Multidisciplinary guidance for safe tracheostomy care during the COVID-19 pandemic: the NHS National Patient Safety Improvement Programme (NatPatSIP).

The COVID-19 pandemic is causing a significant increase in the number of patients requiring relatively prolonged invasive mechanical ventilation and an associated surge in patients who need a tracheostomy to facilitate weaning from respiratory support. In parallel, there has been a global increase in guidance from professional bodies representing staff who care for patients with tracheostomies at different points in their acute hospital journey, rehabilitation and recovery. Of concern are the risks to healthcare staff of infection arising from tracheostomy insertion and caring for patients with a tracheostomy. Hospitals are also facing extraordinary demands on critical care services such that many patients who require a tracheostomy will be managed outside established intensive care or head and neck units and cared for by staff with little tracheostomy experience. These concerns led NHS England and NHS Improvement to expedite the National Patient Safety Improvement Programme's 'Safe Tracheostomy Care' workstream as part of the NHS COVID-19 response. Supporting this workstream, UK stakeholder organisations involved in tracheostomy care were invited to develop consensus guidance based on: expert opinion; the best available published literature; and existing multidisciplinary guidelines. Topics with direct relevance for frontline staff were identified. This consensus guidance includes: infectivity of patients with respect to tracheostomy indications and timing; aerosol-generating procedures and risks to staff; insertion procedures; and management following tracheostomy.

Building Evidence for Health: Green Buildings, Current Science, and Future Challenges.

Civilizational challenges have questioned the status quo of energy and material consumption by humans. From the built environment perspective, a response to these challenges was the creation of green buildings. Although the revolutionary capacity of the green building movement has elevated the expectations of new commercial construction, its rate of implementation has secluded the majority of the population from its benefits. Beyond reductions in energy usage and increases in market value, the main strength of green buildings may be the procurement of healthier building environments. Further pursuing the right to healthy indoor environments could help the green building movement to attain its full potential as a transformational public health tool. On the basis of 40 years of research on indoor environmental quality, we present a summary of nine environment elements that are foundational to human health. We posit the role of green buildings as a critical research platform within a novel sustainability framework based on social-environmental capital assets.

New ventilators for the ICU--usefulness of lung performance reporting.

Monitoring the functional and mechanical properties of the lungs during positive pressure ventilation may assist in confirming the underlying pulmonary diagnosis, allow therapeutic interventions to be accurately assessed and provide information that ensures the optimal setting of the ventilator parameters and encourages timely weaning. This article reviews the range of lung function measurements, both continuous and intermittent, that may be undertaken during mechanical ventilation. The monitoring capability of ICU ventilators is increasing in complexity.

Prolonged resuscitation: a case report.

This report illustrates a case of prolonged resuscitation (without hypothermia) with a return of spontaneous circulation (ROSC) after 1 h of resuscitation in a hospital car park and emergency department. Coronary artery stenting was achieved 2 h and 45 min after collapse. Following a 12-week stay in hospital the patient was discharged home making a full recovery within 12 months. Issues regarding prolonged resuscitation and the key predictors of survival are discussed.

Pulmonary surfactant composition early in development of acute lung injury after cardiopulmonary bypass: prophylactic use of surfactant therapy.

Cardiopulmonary bypass surgery (CPB) causes lung injury and at least 2% of adult patients and more children develop the most severe from acute respiratory distress syndrome (ARDS). Pulmonary surfactant deficiency contributes to the pathogenesis of ARDS. It has been proposed that surfactant therapy immediately after CPB might arrest progression to ARDS. However, many patients develop only mild lung injury after CPB. Thus early markers are needed to identify those patients at highest risk to guide selection for treatment. The aim of this study was to determine whether changes in surfactant phospholipids occur, and reflect severity of lung injury within the first few hours after bypass. Because of the relatively low incidence of ARDS in adult patients, this study was conducted using young pigs highly susceptible to bypass-induced lung injury. Eight pigs were given 2 hours bypass. Six controls underwent 'sham' bypass. At 3 h after bypass pulmonary vascular endothelial permeability was assessed by transcapillary leakage of radiolabelled transferrin. A 4 hour broncho-alveolar lavage (BAL) was used to assess intra-alveolar levels of surfactant, inflammatory cells and oedema protein. Bypass caused falls in arterial oxygenation and lung compliance (P < 0.01), but at this early stage in progression of lung injury BAL surfactant phospholipid and albumin levels were within the control range indicating that the alveolar epithelium had not yet suffered major damage. The main abnormalities were increases in vascular endothelial permeability (P < 0.01), BAL neutrophils (P < 0.01), total protein and sphingomyelin (SM) (P < 0.05). Lung histology showed that the main damage was interstitial oedema located around the bronchioles and their associated vessels. A single instilled dose of surfactant phospholipids in 5 animals caused excess in vivo supplementation and did not reduce the early pathophysiologic changes. Our findings suggest that surfactant phospholipid deficiency does not make a major contribution in the initial stages of lung injury after CPB, and that excessive phospholipid supplementation at this stage can be deleterious.

