Major surgery is still associated with undesirable sequelae such as pain, cardiopulmonary, infective and thromboembolic complications, cerebral dysfunction, nausea and gastrointestinal paralysis, fatigue and prolonged convalescence. The key pathogenic factor in postoperative morbidity, excluding failures of surgical and anaesthetic technique, is the surgical stress response with subsequent increased demands on organ function. These changes in organ function are thought to be mediated by trauma-induced endocrine metabolic changes and activation of several biological cascade systems (cytokines, complement, arachidonic acid metabolites, nitric oxide, free oxygen radicals, etc). To understand postoperative morbidity it is therefore necessary to understand the pathophysiological role of the various components of the surgical stress response and to determine if modification of such responses may improve surgical outcome. While no single technique or drug regimen has been shown to eliminate postoperative morbidity and mortality, multimodal interventions may lead to a major reduction in the undesirable sequelae of surgical injury with improved recovery and reduction in postoperative morbidity and overall costs.

Multimodal approach to control postoperative pathophysiology and rehabilitation.

Institutional Affiliations Co-chairs Feldman D: Minneapolis Heart Institute, Minneapolis, Minnesota, Georgia Institute of Technology and Morehouse School of Medicine; Pamboukian SV: University of Alabama at Birmingham, Birmingham, Alabama; Teuteberg JJ: University of Pittsburgh, Pittsburgh, Pennsylvania Task force chairs Birks E: University of Louisville, Louisville, Kentucky; Lietz K: Loyola University, Chicago, Maywood, Illinois; Moore SA: Massachusetts General Hospital, Boston, Massachusetts; Morgan JA: Henry Ford Hospital, Detroit, Michigan Contributing writers Arabia F: Mayo Clinic Arizona, Phoenix, Arizona; Bauman ME: University of Alberta, Alberta, Canada; Buchholz HW: University of Alberta, Stollery Children’s Hospital and Mazankowski Alberta Heart Institute, Edmonton, Alberta, Canada; Deng M: University of California at Los Angeles, Los Angeles, California; Dickstein ML: Columbia University, New York, New York; El-Banayosy A: Penn State Milton S. Hershey Medical Center, Hershey, Pennsylvania; Elliot T: Inova Fairfax, Falls Church, Virginia; Goldstein DJ: Montefiore Medical Center, New York, New York; Grady KL: Northwestern University, Chicago, Illinois; Jones K: Alfred Hospital, Melbourne, Australia; Hryniewicz K: Minneapolis Heart Institute, Minneapolis, Minnesota; John R: University of Minnesota, Minneapolis, Minnesota; Kaan A: St. Paul’s Hospital, Vancouver, British Columbia, Canada; Kusne S: Mayo Clinic Arizona, Phoenix, Arizona; Loebe M: Methodist Hospital, Houston, Texas; Massicotte P: University of Alberta, Stollery Children’s Hospital, Edmonton, Alberta, Canada; Moazami N: Minneapolis Heart Institute, Minneapolis, Minnesota; Mohacsi P: University Hospital, Bern, Switzerland; Mooney M: Sentara Norfolk, Virginia Beach, Virginia; Nelson T: Mayo Clinic Arizona, Phoenix, Arizona; Pagani F: University of Michigan, Ann Arbor, Michigan; Perry W: Integris Baptist Health Care, Oklahoma City, Oklahoma; Potapov EV: Deutsches Herzzentrum Berlin, Berlin, Germany; Rame JE: University of Pennsylvania, Philadelphia, Pennsylvania; Russell SD: Johns Hopkins, Baltimore, Maryland; Sorensen EN: University of Maryland, Baltimore, Maryland; Sun B: Minneapolis Heart Institute, Minneapolis, Minnesota; Strueber M: Hannover Medical School, Hanover, Germany Independent reviewers Mangi AA: Yale University School of Medicine, New Haven, Connecticut; Petty MG: University of Minnesota Medical Center, Fairview, Minneapolis, Minnesota; Rogers J: Duke University Medical Center, Durham, North Carolina

The 2013 International Society for Heart and Lung Transplantation Guidelines for mechanical circulatory support: executive summary.

