From the Department of Emergency Medicine (I.K., G.M., W.B., F.S., M.M.,
A.N.L.), Institute of Forensic Medicine (A.B.), and Institute of Clinical
Pathology (H.C.B.), General Hospital of Vienna, University of Vienna, Austria.
Correspondence to Univ Prof Dr med Fritz Sterz, Abteilung für Notfallmedizin, Allgemeines Krankenhaus der Stadt Wien, Universitätskliniken, Währinger Gürtel 18–20, 1090 Wien, Austria. E-mail fritz.sterz{at}akh-wien.ac.at
Methods and Results—We retrospectively analyzed the
primarily presumed cause of cardiac arrest as determined by the
emergency room physician on admission in all patients admitted to the
emergency department of one urban tertiary care hospital. This was
compared with the definitive cause as established by clinical evidence
or autopsy. Within 4 years, the initially presumed cause was unclear in
24 (4%) of 593 patients. In the remaining 569 patients, the presumed
cause was correct in 509 (89%) and wrong in 60 (11%) cases. Cardiac
origin was presumed in 421 (71%) and the definitive cause in 408
(69%) cases. Noncardiac origin was presumed in 148 (25%) and the
definitive cause in 185 (31%) patients. Presumed cardiac cause was
sensitive (96%) but less specific (77%). Noncardiac causes such as
pulmonary embolism, cerebral disorders, or exsanguination were
those most frequently overlooked. Asystole occurred significantly more
often in patients in whom presumed cause remained undetermined or
differed from the definitive cause.
Conclusions—Cause of cardiac arrest is not as easily recognized
as anticipated, especially when the initial rhythm is different from
ventricular fibrillation. This might affect comparability
of study results, therapeutic strategies, prognosis, and outcome.
Patients in whom the presumed cause was confirmed as being correct had
significantly better survival and neurological outcome.
The guidelines were developed with the fact in mind that most
out-of-hospital cardiac arrests are of cardiac origin. On the other
hand, cardiac arrest of noncardiac cause was assumed to be "often
obvious and easy to determine," for example, drowning, drug overdose,
and so on.1 Accordingly, data from those patients
who presumably have cardiac arrest from any other cause should not be
used for comparison with those whose arrest was of cardiac origin.
Experience shows that the first presumed cause of cardiac arrest is
sometimes wrong.2 This may be explained by the
fact that at the time of emergency cardiac care, very little
information regarding the patient's medical history is available.
Therefore, any assumption of the cause of cardiac arrest should rather
be regarded as a working hypothesis.
To determine the accuracy of the presumed cause in patients with
cardiac arrest, we analyzed in a retrospective study the
primarily presumed cause of cardiac arrest. This was determined by the
emergency room physician on admission in all patients brought to the
emergency department of one urban tertiary care hospital within July
1991 and July 1995. We then tried to analyze the cases in which
the presumed cause was wrong and to assess the reasons for such
misinterpretations. We also tried to find out whether this makes a
difference in mortality rate and cerebral outcome and attempted to find
common indicators that might function as a warning signal in such
cases.
The study procedures followed were in accordance with the ethical
standards of the responsible committee on human experimentation and
with the Helsinki Declaration of 1975, as revised in 1983.
According to the criteria of the American Heart Association, cardiac
arrest was defined as sudden collapse followed by loss of consciousness
and absence of both spontaneous respiration and pulse that required
cardiopulmonary resuscitation.3 4 Acute
care including basic and advanced cardiac life support performed by the
Vienna Ambulance Service and in-hospital emergency medical personnel
was in accordance with international
guidelines.3 4 The Vienna Emergency Medical
System is based mainly on the municipal ambulance service founded 1881.
Medical emergencies are reported over one emergency telephone number
(144) to the central dispatch center, received by a medical technician,
processed by computer, and passed on to the dispatcher, who assigns a
mobile intensive care unit staffed by a physician and two emergency
medical technicians. Patients with cardiac arrest are usually
successfully resuscitated or pronounced dead by the ambulance
physician. Only patients with special problems such as hypothermia are
transported to the hospital under active cardiopulmonary
resuscitation.
