Inadequate Tissue Perfusion Research Articles

Should corticosteroids be given in shock?

Shock is defined as the inability of the circulation to meet the metabolic needs of tissues. This circulatory failure leads to inadequate tissue perfusion causing hypoxia, metabolic acidosis and cellular injury. Intracellular enzymes, antigens and vasoactive substances such as bradykinin, prostaglandins, renin and catecholamines are then released into the circulation. The syndrome may be complicated by disseminated intravascular coagulation, a respiratory distress syndrome (‘shock lung’) and by acute renal failure (‘shock kidney’).

Recommendations for Continuous Oxygen Therapy in Chronic Obstructive Lung Disease: Report of the Committee on Emphysema American College of Chest Physicians

Although expiratory air flow obstruction is the physiologic sine qua non of chronic obstructive lung disease, tissue hypoxia ultimately accounts for the bulk of systemic physiologic changes. Tissue hypoxia results not only from an inadequate pulmonary gas exchange resulting in decreased oxygenation of arterial blood leaving the lungs (hypoxemia), but also from reductions in hemoglobin concentration and thus oxygen-carrying capacity of the blood. Hypoxia is also caused by inadequate tissue perfusion due to low cardiac output, structurally altered or poorly regulated regional circulation and from an inability of cellular enzymes to utilize the oxygen presented.

Should Corticosteroids Be Used in Shock?

This paper analyzes the available information on the possible mechanisms of corticosteroid action relevant to the correction of shock. Though shock may occur in a number of diseases, the pathophysiological common denominator is inadequate tissue perfusion, and its metabolic consequences: decreased pH, PO2, PCO2, and sodium, and increased lactic acid, potassium, magnesium, fatty acids, ketone bodies, and amino acids. The 4 proposed useful mechanisms of action of corticosteroid for shock treatment are: 1) Corticosteroids are required for normal cardiac function, and their cradiovascular effects are both intropic and vascular (i.e., enhance effects of catecholamines and provide an adrenergic blockade); 2) Corticosteroids stabilize membranes, enhancing the integrity of capillaries and affecting lysosomal membrane stability; 3) they improve tissue metabolism; and 4) catecholamines may also be useful in terms of their other mechanisms of action, which include the prevention of tissue breakdown and direct detoxification of endotoxin. The toxicity and administration of corticosteroids are discussed, and it is pointed out that the only benefit from corticosteroids demonstrated in experimental situations occurred when large doses (more than 300 mg, some up to 1-2 gm., of hydrocortisone or equivalent) were given at the earliest possible decision point and well before extremis, but the authors claim to be in no position to recommend specific agents or dosage regimens for clinical use.

Peripheral and cardiac factors in experimental septic shock.

The insidious and sometimes precipitous development of septic shock in man involves mechanisms not clearly understood. Cardiovascular changes have been reported to occur within seconds following an intravenous injection of endotoxin in dogs £5,7,19,22), and at variable times after injection of endotoxin in monkeys (8,10,13) or live E. coli organisms in the canine and primate species (3,11,14,15). Although the animal shock model has been studied extensively in recent years, the precise mechanisms involved in the early development of shock are not clearly understood. Recent emphasis has been focused on the causes of inadequate tissue perfusion in this form of shock. Of particular importance have been studies in which cardiac output decreased significantly in the early phase of shock. Several explanations have been proposed to account for the early decrease in flow and these will be the subject of this presentation.

Lung pathology in respiratory distress following shock in the adult.

Twenty cases of progressive respiratory distress (PRD) in adult patients following shock in connection with trauma, post‐operative complications or serious acute diseases are reviewed. The development of pulmonary consolidation with the formation of hyaline membranes (HM) in these cases is described in detail. Organization of the HMs may result in fibrous obliteration of respiratory bronchioles and alveolar ducts, if survival is sufficiently long. This is a highly characteristic picture. Thin HMs without organization, interpreted as early lesions, were found among twelve additional cases treated by artificial ventilation; these patients did not develop PRD but died of other causes. The relation of the pathological findings to certain clinical factors, such as length of survival with PRD, duration of mechanical ventilation and oxygen concentration, has been investigated. The results seem to concur with the theory that the pulmonary lesions are precipitated by inadequate tissue perfusion and possibly also intravascular coagulation during shock, leading to endothelial damage and reduced alveolar surfactant. Probably there are many important contributary factors, such as the mechanical effects of artificial ventilation, high oxygen concentration, infection, etc. “The respiratory distress lung” seems to be an appropriate morphological term for this type of lung lesion, which may also be precipitated by uraemia and viral pneumonia, for example, and greatly resembles the hyaline membrane disease in the newborn.

TREATMENT OF THE CRITICALLY ILL CHILD: HEMORRHAGIC SHOCK

Shock in the child is nearly always caused by blood (or fluid) loss, burns, or infection. The goal of the physician is to recognize which of these are causing shock in his patient, and to treat both the underlying disorder and the shock as quickly as possible. This review will touch only on the clinical management of the patient in hemorrhagic shock. The pathophysiology of hemorrhagic shock is characterized by a decrease in cardiac output resulting in inadequate tissue perfusion, tissue hypoxia, and acidosis; and, it is caused by an inadequate circulating blood volume. The patient often arrives in the emergency room with multiple injuries, being hypotensive, tachycardic, tachypneic, and obtunded. First priority is given to establishing an adequate airway, stopping massive hemorrhage (application of manual pressure or tourniquets) , and splinting unstable fractures. Since many resuscitative measures should be undertaken simultaneously, even the most experienced physician should call for assistance as soon as he recognizes the seriousness of a patient's condition. The nurse should start a chart on the patient, recording at frequent intervals vital signs, pupil size and reaction, and fluids and medications given. As quickly as possible, one or more routes for the rapid infusion of fluid should be established. In the child this is best accomplished by cutdown of the greater saphenous vein at the ankle and insertion of a large bore catheter.1 (Efforts at introducing a needle or catheter percutaneously into a collapsed peripheral vein will usually waste valuable time.)

