Prediction of postoperative cardiac surgical morbidity and organ failure at admission to the intensive care unit using esophageal Doppler ultrasonography.
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Publications and source records attributed to M Y Rady.
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OBJECTIVE: To determine whether hospital discharge alone represents a good outcome for patients who had prolonged intensive care after cardiac surgery by studying their postdischarge survival and functional outcome. The secondary objective is to estimate the proportion of intensive care unit (ICU) resources used by the long-stay (> or = 10 initial consecutive ICU days) patients and to identify preoperative patient characteristics that are associated with a prolonged ICU stay and hospital and long-term survival. DESIGN: Inception cohort study. SETTING: The Cleveland Clinic Foundation, a tertiary care, academic teaching institution. PATIENTS: Cardiac surgery patients with an initial ICU stay of 10 or more consecutive days. INTERVENTIONS: Data were collected daily during hospitalization on every adult who underwent coronary artery bypass graft and/or valve surgery at one institution in 1993. Discharged patients who spent >10 initial consecutive days in the ICU after surgery were contacted by telephone to determine vital status and functional capacity using the Duke Activity Status Index. Total ICU and total hospital direct costs were obtained for each patient. MEASUREMENTS AND MAIN RESULTS: The primary outcome measurements were ICU length of stay, hospital mortality, after-surgery and postdischarge mortality and functional capacity, and relative resource utilization. Of the 2,618 cardiac surgery patients who met the inclusion criteria, 142 (5.4%) had an initial ICU length of stay of 10 or more consecutive days. Of these, 47 (33.1%) died in the hospital. Ninety-four of the 95 discharged patients were followed up (median follow-up, 30.6 months), and 44 of the 94 (46.8%) died during the follow-up period. The median Duke Activity Status Index for the 50 survivors was 26 out of a possible 58.2. The 142 long-stay patients used 50% of the total ICU days and 48% of the total ICU direct cost for all 2,618 patients. CONCLUSIONS: Many survivors of prolonged intensive care die soon after hospital discharge and many longer term survivors have a poor functional state. Therefore, hospital discharge is an incomplete measure of outcome for these patients, and longer follow-up is more appropriate. The relatively small number of patients who require prolonged intensive care consumes a disproportionate amount of the total ICU and total hospital direct cost.
OBJECTIVES: To determine perioperative predictors of extubation failure (requirement for reintubation and mechanical ventilation after prior successful weaning from ventilator support and extubation) after cardiac surgery and the effect on clinical outcome. DESIGN: Cohort study. SETTING: A tertiary-care, 54-bed, cardiothoracic intensive care unit (ICU). PATIENTS: ICU admissions (n = 11,330) after cardiac surgery over a 42-month period. INTERVENTIONS: Collection of preoperative, operative, and ICU data from a database. MEASUREMENTS AND MAIN RESULTS: Frequency of extubation failure, total duration of mechanical ventilation, length of stay in ICU and hospital, and death. There were 748 (6.6%) patients who were weaned from mechanical ventilation after cardiac surgery and required reintubation and ventilator support. The predictors of extubation failure were: age of > or =65 yrs; inpatient hospitalization before surgery; arterial vascular disease; chronic obstructive pulmonary disease; pulmonary hypertension; severe left ventricular dysfunction; cardiac shock; hematocrit of < or =34%; blood urea nitrogen of > or =24 mg/dL; serum albumin concentration of < or =4.0 g/dL (< or =40.0 g/ L); systemic oxygen delivery of < or =320 mL/min/m2; redo operation; surgical procedures involving the thoracic aorta; transfusion of blood products of > or =10 units; and cardiopulmonary bypass time of > or =120 mins. Extubation failure prolonged the length of total mechanical ventilation, as well as ICU and hospital stay, independent of the frequency of organ dysfunction or nosocomial infections but did not increase the risk of death after cardiac surgery. CONCLUSIONS: Extubation failure after cardiac surgery is uncommon. Although extubation failure increased the utilization of ICU and hospital resources, it did not affect mortality after cardiac surgery. Protocols for early extubation and ICU discharge should be modified in the presence of certain preoperative and operative predictors of extubation failure to avoid unnecessary increase in the cost of care after cardiac surgery.
