During routine cardiac catheterization of a patient, shock developed, which later was demonstrated to be due to pulmonary embolism and acute cor pulmonale. Hemodynamic studies were made during the preshock period and during the development of shock. In the earlier stage increase in pulmonary vascular resistance was indirectly demonstrated by the rise in right atrial pressure and the increase in the height of the P-wave in the electrocardiogram. During this time a moderate fall in cardiac output and a mild fall in systemic arterial pressure were observed. Onset of clinical shock was signalled by a precipitous fall in systemic arterial pressure, by abrupt fall in right atrial pressure and by bradycardia. This is interpreted as evidence of the neurogenic nature of this shock, to be considered a secondary complication of acute cardiac failure rather than a direct effect of it. The theoretic and practical implications of these observations are discussed.