Abstract / Summary
We have hypothesized that respiratory arrest caused by temporary brainstem dysfunction is the primary cause of death during the hyperacute phase of blast injury and have demonstrated that this is highly likely. To date, we have examined the effects of shock waves on pigs by exposing them to shock waves from both the dorsal and ventral sides. Therefore, in this study, we investigated the effects of lateral shock wave exposure in pigs and identified priority regions for protection against blast injuries. Eight male hybrid pigs (age, 10–12 weeks; mean weight, 36.6 kg) were anesthetized and fitted with a femoral arterial line and subcutaneous electrocardiography leads for continuous monitoring of vital signs and respiration. Pigs were fixed prone with the right lateral thorax aligned to the aperture. A compressed air-driven shock tube generated a shock wave (driving pressure: 3.0 MPa). Arterial blood gases were obtained before and 0, 3, 5, and 10 min post-exposure. Whole-body computed tomography was performed pre- and post-exposure. Survivors were observed for 3 h, then underwent necropsy. Regarding lung injury, since “primary blast lung injury” is defined as “radiological and clinical evidence of acute lung injury occurring within 12 h of exposure and not due to secondary or tertiary injury”, this study focuses on organ injury and mortality in the hyperacute and acute phases. All pigs developed immediate apnea after blast exposure. Two pigs died: one from persistent apnea leading to progressive hypoxia and cardiac arrest and one from delayed cardiac arrest approximately 1 h later. Necropsy in the delayed death revealed thrombus extending from the right subclavian vein into the superior vena cava, suggesting embolism. Marked bradycardia was absent, and hypotension only occurred in one pig. Computed tomography depicted no air embolism and suggested increased right lung injury. Gross anatomy revealed pulmonary contusion and splenic injury in all the pigs; pulmonary bullae were rare. Lateral shock wave exposure can induce profound apnea and death, likely owing to transient brainstem respiratory dysfunction rather than a vagal reflex mechanism. To reduce mortality, protective strategies should prioritize shielding the brainstem region, specifically the lateral and posterior sides of the occipital region and neck.