Physiological aspects of the determination of comprehensive arterial inflows in the lower abdomen assessed by Doppler ultrasound

Non-invasive measurement of splanchnic hemodynamics has been utilized in the clinical setting for diagnosis of gastro-intestinal disease, and for determining reserve blood flow (BF) distribution. However, previous studies that measured BF in a "single vessel with small size volume", such as the superior mesenteric and coeliac arteries, were concerned solely with the target organ in the gastrointestinal area, and therefore evaluation of alterations in these single arterial BFs under various states was sometimes limited to "small blood volumes", even though there was a relatively large change in flow. BF in the lower abdomen (BFAb) is potentially a useful indicator of the influence of comprehensive BF redistribution in cardiovascular and hepato-gastrointestinal disease, in the postprandial period, and in relation to physical exercise. BFAb can be determined theoretically using Doppler ultrasound by subtracting BF in the bilateral proximal femoral arteries (FAs) from BF in the upper abdominal aorta (Ao) above the coeliac trunk. Prior to acceptance of this method of determining a true BFAb value, it is necessary to obtain validated normal physiological data that represent the hemodynamic relationship between the three arteries. In determining BFAb, relative reliability was acceptably high (range in intra-class correlation coefficient: 0.85-0.97) for three arterial hemodynamic parameters (blood velocity, vessel diameter, and BF) in three repeated measurements obtained over three different days. Bland-Altman analysis of the three repeated measurements revealed that day-to-day physiological variation (potentially including measurement error) was within the acceptable minimum range (95% of confidence interval), calculated as the difference in hemodynamics between two measurements. Mean BF (ml/min) was 2951 ± 767 in Ao, 316 ± 97 in left FA, 313 ± 83 in right FA, and 2323 ± 703 in BFAb, which is in agreement with a previous study that measured the sum of BF in the major part of the coeliac, mesenteric, and renal arteries. This review presents the methodological concept that underlies BFAb, and aspects of its day-to-day relative reliability in terms of the hemodynamics of the three target arteries, relationship with body surface area, respiratory effects, and potential clinical usefulness and application, in relation to data previously reported in original dedicated research

Increasing abdominal pressure with and without PEEP: effects on intra-peritoneal, intra-organ and intra-vascular pressures

Intra-organ and intra-vascular pressures can be used to estimate intra-abdominal pressure. The aim of this prospective, interventional study was to assess the effect of PEEP on the accuracy of pressure estimation at different measurement sites in a model of increased abdominal pressure

Increasing abdominal pressure with and without PEEP: effects on intra-peritoneal, intra-organ and intra-vascular pressures

Intra-organ and intra-vascular pressures can be used to estimate intra-abdominal pressure. The aim of this prospective, interventional study was to assess the effect of PEEP on the accuracy of pressure estimation at different measurement sites in a model of increased abdominal pressure

Mitochondrial dysfunction and biogenesis: do ICU patients die from mitochondrial failure?

Mitochondrial functions include production of energy, activation of programmed cell death, and a number of cell specific tasks, e.g., cell signaling, control of Ca2+ metabolism, and synthesis of a number of important biomolecules. As proper mitochondrial function is critical for normal performance and survival of cells, mitochondrial dysfunction often leads to pathological conditions resulting in various human diseases. Recently mitochondrial dysfunction has been linked to multiple organ failure (MOF) often leading to the death of critical care patients. However, there are two main reasons why this insight did not generate an adequate resonance in clinical settings. First, most data regarding mitochondrial dysfunction in organs susceptible to failure in critical care diseases (liver, kidney, heart, lung, intestine, brain) were collected using animal models. Second, there is no clear therapeutic strategy how acquired mitochondrial dysfunction can be improved. Only the benefit of such therapies will confirm the critical role of mitochondrial dysfunction in clinical settings. Here we summarized data on mitochondrial dysfunction obtained in diverse experimental systems, which are related to conditions seen in intensive care unit (ICU) patients. Particular attention is given to mechanisms that cause cell death and organ dysfunction and to prospective therapeutic strategies, directed to recover mitochondrial function. Collectively the data discussed in this review suggest that appropriate diagnosis and specific treatment of mitochondrial dysfunction in ICU patients may significantly improve the clinical outcome

