Lung mechanics and oxygen consumption during spontaneous ventilation and severe heart failure

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.