At the emergency department, a physician stated the presumed cause of
cardiac arrest mainly on the basis of the initial perceptions of the
ambulance physician. In addition, if available, the patient history,
including previous physician reports, bystander information,
preclinical run sheets, and ECG was used. He had to select one of the
following possible causes: cardiac, respiratory, cerebral, near
drowning, hypothermia, drug overdose, metabolic, trauma,
sepsis, exsanguination, others, or unknown cause of cardiac arrest.
Respiratory cause includes pulmonary embolism as well as
asphyxia by upper airway obstruction, status asthmaticus, and
pneumonia. Cerebral cause includes cerebrovascular accident and
intracerebral or subarachnoidal
hemorrhage. Atraumatic exsanguination includes gastrointestinal
bleeding as well as ruptured aortic aneurysm. No patients with
trauma are managed in our department because there is an independent
Department of Traumatology for those cases.
Definitive cause of cardiac arrest in nonsurvivors was determined from
autopsy in almost all cases. Cardiac dissection was performed according
to standard procedures. The coronary artery tree was examined
by transverse cuts at 0.25-cm intervals to localize significant
stenosis of coronary arteries as well as thrombotic
events. Ischemic damage of the myocardium was
evaluated by macroscopic appearance of coagulation necrosis and by
staining with nitroblue tetrazolium. As required by law, persons
without relevant medical history before cardiac arrest were examined by
the Department of Forensic Pathology. In the survivors, we examined
hospital records including the patient's history, clinical
examination, and additional investigations after admission, for
example, laboratory examinations, repeated 12-lead ECGs, radiographs
and computed tomography scans, abdominal ultrasound,
transthoracic and transesophageal
echocardiography, selective coronary
angiography, and electrophysiological
stimulation study. Acute myocardial infarction was diagnosed by 12-lead
ECGs showing ST-segment elevation >0.2 mV in two precordial leads
or >0.1 mV in 2 limb leads and subsequent development of Q waves
within the hospital stay. All surviving patients with cardiac cause and
good neurological outcome underwent coronary angiography.
Additionally, patients in whom a primary rhythm disorder was suspected
underwent electrophysiological
examination.
We assigned the patients to one of two groups: The first group (group
1) consisted of the patients in whom the presumed cause was later
confirmed as being correct. The second group (group 2) consisted of
patients in whom the presumed cause was not determined by the emergency
physician or differed from the definitive cause. The patients in these
two groups were compared for common denominators such as sex; age;
location of cardiac arrest (out-of-hospital versus in-hospital);
initial ECG rhythm observed by any rescue worker, distinguishing
between ventricular fibrillation, pulseless
ventricular tachycardia, asystole, or pulseless
electric activity/electromechanical dissociation (PEA/EMD); lack or
presence of bystander cardiopulmonary resuscitation; and
estimated time until restoration of spontaneous circulation. For the
time interval from cardiac arrest to start of basic and/or advanced
life support, we presumed sufficient systemic blood flow to be absent
(no flow). The time interval from start of life support until return of
spontaneous circulation we presumed to be
representative for reduced systemic blood flow (low
flow).
Mortality and cerebral function were assessed prospectively on arrival
and at regular intervals within 6 months after return of spontaneous
circulation in turns of the cerebral performance categories
(CPC 1 to 5).5 Definitions are CPC 1, conscious
and alert with normal function or only slight disability; CPC 2,
conscious and alert with moderate disability; CPC 3, conscious with
severe disability; CPC 4, comatose or in a persistent vegetative state;
and CPC 5, brain death. The best CPC score achieved within 6 months was
used for the analysis. A CPC score of 1 or 2 was considered as
favorable and a CPC score of 3, 4, or 5 was considered as unfavorable
functional neurological outcome. The investigator assessing the CPC
score was blinded to data concerning resuscitation as well as to other
medical data.
