Invasive and noninvasive hemodynamic monitoring of patients with cerebrovascular accidents.

Seventeen patients with hemodynamic instability from acute cerebrovascular accidents were evaluated shortly after arrival at the emergency department of a university-run county hospital with both invasive Swan-Ganz pulmonary artery catheter placement and a new, noninvasive, thoracic electrical bioimpedance device. Values were recorded and temporal patterns of survivors and nonsurvivors were described. Cardiac indices obtained simultaneously by the 2 techniques were compared. Of the 17 patients, 11 (65%) died. Survivors had higher values than nonsurvivors for mean arterial pressure, cardiac index, and oxygen saturation, delivery, and consumption at comparable times. Cardiac index values, as measured by invasive and noninvasive methods, were correlated. We concluded that hemodynamic monitoring in an acute care setting may recognize temporal circulatory patterns associated with outcome. Noninvasive electrical bioimpedance technology offers a new method for early hemodynamic evaluation. Further research in this area is warranted.

Noninvasive hemodynamic monitoring of critical patients in the emergency department.

OBJECTIVE: To evaluate the feasibility of multicomponent noninvasive hemodynamic monitoring in critical emergency patients and to compare this technique with simultaneous invasive monitoring by the pulmonary artery thermodilution catheter. METHODS: A prospective observational study was done comparing invasive monitoring and noninvasive monitoring in 60 critically ill or injured patients who required hemodynamic monitoring shortly after entering the ED of a university-affiliated country hospital. Cardiac output (CO) values measured by the standard thermo-dilution pulmonary artery catheter technique were compared with simultaneously obtained measurements using a noninvasive bioimpedance method. Concurrent measurements were made of pulse oximetry to screen pulmonary function and transcutaneous oximetry to assess tissue perfusion. RESULTS: The impedance CO values closely approximated those for the thermodilution method; r 0.81, p < 0.001. Significant circulatory abnormalities, including hypotension, reduced cardiac index, arterial hemoglobin desaturation, tissue hypoxia, reduced O2 delivery, and consumption, were found in 54 of the 60 (90%) patients. The cardiac index decreased in 44% of the patients, the transcutaneous O2 decreased in 39%, and the O2 saturation by pulse oximetry fell in 22% during the observation period in the ED (commonly lasting 2-8 hours). CONCLUSIONS: Noninvasive monitoring can provide hemodynamic and perfusion information previously available only by invasive thermodilution catheters. Such noninvasive monitoring can display continuous on-line real-time data, allowing immediate recognition of circulatory abnormalities and providing a means to titrate therapy to appropriate therapeutic goals.

Noninvasive cardiac index monitoring in gunshot wound victims.

OBJECTIVE: To evaluate a bioimpedance device for the noninvasive measurement of cardiac index (CI) against standard thermodilution measurements in patients with gunshot wounds. METHODS: A prospective open-label performance evaluation was done using a convenience sample of gunshot wound victims initially treated in the resuscitation area of a high-volume, urban ED. After initial resuscitation, patients had a flow-directed pulmonary artery catheter placed for thermodilution cardiac output (CO) measurements. The CO measurements were made in triplicate and averaged. Estimates of body surface area were used to convert these measurements to CI estimates. Electrodes for bioimpedance measurements were placed as soon as practical after ED arrival. Simultaneous measurements of CI using the bioimpedance device were made as clinically indicated during each patient's hospital course. RESULTS: There were 54 patients studied, with an overall mean (+/- SEM) age of 32 +/- 3 years, Revised Trauma Score of 6.7 +/- 0.4, and Injury Severity Scale score of 22 +/- 3. There were 42 survivors and 12 nonsurvivors. The CI as estimated by bioimpedance correlated well with that measured by thermodilution (r = 0.79, p < or = 0.02). The precision of the invasive and noninvasive measurements was 1.1 L/min/m2; the bias was -0.011 L/min/m2. In 24 patients with thoracic injuries requiring tube thoracostomy or thoracic surgery, the correlation of the 2 devices was r = 0.71 with precision and bias of 1.4 L/min/m2 and -0.018 L/min/m2, respectively. CONCLUSIONS: Cardiac index can be noninvasively estimated in acutely injured patients with gunshot wounds using a bioimpedance device. Further study of bioimpedance measurements as a guide to volume therapy is warranted.

