Pulmonary vascular obstruction in graded tachypneagenic diffuse embolism

Abstract

One group of experiments revealed minimal doses of 75 µ pulmonary emboli required for eliciting increased frequency and decreased amplitude of breathing in anesthetized dogs. Others measured in vivo lung lobe autoperfusion flow rates at several constant perfusion pressures to determine the fractions of the pulmonary vascular bed obstructed by these and other quantities and to determine concurrent changes in flow-pressure relationships. The fraction of the vascular bed obstructed by threshold tachypneagenic quantities averaged 10% but in some instances was as little as 3%—values so small that the expected hemodynamic consequences in intact animals would be within physiological ranges and therefore seemingly not important as a tachypneagenic mechanism. Following embolization, resistance to blood flow increased in the nonoccluded intralobar vascular bed, particularly at lower perfusion pressures, and associated alterations in flow-pressure and resistance-pressure relationships pointed toward moderate increase in vascular tone as the cause. Quantities of emboli apparently required for completely obstructing the pulmonary vascular bed were considered in relation to established anatomical dimensions.

Effects of pulmonary gas embolism on circulation and respiration in the dog

“…The changes in ventilation and lung mechanics during pulmonary embolism may be induced by a stimulation of lung receptors (irritant receptors). Bernthal et al (1961), and Marazzini et al (1966) found a relationship between the amount of compact emboli, the increase in pulmonary arterial pressure (P ) and the increase in breathing frequency. In this study the same relationship is investigated using gaseous emboli.…”

“…The most prominent effects of pulmonary embolism are tachypnea, polypnea, dyspnea, increased airway resistance, decreased compliance of the lung, and arterial hypoxemia (Behnke et al, 1935(Behnke et al, /1936Bernthal et al, 1961;Derks and Peters, 1974;Dick, 1939;Goodwin and Harmel, 1949;Halmagyi et al, 1963;Hirose et al, 1973;Horres and Bernthal, 1961;Khan et al, 1972;Levy et al, 1963;Marazzini et al, 1966;Megibow et al, 1942;Mills et al, 1969;Nadel et al, 1964;Sasahara et al, 1967;Whitteridge, 1950;Williams, 1956;Wolffe and Robertson, 1935) . The changes in ventilation and lung mechanics during pulmonary embolism may be induced by a stimulation of lung receptors (irritant receptors).…”

Quantitative Studies of Pulmonary Embolism

“…If a careful study were made, you would find probably less than 5 per cent of all cases of sudden death in pulmonary embolism, with the major branches free, which might be due to vasoconstriction. Some investigators have said there must be either a pulmono-coronary or a pulmono-pulmonary reflex operating in such cases.…”