This study describes the integrated cardiovascular response of instrumented turtles to acute anoxic exposure (approximately 2 h) and also determines the factors that regulate these responses. Trachemys scripta were chronically implanted with ultrasonic blood flow probes for the measurement of total pulmonary and systemic blood flows and heart rate. In addition, catheters were implanted into the right aortic arch for the measurement of systemic blood pressure, arterial blood gases, and pH. Animals were free to swim within an aquarium but could only breathe within a small chamber located at the surface. Cardiovascular variables were continuously monitored during normoxia, 2 h of anoxia, and during recovery at normoxia. In addition, some animals were treated with atropine or epinephrine during the anoxic exposure. During the onset of nitrogen breathing there was an increase in ventilation frequency, heart rate, pulmonary blood flow, and systemic blood flow and the development of a net left-to-right cardiac shunt. These changes lasted up to 1 h, followed by bradycardia (heart rate was reduced by 50% from control values) and the development of a large net right-to-left shunt (approximately 80% of the total cardiac output). These changes lasted the duration of the anoxic exposure and were rapidly reversed on return to a normoxic environment. Injections of epinephrine during anoxia had no effect on heart rate, pulmonary blood flow, or systemic blood flow. In contrast, injection of atropine during anoxia resulted in an increase in the heart rate and systemic blood flow, suggesting that the anoxic cardiac response is partially mediated through cholinergic mechanisms.