Noninvasive physiologic monitoring of high-risk surgical patients.

OBJECTIVES: To study the feasibility of multicomponent noninvasive monitoring, consisting of a new bioimpedance method for estimating cardiac output together with routine pulse oximetry and transcutaneous oximetry, and to compare physiologic data obtained noninvasively with hemodynamic and oxygen transport data obtained by standard invasive pulmonary artery thermodilution catheter to evaluate circulatory function in high-risk surgical patients. DESIGN: Prospective descriptive analysis of the time course of physiologic patterns in surgical patients. SETTING: University-run county hospital. PATIENTS: Seventy-one consecutively monitored, high-risk critically ill surgical patients in their perioperative period. OUTCOME MEASURES: Simultaneous measurements by invasive and noninvasive methods to describe and compare the temporal physiologic patterns of survivors and nonsurvivors. RESULTS: The new impedance cardiac output estimations closely approximated those of the thermodilution method (r = 0.82, P < .001). Episodes of hypotension, tachycardia, low cardiac index, arterial hemoglobin desaturation, low transcutaneous oximetry, reduced oxygen delivery, and low oxygen consumption occurred with both groups but were more pronounced in the nonsurvivors than in the survivors. Noninvasive monitoring provided information similar to that of the thermodilution method. Both approaches indicated low flow and poor tissue perfusion (oxygenation) that was worse in the nonsurvivors. CONCLUSIONS: The multicomponent noninvasive monitoring provides continuous online, real-time displays of physiologic data that allow immediate recognition of circulatory dysfunction as well as the means to titrate therapy to appropriate predetermined therapeutic goals. The noninvasive systems are easy to apply, safe, inexpensive, reasonably accurate, and cost-effective.

Prospective, randomized trial of survivor values of cardiac index, oxygen delivery, and oxygen consumption as resuscitation endpoints in severe trauma.

The objective was to test prospectively supranormal values of cardiac index (CI), oxygen delivery index (DO2I), and oxygen consumption index (VO2I) as resuscitation goals to improve outcome in severely traumatized patients. We included patients > or = 16 years of age who had either (1) an estimated blood loss > or = 2000 mL or (2) a pelvic fracture and/or two or more major long bone fractures with > or = four units of packed red cells given within six hours of admission. The protocol resuscitation goals were CI > or = 4.5 L/min/m2, DO2I > or = 670 mL/min/m2, and VO2I > or = 166 mL/min/m2 within 24 hours of admission. The control resuscitation goals were normal vital signs, urine output, and central venous pressure. The 50 protocol patients had a significantly lower mortality (9 of 50, 18% vs. 24 of 65, 37%) and fewer organ failures per patient (0.74 +/- 0.28 vs. 1.62 +/- 0.45) than did the 75 control patients. We conclude that increased CI, DO2I, and VO2I seen in survivors of severe trauma are primary compensations that have survival value; augmentation of these compensations compared to conventional therapy decreases mortality.

Multicenter trial of a new thoracic electrical bioimpedance device for cardiac output estimation.

OBJECTIVE: To evaluate the capacity of a new thoracic electric bioimpedance system to estimate cardiac output compared with the conventional thermodilution method. DESIGN: Prospective, multicenter study. SETTING: A university-run county hospital, a university-run U.S. Veterans Affairs hospital, and a university-affiliated U.S. military hospital. PATIENTS: A series of 68 critically ill patients whose conditions required pulmonary artery catheter insertion. MEASUREMENTS AND MAIN RESULTS: A total of 842 simultaneous pairs of cardiac output estimations by conventional thermodilution and a new thoracic electric bioimpedance system that uses an improved signal processing technique based on an all-integer-coefficient filtering technology, using a time-frequency distribution that provides a high signal/noise ratio were evaluated. The r value was .86, r2 = .74, and p < .001 by regression analysis; the mean difference between the two methods relative to their average value was 16.6 +/- 12.9 (SD) %; the precision was 1.4 L/min or 0.8 L/min/m2; the bias was -0.013 L/min. The mean difference between successive pairs of thermodilution measurements was 8.6 +/- 0.6 (SD) %, which was about half the difference between simultaneous pairs of measurement by the two methods. The changes in impedance estimations were close to simultaneously measured changes in thermodilution estimates of cardiac output. CONCLUSIONS: The new bioimpedance system satisfactorily estimated cardiac output as measured by the thermodilution technique. The difference between the two estimations is more than made up for by the continuous noninvasive capability of the impedance system.

