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PACEMAKERS AND AICDS IN EMERGENCY MEDICINE
155
expect. For example, with a dual-chamber pacemaker,
one might expect to see atrial spikes followed by a P
wave and ventricular spikes followed by a QRS com-
plex. However, if the atrial depolarization is transmit-
ted to the ventricle normally, there may be a normal
native QRS complex with no preceding ventricular
spike. Similarly, if the native heart rate is above that
of the threshold for pacing and AV conduction is not
delayed, both the native P wave and QRS complex
will appear with no preceding pacer activity, provided
the pacemaker is sensing this native activity and is
programmed to inhibit its impulses.
In order to evaluate pacemaker function in this set-
ting, vagal maneuvers and even short-acting medica-
tions such as adenosine, which slow the patient’s heart
rate, have been employed to induce pacing activity for
device evaluation. However, the most effective method
for the emergency physician to assess the device when
native cardiac activity inhibits pacing is the use of a
magnet. A magnet placed over the pacemaker genera-
tor will typically stop the sensing function and put the
device into an asynchronous, fi xed pacing mode. In
this mode, the 12-lead EKG can be assessed to deter-
mine if the pacemaker has malfunctioned as a result
of failure to pace from device or battery failure (no
pacing spikes seen despite the asynchronous mode),
or from failure to capture (no atrial or ventricular
depolarizations despite pacing spikes). However, if
the asynchronous pacing stimulus occurs during the
refractory period (atrial or ventricular), there will not
be a corresponding paced complex (P wave or QRS
complex respectively), and this fi nding would not
necessarily indicate failure to capture. Removal of the
magnet will cause the device to revert back to its nor-
mal programmed mode with sensing.
Sensing malfunctions are more diffi cult to assess
on the 12-lead EKG. The physician must consider the
type of device and the expected response to sensing
to determine what would be expected on the surface
EKG. For example, in dual-chamber pacing, lack
of an intrinsic or paced QRS complex following a
P wave at an appropriate AV interval may indicate
atrial undersensing with the resulting failure to trig-
ger a ventricular stimulus. Alternatively, if the pace-
maker is programmed to inhibit impulses when native
activity is sensed, undersensing could lead to more
asynchronous pacing spikes with variable capture,
depending on whether the stimulus falls during the
refractory periods.
dislodged or disconnected lead has varying and inter-
mittent contact with the ventricular myocardial wall,
resulting in ectopy and ventricular dysrhythmias.
Pacemaker syndrome is a constellation of signs
and symptoms similar to those of a true pacemaker
malfunction. The syndrome is most commonly asso-
ciated with VVI pacemakers, and the onset is usu-
ally soon after implantation. Pathophysiologically,
the syndrome is thought to be the result of loss of
AV synchrony or suboptimal synchronization of the
atria and ventricle by the pacing device, resulting in
an inadequate cardiac pump function.
27
ICD malfunction can occur when there is an abrupt
change in shock frequency or failure to shock or pace
(antitachycardic or antibradycardic) when indicated.
“Electrical storm” refers to a high frequency of shocks
over a short period of time.
28
A sudden increase in
shock frequency can be the result of normal appropri-
ate ICD functioning in the face of frequent episodes of
shockable native rhythms (i.e., VT or VF); however,
increased shocks can also indicate a malfunction of
the device itself, possible lead displacement or break,
as well as oversensing of supraventricular tachydys-
rhythmias, T wave morphologies, or other non-car-
diac signals misinterpreted by the device as malignant
rhythms.
29
Alternatively, the device may fail to shock
or pace appropriately when indicated in the setting of
battery failure, lead problems (break, dislodgement,
disconnection), or suboptimal programmed-threshold
settings.
Testing
The 12-lead EKG is indispensable in the evaluation of
pacemaker function, as single lead rhythm strips and
telemetry monitoring may not display low level ampli-
tude pacemaker impulses. The EKG should be evalu-
ated for pacing spikes (atrial, ventricular, or both), as
well as the usual cardiac waveforms, both native and
paced, and their temporal relation to pacing stimuli
(if any). Because the ventricular pacing lead is usu-
ally placed in the right ventricle, the normal paced
ventricular beat demonstrates a wide QRS complex
waveform similar to left bundle branch block with
left axis deviation, but with a preceding ventricular
pacing spike. ST-segments and T waves should typi-
cally be discordant with the QRS complex.
