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To monitor the ischemic and/or reperfusion injury after porta hepatis occlusion (Pringle maneuver) in livers subjected to hypotension, serum alanine amino transferase (ALT), liver malondialdehyde, (MIDA), and liver glutathione (GSH) levels were measured. MDA is a by-product of oxidant-induced lipid peroxidation, and GSH is an endogenous antioxidant. The effects of lactated Ringer's (LR) and hypertonic saline (7.5%)/Dextran (6%; HSD) resuscitation on liver injury, if any, was investigated. Rats in sham (S, n = 8) and five other groups (n = 8) underwent femoral artery and vein catheterization and laparotomy. The hemorrhage and ischemia (HI) group was bled 30% of their blood volume and had their porta hepatis occluded for 30 min. The HI, LR, and HSD groups underwent both hemorrhage and occlusion. Thirty minutes after hemorrhage, the LR and HSD groups received either LR (equivalent to three times the shed blood) or HSD (10 mL/kg) resuscitation over 30 min. Both LR and HSD resuscitation lowered the increased ALT and liver tissue MDA seen in the HI group. ALT was decreased from 348 +/- 93 IU/L in the HI group to 200 +/- 98 IU/L in the LR and 139 +/- 74 IU/L in the HSD groups. Liver tissue MDA was 353 +/- 22 nmol/g/tissue in the HI group and LR decreased it to 261 +/- 17 nmol/g/tissue, whereas HSD decreased it to 273 +/- 20 nmol/g/tissue. The decrease in ALT and the increase in liver GSH were more pronounced with HSD resuscitation (P < 0.05). HSD seems to be more effective than LR in decreasing the liver tissue damage produced by total hepatic inflow occlusion under hypovolemic conditions.

Background Splanchnic perfusion following hypovolemic shock is an important marker of adequate resuscitation. We tested whether the gap between esophageal partial carbon dioxide tension (PeCO2) and arterial partial carbon dioxide tension (PaCO2) is increased during graded hemorrhagic hypotension and reversed after blood reinfusion, using a fiberoptic carbon dioxide sensor. Materials and method Ten Sprague–Dawley rats were anesthetized, tracheotomized, and cannulated in one femoral artery and vein. A calibrated fiberoptic PCO2 probe was inserted into the distal third of the esophagus for determination of luminal PeCO2 during maintained anesthesia (pentobarbital 15 mg/kg per hour), normothermia (38 ± 0.5°C), and fluid balance (saline 5 ml/kg per hour). Three out of 10 rats were used to determine the limits of hemodynamic stability during gradual hemorrhage. Seven of the 10 rats were then subjected to mild and severe hemorrhage (15 and 20–25 ml/kg, respectively). Thirty minutes after severe hemorrhage, these rats were resuscitated by reinfusion of the shed blood. Arterial gas exchange, hemodynamic variables, and PeCO2 were recorded at each steady-state level of hemorrhage (at 30 and 60 min) and after resuscitation. Results The PeCO2–PaCO2 gap was significantly increased after mild and severe hemorrhage and returned to baseline (prehemorrhagic) values following blood reinfusion. Base deficit increased significantly following severe hemorrhage and remained significantly elevated after blood reinfusion. Significant correlations were found between base deficit and PeCO2–PaCO2 (P < 0.002) and PeCO2 (P < 0.022). Blood bicarbonate concentration decreased significantly following mild and severe hemorrhage, but its recovery was not complete at 60 min after blood reinfusion. Conclusion Esophageal–arterial PCO2 gap increases during graded hemorrhagic hypotension and returns to baseline value after resuscitation without complete reversal of the base deficit. These data suggest that esophageal capnometry could be used as an alternative for gastric tonometry during management of hypovolemic shock.

