George Berberian

Validation of mean arterial pressure as an indicator of acute changes in cardiac output

Changes in mean arterial pressure (MAP) are often assumed to reflect changes in cardiac output (CO). A linear relationship is postulated to exist between these two quantities based upon the circuit model for systemic circulation. Previous studies have correlated changes in CO and MAP. However, to our knowledge, no studies have tested the relationship between CO and MAP in vivo without changes in systemic vascular resistance. Research on baroreceptor stimulation and vasomotor response has shown that vasomotor tone changes 15 to 60 seconds after an acute change in CO. Maximal activation of vasomotor response occurs after approximately 30 seconds. Thus MAP should correlate directly with CO during acute changes (<15 seconds). To test this, we examined the relationship between CO and MAP during 10 second occlusions of the inferior vena cava in anesthetized pigs. A linear relationship existed between CO and MAP in seven pigs (%MAP = 0.60[%CO] − 0.41, p = 0.0001). This study validates the use of MAP as an indicator of acute changes in CO. Fluctuations in MAP correlate well with acute changes in CO in the absence of changes in vascular tone.

Measurement of QRS duration for biventricular pacing optimization.

Optimization of left ventricular pacing site or interventricular pacing delay improves the efficacy of biventricular pacing (BiVP). Cardiac output (CO) based optimization, however, is invasive and slow. QRS duration (QRSd) is noninvasive and responds rapidly. Accordingly, we investigated the utility of QRSd for BiVP optimization in a model of acute right ventricular (RV) pressure overload. In seven anesthetized open-chest pigs, BiVP was implemented with right atrial and RV pacing wires. A 6-electrode array was placed behind the LV. Heart block was established by alcohol ablation. The pulmonary artery was snared to double peak RV pressure. Fifty-four combinations of left ventricular pacing site and interventricular pacing delay were tested in random order over 30-second intervals. QRSd was assessed from electrocardiogram lead II, CO from aortic flow probe, and ventricular function from micromanometers. Comparisons were made with the Pearsons correlation coefficient (r). QRSd narrowing was associated with improved RV function and transseptal synchrony, but correlation with CO was poor. Additionally, QRSd averaged over the last 20 cardiac cycles in each interval was compared with values averaged over successive cardiac cycles following each reprogramming. Seven cardiac cycles after reprogramming, the average r-value went above 0.90 and plateaued. QRSd-based optimization merits further study during BiVP in patients with congestive heart failure.

LOAD DEPENDENCE OF CARDIAC OUTPUT IN BIVENTRICULAR PACING: LEFT VENTRICULAR VOLUME OVERLOAD IN PIGS

OBJECTIVE Previous work from our laboratory has demonstrated that optimization of biventricular pacing is load dependent. Cardiac output was maximized with a ventricular-ventricular delay of +40 milliseconds (right ventricle-first pacing) during right ventricular pressure overload and with a ventricular-ventricular delay of -40 milliseconds (left ventricle-first pacing) during right ventricular volume overload. We hypothesized that a model of left ventricular volume overload would also have specific timing requirements during biventricular pacing for optimization of cardiac output. METHODS After median sternotomy in 6 anesthetized pigs, complete heart block was induced by ethanol ablation. A conduit was grafted from the left ventricle to the left atrium to produce left ventricular volume overload. An ultrasonic flow probe was placed around the conduit to measure retrograde flow that averaged 50% of cardiac output. During epicardial atrial tracking DDD biventricular pacing, atrioventricular delay was varied between 60 and 270 milliseconds in 30-millisescond increments for 20-second intervals. After determination of optimum atrioventricular delay, ventricular-ventricular delay was varied in 20-millisecond increments from +80 to -80 milliseconds for 20-second intervals. RESULTS Ventricular-ventricular delays had no significant effect on cardiac output with the graft clamped (control). With the graft unclamped, however, there was a statistically significant (P = .0001 by repeated-measures analysis of variance) trend toward higher cardiac output with right ventricle-first pacing. CONCLUSIONS Right ventricle-first pacing in swine significantly increased cardiac output during acute left ventricular volume overload, but not during the control state. Understanding load-specific pacing requirements will facilitate the development of perioperative temporary biventricular pacing for acute heart failure.