| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T2 |
11590-11591 |
3652707 |
denotes |
7 |
| T4 |
12285-12679 |
14023293 |
denotes |
2], this group demonstrated a significantly higher mortality. Although the mechanisms relating to the difference in mortality are unknown, it has been suggested that patients with "complicated" shock (defined as multiorgan failure) have greater distortions of cardiorespiratory patterns relative to the degree of hypotension and that this is associated with a higher mortality [8 |
| T3 |
13731-14292 |
13141363 |
denotes |
3) or reported to induce a reduction in the SVR (Table 4).
The largest group of nonseptic patients in this study with hypotension and a low SVR was found to be patients with decompensated cirrhosis. Although occult infections should not be excluded, none of these patients had fever, leukocytosis, an identifiable site of infection, or abnormalities in the peritoneal fluid. Patients with liver cirrhosis often present with systemic hemodynamic disturbances, including hypotension, low SVR, and a reduced sensitivity to vasoconstrictors [10 |
| T1 |
16927-18699 |
3661592 |
denotes |
20]. The hypodynamic state is usually seen early in adrenal insufficiency and is associated with volume depletion from diarrhea, vomiting, and decreased reabsorption of sodium in the distal tubule. CO may also be decreased in adrenal insufficiency as the result of the myofibrillar adenosine triphosphate (ATP) depletion seen with glucocorticoid deficiency [20]. Intravenous fluid therapy most often increases CO and decreases SVR in patients with adrenal crisis. These patients are usually separated from patients with sepsis by a baseline cortisol level below 10μ g/dl or an inadequate response to ACTH [20]. One of our patients with septic shock had baseline cortisol of 22μ g/dl and no response to the cosyntropin stimulation test. This patient could not be weaned off high dose norepinephrine and dopamine until intravenous corticosteroids were instituted. Normal values for basal and stimulated cortisol levels are derived from the adrenal response of healthy individuals. Patients experiencing the severe stress of critical illness demonstrate higher than normal amounts of circulating cortisol. Some patients with critical illness have minimal or no ACTH stimulation above their baseline cortisol levels and may be unable to respond to additional physiologic stress [20]. Several reports suggest a significant number of critically ill patients may have unrecognized adrenal insufficiency [21,22,23,24].
Four cases of idiopathic hypotension with low SVR were identified in our patients. One case was felt to be related to possible anaphylaxis or anaphylactoid reaction but was not well documented. Silverman et al [25] reported a patient who developed anaphylactic shock secondary to penicillin 7 |
