The cardiorespiratory responses were examined in yellowtail, Seriola quinqueradiata exposed to two levels of hypercapnia (seawater equilibrated with a gas mixture containing 1% CO₂ (water PCO₂ = 7 mmHg) or 5% CO₂ (38 mmHg)) for 72 hr at 20°C. Mortality was 100% within 8 hr at 5% CO₂, while no fish died at 1% CO₂. No cardiovascular variables (cardiac output, Q̇; heart rate, HR; stroke volume, SV and arterial blood pressure, BP) significantly changed from pre-exposure values during exposure to 1% CO₂. Arterial CO₂ partial pressure (PaCO₂) significantly increased (P < 0.05), reaching a new steady-state level after 3 hr. Arterial blood pH (pHa) decreased initially (P < 0.05), but was subsequently restored by elevation of plasma bicarbonate ([HCO₃^–]). Arterial O₂ partial pressure (PaO₂), oxygen content (CaO₂), and hematocrit (Hct) were maintained throughout the exposure period. In contrast, exposure to 5% CO₂ dramatically reduced Q̇ (P < 0.05) through decreasing SV (P < 0.05), although HR did not change. BP was transiently elevated (P < 0.05), followed by a precipitous fall before death. The pHa was restored incompletely despite a significant increase in [HCO₃^–]. PaO₂ decreased only shortly before death, whereas CaO₂ kept elevated due to a large increase in Hct (P < 0.05). We tentatively conclude that cardiac failure is a primary physiological disorder that would lead to death of fish subjected to high environmental CO₂ pressures.