Shock

2019 ◽  
Author(s):  
Andrew C Bright ◽  
Yann-Leei L Lee ◽  
Jon D Simmons
Keyword(s):  
Biochemical Markers ◽  
Anaerobic Metabolism ◽  
Tissue Perfusion ◽  
Response To Therapy ◽  
Source Control ◽  
Intravascular Volume ◽  
Volume Responsiveness ◽  
Metabolic Recovery ◽  
Neurogenic Shock ◽  
Volume Tolerance

Shock represents hypoperfusion leading to cellular metabolic failure, with attendant clinical and biochemical markers indicating shock severity and response to therapy. While identifying and treating the underlying cause (source control for sepsis, hemostasis for exsanguination, etc) is paramount, the approach to shock is fundamentally straightforward. Assessment of volume responsiveness or volume tolerance, correction of vasoplegia, and modulation of pump function to improve forward flow aim to recover tissue perfusion at the macroscopic level and facilitate metabolic recovery. These strategies often must be applied simultaneously despite the traditionally used etiology-based classifications of shock. The intensivist should thus be familiar with a variety of invasive and noninvasive tools to determine the approach of greatest perceived yield and evaluate efficacy of interventions.  This review contains 4 figures, 1 table, and 50 references. Key Words: anaerobic metabolism, fluid responsiveness, hemorrhagic shock, lactic acidosis, measurement of intravascular volume, neurogenic shock, septic shock, shock, Swan-Ganz catheter, treatment of shock

Shock

2019 ◽  
Author(s):  
Andrew C Bright ◽  
Yann-Leei L Lee ◽  
Jon D Simmons
Keyword(s):  
Biochemical Markers ◽  
Anaerobic Metabolism ◽  
Tissue Perfusion ◽  
Response To Therapy ◽  
Source Control ◽  
Intravascular Volume ◽  
Volume Responsiveness ◽  
Metabolic Recovery ◽  
Neurogenic Shock ◽  
Volume Tolerance

Shock represents hypoperfusion leading to cellular metabolic failure, with attendant clinical and biochemical markers indicating shock severity and response to therapy. While identifying and treating the underlying cause (source control for sepsis, hemostasis for exsanguination, etc) is paramount, the approach to shock is fundamentally straightforward. Assessment of volume responsiveness or volume tolerance, correction of vasoplegia, and modulation of pump function to improve forward flow aim to recover tissue perfusion at the macroscopic level and facilitate metabolic recovery. These strategies often must be applied simultaneously despite the traditionally used etiology-based classifications of shock. The intensivist should thus be familiar with a variety of invasive and noninvasive tools to determine the approach of greatest perceived yield and evaluate efficacy of interventions.  This review contains 4 figures, 1 table, and 50 references. Key Words: anaerobic metabolism, fluid responsiveness, hemorrhagic shock, lactic acidosis, measurement of intravascular volume, neurogenic shock, septic shock, shock, Swan-Ganz catheter, treatment of shock

Different responses of biochemical markers of bone resorption to bisphosphonate therapy in Paget disease

1995 ◽  
Vol 41 (11) ◽  
pp. 1592-1598 ◽  
Author(s):  
A Blumsohn ◽  
K E Naylor ◽  
A M Assiri ◽  
R Eastell
Keyword(s):  
Bone Resorption ◽  
Biochemical Markers ◽  
Type I Collagen ◽  
Bisphosphonate Therapy ◽  
Response To Therapy ◽  
Tartrate Resistant Acid Phosphatase ◽  
Type I ◽  
Paget Disease ◽  
Markers Of Bone Resorption ◽  
Total Alkaline

