Low Flow States Research Articles

Strategies to Tackle Early Low Flow States in the Extremely Preterm Infant

Strategies to Tackle Early Low Flow States in the Extremely Preterm Infant

Management of Severe Craniofacial Vascular Malformation Operated Under Bypass

Cardiopulmonary bypass (CBP) and circulatory arrest as an assist in the surgical excision of a severe facial vascular malformation were first described by Mulliken et al in 1979. Later on, its use had expanded for resection of intracranial vascular malformations. However, to date, there have not been any published series of these procedures being used in the resection of craniofacial vascular malformations. We sought to review the first 10 surgical procedures performed at McGill University Health Centre for large vascular malformations resection using hypothermic CBP with or without circulatory arrest. All consecutive patients at the McGill University Health Centre who had a craniofacial vascular malformation resected with the aid of CBP were reviewed. A comparison of the classic midline sternotomy with cardiac arrest to percutaneous femoral bypass with hypothermic "low flow" was performed. Charts were reviewed for the operative intervention including bypass parameters and short- and long-term complications of the procedure. Cardiopulmonary bypass was used in 9 patients for 10 surgical procedures for the resection of a variety of craniofacial vascular malformations from 1987 to 2001. All lesions had sclerotherapy and embolization of the feeding vessels 72 to 96 hours preoperatively. The average age of our patients was 21 ± 13.4 years (2-37 years). Procedures were conducted via either an open bypass or a closed femoral approach. There were no mortalities. There were 2 major cardiac intraoperative complications and 1 major postoperative complication, which were managed with no sequelae. The average length of postoperative hospital stay was 10 days. All patients went on to full recovery. The blood transfusions varied from 10 U to 0 U for our last patient. The assistance and adjunct of CBP are a useful procedure in the resection of very large vascular malformations, in selected cases. There were no major long-term complications in this series. With the evolution of our approach, the use of complete circulatory arrest was not required in the majority of cases, and an adequate resection was usually possible with the low-flow state alone as we developed this technique with more experience through the process.

Early Metabolic/Cellular-Level Resuscitation Following Terminal Brain Stem Herniation

Patients with terminal brain stem herniation experience global physiological consequences and represent a challenging population in critical care practice as a result of multiple factors. The first factor is severe depression of consciousness, with resulting compromise in airway stability and lung ventilation. Second, with increasing severity of brain trauma, progressive brain edema, mass effect, herniation syndromes, and subsequent distortion/displacement of the brain stem follow. Third, with progression of intracranial pathophysiology to terminal brain stem herniation, multisystem consequences occur, including dysfunction of the hypothalamic-pituitary axis, depletion of stress hormones, and decreased thyroid hormone bioavailability as well as biphasic cardiovascular state. Cardiovascular dysfunction in phase 1 is a hyperdynamic and hypertensive state characterized by elevated systemic vascular resistance and cardiac contractility. Cardiovascular dysfunction in phase 2 is a hypotensive state characterized by decreased systemic vascular resistance and tissue perfusion. Rapid changes along the continuum of hyperperfusion versus hypoperfusion increase risk of end-organ damage, specifically pulmonary dysfunction from hemodynamic stress and high-flow states as well as ischemic changes consequent to low-flow states. A pronounced inflammatory state occurs, affecting pulmonary function and gas exchange and contributing to hemodynamic instability as a result of additional vasodilatation. Coagulopathy also occurs as a result of consumption of clotting factors as well as dilution of clotting factors and platelets consequent to aggressive crystalloid administration. Each consequence of terminal brain stem injury complicates clinical management within this patient demographic. In general, these multisystem consequences are managed with mechanism-based interventions within the context of caring for the donor's organs (liver, kidneys, heart, etc.) after death by neurological criteria. These processes begin far earlier in the continuum of injury, at the moment of terminal brain stem herniation. As such, aggressive, mechanism-based care, including hormonal replacement therapy, becomes clinically appropriate before formal brain death declaration to support cardiopulmonary stability following terminal brain stem herniation.

Early Metabolic/Cellular-Level Resuscitation Following Terminal Brain Stem Herniation

