2,833 publications from this institution
The underlying cause of sepsis is a dysregulated host response to infection, leading to multiple organ failure. Identifying sepsis is crucial because of the associated pathophysiological, practical, and therapeutic implications, which will determine where and how the patient should be managed. In the absence of an end-of-life decision to limit therapies, the patient should be admitted to the intensive care unit immediately. Importantly, not all patients with sepsis are the same and being able to better characterize them is important. The future will focus on phenotypes to characterize critically ill patients, with or without infection, to enable more appropriate targeting of therapeutic interventions.
It is very important to optimize cardiac output and oxygen delivery by optimizing fluid therapy, and pulse pressure variation can help to identify fluid responsiveness. Dr. Sondergaard is right in underlining all the limitations of pulse pressure variation, but anesthesia provides an ideal setting for the use of pulse pressure variation as there is no spontaneous breathing effort during controlled mechanical ventilation and usually no bronchospasm or right heart failure.Dr. Sondergaard reinforces our provocative statement that we may not have to measure cardiac output during surgery1 when he writes that “YES, we have to measure cardiac output in high-risk surgery to optimize oxygen delivery” without detailing how the measurement can help practically; this sounds to us rather like dogma.
These analyses suggest that outcomes for patients with severe sepsis are closely related to early (baseline to day 1 here) improvement, or lack thereof, in organ function. Also, clinical improvement on subsequent days may have little additional impact on the likelihood of survival.
Summary: Calcium-entry blockers were administered in an attempt to protect myocardium during cardiac arrest due to ventricular fibrillation in mechanically ventilated dogs. An intravenous injection of verapamil, nifedipine, or lidoflazine was administered prior to successively prolonged episodes of ventricular fibrillation, during which no thoracic compression was performed. It is of interest that ventricular defibrillation was more easily obtained after treatment with the three drugs. As previously observed in this model, nine control dogs developed electromechanical dissociation (EMD) after 120 seconds of ventricular fibrillation. In contrast, six of the 11 dogs treated with 0.3 mg/kg of verapamil recovered mechanical systole after 120 seconds of ventricular fibrillation (p < 0.05). Nifedipine administration also postponed the onset of EMD in three of four dogs. However, lidoflazine postponed the onset of EMD in only one of the eight dogs. The later onset of EMD after administration of verapamil or nifedipine in this model was attributed to myocardial protection by calcium-entry blockers during ventricular fibrillation. Decreased energy utilization during cardiac arrest was considered to be the principal protective mechanism. These observations indicate calcium-entry blockers, and especially verapamil and nifedipine, can be valuable drugs during cardiac resuscitation for ventricular fibrillation.
Nobody will argue with the observation that a positive fluid balance is associated with increased mortality rates (1-3). Indeed, this finding is not surprising, because patients who are more severely ill are more likely to develop edema whether or not they have renal failure. Therefore, studies investigating the impact of fluid balance on outcomes must use multivariable or propensity-matched analyses that include many variables in order to determine whether fluid balance is independently associated with outcome. This has been done in several recent studies. In a study conducted in our Department of Intensive Care in Brussels, fluid balance was more positive in non-surviving than in surviving patients with sepsis, and these factors remained related even after adjustment for many variables (2). The monocentric nature of the study may be seen as a weakness, but it is also a strength because it means that variability in patient management was limited. Larger observational studies conducted in Europe (3) and worldwide (1) have shown similar results. These two studies included many variables, enabling quite extensive multivariable analyses to be conducted. In the SOAP study (3), a positive fluid balance had an impressively high prognostic value, just below that of the SAPS II score. In the recent analysis of the ICON database, the effects of a positive fluid balance, again significantly associated with outcome, were particularly important after the first 24 hours (1).
Severe acute arterial hypertension can be associated with significant morbidity and mortality. After excluding a reversible etiology, choice of therapeutic intervention should be based on evaluation of a number of factors, such as age, comorbidities, and other ongoing therapies. A rational pathophysiological approach should then be applied that integrates the effects of the drug on blood volume, vascular tone, and other determinants of cardiac output. Vasodilators, calcium channel blockers, and beta-blocking agents can all decrease arterial pressure but by totally different modes of action, which may be appropriate or contraindicated in individual patients. There is no preferred agent for all situations, although some drugs may have a more attractive profile than others, with rapid onset action, short half-life, and fewer adverse reactions. In this review, we focus on the main mechanisms underlying severe hypertension in the critically ill and how using a pathophysiological approach can help the intensivist decide on treatment options. © 2013 Ribeiro Salgado et al. licensee Springer.