Abstract We examined the response of different biochemical markers of bone resorption to bisphosphonate therapy (400 mg of etidronate daily for 6 months) in mild Paget disease (n = 14). Urinary markers included hydroxyproline (OHP), total (T) and free (F) pyridinolines (Pyds) determined by HPLC, immunoreactive FPyds, immunoreactive TPyds, and the N- and C-terminal telopeptides of type I collage (NTx, CL). Serum measurements included tartrate-resistant acid phosphatase (TRAcP) and the C-terminal telopeptide of type I collagen (ICTP). ICTP and TRAcP showed a minimal response to therapy (% change at 6 months, -13.1 +/- 6.8 and -6.7 +/- 3.4, respectively). The response was greatest for urinary telopeptides (NTx and CL; % change -75.7 +/- 7.5 and -73.4 +/- 8.9, respectively). The response was somewhat greater for TPyds than for FPyds. We conclude that: (a) ICTP and TRAcP are unreliable indicators of changes in bone turnover; (b) oligopeptide-bound Pyds and telopeptide fragments of type I collagen in urine show a somewhat greater response to therapy than do FPyds and may be more sensitive indicators of bone resorption; and (c) as yet no evidence suggests that these markers are substantially better predictors of the clinical response to therapy than serum total alkaline phosphatase or urinary OHP. There are several problems with the interpretation of these measurements in Paget disease, and the clinical utility of these measurements remains uncertain.

Evaluation of three biochemical markers for serially monitoring the therapy of small-cell lung cancer.

1987 ◽  
Vol 5 (3) ◽  
pp. 472-479 ◽  
Author(s):  
P A Ganz ◽  
P Y Ma ◽  
H J Wang ◽  
R M Elashoff
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Biochemical Markers ◽  
Small Cell ◽  
Response To Therapy ◽  
Small Cell Lung ◽  
Single Institution ◽  
Limited Disease ◽  
Acid Glycoprotein

A number of biochemical markers have been proposed for monitoring the therapy of small-cell lung cancer (SCLC). This report reviews the experience at a single institution using three biochemical markers, alpha-1-acid glycoprotein (AGP), carcinoembryonic antigen (CEA), and lactate dehydrogenase (LDH), for serially monitoring the therapy of patients with SCLC. AGP measurements identified limited-disease patients more frequently than LDH or CEA, and a combination of markers (AGP and LDH) improves the accuracy of correctly classifying patients with active disease. Each of the markers correctly tracked the clinical response to therapy in approximately two thirds of the subjects. The use of a combination of markers should be considered for monitoring the therapy of SCLC in future clinical trials.

Biochemical Markers for Monitoring Response to Therapy: Evidence for Higher Bone Specificity by a Novel Marker Compared with Routine Markers

2008 ◽  
Vol 17 (5) ◽  
pp. 1269-1276 ◽  
Author(s):  
Diana Julie Leeming ◽  
Axel Hegele ◽  
Inger Byrjalsen ◽  
Rainer Hofmann ◽  
Per Qvist ◽  
...  
Keyword(s):  
Biochemical Markers ◽  
Response To Therapy ◽  
Monitoring Response

scholarly journals Biochemical Markers of Bone Turnover and Response of Bone Mineral Density to Intervention in Early Postmenopausal Women: An Experience in a Clinical Laboratory

2001 ◽  
Vol 47 (6) ◽  
pp. 1083-1088 ◽  
Author(s):  
La-or Chailurkit ◽  
Boonsong Ongphiphadhanakul ◽  
Noppawan Piaseu ◽  
Sunee Saetung ◽  
Rajata Rajatanavin
Keyword(s):  
Bone Mineral Density ◽  
Postmenopausal Women ◽  
Biochemical Markers ◽  
Bone Markers ◽  
Response To Therapy ◽  
Control Group ◽  
Mineral Density ◽  
Bone Resorption Markers ◽  
Early Postmenopausal Women ◽  
Markers Of Bone Turnover

