Search

Background: The aims are to apply a mathematical search and display model based on noninvasive hemodynamic monitoring, to predict outcome early in a consecutively monitored series of 661 severely injured patients., Methods: A prospective observational study by a previously designed protocol in a Level I trauma service in a university-run inner city public hospital was conducted. The survival probabilities were calculated at the initial resuscitation on admission and at subsequent intervals during their hospitalization beginning shortly after admission to the emergency department. Cardiac function was evaluated by cardiac output (CI), heart rate (HR), and mean arterial blood pressure (MAP), pulmonary function by pulse oximetry (SapO2), and tissue perfusion function by transcutaneous oxygen indexed to FiO2, (PtcO2/FiO2), and carbon dioxide (PtcCO2) tension., Results: The survival probability (SP) averaged 89 +/- 0.4% for survivors and 75.7 +/- 1.6% (p < 0.001) for nonsurvivors in the first 24-hour period of resuscitation. The CI, MAP, SapO2, PtcO2, and PtcO2/FiO2 were significantly higher in survivors than in nonsurvivors in initial resuscitation, whereas HR and PtcCO2 were higher in nonsurvivors., Conclusions: During the initial resuscitation period, misclassifications were 102 of 661 or 15%. The SP provided early objective criteria to evaluate hospital outcome and to track changes throughout the hospital course based on a large database of patients with similar clinical-hemodynamic states.

Objectives: We used noninvasive hemodynamic monitoring in the initial resuscitation beginning in the emergency department (ED) for the following reasons: (1) to describe early survivor and nonsurvivor patterns of emergency patients in terms of cardiac, pulmonary, and tissue perfusion deficiencies; (2) to measure quantitatively the net cumulative amount of deficit or excess of the monitored functions that correlate with survival or death; and (3) to explore the use of discriminant analysis to predict outcome and evaluate the biological significance of monitored deficits., Methods: This is a descriptive study of the feasibility of noninvasive monitoring of patients with acute emergency conditions in the ED to evaluate and quantify hemodynamic deficits as early as possible. The noninvasive monitoring systems consisted of a bioimpedance method for estimating cardiac output together with pulse oximetry to reflect pulmonary function, transcutaneous oxygen tension to reflect tissue perfusion, and BP to reflect the overall circulatory status. These continuously monitored noninvasive measurements were used to prospectively evaluate circulatory patterns in 151 consecutively monitored severely injured patients beginning with admission to the ED in a university-run county hospital. The net cumulative deficit or excess of each monitored parameter was calculated as the cumulative difference from the normal value vs the time-integrated monitored curve for each patient. The deficits of cardiac, pulmonary, and tissue perfusion functions were analyzed in relation to outcome by discriminant analysis and were cross-validated., Results: The mean (+/- SEM) net cumulative excesses (+) or deficits (-) from normal in surviving vs nonsurviving patients, respectively, were as follows: cardiac index (CI), +81 +/- 52 vs -232 +/- 138 L/m(2) (p = 0.037); arterial hemoglobin saturation, -1 +/- 0.3 vs -8 +/- 2.6%/h (p = 0.006); and tissue perfusion, +313 +/- 88 vs -793 +/- 175, mm Hg/h (p = 0.001). The cumulative mean arterial BP deficit for survivors was -10 +/- 13 mm Hg/h, and for nonsurvivors it was -57 +/- 24 mm Hg/h (p = 0.078)., Conclusions: Noninvasive monitoring systems provided continuously monitored on-line displays of data in the early postadmission period from the ED to the operating room and to the ICU for early recognition of circulatory dysfunction in short-term emergency conditions. Survival was predicted by discriminant analysis models based on the quantitative assessment of the net cumulative deficits of CI, arterial hypoxemia, and tissue perfusion, which were significantly greater in the nonsurvivors.

