Effects of fluid administration on renal perfusion in critically ill patients

IntroductionFluid administration is a first-line therapy for acute kidney injury associated with circulatory failure. Although aimed at increasing renal perfusion in these patients, this intervention may improve systemic hemodynamics without necessarily ameliorating intrarenal flow distribution or urine output. We used Doppler techniques to investigate the effects of fluid administration on intrarenal hemodynamics and the relationship between changes in renal hemodynamics and urine output. We hypothesized that, compared to systemic hemodynamic variables, changes in renal hemodynamics would better predict increase in urine output after fluid therapy.MethodsWe measured systemic hemodynamic variables and performed renal interlobar artery Doppler on both kidneys before and after volume expansion in 49 adult patients with acute circulatory failure. We measured systolic and diastolic velocities and computed the resistivity index (RI). We recorded urine output for 3 h before and after the fluid challenge.ResultsFluid administration resulted in a small but consistent decrease in RI (from 0.73 ± 0.09 to 0.71 ± 0.09, p < 0.01). There was a concomitant increase in mean arterial pressure (from 75 ± 15 to 80 ± 14 mmHg, p < 0.01), pulse pressure (49 ± 19 to 55 ± 19 mmHg, p < 0.01) and urine output (55 ± 76 to 81 ± 87 ml/hour, p < 0.01). Changes in RI were negatively correlated with changes in urine output and mean arterial pressure but not in pulse pressure. The increase in urine output was predicted by changes in RI but not by changes in systemic hemodynamics.ConclusionsChanges in renal hemodynamics during a fluid challenge can be observed by Doppler ultrasonography before urine output increases. Moreover, these changes are better predictors of an increase in urine output than are mean arterial pressure and pulse pressure.     

A prospective study of biopsy-proven myocarditis: prognostic relevance of clinical and aetiopathogenetic features at diagnosis.

AIMS: Myocarditis may be idiopathic, viral, and/or immune; frequency of these forms and prognosis are ill-defined. We aimed at identifying aetiopathogenetic and prognostic markers in myocarditis, including viral genome on endomyocardial biopsy (EMB) by polymerase chain reaction (PCR) and serum anti-heart autoantibodies (AHA). METHODS AND RESULTS: We studied 174 patients, 110 males, aged 36 +/- 18 years, median follow-up 23.5 months, range 10-54; 85 patients had active myocarditis and 89 borderline myocarditis (no diffuse or severe inflammation) (Dallas criteria). Serum AHA were detected by indirect immunofluorescence. PCR was used to detect virus. Six-year actuarial survival was 73%. AHA were found in 56% of patients and positive PCR in 26%. Univariate predictors of death/transplantation were young age, longer symptom duration, giant cell myocarditis, NYHA II-IV, positive PCR, presentation with LV dysfunction, clinical signs/symptoms of heart failure, and echocardiographic and haemodynamic indexes of cardiac dysfunction. By Cox univariate analysis, highest risk was conferred by clinical signs/symptoms of left (HR = 4.3, CI 1.7-10.8, P = 0.002) and right heart failure (HR 3.4, CI 1.5-7.3, P = 0.002). CONCLUSION: In myocarditis, biventricular dysfunction at diagnosis was the main predictor of death/transplantation. AHA identified immune-mediated myocarditis in the majority of cases. Viral genome was a univariate predictor of adverse prognosis. Our approach of using AHA and positive PCR as aetiopathogenetic markers should help patient selection and recruitment in future studies on aetiological therapy.     

Genetically determined myocarditis: clinical presentation and immunological characteristics

PURPOSE OF REVIEW: Myocarditis is a clinically heterogeneous myocardial inflammatory disease, diagnosed by endomyocardial biopsy; it may be idiopathic, infectious, or autoimmune and may lead to dilated cardiomyopathy. Myocarditis and dilated cardiomyopathy represent different stages of an organ-specific autoimmune disease in genetically predisposed individuals. RECENT FINDINGS: In animal models, cell-mediated or antibody-mediated autoimmune myocarditis/dilated cardiomyopathy can be induced by viral infection or immunization with heart-specific autoantigens, or can develop spontaneously in genetically predisposed strains. Susceptibility is based on multiple major histocompatibility complex and nonmajor histocompatibility complex genes. In patients the diagnosis of autoimmune myocarditis/dilated cardiomyopathy requires exclusion of viral genome on endomyocardial biopsy and detection of serum heart-reactive autoantibodies. They are directed against multiple antigens that are found in patients and relatives from about 60% of familial and nonfamilial pedigrees. They predict dilated cardiomyopathy development among relatives, years before disease. Some antibodies have functional effects on cardiac myocytes in vitro, in animals and possibly in a dilated cardiomyopathy subset, responsive to extracorporeal immunoadsorption. SUMMARY: In myocarditis/dilated cardiomyopathy, cardiac-specific and disease-specific antibodies of IgG class are potential biomarkers for identifying 'at risk' relatives as well as those patients in whom, in the absence of active infection of the myocardium, immunosuppression, and/or immunomodulation may be beneficial. Future studies should better define the genetic basis of human autoimmune myocarditis/dilated cardiomyopathy.     

Therapeutic hypothermia in Italian Intensive Care Units after 2010 resuscitation guidelines: Still a lot to do

Background

Therapeutic hypothermia (TH) is one of three interventions that have demonstrated to improve patients’ neurological outcome after cardiac arrest. The aim of this study was to investigate the effect of the 2010 resuscitation guidelines on TH implementation in various Italian Intensive Care Units (ICU).

Methods

A structured questionnaire was submitted to Italian ICU. The questionnaire was addressed to determine the procedures of TH in each ICU or, on the contrary, the reason for not employing the therapy.

Results

We obtained complete information from 770 of 847 Italian ICU (91%). Out of 405 Units included in the analysis only 223 (55.1%) reported to use TH in comatose patients after return of spontaneous circulation. The trend of TH implementation shows a stable increase, particularly after 2006 but there is no evident acceleration after the strong indication of the 2010 guidelines. There was a rise of about 3.4 times in the number of Italian ICU using TH as compared to the 2007 survey (an increase of 68% per year). One hundred and eighty-two (44.9%) units did not use TH mainly because of lack of equipment, economic issues or the conviction of the difficulty of execution.

Conclusions

TH is still under-used in Italy (55.1%) even though the therapy is strongly recommended in the 2010 guidelines. However, the increase in the adoption of hypothermia has been significant in the past 5 years (68%/years) and the awareness of the efficacy is almost consolidated among intensivists, being logistic problems the leading cause for non-adoption.     

Myocardial depression in sepsis: From pathogenesis to clinical manifestations and treatment

The cardiovascular system plays a key role in sepsis, and septic myocardial depression is a common finding associated with increased morbidity and mortality. Myocardial depression during sepsis is not clearly defined, but it can perhaps be best described as a global (systolic and diastolic) dysfunction of both the left and right sides of the heart. The pathogenesis of septic myocardial depression involves a complex mix of systemic (hemodynamic) factors and genetic, molecular, metabolic, and structural alterations. Pulmonary artery catheterization and modern echo-Doppler techniques are important diagnostic tools in this setting. There are no specific therapies for septic myocardial depression, and the cornerstone of management is control of the underlying infectious process (adequate antibiotic therapy, removal of the source) and hemodynamic stabilization (fluids, vasopressor and inotropic agents). In this review, we will summarize the pathogenesis, diagnosis, and treatment of myocardial depression in sepsis. Additional studies are needed in order to improve diagnosis and identify therapeutic targets in septic myocardial dysfunction.