Abstract Background: Markers of bone formation and resorption may be useful as early indicators of response to therapy. Our aim in this study was to investigate the use of bone markers for monitoring of intervention for bone loss in early postmenopausal women and to assess the relationships between these markers and changes in bone mineral density (BMD). Methods: Subjects were randomly assigned to the following groups: a control group; a group receiving calcium alone; groups receiving calcium plus low or conventional doses of conjugated equine estrogen; and groups receiving calcium plus low or conventional doses of calcitriol. At baseline and at 1 and 3 months after intervention, we measured serum intact osteocalcin, serum N-terminal midfragment osteocalcin, serum C-terminal telopeptide of type I collagen (CTx), urinary deoxypyridinoline cross-links, and urinary CTx. The BMD of the lumbar spine and the femoral neck was measured at baseline and after 1 and 2 years of intervention. Results: No marker changed significantly in the control group except urinary CTx, which increased at 3 months. Serum CTx decreased in all regimens at 1 or 3 months of intervention. In addition, the changes of all markers at 3 months were inversely associated with the change in the BMD of the lumbar spine at 1 or 2 years (r = −0.144 to −0.314), whereas only the changes of bone resorption markers at 3 months were inversely correlated with the changes in femoral BMD at 1 or 2 years (r = −0.143 to −0.366). Conclusions: Biochemical markers of bone turnover appear to be of use in assessing early response to therapy. Bone resorption markers, especially serum CTx, are better indicators than bone formation markers for estimating the response to intervention in early postmenopausal women. However, the early changes in bone markers were weakly related to the later changes in BMD.

Splanchnic Oxygen Consumption Is Impaired during Severe Acute Normovolemic Anemia in Anesthetized Humans

2006 ◽  
Vol 105 (1) ◽  
pp. 37-44 ◽  
Author(s):  
Mali Mathru ◽  
Daneshvari R. Solanki ◽  
Lee C. Woodson ◽  
J Sean Funston ◽  
Orthan Ozkan ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Oxygen Delivery ◽  
Biochemical Markers ◽  
Anaerobic Metabolism ◽  
Hemoglobin Concentration ◽  
Whole Body ◽  
Before And After ◽  
Normovolemic Anemia ◽  
Splanchnic Oxygen ◽  
Beta Hydroxybutyrate

Background In conscious humans, reduction in hemoglobin concentration to 5 g/dl did not produce inadequate systemic oxygenation. However, systemic measures of inadequate oxygenation may not be sufficiently sensitive to detect inadequate oxygenation in individual organs such as splanchnic organs. The authors tested the hypothesis that acute normovolemic anemia to hemoglobin less than 6.0 g/dl in anesthetized humans reduces splanchnic oxygen consumption because of diminished whole body oxygen delivery. Methods Elective spine (n = 12) and abdominal (n = 7) surgery patients underwent acute normovolemic anemia to decrease the hemoglobin concentration close to 6.0 g/dl. The authors assessed the development of supply-dependent conditions in systemic and regional vascular beds by two primary measures before and after acute normovolemic anemia: oxygen consumption and surrogate biochemical markers of anaerobic metabolism, including plasma lactate, regional lactate kinetics, and ketone body ratio. Results When hemoglobin was reduced from 13.6 +/- 1.2 to 5.9 +/- 0.3 g/dl, oxygen supply dependency occurred in the splanchnic and preportal tissues but not at the systemic level. Regional supply dependency was accompanied by biochemical markers of anaerobic metabolism. Conclusions In anesthetized humans, a reduction in hemoglobin to 5.9 g/dl by acute normovolemic anemia diminished splanchnic and preportal whole body oxygen delivery and impaired splanchnic and preportal oxygen consumption. This was accompanied by increased plasma levels of regional lactate and an increased beta-hydroxybutyrate-to-acetoacetate ratio. These findings suggest that the risk to the gastrointestinal tract during acute normovolemic anemia may be underestimated.

scholarly journals Hemodynamic Monitoring in Sepsis—A Conceptual Framework of Macro- and Microcirculatory Alterations

Diagnostics ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 1559
Author(s):  
Liana Valeanu ◽  
Serban-Ion Bubenek-Turconi ◽  
Carmen Ginghina ◽  
Cosmin Balan
Keyword(s):  
Critical Care ◽  
Fluid Resuscitation ◽  
Antimicrobial Therapy ◽  
Tissue Perfusion ◽  
Healthcare Systems ◽  
Source Control ◽  
Vasopressor Therapy ◽  
Hemodynamic Management ◽  
Hemodynamic Support ◽  
Adequate Tissue

