Background and Aim: Metabolic acidosis could occur due to either accumulation of endogenous acids or bicarbonate loss from the gastrointestinal tract or more commonly from the kidney. This study aimed to investigate the possible underlying mechanism(s) of chronic acidosis-induced cardiac contractile and electrical changes in rats. Materials and Methods: 24 adult Wistar rats, of both sexes, were randomly divided into control group and chronic metabolic acidosis group, which received orally 0.28 M NH4Cl in the drinking water for 2 weeks. At the end of experimental period, systolic and diastolic blood pressures were measured. On the day of sacrifice, rats were anaesthetized by i.p. Pentobarbitone (40 μg/kg B.W.), transthoracic echocardiography and ECG were performed. Blood samples were obtained from abdominal aorta for complete blood count and determination of plasma pH, bicarbonate, chloride, sodium, potassium, troponin I, creatine kinase, interleukin 6 and aldosterone levels. Hearts from both groups were studied histopathologically. SPSS program, version 20.0 was used to compare significance between the two groups. Comparisons were made using unpaired ‘’t” test. Results: Compared to control group, chronic metabolic acidosis group showed anemia, significant systolic and diastolic hypotension accompanied by significant reduction of ejection fraction and fraction of shortening, significant bradycardia, prolonged QTc interval and higher widened T wave, as well as, significantly elevated plasma levels of aldosterone, troponin I, creatine kinase and interleukin 6. The left ventricular wall of acidosis group showed focal areas of degeneration and areas of hypertrophied cardiomyocytes with vacuolated pale acidophilic sarcoplasm and deeply stained pyknotic nuclei. Conclusion: Chronic metabolic acidosis induced negative inotropic and chronotropic effects and cardiomyopathy, possibly by elevated plasma aldosterone and interleukin 6 levels.