Biomedical subjects

T Alexander Quinn

Publications and source records attributed to T Alexander Quinn.

10 recordsLinked to original sources

PubMed2006

Ventricular diastolic stiffness predicts perioperative morbidity and duration of pleural effusions after the Fontan operation.

BACKGROUND: We validated the clinical relevance of ventricular stiffness by examining surgical morbidity in children with univentricular hearts undergoing Fontan operation. We hypothesized that ventricular stiffness affects Fontan morbidity, particularly duration of pleural effusions. METHODS AND RESULTS: Sixteen children with right ventricular (RV) (n =11) or left ventricular (LV) (n =5) dominance were studied intraoperatively at a median age of 3.3 years (1.8 to 5.1). Transesophageal long-axis echocardiograms and ventricular pressure by micromanometer provided end-diastolic pressure (P) area (A) relations during initiation and conclusion of cardiopulmonary bypass. Curve fitting to the equation P=alphae(betaA) defined the ventricular stiffness constant, beta. Changes in beta and clinical correlations were examined. Ventricular stiffness increased after bypass in patients with complete pre-bypass and post-bypass data (n =11, P=0.023, mixed models methodology). Pre-bypass beta correlated well with duration of chest tube (CT) drainage (r=0.90, n =16), net perioperative fluid balance (r=0.71, n=14), and length of stay (LOS) (r=0.81, n =16). CT duration and LOS also correlated significantly with post-bypass beta (r=0.77 for both, n=11), but insignificantly with preoperative catheterization pressures. CONCLUSIONS: Intraoperative beta predicts duration of CT drainage, net perioperative fluid balance, and LOS after the Fontan operation. These observations could improve risk stratification and clinical management of children at high-risk undergoing the Fontan operation.

Chest Tubes↗

PubMed2006

Effects of sequential biventricular pacing during acute right ventricular pressure overload.

Temporary sequential biventricular pacing (BiVP) is a promising treatment for postoperative cardiac dysfunction, but the mechanism for improvement in right ventricular (RV) dysfunction is not understood. In the present study, cardiac output (CO) was optimized by sequential BiVP in six anesthetized, open-chest pigs during control and acute RV pressure overload (RVPO). Ventricular contractility was assessed by the maximum rate of increase of ventricular pressure (dP/dt(max)). Mechanical interventricular synchrony was measured by the area of the normalized RV-left ventricular (LV) pressure diagram (A(PP)). Positive A(PP) indicates RV pressure preceding LV pressure, whereas zero indicates complete synchrony. In the control state, CO was maximized with nearly simultaneous stimulation of the RV and LV, which increased RV (P = 0.006) and LV dP/dt(max) (P = 0.002). During RVPO, CO was maximized with RV-first pacing, which increased RV dP/dt(max) (P = 0.007), but did not affect LV dP/dt(max), and decreased the left-to-right, end-diastolic pressure gradient (P = 0.023). Percent increase of RV dP/dt(max) was greater than LV dP/dt(max) (P = 0.014). There were no increases in end-diastolic pressure to account for increases in dP/dt(max). In control and RVPO, RV dP/dt(max) was linearly related to A(PP) (r = 0.779, P < 0.001). The relation of CO to A(PP) was curvilinear, with a peak in CO with positive A(PP) in the control state (P = 0.004) and with A(PP) approaching zero during RVPO (P = 0.001). These observations imply that, in our model, BiVP optimization improves CO by augmenting RV contractility. This is mediated by changes in mechanical interventricular synchrony. Afterload increases during RVPO exaggerate this effect, making CO critically dependent on simultaneous pressure generation in the RV and LV, with support of RV contractility by transmission of LV pressure across the interventricular septum.

Animals↗

PubMed2006

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.

Animals↗

PubMed2005

Ethanol induction of complete heart block in swine.