According to the Utstein Style, data are expressed as median and
interquartile range (IQR). Percentages were determined for dichotomous
variables. We used the Mann-Whitney U test for the
comparison of groups and the
The emergency physician stated the reason for the cardiac arrest to be
undetermined in 24 (4%) of 593 cases (Figure
In the remaining 569 (96%) of 593 patients, a presumed cause of
cardiac arrest could be stated by the emergency physician. The presumed
causes of cardiac arrest and their specific subcategories are listed
together with the definitive cause in Table 1
Cardiac arrest was described to be of cardiac origin in 421 of these
patients. This assumption was correct in 382 and wrong in 39 patients.
Noncardiac origin was suspected in 148 patients. This was correct in
127 and wrong in 21 patients (Figure
The definitive cause was of cardiac origin in 408 (69%) and noncardiac
origin in 185 (31%) patients (Table 1
We grouped the patients who had a cardiac arrest of noncardiac origin
(n=185) into subcategories according to the most frequent cause, as
presented in Table 1
Presumed cardiac cause was highly sensitive (95%) but less specific
(77%). In comparison, specificity for the different noncardiac causes
was 98% and better. Most often, presumed diagnoses failed to consider
exsanguination, cerebral disorder, respiratory disease, sepsis, and
metabolic disorder as cause of cardiac arrest. In Table 3
We then compared group 1 (n=509), which consisted of the patients in
whom the presumed cause was later confirmed as being correct, with
group 2 (n=84), which consisted of 24 patients with undetermined and 60
patients with erroneous presumed first diagnosis regarding various
parameters at the time of resuscitation. We did not observe
a statistically significant difference between the two groups regarding
the location of cardiac arrest (out-of-hospital versus in-hospital),
whether or not the cardiac arrest was witnessed, the presence or the
lack of bystander CPR, and the sex of the patients, as shown in Table 4
The rate of no restoration of spontaneous circulation was significantly
higher in group 2 (34%) than in group 1 (20%), as seen in Table 5
Silfvast2 has disproved cardiac origin in 25
(31%) of 80 patients who had cardiac arrest of presumed cardiac
origin. A previous study by Kuisma and
Alsspää7 showed that 36% of both
traumatic and nontraumatic out-of-hospital cardiac arrests assumed to
be of cardiac origin were diagnosed to be really of noncardiac origin
after in-hospital investigations or autopsy. Of our patients, only 11%
were misdiagnosed initially. This difference from the above-mentioned
studies could be explained by including in our study patients with all
causes of cardiac arrest and primary in-hospital or out-of-hospital
successful restoration of spontaneous circulation in almost all cases.
When no return of spontaneous circulation could be achieved before
hospitalization, establishing a correct diagnosis is in itself more
difficult because these patients usually do not enter the hospital at
all.
We have shown that in half of the cases in which the emergency
physician was wrong in his assumption about the cause of cardiac
arrest, the initial ECG rhythm was asystole. This problem is enhanced
when there are no relatives who can be questioned about the prior
medical history of those patients. Because asystole is the common
terminal rhythm of all causes of cardiac arrest and is often the result
of the delay before resuscitation, it is evident that a diagnosis is
inherently more difficult. There is also no way of knowing whether in
the case of asystole the rhythm initially was ventricular
fibrillation that deteriorated over time or whether it was an EMD/PEA
that finally converted from mechanical to electrical asystole. In
addition, it might be that because initial resuscitation often fails
and no restoration of spontaneous circulation can be
achieved,8 the emergency physician has less time
to reevaluate the diagnosis and some diagnostic procedures
cannot be performed at all. This further enhances the likelihood of a
mistaken first assessment as to the cause of cardiac arrest. We
therefore suggest that asystole as first rhythm should lead to a high
degree of suspicion as to whether the patient has really arrested
because of cardiac cause, or whether there is any clinical evidence
that a noncardiac reason might be present.
The rate of correct diagnosis was much higher when the initial rhythm
was ventricular fibrillation or EMD/PEA. It is known that
ventricular fibrillation is the most common rhythm in
cardiac arrest of cardiac origin,9 whereas
EMD/PEA is associated with pulmonary
embolism10 and ruptured or dissecting aortic
aneurysm with cardiac tamponade.2
When looking for other factors influencing resuscitation such as age,
sex, absence or presence of basic life support, location (in-hospital
versus out-of-hospital) of cardiac arrest, as well as the times of no
flow and low flow, we did not find significant differences between the
two groups of patients when the presumed cause was later confirmed as
being correct and patients with undetermined and erroneous presumed
first diagnosis. Thus it can be presumed that none of these factors had
any influence on sensitivity or specificity for the initial
diagnosis.