Effects of levarterenol on blood flow in inflammation.

PATIENTS who are in shock associated with infection continue to present difficult therapeutic problems. In addition to the multiple effects of bacterial toxins, patients in septic shock have invariably had associated problems which affect the hemodynamic and metabolic responses to shock, including hypovolemia from dehydration or hemorrhage, and diseases of the heart, lungs, kidneys, liver, or other organ systems. 1 Clinical sepsis is often associated with extensive inflammation, which may impose hemodynamic burdens which the circulation is unable to support. 2 Patients in septic shock are commonly found to have hypotension associated with a normal or cardiac output, ie, low-resistance, or hyperdynamic septic shock. 3-6 Inadequate perfusion of tissues in these patients may result in part, at least, from arteriovenous shunting of blood in areas of inflammation, 2,3,5,7 either through greatly dilated capillary beds or through arteriovenous communications, thereby creating a form of high output cardiac failure. The controversy

Left heart bypass in left ventricular failure due to experimental coronary artery ligation

Summary and conclusions 1. A study of left heart bypass in ischemic left ventricular failure in anesthetized mongrel dogs has been presented. A difference in right and left ventricular end- diastolic pressures suggests that isolated left ventricular failure is present. Functional mitral insufficiency has been observed during the late stages of left ventricular failure due to serial coronary artery ligation. 2. The value of peripheral arterial pressure and central venous pressure as early indications of left ventricular failure is in doubt. 3. The arteriovenous oxygen difference or, by extension, the central venous oxygen saturation is a clinically useful estimate of the effectiveness of the cardiac output in the presence of left ventricular failure and this value becomes abnormal long before arterial hypotension or elevation of the central venous pressure occurs. 4. Hypovolemia, ventricular fibrillation, and inadequate drainage of the left atrium all influence directly the effectiveness of left heart bypass and, when left heart bypass is inadequate in the presence of left ventricular failure, an inadequate tissue perfusion results.

Management of emergencies. IV. Septic shock--pathogenesis and treatment.

SEPTIC shock is a dynamic syndrome induced by infections of varying type in which inadequate perfusion of tissues with blood develops. Although the microcirculation of the capillary loop is the final determinant of the events that occur in this condition, multiple factors are involved in the genesis and persistence of progressive decompensation of the capillary circulation and the cells that it supports. Effective therapy of septic shock requires knowledge of its pathogenesis, anticipation and recognition of the clinical picture, the use of available bedside and laboratory technics for assessing the nature and degree of the derangements and rapid initiation of . . .

Blood Lactate and Pyruvate in Pulmonary Insufficiency

Blood lactate and pyruvate levels and lactate-pyruvate ratios were determined in 20 patients with severe hypoxemia due to pulmonary insufficiency, 18 patients having arterial oxygen tensions (pO2) lower than 50 mm. of mercury, and 8 having tensions lower than 40 mm. of mercury. Most of the patients had normal lactate levels and lactate-pyruvate ratios in spite of severe hypoxemia, and there was no correlation between pO2 or oxygen content and raised levels. All but 1 patient with an elevated lactate level and lactate-pyruvate ratio had a disorder of systemic circulation with hypotension. On the other hand, failure of the right side of the heart with cor pulmonale did not lead to hyperlactatemia. In the resting state generalized tissue hypoxia and increased anaerobic metabolism are seldom due to clinical hypoxemia per se. When present, increased anaerobic metabolism is related to a systemic circulatory disorder, with resultant inadequate tissue perfusion.

Endotoxin shock.

Article1 October 1962Endotoxin ShockWESLEY W. SPINK, M.D., F.A.C.P.WESLEY W. SPINK, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-57-4-538 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptSince world war II extensive investigations on shock have been carried out. Within the past 5 years the subject has been thoroughly reviewed in 3 symposia (1-3). These discussions have emphasized the complexity of the problem and the necessity for more precise information on the nature of shock in the human being.Although hypotension is a cardinal sign in the early stages of shock, a more fundamental concept is necessary in defining the condition. Shock is the inadequate perfusion of tissues and organs with oxygenated blood resulting in hemodynamic changes and metabolic alterations that may be irreversible. Shock can be...

Metabolic aspects of shock.

WE DO NOT PLAN to describe all the metabolic changes which may result from shock but to make some general statements which express our philosophy regarding this problem and then to discuss briefly a few specific points. A detailed discussion of this subject has been presented elsewhere.¹We will use the term "shock" to connote a syndrome whose central feature is a precarious state of the circulation resulting in an overall insufficiency of blood flow. This insufficiency, when prolonged, leads to variable and inadequate perfusion and nourishment of certain organs and tissues and ultimately results in their dysfunction. Are there specific metabolic disturbances which determine "irreversibility" and which lead inexorably to death from shock despite any treatment? This is the point, of course, that Dr. Bing has raised regarding myocardial function.²This general question and its corollary, namely, to what extent and how rapidly can the metabolic defects