30
When evaluating the 12-lead EKG, it is important
to know the type of pacemaker the patient has, to
determine what electrocardiographic fi ndings to
CHAPTER 11
156
In many cases, however, advanced testing to assess
the function of a pacemaker or ICD device will be
required when malfunction is suspected. This device
interrogation requires a highly skilled technician
using manufacturer-specifi c equipment to determine
whether the pacemaker or ICD is functioning prop-
erly or is one that requires adjustment in the device’s
programming. In addition, most devices log recent
events for review during the interrogation to evaluate
the function of the device during this period of time.
Disposition
In the setting of hemodynamic compromise, imme-
diate stabilization and resuscitation are the priority.
External defi brillation can generally be performed
safely in a patient with a pacemaker, so long as the
pads are not in close proximity to the pacer generator.
Life-threatening pacemaker-mediated tachycardias
can often be terminated by placing a magnet over the
device to suspend any device sensing. Similarly, plac-
ing a magnet over an ICD will deactivate the device
and terminate recurrent inappropriate shocks (such as
from oversensing) by disabling the tachydysrhythmia
detection and treatment, but not its backup bradycar-
dia pacing function. However, this maneuver should
be undertaken with caution and only when the ICD
shocks are clearly inappropriate or if external defi bril-
lation and resuscitation treatment is readily available.
As noted above, in many cases, pacemaker and ICD
evaluation in the ED will require interrogation of the
device by a technician either in person or by phone. In
some of these cases, no malfunction will be found or
small adjustments in the device programming will be
required to address the reason for the patient’s clini-
cal presentation. Provided no other acute conditions
are present, these patients can be discharged home
provided close follow-up with their cardiologist is
arranged. Similarly, a single ICD shock that appears
to be an appropriate response to a malignant rhythm
generally does not require admission for further
extensive evaluation.
31
If a major malfunction with the device is found, such
as primary device failure, battery depletion, lead frac-
ture, or dislodgement, the patient will require admis-
sion for close monitoring and, ultimately, repair or
replacement of the device. Other factors to consider
when determining the need for admission include
the patient’s underlying cardiovascular status, the
Similarly, the 12-lead electrocardiogram may pro-
vide clues to the presence of oversensing, depending
on what signals are being detected and the pro-
grammed response of the pacemaker. For example,
if cardiac signals such as the T wave are oversensed
as native QRS complexes, there may be intermit-
tent, irregular, or loss of normal pacing spikes. If
skeletal myopotentials are sensed as native cardiac
activity, isometric movement of the chest wall or arm
musculature may trigger or inhibit pacing activity
inappropriately.
The 12-lead EKG is also helpful in determining the
presence of pacemaker-mediated dysrhythmias. For
ICD devices, 12-lead EKG or continuous monitor-
ing can be helpful to determine if the device is fi ring
in error, such as from oversensing, or is shocking the
patient appropriately in response to a life-threatening
dysrhythmias. In addition, the EKG can demonstrate
evidence of myocardial ischemia or infarction caus-
ing device malfunction as a result of changes at the
electrode-myocardial interface. However, for ICDs,
transient ST elevations or depressions can be seen in
the postshock period without underlying ischemia.
31
A chest X-ray study can often be helpful in identify-
ing the type of pacemaker or ICD. The number and
location of leads seen on radiograph can provide basic
information as to the pacemaker type and function
(such as single- or dual-chamber pacing). Moreover,
many pacemakers have identifi cation information on
the device (such as type and manufacturer) that can
be seen radiographically, particularly with digital
fi lms that allow magnifi cation and overpenetration.
A standard posteroanterior chest radiograph also can
demonstrate any lead problems such as fracture, dis-
connection, dislodgement, or perforation.
Laboratory testing is often necessary to assess for
potential causes of pacemaker failure, including elec-
trolyte disturbances or other metabolic abnormalities
that may result in device malfunction. Serum cardiac
markers may be helpful in assessing for myocar-
dial necrosis or infarction that could have affected
or resulted from pacemaker or ICD malfunction.