Despite massive efforts, the rate of survival after cardiac arrest has
not improved significantly in the last years. Studies have
analyzed a multitude of factors influencing the outcome of
resuscitation.11 12 For obvious reasons, the
outcome after cardiac arrest as shown in our data does not adhere to
the Utstein template. Therefore it should not be compared uncritically
with other published data. The neurological outcome depends largely on
the arrest time. We thought that the poor outcome in the group with
wrong presumed cause might be explained partly by the fact that 50% of
those patients were asystolic and did not achieve restoration
of spontaneous circulation as often as the patients in the other group.
However, in a post hoc analysis, we noticed two things. The
outcome is worse when the first presumed diagnosis is wrong,
irrespective of the initial rhythm. If misclassification occurs,
mortality rate is almost doubled. In addition, our data once more
confirm the well-known fact that patients with ventricular
fibrillation have a much better chance to survive than those with
asystole or EMD/PEA (Table 6
The question remains whether reducing the cardiopulmonary
resuscitation time by establishing the correct cause of cardiac arrest
might improve the primary resuscitation rate and the long-time
prognosis of those patients. Therefore we suggest that not only
improved diagnostic procedures but also more concern by the
treating physicians with regard to the possible definitive cause of
cardiac arrest may help to identify the underlying cause in at least
some of these patients, thereby allowing earlier origin-dependent
advanced treatment.
Unfortunately, there are no reports comparing the efficacy of distinct
treatment on the basis of the underlying pathology in cardiac arrest.
The knowledge of the origin of the cardiac arrest might directly
influence the cause-specific treatment and, because of this, indirectly
influence the outcome. For example, fulminant pulmonary
embolism associated with cardiac arrest has an extremely high mortality
rate.13 However, previous
studies14 demonstrate that a prompt treatment of
systemic thrombolysis or embolectomy, even under
ongoing resuscitation,15 may decrease mortality
rates. While preoperative cardiac arrest in patients with ruptured or
dissecting aortic aneurysm is associated with a high mortality
rate,16 17 prompt treatment results in
significantly better survival.18 Early
sonographic diagnosis of ruptured aortic aneurysm is important,
and the patient may be saved even if this necessitates
cardiopulmonary resuscitation while on the way to the operating
theater.
There is enough evidence that the number of patients discharged from
the hospital after cardiac arrest depends in large part on the way that
judicious therapeutic decisions are made on the basis of presumed
cause. The importance of prehospital medical history-taking,
examination, and resuscitation by ambulance physicians in this respect
cannot be overestimated. Our data corroborate the necessity of
using all available means of proving or—even more
important—excluding a specific diagnosis by the emergency physician,
allowing specific treatment to be initiated. He or she must take into
account the prearrest information as well as the present status and
the results of clinical monitoring, laboratory examinations, bedside
echocardiography, and abdominal ultrasound. These
should be performed as soon as feasible to establish a correct
diagnosis, possibly even in ongoing resuscitation situations. This
implies that after the receipt of the message that the emergency
department is about to receive a patient after cardiac arrest, the
necessary equipment already will be at the bedside, ready for use on
arrival of the patient.
In conclusion, in a significant number of cases particularly of
noncardiac cause, origin of cardiac arrest is not as easily recognized
as initially anticipated. Asystole as first-recorded ECG rhythm and
noncardiac causes such as pulmonary embolism, ruptured aortic
aneurysm, and cerebral disorders frequently led to erroneous
diagnosis. This might affect comparability of study results,
therapeutic strategies, prognosis, and outcome of patients after
cardiac arrest. Those patients in whom the presumed cause was later
confirmed as being correct had a significantly better survival rate and
neurological outcome than patients with undetermined or erroneous
presumed first diagnosis. We therefore believe that it is of paramount
importance to actively procure all relevant information from
bystanders, relatives, and emergency medical service personnel, even
before arrival of the patient in the emergency department. In addition,
early availability of crucial medical information and past medical
history should be provided by an information forwarding service through
the dispatch center. In the emergency department itself, all
diagnostic equipment should be ready on arrival of the
patient, and diagnostic procedures should be performed as
soon as feasible.