Patients with terminal brain stem herniation experience global physiological consequences and represent a challenging population in critical care practice as a result of multiple factors. The first factor is severe depression of consciousness, with resulting compromise in airway stability and lung ventilation. Second, with increasing severity of brain trauma, progressive brain edema, mass effect, herniation syndromes, and subsequent distortion/displacement of the brain stem follow. Third, with progression of intracranial pathophysiology to terminal brain stem herniation, multisystem consequences occur, including dysfunction of the hypothalamic-pituitary axis, depletion of stress hormones, and decreased thyroid hormone bioavailability as well as biphasic cardiovascular state. Cardiovascular dysfunction in phase 1 is a hyperdynamic and hypertensive state characterized by elevated systemic vascular resistance and cardiac contractility. Cardiovascular dysfunction in phase 2 is a hypotensive state characterized by decreased systemic vascular resistance and tissue perfusion. Rapid changes along the continuum of hyperperfusion versus hypoperfusion increase risk of end-organ damage, specifically pulmonary dysfunction from hemodynamic stress and high-flow states as well as ischemic changes consequent to low-flow states. A pronounced inflammatory state occurs, affecting pulmonary function and gas exchange and contributing to hemodynamic instability as a result of additional vasodilatation. Coagulopathy also occurs as a result of consumption of clotting factors as well as dilution of clotting factors and platelets consequent to aggressive crystalloid administration. Each consequence of terminal brain stem injury complicates clinical management within this patient demographic. In general, these multisystem consequences are managed with mechanism-based interventions within the context of caring for the donor’s organs (liver, kidneys, heart, etc.) after death by neurological criteria. These processes begin far earlier in the continuum of injury, at the moment of terminal brain stem herniation. As such, aggressive, mechanism-based care, including hormonal replacement therapy, becomes clinically appropriate before formal brain death declaration to support cardiopulmonary stability following terminal brain stem herniation.

Acute Thrombosis of the Abdominal Aorta Secondary to Low Cardiac Output Syndrome

Acute aortic occlusion is a rare but catastrophic pathology with very high morbidity and mortality. It may result from thrombus formation, saddle embolism and other etiologies related to arteriosclerosis, low flow states or hypercoagulability. The clinical presentations include ischemic and neurologic symptoms of the lower extremities, abdominal symptoms and acute hypertension. We present a case of acute aortic occlusion resulting from in situ thrombosis secondary to a low cardiac output state due to MI. A 61-year-old man underwent sigmoid colon resection for volvulus formation 5 days before his acute presentation. He presented as acute inferior MI with low cardiac output syndrome. Successful stent implantation of the RCA was performed as an emergency via the right brachial artery since the femoral pulses were not palpable. Abdominal aortography showed total occlusion of the abdominal aorta distal to the renal arteries. Emergency bilateral femoral embolectomy was performed with local anesthesia, resulting in good distal pulses. Postoperatively, he deteriorated with acidosis, hypotension, oliguria and increased inotrop requirement. He died of cardiac failure and severe metabolic derangement on the second day after operation. Early diagmosis and treatment is very important for preventing metabolic compromise in these patients. The choice of surgical procedure depends on the general condition of the patient, the presence of chronic aortic occlusive disease, presence of renal and mesenteric ischemia and cardiac function of the patient. (JAREM 2012; 2: 124-6)

Effects of intravenous sulfide during resuscitated porcine hemorrhagic shock*

Controversial data are available on the effects of hydrogen sulfide during hemorrhage. Because the clinical significance of hydrogen sulfide administration in rodents may not be applicable to larger species, we tested the hypothesis whether intravenous Na2S (sulfide) would beneficially influence organ dysfunction during long-term, porcine hemorrhage and resuscitation. Prospective, controlled, randomized study. University animal research laboratory. Forty-five domestic pigs of either gender. Anesthetized and instrumented animals underwent 4 hrs of hemorrhage (removal of 40% of the blood volume and subsequent blood removal/retransfusion to maintain mean arterial pressure at 30 mm Hg). Sulfide infusion was started 2 hrs before hemorrhage, simultaneously with blood removal or at the beginning of retransfusion of shed blood, and continued for 12 hrs. Resuscitation comprised hydroxyethyl starch and norepinenephrine infusion titrated to maintain mean arterial pressure at preshock values. Before, immediately at the end of and 12 and 22 hrs after hemorrhage, we measured systemic and regional hemodynamics (portal vein, hepatic and right kidney artery ultrasound flow probes) and oxygen transport, nitric oxide and cytokine production (nitrate+nitrite, interleukin-6, tumor necrosis factor-α levels). Postmortem biopsies were analyzed for histomorphology (hematoxylin and eosin staining) and DNA damage (terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling staining). The progressive kidney (creatinine levels, creatinine clearance), liver (transaminase activities, bilirubin levels), and cardiocirculatory (norepipnehrine requirements, troponin I levels) dysfunction was attenuated in the simultaneous treatment group only, which coincided with reduced lung, liver, and kidney histological damage. Sulfide reduced mortality, however, irrespective of the timing of its administration. While the sulfide-induced protection against organ injury was only present when initiated simultaneously with blood removal, it was largely unrelated to hypothermia. The absence of sulfide-mediated protection in the pretreatment protocol may be due to the accumulation of sulfide during low flow states. In conclusion, sulfide treatment can be effective in hemorrhagic shock, but its effectiveness is restricted to a narrow timing and dosing window.

