Left ventricular dysfunction in a canine model of chronic cyanosis

States of low cardiac output frequently complicate the postoperative course of patients undergoing repair of cyanotic congenital heart lesions. The relative contribution of chronic cyanosis alone to the postoperative deterioration in left ventricular function remains unknown. To study the effects of chronic cyanosis on left ventricular function, nine dogs underwent inferior vena cava-to-left atrial anastomosis, a model that minimizes abnormal left ventricular hemodynamic loads. After at least 6 months of chronic cyanosis (mean arterial pO2 of 44 mm Hg and mean hematocrit of 61%), the dogs were instrumented with ultrasonic dimension transducers and micromanometers for collection of left ventricular pressure-dimension data. Studies were performed 7 to 10 days after recovery from instrumentation while the dogs were awake and alert. Nine normal dogs were also instrumented and served as controls. Pressure and dimension data were collected during transient vena cava occlusions before and after the combined administration of propranolol and atropine to produce autonomic blockade. Contractile function as measured by dP/dt, ejection fraction, and the stroke work-end diastolic length relationship was decreased by autonomic blockade to a similar extent in both normal and cyanotic dogs. After autonomic blockade, normal dogs were able to maintain stroke volume and cardiac index by utilization of Frank-Starling reserves (increased left ventricular end diastolic volume). In contrast, dogs with cyanosis were unable to maintain stroke volume and cardiac index or to increase left ventricular end diastolic volume after autonomic blockade. Dogs with cyanosis had reduced ventricular diastolic compliance, and they more fully used Frank-Starling reserves to maintain normal stroke volume and cardiac index in the control state when compared with normal dogs. The diminished preload reserves of the cyanotic dogs limited systolic performance (stroke volume and cardiac index) only at reduced levels of contractility produced by autonomic blockade.