OBJECTIVE: Adrenal failure, a treatable condition, can have catastrophic consequences if unrecognized in critically ill ED patients. The authors' objective was to prospectively study adrenal function in a case series of hemodynamically unstable (high-risk) patients from a large, urban ED over a 12-month period. METHODS: In a prospective manner, critically ill adult patients presenting to the ED were enrolled when presenting with a mean arterial blood pressure < or =60 mm Hg requiring vasopressor therapy for more than one hour after receiving fluid resuscitation (central venous pressure of 12-15 mm Hg or a minimum of 40 mL/kg of crystalloid). Patients were excluded if presenting with hemorrhage, trauma, or AIDS, or if steroids were used within the previous six months. An adrenocorticotropic hormone (ACTH) stimulation test was performed and serum cortisol was measured. Treatment for adrenal insufficiency was not instituted. RESULTS: A total of 57 consecutive patients were studied. Of these, eight (14%) had baseline serum cortisol concentrations of <20 microg/dL (<552 nmol/L), which was considered adrenal insufficiency (AI). Three additional patients (5%) had subnormal 60-minute post-ACTH-stimulation cortisol responses (<30 microg/dL) and a delta cortisol < or =9 microg/dL, which is the difference between the baseline and 60-minute levels. This is functional hypoadrenalism (FH). There were no laboratory abnormalities that distinguished patients with AI or FH from those with preserved adrenal function (PAF). Rates of survival to discharge did not differ between the AI group (7 of 8) and PAF patients (21 of 46; p = 0.052). CONCLUSIONS: Adrenal dysfunction is common in high-risk ED patients. Overall, it has a frequency of 19% among a homogeneous population of hemodynamically unstable vasopressor-dependent patients. The effect of physiologic glucocorticoid replacement in this setting remains to be determined.
The purpose of this study was to examine the use of lactic acid levels and continuous central venous oxygen saturation (central venous oximetry) to stratify and treat patients with acutely decompensated end-stage chronic congestive heart failure (CHF) presenting to the emergency department. This prospective, convenience, non-outcome study was performed at an urban tertiary care hospital. Patients with end-stage CHF with an ejection fraction <30% presenting in decompensated CHF were eligible for the study. Patients were assessed using the Killip classification and New York Heart Association criteria. After lactic acid levels were obtained, patients were managed according to a standardized protocol guided by central venous oximetry. The patients were divided into high lactic acid (n = 22), low lactic acid (n = 5), and control groups (stable patients presenting to a cardiology clinic, n = 17) for comparison. There was no statistical difference in vital signs, or Killip and New York Heart Association criteria among the 3 groups. Central venous oxygen saturation was significantly lower in the high lactic acid group (32 +/- 12%) than in the normal lactic acid (51 +/- 13%) and control groups (60 +/- 6%) (p < 0.001). After treatment there was a significant decrease in lactic acid (-3.65 +/- 3.65 mM/L) and an increase in central venous oxygen saturation (32 +/- 13%) in the high lactic acid group compared with the normal lactic acid group (p < 0.001). A significant subset of patients with decompensated end-stage CHF present to the emergency department in occult shock and are clinically indistinguishable from patients with mildly decompensated CHF and stable CHF. Once identified, these patients require aggressive alternative management and disposition. Further study is necessary to identify whether this intervention impacts morbidity, mortality, and health care resource consumption.