OBJECTIVES: A method for the induction of complete heart block (CHB) by ethanol injection and its success rate in a pig model of acute right ventricular failure is reported. Additionally, a review of the literature for the induction of CHB in laboratory animals is detailed. The literature review was undertaken to both compare our rate of success with other methods and provide insight into our technique and refine its implementation. BACKGROUND: Animal models of CHB have facilitated the understanding of therapeutics for various cardiac pathologies in humans. In our laboratory, CHB in pigs is used for complete control of heart rhythm in studies of biventricular pacing. MATERIALS AND METHODS: Experiments carried out on pigs in our laboratory that required the induction of CHB were reviewed retrospectively. In addition, review of the literature for creating CHB in animals was undertaken. Our success rate was compared to that of other groups. RESULTS: Our success rate (93%) is similar to other models of CHB, in general, and to those models that used the injection of caustic substances with thoracotomy. CONCLUSIONS: Review of the literature indicates that our success rate is comparable to other groups and that, although many approaches have been described in both open- and closed-chest models, success is likely dependent on the practice and skill of the experimenter. In addition, review of the literature has afforded us new perspectives on the experimental induction of CHB.

Animals↗

PubMed2005

Optimized biventricular pacing in atrioventricular block after cardiac surgery.

BACKGROUND: Temporary pacing is required after open-heart surgery for treatment of heart block. Atrioventricular delay and ventricular pacing site might be manipulated to increase cardiac output. We hypothesized that by optimizing both atrioventricular delay and ventricular pacing site a 10% improvement in cardiac output would be observed compared with a standard pacing protocol. METHODS: Seven patients in first or third degree heart block after valve replacement surgery had temporary wires sewn to the right atrium, right ventricle, and left ventricle. Cardiac output was measured by integrating flow velocity from an ultrasonic aortic flow probe. After optimization of atrioventricular delays during atrial synchronous right ventricular pacing, the effects of ventricular pacing site were tested at the optimum atrioventricular delay for 10-second intervals. RESULTS: Biventricular pacing was beneficial in all patients with a mean increase of 22% in cardiac index over right ventricular pacing (1.95 L/min/m2 +/- 0.27 standard error of the mean (SEM) to 2.38 L/min/m2 +/- 0.27 SEM, p = 0.0012) and 14% over left ventricular pacing (2.08 L/min/m2 +/- 0.22 SEM to 2.38 L/min/m2 +/- 0.27 SEM, p = 0.0133). Comparing optimized with standard pacing for 30-second intervals yielded a mean increase of 10% in cardiac index over three respiratory cycles (2.87 L/min/m2 +/- 0.33 SEM to 2.60 L/min/m2 +/- 0.37 SEM, p = 0.009) and 17% at the corresponding end-expiratory beats (2.76 L/min/m2 +/- 0.33 SEM to 2.36 L/min/m2 +/- 0.36 SEM, p = 0.011). CONCLUSIONS: Biventricular pacing at optimum atrioventricular delay improves cardiac output in patients with postoperative heart block by at least 10% compared with standard pacing.

Blood Pressure↗

PubMed2005

Optimized perioperative biventricular pacing in setting of right heart failure.

AIMS: A 78-year-old female with prior atrioventricular junctional ablation for paroxysmal atrial fibrillation and implantation of DDDR pacemaker underwent repair of severe tricuspid insufficiency. Effects of biventricular pacing were tested with temporary wires at the conclusion of cardiopulmonary bypass. METHODS: An ultrasonic flow probe was placed on the ascending aorta for real time cardiac output measurements. Atrioventricular delay optimization was performed and biventricular pacing was initiated while right-left ventricular delays were varied. RESULTS: There was no advantage of biventricular pacing (optimum right-left ventricular delay of +80 ms) compared with existing DDD. CONCLUSIONS: This study confirms the physiological effects of right-left ventricular delay on cardiac output after cardiopulmonary bypass.

Aged↗

PubMed2004

Regional functional depression immediately after ventricular septal defect closure.

