Type of Book: A multiauthored textbook for anesthesiologists and others involved in perioperative critical care medicine. The editors, who are affiliated with four major centers for critical care, enlisted contributors under the aegis of the American Society for Critical Care in Anesthesiology. The editors and authors are all well-known experts in their fields.

A 3 year old boy with systemic histiocytosis, diabetes insipidus and a lytic parietal bone lesion experienced episodes of central neurogenic hyperventilation 3 weeks after radiation to the head but was conscious and alert at presentation. At admission, the PaO2 was 133 mmHg, PaCO2 was 8 mmHg and pH 7.65. Magnetic resonance imaging revealed a pontomedullary lesion that resolved during the ensuring year. Central neurogenic hyperventilation has not been described previously as a complication of systemic histiocytosis.

COCKERILL, F. R. III; MULLER, S. R.; ANHALT, J. P.; MARSH, H. M.; FARNELL, M. B.; MUCHA, P.; GILLESPIE, D. J.; ILSTRUP, D. M.; LARSON-KELLER, J. J.; THOMPSON, R. L. Author Information

OBJECTIVE:To determine whether selective decontamination of the digestive tract using oral and nonabsorbable antimicrobial agents and parenteral cefotaxime prevents infection in critically ill patients.DESIGN:Randomized, controlled trial without blinding.SETTING:Surgical trauma and medical intensive care units in a tertiary referral hospital.PATIENTS:One hundred fifty patients admitted to surgical trauma and medical intensive care units during a 3-year interval, whose condition suggested a prolonged stay (greater than 3 days).INTERVENTION:Patients were randomly allocated to an experimental group (n = 75) that received cefotaxime, 1 g intravenously every 8 hours for the first 3 days only, and oral, nonabsorbable antibiotics (gentamicin, polymyxin, and nystatin by oral paste and oral liquid) for the entire stay in the intensive care unit. Control patients (n = 75) received usual care.MEASUREMENTS:The number of infections, total hospital days, and deaths, as well as the number of days in intensive care unit, were recorded.RESULTS:Control patients experienced more infections (36 compared with 12, P = 0.04), including bacteremias (14 compared with 4, P = 0.05) and pulmonary infections (14 compared with 4, P = 0.03). Although total hospital days, days in intensive care, and the overall death rate all were lower in the treatment group, these differences were not statistically significant. Clinically important complications of selective decontamination of the digestive tract were not encountered.CONCLUSIONS:Selective decontamination of the digestive tract decreases subsequent infection rates, especially by gram-negative bacilli, in selected patients during long-term stays in the intensive care unit.

Liver sections removed from phenobarbital induced rats 24 to 48 hours after a 2 hour exposure to 1.0% halothane with 10% oxygen and subjected to immunocytochemical treatment showed evidence of centrilobular damage as well as evidence of the production of a protein which has immunoreactivity with anti HSP 72 antibodies. The cells showing evidence of immunoreactivity were within the area of the centrilobular lesion. The level of immunoreactive protein varied directly with the intensity of the lesion. Liver sections from animals treated with phenobarbital alone, phenobarbital plus 10% oxygen, or phenobarbital plus 20% oxygen and 1.0% halothane all were without lesions as well as the immunoreactive protein.

To determine the extent to which glucose oxidation measured by indirect calorimetry reflects glucose oxidation measured isotopically, subjects were studied during a 6-h hyperinsulinemic euglycemic clamp (1 mU.kg-1.min-1) and during infusion of saline. [6-14C]glucose was infused on both occasions. Breath was collected for determination of the specific activity of carbon dioxide, oxygen consumption, and carbon dioxide production. Glucose turnover during hyperinsulinemia was approximately eightfold higher than during saline infusion. During the final 1.5 h of the hyperinsulinemic glucose clamp, oxidation measured isotopically remained slightly but consistently lower (P less than 0.05) than that measured by indirect calorimetry (13.8 +/- 1.1 vs 16.5 +/- 1.7 mumol.kg-1.min-1, respectively). In contrast, during the saline infusion, glucose oxidation measured isotopically did not differ from that measured by indirect calorimetry (8.3 +/- 0.6 vs 7.2 +/- 2.8 mumol.kg-1.min-1, respectively). We conclude that although net glucose oxidation measured isotopically was slightly lower than that measured by indirect calorimetry, both techniques provide similar estimates of glucose oxidation over a wide range of glucose disposal.