OBJECTIVE: To determine perioperative predictors of morbidity and mortality in patients > or =75 yrs of age after cardiac surgery. DESIGN: Inception cohort study. SETTING: A tertiary care, 54-bed cardiothoracic intensive care unit (ICU). PATIENTS: All patients aged > or =75 yrs admitted over a 30-month period for cardiac surgery. INTERVENTION: Collection of data on preoperative factors, operative factors, postoperative hemodynamics, and laboratory data obtained on admission and during the ICU stay. MEASUREMENTS AND MAIN RESULTS: Postoperative death, frequency rate of organ dysfunction, nosocomial infections, length of mechanical ventilation, and ICU stay were recorded. During the study period, 1,157 (14%) of 8,501 patients > or =75 yrs of age had a morbidity rate of 54% (625 of 1,157 patients) and a mortality rate of 8% (90 of 1,157 patients) after cardiac surgery. Predictors of postoperative morbidity included preoperative intraaortic balloon counterpulsation, preoperative serum bilirubin of >1.0 mg/dL, blood transfusion requirement of >10 units of red blood cells, cardiopulmonary bypass time of >120 mins (aortic cross-clamp time of >80 mins), return to operating room for surgical exploration, heart rate of >120 beats/min, requirement for inotropes and vasopressors after surgery and on admission to the ICU, and anemia beyond the second postoperative day. Predictors of postoperative mortality included preoperative cardiac shock, serum albumin of <4.0 g/dL, systemic oxygen delivery of <320 mL/ min/m2 before surgery, blood transfusion requirement of >10 units of red blood cells, cardiopulmonary bypass time of >140 mins (aortic cross-clamp time of >120 mins), subsequent return to the operating room for surgical exploration, mean arterial pressure of <60 mm Hg, heart rate of >120 beats/min, central venous pressure of >15 mm Hg, stroke volume index of <30 mL/min/m2, requirement for inotropes, arterial bicarbonate of <20 mmol/L, plasma glucose of >300 mg/dL after surgery, and anemia beyond the second postoperative day. During the study period, the study cohort used 6,859 (21.5%) ICU patient-days out of a total 31,867 ICU patient-days. Nonsurvivors used 2,023 (30%) ICU patient-days and patients with morbidity used 5,903 (86%) ICU patient-days. CONCLUSIONS: Severe underlying cardiac disease (including shock, requirement for mechanical circulatory support, hypoalbuminemia, and hepatic dysfunction), intraoperative blood loss, surgical reexploration, long ischemic times, immediate postoperative cardiovascular dysfunction, global ischemia and metabolic dysfunction, and anemia beyond the second postoperative day predicted poor outcome in the elderly after cardiac surgery. Postoperative morbidity and mortality disproportionately increased the utilization of intensive care resources in elderly patients. Future efforts should focus on preoperative selection criteria, improvement in surgical techniques, perioperative therapy to ameliorate splanchnic and global ischemia, and avoidance of anemia to improve the outcome in the elderly after cardiac surgery.
OBJECTIVE: To determine the incidence, diagnostic features, and perioperative predictors of acute cholecystitis after cardiovascular surgery. DESIGN: Inception cohort study. SETTING: A tertiary care 54-bed cardiothoracic ICU. PATIENTS: All patients admitted to an ICU after cardiovascular surgery during a 42-month period. INTERVENTION: Collection of relevant preoperative, operative, and ICU data from a database and medical charts. PRIMARY OUTCOME: Postoperative acute cholecystitis (AC). RESULTS: Out of 11,330 admissions, 876 patients stayed in the ICU more than 7 days and 30 of them (3%) developed postoperative AC. AC was diagnosed a median of 26 days after cardiovascular surgery (interquartile range, 11 to 41 days). All patients with AC developed at least two criteria of the systemic inflammatory response syndrome (SIRS), and 16 of them (53%) were vasopressor-dependent on the day of diagnosis. Trends in biochemical testing of liver function were not diagnostic for AC. Death occurred in seven of 17 patients (41%) who underwent cholecystectomy, three of nine patients (33%) treated with percutaneous cholecystostomy, and one of four patients (25%) treated conservatively (p=not significant). Specific earlier predictors of AC were arterial vascular disease, preoperative oxygen delivery less than 430 mL/min x m2, longer times on cardiopulmonary bypass, surgical re-exploration, ICU course complicated by cardiac arrhythmia, mechanical ventilation > or = 3 days, bacteremia, and nosocomial infections. CONCLUSION: The incidence of AC is low after cardiovascular surgery. Although SIRS and hemodynamic instability were common at the time of diagnosis, the delayed occurrence and lack of specificity of these features for AC limited their utility for early diagnosis. Specific predictors of AC should be sought in the ICU setting to identify patients who are at risk for AC after cardiovascular surgery. When identified, such predictors can prompt earlier diagnosis and treatment. Further evaluation of the selection criteria for different treatment options is needed in order to decrease the morbidity and mortality associated with AC.