However, shocks from a normally functioning ICD
can result in elevated cardiac markers as well.
32
Studies
indicate BNP levels may be useful in assessing cardiac
function and AV synchrony when considering the pos-
sibility of pacemaker syndrome.
33
In addition, looking
at the levels of certain drugs known to alter pacing
thresholds, such as digoxin, may be of utility.
32
PACEMAKERS AND AICDS IN EMERGENCY MEDICINE
157
Placement of a magnet over the device may help •
diagnostically and therapeutically.
Pacemaker malfunction can occur from failures to •
pace, capture, or sense (Tables 11-3, 11-4, 11-5).
dependence on the device (that is, the potential affect
on cardiac function should the device malfunction or
fail), the frequency of underlying life-threatening dys-
rhythmias triggering shocks (in the case of ICDs), and
whether a signifi cant change is required in the program-
ming of the device based on the initial interrogation.
Section IV: Decision making
The key to evaluation is knowing what type of •
device the patient has implanted and understanding
the features and functioning of the different
pacemakers and ICDs (Tables 11-1 and 11- 2).
Evaluation of the device includes an EKG, telemetry, •
chest radiograph, serum electrolytes, and, if indi-
cated, cardiac markers.
Table 11-1. NPG code for pacemakers.
I II III IV V
Chamber(s) Paced Chamber(s) Sensed Sensing Response Rate Modulation Multisite Pacing
O ⫽ none
A ⫽ atrium
V ⫽ ventricle
D ⫽ dual
O ⫽ none
A ⫽ atrium
V ⫽ ventricle
D ⫽ dual
O ⫽ none
T ⫽ triggered
I ⫽ inhibited
D ⫽ dual
O ⫽ none
R ⫽ rate modulation
O ⫽ none
A ⫽ atrium
V ⫽ ventricle
D ⫽ dual
Table 11-2. NPD code for ICDs.
I II III IV
Shock Chamber Antitachycardia
Pacing Chamber
Tachycardia
Detection
Antibradycardia
Pacing Chamber
O ⫽ none
A ⫽ atrium
V ⫽ ventricle
D ⫽ dual
O ⫽ none
A ⫽ atrium
V ⫽ ventricle
D ⫽ dual
E ⫽ electrogram
H ⫽ hemodynamic
O ⫽ none
R ⫽ rate modulation
Table 11-3. Causes of failure to pace (output failure).
Battery Failure
Lead Fracture, Dislodgement, Disconnection
Oversensing
Misinterpreted cardiac potentials
Extracardiac potentials (skeletal myopotentials)
“Make–Break” signals from lead problems
Electromagnetic Interference
Component Failure (i.e., trauma)
Table 11-4. Causes of failure to capture.
Battery Depletion
Lead Fracture, Insulation Break, Dislodgement
Exit Block
Metabolic Abnormalities
Electrolyte imbalance (hyperkalemia)
Hypothyroidism
Acidemia
Medications (antidysrhythmic agents)
External Defi brillation
Long QT Syndrome
Table 11-5. Causes of failure to sense.
Myocardial Infarction
Bundle Branch Block
Dysrhythmias
External Defi brillation
Lead Fracture, Disconnection, Insulation Break
Programming Error
Electrode-Myocardium Interface Infl ammation
CHAPTER 11
158
Hayes DL, Vlietstra RE. Pacemaker malfunction. 12 Ann
Intern Med. 1993;119:828–835.
Gross JN, Platt S, Ritacco R, et al. The clinical rel-13
evance of electromyopotential oversensing in current
unipolar devices. Pacing Clin Electrophysiol. 1992;15:
2023–2027.
Finfer S: Pacemaker failure on induction of anaesthesia. 14
Br J Anaesth. 1991;66:509–512.
Cardall TY, Brady WK, Chan TC, et al. Permanent car-15
diac pacemakers: issues relevant to the emergency physi-
cian, part I. J Emerg Med.1999;17:479–489.
Hayes DL, Wang PJ, Reynolds DW, et al. Interference 16
with cardiac pacemakers by cellular telephones. N Engl
J Med. 1997;336:1473–1479.
