Cardiopulmonary resuscitation: are practitioners being realistic?

Cardiopulmonary resuscitation (CPR) is now established medical practice for all in-hospital cardiac arrests except where a specific 'do not resuscitate' (DNR) order is in place. This article explores many of the ethical and moral issues surrounding CPR and the use of DNR orders. It examines the success rate of in-hospital CPR and raises the question of what constitutes outcome success by illustrating that at best only 15% of resuscitated patients survive to hospital discharge. The article proposes that both patients and healthcare professionals grossly overestimate the success of CPR and suggests that many elderly patients might choose not to be resuscitated if they were allowed to make an informed choice. It concludes by suggesting that further work needs to be undertaken with regard to early assessment of all in-hospital patients, combined with realistic and frank communication between healthcare professionals and patients if futile, undignified and costly deaths are to be avoided.     

Sodium lactate for fluid resuscitation: the preferred solution for the coming decades?

In a recent issue of Critical Care, 0.5 M sodium lactate infusion for 24 hours was reported to increase cardiac output in patients with acute heart failure. This effect was associated with a concomitant metabolic alkalosis and a negative water balance. Growing data strongly support the role of lactate as a preferential oxidizable substrate to supply energy metabolism leading to improved organ function (heart and brain especially) in ischemic conditions. Due to its sodium/chloride imbalance, this solution prevents hyperchloremic acidosis and limits fluid overload despite the obligatory high sodium load. Sodium lactate solution therefore shows many advantages and appears a very promising means for resuscitation of critically ill patients. Further studies are needed to establish the most appropriate dose and indications for sodium lactate infusion in order to prevent the occurrence of severe hypernatremia and metabolic alkalosis.In a recent issue of Critical Care, Nalos and colleagues evaluated the effect of 0.5 M sodium lactate (SL) solution on cardiac function in patients presenting acute heart failure [1]. The key result was that 24-hour infusion of SL resulted in increased cardiac output, whereas it did not change in the control group receiving Ringer lactate. This difference could be accounted for, in large part, by an augmentation in stroke volume. Further, patients receiving SL developed metabolic alkalosis, hypokalemia and hypernatremia, while their water balance was strongly negative. These findings highlight the complexity of the beneficial effects induced by SL infusion.First, hyperlactatemia is a good marker of poor outcome in critically ill patients. Tissue hypoxia is responsible for an increased lactate production resulting from glycolysis [2,3]. Proponents of intensive intervention therefore strongly believed that lactate was, to say the least, a useless waste end product, if not a toxic one. However, the cause–effect relationship is not clearly demonstrated. Indeed, growing data support the notion that lactate production is not deleterious, but rather is an adaptative response allowing one to maintain an appropriate energetic metabolism in the case of shock or organ failure [2-4]. Nevertheless, the effect of solutions containing high lactate concentration in these situations is still a matter of debate.Evidence is now accumulating that lactate is a preferred substrate readily oxidizable in energy crisis conditions [4-6]. In physiological basal situations, the myocardium functions using energy from beta-oxidation of fatty acids. When oxygen availability is limited, myocardial energy metabolism switches from lipid oxidation to carbohydrate oxidation [7]. Previous studies have already shown that lactate infusion was responsible for an improved myocardial function in patients with septic shock or after cardiac surgery [4,8,9]. The current study reproduces these results in patients with acute heart failure [1]. Levy and colleagues demonstrated that lactate deprivation worsened myocardial metabolism and performance in rats with septic shock [4]. This effect is believed to be due to, for the greater part, the preferential lactate metabolism supplying sufficient energy to the myocardium. However, this hypothesis should be confirmed using direct measurements of lactate oxidation in the heart. Similar results have been reported in normal and injured brain, and confirmed the role of lactate as an important source of energy [6,10,11]. Allaman and colleagues described the essential impact of lactate metabolism in the astrocyte–neuron coupling function [12]. In traumatic brain injury, SL infusion was more efficient than mannitol to decrease raised intracranial pressure [11]. In a later study, a systematic SL infusion over 48 hours decreased by 50% the incidence of elevated intracranial pressure episodes [13].The second point raised by Nalos and colleagues is the induction of metabolic alkalosis by SL infusion [1], which reflects the probable lactate oxidation. According to the Stewart concept, the exogenous lactate enters into the cells (metabolized anion) while exogenous sodium remains in the plasma (nonmetabolized cation). These modifications in turn induce an increase in the strong ion difference and in the plasma bicarbonate concentration [14]. In agreement with other studies, SL infusion induced metabolic alkalosis and hypokalemia and prevented hyperchloremic acidosis. The authors emphasized that metabolic alkalosis could improve cardiac function [1]. However, it is known that metabolic alkalosis decreases coronary artery blood flow and worsens cardiac arrhythmias, hypokalemia and cardiac contractility. On the other hand, prevention of hyperchloremic acidosis by the balanced SL solution could lead to an improvement in organ function [15,16]. The global consequences of such multiple and intricate metabolic modifications on cardiac function remain questioned.Third, the infusion of a large amount of sodium in patients with acute heart failure represents a clear danger as sodium restriction is the classic treatment for this condition. Surprisingly, the authors showed that the 24-hour and 48-hour water balances were strongly negative in patients receiving SL compared with the control group. This finding is in agreement with previous studies performed in cardiac surgery and traumatic brain-injured patients [9,11]. The mechanism by which SL influences water balance is not clear. A lower required volume of infusion and/or a higher urine output have been previously reported as a consequence of the sodium/chloride imbalance of this solution [9,11]. Unfortunately, these data are lacking in the study by Nalos and colleagues. Independently of the underlying mechanism, the resulting effect provides a substantial advantage in favor of SL infusion because fluid overload is associated with an increased morbi-mortality in various critical conditions, especially cardiac failure [17].In conclusion, the study by Nalos and colleagues provides additional arguments to strongly consider SL as a valuable means for resuscitation. Thanks to its high lactate and low chloride concentrations, SL offers substantial clinical improvement in organ functions, especially for the heart and brain.     