OBJECTIVE: To determine the effect of preoperative therapy with angiotensin-converting enzyme (ACE) inhibitors on clinical outcome after cardiovascular surgery. STUDY: Inception cohort. SETTING: A tertiary care 54-bed cardiothoracic ICU. PATIENTS: All admissions to an ICU over a 42-month period after cardiovascular surgery. INTERVENTION: Extraction of preoperative, operative, and ICU data from a database. OUTCOME MEASURES: Incidence of acute organ dysfunction, length of mechanical ventilation, ICU stay, and death after cardiovascular surgery. RESULTS: The study cohort consisted of four groups: normal or moderately impaired left ventricular function control (group A, n=6,400); normal or moderately impaired left ventricular function treated with ACE inhibitors (group B, n=1,375); severe left ventricular dysfunction control (group C, n=1,905); and severe left ventricular dysfunction treated with ACE inhibitors (group D, n=1,650). The incidence of three or more organ dysfunction was similar on comparison of group A vs group B (5% vs 6%) or group C vs group D (15% vs 13%). There were no differences in the total duration of mechanical ventilation or length of stay in the ICU in group A vs group B or group C vs group D. Death occurred in 2% of groups A and B, and at 6% in groups C and D. Preoperative severe left ventricular dysfunction in both groups C and D was associated with an increased incidence of three or more organ dysfunction, duration of mechanical ventilation, length of stay in ICU, and death after surgery. Multivariate analysis indicated that therapy with ACE inhibitors did not affect the clinical outcome after cardiovascular surgery. CONCLUSION: Preoperative therapy with ACE inhibitors did not influence the clinical outcome after cardiac surgery. It is unlikely that therapy with ACE inhibitors can alter the clinical sequelae of cardiopulmonary bypass and cardiac surgical procedures performed in high-risk patients because of underlying severe left ventricular dysfunction.
UNLABELLED: We examined the influence of preoperative therapy with amiodarone on the incidence of acute organ dysfunction after cardiac surgery in a matched case-control study. There were 220 case-control pairs matched by day of surgery, source of admission, demographic characteristics, placement of intraaortic balloon pump before surgery, repeat operations, emergency surgery, thoracic aorta surgery and other surgical procedures. History of congestive heart failure was more prevalent in the amiodarone group than in the control group before surgery (60% vs 38%, P < 0.0001). The incidence of acute organ dysfunction, duration of mechanical ventilation, and death was similar in both groups after surgery. The requirement for inotropes (26% vs 17%, P = 0.03) and vasopressors (66% vs 55%, P = 0.02) and the incidence of postoperative nosocomial infections (12% vs 6%, P = 0.04) was greater in the amiodarone group. However, the difference was not significant after adjustment for congestive heart failure (Cochran-Mantel-Haenszel test P = 0.15, P = 0.25, P = 0.16, respectively). Amiodarone did not increase the incidence of acute organ dysfunction or death after cardiac surgery. The requirement for inotropes and vasopressors and the incidence of nosocomial infections were related to the severity of the underlying cardiac disease. The practice of discontinuing amiodarone treatment before surgery to reduce the incidence of postoperative organ dysfunction should be critically reevaluated. IMPLICATIONS: Amiodarone is often used for the treatment of life-threatening rhythm disorder. Amiodarone has been blamed for causing organ injury after cardiac surgery. In a study of 220 patients, amiodarone did not increase the risk of organ injury or death after cardiac surgery when compared with control patients. There was no evidence to support the practice of stopping amiodarone before cardiac surgery to avoid serious complications.
