Introduction: History and Evolution
The discovery of the pulmonary circulation was reported in the 13th century by Ibn al-Nafis (1213–1288) in the “Commentary on Anatomy in Avicenna's Canon” and, probably independently, in the 16th century by Michael Servetus (1511–1553) in the “The Restoration of Christianity.”1 However, it has only been recently realized that the pulmonary circulation as a separate high-flow low-pressure system is the end result of an evolutionary process aimed at the optimization of gas exchange of endothermic birds and mammals.2 Evolution from ancestors of fishes to amphibians, reptiles, and finally birds and mammals has led to progressively greater oxygen consumption requiring thinner pulmonary blood–gas barrier. The alveolocapillary membrane in mammals is a vulnerable structure only 0.3 μm thick. Preservation of the integrity of this barrier has been made possible by the complete separation of the pulmonary circulation from the systemic circulation. This evolution has been accompanied by a progressive unloading and reshaping of the right ventricle (RV) as a thin-walled flow generator.
The extreme potential physiological stresses on the pulmonary circulation are exercise and hypoxia. Exercise increases oxygen uptake and carbon dioxide output up to some 20-fold above resting values, and increases cardiac output up to some sixfold. Strenuous exercise may eventually alter gas exchange because of excessive capillary filtration and stress failure, or expose the RV to excessive loading resulting in a limitation of maximum cardiac output. Hypoxia adds the burden of further increase in pulmonary vascular pressures due to hypoxic pulmonary vasoconstriction.
Pulmonary Vascular Pressures and Resistance
The pulmonary circulation is characterized by an inflow pressure or pulmonary artery pressure (Ppa), an outflow pressure or left atrial pressure (Pla), and a pulmonary blood flow (Q) approximately equal to systemic cardiac output. Pulmonary vascular pressures and flows are pulsatile. However, a simple and clinically useful description of the functional state of the pulmonary circulation may be provided by a calculation of pulmonary vascular resistance (PVR) from mean values of Ppa (mPpa), Pla, and Q.
Measurements of pulmonary vascular pressures and cardiac output are usually performed during a catheterization of the right heart with a fluid-filled balloon-tipped thermodilution catheter (Fig. 13-1). This procedure allows for the estimation of Pla from a balloon-occluded (Ppao) or wedged (Ppw) Ppa and Q by thermodilution.
Right heart catheterization with flow-directed balloon-tipped catheter with successive measurements of right atrial pressure (Pra), right ventricular pressure (Prv), pulmonary artery pressure (Ppa), and occluded Ppa (Ppao). Because of the fractal structure of the arterial and venous branching of the pulmonary vascular tree, occluded or wedged Ppa prolongs the fluid column of the catheter until same diameter pulmonary vein, which is a satisfactory estimate of left atrial pressure or left ventricular end-diastolic pressure.