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1 cts a widespread clinical assumption that in hypovolemic cardiac arrest, the ventricles are collapsed
4 ntilation and various shock states including hypovolemic, cardiogenic, obstructive, and septic shock.
6 d the hypothesis that patients with POTS are hypovolemic compared with healthy controls and explored
7 e changes are of particular importance under hypovolemic conditions, especially when central venous b
10 hen intravenously during ischemia induced by hypovolemic hypotension and bilateral common carotid art
11 set of cardiovascular collapse during severe hypovolemic hypotension in spontaneously breathing human
12 nvasive hemodynamic support in patients with hypovolemic hypotension once the blood loss has been con
15 ontrol (n = 3), control plus L-NAME (n = 5), hypovolemic (n = 4), and hypovolemic plus L-NAME (n = 5)
16 s with pulmonary edema during the study were hypovolemic or euvolemic at the time pulmonary edema dev
17 igh plasma aldosterone levels detected under hypovolemic or hyperkalemic challenge can lead to increa
20 g initial studies with both normovolemic and hypovolemic pigs, sequential increases in inspiratory im
25 The 30-day mortality rate was 18.4%, and hypovolemic shock (odds ratio 4.75; 95% confidence inter
26 tcomes Consortium in patients with traumatic hypovolemic shock (shock) or traumatic brain injury (TBI
27 injured patients, age 15 years or more with hypovolemic shock [systolic blood pressure (SBP) </= 70
28 ude that L-NAME may blunt hypotension during hypovolemic shock by inhibiting nitric oxide synthase an
31 olecular research applies more to protracted hypovolemic shock followed by the systemic inflammatory
36 during a prearrest control period and during hypovolemic shock produced by rapid hemorrhage of 35% of
39 and left ventricular diameter compared with hypovolemic shock values by 34 +/- 2.5% and 20 +/- 2.5%,
42 ied Model for End-Stage Liver Disease score, hypovolemic shock, and bacterial infection at inclusion
43 ortality resulting from intestinal bleeding, hypovolemic shock, and sepsis, even at a very low DSS co
44 cy, Model for End-Stage Liver Disease score, hypovolemic shock, hepatocellular carcinoma, and active
46 randomized, double-blind trial of traumatic hypovolemic shock, HSD (250 mL) versus lactated Ringer's
56 oxone would augment tolerance to hypotensive hypovolemic stress (lower body negative pressure [LBNP])
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