Mrs. E.D. was a 56-year-old woman who presented to the hospital following a suicide attempt. She was obese and an ex-smoker with a medical history of bipolar disease. She was found somnolent at home by her husband with vomit in her hair. She admitted to taking an overdose of her clonazepam, and he called 911.
Mrs. E.D. responded to flumazenil in the emergency department. Her labs were essentially normal including an acetaminophen level. Her CXR [chest x-ray] was interpreted as no active disease. She was admitted by Dr. Hospitalist-1 for continued observation and treatment for possible aspiration pneumonia.
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Both hospitalists missed the ECG clues early in the hospital stay, and further misinterpreted the chest radiographs with respect to heart failure.
For the next 48 hours, Mrs. E.D. was cared for by Dr. Hospitalist-2. Mrs. E.D.’s mental status returned to normal and her SaO2 (arterial oxygen percent saturation) greater than 94% was 2L oxygen/nasal cannula (NC). On day 2, she was noted to have bilateral crackles. An ECG performed that morning showed rate-dependent ST segment depressions in the precordial leads (heart rate, 102 bpm), compared with admission ECG. Dr. Hospitalist-2 made no mention of this finding in his progress note, and no cardiac biomarkers were obtained. Later that evening, Mrs. E.D. was transferred to the inpatient psychiatry ward for ongoing treatment of her bipolar disorder.
Mrs. E.D. participated in her therapies on the psychiatry ward, but complained of dyspnea on exertion (DOE) and shortness of breath (SOB) while lying in bed. Psychiatry ordered a chest radiograph that showed hyperinflation and chronic obstructive pulmonary disease (COPD) with mild fluid overload consistent with heart failure. Dr. Hospitalist-2 was contacted and came to see Mrs. E.D. for an evaluation. He ordered pulmonary function testing (PFT), oral prednisone for COPD, and continued oral antibiotics for aspiration pneumonia.
For the next 2 days, the psychiatry staff continued to document DOE, SOB, and wheezing and crackles on lung auscultation. PFTs demonstrated severe obstructive airway disease. Albuterol nebulizer treatments were initiated along with an ipratropium inhaler. In the early morning hours of day 9, Mrs. E.D. complained of increasing SOB. Her vital signs were BP, 180/110 mm Hg; HR, 104 bpm; and RR, 24 breaths/min. Dr. Hospitalist-2 was contacted. CXR showed bilateral pleural effusions, hyperinflation, with interstitial edema and patchy areas of consolidation. SaO2 was 83% on RA, and Mrs. E.D. was titrated to 3L O2/NC to keep her saturations greater than 92%. Later that morning, the psychiatry staff was informed that Mrs. E.D. would be evaluated by Dr. Hospitalist-1.
On the evening of day 9, Mrs. E.D. was still on the psychiatry floor. Her husband was visiting and was concerned with her breathing. Her SaO2 was 83% on 3L and she was increased to 6L of oxygen. The psychiatry staff contacted Dr. Hospitalist-1, who accepted the transfer to the regular nursing floor. Transfer orders were written by Dr. Hospitalist-1 with a diagnosis of pneumonia/COPD along with therapies for same. There is no evidence in the chart that Dr. Hospitalist-1 evaluated Mrs. E.D. prior to the transfer orders being written. Mrs. E.D. arrived to the regular nursing floor around 9 p.m. She was administered an IV antibiotic dose at 11 p.m. and was noted to be comfortable. At 11:30 p.m., Mrs. E.D. was found apneic and pulseless. She was unable to be resuscitated.
An autopsy was performed with a final anatomic diagnosis of acute subendocardial myocardial ischemic change and necrosis, severe CAD (coronary artery disease), severe chronic ischemic heart disease, severe generalized atherosclerotic vascular disease, severe chronic obstructive lung disease, and patchy bronchopneumonia.
Complaint
The husband felt as if his wife was abandoned. He was aware of her increasing respiratory symptoms while she was on the psychiatry ward and couldn’t understand why it took the doctors so long to do something. When he learned that his wife had essentially died of a "heart attack," he contacted an attorney who filed suit.
The complaint alleged that Dr. Hospitalist-1 and Dr. Hospitalist-2 both failed to diagnose her myocardial ischemia, failed to recognize her heart failure, and failed to initiate appropriate therapies to decrease her cardiac work and save her heart.
Scientific principles
The concept of "demand ischemia" refers to a mismatch between myocardial oxygen demand and supply. The 2012 Joint ESC/ACCF/AHA/WHF Third Universal Definition of MI refers to a type 2 MI when the event is secondary to ischemia due to either an increased oxygen demand or a decreased supply in the absence of an acute primary coronary thrombotic event. Myocardial oxygen demand is increased in a number of clinical settings (sepsis, tachyarrhythmia). Simultaneously, myocardial oxygen delivery may be reduced due to both tachycardia (which reduces diastolic filling time) and reduced perfusion pressure (in the setting of hypotension and/or increased cardiac filling pressures as seen in heart failure).