Nonpulmonary Organ Research Articles

Changing pattern of organ dysfunction in early human sepsis is related to mortality.

We examined the pattern of organ system dysfunction, the evolution of this pattern over time, and the relationship of these features to mortality in patients who had sepsis syndrome. Prospective, multicenter, observational study. Intensive care units in tertiary referral teaching hospitals. A total of 287 patients who had sepsis syndrome were prospectively identified in intensive care units. MATERIALS AND MEASUREMENTS: Cardiovascular, pulmonary, neurologic, coagulation, renal, and hepatic dysfunction were assessed at onset and on day 3 of sepsis syndrome. Organ dysfunction was classified as normal, mild, moderate, severe, and extreme dysfunction. We calculated the occurrence rate and associated 30-day mortality rate of organ dysfunction at the onset of sepsis syndrome. We then measured the change in organ dysfunction from onset to day 3 of sepsis syndrome and determined, for individual organ systems, the associated 30-day mortality rate. At the onset of sepsis syndrome, clinically significant pulmonary dysfunction was the most common organ failure, but was not related to 30-day mortality. Clinically significant cardiovascular, neurologic, coagulation, renal, and hepatic dysfunction were less common at the onset of sepsis syndrome but were significantly associated with the 30-day mortality rate. Worsening neurologic, coagulation, and renal dysfunction from onset to day 3 of sepsis syndrome were associated with significantly higher 30-day mortality than with improvement or no change in organ dysfunction. Increased mortality rate in sepsis syndrome is associated with a pattern characterized by failure of nonpulmonary organ systems and, in particular, worsening neurologic, coagulation, and renal dysfunction over the first 3 days. Although initial pulmonary dysfunction is common in patients with sepsis syndrome, it is not associated with an increased mortality rate.

Nonpulmonary organ failure and outcome in children treated with high-frequency oscillatory ventilation

Purpose: The purpose of this study was to quantitate the contribution of nonpulmonary organ failure to mortality of patients treated with high-frequency oscillatory ventilation (HFOV) and to determine which gas-exchange differences are associated with improvement on HFOV. Materials and Methods: Charts of all patients treated with HFOV in our pediatric intensive care unit from January 1992 until January 1997 were retrospectively reviewed. Results: Sixty-six patients were treated and 21 patients improved during HFOV (group 1); 45 patients did not improve (group 2). Seventeen patients (26%) had isolated respiratory failure and their mortality was 12%. Percentages of patients with 2, and 3 or more organ failure were 45%, 29%, and their mortality was significantly higher, 67% and 95%, respectively. Patients with primary respiratory failure demonstrated a significantly greater risk of improvement on HFOV (RR ratio of 2.5, 95% CI 1.5 to 4.2). There was a significantly greater proportion of patients with primary cardiac failure who did not improve on HFOV compared with all other patients. Oxygenation index significantly improved over the first 72 hours for both groups, but then significantly worsened over the next 48 hours in group 2 but not in group 1. Conclusion: Patients with nonpulmonary organ failure were significantly less likely to improve on HFOV and had a significantly higher mortality than patients with isolated respiratory failure. Children who do not improve on HFOV appear to reach a plateau in oxygenation indices after 3 days of HFOV. Copyright © 2000 by W.B. Saunders Company

EFFECT OF SEVERE SMOKE INHALATION INJURY ON SYSTEMIC MICROVASCULAR BLOOD FLOW IN SHEEP

Multiple nonpulmonary organ dysfunction is frequently associated with acute lung injury; however, the mechanisms underlying the pathogenesis of this process are not completely understood. Decreased oxygen delivery to distant organs due to maldistribution of blood flow may be a contributing factor. We examined the effects of acute lung injury induced by smoke inhalation on microvascular blood flow to various organs in sheep. Seven sheep were prepared with arterial, venous, pulmonary artery, and left atrial catheters. After a 5 day recovery period, a tracheostomy was performed, followed by insufflation with 48 breaths of cool cotton smoke. Determination of microvascular blood flow using colored microspheres, standard hemodynamic measures, and blood gas analysis were performed before and at 12 h intervals after smoke inhalation. Animals were resuscitated to maintain left atrial pressure at +/- 2 mmHg of the baseline value and FiO2 was adjusted to maintain Sao2 at > 90%. After 48 h, sheep were killed and an autopsy was performed. Samples of trachea, left ventricle, ileum, colon, spleen, pancreas, and cortex from both kidneys were obtained for determination of microvascular blood flow. Blood flow to the trachea was substantially increased, while blood flow to the kidneys was preserved near baseline levels. Left ventricular blood flow decreased slightly; however, this decline was not statistically significant. Blood flow to ileum, colon, spleen, and pancreas was significantly decreased, particularly at 36 and 48 h after injury. These decreases were independent of changes in cardiac output or systemic oxygen delivery. It is likely that alteration in microvascular blood flow may contribute to the development of nonpulmonary organ dysfunction after acute lung injury.