Circulatory failure in sepsis is common and places a considerable burden on healthcare systems. It is associated with an increased likelihood of mortality, and timely recognition is a prerequisite to ensure optimum results. While there is consensus that aggressive source control, adequate antimicrobial therapy and hemodynamic management constitute crucial determinants of outcome, discussion remains about the best way to achieve each of these core principles. Sound cardiovascular support rests on tailored fluid resuscitation and vasopressor therapy. To this end, an overarching framework to improve cardiovascular dynamics has been a recurring theme in modern critical care. The object of this review is to examine the nature of one such framework that acknowledges the growing importance of adaptive hemodynamic support combining macro- and microhemodynamic variables to produce adequate tissue perfusion.

The Therapy of Anaphylactic Shock

1984 ◽  
Vol 18 (1) ◽  
pp. 14-21 ◽  
Author(s):  
Joseph F. Dasta ◽  
John J. Fath ◽  
Frank B. Cerra
Keyword(s):  
Anaphylactic Shock ◽  
Volume Expansion ◽  
Systemic Reaction ◽  
Pulmonary Involvement ◽  
Response To Therapy ◽  
Clinical Settings ◽  
Intravascular Volume ◽  
Controlled Ventilation ◽  
Incidence And Mortality ◽  
Life Threatening

Anaphylaxis is an acute, often life-threatening systemic reaction to mediators released by basophils and mast cells. Histamine, leukotrienes, prostaglandins, and other mediators are responsible for complex and varied reactions in man. Serious cardiovascular or pulmonary involvement can lead to death within minutes. Therapy depends on prompt recognition of the disease and rapid administration of epinephrine. Even in ideal clinical settings, response to therapy may be slow and a long resuscitation necessary. Antihistamines, glucocorticoids, intravascular volume expansion, sympathomimetics, bronchodilators, and controlled ventilation all may be necessary. Taking careful allergy histories; using enteral routes for drug administration when possible; observing patients, who have received injections for at least 20 minutes; and rapidly treating patients with epinephrine are the main means of reducing the incidence and mortality of this disease.

scholarly journals Evaluation of tissue perfusion parameters and intravascular volume, emphasizing the inferior vena cava diameter and collapsibility

Critical Care ◽  
2007 ◽  
Vol 11 (Suppl 3) ◽  
pp. P12
Author(s):  
H Missaka ◽  
MA Lima ◽  
H Cal ◽  
NM Otto ◽  
D Moraes ◽  
...  
Keyword(s):  
Inferior Vena Cava ◽  
Inferior Vena ◽  
Vena Cava ◽  
Tissue Perfusion ◽  
Intravascular Volume ◽  
Inferior Vena Cava Diameter

scholarly journals Hemorrhagic shock

2007 ◽  
Vol 54 (1) ◽  
pp. 63-70 ◽  
Author(s):  
V.M. Bumbasirevic ◽  
B. Jovanovic ◽  
I. Palibrk ◽  
A.R. Karamarkovic ◽  
D. Radenkovic ◽  
...  
Keyword(s):  
Hemorrhagic Shock ◽  
Signs And Symptoms ◽  
Tissue Perfusion ◽  
Hemodynamic Instability ◽  
Organ Damage ◽  
Significant Loss ◽  
High Morbidity ◽  
Intravascular Volume ◽  
Compensatory Mechanisms ◽  
Cellular Hypoxia

Hemorrhagic shock is a condition produced by rapid and significant loss of blood which lead to hemodynamic instability, decreases in oxygen delivery, decreased tissue perfusion, cellular hypoxia, organ damage and can be rapidly fatal. Despite improved understanding of the pathophysiology and significant advances in technology, it remains a serious problem associated with high morbidity and mortality. Early treatment is essential but is hampered by the fact that signs and symptoms of shock appear only after the state of shock is well establish and the compensatory mechanisms have started to fail. The primary goal is to stop the bleeding and restore the intravascular volume. This review addresses the pathophysiology and treatment of hemorrhagic shock.

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