The effect of acute traumatic brain injury on the performance of shock index.

BACKGROUND: Shock index (SI) is recognized to be a more reliable early indicator of hemorrhage than traditional vital signs. Acute traumatic brain injury (TBI) can be associated with autonomic uncoupling and may therefore alter the reliability of SI in patients with combined TBI and peripheral hemorrhage. The aim of this study was to evaluate the performance of SI when acute TBI of mild and moderate severity were associated with progressive simple hemorrhage. METHODS: This study was undertaken in a laboratory setting. Brian injury was induced using the lateral fluid percussion model in anesthetized rats. The fluid percussion device delivered an applied cortical pressure of 1.2 atm and 1.8 atm, producing mild and moderate TBI, respectively. Control animals underwent identical procedures but with no applied cortical pressure. Hemorrhage was induced 10 minutes after brain injury, at a rate of 2% of blood volume per minute until 40% blood volume was withdrawn. RESULTS: The SI response to increasing volume of hemorrhage was unaltered when control and mild TBI groups were compared (test of interaction p = 0.39). There was a 50% mortality rate observed 20 to 60 minutes after hemorrhage in the moderate TBI group. The SI response to hemorrhage in the moderate TBI group compared with the control group became significantly different at 40% blood volume loss (test of interaction p = 0.048). Comparison of the SI response with hemorrhage between survivors and nonsurvivors of moderate TBI revealed a significant difference (p = 0.007). SI was markedly attenuated in the presence of increasing hemorrhage in the nonsurvivor subgroup of moderate TBI. CONCLUSIONS: SI significantly underestimated underlying hemorrhage in the presence of acute TBI of moderate severity where attenuation of the biphasic heart rate and blood pressure response was also most pronounced.

Systemic arterial pressure wave reflections during acute hemorrhage.

OBJECTIVE: To determine the effects of hemorrhage on wave-reflection-induced systolic pressure augmentation in the aorta. DESIGN: Randomized, controlled laboratory experiment. SETTING: University research laboratory. SUBJECTS: Twenty-five anesthetized pigs randomized to surgical controls (n = 7), hemorrhage (n = 9, H), and hemorrhage with reinfusion (n = 9, HR). INTERVENTIONS: Hemorrhage of 1 mL/kg/min over 20 mins followed by observation (H) or reinfusion (HR) of shed blood. MEASUREMENTS AND MAIN RESULTS: High-fidelity systemic arterial pressure waveforms, from ascending aorta to femoral artery, were transduced and archived digitally using intravascular semiconductor catheter-tipped pressure transducers. Wave-reflection-induced systolic pressure augmentation was determined using the augmentation index in the ascending aorta (AIaa) and distal descending aorta (AIda). Pulse wave velocity, wave travel times, and lumped pressure wave reflection sites were also calculated. AI values were positive at baseline with greater decreases in AIda compared with AIaa observed following hemorrhage, with negative values achieved for AIda alone. AI returned to control values following reinfusion. Lumped reflection site positions and pressure contour maps suggested that a single lumped reflection site (lower abdomen/pelvis) at baseline was replaced by two discrete sites (upper abdomen and pelvis) following hemorrhage, which only recovered following reinfusion. Hemorrhage was associated with hemodynamic conditions that favored late return of wave reflection from the trunk and with the absence of significant changes in systemic vascular resistance. CONCLUSIONS: Hemorrhage-induced early return of pressure wave reflection from the abdominal vasculature is associated with systolic pressure augmentation in the ascending aorta and has the potential to worsen afterload conditions and decrease coronary artery perfusion and cardiac performance. Hemorrhage-induced splanchnic vasoconstriction causing pressure wave reflection may explain these loading conditions in the ascending aorta, and systolic pressure augmentation may be a more useful guide to left ventricular afterload than systemic vascular resistance.

Estimation of errors in determining intrathoracic blood volume using the single transpulmonary thermal dilution technique in hypovolemic shock.

BACKGROUND: The transpulmonary thermal dilution technique has been widely adopted for monitoring cardiac preload and extravascular lung water in critically ill patients. This method assumes intrathoracic blood volume (ITBV) to be a fixed proportion of global end-diastolic volume (GEDV). This study determines the relation between GEDV and ITBV under normovolemic and hypovolemic conditions and quantifies the errors in estimating ITBV. METHODS: Nineteen pigs allocated to control (n = 9) and shock (n = 10) groups were studied. Shock was maintained for 60 min followed by volume resuscitation. The dual dye-thermal dilution technique was used to measure GEDV and ITBV (ITBVm) at baseline (time 0), shock phase (30 and 90 min), and after resuscitation (150 min). The regression equations estimated from paired GEDV and ITBVm measurements under normovolemic and hypovolemic conditions were used to estimate ITBV from the corresponding GEDV, and the estimation errors were quantified. A more simplified equation, used in a commercially available clinical monitor (ITBV = 1.25 x GEDV), was then used to estimate ITBV. RESULTS: The regression equation in the control group was ITBVm = 1.21 x GEDV + 99 (r = 0.89, P < 0.0001) and in the shock group at 30 and 90 min was ITBVm = 1.45 x GEDV + 0.6 (r = 0.95, P < 0.0001). The 95% confidence interval for the y-intercept was relatively wide, ranging from 31 to 168 and -47 to 49, respectively, for the two equations. The equation estimated in the control group led to overestimation of ITBV and a significant (P < 0.05) increase in errors in the shock group at 30 and 90 min. Errors in estimating ITBV using the simplified commercial algorithm were less than 15% under normovolemic and hypovolemic conditions. CONCLUSIONS: The linear relation between GEDV and ITBV is maintained in hypovolemic shock. Even though the relation between GEDV and ITBV is influenced by circulatory volume and cardiac output, the mean errors in predicting ITBV were small and within clinically tolerable limits.

Muscle wasting and energy balance in critical illness.

BACKGROUND: In nine patients with multiple organ failure ultrasound was able to identify muscle wasting despite the presence of oedema (Campbell et al., J Clin Nutr 62 (1995) 533). AIMS: The purpose of the present study was twofold: one was to determine whether this technique was applicable to a much larger ICU population, many of whom were not as ill as the original subjects. The second reason was to determine whether a relationship could be identified between rates of wasting and energy balance. METHODS: Serial measurements of both mid-upper arm circumference (MAC) and muscle thickness, using ultrasound, were made at 1-3 day intervals between 5 and 39 (median 7) days in 50 critically ill patients. RESULTS: Muscle thickness decreased in 48 of the 50 patients at a median rate of 1.6%/day with a range of 0.2-5.7%/day. In 33 patients, in whom MAC did not change significantly with time, muscle thickness decreased by between 0.3 and 4.2 (median 1.6)%/day. In three patients MAC increased significantly with time but muscle thickness decreased by between 1.3 and 5.7 (median 2.6)%/day. Twelve patients showed a significant decrease in MAC with time and muscle thickness in this group decreased by between 0.2 and 4.0 (median 1.3)%/day. The percentage decrease in muscle thickness between the groups, in whom MAC decreased or did not change, was not significantly different (P = 0.475). CONCLUSION: We have demonstrated that an ultrasound technique devised to identify muscle wasting in the presence of severe fluid retention works in the majority (48/50) of patients when applied to a wider ICU population. Energy balance made no difference to the rate of wasting.