Browsing by Author "Tyberg, J. V."

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    P2.11 Estimation of Lv Stroke Volume by Impedance Cardiography: Its Relation to the Aortic Reservoir
    (2012-11-17) Wang, J. J.; de Vries, G.; Tyberg, J. V.
    Abstract Impedance cardiography (ICG) is a noninvasive technique used to estimate left ventricular stroke volume (SVLV) using thoracic impedance (ΔZ). It remains controversial, partly because ICG parameters have not been successfully related to hemodynamic events.We hypothesized that the change in ΔZ may be proportional to the variation in thoracic blood volumes, primarily aortic blood volume. Nine anaesthetized dogs were divided into two groups: the “Aortic Volume Group” (n=5), where aortic and IVC (inferior vena cava) dimensions were measured ultrasonically, and the “Reservoir Volume Group”, where aortic and IVC reservoir volumes were calculated using the reservoir-wave approach. Measurements were made under control conditions, with nitroprusside, with methoxamine (Mtx), and after volume loading. In both groups, the maximum rate of increase in ΔZ, (dZ/dt)max, strongly correlated with the maximum rate of change in aortic/reservoir blood volume (r2 = 0.85 and 0.95, respectively), which in turn were proportional to SVLV. As shown in the figure, the aortic reservoir volume (VAo reservoir) explains SVLV in that measured aortic flow (QAo) equals the sum of dVAo reservoir/dt and calculated Qout. The LV and IVC contributions to ΔZ were small under control conditions (~5 and 1%, respectively), but the LV contribution increased slightly with administration of Mtx and after volume loading (to 7 and 10%, respectively). We conclude that the change in thoracic impedance (ΔZ) during the cardiac cycle is proportional to the change in aortic reservoir volume, which mechanistically explains why ICG and standard measures of cardiac output have sometimes been shown to correlate well.
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    P3.02 Describing Waves in the Pulmonary Veins: Application of a Reservoir-Wave Model
    (2012-11-17) Bouwmeester, J. C.; Shrive, N. G.; Tyberg, J. V.
    Abstract Background The pulmonary venous pressure waveform is typically described by the downstream events in the left atrium and ventricle. These downstream events create waves that contribute to the overall waveform. Methods In anesthetised open-chest dogs, measurements of pressure and flow were made in the pulmonary artery and vein. Experiments involved increases to blood volume and the application of 10 cm H2O positive end-expiratory pressure (PEEP). The reservoir-wave model describes the reservoir pressure, which is subtracted from measured pressure, to result in the excess pressure (Pexcess). Excess velocity (Uexcess) is similarly formulated. Pexcess and Uexcess are used in wave intensity analysis to calculate wave speed and separate the contributions of waves originating upstream (forward waves) and downstream (backward waves). Results Separated waves are shown in the bottom panel of Figure 1. The effect of PEEP resulted in larger decreases to Pbackward (p < 0.001) after the mitral valve opened. As a result, y was lower than x by ~2.0 mmHg. With PEEP, the delay between arterial and venous forward waves increased from 155 ± 4 ms to 183 ± 4 ms (mean ± SE, p < 0.001). Conclusion The majority of pulmonary venous pressure landmarks can be attributed to the actions of the left atrium and ventricle but the v wave has substantial contributions from waves originating in the pulmonary artery. Diastolic suction has a larger effect with PEEP, presumably from some external constraint applied to the heart and consequently lowered end-systolic left ventricular volume. Figure 1 Common venous markers related to measured pressures (top panel) and the separation of Pexcess into forward and backward components (bottom panel) at control conditions.
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    P3.21 Conductance and Capacitance Effects of Acute, Electrical, Carotid Baroreflex Stimulation
    (2012-11-17) Burgoyne, S.; Tyberg, J. V.; Belenkie, I.; Georgakopoulos, D.
    Abstract Introduction Chronic baroreflex activation is a therapy for resistant hypertension and has potential as a therapy in heart failure. We hypothesized that acute baroreflex activation therapy (CVRx, Inc.) would increase both the capacity of the abdominal venous circulation (lowering “preload”) and aortic conductance (reducing “afterload”). Methods Six 20-kg mongrel dogs were anaesthetized and ventilated. Arterial blood pressure (BP) and diaphragmatic aortic and caval flow (ultrasonic) were measured. Venous capacity changes were evaluated using a modified Brooksby-Donald technique*. A CVRx electrode was affixed to the right carotid sinus. BP and flow data were collected under control conditions and during device activation and drug infusions. Angiotensin II (ANG II) was infused to raise BP to hypertensive levels; the current from the device was then increased. Results Device activation decreased mean aortic BP 22.5±1.3 mmHg, decreased heart rate 14.7±3.4% and cardiac output 10.8±3.9%, increased aortic conductance 16.2±4.9%, and increased abdominal blood volume at a rate of 2.2±0.6 mL/kg/min (5-minute activations). ANG II infusion increased BP 40.3±3.4 mmHg and reduced venous capacitance at a rate of 1.1±0.5 mL/ kg/min. Subsequent electrical stimulation restored BP to baseline while aortic conductance only returned to 82.3±3.3% of control. Venous capacitance increased at a rate of 3.4±0.7 mL/kg/min, reversing the ANG II effects. Conclusions Acute electrical activation of the carotid baroreflex increases arterial conductance, decreases BP, and increases venous capacitance. Modulation of venous capacitance may be an important effect of barore-ceptor activation in hypertension and heart failure.