2,833 publications from this institution
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Measurement of right ventricular ejection fraction (RVEF) by the thermodilution technique has become routinely available at the bedside of the critically ill. We describe 2 patients with tricuspid regurgitation in whom RVEF values were considerably lower by thermodilution than by radionuclide techniques. Discrepancies could be due to the regurgitation of the thermodilution signal and possibly to the different nature of the two measurements (forward stroke volume with the thermodilution technique and total stroke volume with the radionuclide technique). We suggest that lower RVEF measurement by the thermodilution technique could be related to unrecognized tricuspid regurgitation. Measurement of an unexpectedly low RVEF by the thermodilution technique should suggest the presence of tricuspid regurgitation.
The term “nosocomial pneumonia” broadly covers all infections occurring 48 hours or more after hospital admission excluding any infection incubating at the time of admission, and has also been called hospital acquired pneumonia. Intensive care unit (ICU) acquired pneumonia (occurring within 48 hours of admission to the ICU) and ventilator associated pneumonia (occurring within 48 hours of starting mechanical ventilation) are also included in the broader term “nosocomial pneumonia”. The development of nosocomial pneumonia remains a major problem in the ICU with most studies reporting an incidence of between 9% and 45%,1-19 depending on the groups of patients being studied, the definition of nosocomial pneumonia, and the criteria used to diagnose it. It has been shown that nosocomial pneumonia acquired in the ICU markedly increases the length of hospital stay12 16 20 21 and the costs of hospital care.21 22 Mortality rates may also be increased,3 5 7 16 17 19 23 although it is not entirely clear whether all deaths from nosocomial pneumonia are directly related to the development of an infection. The so-called “attributable mortality”, defined as the mortality occurring as the direct result of the nosocomial pneumonia, may be especially high when Pseudomonas or Acinetobacter species are involved as pathogens.19 The diagnosis of nosocomial pneumonia is not straightforward, particularly in patients who are critically ill, as routine parameters do not have a high specificity for pneumonia in these patients.24 For example, infiltrates on chest radiographs consistent with pneumonia may be due to many other processes including oedema, atelectasis, and infarction.25 Positive cultures from tracheal aspirates are also non-specific as the upper respiratory tract of most critically ill patients is colonised by potential pulmonary pathogens.26 Alternative diagnostic techniques such as protected specimen brush biopsies and bronchoalveolar lavage have therefore been …
Personalized hemodynamic management targets personal normal values of hemodynamic variables, which are adjusted to biometric data and adapted to the clinical situation (i.e., adequate values). This approach optimizes cardiovascular dynamics based on the patient's personal hemodynamic profile.
SCOPUS: NotDefined.j
Postoperative salmonella meningitis: suc- cessful treatment with cefotaxime
To study the relationship between the electrical and the mechanical activities of the heart, we have developed a closed chest animal model in which the onset of electromechanical dissociation (EMD) could be predictably observed during cardiac arrest. Ventricular fibrillation, induced by a wire introduced into the right ventricle, was passively observed for successive periods of 60, 90 and 120 seconds, before external defibrillation was performed. When ventricular fibrillation lasted 120 seconds, EMD was consistently observed in each control animal. Adequate electrical activity persisted for more than 10 minutes in each dog. Pretreatment with the calcium antagonists verapamil and nifedipine delayed the onset of EMD, thereby providing myocardial protection during ventricular fibrillation. These observations indicate that the onset of EMD is predictable after ventricular fibrillation. This model can be used to study the effects of pharmacological interventions on the development of EMD.
