Hemodynamic changes after pneumonectomy in the exercising foxhound

Abstract

Pulmonary arterial pressure is higher during exercise after pneumonectomy than before. Several factors may contribute to the elevation, e.g., loss of vascular bed, overinflation of the remaining lung, and active pulmonary vasoconstriction. We measured hemodynamic changes during graded exercise in conditioned foxhounds and compared pulmonary pressure-flow relationships before and after left pneumonectomy. Pulmonary arterial pressure-flow relationship in the remaining lung is not altered by pneumonectomy, suggesting that the increase in pulmonary vascular resistance post-pneumonectomy is largely the passive consequence of increased pulmonary blood flow to the remaining lung. The potential for chronic hyperinflation of the remaining lung to increase pulmonary resistance after pneumonectomy may have been counterbalanced by a concomitant reduction in lung elastic recoil. Unexpectedly, both mean systemic blood pressure and hematocrit were higher with respect to cardiac output after pneumonectomy. Cardiac output and stroke volume at any given work load were lower after pneumonectomy than before, and heart rate response was unaltered. This pattern of responses suggests that increases in left and right ventricular afterload may have contributed to the reduction in cardiac output.

Exercise-induced Arteriovenous Intrapulmonary Shunting in Dogs

“…Perfusion pressure in the isolated dog lung was limited to 29.4 mm Hg, as this was similar to, but did not exceed, the highest estimated driving pressure in the exercising dog of 36 mm Hg (mean pulmonary artery pressure, 40 mm Hg [21]; left atrial pressure, 4 mm Hg [28]). Despite a similar driving pressure, flow through the isolated lungs was no greater than 0.25 L/ minute; substantially lower than pulmonary blood flow (i.e., cardiac output) either at rest or during exercise in the intact dog, indicating greater vascular resistance and an altered pulmonary vasculature in the isolated lung.…”

Long-term Doppler echocardiographic evaluation of the right heart after major lung resections

“…For this reason, some functional parameters may be difficult to evaluate echocardiographically; in particular, RV ejection fraction is usually underestimated [22][23][24], and this is the reason why it was not included among the variables investigated in our study. Cine magnetic resonance imaging [25] could certainly improve understanding and it should be included in future studies.…”

“…The early modifications secondary to major lung resections described by other authors [8,12] were confirmed by our study; pneumonectomy causes an important reduction of the vascular bed resulting in a progressive increase in PASP starting at the end of the first postoperative week and is able to induce modifications of RV morphology; these modifications appear later, and are certainly less impressive than in patients with other types of pulmonary hypertension with much higher PASP values. Clinical and experimental reports [25] suggested that this would be the trigger for right heart modifications along with an increased activity of the adrenergic system early after surgery. As a consequence, the right ventricle progressively enlarges, reaching significance after 6 months; our study documented that PASP and RV diameters continue to increase during the 4 years of follow-up after pneumonectomy; however, at this time point, even if the PASP increase is significant, it is still not enough to elicit hypertrophy of the RV free wall as documented by our measurements.…”

Anesthetic considerations in 65 patients undergoing unilateral pneumonectomy: problems related to fluid therapy and hemodynamic control

“…After unilateral pneumonectomy, pulmonary arterial pressure is markedly increased due to a reduction in the size of the pulmonary vascular bed, hyperinflation of the remaining lung, and pulmonary vasoconstriction [12]. According to Jordan et al [13], the causes of postpneumonectomy pulmonary edema include excessive perioperative fluid infusion and surgical damage resulting from pulmonary collapse and hyperinflation.…”