Background-Dyspnea and fatigue are the main causes of exercise limitation in chronic heart failure (CHF) patients, whose peak inspiratory (Pi max ) and expiratory pressures (Pe max ) are often reduced. The aim of this study was to examine the relationship between respiratory muscle performance and oxygen kinetics. Methods and Results-A total of 55 patients (NYHA class I to III) and 11 healthy subjects underwent cardiopulmonary exercise tests (CPET) on a treadmill. In 45 of the 55 patients (group I) and in healthy subjects (group II), pulmonary function tests, Pi max , and Pe max were measured before and 10 minutes after exercise, and oxygen kinetics were monitored throughout and during early recovery from CPET. The first degree slope of oxygen consumption (V O 2 ) decline during early recovery (V O 2 /t-slope) and V O 2 half-time (T 1/2 ) were calculated. In 10 of the 55 CHF patients (group III), the measurements of Pi max were repeated 2, 5, and 10 minutes after CPET. A Ͼ10% reduction in Pi max after CPET (subgroup IA) was measured in 11 of 45 patients. In contrast, 34 of 45 CHF patients (subgroup IB) and all control subjects (group II) had Pi max Ͼ90% of baseline value after CPET. Subgroup IA patients had significantly lower peak V O 2 (13.5Ϯ2.1 versus 17.8Ϯ5.6 mL ⅐ kg Ϫ1 ⅐ min Ϫ1 ; PϽ0.001), lower anaerobic thresholds (10.1Ϯ2.4 versus 13.6Ϯ4.6 mL ⅐ kg Ϫ1 ⅐ min
The purpose of this study was to determine the role of changes in the parameters of venous return on the homeostatic adaption to the application of PEEP. We studied 13 dogs anesthetized with alpha-chloralose, intubated, and ventilated. We measured central venous pressure (CVP), arterial pressure (Pao) and cardiac output by thermal dilution. The cardiac output was transiently stopped by inflating a balloon in the right atrium, and the subsequent plateau in the CVP was used to obtain mean circulatory filling pressure (MCFP). Total blood volume was measured with Evans blue. To measure vascular capacitance and compliance, we rapidly infused 4 ml/kg or 8 ml/kg of blood and repeated the MCFP measurement. The same volume was withdrawn after the measurement. The volume and MCFP were used to construct pressure-volume (P-V) lines, and the unstressed volume was calculated by extrapolating the P-V to zero pressure. The P-V appeared linear in the range studied. PEEP produced a left shift of the curves and, thus, a decrease in unstressed volume. The shift with 20 cm H2O of PEEP was greater than with 10 cm H2O of PEEP. The rise in MCFP matched the rise in CVP so that the pressure gradient for venous return did not change. However, there was also an increase in the resistance to venous return, which resulted in a lower cardiac output than expected for the rise in MCFP. In conclusion, homeostatic adjustments to PEEP included a decrease in vascular capacitance, which is partially offset by a rise in the resistance to venous return.
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