OBJECTIVE: To define the incidence, risk factors, and clinical outcome of early pulmonary dysfunction after cardiovascular surgery for adults. STUDY: Inception cohort. SETTING: Adult cardiovascular intensive care unit (ICU). PATIENTS: All adult admissions after cardiovascular surgery without preoperative pulmonary parenchyma or vascular disease over a period of 12 consecutive months. INTERVENTION: Collection of data on demographics, preoperative organ insufficiency, emergency surgery, type of surgical procedure, cardiopulmonary bypass time, transfusion of blood products, postoperative arterial blood gases, and systemic hemodynamics on admission to the cardiovascular ICU. MEASUREMENTS AND MAIN RESULTS: Early postoperative pulmonary dysfunction was defined by mechanical ventilation with a PaO2/FIO2 ratio of < or = 150 torr (< or = 20 kPa) and chest radiography on admission to the cardiovascular ICU. Secondary outcome included postoperative renal and neurologic dysfunction, nosocomial infections, length of mechanical ventilation, hospitalization, and death. A total of 3,122 patients were evaluated and 1,461 patients satisfied the entry criteria of the study. Early postoperative pulmonary dysfunction was present in 180 (12%) patients on admission to the cardiovascular ICU. Preoperative variables: age of > or = 75 yrs (odds ratio 1.69, 95% confidence interval [CI] 1.06 to 2.65), body mass index of > or = 30 kg/m2 (odds ratio 1.60, 95% CI 1.09 to 2.32), mean pulmonary arterial pressure of > or = 20 mm Hg (odds ratio 1.60, 95% CI 1.13 to 2.28), stroke volume index of < or = 30 mL/m2 (odds ratio 1.57, 95% CI 1.08 to 2.26), serum albumin (odds ratio 0.71, 95% CI 0.49 to 0.97), history of cerebral vascular disease (odds ratio 1.81; 95% CI 1.08 to 2.96); operative variables: emergency surgery (odds ratio 2.12, 95% CI 1.01 to 4.51), total cardiopulmonary bypass time of > or = 140 mins (odds ratio 1.54, 95% CI 1.0 to 2.34); and postoperative variables (on admission to cardiovascular ICU): hematocrit of > or = 30% (odds ratio 2.46, 95% CI 1.71 to 3.56), systemic mean arterial pressure of > or = 90 mm Hg (odds ratio 1.67, 95% CI 1.13 to 2.42), and cardiac index of > or = 3.0 L/min/m2 (odds ratio 2.09, 95% CI 1.44 to 3.01) were predictors of early postoperative pulmonary dysfunction. Pulmonary dysfunction was associated with a postoperative increase of serum creatinine (1.36 +/- 0.4 vs. 1.24 +/- 0.4 mg/dL, p < .02), neurologic complications (3% vs. 1.6%, p < .001), nosocomial infections (3% vs. 1.6%, p < .001), prolonged mechanical ventilation (2.2 +/- 5.9 vs. 1.7 +/- 5.6 days, p < .001), length of stay in the cardiovascular ICU (4.4 +/- 12.2 vs. 2.6 +/- 6.2 days, p < .001) and hospital (14.8 +/- 13.1 vs. 10.5 +/- 8.0 days, p < .001), and death (4.4% vs. 1.6%, p < .001). CONCLUSIONS: The incidence of early postoperative pulmonary dysfunction is uncommon; however, once developed, it is associated with increased morbidity and mortality after cardiovascular surgery. Advanced age, large body mass index, preoperative increased pulmonary arterial pressure, low stroke volume index, hypoalbuminemia, history of cerebral vascular disease, emergency surgery, and prolonged cardiopulmonary bypass time are risk factors for early onset of severe pulmonary dysfunction after surgery. Postoperative hematocrit and systemic hemodynamics suggest that early postoperative pulmonary dysfunction can be a component of a generalized inflammatory reaction to cardiovascular surgery.