Hyperoxia: good or bad for the injured brain?

PURPOSE OF REVIEW: For decades it was assumed that cerebral ischemia was a major cause of secondary brain injury in traumatic brain injury, and management focused on improving cerebral perfusion and blood flow. Following the observation of mitochondrial dysfunction in traumatic brain injury and the widespread use of brain tissue oxygen tension (P(br)O(2) monitoring, however, recent work has focused on the use of hyperoxia to reduce the impact of traumatic brain injury. RECENT FINDINGS: Previous work on normobaric hyperoxia utilized very indirect measures of cerebral oxygen metabolism (intracranial pressure, brain oxygen tension and microdialysis) as outcome variables. Interpretation of these measures is controversial, making it difficult to determine the impact of hyperoxia. A recent study, however, utilized positron emission tomography to study the impact of hyperoxia on patients with acute severe traumatic brain injury and found no improvement on cerebral metabolic rate for oxygen with this intervention. SUMMARY: Despite suggestive data from microdialysis studies, direct measurement of the ability of the brain to utilize oxygen indicates that hyperoxia does not increase oxygen utilization. This, combined with the real risk of oxygen toxicity, suggests that routine clinical use is not appropriate at this time and should await appropriate prospective outcome studies.     

Lymphocytes in the neighborhood: good or bad for the kidney?

Lupus nephritis (LN) is common in people with systemic lupus erythematosus (SLE) and advances, almost invariably, to end-stage renal disease (ESRD). In this issue of the JCI, Abraham, Durkee, et al. presented a large-scale immune cell landscape of kidney biopsies from patients with LN by combining multiplexed confocal microscopy imaging with customized computer vision and quantification. The presence of diverse CD4^– T cells in small neighborhoods, but not of B cells or CD4⁺ T cells in large neighborhoods, is linked to the development of ESRD. Unexpectedly, B cells in the kidney heralded a good prognosis. The precise location of different types of immune cells allows inference on possible interactions between different immune cells and also between immune and kidney-resident cells. The data have important implications on the development of prognostic tools and effective targeted therapies in patients with LN.     

New airways for resuscitation?

Over the last 15 years supraglottic airway devices (SADs), most notably the classic laryngeal mask airway (LMA) have revolutionised airway management in anaesthesia. In contrast for resuscitation, both in and outside hospital, facemask ventilation and tracheal intubation remain the mainstays of airway management. However there is evidence that both these techniques have complications and are often poorly performed by inexperienced personnel. Tracheal intubation also has the potential to cause serious harm or death through unrecognised oesophageal intubation. SADs may have a role in airway management for resuscitation as first responder devices, rescue devices or for use during patient extraction. In particular they may be beneficial as the level of skill required to use the device safely may be less than for the tracheal tube. Concerns have been expressed over the ability to ventilate the lungs successfully and also the risk of aspiration with SADs. The only SADs recommended by ILCOR in its current guidance are the classic LMA and combitube. Several SADs have recently been introduced with claims that ventilation and airway protection is improved. This pragmatic review examines recent developments in SAD technology and the relevance of this to the potential for using SADs during resuscitation. In addition to examining research directly related to resuscitation both on bench models and in patients the review also examines evidence from anaesthetic practice. SADS discussed include the classic, intubating and Proseal LMAs, the combitube, the laryngeal tube, laryngeal tube sonda mark I and II and single use laryngeal masks.     

New therapies for heart failure: is thalidomide the answer?

The syndrome of advanced heart failure is associated with considerable morbidity and mortality. Ideas about the reasons for the progressive nature of the heart failure syndrome have changed over the years, with the initial view that progression was principally due to pump failure (the 'haemodynamic' hypothesis), giving way to more modern views, which implicate neuro-endocrine activation (including catecholamine excess, renin-angiotensin system activation, etc.). More recently, an excess of inflammatory cytokines has been found in advanced heart failure and implicated in the progression of the disease. Amongst the cytokines found, TNF-alpha seems to be particularly important. The principle therapeutic action of thalidomide appears to be reduction of TNF-alpha levels. We therefore suggest that there may be a role for thalidomide, or its derivatives, in the management of advanced heart failure.