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

Guidelines and Expert Consensus documents aim to present all the relevant evidence on a particular issue in order to help physicians to weigh the benefits and risks of a particular diagnostic or therapeutic procedure. They should be helpful in everyday clinical decision-making.

A great number of Guidelines and Expert Consensus Documents have been issued in recent years by the European Society of Cardiology (ESC) and by different organizations and other related societies. This profusion can put at stake the authority and validity of guidelines, which can only be guaranteed if they have been developed by an unquestionable decision-making process. This is one of the reasons why the ESC and others have issued recommendations for formulating and issuing Guidelines and Expert Consensus Documents.

In spite of the fact that standards for issuing good quality Guidelines and Expert Consensus Documents are well defined, recent surveys of Guidelines and Expert Consensus Documents published in peer-reviewed journals between 1985 and 1998 have shown that methodological standards were not complied with in the vast majority of cases. It is therefore of great importance that guidelines and recommendations are presented in formats that are easily interpreted. Subsequently, their implementation programmes must also be well conducted. Attempts have been made to determine whether guidelines improve the quality of clinical practice and the utilization of health resources.

The ESC Committee for Practice Guidelines (CPG) supervises and coordinates the preparation of new Guidelines and Expert Consensus Documents produced by Task Forces, expert groups or consensus panels. The chosen experts in these writing panels are asked to provide disclosure statements of all relationships they may have which might be perceived as real or potential conflicts of interest. These disclosure forms are kept on file at the European Heart House, headquarters of the ESC. The Committee is also responsible for the …

https://repositorio.chporto.pt/bitstream/10400.16/493/1/pdf.4.pdf

Executive summary of the guidelines on the diagnosis and treatment of acute heart failure: the Task Force on Acute Heart Failure of the European Society of Cardiology.

ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography

To evaluate the extent to which respiratory changes in inferior vena cava (IVC) diameter can be used to predict fluid responsiveness. Prospective clinical study. Hospital intensive care unit. Twenty-three patients with acute circulatory failure related to sepsis and mechanically ventilated because of an acute lung injury. Inferior vena cava diameter (D) at end-expiration (Dmin) and at end-inspiration (Dmax) was measured by echocardiography using a subcostal approach. The distensibility index of the IVC (dIVC) was calculated as the ratio of Dmax − Dmin / Dmin, and expressed as a percentage. The Doppler technique was applied in the pulmonary artery trunk to determine cardiac index (CI). Measurements were performed at baseline and after a 7 ml/kg volume expansion using a plasma expander. Patients were separated into responders (increase in CI ≥15%) and non-responders (increase in CI <15%). Using a threshold dIVC of 18%, responders and non-responders were discriminated with 90% sensitivity and 90% specificity. A strong relation (r=0.9) was observed between dIVC at baseline and the CI increase following blood volume expansion. Baseline central venous pressure did not accurately predict fluid responsiveness. Our study suggests that respiratory change in IVC diameter is an accurate predictor of fluid responsiveness in septic patients.

/pdf/respiratory-changes-in-inferior-vena-cava-diameter-are-43nb3ldsdw.pdf

Respiratory changes in inferior vena cava diameter are helpful in predicting fluid responsiveness in ventilated septic patients

To assess the possible differences in respiratory mechanics between the acute respiratory distress syndrome (ARDS) originating from pulmonary disease (ARDSp) and that originating from extrapulmonary disease (ARDSexp) we measured the total respiratory system (Est,rs), chest wall (Est,w) and lung (Est,L) elastance, the intra-abdominal pressure (IAP), and the end-expiratory lung volume (EELV) at 0, 5, 10, and 15 cm H2O positive end-expiratory pressure (PEEP) in 12 patients with ARDSp and nine with ARDSexp. At zero end-expiratory pressure (ZEEP), Est,rs and EELV were similar in both groups of patients. The Est,L, however, was markedly higher in the ARDSp group than in the ARDSexp group (20.2 +/- 5.4 versus 13.8 +/- 5.0 cm H2O/L, p < 0.05), whereas Est,w was abnormally increased in the ARDSexp group (12.1 +/- 3.8 versus 5.2 +/- 1.9 cm H2O/L, p < 0.05). The IAP was higher in ARDSexp than in ARDSp (22.2 +/- 6.0 versus 8.5 +/- 2.9 cm H2O, p < 0.01), and it significantly correlated with Est,w (p < 0. 01). Increasing PEEP to 15 cm H2O caused an increase of Est,rs in ARDSp (from 25.4 +/- 6.2 to 31.2 +/- 11.3 cm H2O/L, p < 0.01) and a decrease in ARDSexp (from 25.9 +/- 5.4 to 21.4 +/- 55.5 cm H2O/L, p < 0.01). The estimated recruitment at 15 cm H2O PEEP was -0.031 +/- 0.092 versus 0.293 +/- 0.241 L in ARDSp and ARDSexp, respectively (p < 0.01). The different respiratory mechanics and response to PEEP observed are consistent with a prevalence of consolidation in ARDSp as opposed to prevalent edema and alveolar collapse in ARDSexp.

Acute respiratory distress syndrome caused by pulmonary and extrapulmonary disease. Different syndromes

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

Influence of positive end expiratory pressure on left ventricular performance

Influence of Lung and Chest Wall Compliances on Transmission of Airway Pressure to the Pleural Space in Critically Ill Patients

Clinical and hemodynamic results of intra-aortic balloon counterpulsation and surgery for cardiogenic shock

Treatment of post—myocardial infarction angina by intra-aortic balloon pumping and emergency revascularization

Dobutamine was infused at a rate of 8 mcg/kg/min in 17 patients with or without congestive heart failure Cardiac output increased from an average 292 to 445 1/min/m2(p less than 0001) with no change in mean aortic pressure (934 to 978 mmHg) and only a slight increase in heart rate (78 to 87 beats/min) Left ventricular end-diastolic pressure decreased from an average 19 to 137 mmHg (p less than 001) Peak left ventricular dp/dt was doubled (1147 to 2370 mmHg/sec, p less than 0001) and Vmax increased from 108 to 218 circ/sec (p less than 0001) In 10 patients given equi-inotropic doses (100 per cent increase in peak dp/dt) Isoproterenol produced a greater increase in cardiac output (71 percent) than Dobutamine /51 percent) Isoproterenol caused mean aortic pressure to fall significantly (8 percent) while no change was noted with Dobutamine Accordingly, peripheral vascular resistances were reduced to a greater extent with Isoproterenol than with Dobutamine (p less than 005) Mean pulmonary arterial pressure decreased significantly (25 +/- 59 to 22 +/- 57 mmHg, p less than 005) with Isoproterenol infusion and remained unchanged with Dobutamine infusion Dobutamine increased both stroke work (57 percent) and minute work (83 percent) With Isoproterenol however, only minute work was significantly increased (90 percent) Dobutamine therefore is a potent inotropic drug, with mild chronotropic and peripheral vascular effect and may be valuable in the management of severe heart failure not associated with hypotension

Comparative haemodynamic effects of dobutamine and isoproterenol in man

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