Department of Anesthesiology

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The cardiovascular response to digoxin in conscious dogs with left atrial obstruction.

TitleThe cardiovascular response to digoxin in conscious dogs with left atrial obstruction.
Publication TypeJournal Article
Year of Publication1990
AuthorsHeerdt PM, Caldwell RW
JournalJ Cardiothorac Anesth
Volume4
Issue6
Pagination687-94
Date Published1990 Dec
ISSN0888-6296
KeywordsAnimals, Atrial Function, Left, Blood Pressure, Cardiac Output, Catheterization, Consciousness, Digoxin, Dogs, Heart Rate, Hypertension, Pulmonary, Pulmonary Artery, Pulmonary Wedge Pressure, Vascular Resistance, Ventricular Outflow Obstruction
Abstract

In addition to positive inotropic and atrioventricular conduction-blocking properties, digoxin is capable of producing systemic and pulmonary vasoconstriction. However, whether chronic digoxin treatment exacerbates the pulmonary hypertension that results from left atrial (LA) outflow obstruction has not been specifically examined. This study assessed the vascular and inotropic responses to 5 days of digoxin treatment in six conscious dogs before and after filling a permanently implanted LA balloon. Dogs were also instrumented to measure left ventricular (LV) pressure, LV dP/dt, mean systemic arterial (MAP), right atrial (RAP), pulmonary arterial, and pulmonary capillary wedge pressures, as well as cardiac output (CO). Under normal conditions with the balloon empty, digoxin treatment (40 micrograms/kg loading dose and 12 micrograms/kg/d for 5 days) reduced CO (-17%) and increased systemic (SVR) and pulmonary (PVR) vascular resistances 27% and 37%, respectively; heart rate (HR) and LV dP/dt were not changed. Filling the balloon with enough saline to double PVR also increased SVR (52%), HR (42%), and RAP (92%), and reduced CO (-24%). During LA outflow obstruction, 5 days of digoxin reduced HR (-17%), SVR (-29%), and RAP (-23%), but did not alter PVR, CO, or LV dP/dt. This study demonstrates that although systemic and pulmonary vasoconstriction result from chronic digoxin treatment under normal conditions, the drug produces systemic vasodilation and no change in PVR during LA outflow obstruction.

Alternate JournalJ Cardiothorac Anesth
PubMed ID2131897
Grant ListHBLI-17796 / HB / NHLBI NIH HHS / United States