Ventricular function after atrial cardioplegia.
Continuous retrograde coronary sinus cardioplegia (CSCP) has previously been carefully evaluated experimentally and shown to be efficacious during ischemia, even in the presence of coronary lesions and in the hypertrophied state. A new technique of retrograde cardioplegia delivery through the right atrium, using right ventricular distension and pressures of 60 mm Hg, has recently been described with excellent clinical results. This study was designed to specifically examine right ventricular function after atrial cardioplegia and acute passive right ventricular distension. CSCP (n = 10) was compared with cardioplegia delivered through the right atrium both continuously (n = 10) and intermittently (n = 8). When ventricular function was examined with the use of the load-independent relationship of stroke work vs end-diastolic length, there was a profound deterioration of right ventricular function in both atrial cardioplegia groups (44% and 37% of control values, respectively) after 1 hr of reperfusion. In contrast, biventricular function was fully preserved in the CSCP group 1 hr after reperfusion. Left ventricular function measured at the end of reperfusion was preserved in all three groups. Right ventricular ATP levels were slightly but significantly depressed in all groups and in the atrial cardioplegia groups, this metabolic change was also seen in the left ventricle. These metabolic and hemodynamic data may reflect the inability of atrial cardioplegia to cool the myocardium below 16 degrees C. Postoperative right ventricular dysfunction may be more common than has been previously thought when atrial cardioplegia is used, particularly in the absence of topical cooling.
Salter
D R
DR
Department of Surgery, Duke University Medical Center, Durham, NC 27710.
Goldstein
J P
JP
Abd-Elfattah
A
A
Murphy
C E
CE
Brunsting
L A
LA
Wechsler
A S
AS
D000227:Adenine Nucleotides / Q000378:metabolism; D001794:Blood Pressure; D003326:Coronary Circulation; D004734:Energy Metabolism; D006321:Heart / Q000502:physiology*; D006324:Heart Arrest, Induced / Q000379:methods*; D006325:Heart Atria; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism; D010477:Perfusion; D013696:Temperature
D000227:Adenine Nucleotides