Prevention and Management of Graft Thrombosis in Pancreatic Transplant

Pancreatic transplant effectively cures type 1 diabetes mellitus and maintains consistent long-term euglycemia. However, technical failure, and in particular graft thrombosis, accounts for the vast majority of transplants lost in the early postoperative period. The pancreas' inherently low microvascular flow state makes it vulnerable to vascular complications, as does the hypercoagulable blood of diabetic patients. Ultimately, the phenomenon is most definitely multifactorial. Prevention, as opposed to treatment, is key and should focus on reducing these multiple risk factors. This will involve tactical donor selection, optimal surgical technique and some form of anticoagulation. Close monitoring and early intervention will be crucial when treating thrombosis once preventative methods have failed. This may be achieved by further anticoagulation, graft salvage, or pancreatectomy with retransplant. This article will explore the multiple factors contributing to graft thrombus formation and the ways in which they may be addressed to firstly prevent, or more likely, reduce thrombosis. Secondly, we will consider the management strategies which can be implemented once thrombosis has occurred.

Transport, cilia, and PKD: must we in (cyst) on interrelationships? Focus on “Increased Na+/H+ exchanger activity on the apical surface of a cilium-deficient cortical collecting duct principal cell model of polycystic kidney disease”

<i>Transport, cilia, and PKD: must we in (cyst) on interrelationships?</i> Focus on “Increased Na⁺/H⁺ exchanger activity on the apical surface of a cilium-deficient cortical collecting duct principal cell model of polycystic kidney disease”

Nimodipine-Induced Hypotension but Not Nitroglycerin-Induced Hypotension Preserves Long- and Short-Term Memory in Adult Mice

Acute hypotension may be implicated in cognitive dysfunction. L-type calcium channel blockers in the setting of hypoxia are protective of learning and memory. We tested the hypothesis that hypotension induced by nimodipine (NIMO) and nicardipine (NICA) would be protective of long- and short-term memory compared to hypotension induced by nitroglycerin (NTG). Forty Swiss-Webster mice (30 to 35 g, 6 to 8 weeks) were randomized into 4 groups for i.p. injection immediately after passive avoidance (PA) learning on day 0: (1) NTG (30 mg/kg); (2) NICA (40 mg/kg); (3) NIMO (40 mg/kg); and (4) saline. PA training latencies (seconds) were recorded for entry from a suspended platform into a Plexiglas tube where a shock (0.3 mA; 2-second duration) was automatically delivered. On day 2 latencies were recorded during a testing trial during which no shock was delivered. Latencies >900 seconds were assigned this value. Lower testing latency is indicative of an impairment of long-term associative memory. Forty-nine additional mice were randomized into similar groups for object recognition testing (ORT) and given i.p. injections on day 0. ORT measures short-term memory by exploiting the tendency of mice to prefer novel objects where a familiar object is present. On day 5 during training, 2 identical objects were placed in a circular arena and mice explored both for 15 minutes. A testing trial was conducted 1 hour later for 3 minutes after a novel object replaced a familiar one. Mice with intact memory spend about 65% of the time exploring the novel object. Mice with impaired memory devote equal time to each object. Recognition index (RI) is defined as the ratio of time spent exploring the novel object to time spent exploring both objects was the measure of memory. Mean arterial blood pressure (MAP), cerebral bloodflow, and body and brain oxygenation (PO(2)) studies were done in separate groups of mice to determine the dosages for matched degrees of hypotension and the physiological profile of each treatment. The median PA latencies for the different conditions were as follows: NTG (219.5 ± 93.5 second semi-interquartile range [SIQR]), NICA (372.5 ± 75.5 second SIQR), NIMO (540 ± 200 second SIQR) and saline (804 ± 257.5 second SIQR). Rank methods were used to analyze the PA latencies for significant differences. NTG latency was significantly shorter than NIMO latency (P = 0.012) and saline latency (P = 0.006), but not NICA latency (P = 0.126). ORT RI values showed a similar pattern. We found that NTG RI (47.2 ± 5.9% SEM) was different from NIMO RI (60.2 ± 4.6% SEM, P = 0.031) and different from saline RI (66.9 + 3.7% SEM, P = 0.006). Physiological experiments showed that MAP decreased to 45 to 50 mm Hg in all animals who became minimally responsive to external stimuli within 10 to 15 minutes of injection. Intergroup differences for MAP, body and brain oxygenation, and cerebral bloodflow were not statistically significant. Acute hypotension induced by NIMO was protective of 2 categories of memory formation relevant to the clinical posttreatment period. Both immediate long-term associative memory consolidation as measured by the PA learning paradigm and delayed short-term working memory function as measured by the ORT paradigm were significantly improved compared to matched levels of hypotension induced by NTG. These results indicate the utility of further investigation of l-type calcium channel blockers as a potential means of preserving cognition in the setting of hypotensive and low flow states.

