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This website revised:
May, 2009
This is an educational web site by Dr. Dale Dubin (Dale Dubin, M.D.), which includes important EKG (ECG) information about EKG tracings, 12 lead EKG's, and cardiac monitors. All web sites offer free PDF downloads.

To order Rapid Interpretation of EKG's, scroll to the bottom of the page.

Cardiac monitors provide a continuous display of the heart's electrical activity. Some versatile monitors can record twelve classical leads giving us great diagnostic latitude.

Whenever possible, obtain the patient's prior EKG's for comparison; routinely place baseline EKG reference strips in the chart (record time/date). This conventional protocol is ideal for proper patient management, when the patient is first attached to the monitor.

If you wish to share an interesting EKG printout with the author (a devoted collector), please send a copy to the publisher. Your generosity and altruism is appreciated and will help others in the future. 

If any unusual events or changes are seen on cardiac monitor, attempt to record an EKG strip (with time and date) for documentation in the chart. Medication and treatment protocols are not presented.

This section requires a reasonable background in electrocardiography. Page numbers bracketed in yellow relate to the 6th edition of Rapid Interpretation of EKG's. Jump right in, it is easy - and important - to understand!

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The heart has oxygen sensors called ventricular foci ("foci of automaticity"), which discharge a warning stimulus when their oxygen levels diminish. We can humanize that focus and think of him as a committed, sensitive guard whose duty is to watch for low oxygenation. The thing that irritates him the most is ischemia (low blood oxygen). One can assume, with a teleological twist, that foci exist only to warn us of ischemia, which indeed they do.

Upon sensing a reduction in capillary oxygen concentration, a solitary ventricular focus discharges a single premature stimulus, which records as a broad ventricular complex (PVC) of great magnitude on the monitor screen. PVC's are a reliable warning system that the ventricles are experiencing low O2 although certain medications or low K+ can also provoke PVC's.

If low O2 persists or worsens, the ventricular focus becomes more irritable, so it discharges a few more random PVC's, but they all look the same, since they arise from the same focus. The few PVC's alert us that a ventricular focus remains irritable due to low oxygen. 

Now the monitor displays more than six PVC's per minute, and they appear to originate on the terminal portion of the T wave. OK, maybe we had better check the patient to see if the airway is compromised a bit [ pages 135-138 ].

The information below regarding PVC's was demonstrated more than a half century ago by Dr. Thomas Lewis after he ligated a laboratory animal's coronary artery and observed the progression of events portrayed in the first five monitor displays. 

Just place your cursor on the cardiac monitor's lever and click on it.

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Eventually the PVC's are coupled to normal cycles, appearing just after each normal T wave in a bigeminy pattern, so at least half of the ventricular depolarizations are PVC's. Even with a pulse rate of 80/min., there are at least 40 PVC's per min. The solitary ventricular focus is really getting irritable... perhaps the oxygen concentration is getting lower from a coronary spasm? Or slightly obstructed coronary? Better check your patient! [ pages 139, 140 ]. 





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As the patient's O2 sinks lower, the ventricular focus becomes even more irritable and emits a short salvo of rapid discharges, which records on the monitor as back-to-back PVC's. Three or more of these consecutive PVC's are known as ventricular tachycardia, (VT), which drives the heart at 150-250 beats per minute. That's extremely fast for an aged heart, if the VT is sustained. Just to be safe, take a quick look at the ST segments [ pages 266, 267, 271] and check for Q waves [ pages 272-281]. Check the patient's airway, ask the patient about chest discomfort; then consider medications. 




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Sometimes with acute, severe hypoxia, more than one ventricular focus becomes irritable and multiple irritable foci discharge. Because each focus produces its own distinctive PVC, one can see PVC's with different shapes (multifocal PVC's) on the monitor screen. For example, if acute infarction or acute pulmonary embolism is causing sudden ventricular hypoxia, this situation could rapidly deteriorate into a deadly arrhythmia. Check airway and all emergency signs [ pages 266-290 ]. Time to act quickly! [ pages 142, 167-170 ]. 

 



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Extremely irritable ventricular foci can produce Torsades de Pointes or ventricular flutter, either of which can rapidly become ventricular fibrillation. During either of these arrhythmias, the ventricles are contracting at 250 to 350 per minute. Not only is this exceptionally unsafe for even a normal heart, at that rapid rate the ventricles can't effectively fill with blood between beats, so the cardiac output is minimal [ pages 158, 161, 162, 167-170 ]. These arrhythmias may lead to grave consequences. You may need to recruit help immediately. 



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Ventricular fibrillation records as chaotic activity. It requires immediate CPR and defibrillation
[ pages 167-170 ]. Call a code! This is not a simulation or a drill, you must act immediately!




It is obvious that by being attentive to the events on cardiac monitor, you might have prevented or at least have been better prepared to deal with the onset of ventricular fibrillation. If you check the old tracings that were recorded immediately prior to ventricular fibrillation, you will see the progression of these warning signs. Routinely check the patient when these (seemingly innocuous) warning signs appear. Eventually you will prevent a tragedy.