Predictors of pulmonary failure following severe trauma: a trauma registry-based analysis

Background: The incidence of pulmonary failure in trauma patients is considered to be influenced by several factors such as liver injury. We intended to assess the association of various potential predictors of pulmonary failure following thoracic trauma and liver injury. Methods: Records of 12,585 trauma patients documented in the TraumaRegister DGU® of the German Trauma Society were analyzed regarding the potential impact of concomitant liver injury on the incidence of pulmonary failure using uni- and multivariate analyses. Pulmonary failure was defined as pulmonary failure of ≥ 3 SOFA-score points for at least two days. Patients were subdivided according to their injury pattern into four groups: group 1: AIS thorax < 3; AIS liver < 3; group 2: AIS thorax ≥ 3; AIS liver < 3; group 3: AIS thorax < 3; AIS liver ≥ 3 and group 4: AIS thorax ≥ 3; AIS liver ≥ 3. Results: Overall, 2643 (21%) developed pulmonary failure, 12% (n= 642) in group 1, 26% (n= 697) in group 2, 16% (n= 30) in group 3, and 36% (n= 188) in group 4. Factors independently associated with pulmonary failure included relevant lung injury, pre-existing medical conditions (PMC), sex, transfusion of more than 10 units of packed red blood cells (PRBC), Glasgow Coma Scale (GCS) ≤ 8, and the ISS. However, liver injury was not associated with an increased risk of pulmonary failure following severe trauma in our setting. Conclusions: Specific factors, but not liver injury, were associated with an increased risk of pulmonary failure following trauma. Trauma surgeons should be aware of these factors for optimized intensive care treatment

Effects of positive-pressure ventilatory frequency on hepatic blood flow and performance

The liver metabolizes several mediators of sepsis-related acute lung injury, but is frequently dysfunctional during intermittent positive-pressure ventilation (IPPV). With IPPV, increases in intrathoracic pressure (ITP) phasically increase the effective hepatic back pressure owing to compression by the diaphragm and retrograde propagation of swings in right atrial pressure. If intrahepatic flow distribution or the time constant of hepatic outflow are accordingly altered by ventilatory frequency (f), then hepatic performance may be compromised beyond a critical f threshold. In two canine models, we characterized at constant mean ITP the effects of ITP pulses on hepatic blood flow partitioning and performance over a f spectrum (0.4, 1.67, and 2.5 Hz) during IPPV and high-frequency jet ventilation. Portal venous flow (Qpv) and hepatic arterial flow (Qha) were measured by electromagnetic flow probes and performance by the pharmacokinetics of infused indocyanine green (0.25 mg/kg). To assess pressure wave transmission to the portal vein, cardiac cycle-specific (CCS) ITP pulses were used to alter the hepatic venous pressure (Phv) waveform. Measurements were made during control conditions, after graded acute hypovolemia (group 1, n = 7,20 mL/kg bleed; group 2, n = 6, bled to a mean aortic pressure of 45 mm Hg) to change the hepatic critical pressure balance, and after blood reinfusion. Despite decreases in peak-inspiratory transpulmonary pressure with increasing f, phasic reductions in Qpv and the transmural portal venous pressure (Ppv) to Phv gradient were similar at all f. The inspiratory Ppv waveform reflected changes in abdominal pressure, and was not altered by differential swings in Phv with CCS ITP pulses regardless of hypovolemia. We conclude that at f ≤ 2.5 Hz, phasic increases in ITP modulate the hepatic outflow pressure in a post-sinusoidal flow-limiting segment in which diaphragmatic compression increases resistance to Qpv in a f-dependent manner. However, the pharmacokinetics of substances having similar hepatic extraction will primarily vary with inflow over this f spectrum. © 1989

