The effects of acute heart failure on lung mechanics and oxygen consumption (V̇O2) during normocarbic spontaneous ventilation were studied in 21 anesthetized pigs. Heart failure severe enough to double oxygen extraction (O2ex) was induced with intravenous esmolol boluses and infusion. Compared to normal, the inspiratory elastic work of breathing (Wel) increased from 335 ± 371 (X̄ ± SD) to 559 ± 48 mm Hg · ml (p<0.003) during heart failure, lung compliance (CL) fell from 121 ± 144 to 22 ± 15 ml/mm Hg (p<0.05), and respiratory power climbed from 140 ± 200 to 245 ± 214 mm Hg · ml · min-1 (p<0.002). These mechanical changes were accompanied by a decrease in both V̇O2 (221 ± 61 to 191 ± 50 mlO2/min, p<0.05) and oxygen delivery (DO2) (680 ± 240 to 260 ± 90 mlO2/min, p<0.004). The V̇O2/DO2 ratio doubled (p<0.0002), confirming increased O2ex. In conclusion, severe acute heart failure decreased CL, and increased Wel and respiratory power significantly. The depressed cardiac output limits both DO2, and to some extent, V̇O2. However, a greater proportion of the delivered O2 is consumed, supplying indirect evidence which suggests that the respiratory muscles' V̇O2 increases as a consequence of increased power expenditure.
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine
- Critical Care and Intensive Care Medicine
- Cardiology and Cardiovascular Medicine