A 42‐year‐old woman presented to the Emergency Department with intermittent sub‐sternal heaviness, shortness of breath and vomiting. Review of systems was negative for chills, fever, cough, sore throat, headache, abdominal pain, diarrhea, dysuria, palpitations and joint pain. The physical examination revealed blood pressure of 71/41 mm Hg, heart rate of 68/min, respiratory rate of 22/min, temperature of 35oC and bibasilar crackles on chest auscultation. Her significant laboratory results were white count of 21.6 X 103/mm3with bands 14%, lactic acid 54.1 mg/dl, serum creatinine 2.03 mg/dl and troponin <0.01. Chest radiography revealed small right sided pleural effusion and ultrasound of abdomen showed mild gall bladder thickening. An electrocardiogram showed complete atrioventricular dissociation with junctional escape rhythm at 70 beats per minute. She was admitted for severe sepsis from an unclear source and treated with broad‐spectrum antibiotics and intravenous fluids. Given inadequate blood pressure response to intravenous fluids, she was promptly started on nor‐epinephrine drip. She showed remarkable improvement in the next 24 hours. Her white cell count, lactic acid and serum creatinine normalized by then. A repeat electrocardiogram done the next day showed normal sinus rhythm at 80 beats per minute with no evidence of atrioventricular dissociation. Transthoracic echocardiogram did not reveal any structural or functional abnormality. Serial blood cultures did not show any growth and the source of sepsis remained unclear.
It has been well established that skeletal muscles become inexcitable in critically ill septic patients due to reduction in the sodium current availability for generation of action potential. Similar changes in the cardiac muscle fibers of septic patients lead to noticeable electrocardiographic changes. The most common of which are decreased amplitude and widening of QRS complex. Many cases of bundle branch block have also been reported in septic patients but the phenomenon of complete atrioventricular dissociation is an extremely rare occurrence. These changes can be attributed to down regulation of β adrenergic receptors, depressed post receptor signaling pathways, impaired calcium liberation from sarcoplasmic reticulum and impaired electromechanical coupling at the myofibrillar level in septic patients. Most of the time electrocardiographic changes seen in septic patients are transient and revert spontaneously with resolution of sepsis.
Electrocardiographic changes in patients with sepsis may vary from low amplitude of QRS complex to complete atrioventricular dissociation. These are thought to be caused by various electrochemical disturbances, are usually transient and resolve with the resolution of sepsis
To cite this abstract:Wadhwani L, Shah A. Dissociated Heart of a Septic Patient. Abstract published at Hospital Medicine 2014, March 24-27, Las Vegas, Nev. Abstract 669. Journal of Hospital Medicine. 2014; 9 (suppl 2). https://www.shmabstracts.com/abstract/dissociated-heart-of-a-septic-patient/. Accessed July 17, 2019.