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

Viral infections are known to produce hypotension and shock, but the cardiorespiratory patterns associated with viral septic shock have not been described. The clinical course of nine patients who died from overwhelming cytomegalovirus sepsis was reviewed. Viral septicemia was associated with increased cardiac index, decreased systemic vascular resistance index (SVRI), and elevated oxygen delivery. This pattern appeared during early and late stages of shock. In contrast to bacterial sepsis and endotoxemia, the pulmonary vascular resistance index (PVRI) was normal. These results indicate that overwhelming viral infection can produce shock associated with a high cardiac output, low peripheral resistance state similar to that seen with bacterial shock. Relative sparing of the pulmonary circulation in viral shock is consistent with the absence of endotoxemia in these patients.
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PMID:Cardiorespiratory patterns in viral septicemia. 282 98

A 68-year-old female on two-year chronic hemodialysis for chronic renal failure due to chronic pyelonephritis, was admitted to hospital for weakness, dulled sensorium and dizziness. On examination the patient was in a state of circulatory collapse, the electrocardiogram showed an accelerated idioventricular rhythm and laboratory analysis revealed extreme hyperkalemia (K+ 10.1 mmol/l). There were no common causes of shock, such as hypovolemia, sepsis, heart failure and presence of vasodilator drugs. The patient was treated with calcium gluconate, sodium bicarbonate and sodium chloride (to oppose the effects of hyperkalemia on the cell membrane to minimize cardiac and neuromuscular toxicity), insulin and dextrose (to increase the transport of K+ from the extracellular to the intracellular compartment), and hemodialysis (to remove K+ from the body). At the end of the hemodialysis session, the patient was in a clinically good condition, blood pressure was 160/90 mm Hg and the serum K+ concentration was normal. The case appeared to suggest that extreme hyperkalemia may have direct effects on vascular resistance, causing hypotension and shock.
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PMID:A life-threatening complication of extreme hyperkalemia in a patient on maintenance hemodialysis. 748 41

Vascular endothelium releases nitric oxide (NO), an important vasodilator that is continuously synthesised by the constitutive enzyme, endothelial nitric oxide synthase (NOS). This maintains a constant vasodilator tone which is diminished in adult hypertension, due to reduced endothelium-dependent vascular relaxation, which is NO dependent. In childhood, however, hypertension is often secondary, and normalisation of blood pressure by removal of cause (e.g. renal artery stenosis, catecholamine-producing tumour) suggests reversibility of endothelial dysfunction, if it is present. Raised plasma levels of endogenous inhibitors have been found, especially in children with secondary hypertension due to renal parenchymal and renovascular disease, and may contribute to hypertension by more than just inhibition of vascular NO release; e.g. by reduction of glomerular filtration rate and promotion of salt and water retention. These inhibitors also modulate renin release, which may be of relevance in cardiovascular physiology, and may also interfere with the anti-platelet properties of NO, increasing the likelihood of vascular thrombotic events. NO inhibitors also promote endothelial activation, with increased expression of adhesion molecules that may form seedlings of atherosclerosis. In chronic renal impairment, accumulation of NO inhibitors may contribute to hypertension. Efficient long-session dialysis helps better interdialysis control of blood pressure in these subjects, independent of salt and water removal, suggesting that removal of such vasoactive agents may be important for efficient blood pressure control. There are a few studies assessing NO generation in hypertensive children via plasma nitrite and nitrate, the NO end products, which suggest normal or increased production as opposed to a reduction, perhaps as a compensatory phenomenon. In the treatment of hypertension, nitroprusside and nitrates exert their actions via NO donation. Excessive production of NO (usually via inducible NOS) or excessive administration (nitrovasodilators) can be cytotoxic and may cause hypotension and shock, as in severe sepsis. NOS inhibitors and NO therefore appear to play a crucial role in aetiology, complications and therapy of childhood hypertension.
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PMID:Vascular endothelium and nitric oxide in childhood hypertension. 981 94

Waterhouse-Friderichsen syndrome can cause acute death in the baboon without specific signs. Furthermore, this syndrome could result from stress-related intestinal permeability changes that allow macromolecules and/or microbiological entities to enter the systemic circulation. The resulting sepsis could cause adrenocortical insufficiency, hypotension and shock leading to death.
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PMID:Spontaneous Waterhouse-Friderichsen syndrome in a gang-housed baboon. 1151 75

