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Effects of AV Sequential Versus Asynchronous AV Pacing on Pulmonary Hemodynamics
Author(s) -
DREIFUS LEONARD S.,
MITAMURA HIDEO,
RHAUDA ARMIN,
VAIL SYDNEY,
MICHELSON ERIC L.,
BERKOVITS BAROUH V.,
PETERSON DONALD D.,
FIGUEROA WILLIAM F.
Publication year - 1986
Publication title -
pacing and clinical electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.686
H-Index - 101
eISSN - 1540-8159
pISSN - 0147-8389
DOI - 10.1111/j.1540-8159.1986.tb05389.x
Subject(s) - medicine , hemodynamics , cardiology , cardiac output , cardiac pacing , anesthesia , ventricular pacing , atrioventricular node , heart failure , tachycardia
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 O 2 gradient from 23.28 ± 6.97 to 28.74 ± 8.43 mmHg and a decrease in the arterial CO 2 tension from 32.42 ± 3.22 to 29.42 ± 3.22 mmHg. There was also a decrease in arterial CO 2 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 O 2 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 CO 2 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 O 2 increased and CO 2 decreased when the pacing mode was changed from AV100 to VA100. The breath‐by‐breath correlation of end‐expiratory O 2 and CO 2 with left ventricular systolic pressure showed an almost immediate increase in O 2 and reduction in CO 2 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 O 2 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.