Year in review 2005: Critical Care – Respirology: mechanical ventilation, infection, monitoring, and education

We summarize all original research in the field of respiratory intensive care medicine published in 2005 in Critical Care. Twenty-seven articles were grouped into the following categories and subcategories to facilitate rapid overview: mechanical ventilation (physiology, spontaneous breathing during mechanical ventilation, high frequency oscillatory ventilation, side effects of mechanical ventilation, sedation, and prone positioning); infection (pneumonia and sepsis); monitoring (ventilatory monitoring, pulmonary artery catheter and pulse oxymeter); and education (training and health outcome)

Human SP-A and a pharmacy-grade porcine lung surfactant extract can be reconstituted into tubular myelin--a comparative structural study of alveolar surfactants using cryo-transmission electron microscopy.

Cryo-transmission electron microscopy (cryo-TEM) is a rather artefact-free method, well suited to study the alveolar surfactant system. A pharmacy grade porcine lung surfactant extract (HL-10) was mixed with human SP-A and Ringer's solution (for calcium ions), and it was shown by cryo-TEM that the tubular myelin (TM) type of structure was reconstituted. These aggregates were associated to liposomal aggregates, and resulted in macroscopic phase-separation. This phase showed a weak birefringence in the polarising microscope, which is characteristic for a liquid-crystalline type of structure. TM from rabbit lung lavage was also examined, and showed the same periodic arrangement of bilayers as alveolar surface layer from freshly cut rabbit lungs deposited directly on the cryo-TEM grids. The distance between the bilayers of TM was 40-50 nm, and an electron dense material, assumed to be SP-A, was sometimes seen to occur periodically along the bilayers, oriented perpendicularly to the tubuli. The results are consistent with the surface-phase model of the alveolar lining

High tidal volume mechanical ventilation-induced lung injury in rats is greater after acid instillation than after sepsis-induced acute lung injury, but does not increase systemic inflammation: an experimental study

<p>Abstract</p> <p>Background</p> <p>To examine whether acute lung injury from direct and indirect origins differ in susceptibility to ventilator-induced lung injury (VILI) and resultant systemic inflammatory responses.</p> <p>Methods</p> <p>Rats were challenged by acid instillation or 24 h of sepsis induced by cecal ligation and puncture, followed by mechanical ventilation (MV) with either a low tidal volume (Vt) of 6 mL/kg and 5 cm H₂O positive end-expiratory pressure (PEEP; LVt acid, LVt sepsis) or with a high Vt of 15 mL/kg and no PEEP (HVt acid, HVt sepsis). Rats sacrificed immediately after acid instillation and non-ventilated septic animals served as controls. Hemodynamic and respiratory variables were monitored. After 4 h, lung wet to dry (W/D) weight ratios, histological lung injury and plasma mediator concentrations were measured.</p> <p>Results</p> <p>Oxygenation and lung compliance decreased after acid instillation as compared to sepsis. Additionally, W/D weight ratios and histological lung injury scores increased after acid instillation as compared to sepsis. MV increased W/D weight ratio and lung injury score, however this effect was mainly attributable to HVt ventilation after acid instillation. Similarly, effects of HVt on oxygenation were only observed after acid instillation. HVt during sepsis did not further affect oxygenation, compliance, W/D weight ratio or lung injury score. Plasma interleukin-6 and tumour necrosis factor-α concentrations were increased after acid instillation as compared to sepsis, but plasma intercellular adhesion molecule-1 concentration increased during sepsis only. In contrast to lung injury parameters, no additional effects of HVt MV after acid instillation on plasma mediator concentrations were observed.</p> <p>Conclusions</p> <p>During MV more severe lung injury develops after acid instillation as compared to sepsis. HVt causes VILI after acid instillation, but not during sepsis. However, this differential effect was not observed in the systemic release of mediators.</p

