Moomey C B, Fabian T C, Croce M A, Melton S M, Proctor K G
Department of Surgery, University of Tennessee, Memphis, USA.
J Trauma. 1998 Dec;45(6):988-96. doi: 10.1097/00005373-199812000-00003.
This study investigates whether factors that determine myocardial performance (preload, afterload, heart rate, and contractility) are altered after isolated unilateral pulmonary contusion.
Catheters were placed in the carotid arteries, left ventricles, and pulmonary arteries of anesthetized, ventilated (FiO2=0.5) pigs (31.2+/-0.6 kg; n=26). A unilateral, blunt injury to the right chest was delivered with a captive bolt gun (n=17) followed by tube thoracostomy. To control for anesthesia and instrumentation at FiO2 of 0.5, one group received tube thoracostomy only (sham injury; n=6). To control for effects of hypoxia without chest injury, an additional sham-injury group (n=3) was ventilated with FiO2 of 0.12. To generate cardiac function (i.e., Starling) curves, lactated Ringer's solution was administered in three bolus infusions at serial time points; the slope of stroke index versus ventricular filling pressure defines cardiac contractility.
By 4 hours after pulmonary contusion, pulmonary vascular resistance, airway resistance, and dead space ventilation were increased, whereas PaO2 (72+/-6 mm Hg at FiO2=0.5) and dynamic compliance were decreased (all p < 0.05). Despite profound lung injury, arterial blood pressure, heart rate, cardiac filling pressures, and output remained within the normal range, which is inconsistent with direct myocardial contusion. The slope of pulmonary capillary wedge pressure versus left ventricular end-diastolic pressure (LVEDP) regression was reduced by more than 50% from baseline (p < 0.05), but there was no significant change in the slope of the central venous pressure versus LVEDP regression. By 4 hours after contusion, the slope of the stroke index versus LVEDP curve was reduced by more than 80% from baseline (p < 0.05). By the same time after sham injury with FiO2 of 0.12 (PaO2 < 50 mm Hg), the regression had decayed a similar amount, but there was no change in the slope after sham injury with FiO2 of 0.5 (PaO2 > 200 mm Hg).
After right-side pulmonary contusion, the most often used estimate of cardiac preload (pulmonary capillary wedge pressure) does not accurately estimate LVEDP, probably because of changes in the pulmonary circulation or mechanics. Central venous pressure is a better estimate of filling pressure, at least in these conditions, probably because it is not directly influenced by the pulmonary dysfunction. Also, ventricular performance can be impaired by depressed myocardial contractility and increased right ventricular afterload even with normal left ventricular afterload and preload. It is thus conceivable that occult myocardial dysfunction after pulmonary contusion could have a role in the progression to cardiorespiratory failure even without direct cardiac contusion.
本研究调查在单侧肺挫伤后，决定心肌功能的因素（前负荷、后负荷、心率和收缩力）是否发生改变。
将导管插入麻醉、通气（吸入氧分数[FiO₂]=0.5）猪（体重31.2±0.6千克；n=26）的颈动脉、左心室和肺动脉。用栓枪对右胸进行单侧钝性损伤（n=17），随后行胸腔闭式引流术。为了在FiO₂为0.5时控制麻醉和器械操作的影响，一组仅接受胸腔闭式引流术（假损伤；n=6）。为了控制无胸部损伤时缺氧的影响，另一个假损伤组（n=3）用FiO₂为0.12进行通气。为生成心功能（即Starling）曲线，在连续时间点分三次推注乳酸林格氏液；每搏指数与心室充盈压的斜率定义心肌收缩力。
肺挫伤后4小时，肺血管阻力、气道阻力和死腔通气增加，而动脉血氧分压（FiO₂=0.5时为72±6毫米汞柱）和动态顺应性降低（均p<0.05）。尽管有严重的肺损伤，但动脉血压、心率、心脏充盈压和心输出量仍在正常范围内，这与直接心肌挫伤不一致。肺毛细血管楔压与左心室舒张末期压力（LVEDP）回归的斜率较基线降低了50%以上（p<0.05），但中心静脉压与LVEDP回归的斜率无显著变化。挫伤后4小时，每搏指数与LVEDP曲线的斜率较基线降低了80%以上（p<0.05）。在FiO₂为0.12的假损伤后相同时间（动脉血氧分压<50毫米汞柱），回归下降了类似程度，但在FiO₂为0.5的假损伤后（动脉血氧分压>200毫米汞柱）斜率无变化。
右侧肺挫伤后，最常用的心脏前负荷估计值（肺毛细血管楔压）不能准确估计LVEDP，可能是由于肺循环或力学的改变。中心静脉压是充盈压的更好估计值，至少在这些情况下如此，可能是因为它不受肺功能障碍的直接影响。此外，即使左心室后负荷和前负荷正常，心肌收缩力降低和右心室后负荷增加也可损害心室功能。因此可以想象，肺挫伤后隐匿性心肌功能障碍即使在无直接心脏挫伤的情况下也可能在进展为心肺衰竭中起作用。
