This is a nice teaching strip of a slowing sinus bradycardia that began around 40 bpm, and is slowing.  It is a good example of how the sinus node slows down - there is no abrupt change of rates, rather a change with each R-to-R interval.  There is also a first-degree AV block, reflecting slowing of conduction in the AV node.  The PR interval is slightly variable at .28 sec. to about .32 sec.  This is a good strip to begin talking about treatment of bradycardias with beginner students, as there is no second- or third-degee AVB, but the patient is very likely to be symptomatic now, or very soon.  Atropine would probably improve this rate in a symptomatic patient, but if there is time, a 12-Lead would be a good idea to rule out acute M.I.  Inadvertently raising the rate too much in the injured heart can lead to pump failure, while leaving the patient poorly-perfused in a bradycardia will starve the heart.  A transthoracic or temporary IV pacemaker might be a better choice for some patients because of our ability to choose the rate.

This example of sinus arrest, also called sinus pause, shows a spontaneous return to sinus rhythm.  There are many mechanisms by which pauses can occur on the ECG. One concept for beginner students to grasp is that, if the pause contains the equivalent of regular R-to-R intervals, and the first complex after the pause is "on time",  we can expect that the sinus node kept firing, but did not penetrate the atria (exit block). If the pause is irregular in length, with the first beat after the pause seeming to come in randomly, we can call this sinus arrest or pause, understanding that there are many different mechanisms that can be at work here. Because what little we can see of the underlying sinus rhythm is irregular, or speeding up, we cannot discern absolutely that this is sinus arrest. 

The bottom line for the patient, and for any level practitioner, is, "how is the patient tolerating this pause, and what does it mean to the patient's overall prognosis?  In the short term, the patient may require emergency pacing while the cause of the dysfunction is investigated. If pauses are long enough to lower cardiac output, they can cause fainting. More than a few automobile accidents have happened as a result of this type of dysrhythmia. 

For more advanced students, this short rhythm strip (Lead II) reveals sloping ST depression, and indicates the urgent need for a 12-lead ECG and other tests. 

Atrial fibrillation with a controlled ventricular response is often considered to be atrial fib that has been controlled with medication.  While this is often true, it is possible to see atrial fib with a ventricular rate between 50 and 100 bpm in a patient who has not been treated.  The hallmark signs of atrial fib are:  no P waves and irregularly-irregular rhythm.

Multiple, simultaneous leads are advised to be sure there are no P waves, and a long rhythm strip is often needed to prove the irregularly-irregular rhythm.  Remember, even though this rate is adequate (about 90 bpm), the loss of P waves means no "atrial kick".  The atria are not filling the ventricles with a forceful pumping action. Patients can lose a significant percentage - up to 25% - of their cardiac output because of this.  Coupled with the risk of stroke from the formation and embolization of blood clots from the sluggish circulation in the atria, it is much preferable to have sinus rhythm at the same rate.

A good example of ventricular fibrillation.  The patient is pulseless, CPR has been performed, and the ED staff is about to defibrillate.  Characteristics of V Fib are:  a chaotic, wavy baseline without clear P waves, QRS complexes, or T waves.  Baseline artifact (baseline going up and down) can be seen with CPR and other movement of the electrodes on the patient's body as resuscitation efforts are underway.  The patient will ALWAYS be unconscious and pulseless in V Fib.  If this rhythm is seen in a patient who is awake or has pulses, it is ARTIFACT - check your electrodes!