Rationale: Cardiorespiratory insufficiency (CRI) is a term applied to the manifestations of loss of normal cardiorespiratory reserve and portends a bad outcome. CRI occurs commonly in hospitalized patients, but its risk escalation patterns are unexplored.Objectives: To describe the dynamic and personal character of CRI risk evolution observed through continuous vital sign monitoring of individual step-down unit patients.Methods: Using a machine learning model, we estimated risk trends for CRI (defined as exceedance of vital sign stability thresholds) for each of 1,971 admissions (1,880 unique patients) to a 24-bed adult surgical trauma step-down unit at an urban teaching hospital in Pittsburgh, Pennsylvania using continuously recorded vital signs from standard bedside monitors. We compared and contrasted risk trends during initial 4-hour periods after step-down unit admission, and again during the 4 hours immediately before the CRI event, between cases (ever had a CRI) and control subjects (never had a CRI). We further explored heterogeneity of risk escalation patterns during the 4 hours before CRI among cases, comparing personalized to nonpersonalized risk.Measurements and Main Results: Estimated risk was significantly higher for cases (918) than control subjects (1,053; P < 0.001) during the initial 4-hour stable periods. Among cases, the aggregated nonpersonalized risk trend increased 2 hours before the CRI, whereas the personalized risk trend became significantly different from control subjects 90 minutes ahead. We further discovered several unique phenotypes of risk escalation patterns among cases for nonpersonalized (14.6% persistently high risk, 18.6% early onset, 66.8% late onset) and personalized risk (7.7% persistently high risk, 8.9% early onset, 83.4% late onset). Conclusions:Insights from this proof-of-concept analysis may guide design of dynamic and personalized monitoring systems that predict CRI, taking into account the triage and real-time monitoring utility of vital signs. These monitoring systems may prove useful in the dynamic allocation of technological and clinical personnel resources in acute care hospitals.
Dynamic estimates of mean systemic pressure based on a Guytonian analog model (Pmsa) appear accurate under baseline conditions but may not remain so during septic shock because blood volume distribution and resistances between arterial and venous beds may change. Thus, we examined the effect of acute endotoxemia on the ability of Pmsa, estimated from steady-state cardiac output, right atrial pressure, and mean arterial pressure, to reflect our previously validated instantaneous venous return measure of mean systemic pressure (Pmsi), derived from beat-to-beat measures of right ventricular stroke volume and right atrial pressure during positive pressure ventilation. We studied 6 splenectomized pentobarbital-anesthetized close chested dogs. Right ventricular stroke volume was measured by a pulmonary arterial electromagnetic flow probe. Instantaneous venous return measure of mean systemic pressure and Pmsa were calculated during volume loading and removal (±100-mL bolus increments ×5) both before (control) and 30 minutes after endotoxin infusion (endo). Cardiac output increased (2628 ± 905 vs 3560 ± 539 mL/min; P < .05) and mean arterial pressure decreased (107 ± 16 vs 56 ± 12 mm Hg; P < .01) during endo. Changes in Pmsi and Pmsa correlated during both control and endo (r2 = 0.7) with minimal bias by Bland-Altman analysis (mean difference ± 95% confidence interval, 0.47 ± 5.04 mm Hg). We conclude that changes in Pmsa accurately tracts Pmsi under both control and endo.
AimsCurrently, there is no effective resuscitative adjunct to fluid and blood products to limit tissue injury for traumatic hemorrhagic shock. The objective of this study was to investigate the role of inhaled carbon monoxide (CO) to limit inflammation and tissue injury, and specifically mitochondrial damage, in experimental models of hemorrhage and resuscitation.ResultsInhaled CO (250 ppm for 30 minutes) protected against mortality in severe murine hemorrhagic shock and resuscitation (HS/R) (20% vs. 80%; P<0.01). Additionally, CO limited the development of shock as determined by arterial blood pH (7.25±0.06 vs. 7.05±0.05; P<0.05), lactate levels (7.2±5.1 vs 13.3±6.0; P<0.05), and base deficit (13±3.0 vs 24±3.1; P<0.05). A dose response of CO (25–500 ppm) demonstrated protection against HS/R lung and liver injury as determined by MPO activity and serum ALT, respectively. CO limited HS/R-induced increases in serum tumor necrosis factor-α and interleukin-6 levels as determined by ELISA (P<0.05 for doses of 100–500ppm). Furthermore, inhaled CO limited HS/R induced oxidative stress as determined by hepatic oxidized glutathione:reduced glutathione levels and lipid peroxidation. In porcine HS/R, CO did not influence hemodynamics. However, CO limited HS/R-induced skeletal muscle and platelet mitochondrial injury as determined by respiratory control ratio (muscle) and ATP-linked respiration and mitochondrial reserve capacity (platelets).ConclusionThese preclinical studies suggest that inhaled CO can be a protective therapy in HS/R; however, further clinical studies are warranted.
IntroductionTissue reperfusion following hemorrhagic shock may paradoxically cause tissue injury and organ dysfunction by mitochondrial free radical expression. Both nitrite and carbon monoxide (CO) may protect from this reperfusion injury by limiting mitochondrial free radial production. We explored the effects of very small doses of inhaled nitrite and CO on tissue injury in a porcine model of hemorrhagic shock.MethodsTwenty pigs (mean wt. 30.6 kg, range 27.2 to 36.4 kg) had microdialysis catheters inserted in muscle, peritoneum, and liver to measure lactate, pyruvate, glucose, glycerol, and nitrite. Nineteen of the pigs were bled at a rate of 20 ml/min to a mean arterial pressure of 30 mmHg and kept between 30 and 40 mmHg for 90 minutes and then resuscitated. One pig was instrumented but not bled (sham). Hemorrhaged animals were randomized to inhale nothing (control, n = 7), 11 mg nitrite (nitrite, n = 7) or 250 ppm CO (CO, n = 5) over 30 minutes before fluid resuscitation. Mitochondrial respiratory control ratio was measured in muscle biopsies. Repeated measures from microdialysis catheters were analyzed in a random effects mixed model.ResultsNeither nitrite nor CO had any effects on the measured hemodynamic variables. Following inhalation of nitrite, plasma, but not tissue, nitrite increased. Following reperfusion, plasma nitrite only increased in the control and CO groups. Thereafter, nitrite decreased only in the nitrite group. Inhalation of nitrite was associated with decreases in blood lactate, whereas both nitrite and CO were associated with decreases in glycerol release into peritoneal fluid. Following resuscitation, the muscular mitochondrial respiratory control ratio was reduced in the control group but preserved in the nitrite and CO groups.ConclusionsWe conclude that small doses of nebulized sodium nitrite or inhaled CO may be associated with intestinal protection during resuscitation from severe hemorrhagic shock.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-015-0903-z) contains supplementary material, which is available to authorized users.
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