OBJECTIVE: To determine the incidence, predisposing factors, and outcome of early bloodstream infection after cardiopulmonary bypass. DESIGN: A case control study. SETTING: A 54-bed cardiac surgical intensive care in a tertiary referral center. PATIENTS: Patients from a 30-month period with preoperative hospital stay of <48 hrs and subsequent bloodstream infection within 96 hrs of cardiopulmonary bypass were included in a case group. The control group consisted of patients who had cardiac surgery on the same day as the case group. MEASUREMENTS AND MAIN RESULTS: Patient demographics, history of comorbidity, preoperative laboratory testing, details of surgery, transfusion requirement, inotropic infusions, hemodynamics, and arterial blood gases on admission to intensive care were compared in the two groups. Measures of outcome were duration of mechanical ventilation and intensive care stay, serum creatinine on the first postoperative day, highest creatinine and bilirubin concentrations, and hospital mortality. During the study period, 7,928 patients had cardiac surgery. Sixteen (0.2%) patients had early bloodstream infection; the control group consisted of 95 patients. Thirteen of the patients with bloodstream infection had Gram-negative bacilli on blood culture, two had Candida species, and two had Gram-positive bacteria. On multivariate logistic regression analysis, greater prevalence of preoperative pulmonary hypertension (odds ratio 9; 95% confidence interval 2 to 41.8; p = .004), diabetes (odds ratio 4.6; 95% confidence interval 1.4 to 15.8; p = .01), number of blood products transfused (odds ratio 1.09; 95% confidence interval 1.04 to 1.17; p = .005), and infusion of inotropes (odds ratio 4.7; 95% confidence interval 1.3 to 16.4; p = .02) or vasopressors (odds ratio 4.1; 95% confidence interval 1.3 to 15.6; p = .02) were associated with postoperative bloodstream infection. Early bloodstream infection was associated with significantly prolonged duration of mechanical ventilation (117.2 +/- 21.5 vs. 18 +/- 8.8 hrs; p = .0001), intensive care stay (213 +/- 27.5 vs. 53 +/- 11.3 hrs; p < .0001), greater creatinine concentrations on the first postoperative day (1.6 +/- 0.1 vs. 1.2 +/- 0.04 mg/dL; p = .0002), greater maximum creatinine concentration (2.4 +/- 0.2 vs. 1.3 +/- 0.1 mg/dL; p < .0001), and greater maximum bilirubin concentration (4.7 +/- 0.6 vs. 1.3 +/- 0.2 mg/dL; p < .0001) when compared with the control group. Five (32%) of 16 bacteremic patients died vs. none of the 95 control patients (p < .0001). CONCLUSIONS: Early bloodstream infection after cardiac surgery is uncommon and involves predominantly Gram-negative bacteria. The risk factors associated with bloodstream infection were preoperative morbidity and more complex surgery. Bloodstream infection was associated with a significantly adverse impact on outcome after cardiac surgery.
OBJECTIVE: To determine the predictors of outcome in cardiac surgical patients with prolonged ICU stay. DESIGN: Inception cohort with retrospective chart review. SETTING: Adult cardiovascular ICU. PATIENTS: All patients admitted after cardiac surgery who stayed in ICU for at least 14 consecutive days. INTERVENTIONS: Collection of data, including preoperative demographics, comorbidity, routine laboratory testing, surgical procedure, duration of cardiopulmonary bypass and aortic cross-clamping, postoperative requirement for transfusion and intra-aortic balloon counterpulsation, and postoperative indexes of organ dysfunction 14 and 28 days after surgery. An organ failure score (OFS) was calculated for days 1, 14, and 28. OUTCOME MEASURES: Hospital mortality. RESULTS: One hundred forty-one of 324 (43.5%) ICU admissions lasting at least 14 days resulted in hospital mortality. Seventy-four of 166 (45%) ICU admissions lasting at least 28 days resulted in hospital mortality. Preoperative demographics, morbidity, and indexes of organ failure in the first 24 h after surgery were not predictive of hospital mortality. Indexes of organ failure predictive of hospital death at 14 days included requirement for epinephrine infusion, diminished Glasgow coma scale, requirement for dialysis, greater value of BUN, lower value of creatinine, greater value of bilirubin, greater value of arterial PCO2, lower platelet count, and lower value of serum albumin. After a 28-day stay in ICU, the indexes of organ failure predictive of hospital mortality included requirement for dopamine or norepinephrine infusions, diminished Glasgow coma score, greater value of bilirubin, greater value of arterial PCO2, lower value of serum albumin, and advanced age. The area under the receiver operating characteristic curve for the OFS on day 1 was 0.55+/-0.04 (p=0.12), on day 14 it was 0.75+/-0.03 (p<0.0001), and on day 28 it was 0.76+/-0.04 (p<0.0001). CONCLUSION: Preoperative health status and early organ failure were not predictive of late hospital mortality. The pattern of late organ failure associated with hospital mortality changed with time.