Goldschlager N, Epstein A, Freidman P, et al. 17
Environmental and drug effects on patients with pace-
makers and implantable cardioverter/defi brillators. A
practical guide to patient-treatment. Arch Inter Med.
2001;161:649–655.
Cardall TY, Brady WK, Chan TC, et al. P. Permanent 18
cardiac pacemakers: issues relevant to the emergency
physician, part II. J Emerg Med.1999;17:697–709.
Altamura G, Bianconi L, Lo Bianco F, et al. Transthoracic 19
DC shock may represent a serious hazard in pacemak-
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1995;18:194–198.
Dohrmann ML, Goldschlager NF. Myocardial stimula-20
tion threshold in patients with cardiac pacemakers: effect
of physiologic variables, pharmacologic agents, and lead
electrodes. Cardiol Clin. 1985;3:527–537.
Bashour TT. Spectrum of ventricular pacemaker 21
exit block owing to hyperkalemia. Am J Cardiol.
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Tworek DA, Nazari J, Ezri M, Bauman JL. Interference 22
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Sarko JA, Tiffany BR. Cardiac pacemakers: evalua-23
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vibration interference of activity-based rate-respon-
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Inappropriate rate response in a VVI-R pacemaker. Acta
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and predictors of electrical storm in patients with
Disposition should be predicated on evaluation and •
interrogation results, dependence of the patient on
the device, and underlying cardiovascular status
and condition.
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SECTION THREE
Non Ischemic Cardiac Disease
163
Cardiovascular Problems in Emergency Medicine: A discussion-based review, First Edition.
Edited by Shamai A. Grossman and Peter Rosen.
© 2011 John Wiley & Sons, Ltd. Published 2011 by John Wiley & Sons, Ltd.
Section I: Case presentation
A 65-year-old man arrived via EMS in the late after-
noon with a chief complaint of “trouble breathing.”
The crew had placed the patient on 100% oxygen,
through a non-rebreather mask, with minimal improve-
ment en-route to the Emergency Department (ED).
Upon arrival to the ED, the patient appeared in dis-
tress, with increased work breathing. The patient was
accompanied by his wife, who gave the majority of
the history as the patient could only answer in 2–3
word sentences. He denied chest pain, but did feel like
there was a weight on his chest. His symptoms had
progressed slowly over the morning, but more rapidly
over the prior few hours. The prior night, he had slept
sitting up in the living room chair.
His wife stated that he had been in his usual state
of health until the prior night when she noticed him
“huffi ng” when he went up the steps to their bed-
room, and when taking out the trash. She also noted
his legs looked slightly more swollen than usual. The
past medical history included a “heart problem,”
hypertension, and arthritis. She had brought in his
medications, which included metoprolol, furosemide,
and digoxin. The patient stated that he had been com-
pliant with his medications. He had never smoked,
and had only an occasional alcohol drink on special
occasions.
The vital signs were: afebrile; pulse 108 beats/min;
respirations 32 breaths/min; blood pressure 188/106
100% oxygen by non-rebreather mask. A fi nger-stick
glucose was 120 mg/dl.
The patient appeared diaphoretic, in moderate dis-
tress, but awake and alert. He had jugular venous
distention and rales to mid-lung fi elds bilaterally.
The cardiac examination was notable for an S3. The
legs had 2 non-pitting edema without tenderness,
warmth, or palpable cords. The pulses were equal in
all four extremities.
An EKG demonstrated a sinus tachycardia, voltage
criteria for left ventricular hypertrophy, and repolar-
ization changes consistent with a strain pattern in the
lateral leads. There were no changes from prior EKGs.
A chest X-ray study showed cardiomegaly, prominent
vasculature in the upper lung fi elds, Kerley B lines,
and fl uid-fi lled fi ssures. Laboratory studies including
cardiac biomarkers and a BNP (B-type natriuretic
peptide) level were sent to the laboratory.
