Critical care : the official journal of the Critical Care Forum
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The choice of inotropic agent, particularly in catecholamine-resistant septic shock, remains an area of debate. Here we discuss a recent trial examining the use of vasopressin in a carefully controlled trial setting. Yet more data on the use of drotrecogin alfa (activated) in septic shock are described, as are novel but as yet experimental approaches to the treatment of sepsis. Finally, it is important not to forget to read the latest surviving sepsis guidelines.
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Non-invasive evaluation of left ventricular filling pressure has been scarcely studied in critically ill patients. Accordingly, we prospectively assessed the ability of transoesophageal echocardiography (TEE) Doppler to predict an invasive pulmonary artery occlusion pressure (PAOP) < or = 18 mmHg in ventilated patients. ⋯ TEE accurately predicts invasive PAOP < or = 18 mmHg in ventilated patients. This further increases its diagnostic value in patients with suspected acute lung injury/acute respiratory distress syndrome.
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Alveolar dead space reflects phenomena that render arterial partial pressure of carbon dioxide higher than that of mixed alveolar gas, disturbing carbon dioxide exchange. Right-to-left shunt fraction (Qs/Qt) leads to an alveolar dead space fraction (VdAS/VtA; where VtA is alveolar tidal volume). In acute respiratory distress syndrome, ancillary physiological disturbances may include low cardiac output, high metabolic rate, anaemia and acid-base instability. The purpose of the present study was to analyze the extent to which shunt contributes to alveolar dead space and perturbs carbon dioxide exchange in ancillary physiological disturbances. ⋯ In acute respiratory distress syndrome, perturbation of carbon dioxide exchange caused by shunt is enhanced by ancillary disturbances such as low cardiac output, anaemia, metabolic acidosis and hyperventilation. Maintained homeostasis mitigates the effects of shunt.
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Acute kidney injury (AKI) is a common problem, especially in critically ill patients. In Critical Care, Kolhe and colleagues report that 6.3% of 276,731 patients in 170 intensive care units (ICUs) in the UK had evidence of severe AKI within the first 24 hours of admission to ICU. ICU and hospital mortality as well as length of stay in hospital were significantly increased. In light of this serious burden on individuals and the health system in general, the following commentary discusses the current state of knowledge of AKI in ICU and calls for more attention to preventive strategies.
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Recent papers discussed include two large, multicentre, high-positive end-expiratory pressure trials in acute lung injury and reflects upon the usefulness of such trial designs. Further papers considered include the emerging story of beta2-agonists for pulmonary oedema, highlights the newly described, iatrogenic demon, of ventilator-induced diaphragm injury, promotes the addition of B-type natriuretic peptide testing to the prediction of extubation success, and muses again over the oxygen debate.