Cardiovascular determinants of the hemodynamic response to acute endotoxemia in the dog

The cardiovascular changes that occur early in hyperdynamic, hypotensive septic shock are poorly understood. In a splenectomized but otherwise intact pentobarbital-anesthetized canine model (n = 11), we simultaneously characterized the determinants of ventricular and peripheral vascular function in response to a bolus infusion of E. coli endotoxin (1.0 mg/kg). Right-ventricular (RV) and left-ventricular (LV) stroke volumes were measured by electromagnetic flow probes. Instantaneous RV function and venous return curves1,2 and steady state arterial pressure-flow (P/Q) and LV function curves were generated by incremental volume loading both before (control) and 30 minutes after (endo) endotoxin infusion. Blood volume (BV) was determined by indicator dilution. Within five minutes of endotoxin infusion, hypotension and hypoperfusion developed because of a decrease in mean systemic pressure (Pma) with no change in ventricular function of the arterial P/Q relation. However, after 30 minutes endo, compared with control, cardiac output increased (2.4 ± .3 to 3.2 ± .3 L/min, x̄ ± XE. P < .05); arterial pressure fell (132 ± 10 to 87 ± 10 mm Hg, P < .01), while the arterial P/Q slope was unchanged. BV remained constant (2,051 ± 149 to 1,942 ± 194 mL, NS), but Pma decreased further (11.3 ± 0.9 to 9.5 ± 0.9 mm Hg, P < .01). For the same BV, peripheral vascular compliance (ΔBV/ΔPma) was unchanged. Ventricular stroke volumes at similar filling pressures were increased (P < .05), while calculated stroke work was unchanged. The arterial P/Q relation and peripheral vascular compliance were unaffected by subsequent beta-adrenergic blockade, though ventricular function was depressed. We conclude that acute endotoxemia causes a biphasic hemodynamic response comprising an early, disproportionate reduction in venous return and a later, progressive peripheral vasomotor paralysis. © 1986, Grune & Stratton, Inc.. All rights reserved

Effects of positive end-expiratory pressure on hepatic blood flow and performance

Positive end-expiratory pressure (PEEP) may impair extrapulmonary organ function. However, the effects of PEEP on the liver are unclear. We tested the hypothesis that at a constant cardiac output (CO), PEEP does not induce changes in hepatic blood flow (Q̇L) and parenchymal performance. In splenectomized, close-chested canine preparations (group I, n = 6), Q̇L was derived as hepatic outflow using electromagnetic flow probes (Q̇Lemf), and hepatic performance was defined by extraction and clearance of indocyanine green (ICG). In a noninvasive model (group II, n = 7), the effects of PEEP on hepatic performance alone were similarly analyzed. Measurements were taken 1) during intermittent positive-pressure ventilation (IPPV1), 2) after addition of 10 cmH2O PEEP to IPPV (PEEP1), 3) during continued PEEP but after return of CO to IPPV1 levels by intravascular volume infusions (PEEP2), and 4) after removal of both PEEP and excess blood volume (IPPV2). Phasic inspiratory decreases in Q̇Lemf present during positive-pressure ventilation were not increased during either PEEP1 or PEEP2. Mean Q̇Lemf decreased proportionately with CO during PEEP1 (P < 0.05), but was restored to IPPV1 levels in a parallel fashion with CO during PEEP2. The ICG pharmacokinetic responses to PEEP were complex, with differential effects on extraction and clearance. Despite this, hepatic performance was not impaired in either group. We conclude that global Q̇L reductions during PEEP are proportional to PEEP-induced decreases in CO and are preventable by returning CO to pre-PEEP levels by intravascular volume infusions. However, covarying changes in blood volume and hepatic outflow resistance may independently modulate hepatic function