The Patient: This 72-year-old woman called EMS because of a sudden onset of breathlessness and anxiety. She had a history of COPD (asthma), CHF, and Type II diabetes. We do not know her medications or any other history. She was found to have bilateral breath sounds with "minimal" expiratory wheezing. She was alert and very anxious. Her initial pulse rate was recorded at around 60 bpm and irregular. A systolic BP was heard at 140 mm Hg, but the paramedic could not hear a pulse after that. She was given oxygen via CPAP (Continuous positive airway pressure). The first ECG at 15:50 was recorded during this assessment. After appearing to improve, she became neurologically altered, and her level of consciousness varied during the call. She was turned over to emergency department staff conscious and able to speak, but had a cardiac arrest subsequently. The paramedics were unable to obtain followup information regarding the outcome. ECG at 1550: The first QRS on the recording has no associated P wave, and is presumed to be an escape beat, probably junctional, with an interventricular conduction delay (QRS .12 sec.). This is a right bundle branch block pattern with left anterior fascicular block (bifascicular block). The second QRS is about the same width, but with a different morphology and discordant T waves, so probably ventricular. The third QRS is very much like the first, except that it appears to be conducted from the preceding P wave. For the next five seconds, there are only P waves, which are regular at about 130 bpm. The three-beat pattern seen at the beginning repeats itself near the end. This ECG shows evidence of severe conduction blocks. The wide QRS complexes indicate interventricular blocks. In this case, some are probably premature ventricular contractions and some are sinus beats with bifascicular block. Even more worrisome is the intermittent loss of AV conduction. This can be called "intermittent trifascicular block", or "intermittent ventricular standstill". This is not a "third-degree AV block", because there are signs of AV conduction, but it is very close. With two of the three main fasicles of the left bundle branch blocked initially, it only takes a block in the remaining fascicle to produce a complete lack of AV conduction. Of course, there are no pulses during the time of ventricular standstill. The really concerning part of this situation is the lack of an ESCAPE RHYTHM. This is a good time for a temporary pacemaker, either transcutaneous or, if available, transvenous. ECG at 1603: This ECG was obtained enroute to the hospital. The patient is once again alert and anxious. There is some artifact which hampers evaluation, but there are two P waves for every QRS complex. The atrial rate is about 120 bpm and the ventricular rate is about 60 bpm. The non-conducted P waves are buried in the T waves of the preceding beats.

Usually, instructors of basic ECG classes look for examples of the most common conditions that are likely to be encountered by the learners.  But, sometimes, it is advantageous to show students more unusual presentations to remind them of the infinite possibilities when we care for living beings.  This series is a very good example of what can and does happen to some people with cardiovascular disease.  It will give your students an opportunity to think about possible interpretations, and also about anticipating clinical implications and emergencies that may arise.

The Patient:  This patient is a man in his 80s who has been active his whole life.  He considers himself to be healthy, giving no medical history and denying medication use. He states that he has had a yearly health exam.  Today, he felt “tired and dizzy” while raking leaves.  As he walked to his house to rest, he had a syncopal episode and fell, hitting his head. He was unconscious for a few minutes. A family member called for Emergency Medical Services (EMS). Paramedics found him awake and complaining of bilateral “shoulder and wrist” pain. He had no obvious trauma to his extremities, but had some bruising on his head and face.  He denied recent illness and substance abuse.  He was oriented x3. He was pale and diaphoretic, and complained of nausea. He denied chest or back pain.  He denied shortness of breath.  BP 100/60.  Heart rate bradycardic.  SPO2 above 95%.  He was given aspirin and ondasetron, and transported to a hospital.

This pair of ECGs feature one of our recurring themes:  wide-complex tachycardia (WCT). It is a fascinating topic, as tachycardia has many causes and many mechanisms, and wide QRS also has many causes, with the mechanism being slow conduction through the ventricles. 

Sometimes, it is not possible to diagnose the true origin of a WCT from one ECG, or even serial ECGs.  Is the tachycardia due to increased sympathetic activity (fear, dehydration, exercise, hypoxia, hypovolemia, etc.)?  Or is the fast rate due to reentry, where one impulse gets “caught” in a loop, repeating itself rapidly, and depolarizing the myocardium with each pass?  What is the location of the pacemaker that is responsible for the rhythm?  Is it a supraventricular rhythm that has suffered an intraventricular conduction delay, widening the QRS?  Or is the rhythm originating in a ventricular pacemaker, without the ability to travel on the fast highway that is the intraventricular conduction system? 

If you or your students work in an acute care setting, such as pre-hospital or emergency department, you may not be with the patient long enough or be able to conduct enough tests to determine without a doubt the answers to the above questions.  Some WCTs cause such severe symptoms that they must be dealt with quickly, to avoid rapid deterioration to ventricular fibrillation.  For that reason, there is a widely-accepted rule for WTC treatment:

TREAT ALL WIDE-COMPLEX TACHYCARDIA AS IF IT IS V TACH UNTIL PROVEN OTHERWISE.