Probability of survival after prolonged extracorporeal membrane oxygenation in pediatric patients with acute respiratory failure

Extracorporeal membrane oxygenation (ECMO) has been used with increasing frequency for respiratory failure that is unresponsive to conventional therapy. We examined the relationship between duration of ECMO and outcome to understand whether prolonged ECMO (duration of the procedure for > 14 days) was more commonly associated with futile therapy or eventual recovery. A cohort study of all patients reported to the Pediatric ECMO Registry for Acute Respiratory Failure of the Extracorporeal Life Support Organization. Tertiary hospitals (n = 83) capable of providing extracorporeal support for pediatric patients. Children (n = 382) between the ages of 1 wk and 18 yrs of age with severe respiratory failure. Extracorporeal membrane oxygenation. The death or live hospital discharge of ECMO-treated patients, together with the post-ECMO mechanical ventilation course, were examined as a function of duration of ECMO and of pre-ECMO respiratory status. The occurrence of complications and the causes of death were also noted. The criteria used to initiate ECMO, as well as the determination of the futility of further ECMO, were determined by local practice at individual centers. There were 382 patients treated with ECMO, of whom 184 (48%) survived. The proportional survival in the patients treated for the longest duration was similar to the overall group. The cause of death was given for 168 patients: 32 neurologic deaths; nine deaths due to ECMO complications; and 30 deaths due to nonpulmonary organ failure. There were 97 deaths due to elective ECMO termination; 80 of these deaths occurred after the determination of the futility of anticipating pulmonary recovery. The latter deaths occurred at widely varying durations of ECMO, with a median of 282 hrs. However, at that same duration, 47 eventual survivors (26% of all survivors) continued to receive ECMO. By discriminant analysis, the survival rate was independently related (r2 = .18; p < .0001) to peak ventilator inspiratory pressure before ECMO and duration of intubation before ECMO, patient age, and the occurrence of several complications. While the survival rate in pediatric patients receiving ECMO appears related to the severity of lung disease and to the occurrence of ECMO complications, the survival rate in patients treated with ECMO courses of > 2 wks was similar to the survival rate of patients treated for shorter periods of time. ECMO was terminated in some patients for pulmonary futility at durations of ECMO associated with survival in substantial numbers of patients in whom ECMO was continued.

Frequency and importance of barotrauma in 100 patients with acute lung injury.

To determine the occurrence rate of barotrauma in acute lung injury patients, whether barotrauma is an independent risk factor for mortality, and the role of barotrauma in the outcome of those patients who died. Prospective, cohort study. Intensive care units at a university hospital. Consecutive adult patients (n = 100) meeting the usual criteria for a diagnosis of acute lung injury requiring mechanical ventilation. Barotrauma occurred in 13 (13%) of 100 patients. Mortality rates were not different in patients with (76%) and without (64%) barotrauma. Using univariate analysis, barotrauma was not associated with increased mortality (odds ratio 1.85; confidence interval 0.42 to 9.20; p = .53). However, when barotrauma was incorporated into a logistic regression model, along with other potential predictors of mortality, barotrauma was associated with increased mortality (odds ratio 6.15; confidence interval 1.11 to 33.9; p = .017). The presence of nonpulmonary organ dysfunction and sepsis was strongly associated with mortality. In the setting of barotrauma, the mortality rate was 100% if associated with two or more nonpulmonary organ dysfunctions compared with a mortality rate of 40% with one or no nonpulmonary organ failure. Barotrauma contributed directly to the cause of death in only one patient. Barotrauma occurred in only 13% of patients with acute lung injury. Barotrauma was an independent marker of mortality when adjusted for other predictors of mortality. However, barotrauma directly contributed to < 2% of all deaths. We hypothesize that barotrauma is an indication of severity of acute lung injury rather than a major cause of increased mortality.

