Weaning covers the entire process of liberating the patient from mechanical support and from the endotracheal tube. Many controversial questions remain concerning the best methods for conducting this process. An International Consensus Conference was held in April 2005 to provide recommendations regarding the management of this process. An 11-member international jury answered five pre-defined questions. 1) What is known about the epidemiology of weaning problems? 2) What is the pathophysiology of weaning failure? 3) What is the usual process of initial weaning from the ventilator? 4) Is there a role for different ventilator modes in more difficult weaning? 5) How should patients with prolonged weaning failure be managed? The main recommendations were as follows. 1) Patients should be categorised into three groups based on the difficulty and duration of the weaning process. 2) Weaning should be considered as early as possible. 3) A spontaneous breathing trial is the major diagnostic test to determine whether patients can be successfully extubated. 4) The initial trial should last 30 min and consist of either T-tube breathing or low levels of pressure support. 5) Pressure support or assist-control ventilation modes should be favoured in patients failing an initial trial/trials. 6) Noninvasive ventilation techniques should be considered in selected patients to shorten the duration of intubation but should not be routinely used as a tool for extubation failure.

/pdf/weaning-from-mechanical-ventilation-4yn2mbde5t.pdf

Weaning from mechanical ventilation

A 1-d point-prevalence study was performed with the aim of describing the characteristics of conventional mechanical ventilation in intensive care units ICUs from North America, South America, Spain, and Portugal. The study involved 412 medical-surgical ICUs and 1,638 patients receiving mechanical ventilation at the moment of the study. The main outcome measures were characterization of the indications for initiation of mechanical ventilation, the artificial airways used to deliver mechanical ventilation, the ventilator modes and settings, and the methods of weaning. The median age of the study patients was 61 yr, and the median duration of mechanical ventilation at the time of the study was 7 d. Common indications for the initiation of mechanical ventilation included acute respiratory failure (66%), acute exacerbation of chronic obstructive pulmonary disease (13%), coma (10%), and neuromuscular disorders (10%). Mechanical ventilation was delivered via an endotracheal tube in 75% of patients, a tracheostomy in 24%, and a facial mask in 1%. Ventilator modes consisted of assist/control ventilation in 47% of patients and 46% were ventilated with synchronized intermittent mandatory ventilation, pressure support, or the combination of both. The median tidal volume setting was 9 ml/kg in patients receiving assist/control and the median setting of pressure support was 18 cm H(2)O. Positive end-expiratory pressure was not employed in 31% of patients. Method of weaning varied considerably from country to country, and even within a country several methods were in use. We conclude that the primary indications for mechanical ventilation and the ventilator settings were remarkably similar across countries, but the selection of modes of mechanical ventilation and methods of weaning varied considerably from country to country.

https://www.atsjournals.org/doi/pdf/10.1164/ajrccm.161.5.9902018

How is mechanical ventilation employed in the intensive care unit? An international utilization review.

In 2005, the American Thoracic Society marks its 100th year of existence. For over a third of this span, since 1967, clinicians and investigators have struggled with a common, often lethal condition originally termed the adult respiratory distress syndrome (ARDS) (1).* While the syndrome almost certainly occurred in earlier times well before the advent of intensive care units, this date establishes its modern era. Subsequently, ARDS has more correctly come to indicate the acute respiratory distress syndrome because it occurs in children as well as in adults (2). ARDS causes severe acute respiratory failure with dynamic impairment in oxygen and carbon dioxide transfer, with the need for high levels of supplementary oxygen and a high minute ventilation (3, 4). Efforts to understand the pathophysiologic events underlying ARDS, a constellation that is now generally termed acute lung injury (ALI), have been substantial and remain a priority of the National Institutes of Health (5). The expectation has been that basic, translational, and clinical studies will result in new strategies for management of ALI/ARDS based on clear definition of the cellular and molecular events requisite in lung injury and repair. While important discoveries have been made, the goal of fundamental characterization of ALI/ARDS in a way that results in highly effective prevention and treatment remains incomplete and elusive. One major advance in supportive care, a strategy of lung protective mechanical ventilation, has substantially reduced mortality in ALI/ARDS (6, 7). This therapeutic intervention resulted from both experimental and clinical studies that evaluated the effect of different ventilation strategies on the course of ALI, and continues a theme initiated in the original description of ALI/ARDS in which positive end-expiratory pressure was introduced as a management modality (1).

In spite of the advances in supportive care of patients with ALI/ARDS, unacceptable morbidity and mortality persist and formidable challenges remain. Our objective here is to review briefly what we knew in 1967 regarding pathogenesis and what we know in 2005, and to provide a perspective on how insights have evolved over the last four decades.

/pdf/acute-lung-injury-and-the-acute-respiratory-distress-53pznqyrv3.pdf

Acute lung injury and the acute respiratory distress syndrome: four decades of inquiry into pathogenesis and rational management.

Mechanical ventilation is a life-saving intervention for the management of acute respiratory failure. Its objective is to reduce excessive respiratory effort while improving gas exchange. By applying positive pressure to the airway, the mechanical ventilator assumes to a varying extent the work necessary to breathe, thereby unloading the respiratory muscles. In its most basic form, called controlled mechanical ventilation, a pre-set tidal volume is delivered at a fixed rate, irrespective of the patient’s own breathing pattern. If the mechanical and natural respiratory cycles are not matched, however, the patient ‘fights’ the ventilator, causing discomfort, gas exchange deterioration and cardiovascular impairment 1 . To avoid discoordination between the patient and the ventilator, it is often necessary to suppress the patient’s intrinsic respiratory drive with the use of hyperventilation, sedation or even muscle paralysis, which increase the risk of complications due to excessive ventilation 2‐3 , drug-related adverse effects

/pdf/neural-control-of-mechanical-ventilation-in-respiratory-10lscgehi3.pdf

Neural control of mechanical ventilation in respiratory failure.

Although left ventricular dysfunction is common during ventilatory support with positive end-expiratory pressure (PEEP), the mechanism of this disorder remains unclear. In 10 patients with the adult respiratory-distress syndrome we studied the effects of a stepwise increase in PEEP from 0.to 30 cm H2O on left ventricular output, intracardiac transmural pressures, and two-dimensional echocardiographic measurements of left ventricular cross-sectional area at end-systole and at end-diastole. Increasing PEEP was associated with progressive declines in cardiac output, mean blood pressure, and left ventricular dimensions and with equalization of right and left ventricular filling pressures. The radius of septal curvature decreased at both end-diastole and end-systole, implying a leftward shift of the interventricular septum. At the highest PEEP, blood-volume expansion did not restore cardiac output, although left ventricular transmural filling pressures had returned to base-line values. We conclude that decreased cardiac output during PEEP is mediated by a leftward displacement of the interventricular septum, which restricts left ventricular filling.

https://www.nejm.org/doi/pdf/10.1056/NEJM198102123040703?listPDF=true

Nikita Curien

Papers

Influence of positive end expiratory pressure on left ventricular performance