The role of hypoxemia, vasoactive compounds, and acidemia in the pathogenesis of pulmonary edema in the dog with experimental left ventricular overload

Abstract

The pathogenesis of pulmonary edema (PE) in left heart failure involves a consideration of the hydrostatic, osmotic, and permeability changes in the pulmonary circulation. In 14 dogs with isolated left ventricular overload induced by suturing a Teflon graft between the aorta and left atrium, left ventricular end-diastolic pressure (LVEDP) was 36 mmHg (1 mmHg = 133.322 Pa) 3 weeks following surgery. There was no clinical evidence of PE. Seven of these animals developed PE when allowed to breathe 10% O2 in N2 for 15 min. There was no further increase in LVEDP or right ventricular systolic pressure (RVSP). It was postulated that a change in permeability superimposed on increased capillary hydrostatic pressure could result in the overwhelming accumulation of fluid in the alveoli. The release of vasoactive substances from pulmonary mast cells or from the adrenal medulla might alter capillary permeability. However, the infusion of histamine or epinephrine in seven dogs with elevated LVEDP and RVSP failed to precipitate fulminating PE. We have previously observed an increase in plasma renin activity in dogs associated with PE. Nonpressor infusions of angiotensin failed to produce PE. The infusion of lactic acid to decrease the arterial pH to 7.00 (the level observed as a result of hypoxia-induced PE) resulted in fulminating PE. It is concluded that acidemia can be an important factor in the development of severe intra-alveolar pulmonary edema.