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Shock hypovolemic

Hepatic reperfusion injury is not a phenomenon connected solely to liver transplantation but also to situations of prolonged hypoperfusion of the host s own liver. Examples of this occurrence are hypovolemic shock and acute cardiovascular injur) (heart attack). As a result of such cessation and then reintroduction of blood flow, the liver is damaged such that centrilobular necrosis occurs and elevated levels of liver enzymes in the serum can be detected. Particularly because of the involvement of other organs, the interpretation of the role of free radicals in ischaemic hepatitis from this clinical data is very difficult. The involvement of free radicals in the overall phenomenon of hypovolemic shock has been discussed recently by Redl et al. (1993). More specifically. Poll (1993) has reported preliminary data on markers of free-radical production during ischaemic hepatitis. These markers mostly concerned indices of lipid peroxidation in the serum and also in the erythrocytes of affected subjects, and a correlation was seen with the extent of liver injury. The mechanisms of free-radical damage in this model will be difficult to determine in the clinical setting, but the similarity to the situation with transplanted liver surest that the above discussion of the role of XO activation, Kupffer cell activation and induction of an acute inflammatory response would be also relevant here. It will be important to establish whether oxidative stress is important in the pathogenesis of ischaemic hepatitis and in the problems of liver transplantation discussed above, since it would surest that antioxidant therapy could be of real benefit. [Pg.243]

Restore intravascular volume with normal saline if in hypovolemic shock... [Pg.105]

Cardiogenic/distributive/obstructive/hypovolemic shock, carbon monoxide poisoning, severe hypoxemia, severe anemia, and seizures... [Pg.177]

List the most common etiologies of decreased intravascular volume in hypovolemic shock patients. [Pg.195]

Describe the major hemodynamic and metabolic abnormalities that occur in patients with hypovolemic shock. [Pg.195]

Describe the clinical presentation, including signs, symptoms, and laboratory test measurements, for the typical hypovolemic shock patient. [Pg.195]

Prepare a treatment plan with clearly defined outcome criteria for a hypovolemic shock patient that includes both fluid management and other pharmacologic therapy. [Pg.195]

Compare and contrast the relative advantages and disadvantages of crystalloids, colloids, and blood products in the treatment of hypovolemic shock. [Pg.195]

Formulate a stepwise monitoring strategy for a hypovolemic shock patient. [Pg.195]

Hypovolemic shock occurs as a consequence of inadequate intravascular volume to meet the oxygen and metabolic needs of the body. [Pg.195]

In the absence of ongoing blood loss, administration of 2000 to 4000 mL of isotonic crystalloid will normally re-establish baseline vital signs in adult hypovolemic shock patients. [Pg.195]

Blood products are indicated in adult hypovolemic shock patients who have sustained blood loss from hemorrhage exceeding 1500 mL. [Pg.195]

Major treatment goals in hypovolemic shock following fluid resuscitation are as follows arterial systolic blood pressure greater than 90 mm Hg within 1 hour, organ dysfunction reversal, and normalization of laboratory measurements as rapidly as possible (less than 24 hours). [Pg.195]

The principal function of the circulatory system is to supply oxygen and vital metabolic substrates to cells throughout the body, as well as removal of metabolic waste products. Circulatory shock is a life-threatening condition whereby this principal function is compromised. When circulatory shock is caused by a severe loss of blood volume or body water it is called hypovolemic shock, the focus of this chapter. Regardless of etiology, the most distinctive manifestations of hypovolemic shock are arterial hypotension and metabolic acidosis. Metabolic acidosis is a consequence of an accumulation of lactic acid resulting from tissue hypoxia and anaerobic... [Pg.195]

FIGURE 10-1. Hemodynamic relationships between key cardiovascular parameters (panel A). Solid lines represent a direct relationship the broken line represents an inverse relationship. In panel B, the perturbations typically observed in hypovolemic shock are highlighted in blue with arrows depicting the likely direction of the pertubation. (Reprinted from Braunwald E. Regulation of the circulation. I. N Engl J Med 1974,290 1129, with permission.)... [Pg.196]

What type of hypovolemic shock does TJ have ... [Pg.201]

What signs and symptoms of hypovolemic shock would you expect to see in TJ ... [Pg.201]

FIGURE 10-5. Operative forces at the capillary membrane tending to move fluid either outward or inward through the capillary membrane. In hypovolemic shock, one therapeutic strategy is the administration of colloids that can sustain and/or draw fluid from the interstitial space by increasing the plasma colloid osmotic pressure. (Reprinted from Guyton AC, Hall JE. Textbook of Medical Physiology. 8th ed. Philadelphia Saunders,... [Pg.203]

Lactic acidosis, which typically accompanies hypovolemic shock as a consequence of tissue hypoxia, is best treated by reversal of the underlying cause. Administration of alkalizing agents such as sodium bicarbonate has not been demonstrated to have any... [Pg.204]


See other pages where Shock hypovolemic is mentioned: [Pg.203]    [Pg.101]    [Pg.195]    [Pg.195]    [Pg.196]    [Pg.197]    [Pg.197]    [Pg.197]    [Pg.197]    [Pg.197]    [Pg.198]    [Pg.199]    [Pg.199]    [Pg.199]    [Pg.199]    [Pg.201]    [Pg.201]    [Pg.201]    [Pg.201]    [Pg.202]    [Pg.203]    [Pg.203]    [Pg.203]    [Pg.203]    [Pg.204]    [Pg.204]    [Pg.204]    [Pg.205]    [Pg.205]    [Pg.205]   
See also in sourсe #XX -- [ Pg.243 ]

See also in sourсe #XX -- [ Pg.195 , Pg.196 , Pg.197 , Pg.198 , Pg.199 , Pg.200 , Pg.201 , Pg.202 , Pg.203 , Pg.204 , Pg.205 ]

See also in sourсe #XX -- [ Pg.152 ]

See also in sourсe #XX -- [ Pg.247 ]

See also in sourсe #XX -- [ Pg.253 ]




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