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Be vigilant to the spontaneous appearance of subtle conduction problems. These acute changes are valuable prodromal warning signs, but you will only notice them if you are conscientious about detail. Responsible patient care requires constant vigilance.

 

Another patient had a normal appearing nonspecific chest lead EKG on monitor, but coincident with "severe indigestion" (patient's words), his monitor recording changed to that below.


The sudden appearance ST segment elevation signifies acute ischemic injury [ pages 266-267 ]. His T waves are now inverted too [ pages 264, 265 ]. This is the time to quickly compare this finding with the patient's previous tracings to see if this is indeed acute. Rule out non-Q wave infarction [ page 267 ]. By monitoring other limb leads and other chest leads you can locate the general location of the ischemia and even determine which coronary vessel is causing the problem [ pages 275-294 ]. 




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Suddenly the monitor displays Wenckebach (second degree) AV block, a series of successive cycles with progressive lengthening of the PR interval until a final P wave stands alone [ pages 180-184 ]. Although its appearance at rapid heart rates is not of great concern, at normal heart rates, it generally indicates an AV node conduction problem, commonly due to ischemia or degenerative disease of the AV node. Sometimes agents that mimic or induce parasympathetic tone are at fault. 




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While observing a series of normal cycles with consistently normal PR intervals, you note a lone P wave without a QRS response. If the audible beep is on, you may have noticed that one (QRS) beep in the series was obviously missing. Even though one grows "tone deaf" to the monotony of regular beeps, it is interesting that a missing beep (or even a premature one) gets your attention. 

In this case the missing QRS complex represents an intermittent Mobitz (second degree) AV block, a prodromal warning of a serious complete (third degree) AV block. [ pages 181-184, 199, 200, 305 ]. This is always the case if the patient has a pre-existing Bundle Branch Block. 

Like a flickering light bulb warns that the bulb is about to burn out (and fail to conduct electricity), one non-conduction event (missing QRS) of the ventricular conducting system forebodes impending complete AV block. Although seemingly insignificant, this is an important warning sign. Please don't forget it. 




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A resting patient is calmly reading the newspaper. Her monitor displays the MCL1 lead, which is analogous to V1 but it is recorded by three monitor electrodes on the anterior chest. She is comfortable, and she has a normal rate and a regular rhythm. Ho hum...





Soon she acts agitated, and her face looks a little ashen, but she continues reading. Her monitor displays the same regular rhythm and a slightly faster, normal rate. Any need for concern?






The astute care-giver notices little else on the monitor other than evidence of a right Bundle Branch Block (R,R' of the widened QRS in a right chest lead, [ pages 191-196 ]) and perhaps a slightly inverted T wave [ page 313 ]. These subtle and barely perceptible changes on the monitor were the only early sign that the patient had a pulmonary embolus [ pages 312, 313 ]. Acute, spontaneous right Bundle Branch Block is always suspect for pulmonary embolus. And look... the appearance of PVC's tells us that her heart is getting ischemic.


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Another sedated patient is recovering after he was nearly killed in a serious auto accident. He suffered multiple long bone fractures and has just returned to the floor after multiple surgical procedures. His monitor, also recording Lead MCL1, originally displayed a normal rate, normal rhythm, and no signs of cardiac problems. Now you look at the monitor and see the following.





Since MCL1 is really an improvised Lead V1, you know from the increased R wave magnitude and ST segment depression the patient has suddenly developed in Lead V1 ( and because you are so intelligent) that this is a clear warning of a true posterior infarction [ pages 283-288 ]. You can be proud of yourself. Of course this should be verified with a twelve lead EKG and appropriate lab work. Later you notice multifocal PVC's that may presage an impending deadly ventricular arrhythmia. We are so accustomed to looking for significant Q waves, that it is easy to overlook the obvious.

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Another patient is semi-comatose and does not seem to require much immediate care. His monitor, recording Lead I, shows a normal rate and normal rhythm. In general, his tracing looks pretty good, don't you think?





The Lead I recording is very crisp and displays such good detail that the monitor was left on this lead. The care-giver who is observing this monitor notices some very subtle changes. The rate, rhythm, and all other cardiac parameters remain normal. Yawn... Is it time for a little chit-chat with a colleague, or is the monitor displaying a warning that needs attention?





The Lead I initially showed a normal rate and a normal rhythm with normal upright QRS complexes that are typical of a normal QRS axis on the cardiac monitor. The rate and rhythm remain normal. But now, the QRS, although of normal width, is mainly negative in Lead I, so we know that the patient has had an acute shift of QRS axis. 

This monitor is showing us that the patient now has Right Axis Deviation [ page 222 ]. This acute shift from a normal (two thumbs up) axis to RAD is typical of acute posterior hemiblock [ pages 300, 301]. 

Having read Rapid Interpretation of EKG's, the observer knows that acute hemiblock is most often associated with acute infarction. The patient had a serious infarction and the earliest sign was an acute shift in QRS axis out of the normal range. Know this.

If you enjoyed this presentation and found it to be informative and meaningful, please let us hear from you. 

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