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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Current research on the efficacy of CPR in specific patient groups may lead to the withholding of CPR in groups that statistically show minimal success. Prognosticative factors that indicate minimal-at-best success with CPR include age greater than 70, dysrhythmias such as asystole and electromechanical dissociation, sepsis, metastatic cancer, GI hemorrhage, and acute stroke. Although physicians are under no legal or ethical obligation to provide futile treatments, how one defines a treatment as "futile" is unclear. As a patient advocate, the nurse acts to ensure the autonomous patient is fully informed, freely consenting, and actively directing his/her own health care. End-of-life decisions regarding health care must be based on the patient's goals, which will be revealed through the moral discourse among health care professionals, patients, and their loved ones.
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PMID:Limiting care: is CPR for everyone? 235 36

Dobutamine administration has been shown to increase oxygen delivery in various conditions, but there are little data to document its effects in septic shock. We investigated the effects of dobutamine infusion at a rate of 5 micrograms/kg.min in 18 patients (mean 60 +/- 16 yr) with septic shock initially characterized by hypotension, oliguria, and hyperlactatemia in the presence of a documented source of sepsis. Early resuscitation had consisted of fluid administration and vasopressors when required. When added to this standard regimen, dobutamine had no significant effect on mean arterial pressure (MAP) (from 71 +/- 12 to 73 +/- 13 mm Hg), but markedly increased cardiac index (from 3.0 +/- 0.7 to 3.9 +/- 1.0 L/min.m2, p less than .001), stroke index (from 32 +/- 8 to 37 +/- 9 ml/m2, p less than .001) and oxygen transport (from 410 +/- 105 to 530 +/- 146 ml/min.m2, p less than .001). Oxygen consumption (VO2) increased concurrently (from 137 +/- 42 to 162 +/- 66 ml/min.m2, p less than .002). MAP increased (from 68 +/- 9 to 76 +/- 11 mm Hg) in 12 patients and decreased moderately (from 76 +/- 18 to 69 +/- 17 mm Hg) in six patients. The two subgroups of patients had similar hemodynamic profiles before the dobutamine infusion, but vasopressor therapy was already used in one of the 12 patients in the first subgroup and in three of the six patients in the second subgroup (p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dobutamine administration in septic shock: addition to a standard protocol. 236 8

The response of the heart during sepsis has been studied in human and animal models with disparate results. Because sepsis induces marked peripheral vascular changes, to accurately determine the cardiac response, one must use indices of cardiac performance that are independent of loading conditions and heart rate. The slope of the end-systolic pressure-diameter relationship (ESPDR) has been proposed to have these properties. Pigs were equipped with transducers to measure left ventricular pressure, internal short axis diameter (D), and pulmonary and coronary artery blood flows. After 7-10 days of basal observations, an endotoxin-loaded osmotic pump delivering endotoxin at 10 micrograms/kg/hr was implanted into each pig. Fourteen pigs were so treated, and 4 expired before 24 hr of endotoxin challenge. In the surviving pigs, cardiac output, heart rate, dP/dtmax, and peak systolic pressures were elevated. However, both ESPDR and % D shortening were both significantly depressed. These data suggest that the cardiac response to chronic endotoxin challenge includes a loss of inotropic state as indicated by the load-insensitive indicator, ESPDR, and confirmed by depressed % D shortening. One possible mechanism for reduced inotropic state during endotoxin challenge could be the loss of coronary perfusion. The surviving endotoxin-challenged pigs demonstrated a significant increase in coronary perfusion while stroke work remained unchanged, suggesting that depressed cardiac inotropic state during endotoxin challenge was not caused by reduced coronary blood flow. Rather, the myocardium was relatively overperfused. Another possible mechanism for the loss of cardiac inotropism during endotoxin challenge may be endotoxin-induced generation of reactive oxygen free radicals. This possibility was tested by measuring total cardiac gluthathione, a cellular component depleted by oxidant stress. Endotoxemia reduced these levels 50%. These results suggest that cardiac injury may be mediated by the generation of reactive oxygen free radicals. Further study will determine if this mechanism participates in the loss of cardiac inotropism during endotoxin challenge.
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PMID:End-systolic elastance as an evaluation of myocardial function in shock. 240 35