OBJETIVO: Estudar os efeitos da isquemia e reperfusão hepática total sobre acúmulo de neutrófilos no íleo terminal e cólon sigmóide de ratos, em condições de normalidade e submetidos ao estado de choque hemorrágico controlado. MÉTODO: 32 ratos Wistar, machos, foram divididos em quatro grupos de oito animais cada: grupo Sham, submetido aos procedimentos padrões com um período de 60 minutos de observação; grupo Choque, submetido a choque hemorrágico controlado (PAM = 40mmHg, 20min) seguido de reposição volêmica (Ringer lactato + sangue, 3:1) e reperfusão (60min); grupo Pringle, submetido à isquemia hepática total (15min.) e reperfusão (60min); grupo Total submetido a choque hemorrágico controlado (20min) seguido de reposição volêmica (Ringer lactato + sangue, 3:1), isquemia hepática (15min) e reperfusão (60min). Após o sacrifício dos animais, procedeu-se à contagem de neutrófilos nos segmentos intestinais. RESULTADOS: Na contagem de neutrófilos no íleo terminal, apenas o grupo Choque diferiu dos demais (p

OBJETIVO: Estudar os efeitos da isquemia e reperfusão hepática total sobre acúmulo de neutrófilos no interstício pulmonar de ratos, em condições de normalidade e submetidos ao estado de choque hemorrágico controlado. MÉTODOS: 32 ratos Wistar, machos, foram divididos em quatro grupos de oito animais cada: grupo Sham, submetido aos procedimentos padrões com um período de 60 minutos de observação; grupo Choque, submetido a choque hemorrágico controlado (PAM = 40 mmHg, 20 min.) seguido de reposição volêmica (Ringer lactato + sangue, 3:1) e reperfusão (60 min.); grupo Pringle, submetido a isquemia hepática total (15 min.) e reperfusão (60 min.); grupo Total submetido a choque hemorrágico controlado (15 min.) seguido de reposição volêmica (Ringer lactato + sangue, 3:1) e reperfusão (60 min.). Após o sacrifício dos animais, procedeu-se à contagem de neutrófilos no interstício pulmonar. RESULTADOS: Os valores encontrados para contagem de neutrófilos no interstício pulmonar indicaram que, os animais dos grupos Pringle, Total e, também, do grupo Choque, não diferiram dos animais do grupo Sham com valores de (Sham 21,08± 14,12; Choque 35,15± 18,74; Pringle 19,78± 15,38; Total 23,90± 16,37) (p=0.253) CONCLUSÃO: Em ratos submetidos a estado de choque hemorrágico controlado associado a isquemia hepática de 15 minutos, seguida de 60 minutos de reperfusão, não ocorreu acúmulo significativo de neutrófilos no interstício pulmonar. OBJECTIVE: The purpose of this experimental work was to study the effects of total hepatic ischemia and reperfusion on the accumulation of neutrophils in the lung of rats, under normal conditions and submitted to controlled hemorrhagic shock state. METHODS: thirty two adult male Wistar rats, were divided into four groups: the Sham group, was submitted to the standard procedures for a period of 60 min. of observation; Shock group, was submitted to controlled hemorrhagic shock (PAM=40 mmHg, 20 min.) followed by volemic resuscitation (lactated Ringer’s solution + blood, 3:1) and reperfusão for 60 min.; Pringle group, was submitted to total hepatic ischemia for 15 min. and reperfusão for 60 min.; The Total group, was submitted to controlled hemorrhagic shock for 15 min. followed by volemic resuscitation (lactated Ringer’s solution + blood, 3:1) and reperfusão for 60 min.). The counting of neutrophils on the lung tissue was performed after the euthanasia of animals. RESULTS: The values found for the counting of neutrophils on the lung tissue indicate that the animals from the Pringle, Total, and Shock groups, did not differ from the Sham group, having the following values: Sham, 21,08± 14,12; Shock, 35,15± 18,74; Pringle, 19,78± 15,38; Total, 23,90± 16,37) (p=0.253). CONCLUSION: Rats submitted to controlled hemorrhagic shock state associated to total hepatic ischemia for 15 minutes, followed by 60 minutes of reperfusion, did not present significant neutrophils accumulation on the lung tissue.

The clinical charts and contrast mediumenhanced computed tomographic (CT) examinations of 15 adults with a history of serious shock and resuscitation were reviewed. Several hypovolemia-related abnormalities were recognizable and were variably associated with each other. Diminished caliber of the abdominal vessels with intense vascular contrast medium enhancement and renal abnormalities were the most common findings; decreased and/or increased enhancement of the abdominal organs and other hypovolemic changes were also present.