Objective: To evaluate the effect of early optimization in the survival of severely injured patients., Summary Background Data: It is unclear whether supranormal ("optimal") hemodynamic values should serve as endpoints of resuscitation or simply as markers of the physiologic reserve of critically injured patients. The failure of optimization to produce improved survival in some randomized controlled trials may be associated with delays in starting the attempt to reach optimal goals. There are limited controlled data on trauma patients., Methods: Seventy-five consecutive severely injured patients with shock resulting from bleeding and without major intracranial or spinal cord trauma were randomized to resuscitation, starting immediately after admission, to either normal values of systolic blood pressure, urine output, base deficit, hemoglobin, and cardiac index (control group, 35 patients) or optimal values (cardiac index >4.5 L/min/m2, ratio of transcutaneous oxygen tension to fractional inspired oxygen >200, oxygen delivery index >600 mL/min/m2, and oxygen consumption index >170 mL/min/m2; optimal group, 40 patients). Initial cardiac output monitoring was done noninvasively by bioimpedance and, subsequently, invasively by thermodilution. Crystalloids, colloids, blood, inotropes, and vasopressors were used by predetermined algorithms., Results: Optimal values were reached intentionally by 70% of the optimal patients and spontaneously by 40% of the control patients. There was no difference in rates of death (15% optimal vs. 11% control), organ failure, sepsis, or the length of intensive care unit or hospital stay between the two groups. Patients from both groups who achieved optimal values had better outcomes than patients who did not. The death rate was 0% among patients who achieved optimal values compared with 30% among patients who did not. Age younger than 40 years was the only independent predictive factor of the ability to reach optimal values., Conclusions: Severely injured patients who can achieve optimal hemodynamic values are more likely to survive than those who cannot, regardless of the resuscitation technique. In this study, attempts at early optimization did not improve the outcome of the examined subgroup of severely injured patients.

Postoperative survivors' and nonsurvivors' hemodynamic and oxygen transport patterns have been extensively studied, and the early postoperative circulatory events leading to organ failures and death have been documented. Outcome was improved when potentially lethal circulatory patterns were treated during the early (the first 8-12 hours) postoperative period; but after the appearance of organ failure, reversal of nonsurvival patterns did not improve the outcome. The purpose of this study was to describe prospectively intraoperative circulatory deficiencies that precede shock, organ failures, and death. The ultimate aim was to elucidate nonsurvivor patterns at the earliest possible time to develop more effective preventive strategies for lethal organ failures. This approach is based on the assumption that it is easier and more effective to prevent the initiators of shock, such as hypovolemia, hypoxemia, poor tissue perfusion, and tissue hypoxia, than to treat the mediators of organ failure, such as cytokines, antigens, eicosinoids, and heat shock proteins. We monitored 356 high risk elective surgical patients with preoperative and intraoperative hemodynamic monitoring by the pulmonary artery (PA) thermodilution catheter. The conventionally monitored mean arterial pressure and heart rate remained in the normal range in both groups; the nonsurvivor pattern included decreased cardiac index, stroke index, stroke work, oxygen delivery, and oxygen consumption. Low oxygen consumption was partly compensated by increased oxygen extraction rates, and arterial pressures were maintained by increasing systemic vascular resistance. The early temporal pattern of nonsurvivors' changes were similar to those described during the postoperative period that preceded development of organ failure and death. This suggests that lethal circulatory dysfunctions may begin during the intraoperative period but become more apparent before and after organs fail during later postoperative stages.

Pulmonary artery catheterization is usually not available to critically injured patients before admission to the intensive care unit, where action to correct values derived from such monitoring may be too late. Methods allowing hemodynamic monitoring during the early stages after trauma need to be explored. We used non-invasive monitoring systems (bioimpedance cardiac output monitoring, pulse oximetry and transcutaneous oximetry) to evaluate early temporal hemodynamic patterns after blunt trauma, and compared these to invasive PA monitoring. We included prospectively 134 patients monitored shortly after admission to the emergency department. The non-invasive impedance cardiac output estimations under extenuating emergency conditions approximated those of the thermodilution method: r = 0.83, r2 = 0.69, P<0.001; bias and precision were -0.02+/-0.78 l/min/m2. In the intensive care unit, these values improved further to: r = 0.91, r2 = 0.83, P<0.001; bias and precision = 0.36+/-0.59 l/min/m2. Monitoring revealed episodes of hypotension, low cardiac index, arterial hemoglobin desaturation, low transcutaneous oxygen and high transcutaneous carbon dioxide tensions, and low oxygen consumption during initial resuscitation. Low flow and poor tissue perfusion were more pronounced in non-survivors by both methods. Multicomponent non-invasive monitoring systems give continuous on-line, real-time displays of physiological data that allow early recognition of circulatory dysfunction. Such systems provide information similar to that provided by the invasive thermodilution method, and are easier and safer to use.

