36 research outputs found
Near-infrared spectroscopy during stagnant ischemia estimates central venous oxygen saturation and mixed venous oxygen saturation discrepancy in patients with severe left heart failure and additional sepsis/septic shock
Skeletal muscle oxygen saturation does not estimate mixed venous oxygen saturation in patients with severe left heart failure and additional severe sepsis or septic shock
Measurement of skeletal muscle tissue oxygenation in the critically ill
Shock is a state of acutely reduced tissue oxygenation. In cardiogenic shock oxygen delivery (DO2) is reduced, but oxygen extraction is preserved. In septic shock DO2 is preserved, but oxygen extraction is decreased because of microvascular changes and disturbed metabolism. Global assessment of DO2 and oxygen consumption does not tell us enough about adequacy of regional perfusion. The aim of this study was to assess the value of near infrared spectroscopy (NIRS) in detecting skeletal muscle tissue oxygenation (StO2) in critically ill patients.
Patients in cardiogenic shock (n=17), septic shock (n=14), without shock but with localized infection (n=14) and healthy volunteers (n=15) were included. Thenar StO2 was measured with NIRS before (baseline StO2, %), between (downward StO2 slope, %/min) and after 90 seconds of upper arm stagnant ischemia (hyperemic StO2, %). Muscle oxygen extraction (mOER) was calculated as follows: mOER (%) = (1-baselineStO2/hyperemic StO2)*100. Repeatability was assessed using the Bland Altman method (95 % of values within limits of agreement), comparing 55 pairs of measurements performed in 5-minute intervals.
Repeatability of measurements was clinically acceptable. Compared to septic shock patients, cardiogenic shock patients had lower baseline StO2 (68.9 ± 10.0 % vs. 84.3 ± 10.4 %; p < 0.05) and hyperemic StO2 (80.8 ± 7.8 % vs. 91.8 ± 8.3 %; p < 0.05), and a higher downward StO2 slope (-17.4 ± 31.7 %/min vs. -9.1 ± 2.6 %/min; p < 0.05). mOER was higher in healthy volunteers (11.9 ± 3.8 %) and volunteers with cardiogenic shock (14.8 ± 7.3 %) compared to septic shock patients (8.1 ± 7.8 %) and those with localized infection (7.6 ± 5.4 %) (p < 0.05).
Repeatability of baseline StO2 and hyperemic StO2 is clinically acceptable. Results support the hypothesis that skeletal muscle oxygen extraction capability is preserved and extraction is increased in cardiogenic shock compared to septic shock
Do we need an individual approach to atrial fIbrillation and adrenergic overload in the critically ill?
Despite catecholamines being lifesaving
drugs, they can also be harmful. Adrenergic
overload is one of the major promoters of
supra- and ventricular arrhythmias, which
induce hemodynamic instability in the critically
ill. In this paper we will focus on the
pathophysiology of atrial fbrillation (AF),
the importance of adrenergic overload for
triggering AF, the importance of the autonomic
nervous system and fnally, we will
challenge the importance of decreasing
adrenergic load with selective and nonselective
β-blockers, which have diferent
efects on the metabolism in the severely
ill. We will also emphasize the importance
of an individual approach due to pharmacogenetic
diferences in β-adrenergic signalling
Do we need an individual approach to atrial fibrillation and adrenergic overload in the critically ill?
Despite catecholamines being lifesaving
drugs, they can also be harmful. Adrenergic
overload is one of the major causes of
supra- and ventricular arrhythmias, which
induce haemodynamic instability of critically
ill patients. In this paper we will focus
on the pathophysiology of atrial fibrillation
(AF), the importance of adrenergic overload
for triggering AF, the importance of
the autonomic nervous system and we will
challenge the importance of decreasing
adrenergic load with selective and nonselective
β-blockers, which have different
effects on the metabolism of the severely
ill. We will also emphasize the importance
of an individual approach due to pharmacogenetic
differences in β-adrenergic signalling
Long-term outcome and quality of life of patients treated in surgical intensive care: a comparison between sepsis and trauma
INTRODUCTION: Our aim was to determine long-term survival and quality of life of patients admitted to a surgical intensive care unit (ICU) because of sepsis or trauma. METHODS: This was an observational study conducted in an 11-bed, closed surgical ICU at a 860-bed teaching general hospital over a 1-year period (January 2003 to December 2003). Patients were divided into two groups according to admission diagnoses: group 1 included patients with sepsis; and group 2 included patients with trauma (polytrauma, multiple trauma, head injury, or spinal injury). Quality of life was assessed after 2 years following ICU admission using the EuroQol 5D questionnaire. RESULTS: A total of 164 patients (98 trauma patients and 66 patients with sepsis) were included in the study. Trauma patients were younger than patients with sepsis (53 ± 21 years versus 64 ± 13 years; P ≤ 0.001). There was no significant difference between groups in Acute Physiology and Chronic Health Evaluation II score or length of stay in the surgical SICU. Trauma patients stayed longer on the general ward (35 ± 44 days versus 17 ± 24 days; P < 001). Surgical ICU survival, in-hospital survival, and post-hospital and cumulative 2-year survival were lower in the sepsis group than in the trauma group (surgical ICU survival: 60% versus 74%; in-hospital survival: 42% versus 62%; post-hospital survival: 78% versus 92%; cumulative 2-year survival: 33% versus 57%; P < 0.05). There was no significant difference in quality of life in all five dimensions of the EuroQol 5D between groups: 60% of patients had signs of depression, almost 60% had problems in usual activities and 56% had pain. CONCLUSION: Patients with sepsis treated in a surgical ICU have higher short-term and long-term mortality than do trauma patients. However, quality of life is reduced to the same level in both groups
Total plasma sulfde in mild to moderate diastolic heart dysfunction
Background. Te early pathophysiological mechanisms of diastolic dysfunction are not understood well. Hydrogen sulfde is
an important endogenous gaseous transmitter that can infuence heart remodeling. The aim was to determine total plasma
sulfde (TPS) levels, as a surrogate marker of hydrogen sulfde, in patients with mild diastolic dysfunction.
