Preoperative risk models for minimally invasive coronary bypass: a preliminary study.

OBJECTIVE: Available risk assessment models are designed for standard coronary artery bypass grafting. We hypothesized that minimally invasive coronary bypass could improve on predicted outcome in extremely high-risk patients (Parsonnet score > 20%) by the current risk models. METHODS: From September 1996 to September 1997, 27 consecutive extremely high-risk patients underwent minimally invasive coronary bypass. Seventeen patients were male; age was 73 +/- 12 years, and 63% of patients were older than 75 years. Left ventricular ejection fraction was 33.7% +/- 15% and 63% had an ejection fraction of less than 35%. The predicted 30-day mortality according to the System 97 model was 25.6% +/- 11.3%. The Parsonnet risk score was 36.2% +/- 11%; the predicted length of stay in the hospital was 15.3 +/- 3 days. The predicted risk of stroke according to the Multicenter Perioperative Stroke Risk Index was 22.3% +/- 11.7%. RESULTS: Minimally invasive coronary bypass was isolated in 20 patients and integrated with angioplasty and stenting in 7 patients. The observed 30-day mortality was 0% (P < .01 vs predicted): at an average follow-up of 10.8 +/- 4.1 months, 26 patients (96.3%) are alive without angina; one patient with acquired immunodeficiency syndrome died on postoperative day 40 of acute pancreatitis. No patient had a stroke or neurologic deficit (P < .01 vs predicted). Patency of internal thoracic artery anastomosis was confirmed by angiography in all 27 patients. No patient required reoperation. Eighteen patients (67%) were extubated in the operating room. The observed length of hospital stay after minimally invasive coronary bypass was 3.8 +/- 2.6 days (P < .01 vs predicted). CONCLUSION: On the basis of our results on a relatively small series of patients, we suggest that risk models geared for standard coronary bypass grafting may not be appropriate for minimally invasive coronary bypass.

Hypotension.

Advanced practice nurses are responsible for diagnosing and treating patients with acute onset hypotension. The potential diagnostic hypotheses for hypotension are related to a wide variety of pathophysiologic processes. These processes are represented by the acronym VINDICATE--Vascular (and cardiac), Inflammatory, Neoplastic, Degenerative, Intoxication/Iatrogenic, Congenital, Allergic/Autoimmune, Traumatic, Endocrine/Metabolic However, acute onset hypotension experienced by the adult patient in the hospital is likely to be caused by the vascular (and cardiac) processes of absolute hypovolemia, relative hypovolemia, and pump failure. Developing the differential diagnosis for acute onset hypotension involves making a series of clinical decisions in a stepwise manner. The clinician bases these decisions on information contained in a subjective and objective database and on recognizing patterns in the central findings. However, treatment of hypotension may be necessary before or during the diagnostic process, depending on the severity of the patient's symptoms.

Reperfusion injury in single-lung transplant recipients with pulmonary hypertension and emphysema.

BACKGROUND: The early postoperative course of single-lung transplant recipients depends on the recipient's underlying lung pathophysiology and the degree of ischemic-reperfusion injury. We examined the effect of pulmonary hemodynamics and preoperative diagnosis on early allograft function and the effects of pulmonary hemodynamics, allograft blood flow, and chest radiographs on length of mechanical ventilation and intensive care unit length of stay. METHODS: We retrospectively collected data on 30 single-lung transplant recipients, 15 each with pretransplantation pulmonary hypertension and emphysema. Blood flow to the allografts was quantitated by perfusion scans obtained on the first postoperative day. Chest radiographs were graded for reperfusion injury. Pulmonary and hemodynamic data, gas exchange parameters, duration of mechanical ventilation, and intensive care unit stay were recorded. RESULTS: Patients with pulmonary hypertension had a prolonged intensive care unit stay compared with emphysema patients, but pulmonary artery pressures were not quantitatively related to duration of ventilation during the intensive care unit stay. There was no difference in the severity of allograft infiltrate between the emphysema and pulmonary hypertensive patients. The day 1 chest radiograph score was highly predictive of an intensive care unit stay of > or = 7 days, although the threshold score of those with pulmonary hypertension was significantly lower than in emphysema patients. Allograft blood flow and pulmonary hypertension were not contributors to early graft dysfunction. Allograft perfusion decreased with increasing radiographically demonstrated infiltrate in those with emphysema but not in those with pulmonary hypertension. CONCLUSIONS: Elevated allograft blood flow and pressures do not exacerbate radiographically confirmed reperfusion injury. Reperfusion injury is the major cause of early respiratory morbidity after single-lung transplantation. Allograft perfusion in emphysema patients decreases in response to reperfusion injury, but pulmonary hypertension patients remain almost entirely dependent on allograft function, even with severe chest radiograph scores. This may be an important mechanism by which single-lung transplant recipients with emphysema, unlike those with pulmonary hypertension, are able to mitigate the degree of respiratory impairment associated with reperfusion injury.

