phase relationships during single-breath tests performed in microgravity

Lauzon, Anne-Marie, Ann R. Elliott, Manuel Paiva, John B. West, and G. Kim Prisk. Cardiogenic oscillation phase relationships during single-breath tests performed in microgravity. J. Appl. Physiol. 84(2): 661–668, 1998.—We studied the phase relationships of the cardiogenic oscillations in the phase III portion of single-breath washouts (SBW) in normal gravity (1 G) and in sustained microgravity (μG). The SBW consisted of a vital capacity inspiration of 5% He-1.25% sulfurhexafluoride-balance O2, preceded at residual volume by a 150-ml Ar bolus. Pairs of gas signals, all of which still showed cardiogenic oscillations, were cross-correlated, and their phase difference was expressed as an angle. Phase relationships between inspired gases (e.g., He) and resident gas (N2) showed no change from 1 G (211 ± 9°) to μG (163 ± 7°). Ar bolus and He were unaltered between 1 G (173 ± 15°) and μG (211 ± 25°), showing that airway closure in μG remains in regions of high specific ventilation and suggesting that airway closure results from lung regions reaching low regional volume near residual volume. In contrast, CO2 reversed phase with He between 1 G (332 ± 6°) and μG (263 ± 27°), strongly suggesting that, in μG, areas of high ventilation are associated with high ventilation-perfusion ratio (V˙a/Q˙). This widening of the range ofV˙a/Q˙in μG may explain previous measurements (G. K. Prisk, A. R. Elliott, H. J. B. Guy, J. M. Kosonen, and J. B. West. J. Appl. Physiol. 79: 1290–1298, 1995) of an overall unaltered range ofV˙a/Q˙in μG, despite more homogeneous distributions of both ventilation and perfusion.

Contributions of diffusion jet flow and cardiac activity to regional ventilation in CFV

The magnitude and regional distribution of local gas transport during constant-flow ventilation (CFV) were quantified by imaging the washout of nitrogen 13 (13NN) from anesthetized and paralyzed mongrel dogs with positron emission tomography. Equal jet flows, through two 2-mm-ID bronchial catheters 1 cm distal to the carina, were adjusted to provide eucapnic CFV (total flow = 57.6 ml.s-1.kg-1). Basal, midheart, and apical transverse sections were studied in supine and prone anesthetized dogs. The ventilation per unit volume (sV) of selected areas was computed from local 13NN concentration vs. time curves during washout. To separate the regional contributions of CFV and cardiogenic oscillation to enhanced molecular diffusion, additional supine dogs were also studied during unilateral CFV. In this protocol the CFV jet flow was delivered to a single lung while the contralateral lung was left apneic. For each lung, washout data were obtained under CFV and apnea both living and postmortem animals. The local contributions of diffusion, CFV jet effects, and cardiac activity to gas transport were evaluated and tested for additive and multiplicative synergistic interactions. The regional distribution of gas transport during CFV was found to be highly nonuniform and characterized by higher ventilation to regions located close to the main bronchi and those located in the direction in which the CFV jet pointed. No major differences were observed between supine and prone positions. This regional pattern of ventilation distribution was found to be the result of complementary and nearly multiplicative interaction between the regional effects of the CFV jet, concentrated in the central airways, and the preferential cardiogenic gas transport enhancement in ventral regions close to the heart. The data were also analyzed with a model that divides the regional diffusive gas transport resistance into a central component, affected by the CFV jet, and a peripheral component, affected only by cardiac activity. This analysis showed substantial regional heterogeneities in the effects of the different gas transport mechanisms, which are consistent with the geometry of the bronchial tree and the location of the heart in the dog. The results indicate that regional nonuniformities must be considered when modeling gas transport in CFV.