Temporal patterns of radiographic infiltration in severely traumatized patients with and without adult respiratory distress syndrome.

We prospectively evaluated the patterns of pulmonary structural and functional changes in 100 consecutive surgical intensive care unit trauma patients who had (1) emergent major surgery, (2) a pelvic fracture, or (3) two or more major long bone fractures. For each patient, arterial blood gas measurements (ABGs), central venous pressure (CVP), pulmonary capillary occlusion pressure (PAOP), thoracic compliance, arterial oxygen tension/fraction of inspired oxygen (PAO2/FIO2), pulmonary venous admixture (Qs/Qt), and portable chest roentgenograms were sequentially tracked. The senior staff radiologist interpreted all chest roentgenograms. Pulmonary infiltration was quantitated in each of six fields using a scale ranging from 0 to 4, with 0 being no infiltration and 4 being the maximum. Adult respiratory distress syndrome (ARDS) was defined as follows: Qs/Qt > or = 20%, PAO2/FIO2 < 250 or both; dependence on mechanical ventilation for life support for > or = 24 hours; PAOP or CVP or both < 20 mm Hg; and thoracic compliance < 50 mL/cm H2O. Time zero (T0) the time of onset of ARDS, was defined as the time these criteria were met. Eighty-three of 100 study group patients had penetrating injuries, and 17 were admitted with blunt trauma. Fifty-one of 100 patients developed ARDS: 36 of 51 died. Only 4 of 49 (8%) patients without ARDS died. The injured lungs of patients with and without ARDS had similar amounts of infiltration over most measured time intervals. The noninjured lungs of the ARDS patients, however, had significantly greater infiltration than those without ARDS at T0 and over subsequent time intervals.(ABSTRACT TRUNCATED AT 250 WORDS)

Temporal patterns of hemodynamics, oxygen transport, cytokine activity, and complement activity in the development of adult respiratory distress syndrome after severe injury.

The aim of this study was to search for early inflammatory mediators in severely traumatized patients that could predict the occurrence of adult respiratory distress syndrome (ARDS). We measured sequential plasma levels of tumor necrosis factor (TNF), interleukin 1 (IL-1), interleukin 6 (IL-6), interleukin 8 (IL-8), complement fragment C3a, and endotoxin. In addition, we measured sequentially the values of hemodynamics, oxygen transport, and pulmonary function. The temporal patterns seen in the patients who developed ARDS were compared with those who did not. In the patients who developed ARDS, the first observed findings were low cardiac index (CI) and oxygen delivery (DO2) followed by progressive increases in IL-6, IL-8 and C3a levels, worsening of pulmonary function, and increases in hemodynamic values. The maximum values of IL-6, IL-8, and C3a occurred after the onset of ARDS. In the patients who did not develop ARDS, initial oxygen transport values were not low, the levels of IL-6, IL-8, and C3a decreased rapidly from their initial peaks, and there were no further increases in hemodynamic values. In both ARDS and nonARDS patients, no measurable quantities of TNF, IL-1, or endotoxin were found. We concluded that none of the mediators we measured reached their peaks before the onset of ARDS and none were found to be predictive of posttraumatic ARDS. However, these and other mediators may augment or intensify the development of ARDS.

Sequence of physiologic patterns in surgical septic shock.

