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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.
