Abstract
Autonomic control of blood pressure (BP) and heart rate (HR) is crucial during bleeding and hemorrhagic shock (HS) to compensate for hypotension and hypoxia. Previous works have observed that at the point of hemodynamic decompensation a marked suppression of BP and HR variability occurs, leading to irreversible shock. We hypothesized that recovery of the autonomic control may be decisive for effective resuscitation, along with restoration of mean BP. We computed cardiovascular indexes of baroreflex sensitivity and BP and HR variability by analyzing hemodynamic recordings collected from five pigs during a protocol of severe hemorrhage and resuscitation; three pigs were sham-treated controls. Moreover, we assessed the effects of severe hemorrhage on heart functionality by integrating the hemodynamic findings with measures of plasma high-sensitivity cardiac troponin T and metabolite concentrations in left ventricular (LV) tissue. Resuscitation was performed with fluids and norepinephrine and then by reinfusion of shed blood. After first resuscitation, mean BP reached the target value, but cardiovascular indexes were not fully restored, hinting at a partial recovery of the autonomic mechanisms. Moreover, cardiac troponins were still elevated, suggesting a persistent myocardial sufferance. After blood reinfusion all the indexes returned to baseline. In the harvested heart, LV metabolic profile confirmed the acute stress condition sensed by the cardiomyocytes. Variability indexes and baroreflex trends can be valuable tools to evaluate the severity of HS, and they may represent a more useful end point for resuscitation in combination with standard measures such as mean values and biological measures.NEW & NOTEWORTHY Autonomic control of blood pressure was highly impaired during hemorrhagic shock, and it was not completely recovered after resuscitation despite global restoration of mean pressures. Moreover, a persistent myocardial sufferance emerged from measured cardiac troponin T and metabolite concentrations of left ventricular tissue. We highlight the importance of combining global mean values and biological markers with measures of variability and autonomic control for a better characterization of the effectiveness of the resuscitation strategy.
Highlights
Hemorrhage and unresolved hemorrhagic shock (HS) still represent the leading cause of mortality after trauma in both civilian and military settings, with the majority of deaths occurring because of the inability to control bleeding and to effectively resuscitate hemorrhage patients [27, 67].much effort has been spent on investigation of the fundamental underlying pathophysiology of HS in order to develop innovative approaches or to discover new biological parameters capable of detecting the severity of blood loss, controlling bleeding, and guiding resuscitation.HS is a form of hypovolemic shock in which an acute reduction in central blood volume causes organ hypoperfusion and an inadequate oxygen supply at the cellular level
Bleeding caused a significant decrease in MAP, cardiac output (CO), and filling pressures and a concomitant significant increase in heart rate (HR), heart contractility and lactate compared with shamtreated animals (Fig. 1, Table 1)
After resuscitation with fluids and norepinephrine, MAP recovered to the target of 60 mmHg in all animals except one, but HR and heart contractility remained significantly higher than baseline values
Summary
HS is a form of hypovolemic shock in which an acute reduction in central blood volume causes organ hypoperfusion and an inadequate oxygen supply at the cellular level. Clinical signs of this condition are severe hypotension and hypoxia, pronounced tachycardia and tachypnea, diffused coagulopathy, hypothermia, and metabolic acidosis [14]. Physiological compensatory mechanisms are usually elicited in trying to maintain homeostasis. The cardiovascular system activates physiological responses with the aim of maintaining cerebral oxygenation and blood supply to central organs; for example, neuroendocrine-mediated modifications of peripheral vascular resistance cause a redistribution of fluids that leads to nonuniform regional blood loss. Other compensatory mechanisms consist of an increase in heart rate (HR) and myocardial contractility to increase cardiac output (CO) [62]
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