The Transcutaneous Oxygen Challenge Test

The transcutaneous partial pressure of oxygen (PtcO₂) index has been used to detect low-flow state in circulatory failure, but the value of the transcutaneous oxygen challenge test (OCT) to estimate low cardiac output has not been thoroughly evaluated. The prospective observational study examined 62 septic patients requiring PiCCO-Plus for cardiac output monitoring. Simultaneous basal blood gases from the arterial, central venous catheters were obtained. Cardiac indices were measured by the transpulmonary thermodilution technique at the same time, then the 10-min inspired 1.0 fractional inspired oxygen concentration (FIO₂) defined as the OCT was performed. Transcutaneous partial pressure of oxygen was measured continuously by using a noninvasive transcutaneous monitor throughout the test. The values for arterial pressure of oxygen (PaO₂) were examined on inspired of 1.0 FIO₂. We calculated the PtcO₂ index = (baseline PtcO₂/baseline PaO₂), 10-min OCT (10 OCT) = (PtcO₂ after 10 min on inspired 1.0 O₂) - (baseline PtcO₂), and the oxygen challenge index = (10 OCT) / (PaO₂ on inspired 1.0 O₂ - baseline PaO₂). Patients were divided into two groups: a normal cardiac index (CI) group with CI of greater than 3 L/min per m (n = 41) and a low CI group with CI of 3 L/min per m or less (n = 21). The 10 OCT and the oxygen challenge index predicted a low CI (≤ 3 L/min per m) with an accuracy that was similar to central venous oxygen saturation, which was significantly better than the PtcO₂ index. For a 10 OCT value of 53 mmHg, sensitivity was 0.83; specificity, 0.86; a positive predictive value, 0.92; and a negative predictive value, 0.72 for detecting CI of 3 L/min per m or less. We propose that the OCT substituted for the PtcO₂ index as an accurate alternative method of PtcO₂ for revealing low CI in septic patients.

Pre-industrial multiple equilibrium sea-ice flow states due to plastic ice mechanics

Abstract Because the Arctic Ocean is largely surrounded by land masses, sea ice mechanics significantly affects the outflow of ice from the Arctic Basin. An important legacy of Dr. Max Coon has been the recognition that Arctic ice pack fails and flows in a plastic manner. Building on this concept we demonstrate here that with reasonable simulation of plastic scaling of sea-ice flow through narrow channels, dynamic–thermodynamic sea ice models have the potential to yield multiple equilibrium flow and hence thickness states for appropriate seasonal daily wind and thermodynamic forcing. These multiple states are due to ‘plastic’ ice mechanics and are not ‘Budyko-Sellers’ albedo feedback multiple states. Each state consists of a mean seasonal ice thickness with annual outflow balancing net growth. Low flow states are thicker. In this paper we first demonstrate that with some caveats, a properly formulated ‘viscous plastic’ sea ice model where ‘rigid’ ice is approximated by very slow flow can successfully simulate plastic ice flow and stoppage of ice flow through narrow channels in agreement with observations and theory. The characteristics of this flow and stoppage are methodically examined by a series of initial value problems of ice flow and advection through various narrowing channels with different ice thicknesses being advected into the channel. Different rheologies are examined and the effect of different creep closure rates on stoppage is investigated using several day mechanistic simulations of flow into the channel employing explicit time stepping. In the case of parallel channels, numerical results are examined in light of analytic solutions. Together with idealized growth rates this simple channel model is used to illustrate the principle of multiple equilibrium states due to ice mechanics. Following this we utilize a 40 km resolution dynamic thermodynamic sea ice model with multiple openings from the Arctic Basin to examine the potential for multiple equilibrium flow states under pre-industrial atmospheric thermodynamic forcing together with daily wind field forcing taken from more current conditions. This potential is assessed by carrying out five year seasonal simulations initialized with different ice thicknesses. Intersection of seasonal averaged net growth and outflow thus obtained are then used to identify potential multiple states and assess their stability. With a coulombic rheology with modest cohesive strength, the results show three states two of which are stable. With an elliptical yield curve having higher cohesive strength only one low flow state is identified. Several ~ 100 year simulations are then carried out to show the existence of the two stable states and their seasonal flow and thickness characteristics. The decay time scales between pre-industrial low flow states and present high flow states are also examined via long term simulations. Finally, a simulation from 1960 to 2040 with estimated climatic warming is carried out and compared with equilibrium thickness states at discrete intervals to show the effect of inertia in the rate of ice decay due to ice mechanics. Forcing data reported in this paper are adequate to test the capability of other dynamic thermodynamic sea ice models to yield multiple flow states.