Measurement of lung volume and DLCO in acute respiratory failure.

We have undertaken rebreathing measurements of functional residual capacity (FRC), carbon monoxide diffusing capacity (DLCO), and diffusing coefficient (KCO) during positive pressure ventilation in 15 patients with adult respiratory distress syndrome (ARDS). Measurements of oxygenation (PaO2:FIO2 ratio) and lung injury score (LIS) were also recorded. Eight patients subsequently died (mortality of 53%). There was no significant difference in mean FRC, PaO2:FIO2, or LIS at presentation between survivors and nonsurvivors. However, both DLCO and KCO at presentation were significantly greater in survivors than nonsurvivors. In a separate study of nine patients with less severe lung injury, pulmonary capillary blood volume, derived from values of DLCO measured at two different values of FIO2, correlated with invasive pulmonary vascular resistance (PVR) measurements (r = 0.84, p < 0.01). DLCO measurements can be successfully undertaken in patients being ventilated with acute lung injury and may be a useful, noninvasive method of assessing the pulmonary circulation. The lowest values of DLCO were recorded in patients who subsequently did not survive.

Surfactant replacement therapy in late-stage adult respiratory distress syndrome.

In four adult patients with late-stage acute respiratory distress syndrome (ARDS), a single dose of the artificial surfactant ALEC was given by intrabronchial instillation. There was no sustained clinical improvement, but bronchoalveolar lavage measurements indicated that phosphatidylcholine (PC) at 24 h after treatment had increased up to 4.4 fold and phosphatidylglycerol up to 34.7 fold. However, PC relative to total phospholipid remained below normal, and protein contamination relative to PC remained above normal. Thus, therapeutic formulations and regimens to achieve greater and more sustained supplementation of PC may be required in patients with late-stage ARDS.

The effect of exogenous surfactant therapy on lung function following cardiopulmonary bypass.

OBJECTIVE: Pilot study to investigate the effect of exogenous surfactant therapy on lung function following cardiopulmonary bypass (CPB). DESIGN: Prospective randomized controlled study. SETTING: Adult intensive care unit of a postgraduate cardiothoracic hospital. PATIENTS: Sixteen adult patients undergoing elective coronary artery revascularization surgery without a history of preoperative respiratory disease. INTERVENTIONS: Artificial lung-expanding compound (ALEC, Britannia Pharmaceuticals, Crawley, UK) 3.2 g, was given via a bronchoscope 60 min after bypass in eight patients. Eight control subjects received air. MAIN OUTCOME MEASUREMENTS: Lung function tests during IPPV (arterial blood gas tensions, Crs, FRC, TLco, KCO) were measured prior to CPB, before therapy, and at regular intervals up to 180 min afterwards. RESULTS: The CPB caused a significant impairment of lung function in both groups with an increase in A-a gradient (+47 +/- 11 mm Hg in the ALEC group and +44 +/- 17 mm Hg in controls) and reductions in FRC (-290 +/- 121 ml in the ALEC group and -470 +/- 132 ml in controls), TLco (-1.6 +/- 0.3 ml/min/mm Hg in the ALEC group and -2.2 +/- 0.3 ml/min/mm Hg in controls), and Crs (-10 +/- 1 ml/cm H2O in the ALEC group and -21 +/- 4 ml/cm H2O in controls). The ALEC therapy did not affect A-a gradient, FRC, and Crs compared with controls. However, TLco was significantly lower in the ALEC group following therapy (120 min after treatment -0.1 +/- 0.3 ml/min/mm Hg in ALEC group and +1.0 +/- 0.3 ml/min/mm Hg in controls). CONCLUSIONS: A single 3.2-g dose of ALEC administered as a bolus bronchoscopically does not improve lung function following CPB and may impair gas transfer.

Measurement of carbon monoxide transfer and lung volume in ventilated subjects.

A simple method for measuring lung volume and carbon monoxide transfer factor (TLCO) by a rebreathing technique was assessed in nine healthy volunteers undergoing intermittent positive pressure ventilation (IPPV). Measurements of TLCO, alveolar volume (VA) and carbon monoxide transfer coefficient (KCO) made at three inspired oxygen concentrations (21, 35 and 70%) during IPPV were compared to those obtained during spontaneous breathing. The effects of 10 cmH2O positive end expiratory pressure (PEEP) were also studied. Pulmonary capillary blood volume (Vc) and the diffusing capacity of the alveolar capillary membrane (Dm) were derived. There was a close correlation between measurements of TLCO during IPPV (TLCOIPPV) and spontaneous breathing (TLCOSV) (r = 0.92). Ventilated TLCO was 64 +/- 8% of spontaneously breathing TLCO. There was a close agreement between ventilated and spontaneously breathing measurements of KCO (r = 0.95; mean difference 0.14, 95% limits of agreement +0.37 to -0.09 mmol.min-1 x kPa-1 x l-1). Vc was 92 +/- 23 ml during spontaneous breathing and 72 +/- 21 ml during IPPV (p < 0.05). PEEP of 10 cmH2O significantly increased functional residual capacity (2.3 +/- 0.5 to 3.5 +/- 0.6 l) and decreased TLCO (5.9 +/- 1.0 to 5.3 +/- 1.2 mmol.min-1 x kPa-1), KCO (1.7 +/- 0.2 to 1.1 +/- 0.3 mmol.min-1 x kPa-1 x l-1) and Vc (82 +/- 22 to 56 +/- 20 ml). Dm did not change with PEEP. This simple method may be a useful means of assessing gas exchange and lung volume in ventilated subjects. It showed that PEEP increased lung volume but reduced TLCO and that this reduction appeared to be due to a reduction in capillary blood volume.