Received December 16, 1997;
revision received March 27, 1998;
accepted April 20, 1998.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Accuracy and Impact of Presumed Cause in Patients With Cardiac Arrest
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
Background—International guidelines
recommend differentiation between cardiac and noncardiac causes of
cardiac arrest. The aim of this study was to find the rate of agreement
between primarily postulated and definitive causes of cardiac
arrest.
Key Words: resuscitation • epidemiology • heart arrest • pathology
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References
To ensure
comparability of data regarding out-of-hospital cardiac arrest, a
uniform reporting style of gathering and presenting such material,
the Utstein guidelines have been published.1
Since 1990 most scientific publications in the field of resuscitation
adhere to this de facto standard. In this
protocol1 the differentiation between cardiac and
noncardiac causes is obligatory.
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References
Between July 1991 and July 1995, all patients admitted to the
Department of Emergency Medicine of the University Hospital of Vienna
after either in-hospital or out-of-hospital cardiac arrest were
documented on arrival according to a specific protocol (Utstein
Style).1 Patients with in-hospital cardiac arrest
include mainly patients from our department. In addition, because beds
in the intensive care units (ICU) are limited, almost all those
patients with cardiac arrest in one of the regular wards or outpatient
departments are first brought to the emergency department for
stabilization before being admitted to an ICU. 
2 test for
comparison of proportions. We reviewed the accuracy of presumed cause
of cardiac arrest by comparing the number of cases in which presumed
cause was correct or wrong, calculating sensitivity and specificity of
each factor.6 A value of P<0.05 was
considered statistically significant.
Results
Top
Abstract
Introduction
Methods
Results
Discussion
References
Of the 612 patients admitted between July 1991 and July 1995, 19
had to be excluded because we were unable to establish any cause of
cardiac arrest (Figure
). Of the remaining 593 patients,
193 (33%) were female, the median age was 62 years (IQR 51 to 71), and
cardiac arrest occurred out-of-hospital in 424 (72%) patients. Within
the observation period of 6 months after cardiac arrest, 435 (74%) of
593 patients died. Autopsy was performed on 398 patients (91%), 40 of
those at the Department of Forensic Pathology and the rest at the
Department for Clinical Pathology.
View larger version (14K):
[in a new window]
Figure 1. Distribution of presumed versus definitive causes of cardiac
arrest. 
). We were able to
establish a definitive diagnosis in all of these patients. The cause
was of cardiac origin in 11 patients, cerebral in 4, and respiratory in
another 4 patients. In 3 patients the underlying cause was
metabolic, in 1 patient it was sepsis, and in 1 it was
exsanguination. . Noncardiac causes were
primarily underestimated. The presumed cause was correct in 509 (89%)
cases and wrong in 60 (11%) cases. Data for subgroups and sensitivity
and specificity of presumed cause in patients with cardiac arrest of
cardiac or noncardiac origin are shown in Table 2.