Increased nitric oxide (NO) production is the cause of hypotension and shock during sepsis. In the present experiments, we have measured the contribution of endothelial (e) and inducible (i) nitric oxide synthase (NOS) to systemic NO production in mice under baseline conditions and upon LPS treatment (100 microg/10 g ip LPS). NO synthesis was measured by the rate of conversion of l-[guanidino-15N2]arginine to l-[ureido-15N]citrulline, and the contribution of the specific NOS isoforms was evaluated by comparing NO production in eNOS-deficient [(-/-)] and iNOS(-/-) mice with that in wild-type (WT) mice. Under baseline conditions, NO production was similar in WT and iNOS(-/-) mice but lower in eNOS(-/-) mice [WT: 1.2 +/- 0.2; iNOS(-/-): 1.2 +/- 0.2; eNOS(-/-): 0.6 +/- 0.3 nmol. 10 g body wt-1. min-1]. In response to the challenge with LPS (5 h), systemic NO production increased in WT and eNOS(-/-) mice but fell in iNOS(-/-) mice [WT: 2.7 +/- 0.3; eNOS(-/-): 2.2 +/- 0.6; iNOS(-/-): 0.7 +/- 0.1 nmol. 10 g body wt-1. min-1]. After 5 h of LPS treatment, blood pressure had dropped 14 mmHg in WT but not in iNOS(-/-) mice. The present findings provide firm evidence that, upon treatment with bacterial LPS, the increase of NO production is solely dependent on iNOS, whereas that mediated by cNOS is reduced. Furthermore, the data show that the LPS-induced blood pressure response is dependent on iNOS.
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PMID:NO production by cNOS and iNOS reflects blood pressure changes in LPS-challenged mice. 1272 Nov 55

In the setting of intensive care, patients with acute renal failure often present a clinical picture of the systemic inflammatory response syndrome (SIRS). SIRS can be caused by bacterial stimuli or by non-microbiological stimuli that induce a significant inflammatory response. When this response is exaggerated, the patient experiences multiple organ system failure and a condition of sepsis also defined as a systemic malignant inflammation. This is mostly characterized by an invasion of cytokines and other pro-inflammatory mediators into the systemic circulation where major biological effects take place, including vasopermeabilization, hypotension and shock. At the same time, the monocyte of the septic patient seems to be hyporesponsive to inflammatory stimuli to a certain extent. In this condition, the patient faces a situation of hyperinflammation but at the same time of immunodepression expressing a clinical entity defined as counter anti-inflammatory response syndrome. The general picture of the clinical disorder is therefore better characterized by an immunodysregulation than by a simple pro- or anti-inflammatory disorder. Due to the short half-life of cytokines and other mediators spilled over into the circulation, it is extremely difficult to approach the problem at the right moment with the right pharmacological agent. For these reasons, the peak concentration hypothesis suggests that continuous renal replacement therapies, due to their continuity and unspecific capacity of removal, might be beneficial in cutting the peaks of the concentrations of both pro- and anti-inflammatory mediators, restoring a situation of immunohomeostasis. Thus the patient may benefit from a lesser degree of immunodysregulation and he/she may restore a close-to-normal capacity of response to exogenous stimuli.
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PMID:Extracorporeal therapies in non-renal disease: treatment of sepsis and the peak concentration hypothesis. 1473 25

Hypotension and shock can be classified as hypotension caused by reduced or maintained left ventricular (LV) ejection. Reduced left ventricular ejection can result from intrinsic left ventricular, aortic valve or mitral valve failure, which includes dilated or ischemic cardiomyopathy, left main trunk disease, acute myocarditis, etc. Acute and subacute severe aortic regurgitation can also cause shock. Echocardiography allows noninvasive diagnosis of infective endocarditis and Takayasu's arteritis to cause severe arotic regurgitation and can also be used to diagnose obstruction of the left ventricular outflow tract. Reduced left ventricular preload can be caused by pericardial effusion and right ventricular ejection failure, and can result from pulmonary embolism, tricuspid regurgitation, right ventricular infarction, tension pneumothorax, hypovolemia and others characterized by a small left ventricle with good ejection fraction. Normal left ventricular ejection may be associated with hypotension. Sepsis, anaphylactic shock and neural disorder are associated with hypotension and normal cardiac output. Pseudohypotension may result from aortic dissection, Takayasu's arteritis, arteriosclerosis obliterans and aortic coarctation. A right parasternal approach enables better visualization of the ascending aorta. Fundamental echochocardiographic scanning allows approximate yet useful diagnosis of hypotension and shock.
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PMID:[Easy echo diagnosis for hypotension and shock]. 1908 1

A 55 year old male patient with a diagnosis of hypertrophic cardiomyopathy was admitted with features of sepsis related to cholangitis. Initial management with intravenous (i.v.) fluids and antibiotics did not cause any change in his general condition mandating an emergency endoscopic retrograde cholangio-pancreatography (ERCP). After successful retrieval of CBD stone on ERCP, patient had massive upper gastrointestinal bleed leading to hypotension and shock. Addition of inotropes had led to further deterioration in his clinical status with a mean arterial BP falling to 44 mm of Hg. His echocardiography showed a resting left ventricular outflow tract (LVOT) gradient of 90 mm of Hg and thus was taken up for emergency alcohol septal ablation (ASA). Immediately after ASA, patient had significant decrease in LVOT obstruction and rise of systemic arterial pressures. After 10 days of antibiotic therapy patient was discharged with a residual LVOT obstruction of 28 mm of Hg.
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PMID:Rescue alcohol septal ablation in sepsis with multiorgan failure. 2325 12