Diaphragmatic function is preserved during severe hemorrhagic shock in the rat.

BACKGROUND: Acute diaphragmatic dysfunction has been reported in septic and cardiogenic shock, but few data are available concerning the effect of hemorrhagic shock on diaphragmatic function. The authors examined the impact of a hemorrhagic shock on the diaphragm. METHODS: Four parallel groups of adult rats were submitted to hemorrhagic shock induced by controlled exsanguination targeting a mean arterial blood pressure of 30 mmHg for 1 h, followed by a 1-h fluid resuscitation with either saline or shed blood targeting a mean arterial blood pressure of 80 mmHg. Diaphragm and soleus strip contractility was measured in vitro. Blood flow in the muscle microcirculation was measured in vivo using a Laser Doppler technique. Muscle proinflammatory cytokine concentrations were also measured. RESULTS: Hemorrhagic shock was characterized by a decrease in mean arterial blood pressure to 34 ± 5 mmHg (-77 ± 4%; P< 0.05) and high plasma lactate levels (7.6 ± 0.9 mM; P < 0.05). Although tetanic tension of the diaphragm was not altered, hemorrhagic shock induced dramatic impairment of tetanic tension of the soleus (-40 ± 19%; P < 0.01), whereas proinflammatory cytokine levels were low and not different between the two muscles. Resuscitation with either blood or saline did not further modify either diaphragm or soleus performance and proinflammatory cytokine levels. The shock-induced decrease in blood flow was much more pronounced in the soleus than in the diaphragm (-75 ± 13% vs. -17 ± 10%; P = 0.02), and a significant interaction was observed between shock and muscle (P < 0.001). CONCLUSION: Diaphragm performance is preserved during hemorrhagic shock, whereas soleus performance is impaired, with no further impact of either blood or saline fluid resuscitation.

Use of nuclear magnetic resonance spectroscopy to assess renal dysfunction after hypertonic-hyperoncotic resuscitation in rats.

BACKGROUND: The aim of this study was to evaluate the renal tolerance of a hypertonic-hyperoncotic solution (HHS) administration during uncontrolled hemorrhagic shock (UHS). METHODS: UHS was produced in rats by a preliminary bleed followed by tail amputation. Hydroxyethylstarch (HHS) 200/0.5 6% in NaCl 7.2% was administered to the HHS groups (n = 20) and normal saline (NS) to the NS group (n = 20). Infusion rates were adjusted to prevent mean arterial pressure (MAP) from falling either below 40 mm Hg in the HHS40 (n = 10) and NS40 groups (n = 10), or below 80 mm Hg in the HHS80 (n = 10) and NS80 groups (n = 10). Data obtained were compared with a sham group and a no resuscitation (NR) group. Nephrotoxicity was evaluated by nuclear magnetic resonance analysis in urine samples. RESULTS: Survival was 60% in the NS40 group and 40% in the NS80 group, 70% in the HHS40 group, and 60% in the HHS80 group (p = not significant). Within and between target groups of 40 mm Hg MAP and 80 mm Hg MAP, there was no significant difference in survival. The mean values of renal metabolites to creatinine (ct) ratios were not significantly different among the six groups. Principal component analysis showed that the HHS80 group was characterized by an increase in allantoin/ct and urea/ct ratios demonstrating acute renal dysfunction and failure of nitrogen metabolism. CONCLUSION: In prolonged UHS, an infusion of HHS may not increase the rate of survival. HHS infusion in normotensive resuscitation appears to be associated with renal toxicity.

Survival of severely shocked patients who present with absent radial pulse and unrecordable blood pressure in the pre-hospital phase.

OBJECTIVES: To determine the mortality and clinical features of patients presenting with severe hypotension in the pre-hospital phase of care. DESIGN: A prospective observational study. The medical records of patients attended by a physician-led pre-hospital medical service were examined prospectively. Inclusion criteria were severe shock characterized by a non-palpable radial pulse and unrecordable blood pressure at clinical presentation. All consecutive records between September 2002 and September 2003 were included. SETTING: Seine Saint-Denis, an urban area with a population of 1.5 million located in the northern suburbs of Paris, France. INTERVENTIONS: None. RESULTS: One hundred and thirty one patients met the inclusion criteria. The overall mortality was 50% (66/131). Of the deaths, 20% (13/66) occurred in the pre-hospital phase and 80% (53/66) after arrival in hospital. Clinical features significantly associated with increased mortality were: more than one pre-existing co-morbidity, increased age, high Knaus score, a low Glasgow Coma Score, vasopressor administration, pre-hospital cardiac arrest and hypotension on arrival at hospital. The presence of anaphylactic shock was associated with low mortality. In multivariate analysis, occurrence of cardiac arrest (OR=13.5 [2.8; 64.5]), age (OR=1.03 [1.01; 1.05]) and low Glasgow Coma Scale score value (OR=1.15 [1.05; 1.29]) were independently associated with mortality. CONCLUSION: Patients presenting with profound hypotension in the pre-hospital phase have a high mortality. Patients who recover their blood pressure with interventions before hospital admission and those with anaphylactic shock have a better outcome than other patient sub-groups.

Improved survival after resuscitation with norepinephrine in a murine model of uncontrolled hemorrhagic shock.

BACKGROUND: Recent studies have challenged current guidelines on fluid resuscitation. However, studies on resuscitation using norepinephrine in uncontrolled hemorrhagic shock are lacking. The authors examined the effects of norepinephrine in combination with saline infusion in uncontrolled hemorrhage in rats. METHODS: Rats subjected to a 15-min controlled hemorrhage (withdrawal of 3 ml blood/100 g body mass) followed by a 60-min uncontrolled hemorrhage (75% tail amputation) were randomly assigned to one of several treatment groups (10 rats/group) receiving different doses of norepinephrine (0 [NE0], 5 [NE5], 50 [NE50], or 500 [NE500] microg.100 g(-1).h(-1)). In the four hypotensive resuscitation groups (n = 40), mean arterial pressure was not allowed to fall below 40 mmHg by titrated infusion of normal saline. In the four normotensive resuscitation groups (n = 40), it was not allowed to fall below 80 mmHg. The endpoint was survival at 210 min. RESULTS: There was a significant difference (P < 0.05) in survival rate among groups. Among the hypotensive rats, 6 (60%) survived in the NE0 and NE5 dose groups, 9 (90%) survived in the NE50 dose group, and none survived in the NE500 dose group. Among the normotensive rats, none survived in the NE0 group, 4 (40%) survived in the NE5 dose group, all 10 (100%) survived in the NE50 group, and none survived in the NE500 group. CONCLUSIONS: The early use of norepinephrine in uncontrolled hemorrhagic shock in rats significantly improved survival when infused at a rate of 50 microg.100 g(-1).h(-1) in normotensive and hypotensive resuscitation strategies.