Effects of AV Sequential Versus Asynchronous AV Pacing on Pulmonary Hemodynamics

We studied the effects of various pacing modes on cardiac hemodynamics and pulmonary gas alterations in chronic heart blocked dogs. Changing the pacing mode from an atrioventricular interval of 100 ms (AV100) to a ventriculo‐atrial interval of 100 ms (VA100) caused a significant fall in left ventricular pressure (117.64 ± 11.91 to 95.60 ± 16.58 mmHg) and cardiac output from 2.18 ± 0.24 to 1.46 ± 0.20 L/min. Following the change in pacing mode from AV100 to VA 100, there was an increase in the alveolar‐arterial O2 gradient from 23.28 ± 6.97 to 28.74 ± 8.43 mmHg and a decrease in the arterial CO2 tension from 32.42 ± 3.22 to 29.42 ± 3.22 mmHg. There was also a decrease in arterial CO2 tension when the AV100 pacing mode was compared to asynchronous ventricular pacing (32.42 ± 3.22 versus 30.56 ± 2.82 mmHg). The minute volume of O2 also decreased when the pacing mode was changed from AV100 to asynchronous ventricular pacing (0.134 ± 0.01 versus 0.126 ± 0.01 L/min) and decreased further at VA100 to 0.114 ± 0.01 L/min. Other significant changes were also observed: the percent of expired CO2 decreased when the pacing mode was changed from AV100 to VA100 (3.68 ± 0.13 versus 3.37 ± 0.26%) or to asynchronous ventricular pacing (3.40 ± 0.31%). The end‐expiratory O2 increased and CO2 decreased when the pacing mode was changed from AV100 to VA100. The breath‐by‐breath correlation of end‐expiratory O2 and CO2 with left ventricular systolic pressure showed an almost immediate increase in O2 and reduction in CO2 concentration associated with decreasing systolic pressure. The decrease in pulmonary gas exchange appeared in part related to alterations in cardiac hemodynamics and particularly to the fall in cardiac output. It is speculated but not proven by these studies that alterations could be further explained by a fall in O2 consumption or reflex shunting of blood in vascular beds due to the fall in cardiac output. However, the additional deleterious effects of atrial contraction against a closed AV valve on pulmonary gas exchange and hemodynamics were also apparent. Notably, these studies could provide a physiologic basis for some symptoms associated with the pacemaker syndrome produced by the absence of AV synchrony.