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.    

The patient:  This ECG is taken from a 55-year-old man whose wife called 911 because he had a syncopal episode.  When the paramedics arrived, he was conscious and alert, and denied any symptoms.  He gave a history of "cardiac", diabetes, and opiate abuse.  We do not know the nature of his cardiac history or his medications.  

It is difficult to pinpoint a definite diagnosis with this lack of information and a clearly abnormal ECG.  We will limit our discussion to listing the abnormalities seen:

The ECG rhythm:  There is a fast, regular rhythm that is supraventricular in origin (there are P waves).  When a supraventricular rhythm has a rate of about 150 per minute, we should ALWAYS consider ATRIAL FLUTTER WITH 2:1 CONDUCTION.  Atrial flutter produces P waves (flutter waves) at approximately 250-350 per minute.  The normal AV node is able to conduct half of these, at a rate of about 150 per minute. Atrial flutter with 2:1 conduction is the most common presentation of new-onset atrial flutter.  It is often missed by people who expect to see several flutter waves in a row, producing the "sawtooth pattern".  That being said, atrial flutter is usually discernable in at least a few leads if it is present.  We do not see any signs of flutter waves in this ECG.

That leaves us with a differential diagnosis of sinus tachycardia vs. one of the regular supraventricular tachycardias like reentrant tachycardias or atrial tachycardia.  Sinus tachycardia can be recognized by several features. If we are fortunate enough to witness the onset or offset of the fast rhythm, will will recognize sinus tachycardia by a "warm up" or gradual speeding up of the rate, and a "cool down", or gradual slowing.  On the other hand, SVTs often have abrupt onset and offset.  Sinus tachycardia often has a very obvious cause, such as hypovolemia, fever, pain, anxiety, vigorous exercise, or hypoxia.  Sinus tachycardia usually has a distinct, upright P wave in Lead II, and a clearly-seen, often negative, P wave in Lead V1.  This ECG does not show the onset of the tachycardia, and is not long enough to evaluate for rate changes. Lead II appears to have upright P waves on the downslope of the previous T waves. V1 has deeply negative P waves, and V4 has the most clearly-seen P waves.  Without being positive, this looks more like sinus tachycardia than a reentrant tachycardia.  It would help to know more about the patient's condition.

This ECG is taken from an 82-year-old man who called 911 because of chest pain.  He has an unspecified “cardiac” history, but we do not know the specifics. 

WHAT IS THE RHYTHM?  The heart rate is 69 bpm, and there are P waves before every QRS complex. The underlying rhythm is regular, with one premature beat that is wide without a P wave.  The PR interval is slightly prolonged at .25 seconds.  The rhythm is normal sinus rhythm with first-degree AV block and one PVC. 

WHY THE WIDE QRS?   The QRS complex is wide at .14 seconds. The QRS in V 1 has a wide R wave after a small Q wave.  This in consistent with right bundle branch block pattern, with loss of the normal initial small r wave (pathological Q waves).  The diagnosis of RBBB is further corroborated by the wide little S waves in Leads I and V6.  The QRS frontal plane axis is -66 degrees per the machine, and clearly “abnormal left” because the QRS in Lead II is negative, while the QRS in Leads I and aVL are positive.  This is left anterior fascicular block, also called left anterior hemiblock.  The combination of RBBB and LAFB is a common one, as the two branches have the same blood supply.  It is also called bi-fascicular block. 

WHAT ABOUT THE ST SEGMENTS?  The ST segments in leads V2 through V6 are elevated, and their shape is very straight, as opposed to the normal shape of coved upward (smile). Even though the amount of ST elevation at the J points appears subtle, the shape of the segments, the fact that they appear in related leads, and the fact that the patient is an elderly male with chest pain all point to the diagnosis of ANTERIOR WALL ST elevation M.I. (STEMI).  Additional ST changes include a straight shape in Leads I and aVL and ST depression in V1 and aVR.  

PATIENT OUTCOME  The patient was transported to a cardiac center, where he received angioplasty in the cath lab.  The left coronary artery was found to be occluded, and was repaired and stented.  He recovered without complications and was sent home in a few days.