MECHANISM OF ADENOSINE-INDUCED ELEVATION OF PULMONARY CAPILLARY WEDGEPRESSURE IN HUMANS

Background Continuous intravenous administration of adenosine to human s often results in a paradoxical rise in pulmonary capillary wedge pre ssure (PCWP), whereas arterial resistance is lowered and cardiac outpu t and heart rate increase. This is believed to be due to diastolic sti ffening of the ventricle or to a negative inotropic effect. In the pre sent study, we tested these and other mechanisms by using pressure vol ume (PV) analysis and echocardiography. Methods and Results Fifteen pa tients with normal rest left ventricular function underwent cardiac ca theterization and received adenosine at a rate of 140 mu g/kg per minu te IV for 6 to 10 minutes. PV relations were measured in 9 patients (w ithout coronary artery disease) using the conductance catheter method. In 6 additional patients with coronary artery disease, echocardiogram s were used to assess wall thickness and function, and aortic and coro nary sinus blood, lactate, oxygen, and adenosine levels were measured. Adenosine increased PCWP by 19% (+2.6 mm Hg) in both patient groups w hile lowering arterial load by 30% and increasing cardiac output by 45 % (all P<.001). There was no significant effect of adenosine on mean l inear chamber compliance or monoexponential elastic stiffness, as the diastolic PV relation was unchanged in most patients. Diastolic wall t hickness also was unaltered. Thus, the PCWP rise did not appear to be due to diastolic stiffening. Adenosine induced a rightward shift of th e end-systolic PV relation (ESPVR) (+12.7+/-3.7 mL) without a slope ch ange. This shift likely reflected effects of afterload reduction, as o ther indexes (stroke work-end-diastolic volume relation and dP/dt(max) at matched preload) were either unchanged or increased. Furthermore, this modest shift in ESPVR was more than compensated for by vasodilati on and tachycardia, so reduced systolic function could not explain the increase in PCWP. There also was no net lactate production to suggest ischemia. Rather than arising from direct myocardial effects, PCWP el evation was most easily explained by a change in vascular loading, as both left ventricular end-diastolic volume and right atrial pressure i ncreased (P<.05). This suggests that adenosine induced a redistributio n of blood volume toward the central thorax. Conclusions PCWP elevatio n in response to adenosine primarily results from changes in vascular loading rather than from direct effects on cardiac diastolic or systol ic function.