Clinical disorders of the pulmonary circulation [antikvár]

FOREWORD By PAUL WOOD, O.B.E., M.D., F.R.C.P. This monograph on the pulmonary circulation is a timely and much needed contribution to medical knowledge, for a great deal of work has been done on this subject since the introduction of reliable means of measuring pressure and flow in the pulmonary arteries and veins. That the majority of its authors are on the staff of the Postgraduate Medical School of London or have at one time been connected with that institution is seemly, for it was here that McMichael and Sharpey-Schafer helped to develop the technique that made so many of these observations possible. In their choice of other authors the editors have selected wisely, particularly perhaps in relation to Donald and Lee, whose contributions are outstanding. For a book of this kind there is remarkably little overlapping or conflict of opinion; only with regard to nomenclature is there any confusion. Being in a privileged position perhaps I may be allowed to comment on this, especially because with the help of J. B. Lowe I was responsible for introducing several of the expressions around which much of the confusion seems to circulate. Physiologically there are only three fundamentally different kinds of pulmonary hypertension; these may logically be called passive, hyperkinetic and vaso-occlusive. The word passive implies the absence of any active agent on the arterial side that might lead to a raised pulmonary artery pressure, and this denies its use in relation to increased pulmonary blood flow. It should be used solely when pulmonary hypertension results only because the pulmonary venous pressure is raised. The term hyperkinetic pulmonary hypertension best describes a high pulmonary artery pressure caused chiefly by increased blood-flow. The adjective was selected because it had long been used to describe a high cardiac output (Tinsley Harrison's hyperkinetic circulatory states), and because kinetic refers to movement whereas dynamic refers to force. Hyperdynamic pulmonary hypertension would mean that a raised pulmonary blood pressure was caused primarily by more forceful contraction of the right ventricle, a situation that does not exist. Hyperkinetic pulmonary hypertension is not passive, because there is an active blood pressure raising agent (increased flow) on the arterial side. The third great group results physiologically from an increased pulmonary vascular resistance, however caused, and this may be called vaso-occlusive pulmonary hypertension. Its chief subdivisions are (vaso) obstructive, e.g. thrombo-embolic, (vaso) obliterative, e.g. from endarteritis fibrosa, and vasoconstrictive (functional), e.g. hypoxic. When an increased pulmonary vascular resistance is secondary to passive or hyperkinetic pulmonary hypertension, the word reactive may be used with advantage when it is desired not to beg the question of mechanism. The term active pulmonary hypertension (once used in cases of mitral stenosis with a high pulmonary vascular resistance to distinguish them from cases of passive pulmonary hypertension) should now be abandoned, for the implication that the reaction is necessarily vasoconstrictive is not justified, and when it is vasoconstrictive that word itself identifies it.