Methods. Total plasma sulfde and N-terminal pro brain-type natriuretic peptide (NT-proBNP) levels were determined in ambulatory patients with arterial hypertension or diabetes mellitus and echocardiographically mild to moderate diastolic dysfunction.
Results. Twenty-four patients were included: nine with normal diastolic function (Grade 0), eight with an impaired relaxation pattern (Grade 1), and seven with a pseudo-normalized pattern (Grade
2). TPS levels were highest in patients with normal diastolic function (Grade 0), and lowest in patients with Grade 2 diastolic
dysfunction, with this diference between Grade 0 and Grade 2 showing statistical signifcance (p = 0.017). NT-proBNP levels showed the reverse behavior, with this diference again showing statistical signifcance (p = 0.042).
Conclusions. Total plasma sulfde levels decrease with worsening of diastolic function from normal to moderate diastolic
dysfunction
Cytokine Response of Cultured Skeletal Muscle Cells Stimulated with Proinflammatory Factors Depends on Differentiation Stage
Myoblast proliferation and myotube formation are critical early events in skeletal muscle regeneration. The attending inflammation and cytokine signaling are involved in regulation of skeletal muscle cell proliferation and differentiation. Secretion of muscle-derived cytokines upon exposure to inflammatory factors may depend on the differentiation stage of regenerating muscle cells. Cultured human myoblasts and myotubes were exposed to 24-hour treatment with tumor necrosis factor (TNF)-α or lipopolysaccharide (LPS). Secretion of interleukin 6 (IL-6), a major muscle-derived cytokine, and interleukin 1 (IL-1), an important regulator of inflammatory response, was measured 24 hours after termination of TNF-α or LPS treatment. Myoblasts pretreated with TNF-α or LPS displayed robustly increased IL-6 secretion during the 24-hour period after removal of treatments, while IL-1 secretion remained unaltered. IL-6 secretion was also increased in myotubes, but the response was less pronounced compared with myoblasts. In contrast to myoblasts, IL-1 secretion was markedly stimulated in LPS-pretreated myotubes. We demonstrate that preceding exposure to inflammatory factors stimulates a prolonged upregulation of muscle-derived IL-6 and/or IL-1 in cultured skeletal muscle cells. Our findings also indicate that cytokine response to inflammatory factors in regenerating skeletal muscle partially depends on the differentiation stage of myogenic cells
Can echocardiographic assessment of interatrial septum shape and motion improve the accuracy of the BLUE protocol?
Acute respiratory failure is one of the most challenging critical conditions due to a wide variety of differential diagnosis. Bedside lung ultrasound in emergency (BLUE) protocol allows accurate differentiation between the most common underlying causes of acute respiratory failure in up to 90% of the cases. The assessment of left atrial pressure affecting left ventricular filling is essential in critically ill patients guiding volume substitution, optimization of left ventricular function and prevention of pulmonary congestion, thus ensuing haemodynamic stability. A simple, non-invasive method of left atrial pressure evaluation is the echocardiographic assessment of interatrial septum shape and motion, which is affected by interatrial pressure gradient. Aiming to improve the accuracy of the BLUE protocol, we propose the simple, non-invasive echocardiographic assessment of interatrial septum shape and motion as an upgrade, providing additional information of the loading of left and right atrium thus distinguishing the most common causes of acute respiratory failure
Echocardiography of isolated subacute left heart tamponade in a patient with cor pulmonale and circumferential pericardial effusion
Patients with advanced idiopathic pulmonary artery hypertension have often a chronic pericardial effusion. It is the result of increased transudation and impaired re-absorption due to elevated venous pressure. These patients have pre-existent symptoms and signs of chronic right heart failure. High degree of suspicion is required to detect of development of an atypical form of tamponade with isolated compression of left heart chambers as shown in present case report. Transthoracic echocardiography provides a rapid access to the correct diagnosis, a prompt relief of symptoms following the ultrasound guided pericardiocentesis and important diagnostic tool for regular follow up of patients thereafter as shown in our case report