Introduced in 1976, atenolol was developed as a replacement for propranolol in the treatment of hypertension. It works by slowing down the heart and reducing its workload. Unlike propranolol, atenolol does not pass through the blood–brain barrier to a large extent thus decreasing the incidence of various central nervous system side effects. (1)

Symptoms of overdose are due to excessive pharmacodynamic actions on β₁ and also β₂-receptors. These include bradycardia (slow heartbeat), severe hypotension with shock, acute heart failure, hypoglycemia and bronchospastic reactions. Treatment is largely symptomatic. 

Hospitalization and intensive monitoring is indicated.

dobutamine can be given against hypotension and the inhalation of a β₂-mimetic as  salbutamol will terminate bronchospasms. Blood or plasma atenolol concentrations may be measured to confirm a diagnosis of poisoning in hospitalized patients or to assist in a medicolegal death investigation. Plasma levels are usually less than 3 mg/L during therapeutic administration, but can range from 3–30 mg/L in overdose victims (2) (3)

Atenolol  identified as carrying a higher risk of provoking type 2 diabetes, leading to its downgrading in the United Kingdom in June 2006 to fourth-line agent in the management of hypertension (4) (7) (8)

Some other studies did NOT find this correlation tho (5) (6)

Abrupt withdrawal of atenolol can provoke a thyroid storm (9) => monitor pt closely if you are to withdraw beta blockers. (9)

1.  DeLima LG, Kharasch ED, Butler S (1995). "Successful pharmacologic treatment of massive atenolol overdose: sequential hemodynamics and plasma atenolol concentrations". Anesthesiology 83 (1): 204–207. doi:10.1097/00000542-199507000-00025. PMID 7605000.

1.  R. Baselt (2008). Disposition of Toxic Drugs and Chemicals in Man (8th ed.). Foster City, CA: Biomedical Publications. pp. 116–117