This strip shows a second-degree AV block.  During most of the strip, 2:1 conduction is present.  At the beginning, however, two consecutive p waves are conducted, revealing progressive prolongation of the PR interval.  This usually represents a Type I , or nodal, block:  progressive refractoriness of the AV node.   However, the wide QRS ( possibly left bundle branch block), and the fact that the non-conducted p waves are "out in the open" where they should have conducted, points to Type II - an intermittant tri-fascicular block. Wenckebach periods in patients with LBBB can be caused by progressive conduction delay in the right bundle branch.

Narrow-complex tachycardias can be very confusing to students of basic-level ECG.  There are very many rhythms that fall into the broad category of narrow-complex tachycardia.  We usually further divide them into sinus tachycardia and other "supraventricular tachycardias".  The basic student will want to make this distinction, as well as be able to differentiate atrial fib and atrial flutter from the other SVTs.  The more advanced student will want to go into more detail about which mechanism for supraventricular tachycardia is present.

Just the basics, please.   When the tachycardia is regular, it is most important to determine whether it is a SINUS TACHYCARDIA or a SUPRAVENTRICULAR TACHYCARDIA.  (Yes, we are aware that sinus rhythms are supraventricular, but the term "supraventricular tachycardia" or "SVT" is usually reserved for the fast, regular rhythms that are not sinus.)  So, what clues will be most helpful to our beginner students?

Rate    SVTs tend to be faster than sinus tachycardia.  More importantly, they are fast regardless of the patient's situation.  Sinus tachycardia almost always is reacting to the patient's situation.  For instance, a 22-year-old woman resting in a chair with a heart rate of 150 is likely to have an SVT.  A 22-year-old woman who is running in a 10 k marathon race and has a heart rate of 160 is responding appropriately to an increased need for oxygen and nutrients to her cells. Sinus tachycardia will ususally be 160 or less, and have an obvious reason for being, such as fever, pain, anxiety, exercise, hypovolemia, hypoxia, or drugs.  Unfortunately, many beginning students are told that any narrow-complex tachycardia with a rate of 150 or less is sinus, and over 150 is SVT. While they may be right most of the time, or on the written test they are about to take, this rule should not be applied in "real life".  Sinus rhythms can go over 150, and SVTs can be slower than 150.  So, what other clues should we be teaching beginners?

Consider the clinical situation    Look for an obvious cause for sinus tachycardia.  If none is found, strongly consider SVT.  Remember that pediatric patients have faster heart rates, especially infants.  If the strip is on a test, with no clinical information, consider these:

This ECG rhythm strip has all the hallmarks of atrial fibrillation:  the rhythm is irregularly irregular and there are no P waves.  The rate is about 150 beats per minute. There is no P wave because the atria are being irregularly depolarized by many ectopic pacemakers at once, causing the atria to "quiver".  This patient has new-onset atrial fib, and has been medicated with a calcium channel blocker.  The rate shows signs of slowing, but has not reached the target rate for this patient of less than 80 bpm.

At the onset of atrial fib, the rate is usually fast, because the AV node is being bombarded by numerous impulses from the atria.  The impulses arrive irregularly, and with different "strengths".  The AV node conducts as many impulses as it is able to, usually resulting in a rate over 110-120 bpm.  Medications can affect the rate, of course, and we use medications to slow AV conduction and allow a more normal heart rate.  

There are many methods of correcting atrial fib, not always with permanent success. Some patients tolerate this rhythm well as long as the rate is kept in check.  But others suffer a loss of cardiac output due to the loss of "atrial kick", which is the forceful filling of the ventricles by the contracting atria.  This loss of cardiac output can severely impair some people, making it necessary to try to convert the atrial fibrillation.  In addition, people living with atrial fib must be anticoagulated, as the loss of forceful emptying of the atria can cause collections of blood clots which can break free and embolize.

This Lead II rhythm strip shows a regular rhythm with narrow QRS complexes and retrograde P waves.  The strip was taken from a nine-year-old girl.  The rate is about 110 per minute and the PR interval is .12 seconds (120 ms).

When retrograde conduction is seen in the atria, it is often assumed that the rhythm is originating in the junction.  When a junctional pacemaker is initiating the rhythm, the atria and ventricles are depolarized almost simultaneously.  This can produce a P wave in front of the QRS with a short PR interval, during the QRS, or after the QRS.  Sometimes, in junctional rhythm, a block prevents the impulse from entering the atria, producing NO P wave.  Junctional rhythms are usually slow "escape" rhythms, but can be accelerated or tachycardic.

The fact that this rate is 110 / minute and the PR interval is normal at .12 seconds, we should consider that this rhythm could also be from an ectopic pacemaker low in the atria.  From this low starting point, the impulse will travel backward, in a "retrograde" fashion, through the atria, producing a negatively-deflected P wave in Lead II.

We do not have clinical data on this patient, and so do not know what possible causes of arrhythmia might be present, and what the expected rate should be in this situation.