Introduction: Current guidelines for cardiopulmonary resuscitation (CPR) recommend the bystander should begin external chest compression if any sign of circulation is not present or carotid pulse is not palpable. However, there have been no reports regarding the hemodynamic effect of external chest compression in the state the heart is not stopped, such as pulseless ventricular tachycardia. Purpose: The purpose of this study is to evaluate the hemodynamic effects of external chest compression in state the heart is beating in a model of simulated ventricular tachycardia. Subjects and Methods: Ten mongrel dogs were used in this study. Ventricular tachycardia was simulated by a rapid ventricular pacing and ventricular rate was adjusted and maintained at the rate to achieve a 50 mm Hg fall of baseline systolic aortic pressure. External chest compression was initiated after 4 minutes of simulated ventricular tachycardia and continued for 4 minutes. Hemodynamic measurements including systolic and diastolic aortic pressure, right atrial pressure, carotid blood flow, and end tidal CO2 tension were done at baseline, during simulated ventricular tachycardia (VT), and simulated ventricular tachycardia with external chest compression (VT+ECC). Results: Systolic aortic pressure, diastolic aortic pressure, and mean right atrial pressure was increased during VT+ECC than during VT (98짹11 vs 82짹7 p=0.00, 67짹10 vs 63짹11 p=0.022, and 13짹5 vs 4짹3 mmHg p=0.00, respectively). Carotid blood flow was increased during VT+ECC than during VT (243짹185 vs 137짹73 ml/min., p=0.023). Calculated coronary perfusion pressure was decreased during VT+ECC than during VT (59짹10 vs 54짹11 mmHg, p=0.009). End tidal CO2 tension was not different between VT+ECC and VT. Conclusion: In a canine model of simulated ventricular tachycardia, external chest compression had a contradictory hemodynamic effect including an increase in cerebral blood flow and a decrease in coronary perfusion pressure.