Circulating xanthine oxidase mediates lung neutrophil sequestration after intestinal ischemia-reperfusion.

Injury to nonpulmonary organ systems often initiates systemic processes that cause recruitment of neutrophils to the lung. We found that rats subjected to intestinal ischemia-reperfusion (I/R) had increased transvascular leak of 125I-labeled albumin into lungs and decreased lung ATP levels (P less than 0.05). In addition, rats subjected to intestinal I/R had increased plasma xanthine oxidase (XO) activity, plasma leukotactic activity for neutrophils, and lung neutrophil retention (assessed by morphometry and myeloperoxidase activity) compared with sham-treated rats (P less than 0.05). By comparison, after intestinal I/R, rats fed an allopurinol- or tungsten-enriched diet had decreased plasma and intestinal XO activities, decreased plasma leukotacic and lung myeloperoxidase (MPO) activities, decreased lung leak, and increased lung ATP levels compared with rats fed control diets (P less than 0.05). Further studies suggested a more specific role for circulating rather than tissue XO in mediating lung neutrophil accumulation but not lung leak. Plasma XO, plasma leukotactic, and lung MPO activities, but not lung leak, increased in rats administered purified XO intravenously. In addition, plasma XO, plasma leukotactic, and lung MPO activities, but not lung leak, decreased in rats administered antisera against XO and then subjected to intestinal I/R. We conclude that circulating XO increases acutely and may contribute to pulmonary retention of neutrophils after an ischemic intestinal insult.

The Effects of Prostaglandin E1 on Non-Pulmonary Organ Function During Clinical Acute Respiratory Failure

The Effects of Prostaglandin E1 on Non-Pulmonary Organ Function During Clinical Acute Respiratory Failure

Increased Intestinal Protein Permeability in a Model of Lung Injury Induced by Phorbol Myristate Acetate

Multiple nonpulmonary organ failure is a frequent complication of the adult respiratory distress syndrome (ARDS), and contributes significantly to the high mortality rate associated with this disorder. Although previous studies suggest that systemic organ injury may be an integral component of ARDS, little is known about the specific functional alterations that occur in these target organs. The present study was designed, therefore, to test the hypothesis that endothelial damage, as assessed by microvascular permeability changes, develops in systemic organs in a model of acute lung injury. To test this postulate, the microvascular permeability for total protein was estimated using the steady-state relationship between the lymph (CL) to plasma (Cp) protein concentration ratio (i.e., CL/Cp) and lymph flow in autoperfused cat ileum preparations. Specifically, CL/Cp was measured in five cats, 2 h after acute lung injury was induced by intravenously administered phorbol myristate acetate (PMA), 15 micrograms/kg, and the results were compared with those of seven time-matched control animals. Prior to PMA infusion, the PaO2/FIO2 ratio was 451 +/- 28 in both groups and remained unchanged (486 +/- 26) in the control group. By contrast, the PaO2/FIO2 ratio fell to 275 +/- 95 after PMA infusion (p less than 0.05). In addition, whereas CL/Cp was 0.099 +/- 0.008 in the control animals, it increased to 0.36 +/- 0.06 in the PMA-injured animals (p less than 0.01). In summary, this study demonstrated that in this model of acute lung injury produced by PMA-induced activation of circulating inflammatory cells, both acute lung injury and systemic organ injury (i.e., morphologic and permeability alterations) occurred.

The Adult Respiratory Distress Syndrome: Definition and Prognosis

This article provides an expanded definition of acute lung injury and the adult respiratory distress syndrome and describes the value of using this definition for establishing prognosis by discussing the basis for the acute lung injury scoring system, the various clinical disorders that may be associated with acute lung injury and how they affect outcome, and the influence of nonpulmonary organ failure on the outcome of patients with acute lung injury.