OBJECTIVES: Gradual, almost imperceptible transitions occur between localized infection, generalized infection, systemic manifestations of the sepsis syndrome, septic shock, and death. The aim of this study was to describe the sequential pattern of hemodynamic and oxygen transport patterns of survivors and nonsurvivors of septic shock, so as to differentiate primary from secondary and tertiary events, to evaluate possible physiologic mechanisms, and to provide a template to relate the appearance of biochemical mediators to the sequence of physiologic events. DESIGN: Prospective, cohort study. SETTING: University-run county hospital. PATIENTS: A series of 300 consecutive surgical patients with septic shock; 85 survived and 215 died. INTERVENTIONS: We used specific criteria to define stages as: a) early period, the first recorded increase in cardiac output; b) middle period, time of maximal metabolic activity defined as the highest recorded oxygen consumption (VO2); and c) late period, the time of death or recovery. MEASUREMENTS AND MAIN RESULTS: Hemodynamic and oxygen transport variables were measured at frequent intervals throughout the course of septic shock. Beginning with increased cardiac index and oxygen delivery (Do2), which were the earliest observed hemodynamic changes, there were progressive increases in cardiac index, DO2, and VO2. The values of these variables in the survivors were both greater than normal and greater than those values of the nonsurvivors at comparable time periods. These values decreased in the late stage in nonsurvivors. There were early transient reductions in VO2 that preceded the increase in temperature and the decrease in blood pressure in both survivors and nonsurvivors. Although 86% of the septic patients were hyperdynamic, there were transient hypodynamic episodes (defined as cardiac index < 2.5 L/min/m2) in < 10% of the measurements. Transient preterminal hypermetabolic periods occurred in 9% of the nonsurvivors. CONCLUSIONS: Increased cardiac index and DO2 represent compensations for circulatory deficiencies that limit body metabolism, as reflected by inadequate VO2. Survivors have higher cardiac index, DO2, and VO2 values than those values of both the nonsurvivors and normal values. These data suggest that therapy should be directed toward increasing cardiac index to > 5.5 L/min/m2, DO2 to > 1000 mL/min/m2, and VO2 to > 190 mL/min/m2 as therapeutic goals; these supranormal values were empirically determined by the patterns of the survivors. Further studies to describe temporal relationships of biochemical mediators of these physiologic patterns are needed.

Temporal hemodynamic and oxygen transport patterns in medical patients. Septic shock.

STUDY DESIGN: Because of the gradual insidious transitions between localized infection, generalized infection, and septic shock, it is difficult to compare data of patients in various stages and to differentiate primary from secondary and tertiary events. The aim of the present study was to describe the sequential pattern of hemodynamic and oxygen transport patterns of survivors and nonsurvivors of septic shock in order to evaluate possible physiologic mechanisms and to provide a template to relate the sequence of physiologic events to biochemical mediators. PROCEDURE: A previously described defined protocol was used prospectively to study the sequence of physiologic events using specific criteria to define stages as: (a) early period, the first recorded change in cardiac output; (b) middle period, time of maximal metabolic activity defined as the highest recorded oxygen consumption (VO2); and (c) late period, the time of death or recovery. In addition, three time lines were defined as the first time mean arterial pressure fell below 70 mm Hg, the first time temperature rose above 38 degrees C, and the earliest fall in VO2. Physiologic data were aligned in actual time before or after the time these criteria were met. Invasive hemodynamic and oxygen transport variables were measured with systemic and pulmonary artery catheters; intravascular pressures, arterial and mixed venous gas levels, cardiac output, and derived calculations were made at frequent intervals and keyed to the time of the cardiac output; each set of measurements in turn was keyed to the aforementioned time periods to describe the early, middle, and late periods. RESULTS: Beginning with increased cardiac index and oxygen delivery (DO2) as the early physiologic changes, there were progressive increases in cardiac index, DO2, and VO2 throughout the early and middle periods. They were maintained above the normal range in the late stage of survivors, but fell in the last 16 h in nonsurvivors. These values were greater in survivors than in nonsurvivors throughout. There were early transient reductions in VO2 that preceded the rise in temperature and the fall in mean arterial pressure (MAP). Although 84 percent of the septic patients were hyperdynamic, there were transient hypodynamic episodes defined as cardiac index of less than 2.5 L/min.m2 in approximately 10 percent of the measurements. There were also transient preterminal hypermetabolic periods in about 8 percent of the nonsurvivors. CONCLUSION: We conclude that increased cardiac index and DO2 represent compensations for circulatory inadequacies that limit body metabolism as reflected by VO2. Cardiac index, DO2, and VO2 values of survivors were higher than those of nonsurvivors and normal values. Therapy directed toward increasing cardiac index to supranormal values empirically determined by survivors has been reported to improve outcome. Additional studies to describe temporal relationships of biochemical mediators of these physiologic patterns are needed.