Successful management of secondary aortoesophageal fistula.

Aortoesophageal fistula is a rare complication after thoracic aortic aneurysm repair. Six previously reported cases of aortoesophageal fistula management have been uniformly fatal. We present our successful management and review the literature of this topic.

Respiratory care of the postoperative lung transplantation patient.

The management of patients receiving lung transplantation has been evolving during the last thirty years. Transplant programs have continued to develop both in United States and internationally. Patient evaluations and experiences with procedures help guide the decision as to which type of transplant would best benefit the patient. To care for lung transplantation patients, nurses need an understanding of the alterations in physiology from the procedure. An understanding of the clinical experiences in the areas of immunosuppression, preoperative conditioning, surgical techniques, preservation techniques, ventilatory management, and nursing care have made significant contributions to patient survival.

Predicting ICU length of stay following single lung transplantation.

STUDY OBJECTIVE: The aim was to identify potential predictors of ICU length of stay (LOS) for single lung transplant patients. DESIGN: Retrospective chart review. SETTING: University medical center. PATIENTS: All single lung transplant recipients for 1992 and 1993 at our institution. RESULTS: Data were collected from 69 patients. The median ICU LOS was 5 days, and this was highly correlated with the duration of mechanical ventilation. The mean acute physiology and chronic health evaluation (APACHE II) score was 10. Patients with pulmonary hypertension had the longest ICU LOS. Similarly, patients with a measured transpulmonary gradient of 20 mm Hg or less had a significantly shorter ICU LOS. Patients with an immediate postoperative PaO2/fraction of inspired oxygen (FIo2) ratio greater than 200 mm Hg and a flow mismatch between the two lungs of 30% or less also had a significantly shorter ICU LOS. Positive and negative predictive values for the immediate postoperative PaO2/FIo2 ratio of 200 mm Hg or less were 77% for an ICU LOS greater than 5 days, and the calculated receiver operating characteristic (ROC) curve area was 0.74. CONCLUSION: Overall, the immediate postoperative PaO2/FIo2 ratio of 200 mm Hg or less had the best positive and negative predictive values as well as the highest ROC curve area for predicting an ICU LOS greater than 5 days.

Use of bronchial blocker to improve gas exchange in respiratory failure and differential lung disease.

The use of bronchial blocker to optimize gas exchange in a patient with marked differential lung disease is reported. This technique proved to be a useful alternative in an ICU setting to independent lung ventilation.

ECMO support for adult patients with acute respiratory failure.

The authors analyzed factors that may influence the outcome of adult patients with respiratory failure who were treated with ECMO. Between December 1990 and July 1995, the authors used ECMO to support 33 patients (age range, 17-56 years) with respiratory failure from adult respiratory distress syndrome (ARDS; n = 9), primary graft failure after lung transplantation (n = 16), late graft failure after lung transplantation (n = 5), and miscellaneous reasons (n = 3). Twenty (61%) patients were successfully weaned from ECMO, and 13 (39%) survived to hospital discharge. Venoarterial ECMO was used in 46% of survivors, compared with 60% of nonsurvivors (p = 0.43). The time on mechanical support before ECMO and the duration on ECMO for survivors and nonsurvivors was 2.9 +/- 1.8 days vs 5.0 +/- 1.3 days (p = 0.35), and 6.5 +/- 1.8 days vs 5.7 +/- 1.1 days (p = 0.68), respectively. Compared with the nonsurvivors, survivors had higher PF ratios (PaO2/FIO2; 104 +/- 33 vs 81 +/- 8, p = 0.43) before ECMO was initiated, although the differences were not significant. Among the patients who received ECMO for primary graft failure, 75% were weaned from ECMO, and 56% survived to discharge. ECMO is beneficial for adult patients with respiratory failure, especially those with primary graft failure after lung transplantation.

Mechanical circulatory assist devices.

A ventricular assist device (VAD) is a heterotopic mechanical pump that augments or replaces the output of a failing ventricle. In the past decade, investigation and use of these devices has greatly improved our understanding of their potential roles and limitations. Successful univentricular and biventricular support has allowed for myocardial recovery and survival in several settings of intractable cardiogenic shock. The development of long-term VADs has allowed for successful bridging of patients to heart transplantation, and it has laid the groundwork for a permanent implantable replacement ventricle. In this review, we address indications, complications, management, and results of mechanical support in postcardiotomy, bridge to recovery, and bridge to transplantation settings. The tools to achieve ventricular support in the United States, and the VADs themselves, are described, with emphasis on unique features, indications, and limitations.

