Biomedical subjects

John V Tyberg

Publications and source records attributed to John V Tyberg.

6 recordsLinked to original sources

PubMed2003

Pericardium modulates left and right ventricular stroke volumes to compensate for sudden changes in atrial volume.

The pericardium may modulate acute compensatory changes in stroke volumes seen with sudden changes in cardiac volume, but such a mechanism has never been clearly demonstrated. In eight open-chest dogs, we measured left and right ventricular pressures, diameters, stroke volumes, and pericardial pressures during rapid (approximately 300 ms) systolic infusions or withdrawals of approximately 25 ml blood into and out of the left atrium and right atrium. Control beats, the infusion/withdrawal beat, and 4-10 subsequent beats were studied. With infusions, ipsilateral ventricular end-diastolic transmural pressure, diameter, and stroke volume increased. With the pericardium closed, there was a compensatory decrease in contralateral transmural pressure, diameter, and stroke volume, mediated by opposite changes in transmural end-diastolic pressures. The sum of the ipsilateral increase and contralateral decrease in stroke volume approximated the infused volume. Corresponding changes were seen with blood withdrawals. This direct ventricular interaction was diminished when pericardial pressure was <5 mmHg and absent when the pericardium was opened. Pericardial constraint appears essential for immediate biventricular compensatory responses to acute atrial volume changes.

Animals↗

PubMed2002

Time-domain representation of ventricular-arterial coupling as a windkessel and wave system.

The differences in shape between central aortic pressure (P(Ao)) and flow waveforms have never been explained satisfactorily in that the assumed explanation (substantial reflected waves during diastole) remains controversial. As an alternative to the widely accepted frequency-domain model of arterial hemodynamics, we propose a functional, time-domain, arterial model that combines a blood conducting system and a reservoir (i.e., Frank's hydraulic integrator, the windkessel). In 15 anesthetized dogs, we measured P(Ao), flows, and dimensions and calculated windkessel pressure (P(Wk)) and volume (V(Wk)). We found that P(Wk) is proportional to thoracic aortic volume and that the volume of the thoracic aorta comprises 45.1 +/- 2.0% (mean +/- SE) of the total V(Wk). When we subtracted P(Wk) from P(Ao), we found that the difference (excess pressure) was proportional to aortic flow, thus resolving the differences between P(Ao) and flow waveforms and implying that reflected waves were minimal. We suggest that P(Ao) is the instantaneous summation of a time-varying reservoir pressure (i.e., P(Wk)) and the effects of (primarily) forward-traveling waves in this animal model.

Animals↗

PubMed2002

How changes in venous capacitance modulate cardiac output.

Pressure-volume relations, which most directly represent changes in venous capacitance, are useful tools in understanding how changing venous tone modulates cardiac output under both normal physiologic conditions and in disease states. A conceptual model is presented, followed by a discussion of experimental results.

Animals↗

PubMed2002

Comparative effects of nitroglycerin on intestinal vascular capacitance and conductance.

BACKGROUND: Nitroglycerin (NTG) dilates capacitance veins and resistance arterioles, but its relative effects on veins and arterioles are not known. OBJECTIVES: To compare NTG-induced changes in capacitance and conductance. ANIMALS AND METHODS: Aortic, left ventricular and portal venous (P(port)) pressures, portal flow and relative changes in intestinal blood volume (IBV) ((99m)technetium blood-pool scintigraphy) were measured in seven isoflurane-anesthetized, splenectomized dogs. Changes in intestinal vascular capacitance and conductance (mean portal flow/[mean aortic pressure - mean P(port)]) were determined when NTG was continuously administered (0.8 to 150 microg/kg/min) into a jugular vein. Pressure-volume (ie, P(port)-IBV) curves were defined by impeding portal flow, and capacitance was defined as the IBV at P(port)=7.5 mmHg. RESULTS: At lower doses, NTG increased capacitance without increasing conductance, but conductance increased considerably with little further increase in capacitance at higher doses. Dose-response analysis revealed that the half-maximum capacitance effect was achieved at an NTG infusion rate of 3.5 microg/kg/min, whereas a rate of 35 microg/kg/min was required for the half-maximum conductance effect. CONCLUSIONS: At lower doses, NTG dilates capacitance vessels primarily, and that effect approaches its maximum before significant dilation of conductance vessels is manifest. However, at higher doses, the increase in conductance is substantial with little additional effect on capacitance.

Analysis of Variance↗

PubMed2002

Effects of acute volume loading and hemorrhage on intestinal vascular capacitance: a mechanism whereby capacitance modulates cardiac output.

BACKGROUND: Changes in intestinal vascular capacitance during acute volume loading and hemorrhage have not been described. OBJECTIVES: To determine the effects of volume loading and hemorrhage on the intestinal vascular pressure-volume relationship and cardiac output. PATIENTS AND METHODS: In 11 alpha-chloralose-anesthetized dogs, a pneumatic portal venous constrictor and catheter were positioned to increase and measure portal venous pressure (Ppv), respectively. Relative changes in intestinal blood volume (IBV) were determined by blood-pool scintigraphy and expressed as the percentage change from control values (taken as 100%). Ppv-IBV relationships were constructed by graded portal vein constriction. RESULTS: IBV and cardiac output increased by 60 6% and 178 48%, respectively, and Ppv increased from 5.8 0.9 mmHg to 13.2 1.8 mmHg after initial volume loading (40 mL/kg of an isotonic glucose-saline solution over 7 min). IBV gradually decreased and reached near-control values after 75 min. In seven dogs, hemorrhage (sufficient to decrease mean aortic pressure by 56 4%) decreased IBV and cardiac output to 88 4% and 52 3% of control values, respectively, and Ppv decreased to 3.2 0.8 mmHg. CONCLUSIONS: A sigmoid function curve defined the relationship between cardiac output and IBV. Cardiac output remained constant over a wide range (between approximately 95% and 135% of control IBV). Outside this range, insufficient dilation or constriction resulted in a marked increase or decrease in venous pressures and cardiac output. These data indicate that vasculature capacitance modulates cardiac output during acute volume loading and hemorrhage, thereby maintaining cardiac output relatively constant over a wide range of total vascular blood volume.

Animals↗

PubMed2002

Evidence for left ventricular constraint during open heart surgery.

BACKGROUND: The degree to which the lungs and other mediastinal structures constrain the heart during cardiac surgery is uncertain. OBJECTIVES: To assess the degree of constraint to left ventricular (LV) filling that is present during cardiac surgery. PATIENTS AND METHODS: Central venous (CVP) and pulmonary capillary wedge pressures (PCWP), and an index of LV end-diastolic volume (LVEDV) - LV area, transesophageal echocardiography - were measured before and after sternotomy, after volume loading, after pericardiotomy, and before and after sternal closure following the clinically indicated procedure in 12 patients undergoing cardiac surgery. PCWP and estimated transmural LVEDP (PCWP-CVP) were plotted against the LV area. RESULTS: In all patients, the difference between PCWP and estimated transmural LVEDP-LV area relations over the full range of LV areas was substantial, indicating the presence of important constraint to filling. Even at small LV areas, when transmural LVEDP approached zero, PCWP was almost always greater than 10 mmHg. Because transmural LVEDP approached zero when areas were smallest, transmural LVEDP-LV area relations were judged to be more plausible than the corresponding PCWP-LV area relations. CONCLUSIONS: Considerable constraint to cardiac filling is effected by the lungs and other mediastinal structures. This constraint must be considered when assessing LV filling pressure - PCWP is not a reliable measure of LV preload in these circumstances.

Aged↗