Rates of hemorrhage from an arterial injury are related to changes in mean arterial pressure. In this animal model, early aggressive fluid resuscitation in penetrating thoracic trauma exacerbates total hemorrhage volume. Despite resumption of hemorrhage from the site of injury, delaying fluid resuscitation results in the best hemodynamic parameters.
Abstract. Objectives:To determine the effects of delaying fluid on the rate of hemorrhage and hemodynamic parameters in an injury involving the arterial system. Methods: Twenty-one adult, anesthetized sheep underwent left anterior thoracotomy and transection of the left internal mammary artery. A chest tube was inserted into the thoracic cavity to provide a continuous measurement of blood loss. The animals were randomly assigned to one of three resuscitation protocols: 1) no fluid resuscitation (NR), 2) standard fluid resuscitation (SR) begun 15 minutes after injury, or 3) delayed fluid resuscitation (DR) begun 30 minutes after injury. All of the animals in the two resuscitation groups received 60 mL/kg of lactated Ringer's solution over 30 minutes. Blood loss and hemodynamic parameters were measured throughout the experiment. Results: Total hemorrhage volume (mean Ϯ SD) at the end of the experiment was significantly lower (p = 0.006) in the NR group (1,499 Ϯ 311 mL) than in the SR group (3,435 Ϯ 721 mL) or the DR group (2,839 Ϯ 1549 mL). Rate of hemorrhage followed changes in mean arterial pressure in all groups. Hemorrhage spontaneously ceased significantly sooner (p = 0.007) in the NR group (21 Ϯ 14 minutes) and the DR group (20 Ϯ 15 minutes) than in the SR group (54 Ϯ 4 minutes). In the DR group, after initial cessation of hemorrhage, hemorrhage recurred in five of six animals (83%) with initiation of fluid resuscitation. Maximum oxygen (O 2 ) delivery in each group after injury was as follows: 101 Ϯ 34 mL O 2 /kg/min at 45 minutes in the DR group, 51 Ϯ 20 mL O 2 /kg/min at 30 minutes in the SR group, and 35 Ϯ 8 mL O 2 /kg/min at 60 minutes in the NR group. Conclusions: Rates of hemorrhage from an arterial injury are related to changes in mean arterial pressure. In this animal model, early aggressive fluid resuscitation in penetrating thoracic trauma exacerbates total hemorrhage volume. Despite resumption of hemorrhage from the site of injury, delaying fluid resuscitation results in the best hemodynamic parameters.
Introduction: In individuals with dyspnea on exertion (DOE) and suspected exercise pulmonary hypertension (exPH), oxygen uptake (VO 2 ), cardiac output (CO), peripheral oxygen extraction (Ca-vO 2 ), and mean pulmonary artery pressure (mPAP) have been well characterized during incremental exercise but less is known about the kinetics of post-exercise recovery patterns. Hypothesis: Exercise recovery cardiac output kinetics are slowed in patients with exPH. Methods: Upright maximum incremental ramp cycle ergometry cardiopulmonary exercise testing with invasive hemodynamic monitoring and serial blood gas measurements during exercise and recovery was performed in 50 consecutive patients referred for evaluation of DOE of unclear etiology. VO 2 , arterial and venous oxygen content (Ca-vO 2 ), Fick cardiac output, and mPAP were analyzed from rest, peak exercise, and 2 minutes post-exercise. ExPH was defined in a consistent manner with recent consensus statements (ΔmPAP/ΔCO >3.0 mmHg/L/min) from rest to peak exercise. Results: Among 50 patients with DOE, [62% female, Age 61.7±11.8, BMI 30.7±8.2] 2-min post-exercise VO 2 was -56±11%, CO: -22±19%, Ca-vO 2 :-42±15% compared to peak exercise values. The % fall in CO at 2min was significantly lower in the 26 patients with exPH compared to the 24 patients without exPH (Table). The average mPAP remained elevated at 2 min post-exercise (>20mmHg) in exPH despite normal average resting values. Conclusions: Patients with exPH demonstrate slowed CO recovery kinetics in conjunction with persistent PAP elevation 2-min post-exercise. Persistent elevation in blood flow through the pulmonary circuit at a time conducive to non-invasive assessment of PAP (i.e. by echocardiography) may lend itself to non-invasive detection of exercise-PH in patients undergoing evaluation of dyspnea on exertion.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.