The following figures are from: M. Malbrain: Abdominal Perfusion Pressure
as a Prognostic Marker in Intra-abdominal Hypertension, Yearbook of
Intensive Care and Emergency Medicine 2002, edited by
Jean-Louis Vincent, pg. 792-814
Cardiac preload is diminished due to a direct compressive effect on
the vessels and the heart. Cardiac contractility is diminished due
to cardiac compression and raised intrathoracic pressures mediated
by diaphragm elevation which erroneously increases central venous
pressure (CVP) and pulmonary capillary wedge pressure (PCWP). Organ
compression and compression of the venous capacitance vessels in the
abdomen result in elevated afterload either by a direct effect or
by the mediation of renin-angiotensin aldosteron and endothelin. Finally,
cardiac output (CO) and mean arterial pressure (MAP) drop resulting
in a low abdominal perfusion pressure (APP), which then may lead to
splanchnic hypoperfusion. DVT: deep venous thrombosis; PE: pulmonary
embolism; EDV: end-diastolic volume; Ptrans: trans-mural pressure.
In the absence of correct blood volume measurements, traditional filling
pressures can be used adapting the thresholds according to the degree
of IAH, values are given between brackets as a directive. Since no
clear-cut thresholds could be obtained from the literature, values
for right ventricular end-diastolic volume index (RVEDVI) are preceded
by a question mark. APP: abdominal perfusion pressure; MAP: mean arterial
pressure; CI: cardiac index; ITBVI: intrathoracic blood volume index;
EVLWI: extravascular lung water index.
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