The use of a differential quantitative blood culture technique (Isolator) to diagnose intravascular-device-related bacteremia (IDRB) was studied prospectively. During septic episodes in 44 patients, blood was obtained simultaneously through the suspected infected device and from a peripheral venipuncture. The blood samples were processed by the Isolator technique, which enables easy quantification of microorganisms. The cannula was removed, and its tip was cultured semiquantitatively. Of the 52 cannulas studied, 15 were the cause of IDRB, but only 7 of these showed a significantly higher bacterial count in blood obtained through the device compared with peripheral blood. The bacterial count was higher in blood drawn through the device than in peripheral blood in four of six cases that did not fulfill the definition of IDRB. Some blood cultures obtained through the device were positive despite negative cultures of peripheral blood and cannula tips (six cannulas). Quantitative blood cultures were not useful in diagnosing IDRB in this study.

We conducted studies to determine whether the Mayo whole-body counter could be used to measure body potassium, and thus lean body mass (LBM), and whether moderate obesity alters resting energy expenditure when corrected for LBM. Twenty-four nonobese and 18 moderately obese adults underwent body potassium (40K) counting, as well as tritiated water space measurement and indirect calorimetry. LBM values predicted from 40K counting and tritiated water space measurements were highly correlated (P = 0.001; r = 0.88). Resting energy expenditure was closely related to LBM (P less than 0.0001; r = 0.78): kcal/day = 622 kcal + (LBM.20.0 kcal/kg LBM). In this relationship, the obese subjects did not differ from nonobese subjects. In summary, the Mayo whole-body counter can accurately measure LBM, and moderate obesity has no detectable effect on corrected resting energy expenditure.

A retrospective review of Mayo Clinic records through 1983 revealed 84 patients (24 male and 10 female; mean age, 41 years) with the diagnosis of pulmonary alveolar phospholipoproteinosis. The major clinical features were dyspnea, cough, fever, and chest pain. Chest roentgenograms usually showed bilateral symmetric alveolar infiltrates, but asymmetric, unilateral, and chronic patchy patterns were also noted. Diagnosis was established by thoracotomy-lung biopsy in 26 patients. Histologic analysis revealed uniform filling of the alveoli by periodic acid-Schiff-positive material and maintenance of normal alveolar architecture. Electron microscopy showed enlarged alveolar macrophages with lamellar osmiophilic inclusions, dense granules, and myeloid bodies. Of the 21 patients who underwent therapeutic bronchoalveolar lavage, 13 had no recurrence of the disease during a mean follow-up of 8.8 years. In patients who underwent pulmonary function testing both before and after lavage, significant restrictive dysfunctions present before the procedure were alleviated afterward. Three deaths occurred among the 34 patients. Pulmonary alveolar phospholipoproteinosis may result from defective clearance of phospholipids by the alveolar macrophages, excessive production of phospholipids by type II pneumocytes, or both. It is likely a nonspecific response to a variety of injuries to the alveolar macrophage or type II pneumocyte or both, including exposure to certain dusts and chemicals and occurrence of hematologic diseases or infections. The uncommon occurrence of this disorder suggests individual susceptibility.

The sections in this article are: 1 Effects of Anesthesia on the Chest Wall 1.1 Anesthesia With Spontaneous Breathing 1.2 Anesthesia-Paralysis With Mechanical Ventilation of the Lungs 2 Effects of Anesthesia on FRC 3 Effects of Anesthesia on Pressure-Volume Relationships 3.1 Total Respiratory System 3.2 Lungs 3.3 Chest Wall 3.4 Mechanisms for Changes in Pressure- Volume Relationships 4 Effects of Anesthesia on Pressure-Flow Relationships 5 Effects of Anesthesia on Intrapulmonary Inspired-Gas Distribution 5.1 Anesthesia With Spontaneous Breathing 5.2 Anesthesia-Paralysis With Mechanical Ventilation of the Lungs 6 Conclusions

This book aims to be a complete, state-of-the-art text on monitoring and to provide a general reference source for the field. It has, in general, accomplished these goals and will be a useful addition to most anesthesia and critical-care reference libraries. The information included will be of interest to both residents and consultants.