Extensive colonic necrosis following cardiac arrest and successful cardiopulmonary resuscitation: report of a case and literature review

Non-occlusive colonic ischaemia is a recognized albeit rare entity related to low blood flow within the visceral circulation and in most reported cases the right colon was affected. This is the second case report in the literature of extensive colonic necrosis following cardiac arrest and cardiopulmonary resuscitation (CPR). A 83-year-old Caucasian woman was admitted to our hospital due to a low energy hip fracture. On her way to the radiology department she sustained a cardiac arrest. CPR started immediately and was successful. A few hours later, the patient developed increasing abdominal distension and severe metabolic acidocis. An abdominal multidetector computed tomography (MDCT) scan was suggestive of intestinal ischaemia. At laparotomy, the terminal ileum was ischaemic and extensive colonic necrosis was found, sparing only the proximal third of the transverse colon. The rectum was also spared. The terminal ileum and the entire colon were resected and an end ileostomy was fashioned. Although the patient exhibited a transient improvement during the immediate postoperative period, she eventually died 24h later from multiple organ failure. Histology showed transmural colonic necrosis with no evidence of a thromboembolic process or vasculitis. Therefore, this entity was attributed to a low flow state within the intestinal circulation secondary to the cardiac arrest.

Abstract 86: CPR Parameters as Predictors of Return of Spontaneous Circulation Following Inpatient Cardiac Arrest

Background: The quality of cardiopulmonary resuscitation (CPR) parameters, including chest compression fraction (CCF) and compression depth, appear to be associated with return of spontaneous circulation (ROSC) in out-of-hospital cardiopulmonary arrest (CPA). In addition, end tidal carbon dioxide (EtCO2) may be useful as a marker for ROSC during low flow states such as CPA. Objective: To explore the relationship between CCF, compression depth, and EtCO2 for inpatient CPA. Methods: This study was conducted in two urban university hospitals. Defibrillator data are exported for analysis following all CPA events. Inpatient medical records were reviewed to determine baseline characteristics and outcomes. CPR data were analyzed in 1-min intervals over the entire CPA resuscitation. The pattern of CCF, compression depth, and EtCO2 were explored in ventricular fibrillation (VF) and non-VF patients and in those with and without ROSC. Results: A total of 23 CPAs were analyzed between 5/31/09 and 4/23/11. There were 14 with ROSC and 9 without ROSC. The majority of arrests were non-VF (87%). The mean values were calculated for code duration (13 min), CCF (92%), compression depth (2.8 inches), and EtCO2 (20.3 mm Hg). Code duration was shorter (8.8 vs. 19.8 min) and CCF values higher (93.1% vs. 89.5%) in patients with ROSC. EtCO2 values were higher in VF patients with ROSC (17 vs. 11 mmHg) but not for all rhythms. In addition, terminal EtCO2 values were higher when compared to mean EtCO2 values in ROSC patients than for non-ROSC patients. Conclusion: For this small sample of inpatient cardiac arrests, patients with ROSC had shorter code durations, higher CCF values, deeper compressions, and higher terminal EtCO2 values. These data support the importance of optimal CPR in the inpatient setting.