Laboratory models of sepsis and septic shock

That there are so many models of sepsis and septic shock is tacit evidence that none of them are perfect. Although sepsis presents in many forms clinically, most clinicians would probably agree that virtually all severely septic patients manifest respiratory failure and ventilator dependence. Furthermore, failure of organs other than the lungs typically occurs days to weeks after the onset of the septic process. Although early deaths occur commonly in some situations (e.g., meningococcemia, pneumococcal bacteremia in asplenic individuals, Gram-negative bacteremia in the setting of profound granulocytopenia), most deaths due to sepsis occur after a protracted course in an intensive care unit. Thus, for certain important experiments, there is a need for an animal model of severe chronic sepsis characterized by these features: persistent hypermetabolism, low systemic vascular resistance, respiratory failure severe enough to require mechanical ventilation, late (nonpulmonary) organ system failure, and death. Obviously, creation of such a model will require a major commitment of resources, because it will require, in essence, the creation of an animal intensive care unit. Nevertheless, we believe that progress in sepsisrelated research would be substantially facilitated were such a model available. Even without such a model, progress will continue in this field. A wide variety of good animal models are already available to investigators. In the next decade, as new methods, such as the powerful tools of molecular biology, are applied to problems related to the sepsis syndrome, these models will be invaluable in improving our understanding of pathophysiology and in developing new and more effective approaches toward therapy.

Elevated von Willebrand factor antigen is an early plasma predictor of acute lung injury in nonpulmonary sepsis syndrome.

In this prospective study of 45 patients, we tested the hypothesis that markedly elevated levels of plasma von Willebrand antigen (vWf-Ag) a marker of endothelial cell injury, might predict the development of acute lung injury in patients with nonpulmonary sepsis syndrome. Acute lung injury was quantified on a four-point scoring system. At the time of entry into the study, none of the 45 patients had evidence of lung injury. Subsequently, 15 patients developed lung injury and 30 patients did not develop lung injury. The mean plasma vWf-Ag level was markedly elevated in the 15 patients who developed lung injury compared with the 30 patients who did not develop lung injury (588 +/- 204 vs. 338 +/- 196, percentage of control, P less than 0.01). Furthermore, a plasma vWf-Ag level greater than or equal to 450 was 87% sensitive and 77% specific for predicting the development of acute lung injury in the setting of nonpulmonary sepsis. In addition, the combination of a plasma vWf-Ag greater than 450 and nonpulmonary organ failure at the time of entry into the study had a positive predictive value of 80% for acute lung injury. Also, a plasma vWf-Ag level greater than 450 had a positive predictive value of 80% for identifying nonsurvivors. Thus, in patients with nonpulmonary sepsis, an elevated level of plasma vWf-Ag is a useful, early biochemical marker of endothelial injury and it has both predictive and prognostic value.

Mechanisms of Multiple Nonpulmonary Organ Failure in ARDS

Since the original description by Asbaugh and colleagues,1 much has been learned about ARDS.2-4 Specifically, ARDS is now recognized to be a catastrophic form of acute lung injury that affects more than 150,000 patients each year.5 Moreover, unlike most lung disorders, there is a propensity for ARDS to afflict previously healthy individuals in a variety of clinical settings, including gastric aspiration, pancreatitis, multiple trauma wounds, and severe bacterial infection.

Multiple Organ Damage Caused by Tumor Necrosis Factor and Prevented by Prior Neutrophil Depletion

The effect of TNF on nonpulmonary multiple organ damage (MOD) was studied. Since polymorphonuclear leukocytes (PMN) are thought to play an important role in septic or TNF-induced MOD, we investigated both neutrophil sufficient (PMN+) and neutropenic (PMN-) guinea pigs. Sepsis was induced by Escherichia coli administration (2 x 10(9)/kg) or recombinant human TNF (1.4 x 10(6) U/kg) was infused into PMN+ and PMN- guinea pigs. During necropsy, the PMN+/TNF and PMN+/E coli animals exhibited marked damage in the adrenal glands, kidneys and liver as evidenced by hemorrhage, congestion, and PMN sequestration on histopathologic examination. There was also increased tissue albumin accumulation in the adrenal glands, kidneys, spleen, heart, and liver as demonstrated by 125I-labeled albumin determinations. In contrast, the PMN-/TNF group did not reveal histopathologic damage in any organ system and there was no abnormal organ accumulation of 125I-albumin. However, in PMN-/E coli animals, marked histopathologic damage in the adrenal glands and liver was evident. Furthermore, there were marked accumulations of 125I-albumin in the adrenals, heart, kidneys, liver, and spleen. Moreover, the PMN-/E coli guinea pigs had a much greater accumulation (p less than 0.01) of 125I-albumin in the kidneys than any other group including the PMN+/E coli group. Thus, nonpulmonary MOD in guinea pigs is caused by TNF administration and can be prevented by PMN depletion. However, while E coli administration also caused marked nonpulmonary MOD in neutrophil sufficient guinea pigs, equivalent or greater damage was produced in neutropenic animals. This suggests that while TNF-induced MOD may be primarily mediated by PMN, E coli-induced MOD seems to be mediated by more than PMN.