On earth, human beings live under the influence of gravity. The orientation of gravity to the body may be altered by change in body position, which in turn alters cardiopulmonary function. Despite the well-recognized effects of gravity, postural changes in symptoms are often neglected by the clinician. An interesting series of case reports, which appear in this issue of the Proceedings (pages 221 to 231), deals with such symptoms—namely, platypnea and orthodeoxia. These terms, originally coined by Robin and co-workers,1Altman M Robin ED Platypnea (diffuse Zone I phenomenon?).N Engl J Med. 1969; 281: 1347-1348Crossref PubMed Scopus (94) Google Scholar, 2Robin ED Laman D Horn BR Theodore J Platypnea related to orthodeoxia caused by true vascular lung shunts.N Engl J Med. 1976; 294: 941-943Crossref PubMed Scopus (165) Google Scholar are defined, respectively, as dyspnea and hypoxemia occurring in the upright position (sitting or standing) but not in the recumbent position. Dyspnea occurring in one recumbent position but not in others is termed “trepopnea.” In the clinician's mind, postural changes in the degree of cyanosis and dyspnea are most commonly associated with tetralogy of Fallot. William Hunter3Hunter W Three cases of mal-formation in the heart.Med Obs Inq Soc Phys Lond. 1784; 6: 291-309Google Scholar in 1784 described such changes in one patient in graphic detail, but it remained for Helen Taussig4Taussig HB Congenital Malformations of the Heart. Commonwealth Fund, New York1947Google Scholar to point out that most patients with tetralogy of Fallot show spontaneous preference for certain postures in which their cyanosis and dyspnea are minimized. The possible hemodynamic mechanisms underlying these postural effects on the degree of cyanosis and dyspnea in patients who have tetralogy of Fallot were later examined by using cardiac catheterization and oximetry.5Hamilton WF Winslow JA Hamilton Jr, WF Notes on a case of congenital heart disease with cyanotic episodes.J Clin Invest. 1950; 29: 20-27Crossref PubMed Scopus (5) Google Scholar, 6Lurie PR Postural effects in tetralogy of Fallot.Am J Med. 1953; 15: 297-306Abstract Full Text PDF PubMed Scopus (12) Google Scholar Two mechanisms contribute to the increased cyanosis that occurs when patients with right-to-left intracardiac shunts assume the erect posture. 1.A change in the pressure gradient between right and left atria produces a right-to-left shunt or increases the magnitude of an existing shunt. Such a change in the pressure gradient can result from an increase in the impedance of the pulmonary circulation relative to the systemic circulation or from an alteration in the position of the two atria relative to each other.2.The saturation of mixed venous blood decreases with an unchanged right-to-left shunt fraction, as may occur if total cardiac output decreases in the presence of unchanged oxygen consumption. Postural cyanosis and dyspnea have also been reported in association with patent foramen ovale in patients who have sustained thoracic trauma7Wright JL Burchell HB Kirklin JW Wood EH Congenital displacement of the tricuspid valve (Ebstein's malformation): report of a case with closure of an associated foramen ovale for correction of the right-to-left shunt.Proc Staff Meet Mayo Clin. 1954; 29: 278-284PubMed Google Scholar or who have undergone pneumonectomy.8Schnabel Jr, TG Ratto O Kirby CK Johnson J Comroe Jr, JH Postural cyanosis and angina pectoris following pneumonectomy: relief by closure of an interatrial septal defect.J Thorac Surg. 1956; 32: 246-250PubMed Google Scholar In these patients, the underlying mechanisms are less clear. A change in the position of the two atria relative to each other when the patient shifts from the supine to the erect posture has been suggested as a possible factor. Such a change of atrial position may increase blood flow from the nondependent right atrium to the dependent left atrium by increasing the hydrostatic force. A similar mechanism may be responsible for the increase in cyanosis when such patients turn from the right to the left lateral decubitus position. Other mechanisms may include distortion of the atrial septum with change in position, which would alter the size of the atrial septal defect.8Schnabel Jr, TG Ratto O Kirby CK Johnson J Comroe Jr, JH Postural cyanosis and angina pectoris following pneumonectomy: relief by closure of an interatrial septal defect.J Thorac Surg. 1956; 32: 246-250PubMed Google Scholar Preferential streaming of blood from the inferior vena cava through an atrial septal defect may also contribute to hypoxemia by deflecting blood from the right to the left atrium, even in the presence of normal or low pressures in the right side of the heart.9Winters Jr, WL Cortes F McDonough M Tyson RR Baier H Gimenez J Davila JC Venoarterial shunting from inferior vena cava to left atrium in atrial septal defects with normal right heart pressures: report of two cases.Am J Cardiol. 