Moribund Stomach

Question: A 75-year-old Caucasian man sustained traumatic rib fractures with right-sided pneumothorax and right hip fracture after falling off a ladder. He underwent tube thoracostomy and repair of his hip fracture, and was doing relatively well until he suffered cardiopulmonary arrest 4 days later. He was successfully resuscitated after about 15 minutes and transferred to the intensive care unit. Mechanical ventilation and vasopressor support was required postresuscitation. Before cardiopulmonary arrest, there was no documented evidence of hypotension or tachycardia, and the triggering event was considered to be aspiration with attendant respiratory failure. It was discovered that the patient had a significant, 3-g decline in his hemoglobin over the preceding 24 hours, associated with some coffee-ground output from the nasogastric tube. The patient underwent emergent esophagogastroduodenoscopy (Supplementary Videos 1 and 2). He was found to have severe ulcerative esophagitis. There was no evidence of active bleeding. There was loss of normal mucosal vascular pattern throughout the entire stomach, and multiple diminutive ulcers and subepithelial hemorrhage, noted in the proximal and mid corpus (Figure A, B). Examination of the duodenum up to the third portion revealed diffuse patchy mucosal erythema. What is the diagnosis explaining these endoscopic findings? See the Gastroenterology web site (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI. The endoscopic findings are consistent with acute and diffuse ischemic insult due to the low-flow state resulting from the patient's cardiopulmonary arrest and persistent shock. In this patient, the low-flow state likely persisted for some time after resuscitation given the need for multiple vasopressors. Clinical ischemia of the stomach is very rare in view of its rich vascular supply and intramural anastomoses. It has been shown that both arterial and venous circulation must be compromised before gastric ischemia ensues.1Abdu R.A. Garritano D. Culver O. Acute gastric necrosis in anorexia nervosa and bulimia Two case reports.Arch Surg. 1987; 122: 830-832Crossref PubMed Scopus (96) Google Scholar Lee et al2Lee T.C. Lin J.T. Liang C.W. et al.Ischemic gastropathy: leopard skin in the stomach.Endoscopy. 2005; 37: 927Crossref PubMed Scopus (6) Google Scholar have previously reported ischemic gastropathy on endoscopy performed after cardiac arrest. Most other cases of gastric ischemia reported in the literature have been in the setting of acute massive gastric dilatation, either in the setting of gastric volvulus or binge eating associated with primary eating disorders.1Abdu R.A. Garritano D. Culver O. Acute gastric necrosis in anorexia nervosa and bulimia Two case reports.Arch Surg. 1987; 122: 830-832Crossref PubMed Scopus (96) Google Scholar Increased intragastric pressure >20 cm H2O, which exceeds venous pressure, results in gastric mucosal ischemia and necrosis.3Edlich R.F. Borner J.W. Kuphal J. et al.Gastric blood flow Its distribution during gastric distention.Am J Surg. 1970; 120: 35-37Abstract Full Text PDF PubMed Scopus (43) Google Scholar The predominantly mid corpus distribution of ischemic ulcerations in this case is likely explained by the watershed area of gastric vascular supply. Hemodynamic instability during esophagogastroduodenoscopy precluded us from obtaining biopsies. This patient had increasing intra-abdominal pressure as confirmed by increasing bladder pressures, and an emergent laparotomy was undertaken. The patient was found to have extensive ischemic changes involving the gastrointestinal tract as well as other intra-abdominal viscera, further corroborating an ischemic etiology from a low-flow state as the explanation for these rare endoscopic findings. eyJraWQiOiI4ZjUxYWNhY2IzYjhiNjNlNzFlYmIzYWFmYTU5NmZmYyIsImFsZyI6IlJTMjU2In0.eyJzdWIiOiJlOTgwNDI3NjJjMGIwZDA1NDJlYWVkZDliN2U3NTg2ZCIsImtpZCI6IjhmNTFhY2FjYjNiOGI2M2U3MWViYjNhYWZhNTk2ZmZjIiwiZXhwIjoxNjgxMjM3MjAyfQ.g2MPoxwS8j4vCybyxrQqE4z1baeTznOcJYrZ8JTooBo7slmg_dpz8iVBioS-U3Ut4xyif46aqf5Dygdh0Q_TMJVnV2QNsPG4XtiXgoGfHrIvasOUJ8AGwnQpsN5FHf25GXg9JG8VHy2MXbgc6vjXJAVvAuNRbd7hoJ6XHAGvGO8Z4HxsJ80LKYzUuj1fffkS0Cu2EkEvhEwJDQPps3JBtmpvAiODiwsSnd6IzlKrBUZVMHrJ_bxlwwqHVLY-a6rEUc6Lj16NfuZ46VvzfbLD6-vUrrrGz72_zIetKTtJ2F4qzgDuYkkeDwOqAuyEWeK404vvdgv0A4Od1PMyWCawIw Download .mp4 (16.33 MB) Help with .mp4 files Supplementary Video 1eyJraWQiOiI4ZjUxYWNhY2IzYjhiNjNlNzFlYmIzYWFmYTU5NmZmYyIsImFsZyI6IlJTMjU2In0.eyJzdWIiOiIxMDlmZWQwZDQ2YmU3M2EzNWQwZTE1MWVmOTIzODYwMCIsImtpZCI6IjhmNTFhY2FjYjNiOGI2M2U3MWViYjNhYWZhNTk2ZmZjIiwiZXhwIjoxNjgxMjM3MjAyfQ.VlOIh7RMAdyyzik17pNvAp9gHD1go1tfVICZsIUR_IG3O_RDWKpvTEUeRbxR_p49LwkVlyG7HvbdgccwvN1n_D46lcvuOG1_0Vwf4ZAADJEC1So2VnxAJsnOPTgR37MkJ-8dB7M2gHhPEMD8tEU0QzZeFqEORX4oSXPF9zFVVPqQ-Op8WBRsKySy5WLvowQ_UrnT69KjBHd3-eg0owUpBm1_eLUFl6ksgWlCRZyb2sATPBl_UuiYSomNSTgl5lLA3q5QqUVonqqM9-0OQJrBsBhmCNmLAsuTze1aNDq0Xm5Z_L5Zj-tVFCDRPGWFsLRGlCRVC0b_lQrOJAbSpGLN5w Download .mp4 (4.3 MB) Help with .mp4 files Supplementary Video 2

