Case Presentation: A 38-year-old female with past medical history significant for poorly controlled, insulin dependent, type two diabetes mellitus presented with shortness of breath, abdominal pain, polyuria, and polydipsia for two days. Patient had been noncompliant with her insulin regimen for at least one month. On admission, ABG showed a pH of 6.97, pCO2 of ten (10), bicarbonate of two (2), and a beta hydroxybutyrate of 76.87. Patient was given a three liter bolus of normal saline, ten units insulin, one amp bicarbonate, and started on insulin drip. Subsequently, the patient developed acute hypoxic respiratory distress with pulmonary edema requiring bipap. Patient was then given a dose of intravenous 40mg Lasix with repeat ABG showing worsening acidosis with pH of 6.84. As the patients respiratory status continued to deteriorate, she was intubated and mechanical ventilation was started in addition to bicarbonate drip. Four hours later, code blue was called and patient had 3 PEA arrest, one ventricular fibrillation arrest. ROSC was achieved and 12 lead EKG showed ST segment elevations in the anterior leads, activating code STEMI. Stat ECHO showed ejection fraction (EF) of 10-15% with global hypokinesis. Cardiac catheterization showed nonobstructive coronaries, severely depressed EF consistent with cardiogenic shock requiring vasopressors and intra aortic balloon pump. Patient had a cardiac output of 4.5L and required extracorporeal membrane oxygenation (ECMO). Patient had ECMO initiated and was then transferred to a tertiary center. Ultimately, Patient was stabilized and had a full recovery.

Discussion: Diabetic ketoacidosis (DKA) can lead to many complications including but not limited to cardiac manifestations. Rarely seen in patients without preexisting heart disease, acidosis can cause reduced contractility of cardiac myocytes due to derangements of the concentrations of different cations. Cardiac myocytes depend on action potentials created by ion channels dependent on potassium, sodium, and calcium. These patients are often hypokalemic. Severe acidosis and decreased myocardial contractility predispose patients to arrhythmias and impaired oxygen delivery. Patients with DKA and severely low pH below 6.9 are recommended to receive supplemental bicarbonate in order to help correct the metabolic acidosis.

Conclusions: Diastolic and systolic heart failure, and DKA can often be seen in clinical practice. It is rare to see DKA leading to systolic heart failure. It is important to understand the effect of acidosis on cardiac contractility and the hearts ability to function. Acidosis causes ion shifts affecting action potentials, contractility of cardiac myocytes, pump function of the heart, and impaired oxygen delivery. Timely response to correct metabolic derangements can help avert these detrimental complications. It is extremely rare to see severe acidosis lead a fairly healthy 38-year-old female to severe heart failure with reduced ejection fraction, stress cardiomyopathy, cardiogenic shock requiring vasopressors, and ECMO.