The cardiac mechanisms responsible for endotoxin-mediated disruptions in left ventricular (LV) contraction-relaxation dynamics have been controversial. Recently, a combination of clinical cardiodynamic studies in patients along with experimental cardiodynamic studies in endotoxemic/septic animals and isolated heart tissue has yielded corroborating evidence for a consistent deleterious alteration(s) of intrinsic LV contractility during shock syndromes. Cardiac dysfunction in shock patients and intact animals was characterized by reduced LV ejection fraction in the presence of unchanging LV stroke volume, or by reduced LV end-systolic pressure-volume ratio. In hearts isolated from experimental shock subjects, LV contractile abnormality was characterized by reduced isovolumetric intraventricular pressure development and stroke volume, even in the presence of maximally effective increments in end-diastolic volume or preload. Cardiodynamic changes developed early in experimental septicemic shock syndromes (less than 4 hr) and were not irreversible. Furthermore, and this is a key element, both clinical and experimental study indicated that coronary perfusion inadequacy was not an obligatory etiologic factor in the shock-associated loss of cardiac contractile function. Thus, clinical and experimental data are now available to assemble a consensus that 1) intrinsic LV contractile reserves are diminished early during endotoxemia and sepsis and 2) this diminution is not simply a consequence of global myocardial ischemia.
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PMID:Intrinsic myocardial dysfunction during endotoxemia: dependent or independent of myocardial ischemia? 240 37

At 31 critically ill surgical patients who on clinical grounds required fluid therapy, hemodynamic and oxygen transport, responses were measured after volume expansion with 500 ml 6% HES 450/0,7. There were statistically significant increases in cardiac index (CI) from 3,5 +/- 2,1 to maximal values of 4,4 +/- 0,2 (l/min/m2) and in wedge pressure (WP) from 9,3 +/- 0,7 to maximal values of 13,6 +/- 0,8 (mm Hg) and a significant reduction of systemic vascular resistance index (SVRI) from 2018 +/- 128 to 1641 +/- 102 (dynsec/cm5 m2). There were also observed statistically significant maximal increases of left ventricular stroke work index (LVSWI) from 41 +/- 3,1 to 53 +/- 3,2 (gm/m2) of oxygen delivery (DO2) from 489 +/- 24 to 587 +/- 29 (ml/min/m2) and of oxygen consumption (VO2) from 111 +/- 6 to 130 +/- 7 (ml/min/m2) which took place at the time of the maximum CI-increase. Moreover MAP-, CI- and VO2-responses of patients were stratified according to clinical conditions like time of operation, age, prognosis, ARDS, sepsis, hyperdynamic- and blood volume status.
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PMID:[Reactions of critically ill patients to volume therapy with hydroxyethyl starch (6% HES 450/0.7)]. 242 57

Twenty consecutive patients with severe sepsis were randomized to fluid challenge with 5% albumin or 10% low MW hydroxyethyl starch (pentastarch) solutions. Fluid challenge was administered iv as 250 ml of test colloid every 15 min until the pulmonary artery wedge pressure (WP) was greater than or equal to 15 mm Hg or a maximum dose of 2000 ml was infused. Hemodynamic, respiratory, and coagulation profiles were measured before and after fluid infusion. The amount of colloid required to achieve a WP of 15 mm Hg was comparable between groups. Both colloid infusions resulted in similar increases in cardiac output, stroke output, and stroke work. The effect of fluid infusion with pentastarch on coagulation was not significantly different from albumin, although pentastarch was associated with a 45% decrease in factor VIII:c. We conclude that pentastarch is equivalent to albumin for fluid resuscitation of patients with severe sepsis.
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PMID:Effects of pentastarch and albumin infusion on cardiorespiratory function and coagulation in patients with severe sepsis and systemic hypoperfusion. 246 47