Ischémie aiguë du mésentère : apports de l’imagerie en coupes

Acute mesenteric ischemia (AMI) is a life-threatening emergency with prognosis directly correlated with the delay in diagnosis and treatment. Clinical and laboratory findings are nonspecific and it is imperative to look for findings of AMI on CT and ultrasound examinations performed in patients with acute abdomen. Arterial and venous ischemia are different entities with different clinical and imaging features, treatment and prognosis. The main causes of AMI are arterial thromboembolic disease and low-flow state. Venous ischemia is less frequent. Due to its high reported sensitivity (90%), CT should be performed as a firstline imaging modality when AMI is suspected. CT and ultrasound imaging features of AMI include: bowel wall thickness and enhancement abnormalities, pneumatosis, portal venous gas, demonstration of intravascular thrombus, bowel dilatation and ascitis.

The Endothelial Glycocalyx as a Barrier to Leukocyte Adhesion and Its Mediation by Extracellular Proteases

The endothelial cell (EC) surface is coated with a layer of polysaccharides linked to membrane-bound and trans-membrane proteoglycans that comprise the glycocalyx, which is augmented by adsorbed proteins derived from the blood stream. This surface layer has been shown to affect hemodynamics in small blood vessels of the microcirculation, the resistance to flow, and leukocyte (WBC) to EC adhesion. Parallel studies of WBC-EC adhesion in response to chemoattractants and cytokines, and shedding of constituents of the glycocalyx, have suggested a role for activation of extracellular proteases in mediating the dynamics of WBC adhesion in response to inflammatory and ischemic stimuli. Likely candidates among the many proteases present are the matrix metalloproteases (MMPs). Inhibition of MMP activation with sub-antimicrobial doses of doxycycline, or zinc chelators, has also inhibited WBC adhesion and shedding of glycans from the EC surface in response to the chemoattractant fMLP. Taken together, these studies suggest that shedding of the EC glycocalyx exposes adhesion receptors and thus enhances WBC-EC adhesion. Future therapeutic strategies for treating pathologies such as the low flow state and inflammation may benefit by further exploration of the mechanics of the glycocalyx in light of protease activation and shear-dependent effects.

Vascular and Extravascular Volume Expansion of Dobutamine and Norepinephrine in Normovolemic Sheep

In low-flow states, such as circulatory shock, both fluids and catecholamines are often coadministered. We have previously found that adrenergic agents alter volume expansion after a fluid bolus. The present study tested the volume expansion properties of dobutamine and norepinephrine in sheep treated with (series 1) and without (series 2) a fluid bolus. Series 1 (n = 6 per group): no drug (control), dobutamine (10 μg x kg(-1) x min), or norepinephrine (1.0 μg x kg(-1) x min(-1)) was begun 30 min before a 24-mL x kg(-1), 20-min, 0.9% NaCl bolus. The effect of drug and fluid on plasma volume (ΔPV), urinary output (UOP), and extravascular volume (ΔEVV) was determined. Series 2: Identical protocol but no fluid bolus. Series 1: the fluid bolus resulted in a peak and sustained ΔPV expansion. Norepinephrine (7.5 ± 0.9 mL x kg(-1)) and dobutamine (9.5 ± 1.1 mL x kg(-1)) significantly increased ΔPV compared with control (3.8 ± 1.1 mL x kg(-1)). Cumulative UOP was reduced by dobutamine (3.8 ± 1.4 mL x kg) compared with norepinephrine (25.1 ± 3.9 mL x kg(-1)) and control (16.9 ± 4.0 mL x kg(-1)). Norepinephrine increased ΔPV, while reducing ΔEVV after bolus. Series 2: ΔPV was unchanged in the control group. Dobutamine and norepinephrine increased ΔPV over time, 5.1 ± 0.5 and 4.0 ± 0.5 mL x kg(-1), respectively. At study end, UOP was lowest in dobutamine. Norepinephrine resulted in loss of ΔEVV fluid. data suggest a novel role for adrenergic receptors in regulating vascular and EVV expansion. β-Adrenergic agonists enhance vascular volume expansion, whereas α-adrenergic agonists eliminate extravascular fluid.

