An irregularly irregular tachycardia at 180/minute, this rhythm could be mistaken for atrial fibrillation, but notice the large upright waves between QRS complexes – these are not T waves, but are P waves of varying morphology. They are so large in a lead II rhythm strip because this woman with COPD has R atrial enlargement and these are resulting “P pulmonale”. This rhythm is multifocal atrial tachycardia (MAT).

MAT – rapid, irregularly irregular rhythm with P waves of varying morphology

MAT can be caused by several conditions including: electrolyte abnormalities, exacerbation of respiratory disease, drug toxicity (theophylline toxicity), and almost any severe illness – it is said that MAT is one of the common arrhythmias noted in an ICU population.

This patient had recently been discharged home after an admission for exacerbation of COPD, but had no respiratory complaints on this presentation. Her theophylline level was 40μg/mL (>2x normal), and a review of her discharge medications found an incorrectly written prescription for twice the usual daily dose of theophylline.

Rate:36/minute
Rhythm: progressive lengthening of the PR intervals, until a P wave is dropped 2° AV block, Type I (Wenckebach).
Axis:normal

Intervals
PR: progressive lengthening with AV block
QRS: normal
QTc: normal
Chamber enlargement: none

Ischemia/Infarction: broad T waves in inferior leads (II, III, aVF) which begin at the J point of the QRS and seem to be “tugging” the ST-segment upwardà these broad and tall T waves are early, hyperacute T waves of transmural infarction. There are also “reciprocal changes” in V_2-3 with ST-segment depression and T-wave inversion. These changes often represent infarction of the posterior wall.

Interpretation: This EKG represents an acute inferior-posterior MI with 2° AV block, type I (Wenckebach).

The pacemaker is firing at a ventricular rate of 125/minute. There is a PVC approximately half-way across the rhythm strip with a compensatory pause which allows you to notice a P wave – and the ventricular pacer follows the atrial activity. This is a dual chamber pacer, which is more physiologic than a single lead ventricular pacemaker. The pacer allows the ventricle to follow the sinus rate during exercise or other situations of appropriate increased heart rate.

Rhythm strip – 4^th beat is PVC with following compensatory pause revealing P waves with following ventricular paced beats.

This elder man is febrile and dehydrated – both good reasons for sinus tachycardia at 125/minute. Appropriate treatment of this pacemaker-mediated tachycardia is fluid resuscitation and acetaminophen!

This is an excellent example of EKG changes of COPD.

Findings suggestive of COPD include (but you don’t need to have all):

1. P waves >0.25 mV in II, III, or aVF (P “pulmonale”)
2. Lead I sign – isoelectric P wave, QRS amplitude <0.15 mV, and T wave <0.05mV in lead I
3. QRS amplitude in all limb leads <0.5 mV
4. QRS axis > 90° (right axis deviation)

Just in case you’re still not a believer, here’s her CXR…

Note the impressive changes of emphysema: flat and depressed diaphragms and the “vertical” heart.

Answer:
This unfortunate young man spent a very cold night on the streets of New York City in February. His rectal temperature on arrival in the ED was 84°F (28.⁸C). This EKG is a beautiful example of some of the changes of hypothermia.

Explanation:
As core temperature falls below 32°C (90° F), sinus bradycardia develops, associated with progressive prolongation of the PR interval, QRS complex, and QT interval. As temperature approaches 30°^C (86° F), atrial fibrillation commonly develops.

By 30°C, Osborn waves (or J waves) develop in 80% of patients. These additional terminal deflections of the QRS complex are most prominent in the leads with the greatest voltage, and they tend to follow the axis of the QRS complexes. They become more prominent as body temperature drops, and regress gradually with rewarming.

 Osborne wave of hypothermia

This patient has a slightly irregular rhythm which corresponds to her sensation of “a skipped beat”.  The rhythm is essentially sinus at 75/minute with occasional pauses in the regular rhythm.  The pauses are caused by an early atrial depolarization (a PAC) which does not conduct because it occurs so early that the conducting system is still refractory to further beats (a blocked PAC). This is evident in the rhythm strip as a deformed T wave of the complex preceding the pause (P wave within the usual T wave).

“The most common cause of a pause during sinus rhythm is a blocked PAC”.

Answer:
In a patient with a concerning history of chest pain, the most striking part of this EKG is the ST-segment depression in V2-3—the EKG depiction of an acute isolated posterior MI.

Explanation:
Posterior wall MI usually accompanies an inferior MI, identified as ST-segment depression in V2-4 (often referred to as “reciprocal” changes). Rarely, in maybe 3-5% of all acute MIs, an occlusion of the circumflex artery may cause identifiable infarction in only the posterior wall.

Remember, the posterior wall of the heart has no direct EKG representation—we see “reverse” changes in the EKG as the anterior leads (V2-4) reveal the posterior wall changes. Instead of the ST-elevation of an acute transmural MI of the anterior surface of the heart, these leads will depict ST-segment depression with a posterior wall infarct. Imagine picking the EKG up from the bottom and flipping it over—these same leads now reveal typical ST-segment elevation (a visual aid to help you believe!).

This presentation is important to recognize because it is an appropriate opportunity for acute intervention. These patients should be referred to interventional cardiology for catheterization and angioplasty. If interventional cath is unavailable, thrombolytics should be considered.

Note:
Life in the Fast Lane has a particularly good page on this topic.
http://lifeinthefastlane.com/ecg-library/pmi/

Answer:

This EKG reveals a regular rhythm at 72 bpm but no P waves. The baseline in V1 has some irregular oscillations as with atrial fibrillation, and in fact this rhythm is atrial fibrillation with complete heart block and an accelerated junctional rhythm. This has also been described as “regularization” of atrial fibrillation due to digoxin toxicity.

Explanation:

The main symptoms of digoxin toxicity are neuro-psychiatric, gastrointestinal, and cardiac. GI complaints often appear first with anorexia, and then nausea, vomiting, and diarrhea.

The hallmarks of cardiac effects are:

• Increased automaticity (atrial tachycardias, ventricular ectopy, accelerated junctional rhythms), and
• Excessive AV blocking (2° or 3° block).

A rhythm which demonstrates features of both effects should definitely suggest digoxin toxicity.

This elderly woman complained only of GI symptoms. Her medication did include digoxin 0.25 mg daily. Her digoxin level in the ED was 3.5! Labs also revealed worsening renal insufficiency with BUN 42 and creatinine 2.6, the likely cause of the digoxin toxicity.

Notice the good example of digoxin effect on the ST-segments and T waves in V4-6. This gradual down-sloping is what Dubin refers to as Salvador Dali’s moustache. These changes do not necessarily correspond to digoxin levels, and therefore are not an indicator of toxicity.