Background: Recent reports showed lack of effectiveness of pulmonary artery catheterization in critically ill medical patients and relatively late-stage surgical patients with organ failure. Since invasive monitoring requires critical care environments, the early hemodynamic patterns may have been missed. Ideally, early noninvasive hemodynamic monitoring systems, if reliable, could be used as the "front end" of invasive monitoring to supply more complete descriptions of circulatory pathophysiology., Objectives: To evaluate the accuracy and reliability of noninvasive hemodynamic monitoring consisting of a new bioimpedance method for estimating cardiac output combined with arterial BP, pulse oximetry, and transcutaneous PO2 and PCO2; we compared this system of noninvasive monitoring with simultaneous invasive measurements to evaluate circulatory deficiencies in acutely ill patients shortly after hospital admission where invasive monitoring was not readily available. We also preliminarily explored early differences in temporal hemodynamic patterns of survivors and nonsurvivors., Design and Setting: Prospective comparison of simultaneous invasive and noninvasive measurements of circulatory function with retrospective analysis of data in university-run county hospitals, university hospitals and affiliated teaching hospitals, and a community private hospital., Patients: We studied 680 patients, including 139 severely injured or hemorrhaging patients in the emergency department (ED), 129 medical (nontrauma) patients on admission to the ED, 274 high-risk surgical patients intraoperatively, and 138 patients recently admitted to the ICU., Results: A new noninvasive impedance device provided cardiac output estimations under conditions in which invasive thermodilution measurements were not usually applied. There were 2,192 simultaneous bioimpedance and thermodilution cardiac index measurements; the correlation coefficient, r = 0.85, r2 = 0.73, p < 0.001. The precision and bias was -0.124+/-0.75 L/min/m2. Both invasive and noninvasive monitoring systems provide similar information and identified episodes of hypotension, low cardiac index, arterial hemoglobin desaturation, low transcutaneous O2, high transcutaneous CO2, and low oxygen consumption before and during initial resuscitation. The limitations of noninvasive systems were described., Conclusions: Noninvasive monitoring systems gave continuous displays of physiologic data that provided information allowing early recognition of low flow and poor tissue perfusion that were more pronounced in the nonsurvivors. Noninvasive systems may be acceptable alternatives where invasive monitoring is not available.

The aim of the present study was to explore methods, concepts, and techniques that provide recognition of circulatory deficiencies at the earliest possible time in the patient's illness. We used both the standard invasive pulmonary artery thermodilution catheter and noninvasive hemodynamic monitoring systems consisting of a new bioimpedance cardiac output device, pulse oximetry, transcutaneous oxygen (PtCO2) and carbon dioxide tensions as well as the transcutaneous oxygen tension/fraction of inspired oxygen ratio (PtCO2/FIO2). These three noninvasive systems were used to evaluate cardiac function, pulmonary function, and tissue perfusion, respectively. This approach to early noninvasive monitoring is based on recent evidence suggesting that poor tissue perfusion and oxygenation initiate circulatory dysfunction that leads to shock and organ failure. We studied 303 acute episodes of circulatory dysfunction and shock in 261 patients in a university-run county hospital; 75 were acute traumatic injuries and 109 acute nontrauma medical emergencies on admission to the emergency department, and 77 ICU patients with an acute illness or exacerbation of their current illness. The study was a prospective, descriptive study to identify early abnormal circulatory patterns reflecting the cardiac, pulmonary, and perfusion functions associated with death and with survival. We described noninvasively monitored patterns in individual illustrative cases, in common etiologic groups, and in physiologic categories representing various abnormal functional patterns. We found that hypotensive shock usually was preceded by episodes of high flow followed by low flow and inadequate tissue perfusion indicated by reduced PtCO2; this frequent pattern was modified by associated co-morbid conditions, especially hypovolemia, limited cardiac reserve capacity, age, hypertensive states, and increased body metabolism from infection, trauma, stress, exercise, temperature, and endocrine disorders. Reduced pulmonary function occurred in 18% of emergency patients; these were usually patients with thoracic trauma, severe hypovolemia, head injuries, chronic obstructive pulmonary disease, asthma, drug overdose, and central nervous system failure (massive stroke and coma). We concluded that noninvasive measurements identify early circulatory problems reliably and provide objective criteria for physiologic analysis as well as for definition of therapeutic goals and titration of therapy.