Multimodal Approach to Control Postoperative Pathophysiology and Rehabilitation

Introduction Morphological Analysis of the CT Images Early Phase [First Week] Late Stage [Second Week and Beyond] Long-Term Follow-up Pathogenesis Alters Morphology Quantitative Analysis of CT Scan Images CT Frequency Distribution Lung Compartments CT Scan Protocols and Analysis Influence Results One to Three Slices versus Whole Lung CT Scan Recruitment Hyperinflation and Overstretching Structure–Function Correlation in the Whole Lung Gas Exchange Lung Mechanics CT—Regional Analysis Edema Distribution and Lung Volume Superimposed Pressure and PEEP The CT Scan and Mechanical Ventilation Settings Opening the Lung Interaction between End Expiration and End Inspiration Distribution of Gas in Mechanical Ventilation Intratidal Collapse and Decollapse The Impact of CT Scanning in Clinical Practice New Developments and Future Areas of Research

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What Has Computed Tomography Taught Us about the Acute Respiratory Distress Syndrome

Rationale: Lung injury caused by a ventilator results from nonphysiologic lung stress (transpulmonary pressure) and strain (inflated volume to functional residual capacity ratio).Objectives: To determine whether plateau pressure and tidal volume are adequate surrogates for stress and strain, and to quantify the stress to strain relationship in patients and control subjects.Methods: Nineteen postsurgical healthy patients (group 1), 11 patients with medical diseases (group 2), 26 patients with acute lung injury (group 3), and 24 patients with acute respiratory distress syndrome (group 4) underwent a positive end-expiratory pressure (PEEP) trial (5 and 15 cm H2O) with 6, 8, 10, and 12 ml/kg tidal volume.Measurements and Main Results: Plateau airway pressure, lung and chest wall elastances, and lung stress and strain significantly increased from groups 1 to 4 and with increasing PEEP and tidal volume. Within each group, a given applied airway pressure produced largely variable stress due to the variability of...

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Lung Stress and Strain during Mechanical Ventilation for Acute Respiratory Distress Syndrome

Twenty patients (23-76 yr) were studied with regard to lung tissue changes prior to and following induction of general anesthesia with muscular relaxation, and another four subjects were studied for a longer period awake. The transverse thoracic area and the structure of the lung tissue were determined by computerized tomography. No abnormalities in the lung tissue were noted before anesthesia. Within 5 min after induction, including muscular relaxation, all subjects had developed crest-shaped changes of increased density in the dependent regions of both lungs. They were largest in the most caudal segment (4.8 +/- 0.8% of the transverse lung area, mean +/- SE) and smaller in the cephalad exposures (3.4 +/- 0.7% of the transverse area). The size of the densities showed no correlation to age. The densities did not increase after a further 20 min of anesthesia and were not affected by the inspiratory oxygen fraction. When the subjects were moved from the supine to the lateral position, the crest-shaped densities disappeared in the nondependent lung and remained in the dorsal part of the dependent lung. The application of positive end-expiratory pressure of 10 cmH2O eliminated or reduced the densities. The four awake subjects showed no lung densities after 90 min in the supine position. It is suggested that these crest-shaped densities represent atelectases, which develop by compression of lung tissue rather than by resorption of gas.

Pulmonary densities during anesthesia with muscular relaxation--a proposal of atelectasis.

