Matuschak, GM and Pinsky, MR
(1989)
Effects of positive-pressure ventilatory frequency on hepatic blood flow and performance.
Journal of Critical Care, 4 (3).
153 - 165.
ISSN 0883-9441
![[img]](http://d-scholarship.pitt.edu/style/images/fileicons/text_plain.png) |
Plain Text (licence)
Available under License : See the attached license file.
Download (1kB)
|
Abstract
The liver metabolizes several mediators of sepsis-related acute lung injury, but is frequently dysfunctional during intermittent positive-pressure ventilation (IPPV). With IPPV, increases in intrathoracic pressure (ITP) phasically increase the effective hepatic back pressure owing to compression by the diaphragm and retrograde propagation of swings in right atrial pressure. If intrahepatic flow distribution or the time constant of hepatic outflow are accordingly altered by ventilatory frequency (f), then hepatic performance may be compromised beyond a critical f threshold. In two canine models, we characterized at constant mean ITP the effects of ITP pulses on hepatic blood flow partitioning and performance over a f spectrum (0.4, 1.67, and 2.5 Hz) during IPPV and high-frequency jet ventilation. Portal venous flow (Qpv) and hepatic arterial flow (Qha) were measured by electromagnetic flow probes and performance by the pharmacokinetics of infused indocyanine green (0.25 mg/kg). To assess pressure wave transmission to the portal vein, cardiac cycle-specific (CCS) ITP pulses were used to alter the hepatic venous pressure (Phv) waveform. Measurements were made during control conditions, after graded acute hypovolemia (group 1, n = 7,20 mL/kg bleed; group 2, n = 6, bled to a mean aortic pressure of 45 mm Hg) to change the hepatic critical pressure balance, and after blood reinfusion. Despite decreases in peak-inspiratory transpulmonary pressure with increasing f, phasic reductions in Qpv and the transmural portal venous pressure (Ppv) to Phv gradient were similar at all f. The inspiratory Ppv waveform reflected changes in abdominal pressure, and was not altered by differential swings in Phv with CCS ITP pulses regardless of hypovolemia. We conclude that at f ≤ 2.5 Hz, phasic increases in ITP modulate the hepatic outflow pressure in a post-sinusoidal flow-limiting segment in which diaphragmatic compression increases resistance to Qpv in a f-dependent manner. However, the pharmacokinetics of substances having similar hepatic extraction will primarily vary with inflow over this f spectrum. © 1989.
Share
| Citation/Export: |
|
| Social Networking: |
|
Details
Metrics
Monthly Views for the past 3 years
Plum Analytics
Altmetric.com
Actions (login required)
 |
View Item |
![[feed]](/images/feed-icon-32x32.png){kind=icon}