Thirty-five year-old Amadeus Mozart died in Vienna after an acute illness that lasted only 15 days but no consensus has been reached on the cause of his death. From many letters written by his farther it is almost certain that he experienced at least three episodes of acute rheumatic fever attack in his childhood, and a relapse of rheumatic fever was suggested to have killed Mozart, although death from acute rheumatic fever is very rare in adults. His last illness was characterized by high fever, massive edema, vomiting and skin rash. His last illness can be explained by infectious endocarditis and heart failure. During his last hours, he was given phlebotomy, possibly for the third time in two weeks, and soon after he became unconscious and died. As such, phlebotomy performed on a man dehydrated by high fever and vomiting may have caused systemic shock. In summary, Mozart probably died from chronic rheumatic heart disease complicated by infective endocarditis and heart failure, and repeated phlebotomy-induced hypovolemic shock.

In a rat model of severe hypotension and respiratory depression induced by step-wise bleeding, protoveratrines cause a prompt and sustained improvement of cardiovascular and respiratory functions, both in anesthetized and in conscious animals, seemingly through a magnification of the reflex response originated by the chemoreceptors of aortic and carotid bodies. The restoration of cardiovascular function is attributable to an increase both in total peripheral resistance and cardiac output. The finding could provide the basis for a new approach to the first-aid management of massive blood losses.

The fundamental abnormality in nephrotic syndrome is the structural and electrochemical changes that have been documented to occur in the glomerular basement membrane lead to proteinuria. It is the proteinuria itself which most likely causes hypoalbuminemia and associated complications such as infections, hypercoagulability and hypovolemia. Hypovolemia may cause postural hypotension, acute renal failure, circulatory collaps or sudden death. An eleven-year-old boy was referred to the Child Health Department of Dr. Kariadi Hospital Semarang with a diagnosis of corticosteroid resistant nephrotic syndrome and acute renal failure. Physical examination showed a severely ill boy with general edema, shock, hemoconcentration, hypoalbuminemia, hypercholesterolemia, massive proteinuria and disturbed renal function. The treatment consisted of infusion of dextrose 10% followed by human plasma and furosemide to restore plasma volume and enhance urine production. Two days later he was in better condition, normovolemia, slight edema, good diuresis, but his blood pressure increased, and ophtalmologic examination supported the diagnosis of grade I hypertensive retinopathy. Intravenous clonidine and furosemide were given and were very effective. Kidney biopsy revealed minimal lesion with slight proliferation.

In an experimental model of bleeding-induced hypovolemic shock causing the death of all saline-treated rats within 26 ± 4 min, the intravenous injection of bombesin (2.5, 5 or 10 μg/kg) dose-dependently restored blood pressure, pulse amplitude, heart rate and respiratory function, and improved survival rate as assessed at the end of the experiment (2 h). The effect on cardiovascular and respiratory functions was prompt (within 1–2 min) and sustained. The release of cholecystokinin seems to be the main mechanism of action, because the anti-shock effect of bombesin is largely prevented by the CCK-antagonist, L-364, 718.