1967; 19: 293-300Abstract Full Text PDF PubMed Scopus (33) Google Scholar Postural hypoxemia can also occur in the absence of right-to-left intracardiac shunts, in association with hepatic disease10Wolfe JD Tashkin DP Holly FE Brachman MB Genovesi MG Hypoxemia of cirrhosis: detection of abnormal small pulmonary vascular channels by a quantitative radionuclide method.Am J Med. 1977; 63: 746-754Abstract Full Text PDF PubMed Scopus (151) Google Scholar or with acute11Douglas WW Rehder K Beynen FM Sessler AD Marsh HM Improved oxygenation in patients with acute respiratory failure: the prone position.Am Rev Respir Dis. 1977; 115: 559-566PubMed Google Scholar or chronic1Altman M Robin ED Platypnea (diffuse Zone I phenomenon?).N Engl J Med. 1969; 281: 1347-1348Crossref PubMed Scopus (94) Google Scholar pulmonary disease. Underlying mechanisms include posturally induced increases in right-to-left intrapulmonary shunting (through arteriovenous malformations, spider nevi, or other unusual vascular channels in the basal portion of the lung) and posturally induced increases in the ventilation-perfusion mismatching, with an increase in blood flow to regions with low ventilation-perfusion ratios. Posture also can affect the function of respiratory muscles, particularly the diaphragm. For instance, in the upright posture, dyspnea may develop in quadriparetic patients who have paralyzed intercostal and abdominal muscles. Seward and associates, the authors of the aforementioned report appearing in this issue of the Proceedings, are to be congratulated for demonstrating variable right-to-left intracardiac shunts at the atrial level by using a minimally invasive test—namely, tilt-table two-dimensional echocardiography with peripheral venous echocardiographic contrast medium. They have also confirmed, in a relatively large series, previous reports of elimination of symptoms by surgical closure of such defects. The risk for development of right-to-left shunting at the atrial level when pulmonary hypertension or increased pulmonary vascular impedance occurs may be higher than previously appreciated, inasmuch as about 30% of the population have a probe-patent foramen ovale with a mean diameter of 3.4 mm in the first decade of life and increasing to 5.8 mm in the 10th decade of life.12Hagen PT Scholz DG Edwards WD Incidence and size of patent foramen ovale during the first 10 decades of life: an autopsy study of 965 normal hearts.Mayo Clin Proc. 1984; 59: 17-20Abstract Full Text Full Text PDF PubMed Scopus (2030) Google Scholar The report by Seward and colleagues leaves unanswered several questions that may be of clinical relevance. The authors did not determine whether and how much ventilation-perfusion mismatching contributed to deoxygenation in these patients. Ventilation-perfusion mismatching can be estimated by determining arterial oxygen tensions during breathing of air and of oxygen. The “inert” gas elimination method13Wagner PD Saltzman HA West JB Measurement of continuous distributions of ventilation-perfusion ratios: theory.J Appl Physiol. 1974; 36: 588-599PubMed Google Scholar may be used to “quantitate” the degree of ventilation-perfusion mismatching and right-to-left shunting. A reduction in cardiac output might also have contributed to the deoxygenation. If cardiac output is reduced when the patient assumes the upright position, perhaps as a result of failed orthostatic compensation, mixed venous oxygen saturation will be reduced. Thus, the blood shunted at the atrial level would become more desaturated and would contribute to reduced arterial saturation. No mention was made of changes in arterial oxygenation associated with different recumbent positions. This information would be of clinical value, particularly to anesthesiologists, who have the responsibility of caring for these patients during corrective surgical interventions. Both the anesthesiologist and the intensive-care specialist may also wonder how the right-to-left shunt would respond to increased intrathoracic pressure, because mechanical ventilation of the lungs may be necessary during the operative or postoperative period. It is unfortunate that the postural deoxygenation in the seven patients described by Seward and colleagues was incompletely substantiated. Arterial oxygen tensions (PaO2) were not measured in both the supine and the erect position in all patients, and control of inspired oxygen concentration was inadequate in one patient. Finally, PaO2 values were not reported for the patients after correction of the patent foramen ovale, to ensure that this was the entire source for the shunt. Despite these shortcomings, inevitable in clinical investigations of this nature, the authors have made a substantial contribution by increasing the clinician's awareness of this interesting and perhaps underdiagnosed syndrome.

Mean airway pressure (Paw) calculated by 4 methods was compared with measured Paw, using 833 observations on 16 infants requiring constant-flow, pressure-limited mechanical ventilation. Measured Paw was most accurately predicted by determining a waveform constant for each infant every 12 h, and then using the waveform constant in a general Paw equation for the ensuing 12 h. However, this method is impractical for clinical use. A square-waveform equation more accurately predicted Paw than did triangular or sine-like waveform equations. Because there was considerable interindividual variation in the accuracy of all methods, due to different individual respiratory waveforms and waveform constants, Paw should be measured and not calculated.

A patient had the rare combination of central neurogenic hyperventilation (PaCO2 of 9 torr) and a normal level of consciousness for eight days. Morphine attenuated but never corrected the hyperventilation. Experimental effects of hypocapnia, which decreases both cerebral blood flow and metabolism in humans, are at odds with the normal mentation initially seen in this patient despite her marked and persistent hypocapnia. Death occurred after progressive brainstem dysfunction. Pathological study showed a well-differentiated astrocytoma involving primarily the medulla and pons, with scattered tumor foci throughout the entire neuraxis. Possible mechanisms for central neurogenic hyperventilation are discussed briefly in relation to the pathological findings and the observed response to morphine.