A paramedic crew responded to the office of a local physician. A 61-year-old male presented with a one-week history of chest pain and shortness of breath. He had a previously undiagnosed atrial fibrillation with rapid ventricular response and left bundle branch block, but was alert. Shortly after transport commenced, the patient became unresponsive with Torsades de Pointes, which rapidly degenerated into ventricular fibrillation. The paramedic placed pads and defibrillated within one minute.  After two minutes of compressions, the patient had a fairly regular rhythm with return of spontaneous circulation.  Transport time was short.  On catheterization, the patient was found to have severe coronary artery disease, requiring coronary artery bypass graft surgery (CABG) A balloon pump was inserted in an attempt to strengthen him for surgery.

What is the rhythm?   The 12-lead ECG presented here shows atrial fibrillation at a rate of 138 per minute.  The rhythm is irregularly-irregular with no P waves.  Since the patient had not yet been diagnosed with atrial fib, obviously no therapy had been initiated to control the rate. There is a PVC near the end of the strip.

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 patient was diagnosed by the rescue crew as having atrial fibrillation, based on the fact that they thought the rhythm was irregular, and they could not see P waves.  They also noted a wavy baseline, and considered it to be fibrillatory waves.  In reality, the underlying rhythm is regular, with some PACs (regularly irregular). The P waves are small and hard to see in the baseline artifact.  We have marked the P waves in Lead I with small dots.  

It pays to look at multiple leads, reduce artifact as much as possible, and look at the strip for evidence of an underlying rhythm.  

It is not shown here, but the ECG machine is often able to show that the P waves are present by giving a PR interval and P wave axis in the diagnostics.

This 31-year-old man presented to the Emergency Dept. complaining of chest pain, shortness of breath, and nausea. His heart rate on admission was 120 - 130 bpm and irregular, and the monitor showed atrial fibrillation. His rate slowed with the administration of diltiazem. His 12-lead ECG shows the classic ST elevation of inferior wall M.I. in Leads II, III, and aVF. This patient also had JVD, bibasilar rales, orthopnea, and exertional dyspnea, signs of CHF. He had no history of acute M.I., CHF, or atrial fibrillation. He offered no history of drug use or medications.

This ECG is very useful for the basic student, in that the ST elevations are readily seen, and the atrial fib is definitely irregularly-irregular. For the more advanced student, the ST depression in V2 indicates posterior wall injury, while the flat ST segment in V1 indicates a possible right ventricular M.I.  While the posterior wall is trying to depress the ST segment, the right ventricle is trying to elevate it, resulting in flattening. Also, Lead III has a greater STE than Lead II, which has been shown to be a reliable indicator of RV infarction.  This should be confirmed with a V4 right, or all chest leads done on the right side. Right ventricular injury has been shown to increase mortality, and it also requires different management of hemodynamics.

It is unusual for a 31-year-old to experience acute M.I.  That makes it important to rule out other causes of ST elevation and chest pain.  Benign early repolarization and pericarditis should be considered.  Some of the ECG signs that FAVOR the diagnosis of STEMI are:  1) ST segments are straight, rather than curved downward like a smile.  2)  ST elevations are seen in related leads - leads oriented over the inferior wall and right ventricle (II, III, aVF, V1).  3) Reciprocal ST depressions are seen in leads known to be reciprocal to the inferior leads (I, aVL) and leads reciprocal to the "upper" inferior wall, or posterior wall.  4) There is an acute dysrhythmia (atrial fib).  Atrial fibrillation is a fairly common complication of acute M.I., and also leads to increased mortality, especially when associated with CHF.