A structural model of perfusion and oxygenation in low-flow states

Background Recent investigations underscore the critical importance of ventilation strategies on resuscitation outcomes. In low perfusion states, such as cardiac arrest and traumatic shock, the rise in intrathoracic pressure that accompanies positive-pressure ventilation can significantly impede venous return and lead to a decrease in cardiac output. The optimal ventilation strategy in these “low-flow” states remains unclear. Objective To create a mathematical model of perfusion and oxygenation to predict the effects of PPV with both normotension and hypotension. Methods The lung pressure–volume relationship was modeled using a novel formula allowing manipulation of various lung characteristics. A separate formula was then derived to predict mean intrathoracic pressure (MITP) for specific minute ventilation values using the pressure–volume formula. The addition of positive end-expiratory pressure was also modeled. Finally, a formula was derived to model oxygen absorbance as a function of alveolar surface area and flow based on ventilation rate and MITP. Results Mathematical models of the lung pressure–volume relationship, MITP, and absorbance were successfully derived. Manipulation of total lung capacity, compliance, upper and lower inflection points, positive end-expiratory pressure, and minute ventilation allowed prediction of optimal ventilation rate and tidal volume for a normal lung and with various abnormal characteristics to simulate particular disease states, such as acute respiratory distress syndrome (ARDS). For a normal lung, ventilation rates of 4–6 breaths/min with higher tidal volumes (15–20 mL/kg) resulted in the lowest predicted MITP values (5 cm H 2O) and the highest absorbance. The input of lung parameters that would simulate ARDS resulted in optimal ventilation rates of 10–12 breaths/min with lower tidal volumes (8–10 mL/kg) and higher predicted MITP values (10–15 cm H 2O). Conclusions A mathematical model of ventilation was successfully derived allowing manipulation of multiple pulmonary physiological variables to predict MITP and potentially identify optimal ventilation strategies. This model suggests the use of lower ventilation rates and larger tidal volumes to minimize the hemodynamic effects of positive pressure ventilation in patients with hypoperfusion but normal lung characteristics.

Intensive management of electrical storm and incessant ventricular arrhythmias

Abstract Electrical storm (ES) is defined as ventricular tachycardia or ventricular fibrillation occurring at least three times in 24 h leading to hemodynamic unstable state that needs cardioversion or defibrillation. ES may cause fast hemodynamic impairment, leading to “low-perfusion” or “no perfusion” state of the organs, a vicious circle pointing toward cardiogenic shock, multi-organ failure, and pulseless electrical activity. ES in ICD patients may be a strong predictor of arrhythmic and nonarrhythmic death, as well as of rehospitalization. The first step is to start cardiopulmonary resuscitation to achieve complete hemodynamic stabilization to prevent the low-flow or no-flow state. The patient has to be transported to an intensive care unit for further specific treatment. The arrhythmia should be treated with specific antiarrhythmic agents, for example, amiodarone, lidocain and bretylium, and then all the reversible causes have to be detected and treated as fast as possible. Underlying heart disease determines the specific treatment such as coronary revascularization, mechanical circulatory and respiratory support, and ablation of the arrhythmic foci.

MR measures of renal perfusion, oxygen bioavailability and total renal blood flow in a porcine model: noninvasive regional assessment of renal function

Magnetic resonance imaging (MRI) may be a useful adjunct to current methods of evaluating renal function. MRI is a noninvasive imaging modality that has the ability to evaluate the kidneys regionally, which is lacking in current clinical methods. Other investigators have evaluated renal function with MRI-based measurements, such as with techniques to measure cortical and medullary perfusion, oxygen bioavailability and total renal blood flow (TRBF). However, use of all three techniques simultaneously, and therefore the relationships between these MRI-derived functional parameters, have not been reported previously. To evaluate the ability of these MRI techniques to track changes in renal function, we scanned 11 swine during a state of hyperperfusion with acetylcholine and a saline bolus and subsequently scanned during a state of hypoperfusion with the prolonged use of isoflurane anesthesia. For each time point, measurements of perfusion, oxygen bioavailability and TRBF were acquired. Measurements of perfusion and oxygen bioavailability were compared with measurements of TRBF for all swine across all time points. Cortical perfusion, cortical oxygen bioavailability, medullary oxygen bioavailability and TRBF significantly increased with the acetylcholine challenge. Cortical perfusion, medullary perfusion, cortical oxygen bioavailability and TRBF significantly decreased during isoflurane anesthesia. Cortical perfusion (Spearman's correlation coefficient = 0.68; P < 1 × 10(-6)) and oxygen bioavailability (Spearman's correlation coefficient = -0.60; P < 0.0001) correlated significantly with TRBF, whereas medullary perfusion and oxygen bioavailability did not correlate with TRBF. Our results demonstrate expected changes given the pharmacologically induced changes in renal function. Maintenance of the medullary oxygen bioavailability in low blood flow states may reflect the autoregulation particular to this region of the kidney. The ability to non-invasively measure all three parameters of kidney function in a single MRI examination and to evaluate the relationships between these functional parameters is potentially useful for evaluating the state of the human kidneys in situ in future studies.