![]() ![]() Indications, advantages, and disadvantages of different pacing modes are reviewed in Table 34-3. Period after a ventricular paced or sensed event that prevents inappropriate pacing during vulnerable periodĪvailable pacing modes depend on the location and number of leads implanted. Period after a ventricular event when the device can sense but not track an atrial eventĪV delay that adjusts by shortening as the rate increases.ĬARDIAC RESYNCHRONIZATION THE RAPY/PACEMAKERSīiventricular pacing interval or LV offset (V–V)Īn RV sensed event maybe noted but ignored, without affecting RV pacing timing cycleĪn LV sensed event maybe noted but ignored, without affecting LV pacing timing cycle Post-ventricular atrial refractory period (PVARP) Period when atrial sensing is “OFF” after a ventricular paced or sensed event Post-ventricular atrial blanking period (PVAB) Period when ventricular sensing is “OFF” after an atrial paced event Postatrial ventricular blanking period (PAVB) Maximum ventricular pacing rate allowed in response to high sensed atrial rates Programmed atrioventricular pacing intervalĪV interval/delay from atrial paced event (A) to ventricular paced event (V)ĪV interval/delay from atrial sensed event (P) to ventricular paced event (V) Interval from ventricular sensed or paced event to atrial paced eventĪtrial paced event followed by ventricular sensed event Maximum pacing rate by rate-responsive sensorĭUAL-CHAMBER (ATRIAL AND VENTRICULAR) PACEMAKERĪtrial paced event followed by paced ventricular eventĪtrial sensed event followed by paced ventricular event Ventricular sensing amplifier is “blind” and will not detect or respond to any ventricular sensed eventĪn atrial sensed event will be noted but ignored, without affecting pacemaker timing cycleĪ ventricular sensed event will be noted but ignored, without affecting pacemaker timing cycle Sensed a native Ventricular depolarization (Q RS complex)Ītrial sensing amplifier is “blind” and will not detect or respond to atrial sensed event Sensed a native Atrial depolarization ( P wave) SINGLE-CHAMBER (ATRIAL OR VENTRICULAR) PACEMAKER ![]() Table 34-2 Abbreviations and Description of Cardiac Events and Timing Cycles in Single-Chamber, Dual-Chamber, and Biventricular Pacemakers/DevicesĬARDIAC EVENTS/TIMING CYCLES (ABBREVIATION) Notably, these studies could provide a physiologic basis for some symptoms associated with the pacemaker syndrome produced by the absence of AV synchrony.Table 34-1 Revised NASPE/BPEG Generic Code for Antibradycardia, Adaptive-Rate, and Multiple-Site Pacing However, the additional deleterious effects of atrial contraction against a closed AV valve on pulmonary gas exchange and hemodynamics were also apparent. 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. The decrease in pulmonary gas exchange appeared in part related to alterations in cardiac hemodynamics and particularly to the fall in cardiac output. 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 end-expiratory O 2 increased and CO 2 decreased when the pacing mode was changed from AV100 to VA100. 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 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. 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). 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. 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. We studied the effects of various pacing modes on cardiac hemodynamics and pulmonary gas alterations in chronic heart blocked dogs.
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