Neutrophil attractant protein-1 and monocyte chemoattractant protein-1 in human serum. Effects of intravenous lipopolysaccharide on free attractants, specific IgG autoantibodies and immune complexes.

We recently found that normal human sera contain IgG antibodies against two chemoattractants, neutrophil attractant protein-1 (NAP-1/IL-8) and monocyte chemoattractant protein-1 (MCP-1), as well as immune complexes of these proteins. Intravenously administered LPS was reported to cause a sharp rise in serum NAP-1 concentration. Our study was designed to determine if LPS also caused an increase in MCP-1 and to measure associated changes in concentrations of antibody and immune complex. LPS caused a rise to peak within 2 to 3 h in serum concentrations of free NAP-1 and MCP-1, followed by an almost equally rapid fall toward base-line levels by about 5 h postinjection. MCP-1 concentration in sera from the 11 subjects rose to a peak of 330 +/- 52 pM. The peak value for NAP-1 was 80 +/- 11 pM. In 10 of the 11 subjects, free IgG autoantibody to MCP-1 decreased from a mean pre-LPS value of 1820 +/- 660 pM to a mean low of 53% of the respective initial values. Corresponding data for IgG anti-NAP-1 were a pre-LPS concentration of 216 +/- 7 pM, which decreased to a mean low of 44% of the respective initial values. The finding in some subjects of a rapid rise in free antibody after the nadir suggests the possibility of acute regulation of autoantibody secretion rates. Although the results suggested that LPS-induced chemoattractant combined with free antibody, serum concentrations of MCP-1-IgG or NAP-1-IgG did not increase, which points to an as yet unknown mechanism for trapping and elimination of the immune complexes.

Compartmentalization of the acute cytokine response in humans after intravenous endotoxin administration.

Lung cytokine production was examined after the intravenous administration of endotoxin to 23 normal human subjects. Bronchoalveolar lavage (BAL) was performed 7 days before and 1.5 or 5 h after endotoxin (4 ng/kg). Cytokine mRNA was evaluated in cell pellets (> 98% macrophages) by use of reverse transcription and the polymerase chain reaction. Immunoreactivity was measured by enzyme-linked immunosorbent assay of 20- to 40-fold concentrated BAL. Interleukin- (IL) 8 was detected in BAL (4-130 pg/ml) but not in the serum at baseline. Few neutrophils were found in BAL (< 1%) despite this IL-8 gradient. Peak serum IL-8 levels occurred 2 h after endotoxin (3,930 +/- 241 pg/ml), but BAL neutrophils and IL-8 did not increase. Peak serum tumor necrosis factor (TNF) levels occurred 1.5 h after endotoxin (1,844 +/- 210 pg/ml), but TNF was detected in only 1 of 20 BAL samples. TNF and IL-8 mRNA were detected by polymerase chain reaction in > 70% of the BAL samples before endotoxin, whereas IL-1 alpha, IL-1 beta, and IL-6 were detected in < 25% of the BAL samples. After endotoxin, no change was detected in cytokine mRNA expression. Actinomycin D treatment of the BAL did not alter the pattern of cytokine mRNA expression. These data suggest that mechanisms exist to insulate the alveolar space from the stimulatory effects of endotoxin and high circulating levels of cytokines. Additional factors appear to control the chemotactic effects of IL-8 on neutrophils in the air spaces during acute systemic inflammation.

Response of man to endotoxin.

Endotoxin, a cell wall component of Gram-negative bacteria, plays a central role in the pathogenesis of septic shock. By administering small doses of intravenous endotoxin to humans, a variety of acute inflammatory responses are induced which are qualitatively similar to those that occur during the early stages of septic shock. Within hours of the administration of intravenous endotoxin to human volunteers, changes occur in systemic hemodynamics, ventricular function, pulmonary gas exchange and permeability. In conjunction with these changes in organ function, a wide variety of inflammatory mediators are released which appear to contribute to these responses. These include the release of proinflammatory cytokines (e.g. tumor necrosis factor-alpha, IL-1 beta, IL-6, IL-8), activation of the fibrinolytic system, kallikrein-kinin generation and phospholipase A2 release. Phagocytic leukocytes are primed for enhanced inflammatory responses following endotoxin administration. Counter-regulatory responses are initiated in parallel and may serve to limit some of the end-organ responses by the inflammatory mediators. This human model provides a unique opportunity to extend previous concepts of acute inflammation and to evaluate the earliest responses activated after exposure to an important bacterial component. Defining the pathways and responses initiated during acute human endotoxemia may allow a better understanding of host responses that are critical to the development of organ dysfunction and shock due to severe infections.