The recognition of tissue hypoxia or cumulative oxygen debt is of fundamental importance for triage and resuscitation of critically ill patients during the ¿golden hour¿ in the emergency department (ED). The measurement of central venous blood oxygen saturation, plasma lactate concentration, cardiac output, systemic oxygen transport and use, and non-vital organ oxygenation and function can enhance the detection of systemic and regional hypoperfusion and tissue hypoxia. Systemic and organ-specific oxygenation indices may guide the choice of therapy to optimize resuscitation of the macrocirculation and microcirculation in critically ill ED patients.
To describe the simultaneous responses of systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial blood pressure (MAP), heart rate (HR), shock index (SI = HR/SBP), central venous oxyhemoglobin saturation (ScvO2), and arterial blood lactate concentration (Lact) to resuscitation of critically ill patients in the emergency department (ED), an observational descriptive study was conducted in the ED of an urban teaching hospital. Thirty- six patients admitted from the ED to the medical intensive care unit were studied. Vital signs were measured immediately on arrival to the ED (phase 1). After initial resuscitation and stabilization, ie, HR between 50 and 120 beats/min and MAP between 70 and 110 mm Hg (phase 2), ScvO2 and Lact were measured and additional therapy was given in the ED to increase ScvO2 to > 65% and decrease Lact to < 2 mmol/L, if needed (phase 3). SBP, DBP, MAP, HR. SI, ScvO2, and Lact were measured. Initial resuscitation increased SBP from 103 +/- 39 to 118 +/- 29 mm Hg (P < .05) and MAP from 67 +/- 35 to 82 +/- 22 mm Hg (P < .05) but did not affect DBP (53 +/- 35 to 63 +/- 22 mm Hg, P = NS), HR (110 +/- 26 to 110 +/- 22 beats/min, P = NS) or SI (from 1.3 +/- 0.7 to 1.0 +/- 0.3, P =NS) from phase 1 to phase 2. ScvO2 remained < 65% and/or Lact > 2.0 mmol/L in 31 of 36 patients at phase 2, and additional therapy was required. Lact was decreased (from 4.6 +/- 3.8 to 2.6 +/- 2.5 mmol/L, P < .05) and ScvO2 was increased (from 52 +/- 18 to 65 +/- 13%, P < .05) without significant additional changes in SBP, DBP, MAP, HR, or SI at phase 3. The in-hospital mortality was 14% for this group of patients. It was concluded that additional therapy is required in the majority of critically ill patients to restore adequate systemic oxygenation after initial resuscitation and hemodynamic stabilization in the ED. Additional therapy to increase ScvO2 and decrease Lact may not produce substantial responses in SBP, DBP, MAP, HR, and SI. The measurement of ScvO2 and Lact can be utilized to guide this phase of additional therapy in the ED.