Diaphragmatic dysfunction in mechanical ventilation

Purpose of Review: It has become clear from experimental data that prolonged mechanical ventilation can induce diaphragm dysfunction, also known as ventilator-induced diaphragm dysfunction. In this article we will discuss most recent understanding on ventilator-induced diaphragm dysfunction and data on diaphragm dysfunction in patients. Recent Findings: Over the last year several studies confirmed the existence of diaphragm dysfunction in patients. Known atrophy pathways are activated in patients undergoing prolonged conventional ventilation resulting in muscle proteolysis and a decrease in myofiber content. The loss of diaphragm force is time-dependent, but current data do not distinguish between the role played by other factors involved in diaphragm dysfunction. Summary: Diaphragm dysfunction occurs in patients, especially when ventilated with controlled modes of ventilation that minimize diaphragm activity. Time on the ventilator seems to be one of the biggest risk factors resulting in difficulties in weaning patients and prolonging time on the ventilator. Future trials should investigate whether improved patient-ventilator synchrony can reduce ventilator-induced diaphragm dysfunction and decrease weaning failure

Physiology of Mechanical Ventilation

Mechanical ventilation, although essential in taking care of acute lung injury and widely used during surgical procedures worldwide, remains a highly debated field. Clinical trials in the last decade have shown convincingly that mechanical ventilation can result in additional mortality in patients with acute lung injury. This understanding has resulted in a resurged interest in mechanical ventilation, and especially in techniques and strategies to further improve mechanical ventilation. This article discusses physiological principles to improve the understanding of mechanical ventilation

Surfactant therapy

Pulmonary surfactant covers our lung epithelial, allowing normal tidal breathing at the air/water interface. Initially, surfactant abnormalities were found in respiratory distress syndrome (RDS); later on, changes in the surfactant system were also demonstrated in acute respiratory distress syndrome (ARDS) In neonates, Fujiwara et al. in 1980 reported that exogenous surfactant therapy reduced mortality and morbidity. And surfactant replacement therapy is now well established in the management of RDS, and represents standard care for neonates requiring mechanical ventilation. In Acute Lung Injury/Acute Respiratory Distress Syndrome (ALI/ARDS) similar dysfunction of the pulmonary surfactant system are observed. This has resulted in several trials of surfactant therapy in adults with ARDS. No effect of exogenous surfactant has been shown on survival in phase III studies in adult patients, but a phase III study performed on pediatric population did show beneficial effects of surfactant on oxygenation and survival. However, due to the results of the randomized controlled trials performed so far, exogenous surfactant is not recommended for routine use in patients with ALI/ARDS. But natural surfactants are standard of care in pre-term babies at risk for RDS. In the current manuscript we will discuss the rationale behind surfactant therapy, outcome of trials, and try to explain why current trials have failed to show efficacy

The role of coagulation in ventilator-associated pneumonia

Ventilator-associated pneumonia (VAP) is the most common nosocomial infection in the intensive care unit, and it is associated with prolonged hospitalization, increased health care costs, and high attributable mortality. Inflammatory changes in the pulmonary compartment as observed in acute lung injury are also often seen in VAP, and similar observations are now made regarding pulmonary coagulation changes. In the current review we will discuss the role of these coagulation changes in VAP (coagulopathy). We will discuss how mechanical ventilation affects both VAP and coagulopathy. As well as the role of anticoagulant therapies to reduce coagulopathy; from a theoretical perspective and from limited experimental research. And finally we will outline future research in this field

Surfactant therapy in adults with acute lung injury/acute respiratory distress syndrome

Purpose of review: Several phase II and phase III studies have been performed to investigate safety, efficacy and the improvement of survival due to exogenous surfactant instillation in patients with acute lung injury or acute respiratory distress syndrome. In this review we will discuss the most recent of these studies, paying particular attention to differences in the composition of the exogenous surfactant used, the diverse modes of delivery and dose of therapy and the influence of mechanical ventilation. Recent findings: Several phase II studies performed on patients with acute lung injury or acute respiratory distress syndrome and a phase III study performed on a pediatric population have shown beneficial effects of surfactant on oxygenation and survival. No effect of exogenous surfactant has been shown on survival in phase III studies in adult patients. Summary: The changes in the surfactant system of patients with acute lung injury and acute respiratory distress syndrome form the rationale for the instillation of exogenous surfactant. There is enough evidence to use surfactant instillation for pediatric patients with acute lung injury. Due to the results of the randomized controlled trials performed so far, however, exogenous surfactant is not recommended for routine use in patients with acute lung injury or acute respiratory distress syndrome. In the future, other surfactants with different compositions may show beneficial effects