The cardiovascular response of the patient with acute spinal cord injury (SCI) is known to be altered secondary to the cord injury. Our current protocol of managing the acute phase of patients with SCI includes invasive hemodynamic monitoring (with arterial line and Swan-Ganz catheter) and support with fluids and dopamine and/or dobutamine, titrated to maintain a hemodynamic profile with adequate cardiac output (to be determined by oxygen consumption and delivery) and a mean blood pressure of > 90 mm Hg. We feel that this protocol provides two benefits: 1) maintaining the mean blood pressure improves the morbidity of these patients by deterring ischemia and accompanying secondary insults; 2) aggressive monitoring and hemodynamic intervention help stabilize the hemodynamic status of these patients and make it possible to consider early surgery in selected cases. Our hypothesis is that the pulmonary vascular bed is more sensitive to the sympathectomized effect of acute complete cervical SCI. We analyzed the demographic, neurologic, and hemodynamic data of 50 consecutive patients during their first week postinjury. All had signs of myelopathy; 31 (62%) were considered clinically complete. Of the 50 patients, 9 (18%) died, 20 did not improve functionally, and 21 improved. The mean heart rate (82.1 +/- 13.3), blood pressure (94.4 +/- 9.4), pulmonary artery pressure (22 +/- 5) and wedge (12.7 +/- 3.4), cardiac index (4.5 +/- 0.9), systemic vascular resistance index (SVRI) (1637 +/- 399), pulmonary vascular resistance index (PVRI) (181 +/- 80), and oxygen transport (694 +/- 156) showed good response to the treatment. Because the measurements were obtained during treatment, they differ from the expected "classic sympathectomized" response, but they provide a database for further analysis of hemodynamic manipulation in SCI. An analysis of the hemodynamic parameters did not differentiate between complete and incomplete lesions or between patients with functional improvement. We determined, on the basis of the initial hemodynamic measurements, that no patient with a clinically complete motor deficit (Frankel Grade A+B) improved of the 10 who had measurements compatible with either: 1) PVRI < 100 with SVRI < 1200; or 2) PVRI < 115 with SVRI < 1300 or PVR/SVR ratio of < 0.08 when SVRI was < 1600. These patients could not have other measurements that showed low SVRI < 1350 with PVRI > 139. At odds with this unique group, 13 of 29 patients with the same clinical picture and without the above physiological criteria of severe hemodynamic deficit eventually improved (P < 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)

In an acute trauma patient with unrecognized scimitar syndrome, physiologic measurements used in patient management decisions were misleading due to the anatomic and physiologic anomalies of the syndrome. Pulmonary artery catheter measurements believed to reflect left atrial pressures were actually measuring central venous pressures because the catheter was terminating in the scimitar vein. These erroneous measurements led to overly aggressive fluid resuscitation and iatrogenic pulmonary edema. The pathologic features of scimitar syndrome are reviewed, and the mechanism for potential mismanagement of patient volume status created by aberrant pulmonary hemodynamics is discussed.