Acute pulmonary edema in puppies generally occurs due to congenital left-right shunts such as patent ductus arteriosus or large ventricular septal defects. Herein, we presented two cases of puppies with no apparent congenital cardiovascular disease. Case 1: A 12-day-old male Labrador Retriever, weighing 1.15 kg, was unable to suckle sufficiently from its dam and exhibited laboured breathing. Pulmonary edema was identified in all lung lobes by radiography, furthermore, echocardiography revealed significant enlargement of the left side of the heart. Pulmonary edema secondary to volume overload was suspected and furosemide was administered. The respiratory status was improved on the following day. Pimobendan was administered orally in addition to furosemide and both were withdrawn 6 weeks later when the heart size was normalized. Case 2: A 15-day-old female Standard Poodle, weighing 0.68 kg, was less active than other littermates and exhibited laboured breathing. Radiography revealed pulmonary edema in the right posterior lobe, dilatation of the caudal vena cava and ascites. Echocardiography revealed significant enlargement of the left atrium and ventricle perhaps owing to decreased left ventricular contractility. Furosemide and pimobendan were administered. One week later, appetite was improved and supraventricular tachycardia of 375 bpm was observed. Therefore, tachycardia-induced dilated cardiomyopathy was suspected which returned to sinus rhythm with diltiazem treatment, however, it was recurred. Upon sotalol monotherapy, a normal heart size was observed seven months later. In conclusion, we encountered two new-born puppies with transient pulmonary edema that were temporarily treated with pimobendan and furosemide.