Neutrophil accumulation and structural changes in nonpulmonary organs after acute lung injury induced by phorbol myristate acetate.

Multiple nonpulmonary organ failure contributes significantly to the high mortality rate associated with the adult respiratory distress syndrome (ARDS). However, little is known about specific structural and/or functional alterations that occur in nonpulmonary organs in this syndrome. Therefore, the present study was designed to test the hypothesis that inflammatory cell infiltration and structural changes occur both in the lungs and in nonpulmonary organs in ARDS. To test this hypothesis, neutrophil accumulation and structural alterations were evaluated in nonpulmonary organs from dogs with acute lung injury produced by intravenous phorbol myristate acetate (PMA) (30 micrograms/kg; n = 5). As expected, morphologic changes were present in the lungs of the PMA-treated animals and included a diffuse neutrophilic pneumonitis with interstitial, vascular, and alveolar components. PMA-treated dogs had significant increases in neutrophils (expressed as PMN/mm2 tissue section area) compared with those in control animals in the following organs: heart, 14 +/- 3 versus 4 +/- 1; brain, 2.5 +/- 0.3 versus 0.7 +/- 0.3; duodenum, 34 +/- 7 versus 10 +/- 2; liver, 397 +/- 16 versus 103 +/- 12 (p less than 0.025, all comparisons). In addition, severe necrosis and inflammation of vessels, sinusoidal thrombosis, and hepatic necrosis were noted in the liver. Like the changes noted in the lung, hepatic lesions appeared to be vascular in origin and were consistent with lesions produced by the intravascular activation of neutrophils. No microscopic lesions were detected in the brain, kidney, duodenum, and heart. Taken together, the finding of concurrent lung injury, liver injury, and nonpulmonary organ neutrophil accumulation suggests the possibility of a common pathway of injury in this model of ARDS.

Ibuprofen Plus Prostaglandin E1 in a Septic Porcine Model of Adult Respiratory Distress Syndrome

Prostaglandin manipulation has been shown to improve pulmonary dysfunction in animal models of acute respiratory distress syndrome. Using our previously reported porcine model of Pseudomonas-induced respiratory failure, we examined the therapeutic effects of a vasodilating prostaglandin, PGE1, and a reversible cyclooxygenase inhibitor, ibuprofen. Forty-two animals were randomized to seven groups: I--ibuprofen; II--PGE1; III--ibuprofen + PGE1; IV--Pseudomonas + ibuprofen; V--Pseudomonas + PGE1; VI--Pseudomonas + ibuprofen + PGE1; VII--Pseudomonas. Ibuprofen significantly improved pulmonary vasoconstriction, pulmonary hypertension, and hypoxemia, as well as increased survival slightly. PGE1 had no effect on pulmonary dysfunction, but prevented the rise in systemic vascular resistance that occurred in untreated, infected animals and animals treated with ibuprofen alone. Combination therapy improved stroke volume index, a measure of nonpulmonary organ function.

Miliary tuberculosis and adult respiratory distress syndrome.

Although, miliary tuberculosis is an unusual cause of severe acute respiratory failure, we describe nine patients with miliary tuberculosis who developed adult respiratory distress syndrome. This complication occurred in seven patients despite treatment with antituberculous drugs. In two patients who developed the syndrome, miliary tuberculosis was diagnosed only at postmortem. The presence of pulmonary hypertension in all cases and disseminated intravascular coagulation in seven cases suggests a possible pathophysiologic relationship with severe pulmonary vascular damage. The high mortality rate (88.8%) was associated with nonpulmonary organ system failure. Miliary tuberculosis should be considered in patients with adult respiratory distress syndrome of unknown etiology, and simple diagnostic procedures such as sputum, bronchial brushing, and gastric examination should be followed by invasive diagnostic procedures to confirm this etiology. Since untreated miliary tuberculosis is usually fatal, early recognition of this disease is of great importance, and specific therapy may play a lifesaving role.

