Effects of intra-abdominal CO2-insufflation on normal and impaired myocardial function: an experimental study.
BACKGROUND
Intra-abdominal pressure (IAP) elevation during CO2-pneumoperitoneum increases cardiac afterload and may enhance dysfunction of the already compromised heart. This study focused on the effects of acute IAP increases on left and right ventricular loadings and contractility in the heart with impaired global function.


METHODS
Impairment of myocardial function (IMF) was pharmacologically induced in 16 pigs by administration of halothane and propranolol, while baseline arterial pressure was maintained by intravenous phenylephrine. Intra-abdominal pressure was gradually increased by 10 mmHg up to 30 mmHg in the supine position (IMF group 1, n = 8) or in a head-down tilted position (IMF group 2, n = 8). In two control groups with normal myocardial function, IAP was also increased in the supine position or the head-down tilted position. Cardiac function in all groups was assessed by epicardial echocardiography, intraventricular pressure measurements and pulmonary artery catheterization.


RESULTS
The increase in IAP was accompanied by a transient rise in LV end-systolic wall stress and reduced cardiac output significantly by 16-24% in all groups. In the IMF groups, LV end-diastolic transmural pressure increased by 34-60% to peak values of 24 mmHg, while cross-sectional LV end-diastolic areas remained unchanged. Increases in right ventricular end-diastolic volume and decreases in right ventricular ejection fraction as well as in cardiac output were most pronounced at IAP 20 mmHg and significantly stronger in both IMF groups than in the control groups (P < 0.001).


CONCLUSIONS
Following the acute elevation of IAP, the right ventricular volume load shifted more extensively in the IMF groups than in the animals with normal myocardial function. Myocardial function in the impaired heart may worsen during IAP elevation due to right ventricular load alterations rather than a LV afterload increase.
Greim
C A
CA
Klinik für Anaesthesiologie, Universitätsklinikum Würzburg, Germany. greim@anaesthesie.uni-wuerzburg.de
Broscheit
J
J
Kortländer
J
J
Roewer
N
N
Schulte am Esch
J
J
D000005:Abdomen / Q000502:physiology*; D000319:Adrenergic beta-Antagonists; D018685:Anesthetics, Inhalation; D000818:Animals; D002245:Carbon Dioxide; D002302:Cardiac Output / Q000502:physiology; D002406:Catheterization, Peripheral; D004452:Echocardiography; D006221:Halothane; D006331:Heart Diseases / Q000139:chemically induced / Q000503:physiopathology*; D006439:Hemodynamics / Q000502:physiology; D007327:Insufflation / Q000009:adverse effects*; D010656:Phenylephrine / Q000494:pharmacology; D011433:Propranolol; D013318:Stroke Volume / Q000502:physiology; D013552:Swine; D013556:Swine, Miniature; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D016277:Ventricular Function, Left / Q000502:physiology; D016278:Ventricular Function, Right / Q000502:physiology
D000319:Adrenergic beta-Antagonists; D018685:Anesthetics, Inhalation; D014662:Vasoconstrictor Agents; D002245:Carbon Dioxide; D010656:Phenylephrine; D011433:Propranolol; D006221:Halothane