Changes in lung function and pulmonary capillary permeability after cardiopulmonary bypass.

OBJECTIVE: To assess the possibility that changes in lung function following cardiopulmonary bypass are associated with increased pulmonary capillary permeability. DESIGN: A prospective, descriptive study. SETTING: Adult cardiothoracic ICU in a post-graduate teaching hospital. PATIENTS: Ten sequential patients undergoing cardiac surgery requiring cardiopulmonary bypass. MEASUREMENTS: Arterial blood gas tensions, helium dilution end-expiratory lung volume, and carbon monoxide transfer were measured by a rebreathing technique preoperatively and 2 hrs postoperatively. Lung extravascular protein accumulation index was measured by a double-isotope technique 2 hrs postoperatively and in a group of normal controls. RESULTS: Mean +/- SEM alveolar-arterial PO2 gradient increased from 77 +/- 14 torr (10.3 +/- 1.8 kPa) to 138 +/- 24 torr (18.5 +/- 3.2 kPa) (p less than .01). Functional residual capacity decreased by 20.2 +/- 5.6% (p less than .01). Carbon monoxide transfer decreased by 26.7 +/- 5.3% (p less than .01) for the lung as a whole and by 17.9 +/- 3.2% (p less than .01) per liter of accessible gas volume. Protein accumulation index ranged from 0.03 to 3.2 x 10(-3) (median 0.6) postoperatively (median for normal subjects 0.4; p less than .05), although only one patient had a value indicative of clinically important endothelial injury. CONCLUSIONS: Cardiac surgery involving cardiopulmonary bypass results in a deterioration in lung function characterized by a loss of lung volume, a reduction in carbon monoxide transfer, and an increase in the alveolar-arterial PO2 gradient. These changes do not appear to be mediated by an increase in pulmonary endothelial permeability.

Blood lactate and mixed venous-arterial PCO2 gradient as indices of poor peripheral perfusion following cardiopulmonary bypass surgery.

Conventional indices of tissue perfusion after surgery involving cardiopulmonary bypass (CPB) may not accurately reflect disordered cell metabolism. Venous hypercarbia leading to an increased veno-arterial difference in CO2 tensions (V-aCO2 gradient) has been shown to reflect critical reductions in systemic and pulmonary blood flow that occur during cardiorespiratory arrest and septic shock. We therefore measured plasma lactate levels and V-aCO2 gradients in 10 patients (mean age 57.2 years) following CPB and compared them with conventional indices of tissue perfusion. Plasma lactate levels, cardiac index (CI) and oxygen uptake (VO2) all increased significantly (p less than 0.05 vs baseline levels) up to 3 h following surgery. Oxygen delivery (DO2) did not change. Plasma lactate levels correlated significantly with CI (r = 0.47, p less than 0.01). V-aCO2 fell significantly with time (p less than 0.01 vs baseline). There was an inverse relationship between V-aCO2 and cardiac index and V-aCO2 and lactate (r = -0.37, p less than 0.05; r = -0.3, p less than 0.05 respectively). We conclude that blood lactate, CI and VO2 increase progressively following CPB. An increase in lactate was associated with a decrease in V-aCO2. An increase in V-aCO2 was not therefore associated with evidence of inadequate tissue perfusion as indicated by an increased blood lactate concentration.

Pulmonary function testing in the intensive care unit.

A number of tests of pulmonary function have been successfully developed for use in the intensive care unit. When performed in the ICU on critically ill patients, many of the traditional laboratory-based tests will have different clinical implications than when performed in ambulatory patients, for example vital capacity measurement. Also, the clinical questions posed in the ICU are often different, such that estimates of lung water may be clinically more useful than more traditional measures, such as the flow-volume loop. There is a need for further research to identify the clinical utility of these measurements. As the understanding of ARDS and MOF improves, new therapies may be developed which will require sensitive methods in order that they can be evaluated accurately. Similarly, the potential for new methods of respiratory support such as jet ventilation, extracorporeal techniques and lung transplantation reinforce the need for the pulmonary physician to be able to make an accurate assessment of respiratory function on the intensive care unit.