Background Large registries are important data sources in epidemiological studies of shock, if these registries are valid. Therefore, we examined the positive predictive value (PPV) of diagnosis codes for shock, the procedure codes for inotropic/vasopressor therapy among patients with a diagnosis of shock, and the combination of a shock diagnosis and a code for inotropic/vasopressor therapy in the Danish National Patient Registry (DNPR). Methods We randomly selected 190 inpatients with an International Classification of Diseases, 10th revision (ICD-10) diagnosis of shock at Aarhus University Hospital from 2005–2012 using the DNPR; 50 patients were diagnosed with cardiogenic shock, 40 patients with hypovolemic shock, and 100 patients with septic shock. We used medical charts as the reference standard and calculated the PPV with 95% confidence intervals (CI) for overall shock and for each type of shock separately. We also examined the PPV for inotropic/vasopressor therapy and the PPV for shock when a concurrent code for inotropic/vasopressor therapy was also registered. Results The PPV was 86.1% (95% CI: 79.7–91.1) for shock overall, 93.5% (95% CI: 82.1–98.6) for cardiogenic shock, 70.6% (95% CI: 52.5–84.9) for hypovolemic shock, and 69.2% (95% CI: 57.7–79.2) for septic shock. The PPV of use of inotropes/vasopressors among shock patients was 88.9% (95% CI: 79.3–95.1). When both a shock code and a procedure code for inotropic/vasopressor therapy were used, the PPV for shock overall was 93.1% (95% CI: 84.5–97.7). ICD-10 codes for subtypes of shock and simultaneously registered use of inotropes/vasopressors provided PPVs of 96.0% (95% CI: 79.6–99.9) for cardiogenic shock, 69.2% (95% CI: 38.6–90.9) for hypovolemic shock, and 82.4% (95% CI: 65.5–93.2) for septic shock. Conclusions Overall, we found a moderately high PPV for shock in the DNPR. The PPV was highest for cardiogenic shock but lower for hypovolemic and septic shock. Combination diagnoses of shock with codes for inotropic/vasopressor therapy further increased the PPV of shock overall, and for cardiogenic and septic shock diagnoses. Electronic supplementary material The online version of this article (doi:10.1186/s12874-015-0013-2) contains supplementary material, which is available to authorized users.

Purpose: To describe and discuss the thoracic CT features of hypovolemic shock. Material and Methods: From a group of 18 patients with signs of hypovolemia on contrast-enhanced abdominal CT, 11 were selected for our study as having also undergone a complete chest examination. Pulse rate, blood pressure, trauma score value, Glasgow coma scale value, surgical result, and final outcome were retrospectively evaluated. The CT features analyzed were: decreased cardiac volume, reduced caliber of the thoracic aorta, aortic branches and caval venous system, increased enhancement of the aorta, and increased enhancement of the pulmonary collapses/contusions. Results: All 11 subjects presented severe injuries and hemodynamic instability; 7 were stable enough to undergo surgery; only 1 of the 11 survived. Two patients showed none of the features of thoracic hypovolemia. All the other patients presented at least two signs: reduced caliber of the thoracic aorta in 7 cases; decreased volume of the cardiac chambers and increased aortic enhancement in 6; decreased caliber of the aortic vessels in 4; decreased caliber of the caval veins in 3; and increased enhancement of the pulmonary collapses/contusions in 3. Conclusions: In patients with hypovolemia, CT may show several thoracic findings in addition to abdominal ones. Knowledge of these features is important for distinguishing them from traumatic injuries.

BACKGROUND The assessment of hemodynamic status is a crucial task in the initial evaluation of trauma patients. However, blood pressure and heart rate are often misleading, as multiple variables may impact these conventional parameters. More reliable methods such as pulmonary artery thermodilution for cardiac output measuring would be necessary, but its applicability in the Emergency Department is questionable due to their invasive nature. Non-invasive cardiac output monitoring devices may be a feasible alternative. METHODS A systematic literature review was conducted. Only studies that explicitly investigated non-invasive hemodynamic monitoring devices in trauma patients were considered. RESULTS A total of 7 studies were identified as suitable and were included into this review. These studies evaluated in a total of 1,197 trauma patients the accuracy of non-invasive hemodynamic monitoring devices by comparing measurements to pulmonary artery thermodilution, which is the gold standard for cardiac output measuring. The correlation coefficients r between the two methods ranged from 0.79 to 0.92. Bias and precision analysis ranged from -0.02 +/- 0.78 l/min/m(2) to -0.14 +/- 0.73 l/min/m(2). Additionally, data on practicality, limitations and clinical impact of the devices were collected. CONCLUSION The accuracy of non-invasive cardiac output monitoring devices in trauma patients is broadly satisfactory. As the devices can be applied very early in the shock room or even preclinically, hemodynamic shock may be recognized much earlier and therapeutic interventions could be applied more rapidly and more adequately. The devices can be used in the daily routine of a busy ED, as they are non-invasive and easy to master.