Management of Atelectasis and Pneumonia

Although many of the authors in this book discuss the pathogenesis of lung dysfunction, the review by Demling deserves particular scrutiny. He stretches the pertinent literature over a framework of pulmonary physiology in a fashion that is uniquely readable and understandable. With the breadth of background provided by this article, the reader is ready tor Lewis’ scholarly review of atelectasis and pneumonia and the parallel piece by Weinstein and Skillman on the overall management of respiratory failure. There is no chapter on "acute respiratory distress syndrome" (ARDS) in this book because the term is too vague and ill-defined to be helpful to the clinician. However, for those who recognize a syndrome of diffuse atelectasis combined with interstitial edema at normal hydrostatic pressure, (that is, ARDS) that disorder is discussed in these three articles. Protocols for management of respiratory failure on the surgical service at the Beth Israel Hospital, Boston, and San Francisco General Hospital are presented in this section. A Serious student of respiratory care would do well to compare the similarities and differences of the various protocols presented in this book. Good respiratory care assumes expert management of the other nonpulmonary organ systems. Waxman and Shoemaker present a protocol for such care, with reference to their own methods.

Management of Severe Respiratory Failure

Although many of the authors in this book discuss the pathogenesis of lung dysfunction, the review by Demling deserves particular scrutiny. He stretches the pertinent literature over a framework of pulmonary physiology in a fashion that is uniquely readable and understandable. With the breadth of background provided by this article, the reader is ready tor Lewis’ scholarly review of atelectasis and pneumonia and the parallel piece by Weinstein and Skillman on the overall management of respiratory failure. There is no chapter on "acute respiratory distress syndrome" (ARDS) in this book because the term is too vague and ill-defined to be helpful to the clinician. However, for those who recognize a syndrome of diffuse atelectasis combined with interstitial edema at normal hydrostatic pressure, (that is, ARDS) that disorder is discussed in these three articles. Protocols for management of respiratory failure on the surgical service at the Beth Israel Hospital, Boston, and San Francisco General Hospital are presented in this section. A Serious student of respiratory care would do well to compare the similarities and differences of the various protocols presented in this book. Good respiratory care assumes expert management of the other nonpulmonary organ systems. Waxman and Shoemaker present a protocol for such care, with reference to their own methods.

Management of Postoperative and Posttraumatic Respiratory Failure in the Intensive Care Unit

Although many of the authors in this book discuss the pathogenesis of lung dysfunction, the review by Demling deserves particular scrutiny. He stretches the pertinent literature over a framework of pulmonary physiology in a fashion that is uniquely readable and understandable. With the breadth of background provided by this article, the reader is ready tor Lewis’ scholarly review of atelectasis and pneumonia and the parallel piece by Weinstein and Skillman on the overall management of respiratory failure. There is no chapter on acute respiratory distress (ARDS) in this book because the term is too vague and ill-defined to be helpful to the clinician. However, for those who recognize a syndrome of diffuse atelectasis combined with interstitial edema at normal hydrostatic pressure, (that is, ARDS) that disorder is discussed in these three articles. Protocols for management of respiratory failure on the surgical service at the Beth Israel Hospital, Boston, and San Francisco General Hospital are presented in this section. A Serious student of respiratory care would do well to compare the similarities and differences of the various protocols presented in this book. Good respiratory care assumes expert management of the other nonpulmonary organ systems. Waxman and Shoemaker present a protocol for such care, with reference to their own methods.

The Pathogenesis of Respiratory Failure After Trauma and Sepsis

Although many of the authors in this book discuss the pathogenesis of lung dysfunction, the review by Demling deserves particular scrutiny. He stretches the pertinent literature over a framework of pulmonary physiology in a fashion that is uniquely readable and understandable. With the breadth of background provided by this article, the reader is ready tor Lewis’ scholarly review of atelectasis and pneumonia and the parallel piece by Weinstein and Skillman on the overall management of respiratory failure. There is no chapter on acute respiratory distress (ARDS) in this book because the term is too vague and ill-defined to be helpful to the clinician. However, for those who recognize a syndrome of diffuse atelectasis combined with interstitial edema at normal hydrostatic pressure, (that is, ARDS) that disorder is discussed in these three articles. Protocols for management of respiratory failure on the surgical service at the Beth Israel Hospital, Boston, and San Francisco General Hospital are presented in this section. A Serious student of respiratory care would do well to compare the similarities and differences of the various protocols presented in this book. Good respiratory care assumes expert management of the other nonpulmonary organ systems. Waxman and Shoemaker present a protocol for such care, with reference to their own methods.