Central venous oxygen saturation and emergency intubation – another piece in the puzzle?

A recent multicentre observational study examined the effect of emergency intubation on central venous oxygen saturation (SCVo2) in critically ill patients. The main finding was that SCVo2 significantly increases 15 minutes after emergency intubation and institution of mechanical ventilation with 100% oxygen, especially in those patients with pre-intubation SCVo2 values <70%, regardless of whether these patients suffered from severe sepsis. However, in only one-quarter of this subgroup was the SCVo2 normalized to ≥70% solely by this intervention. In contrast, in patients with pre-intubation SCVo2 ≥70%, the SCVo2 failed to increase after intubation. A rise in SCVo2 can be expected when whole body oxygen extraction remains unchanged after intubation and ventilation with pure oxygen

Sepsis therapy: what's the best for the mitochondria?

It is suspected that mitochondrial dysfunction is a major cause of organ failure in sepsis and septic shock. A study presented in this issue of Critical Care revealed that liver mitochondria from pigs treated with norepinephrine during endotoxaemia exhibit greater in vitro respiratory activity. The investigators provide an elegant demonstration of how therapeutic interventions in sepsis may profoundly influence mitochondrial respiration, but many aspects of mitochondrial function in sepsis remain to be clarified

Which variables are associated with blood glucose levels outside the target range in surgical critically ill patients? A retrospective observational study

<p>Abstract</p> <p>Background</p> <p>The aim of the present study is to determine the variables affecting blood glucose concentrations outside the target range of 80 and 150 mg/dl in critically ill surgical patients.</p> <p>Methods</p> <p>All critically ill surgical patients admitted to a university ICU, from 01/2007 to 12/2008, were surveyed daily using computer assistance with respect to minimal and maximal daily blood glucose concentrations, application of insulin and demographic/clinical variables. Multiple logistic regression for clustered data with backward elimination was performed to identify variables strongly associated with blood glucose concentrations < 80 mg/dl or ≥ 150 mg/dl in 804 patients with an ICU stay > 72 hours.</p> <p>Results</p> <p>Application of insulin (odds ratio (OR) 2.1, with corresponding 95% confidence interval (CI) 1.7; 2.6), noradrenaline (OR 1.4, 95% CI 1.2 - 1.8) or steroids (1.3, 1.003 - 1.7), and age (per year) (1.02, 1.01 - 1.03) were associated with an increased risk of blood glucose concentrations < 80 mg/dl. In analogy, application of insulin (OR 2.4, 95% CI 2.0 - 2.7), noradrenaline (1.4, 1.2 - 1.6) or steroids (1.4, 1.2 - 1.7), severe sepsis (1.2, 1.1 - 1.4), neurosurgery (OR 1.0) compared to abdominal, vascular and trauma surgery, and age (per year) (1.01, 1.01 - 1.02), were associated with an increased risk of blood glucose concentrations ≥ 150 mg/dl.</p> <p>Conclusions</p> <p>Critically ill surgical patients are at an increased risk for fluctuating blood glucose concentrations ranging < 80 mg/dl or ≥ 150 mg/dl in particular if they are of advanced age and require administration of insulin, noradrenaline, and/or steroids. Patients who underwent neurosurgery and/or presented with severe sepsis/shock are those in particular at risk for blood glucose concentrations ≥ 150 mg/dl.</p

Year in review 2007: Critical Care – shock

The research papers on shock published in Critical Care throughout 2007 are related to three major subjects: the modulation of the macrocirculation and microcirculation during shock, focusing on arginine vasopressin, erythropoietin and nitric oxide; studies on metabolic homeostasis (acid–base status, energy expenditure and gastrointestinal motility); and basic supportive measures in critical illness (fluid resuscitation and sedation, and body-temperature management). The present review summarizes the key results of these studies and provides a brief discussion in the context of the relevant scientific and clinical background

Vasopressin in vasodilatory shock: is the heart in danger?

In patients with hyperdynamic hemodynamics, infusing arginine vasopressin (AVP) in advanced vasodilatory shock is usually accompanied by a decrease in cardiac output and in visceral organ blood flow. Depending on the infusion rate, this vasoconstriction also reduces coronary blood flow despite an increased coronary perfusion pressure. In a porcine model of transitory myocardial ischemia-induced left ventricular dysfunction, Müller and colleagues now report that the AVP-related coronary vaso-constriction may impede diastolic relaxation while systolic contraction remains unaffected. Although any AVP-induced myocardial ischemia undoubtedly is a crucial safety issue, these findings need to be discussed in the context of the model design, the dosing of AVP as well as the complex direct, afterload-independent and systemic, vasoconstriction-related effects on the heart

Cardiac magnetic resonance imaging derived quantification of myocardial ischemia and scar improves risk stratification and patient management in stable coronary artery disease

Background: Quantification of myocardial ischemia and necrosis might ameliorate prognostic models and lead to improved patient management. However, no standardized consensus on how to assess and quantify these parameters has been established. The aim of this study was to quantify these variables by cardiac magnetic resonance imaging (CMR) and to establish possible incremental implications in cardiovascular risk prediction. Methods: This study is a retrospective analysis of patients with known or suspected coronary artery disease (CAD) referred for adenosine perfusion CMR was performed. Myocardial ischemia and necrosis were assessed and quantified using an algorithm based on standard first-pass perfusion imaging and late gadolinium enhancement (LGE). The combined primary endpoint was defined as cardiac death, non-fatal myocardial infarction, and stroke. Results: 845 consecutive patients were enrolled into the study. During the median follow-up of 3.64 [1.03; 10.46] years, 61 primary endpoints occurred. Patients with primary endpoint showed larger extent of ischemia (10.7 ± 12.25% vs. 3.73 ± 8.29%, p &lt; 0.0001) and LGE (21.09 ± 15.11% vs. 17.73 ± 10.72%, p &lt; 0.0001). A risk prediction model containing the extent of ischemia and LGE proved to be superior in comparison to all other models (χ² increase: from 39.678 to 56.676, integrated discrimination index: 0.3851, p = 0.0033, net reclassification index: 0.11516, p = 0.0071). The ben­eficial effect of revascularization tended to be higher in patients with greater extents of ischemia, though statistical significance was not reached. Conclusions: Quantification of myocardial ischemia and LGE was shown to significantly improve existing risk prediction models and might thus lead to an improvement in patient management

Of mice and men (and sheep, swine etc.): The intriguing hemodynamic and metabolic effects of hydrogen sulfide (H2S)

Whether the hydrogen sulfide (H2S)-induced metabolic depression observed in awake rodents exists in larger species is controversial. Therefore, Derwall and colleagues exposed anesthetized and ventilated sheep to incremental H2S concentrations by means of an extracorporeal membrane oxygenator. H2S caused pulmonary vasoconstriction and metabolic acidosis at the highest concentration studied. Oxygen uptake and carbon dioxide production remained in the physiological range. The authors concluded that, beyond the effect of temperature, H2S hardly modifies metabolism at all. Since the highest H2S concentration caused toxic side effects (possibly due to an inhibition of mitochondrial respiration), the therapeutic use of inhaled H2S should be cautioned