Temporal patterns of blood volume, hemodynamics, and oxygen transport in pathogenesis and therapy of postoperative adult respiratory distress syndrome.

Time relationships of physiologic patterns that are relevant to the pathogenesis of adult respiratory distress syndrome (ARDS) have not been well studied. The purpose of this review is to summarize the temporal relationship of blood volume, hemodynamics, and oxygen transport patterns occurring in postoperative patients before and after ARDS in order to develop a more complete mechanistic evaluation of its pathophysiology and to propose more rational therapeutic strategies. The data indicate that hypovolemia, reduced or uneven blood flow, inadequate delivery of oxygen, and insufficient consumption of oxygen precede the appearance of ARDS and are the primary precipitating physiologic events. This is contrary to conventional thinking which emphasizes capillary leak and fluid overload as the primary problems. The conventional approach also ignores events antecedent to ARDS that produce hypoxia of the lung tissue, result in pulmonary vasoconstriction, and increased pulmonary venous admixture (shunt). Therapy to prevent or rapidly treat these antecedent events has been shown to prevent or attenuate postoperative and posttraumatic ARDS. Various mediators such as interleukin (IL)-1, IL-6, and IL-8 and tumor necrosis factor as measured by plasma concentrations do not precede diagnostic criteria of ARDS, but may accelerate and augment the disorder as it is occurring.

Unreliability of blood pressure and heart rate to evaluate cardiac output in emergency resuscitation and critical illness.

OBJECTIVE: To evaluate the reliability of the vital signs to evaluate circulatory stability as reflected by cardiac index. DESIGN: Descriptive analysis based on data gathered prospectively, using a predetermined protocol. SETTING: University-run county hospital, with a large trauma service. PATIENTS: Sixty-one high-risk trauma patients with accidental injury who were studied immediately after admission to the Emergency Department, and subsequently, 163 critically ill postoperative ICU patients. INTERVENTIONS: Standard fluid therapy, usually crystalloids, but occasionally packed red cell transfusions and colloids, as indicated by clinical criteria. MEASUREMENTS AND RESULTS: Arterial BP was measured by pressure transducer and arterial catheter; heart rate (HR) was measured by electrocardiograph signal, and cardiac output was measured by thermodilution. In sudden severe hypovolemic hypotension, the mean arterial pressure (MAP) nadir (lowest) roughly correlated (r2 = .25) with flow, but there was poor correlation (r2 = .0001) when all pressure and flow values were evaluated. The pressure and flow values were obtained throughout the course of the hypotensive episodes during the initial resuscitation in ICU patients and during terminal illnesses. CONCLUSIONS: Observations at the time of acute severe hypotensive crises that show rough correlation of MAP and cardiac index should not be extrapolated throughout the entire hypotensive period or to other less extreme clinical situations. The stress response to hypovolemia, with endogenous catecholamines and neural mechanisms, tends to maintain arterial pressure in the face of decreasing flow for a variable period of time. However, when these mechanisms are overwhelmed by prolonged hypovolemia, the pressure decreases precipitously, but not synchronously, with flow. We conclude that blood flow cannot reliably be inferred from arterial pressure and heart rate measurements until extreme hypotension occurs.

Relationship between supranormal circulatory values, time delays, and outcome in severely traumatized patients.

