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<p>Strenuous respiratory effort has been proposed as a second hit for the lungs, labeled as <i>“patient self-inflicted lung injury”</i> (P-SILI). This secondary exploratory analysis evaluated whether insufficient respiratory support is associated with biventricular myocardial injury and pulmonary microvascular ultrastructural changes in experimental acute lung injury. In rats, lung injury was induced through surfactant depletion, followed by 3&#xa0;h of unsupported (standard oxygen therapy, 2L/min) or supported ventilation: protective mechanical ventilation (MV), continuous positive airway pressure (CPAP) 6 cmH<sub>2</sub>O, or high-flow nasal oxygen (HFNO) 4L/min. Subjects were assessed through general monitoring, arterial blood gas analysis, esophageal manometry (inspiratory effort), surface electromyography on the abdominal wall (expiratory effort), echocardiography (right ventricular outflow), and coagulation dysfunction analysis. An exploratory histological hypothesis-generating study on the right and left ventricular (RV and LV) myocardium was performed in all animals, and a quantitative scanning electron microscopy-based analysis of luminal permeability in small pulmonary vessels was completed only in four subjects per injured group. The primary endpoint was RV myocardial injury, while LV injury and pulmonary microvascular changes were considered secondary endpoints. The unsupported group presented higher heart rate, hypercapnia, increased arterial lactate levels, respiratory variation in pulmonary peak flow velocity, RV and LV myocardial injury, and incipient alterations in coagulation compared to MV and CPAP (all <i>p</i> &lt; 0.05). All support therapies were associated with lower myocardial injury score: MV and CPAP showed the lowest RV injury, and HFNO the highest. Only MV was strongly associated with lower LV injury score (all <i>p</i> &lt; 0.05). The Standard oxygen therapy and HFNO groups showed significantly higher luminal occlusion in small pulmonary vessels, consisting of erythrocyte-rich intravascular aggregates and amorphous material adherent to the vascular wall (all <i>p</i> &lt; 0.05). Unsupported respiratory effort was associated with biventricular myocardial injury and pulmonary microvascular ultrastructural findings characterized by occlusive intravascular aggregates compatible with early microthrombotic changes. These findings support the concept that underassistance injury may extend beyond the lung parenchyma and respiratory muscles to involve cardiovascular and pulmonary microvascular domains.</p>

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Unsupported respiratory effort is associated with myocardial injury and pulmonary occlusive microvascular changes in experimental acute lung injury

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月31日

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  • Felipe M. Llancalahuen,
  • Sonia Reveco,
  • Paola Caviedes,
  • Andrés Silva,
  • Carlos González,
  • Agustín Pérez,
  • Juan P. Cruces,
  • Jaime Retamal,
  • Daniel E. Hurtado,
  • Pablo Cruces

摘要

Strenuous respiratory effort has been proposed as a second hit for the lungs, labeled as “patient self-inflicted lung injury” (P-SILI). This secondary exploratory analysis evaluated whether insufficient respiratory support is associated with biventricular myocardial injury and pulmonary microvascular ultrastructural changes in experimental acute lung injury. In rats, lung injury was induced through surfactant depletion, followed by 3 h of unsupported (standard oxygen therapy, 2L/min) or supported ventilation: protective mechanical ventilation (MV), continuous positive airway pressure (CPAP) 6 cmH2O, or high-flow nasal oxygen (HFNO) 4L/min. Subjects were assessed through general monitoring, arterial blood gas analysis, esophageal manometry (inspiratory effort), surface electromyography on the abdominal wall (expiratory effort), echocardiography (right ventricular outflow), and coagulation dysfunction analysis. An exploratory histological hypothesis-generating study on the right and left ventricular (RV and LV) myocardium was performed in all animals, and a quantitative scanning electron microscopy-based analysis of luminal permeability in small pulmonary vessels was completed only in four subjects per injured group. The primary endpoint was RV myocardial injury, while LV injury and pulmonary microvascular changes were considered secondary endpoints. The unsupported group presented higher heart rate, hypercapnia, increased arterial lactate levels, respiratory variation in pulmonary peak flow velocity, RV and LV myocardial injury, and incipient alterations in coagulation compared to MV and CPAP (all p < 0.05). All support therapies were associated with lower myocardial injury score: MV and CPAP showed the lowest RV injury, and HFNO the highest. Only MV was strongly associated with lower LV injury score (all p < 0.05). The Standard oxygen therapy and HFNO groups showed significantly higher luminal occlusion in small pulmonary vessels, consisting of erythrocyte-rich intravascular aggregates and amorphous material adherent to the vascular wall (all p < 0.05). Unsupported respiratory effort was associated with biventricular myocardial injury and pulmonary microvascular ultrastructural findings characterized by occlusive intravascular aggregates compatible with early microthrombotic changes. These findings support the concept that underassistance injury may extend beyond the lung parenchyma and respiratory muscles to involve cardiovascular and pulmonary microvascular domains.