The Patient: Paramedics were summoned to the home of a 74-year-old woman who had a complaint of shortness of breath. She was found sitting, alert and oriented, with labored respirations at 30/min. She stated that the shortness of breath came on suddenly. She denied any cardiac or pulmonary medical history, and said she took no medications. The patient was ambulatory. Her skin was cool and moist. Her SpO2 on room air was 85%, improving to 90% on oxygen via 15 lpm non-rebreather mask. Her lungs sounded clear.
When the patient was moved to the transport vehicle, she suddenly became nonverbal, with a leftward gaze. Her pupils were noted to be unequal and non-reactive (we do not know which was larger). Her BP was 67/43.
During transport, her heart rate declined into the 20’s and became apneic and pulseless. Recorded BP was 46/25. CPR was done until and after arrival at the hospital, where efforts to resuscitate were halted after some time.
ECG Number 1: The first ECG, shown here, was taken approximately 8 minutes after arrival of EMS. There is significant artifact, making it difficult to comment with certainty on the QRS width, P waves, and J points. P waves are best viewed in the right-sided chest leads, V1 through V3. The QRS morphology appears normal and the intervals are within normal ranges.
The ST segments appear to be elevated in V2 through V5, and the machine’s interpretation confirms this (although the artifact can make measurement difficult for the machine also). In addition to J point elevation, the SHAPE of the ST segments in the precordial leads is abnormal –straightening and losing the “smile” shape that is normal. There is some mild ST depression in Lead III.
ECG Number 2: The second ECG, performed about nine minutes later, shows what happened when the patient’s condition suddenly declined. Her heart rate declined to about 20 bpm, and she was pulseless. Keeping in mind that the three channels of this 12-lead ECG are run simultaneously. So, Leads I, II, and III are recorded together, and the QRS morphology matches that of ECG No. 1. Then, when aVR, aVL, and aVF are recorded, the QRS morphology changes and becomes wider at around .12 seconds (120 ms) or more. This represents an “escape” rhythm. Even though the ECG machine records an axis for the P wave, and a PR interval, P waves appear very flat in the first 3 seconds of the ECG, and non-existent in the rest of the leads.
Assessment: It is obvious that an acute catastrophic event happened to this patient. Because she died before definitive tests could be performed, we will never know what it was. The ECG signs of ST elevation and failure of the primary pacemaker certainly fall within the realm of acute myocardial infarction, but the only symptom initially was shortness of breath, which would be a possible, but atypical, presentation. She also exhibited some clinical signs of many other life-threatening illnesses, such as stroke or pulmonary embolism, but without “typical” ECG changes.
In retrospect, we are left wondering if an M.I. caused loss of perfusion, which led to the other symptoms, or if another condition lowered perfusion, causing STEMI signs on the ECG. The common denominator here is perfusion, and our goal should be to restore perfusion in order to gain time to find and treat the culprit disorder. Depending upon the setting we operate in, we might use I.V. fluids, temporary transvenous or transcutaneous pacing, mechanical ventilation, drugs, or chest compressions to try to maintain perfusion to the brain and coronary arteries. Of course, some catastrophic medical events are just that – catastrophic – and, sadly, our efforts fail.
Our thanks to Lt. Vincent Levin for donating these ECGs.