Lung densities (atelectasis) and pulmonary gas exchange were studied in 13 supine patients with no apparent lung disease, the former by transverse computerized tomography (CT) and the latter by a multiple inert gas elimination technique for assessment of the distribution of ventilation/perfusion ratios. In the awake state no patient had clear signs of atelectasis on the CT scan. Lung ventilation and perfusion were well matched in most of the patients. Three patients had shunts corresponding to 2-5% of cardiac output, and in one patient there was low perfusion of poorly ventilated regions. CT scans after 15 min of halothane anesthesia and mechanical ventilation showed densities in dependent lung regions in 11 patients. A shunt was present in all patients, ranging from 1% in two patients (unchanged from the awake state) to 17%. Ventilation of poorly perfused regions was noted in nine patients, ranging from 1-19% of total ventilation. The magnitude of the shunt significantly correlated to the size of dependent densities (r = 0.84, P less than 0.001). Five patients studied during spontaneous breathing under anesthesia displayed both densities in dependent regions and a shunt, although of fairly small magnitude (1.8% and 3.7%, respectively). Both the density area and the shunt increased after muscle paralysis. PEEP reduced the density area in all patients but did not consistently alter the shunt. It is concluded that the development of atelectasis in dependent lung regions is a major cause of gas exchange impairment during halothane anesthesia, during both spontaneous breathing and mechanical ventilation, and that PEEP diminishes the atelectasis, but not necessarily the shunt.

Lung collapse and gas exchange during general anesthesia: effects of spontaneous breathing, muscle paralysis, and positive end-expiratory pressure

Functional residual capacity (FRC), rib cage and abdominal dimensions (rc-ab), central blood volume (CBV), and extra vascular lung water (EVLW) were measured in six lung-healthy subjects awake and during halothane anesthesia, muscle paralysis, and mechanical ventilation. FRC was assessed by multiple breath nitrogen washout, rc-ab dimensions by computerized tomography, and CBV and EVLW by a double-indicator dilution technique (thermo-dye). During anesthesia, FRC decreased by 0.5 1 (17%). The cross-sectional chest area was reduced by 12-20 cm2, causing an approximate reduction in thoracic volume by 0.3 1. Concomitantly, the diaphragm was moved cranially by an average of 1.9 cm, diminishing the thoracic volume a further 0.5 1. The abdominal cross-sectional area did not alter significantly, despite the shift of the diaphragm. CBV decreased by 0.3 1. EVLW did not change significantly. It is concluded that the thoracic volume is reduced during halothane anesthesia, muscle paralysis, and mechanical ventilation as a result of cranial shift of the diaphragm and reduction in transverse area. The decrease in thoracic volume is accompanied by a reduction in FRC and a displacement of blood from the thorax to the abdomen, the transverse area of the latter thus being maintained despite the shift of the diaphragm.

Functional residual capacity, thoracoabdominal dimensions, and central blood volume during general anesthesia with muscle paralysis and mechanical ventilation.

Purpose:We aimed to describe the frequency of atelectasis occurring during anaesthesia, to describe the size and pattern of the atelectasis, and to standardise the method of identifying the atelectasis and calculate its area.Material and Methods:Patients (n=109) scheduled for elective abdominal surgery were examined with CT of the thorax during anaesthesia.Results:In 95 patients (87%) dependent pulmonary densities were seen, interpreted as atelectasis. Two different types of atelectasis were found — Homogeneous (78%) and non-homogeneous (9%). Attenuation values in histograms of the lung and atelectasis were studied using 2 methods of calculating the atelectatic area.Conclusion:On the basis of the present findings, we defined atelectasis as pulmonary dependent densities with attenuation values of —100 to +100 HU.

CT-Assessment of Dependent Lung Densities in Man during General Anaesthesia

Tokics, Leif, Goran Hedenstierna, Leif Svensson, Bo Brismar, Torsten Cederlund, Hans Lundquist, and Ake Strandberg. V˙/Q˙ distribution and correlation to atelectasis in anesthetized paralyzed human...

H Lundquist

Papers

Pulmonary densities during anesthesia with muscular relaxation--a proposal of atelectasis.

Lung collapse and gas exchange during general anesthesia: effects of spontaneous breathing, muscle paralysis, and positive end-expiratory pressure

Functional residual capacity, thoracoabdominal dimensions, and central blood volume during general anesthesia with muscle paralysis and mechanical ventilation.

CT-Assessment of Dependent Lung Densities in Man during General Anaesthesia

V/Q distribution and correlation to atelectasis in anesthetized paralyzed humans.