Although adequate volume resuscitation has decreased mortality from hemorrhagic shock, recovery in many patients is complicated by sepsis. To determine whether a subject debilitated by hemorrhagic shock would exhibit greater cardiocirculatory dysfunction when challenged with sepsis, ten dogs (Group I) were hemorrhaged to a mean arterial blood pressure of 30 mm Hg. After 2 hours of hypotension, shed blood and lactated Ringer's solution (50 ml/kg) were given, and the dogs were observed for 3 to 6 days. Ten dogs were sham hemorrhage and served as controls (Group II). On the experimental day, all cardiovascular and hemodynamic parameters were measured in both groups of animals before endotoxin challenge. There was no significant difference in cardiac output, stroke volume, stroke work, +dP/dt max, myocardial blood flow, myocardial oxygen metabolism, or acid-base balance in the two groups. Compared to sham-hemorrhaged dogs, resuscitated shock dogs had a significantly lower mean arterial blood pressure (127 +/- 7 vs. 110 +/- 6 mm Hg; p less than 0.05), and heart rate was significantly higher (86 +/- 6 vs. 109 +/- 7 beats/minute; p less than 0.05). Furthermore, maximal rate of left ventricular pressure fall (-dP/dT max) was significantly lower in the animals previously hemorrhaged, suggesting a persistent defect in left ventricular relaxation. Blood glucose and insulin levels were significantly elevated in the resuscitated shocked dogs, likely due to increased circulating catecholamine concentrations and enhanced glycogenolysis. Endotoxin shock caused significant hypotension, acidosis, and impaired regional perfusion in all dogs. In addition, cardiac output, stroke volume, dP/dT, and left ventricular end-diastolic pressure fell and hyperglycemia and hyperinsulinemia occurred in all dogs after endotoxin injection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The cardiocirculatory and metabolic effects of endotoxin challenge after canine resuscitated hemorrhagic shock. 256 78

105 patients with acute calculous cholangitis who did not respond to conservative management underwent urgent endoscopic drainage of the biliary system at a mean of 1.5 days after admission. Treatment was successful in 102 (97%) patients. 3 of the patients in whom drainage was not successful underwent emergency surgery, with 1 death. 3 patients died of uncontrolled sepsis despite successful endoscopic drainage. 1 patient died of a stroke. The overall mortality was 4.7%. Among those in shock 2 out of 4 drained after 72 h died, compared with 3 out of 38 drained before 72 h. There were no deaths in the group without shock irrespective of the timing of drainage.
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PMID:Urgent endoscopic drainage for acute suppurative cholangitis. 256 34

A young woman presented with a 4-month history of retinal and vertebrobasilar ischemia. Angiography demonstrated narrowing of major branches of the aortic arch. Intractable, severe retroorbital pain of the right eye developed after a middle cerebral artery stroke. During 4 weeks of aggressive immunosuppressive therapy including IV high dose bolus corticosteroids and pulse cyclophosphamide, her neurologic deficit improved transiently, but her retroorbital pain persisted. She died of staphylococcal sepsis and pneumonia. An autopsy demonstrated thrombotic or fibrous occlusion, with minimal inflammation, of extracranial arteries.
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PMID:Takayasu arteritis presenting as retinal and vertebrobasilar ischemia. 257 Jan 49

We retrospectively evaluated the clinical features and therapeutic outcomes in 13 consecutive patients with the diagnosis of fusiform aneurysm of the vertebrobasilar system. Four patients (31%) presented with compressive symptoms and 10 (77%) with ischemic symptoms; one patient presented with both types of symptoms. No patient presented with rupture of the fusiform aneurysm. Based on the attending physician's choice, treatment included antiplatelet therapy in five patients, anticoagulation in seven, and no medication in one. Five patients died, four treated with antiplatelet agents and one not treated with any medication. The cause of death was progressive brainstem ischemia in three, sepsis in one, and gastrointestinal bleeding in one patient. All seven patients who received anticoagulants were alive, with no recurrence of symptoms or hemorrhagic complications after a mean follow-up period of 18 months. Based on previous and current series, we conclude that rupture of fusiform aneurysms is rare. Our results suggest a more favorable outcome in the management of these aneurysms with anticoagulation therapy to prevent progressive thrombosis and embolization.
Stroke 1989 Dec
PMID:Fusiform aneurysm of the vertebrobasilar arterial system. 259 37


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