Journal of applied physiology
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After shock, persistent oxygen extraction deficit despite the apparent adequate recovery of systemic hemodynamic and oxygen-derived variables has been a source of uncertainty and controversy. Dysfunction of oxygen transport pathways during intensive care underlies the sequelae that lead to organ failure, and the limitations of techniques used to measure tissue oxygenation in vivo have contributed to the lack of progress in this area. Novel techniques have provided detailed quantitative insight into the determinants of microcirculatory and mitochondrial oxygenation. ⋯ Studies identified loss of coherence between the macrocirculation and the microcirculation, in which resuscitation successfully restored systemic circulation but did not alleviate microcirculatory perfusion alterations. Various mechanisms responsible for these alterations underlie the loss of hemodynamic coherence during unsuccessful resuscitation procedures. Therapeutic resolution of persistent heterogeneous microcirculatory alterations is expected to improve outcomes in critically ill patients.
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The earliest description of what is now known as the acute respiratory distress syndrome (ARDS) was a highly lethal double pneumonia. Ashbaugh and colleagues (Ashbaugh DG, Bigelow DB, Petty TL, Levine BE Lancet 2: 319-323, 1967) correctly identified the disease as ARDS in 1967. Their initial study showing the positive effect of mechanical ventilation with positive end-expiratory pressure (PEEP) on ARDS mortality was dampened when it was discovered that improperly used mechanical ventilation can cause a secondary ventilator-induced lung injury (VILI), thereby greatly exacerbating ARDS mortality. ⋯ The mechanical breath will be deconstructed to show that multiple parameters that comprise the breath-airway pressure, flows, volumes, and the duration during which they are applied to each breath-are critical to lung injury and protection. Specifically, the mechanisms by which a properly set mechanical breath can reduce the development of excessive fluid flux and pulmonary edema, which are a hallmark of ARDS pathology, are reviewed. Using our knowledge of how multiple parameters in the mechanical breath affect lung physiology, the optimal combination of pressures, volumes, flows, and durations that should offer maximum lung protection are postulated.
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Review Meta Analysis
Clinical outcomes and cardiovascular responses to exercise training in heart failure patients with preserved ejection fraction: a systematic review and meta-analysis.
Exercise training induces physical adaptations for heart failure patients with systolic dysfunction, but less is known about those patients with preserved ejection fraction. To establish whether exercise training produces changes in peak V̇o2 and related measures, quality of life, general health, and diastolic function in heart failure patients with preserved ejection fraction. We conducted a MEDLINE search (1985 to October 10, 2014), for exercise-based rehabilitation trials in heart failure, using search terms "exercise training, heart failure with preserved ejection fraction, heart failure with normal ejection fraction, peak V̇o₂, and diastolic heart dysfunction". ⋯ The corresponding data are provided for the following exercise test variables: V̇e/V̇co₂ slope, MD 0.85 ml·kg(-1)·min(-1) (95% CI 0.05 to 1.65, P = 0.04); maximum heart rate, MD 5.60 beats per minute (95% CI 3.95 to 7.25, P < 0.00001); Six-Minute Walk Test, MD 32.1 m (95% CI 17.2 to 47.1, P < 0.0001); and indices of diastolic function: E/A ratio, MD 0.07 (95% CI 0.02 to 0.12, P = 0.005); E/E' ratio MD -2.31 (95% CI -3.44 to -1.19, P < 0.0001); deceleration time (DT), MD -13.2 ms (95% CI -19.8 to -6.5, P = 0.0001); and quality of life: Minnesota Living with Heart Failure Questionnaire, MD -6.50 (95% CI -9.47 to -3.53, P < 0.0001); and short form-36 health survey (physical dimension), MD 15.6 (95% CI 7.4 to 23.8, P = 0.0002). In 3,744 h patient-hours of training, not one death was directly attributable to exercise. Exercise training appears to effect several health-related improvements in people with heart failure and preserved ejection fraction.
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Review Meta Analysis
Clinical outcomes and cardiovascular responses to exercise training in heart failure patients with preserved ejection fraction: a systematic review and meta-analysis.
Exercise training induces physical adaptations for heart failure patients with systolic dysfunction, but less is known about those patients with preserved ejection fraction. To establish whether exercise training produces changes in peak V̇o2 and related measures, quality of life, general health, and diastolic function in heart failure patients with preserved ejection fraction. We conducted a MEDLINE search (1985 to October 10, 2014), for exercise-based rehabilitation trials in heart failure, using search terms "exercise training, heart failure with preserved ejection fraction, heart failure with normal ejection fraction, peak V̇o₂, and diastolic heart dysfunction". ⋯ The corresponding data are provided for the following exercise test variables: V̇e/V̇co₂ slope, MD 0.85 ml·kg(-1)·min(-1) (95% CI 0.05 to 1.65, P = 0.04); maximum heart rate, MD 5.60 beats per minute (95% CI 3.95 to 7.25, P < 0.00001); Six-Minute Walk Test, MD 32.1 m (95% CI 17.2 to 47.1, P < 0.0001); and indices of diastolic function: E/A ratio, MD 0.07 (95% CI 0.02 to 0.12, P = 0.005); E/E' ratio MD -2.31 (95% CI -3.44 to -1.19, P < 0.0001); deceleration time (DT), MD -13.2 ms (95% CI -19.8 to -6.5, P = 0.0001); and quality of life: Minnesota Living with Heart Failure Questionnaire, MD -6.50 (95% CI -9.47 to -3.53, P < 0.0001); and short form-36 health survey (physical dimension), MD 15.6 (95% CI 7.4 to 23.8, P = 0.0002). In 3,744 h patient-hours of training, not one death was directly attributable to exercise. Exercise training appears to effect several health-related improvements in people with heart failure and preserved ejection fraction.