OBJECTIVE: To examine if either nociceptive somatic nerve stimulation or skeletal muscle injury modified systemic hemodynamics and oxygen transport and utilization after resuscitation from hemorrhage in anesthetized pigs. DESIGN: Prospective, randomized, controlled laboratory study. SETTING: Animal laboratory. SUBJECTS: Twenty isoflurane-anesthetized and mechanically ventilated large white pigs. INTERVENTIONS: Three groups of animals were instrumented with femoral arterial and thermodilution pulmonary artery catheters. One group of animals had bilateral brachial nerve electric stimulation before hemorrhage (brachial nerve stimulation + hemorrhage, n = 7). The second group of animals had bilateral hindlimbs skeletal muscle injury induced by firing a captive-bolt handgun with standard charges before hemorrhage (skeletal muscle injury + hemorrhage, n = 6). The third group had neither insult before hemorrhage (control, n = 7). Controlled bleeding was initiated to reduce the cardiac index and systemic oxygen delivery (Do2) by 50% in all animals. Animals were then left for 30 mins before resuscitation. All animals were resuscitated with 4.5% human serum albumin at 45 mL/kg and observed for 2 hrs. MEASUREMENTS AND MAIN RESULTS: Plasma volume, systemic hemodynamics, and oxygen transport variables were measured and calculated after resuscitation. Similar increases of plasma volume and supranormal cardiac index were observed in all groups immediately after resuscitation. The branchial nerve stimulation and hemorrhage group maintained higher heart rate, cardiac index, Do2, and oxygen consumption (Vo2) than the hemorrhage group. In contrast, the skeletal muscle injury and hemorrhage group had lower systemic mean arterial pressure and vascular resistance, and a tendency for decrease in Vo2, than the hemorrhage group, although heart rate, cardiac index, and Do2 were similar in both groups. Hemorrhage increased the arterial plasma lactate concentration, which was later normalized in all groups 60 mins after resuscitation. CONCLUSIONS: Neither nociceptive brachial nerve stimulation nor skeletal muscle injury attenuated the increase in plasma volume, cardiac index, or the repayment of systemic oxygen debt after resuscitation from hemorrhage. Brachial nerve stimulation was associated with augmented cardiac index, systemic Do2, and increased Vo2 requirements related to increased sympathetic nervous system activation. Skeletal muscle injury produced early systemic arterial hypotension and vasodilation, and a decrease in Vo2 that was suggestive of pathologic supply dependency on systemic Do2.
Cardiac ischemia can present as distinctive clinical syndromes such as acute myocardial infarction, cardiogenic shock, sudden cardiac arrest or chronic congestive heart failure. All of the clinical syndromes share common pathophysiological events including reduction of cardiac output and systemic oxygen delivery (DO2) and activation of neurohumoral stress response. The balance between systemic DO2 and oxygen consumption (VO2) is maintained by modification of systemic oxygen utilization and demands which are essential for tissue viability and survival in cardiac ischemic syndromes. Low blood flow and the neurohumoral response may influence cellular metabolism (e.g., acute ischemia preconditioning and chronic downregulation of aerobic metabolism) and microcirculatory perfusion patterns to decrease systemic oxygen demands and VO2 in harmony with low cardiac output and systemic DO2. The clinical relevance of these metabolic adaptations and their influence on the outcome in cardiac ischemic syndromes remains unknown.
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STUDY OBJECTIVE: Shock index (SI) (heart rate/systolic blood pressure; normal range, 0.5 to 0.7) and conventional vital signs were compared to identify acute critical illness in the emergency department. DESIGN: Quasi-prospective study. PATIENTS: Two hundred seventy-five consecutive adults who presented for urgent medical care. INTERVENTIONS: Patients had vital signs, SI, and triage priority recorded on arrival in the ED and then their final disposition. RESULTS: Two groups were identified retrospectively by the SI; group 1 (41) had an SI of more than 0.9, and group 2 (234) had an SI of less than 0.9 on arrival in the ED. Although both groups had apparently stable vital signs on arrival, group 1 had a significantly higher proportion of patients who were triaged to a priority requiring immediate treatment (23 versus 45; P < .01) and required admission to the hospital (35 versus 105; P < .01) and continued therapy in an ICU (10 versus 13; P < .01). CONCLUSION: With apparently stable vital signs, an abnormal elevation of the SI to more than 0.9 was associated with an illness that was treated immediately, admission to the hospital, and intensive therapy on admission. The SI may be useful to evaluate acute critical illness in the ED.