TY - JOUR
T1 - Canine biventricular performance during acute progressive pulmonary microembolization
T2 - Regional myocardial perfusion and fatty acid uptake
AU - Hurford, William E.
AU - Barlai-Kovach, Martha
AU - Strauss, H. William
AU - Zapol, Warren M.
AU - Lowenstein, Edward
N1 - Funding Information:
From the Anesthesia and Radiology Services of the Massachusetts General Hospital and the Departments of Anesthesia and Radiology, Harvard Medical School, Boston. Supported by NHLBI SCOR grant HL23591 and HL32636. Dr Hurford is a recipeint of USPHS National Research Service Award HLO7416-07. Address reprint requests to William Department of Anesthesia, Massachusetts tal, Boston, MA 02114. o I987 by Grune & Stratton, Inc. OSS3-9441/87/0204-0005$05.00/O
PY - 1987/12
Y1 - 1987/12
N2 - The cardiac output during acute pulmonary artery hypertension (PAH) may be compromised by right ventricular (RV) outflow obstruction, myocardial ischemia, or adverse ventricular interactions. To study the relative contributions of these mechanisms to impaired biventricular function during PAH, we injected 75 to 105-μm glass beads into the pulmonary vasculature of 11 dogs and correlated the hemodynamic alterations with changes in biventricular function. Biventricular ejection fractions and interventricular septal motion were evaluated by gated blood pool angiocardiograms. Regional myocardial blood flow (n = 8 dogs) was measured with microspheres, and regional myocardial fatty acid metabolism during PAH (n = 8 dogs) was assessed by measuring the regional myocardial extraction of the radioiodinated fatty acid analog, 15-(p-iodophenyl)-3-methylpentadecanoic acid (3m-PIP/PDA). Following microembolization, the mean pulmonary artery pressure increased from 14 ± 1 to 48 ± 2 mm Hg (P < .001) and cardiac output decreased from 3.5 ± 0.3 to 2.6 ± 0.3 1 /min (P < .05). Right ventricular volume increased and RV ejection fraction decreased progressively. Abnormal septal motion during PAH occurred in 5 of 11 dogs and was associated with decreased LV diastolic compliance. Right ventricular myocardial blood flow remained increased during PAH while the regional extraction of 3m-PIP/PDA was uniform throughout the heart. These findings suggest that during moderate PAH the canine cardiac output is limited by RV outflow obstruction and decreased LV diastolic compliance rather than by ischemia.
AB - The cardiac output during acute pulmonary artery hypertension (PAH) may be compromised by right ventricular (RV) outflow obstruction, myocardial ischemia, or adverse ventricular interactions. To study the relative contributions of these mechanisms to impaired biventricular function during PAH, we injected 75 to 105-μm glass beads into the pulmonary vasculature of 11 dogs and correlated the hemodynamic alterations with changes in biventricular function. Biventricular ejection fractions and interventricular septal motion were evaluated by gated blood pool angiocardiograms. Regional myocardial blood flow (n = 8 dogs) was measured with microspheres, and regional myocardial fatty acid metabolism during PAH (n = 8 dogs) was assessed by measuring the regional myocardial extraction of the radioiodinated fatty acid analog, 15-(p-iodophenyl)-3-methylpentadecanoic acid (3m-PIP/PDA). Following microembolization, the mean pulmonary artery pressure increased from 14 ± 1 to 48 ± 2 mm Hg (P < .001) and cardiac output decreased from 3.5 ± 0.3 to 2.6 ± 0.3 1 /min (P < .05). Right ventricular volume increased and RV ejection fraction decreased progressively. Abnormal septal motion during PAH occurred in 5 of 11 dogs and was associated with decreased LV diastolic compliance. Right ventricular myocardial blood flow remained increased during PAH while the regional extraction of 3m-PIP/PDA was uniform throughout the heart. These findings suggest that during moderate PAH the canine cardiac output is limited by RV outflow obstruction and decreased LV diastolic compliance rather than by ischemia.
UR - https://www.scopus.com/pages/publications/0023630639
U2 - 10.1016/0883-9441(87)90070-0
DO - 10.1016/0883-9441(87)90070-0
M3 - Article
AN - SCOPUS:0023630639
SN - 0883-9441
VL - 2
SP - 270
EP - 281
JO - Journal of Critical Care
JF - Journal of Critical Care
IS - 4
ER -