View this table:
[in a new window]
Table 1. Presumed and Definitive Causes of Cardiac Arrest in
593
Patients
View this table:
[in a new window]
Table 2. Specificity and Sensitivity of Presumed Cause of
Cardiac
Arrest and Table 2). ). Of those 408 patients, acute
myocardial infarction was the most common cardiac cause of cardiac
arrest [255 (63%)]. Of the remaining 153 patients (37%), sudden
cardiac death was the result of a primary electric event in 116 (28%)
patients and the result of hypoxia caused by cardiac
pulmonary edema in 37 (9%) patients. In this group of 153
patients without acute myocardial infarction, coronary artery
disease was found in 50 (12%), dilated
cardiomyopathy in 33 (8%), ischemic
cardiomyopathy in 28 (7%), and hypertensive
cardiomyopathy in 11 (3%) patients. Other cardiac
causes were established in 31 (8%) cases, including 4 with idiopathic
ventricular fibrillation and 2 with complete heart block
degenerating into ventricular fibrillation. . Of 59 patients with cardiac arrest of
respiratory origin, 27 had cardiac arrest after pulmonary
embolism (23 of them had deep vein thrombosis) and 12 after status
asthmaticus. Of 27 patients with cardiac arrest caused by
exsanguination, 17 had ruptured aortic aneurysm (13 abdominal
and 4 thoracic). , we show the distribution
of erroneously presumed causes within the definitive causes. We found
that in 39 cases in which a cardiac origin had been primarily
suspected, 14 patients had cardiac arrest from respiratory origin (10
pulmonary embolism), 10 because of exsanguination after a
ruptured aortic aneurysm (2 thoracic, 5 abdominal) and 7 for
cerebral reasons. Of 12 cases with suspected respiratory origin of
cardiac arrest, 9 were in fact of cardiac origin (6 acute myocardial
infarction).
View this table:
[in a new window]
Table 3. Distribution of Erroneous Presumed Cause Within
Definitive Cause of Cardiac
Arrest . When comparing the most
frequently documented initial rhythms, we found a significant
difference between the two groups for ventricular
fibrillation and asystole as described in Table 4. In group 2, asystole
was found as the initial rhythm in 50% of the cases compared with 20%
in group 1. The times of no flow and low flow were not different in the
two groups. For all groups, the median no-flow time was 1 minute (IQR 0
to 7 minutes) and the low-flow time was 10 minutes (IQR 3 to 20
minutes).
View this table:
[in a new window]
Table 4. Factors at Time of
Resuscitation (P<0.003). Of
all patients who achieved restoration of spontaneous circulation
initially, 306 (52%) died within 6 months, with a median survival of 1
day (IQR 1 to 8) [group 1, 2 days (IQR 1 to 8) and group 2, 7 days
(IQR 2 to 35)]. Out of all patients, 158 (26%) were discharged alive.
When comparing the two groups, group 1 had a significantly better
outcome (P<0.001). Of all surviving patients, 138 patients
(87%) had a good neurological outcome with a CPC score of 1 or 2.
Those patients in whom the presumed cause was later confirmed as being
correct had a significantly better neurological outcome than patients
with undetermined or erroneous presumed first diagnosis (<0.001)
(Table 5).
View this table:
[in a new window]
Table 5. Outcome of Cardiac Arrest Within 6
Months
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References
Comparing the initial assumption regarding the cause of cardiac
arrest with the definitive diagnosis, the first presumed cause of
cardiac arrest is disproved in 11% of the studied cases. In another
4% of the patients the emergency physician could not reach a
conclusion regarding the cause of cardiac arrest. In our study, cardiac
arrest of cardiac origin is most common (69%) and is recognized with a
sensitivity of 95%. This might be explained by the fact that in most
patients with ventricular fibrillation as the first
documented rhythm, a cardiac cause is the most likely cause of cardiac
arrest.4 The relatively low specificity of 77%
reflects those patients who were erroneously assumed to have suffered
cardiac arrest of cardiac origin, although it was actually of
noncardiac origin. When we examined the real cause for this group of
patients, we found that especially pulmonary embolism, ruptured
aortic aneurysm, and neurological disorders such as
intracerebral and subarachnoidal
hemorrhage were erroneously classified as cardiac arrest of
cardiac origin. Silvfast2 and Kuisma and
Alsspää7 came to similar proportions
in their studies. The reason might be that although these diseases are
not uncommon, the patients rarely have cardiac arrest as first
manifestation. Because of this, there might be a lack of experience in
interpreting the possible prearrest clinical symptoms correctly. In
addition, these patients may have symptoms quite similar to cardiac
arrest of cardiac origin. ).
View this table:
[in a new window]
Table 6. Outcome of Cardiac Arrest Grouped According to
Initial ECG and Misclassification of
Cause
Acknowledgments
Wilhelm Behringer is supported by the Austrian Ministry of
Science and Transport (BMWV).
References
Top
Abstract
Introduction
Methods
Results
Discussion
References
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