Section II: Case discussion
Dr Peter Rosen: There was a study that suggested a
diurnal variation to episodes of acute pulmonary
edema. Patients who arrive in the daytime are more
Acute heart failure
Kevin Reed
1
& Amal Mattu
2
1
Assistant Professor of Clinical Emergency Medicine, Georgetown University
School of Medicine, Department of Emergency Medicine, Washington, USA
2
Professor and Residency Director, Department of Emergency Medicine,
University of Maryland School of Medicine, Baltimore, Maryland, USA
12
CHAPTER 12
164
PR: One of the early clues is in the blood pressure,
as patients who are volume overloaded tend to have
high resistance failure and present, as this man did,
with hypertension; in patients with pump failure, the
initial blood pressures are often normal to low since
when these patients are well, their blood pressures
are usually elevated. Another clue that the patient’s
CHF is related to high resistance failure is respira-
tory distress. When you see a patient with acute onset
of respiratory distress, someone who is in the classic
bubbling pulmonary edema, do you think that there
are any clues as to what’s going on in the heart that
causes this, or do you think that there is always just
volume overload and high resistance?
Dr Amal Mattu: I look at CHF as having two distinct
major causes. One of them is fl uid overload or vol-
ume dysfunction, and the other is vascular dysfunc-
tion, or in other words, very high resistance. When
people come in with acute onset CHF, it tends to be
associated with more of a vascular problem, often-
times with acute afterload dysfunction. They pres-
ent with very high blood pressures. Patients who are
fl uid overloaded tend to present with a more gradual
onset of symptoms. When people come in with a more
abrupt onset of symptoms, and appear to be doing
pretty well but over the course of an hour they go
from looking well to looking very sick, then I steer
away from diuretics. In this case, I’m not worried
about fl uid overload. The most important therapy for
these patients is to improve their resistance with quick
afterload and preload reduction rather than focusing
on diuretics and their volume.
PR: There is one fi nding on physical examination that
can really help you in the face of acute rapid decom-
pensation. When you hear a loud murmur in a patient
who suddenly presents with acutely decompensated
CHF, you must suspect the patient has a rupture of
a papillary muscle. It’s helpful to pick up this mur-
mur as these patients need acute cardiac surgery more
than they need medical manipulation. What would be
your initial approach to management of the patient
in this case? Which patients need emergent airway
management?
SG: Any patient who presents with airway compro-
mise will need some sort of airway management.
Generally, we reserve intubation for those patients
who cannot tolerate a noninvasive type of ventilation.
likely to have a heart attack as the underlying cause of
their congestive failure than patients who arrive in the
middle of the night. Have you noticed a similar diurnal
variation, and what do you believe is the most common
trigger in decompensated congestive heart failure?
Dr Edward Ullman: This is somewhat dependent on
your patient population and practice environment.
When I was in residency training, most of the cases
of congestive heart failure (CHF) I encountered were
related to medicinal noncompliance and dietary
indiscretion. Now I tend to see more ischemia as a
trigger. This may refl ect a more savvy patient popu-
lation who tend not to cheat on their diets as much,
and are more compliant with their medications.
However, I have not noticed a diurnal variation in
either of these populations.
PR: When you see a patient like this who is not yet
in fulminant pulmonary edema, but who seems well
on the way, what makes you decide whether he is
sliding in to hypervolemic high resistance failure
as opposed to pump failure? I think this is the fi rst
distinction we need to make in congestive failure,
since the management is very different. Are there any
clues, either from the initial appearance or during
the evaluation?
Dr William Brady: Patients who have true pump fail-
ure most often are having a large myocardial infarc-
tion (MI), and usually appear sicker. They often are
in shock. They have an ashen appearance. They have
cold extremities. They are not perfusing in any shape,
manner, or form. When you look at these patients’
EKGs and serum cardiac markers, they will be very
abnormal with the waveforms of an acute or subacute
MI. Sometimes the EKG may show an old infarction,
refl ecting acute pump failure related to prior cardiac
disease. The blood work will show hypoperfusion
demonstrated by a low serum bicarbonate level or
a signifi cantly elevated lactate level. Nevertheless,
patients in volume overload can also be very ill with
acute respiratory failure, and also develop shock
and all the sequalae of the pump failure. In general,
not only are they are less ill, in some ways they are
easier to treat. I believe that looking at the patient’s
history of present illness, their medical history, and
your analysis of what is likely going on can point you
in the right direction diagnostically and ultimately
therapeutically.