OBJECTIVE: To describe the temporal patterns of hemodynamics and oxygen transport in survivors and nonsurvivors of severe trauma in relation to time delays, mortality, and morbidity. DESIGN: Prospective, empiric analysis. SETTING: University-run, inner city county hospital with a Level I trauma center. PATIENTS: A series of 90 consecutively monitored, severely ill trauma patients. METHODS: We followed 90 patients from admission through their hospital course, and divided the study group into patients with estimated blood loss of < or = 3000 mL and those patients with an estimated blood loss of < 3000 mL. For each patient, vital signs were recorded in the Emergency Department, operating room, recovery room, and surgical ICU. Hemodynamic and oxygen transport variables were measured at least every 12 hrs for 96 hrs postadmission. Final outcome and complications were recorded. RESULTS: In the first 24 hrs, the values of 60 survivors were significantly higher than the values of 30 nonsurvivors for mean cardiac index (4.52 +/- 1.45 vs. 3.80 +/- 1.20 L/min/m2; p < .05), oxygen delivery (670 +/- 230 vs. 540 +/- 200 mL/min/m2; p < .01), and oxygen consumption (166 +/- 48 vs. 134 +/- 47 mL/min/m2; p < .01). Thirteen (50%) of 26 patients who never attained mean survivors' values (defined as the mean survivors' values listed above) died. Also, 12 (57%) of 21 patients who took > 24 hrs to attain these values died. In contrast, only five (12%) of 43 patients who reached mean survivors' values in < or = 24 hrs died. Thirty-five of 90 patients lost < 3000 mL of blood; 17 of these 35 patients failed to reach survivors' values within 24 hrs, and 12 (71%) patients died. However, of 18 patients with an estimated blood loss of > 3000 mL, who reached survivors' values in < or = 24 hrs, only two (12%) died. The patients reaching survivors' values in < or = 24 hrs, > 24 hrs, or not at all had similar Injury Severity Scores (28 +/- 13, 26 +/- 13, and 26 +/- 12, respectively) and Trauma Scores (12 +/- 3, 13 +/- 3, and 12 +/- 3, respectively). Only six (12%) of 43 patients reaching survivors' values in < or = 24 hrs developed adult respiratory distress syndrome (ARDS), while 27 (57%) of 47 patients showed these values in > 24 hrs or never developed ARDS. CONCLUSIONS: Reaching supranormal circulatory values, especially within 24 hrs of injury, may improve survival and reduce the frequency of shock-related organ failure in severely traumatized patients.

The relationship between ARDS, pulmonary infiltration, fluid balance, and hemodynamics in critically ill surgical patients.

Hypervolemia from fluid overload with resultant pulmonary edema is thought to be a frequent cause of Adult Respiratory Distress Syndrome (ARDS). However, ARDS may also occur as a result of the hypovolemic shock of surgery or trauma. To develop an appropriate rationale for fluid therapy in high-risk surgical patients, the relationship between fluid balance, hemodynamics, the onset of ARDS by physiologic criteria (shunt greater than or equal to 20%, and/or PaO2/FiO2 ratio less than 250) and the onset of pulmonary infiltration (PI) associated with ARDS were examined. Fifty patients were prospectively followed from admission throughout their hospitalizations; 38 (76%) had trauma and 12 (24%) were postoperative. Cardiac index, central venous pressure (CVP), wedge pressure (WP), and shunt (Qsp) were measured. All chest x rays were read by one staff radiologist who was blinded to the patients' identities. PI was graded from "0" to "4" (0 = no PI, 4 = maximum PI). The first x ray reading of "2" or greater was used as the time of onset of PI. ARDS by physiologic criteria occurred in 29 of 50 (58%) patients; 27 of these 29 (94%) also developed +2 or greater PI. The mean onset times of ARDS and of +2 PI were 40 +/- 41 hours and 40 +/- 38 hours, respectively. The ARDS patients had a significantly smaller net positive fluid balance than the non-ARDS patients over the first 40 hours after admission (+6,831 ml +/- 4,909 ml vs 12,440 ml +/- 7,817 ml, (P less than 0.01)).(ABSTRACT TRUNCATED AT 250 WORDS)