Left ventricular ejection is depressed immediately after repair of ventricular septal defect (VSD). Postrepair functional depression seen after VSD closure could result from a reduction in preload. However, other mechanisms could be at work. Functional depression could also be caused by closure of a low-impedance path for left ventricular ejection, the introduction of a stiff akinetic patch, or the operation itself. We reasoned that functional depression mediated by changes in preload or afterload should symmetrically affect end-diastole and end-systole, whereas depression resulting from changes in septal mechanics should be localized. We, therefore, performed segmental wall-motion analysis on intraoperative echocardiograms from patients undergoing VSD and atrial septal defect repair. After VSD closure, there was an asymmetric change in left ventricular end-systolic segment length and a decrease in fractional segment shortening localized to the septal and lateral walls, whereas patients with atrial septal defect had a symmetric increase in fractional shortening. These results suggest that acute functional depression after VSD repair is a result of localized impairment of septal function.

Cardiac Surgical Procedures↗

PubMed2004

Mechanisms of optimized biventricular pacing in pulmonary stenosis: effects on left ventricular geometry in swine.

We tested the hypothesis that optimized biventricular pacing (BiVP) enhances cardiac output (CO) during critical pulmonary stenosis (PS) by attenuating distortions in left ventricular (LV) geometry. Following median sternotomy in six anesthetized pigs, heart block was induced by ethanol ablation. During epicardial, DDD BiVP, atrioventricular delay (AVD) was varied from 60 ms to 180 ms in 30 ms increments. At the AVD with the highest CO right-left delay (RLD) was varied from (+) 80 ms (RV first) to (-) 80 ms (LV first) in 20 ms increments. At each pacing setting, aortic flow, ECG, and LV diameter were measured in the control state (CON) and during PS, created by snaring the pulmonary artery until CO decreased 50%. Short axis LV echocardiograms were obtained at (+) and (-) 80 ms. In CON, RLD had no effect on function or geometry. During PS optimum BiVP resulted in significant increases in CO (1.12 L/min +/- 0.13 SEM at RLD =+ 40 ms versus 0.92 +/- 0.12 at RLD = 0 and 0.73 +/- 0.08 at RLD =-80), and LV fractional shortening (8.97%+/- 0.51% at RLD =+ 40 ms versus 7.34%+/- 0.58% at RLD = 0 and 6.21%+/- 0.66% at RLD =-80). In addition, LV eccentricity with (-) RLD was significantly different versus CON at both end-diastole (0.79 +/- 0.07 vs 1.02 +/- 0.03, P = 0.011 Student's t-test) and end-systole (0.83 +/- 0.05 vs 1.00 +/- 0.02, P = 0.017). However, with (+) RLD differences versus CON were not significant at either end-diastole (0.88 +/- 0.06 vs 0.99 +/- 0.03) or end-systole (0.92 +/- 0.03 vs 1.01 +/- 0.03). In swine hearts with PS, optimized BiVP increases CO, fractional shortening, and LV symmetry. BiVP warrants further study as treatment for acute postoperative heart failure.

Animals↗

PubMedDate not supplied

Validation study of PulseCO system for continuous cardiac output measurement.

Ultrasonic flow probes have been used to optimize biventricular pacing immediately after cardiopulmonary bypass, improving cardiac output (CO) by 10%; however, flow probes must be removed with chest closure. The PulseCO system (LiDCO Limited, Cambridge, UK) may extend optimization into the postoperative period, but controlled validations have not been reported. Six anesthetized pigs were instrumented for right heart bypass. Flow was varied from 3 to 1 L/min and then back to 3 in 0.5 L/min increments for 60 second intervals. CO was measured by ultrasonic flow probe on the aorta and by PulseCO using a femoral arterial line. PulseCO and flow probe accurately measured CO (PulseCO R2: 0.79-0.95; flow probe R2: 0.96-0.99). At flow of 2 L/min, when the heart was paced 30 bpm over the sinus rate, PulseCO falsely indicated an increase in CO (2.13 vs. 2.30 L/min, p = 0.014). When mean arterial pressure was increased by 20% using a phenylephrine infusion, PulseCO falsely indicated an increase in CO (2.13 vs. 2.47 L/min, p = 0.014). When mean arterial pressure was decreased by 20% using a nitroprusside infusion, PulseCO falsely indicated a decrease in CO (2.13 vs. 1.79 L/min, p = 0.003). PulseCO appears to be useful for assessing acute changes in CO if its limitations are recognized.

Animals↗

PubMedDate not supplied

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.

Animals↗