ArticlePDF Available

Pulmonary embolism as a cause of cardiac arrest: Diagnosis and management

Authors:
766 Janata et al., Mortality of patients with pulmonary embolism
Wien Klin Wochenschr (2002) 114/17–18: 766–772
© Springer-Verlag 2002
Mortality of patients with pulmonary embolism
Karin Janata1, Michael Holzer1, Hans Domanovits1, Marcus Müllner1, Alexander Bankier2,
Amir Kurtaran3, Hans C. Bankl4, and Anton N. Laggner1
1Universitätsklinik für Notfallmedizin, 2Universitätsklinik für Radiodiagnostik, 3Universitätsklinik für Nuklearmedizin, and
4Klinisches Institut für Klinische Pathologie, Allgemeines Krankenhaus der Stadt Wien, Vienna, Austria
wiener klinische
wochenschrift
the middle european journal
of medicine
Printed in Austria
Original Article
Prognose von Patienten mit Pulmonalembolie
Zusammenfassung.
Hintergrund:
Die akute Pulmo-
nalembolie (PE) ist eine potentiell tödliche Erkrankung
mit unterschiedlichen Angaben zur Mortalität. Um klare
Informationen für prospektive Interventionsstudien zur
erhalten haben wir bei unseren Patienten mit PE klinisch
relevante Subgruppen definiert und diese hinsichtlich
Mortalität untersucht.
Methoden:
Analysiert wurden die Daten von 283 Pa-
tienten mit nachgewiesener PE in Hinblick auf demogra-
phische Daten, Risikofaktoren für thromboembolische
Erkrankungen, klinische Befunde und sowie diagnosti-
sche und therapeutische Interventionen wie Blutgasana-
lyse (BGA), Laktat- und D-dimer Bestimmung, Elektrokar-
diographie (EKG), Echokardiographie, Spiral Computer-
tomographie (Spiral CT), Ventilations/Perfusionsszintigra-
phie (V/Q-Scan), Thrombolyse, mechanische Beatmung
und kardiopulmonale Reanimation (CPR). Studienend-
punkt war das Versterben innerhalb 72 Stunden nach
Aufnahme.
Ergebnisse:
Die Mortalität des Gesamtkollektivs von
283 Patienten lag bei 15%. Die Mortalitätsraten der ein-
zelnen Subgruppen zeigten erhebliche Differenzen und
betrugen 95% bei Patienten mit Herzstillstand bei Auf-
nahme (21 von 22), 85% bei Patienten mit präklinischem
Herzstillstand (28 von 33), 80% bei Patienten, die ma-
schinell beatmet wurden (40 von 50), 77% bei Patienten,
die in den ersten 24 Stunden reanimiert werden mussten,
37% bei Patienten, die eine Synkope erlitten hatten (18
von 49), 30% bei thrombolysierten Patienten (25 von 87),
26% bei Patienten, bei denen eine Laktatbestimmung
durchgeführt wurde (36 von 139), 18% bei Patienten, bei
welchen eine BGA-Analyse durchgeführt wurde (35 von
197), 17% bei Patienten, die eine Echokardiographie er-
halten hatten (34 von 195), 8% bei Patienten mit EKG-
Diagnostik (21 von 262) bzw. D-dimer Bestimmung (12/
148), 2% bei Patienten mit Spiral CT (5 von 226) und 1%
bei Patienten mit V/Q-Scan (1 von 74) Diagnostik.
Konklusion:
Patienten mit akuter PE, die eine maschi-
nelle Beatmung, eine kardiopulmonale Reanimation oder
eine Thrombolysebehandlung benötigen haben extrem
hohe Mortalitätsraten von von 80, 77 bzw. 30%. Ist die
hämodynamische Situation der Patienten mit PE stabil ge-
nug, dass Diagnostik mit Spiral CT bzw. V/Q-Scan betrie-
ben werden kann, reduziert sich die Mortalität auf 1 bis 2%.
Diese Tatsachen sind bei der Planung von prospektiven
Interventionsstudien zu berücksichtigen, insbesondere
dann, wenn die Mortalität ein definierter Endpunkt sein soll.
Schlüsselwörter: Pulmonalembolie, Mortalität,
Thrombolyse, Echokardiographie, Elektrokardiographie,
Spiral Computertomographie, Lungenszintigraphie.
Summary.
Background:
Pulmonary embolism (PE)
is a potentially fatal disorder with highly varying mortality
rates. To provide information that is more precise for
prospective intervention studies, we analysed the data of
our patients with PE, defining clinically relevant sub-
groups with respect to their individual mortality rates.
Methods:
We studied 283 consecutive patients with
confirmed PE diagnosis, with respect to demographic
data, risk factors for thromboembolic disease and clinical
signs. In addition, diagnostic and therapeutic interven-
tions such as blood gas analysis (BGA), lactate and
D-dimer determination, electrocardiography (ECG),
echocardiography, spiral computer tomography (Spiral
CT), ventilation/perfusion lung scintigraphy (V/Q-Scan),
thrombolytic therapy, mechanical ventilation, and cardio-
pulmonary resuscitation (CPR), were accounted for.
Study endpoint was mortality rates on day three.
Results:
Overall, mortality rate was 15% (42 of 283).
Mortality rates differed considerably; 95% of patients with
cardiac arrest on arrival (21 of 22), 85% of patients with
cardiac arrest – not in hospital (28 of 33), 80% of patients
receiving mechanical ventilation (40 of 50), 77% of pa-
tients needing cardiopulmonary resuscitation within the
first 24 hours (37 of 48), 37% of patients with syncope (18
of 49), 30% of patients receiving thrombolytic treatment
(25 of 87), 26% of patients on whom lactate measure-
ment was performed (36 of 139), 18% of patients on
whom blood gas analysis was done (35 of 197), 17% of
patients on whom echocardiography was performed (34
of 195), 8% of patients with twelve complete lead ECG
recordings (21 of 262) and D-Dimer determination (12 of
148), 2% of patients tested on Spiral CT (5 of 226) and
1% where a V/Q-Scan was performed (1 of 74).
767Janata et al., Mortality of patients with pulmonary embolism
Conclusion:
Patients with PE who received mechan-
ical ventilation, cardiopulmonary resuscitation, and
thrombolytic treatment had very high mortality rates of
80, 77 and 30% respectively. However, patients stable
enough for diagnostic procedures as Spiral CTs and V/Q-
Scans had mortality rates of 1 to 2%. These facts are to
be considered when planning pulmonary embolism inter-
vention trials in which reduction of mortality is a defined
endpoint.
Key words: Pulmonary embolism, outcome, cardio-
pulmonary resuscitation, thrombolysis, spiral CT.
Introduction
Pulmonary embolism (PE) afflicts more than 100 000
people annually in the United States of America and has a
high case fatality rate [1]. A recent 25-year observational
study revealed that the male sex, increased age, lower
body mass index, history of malignancy, congestive heart
failure, neurological disease or chronic lung disease as
well as patients location at hospital or nursing home, were
independent predictors of reduced short term survival [2].
The German multi-centre registry (MAPPET Study) dem-
onstrated that short-term prognosis was mainly dependent
on the hemodynamic situation of the patient at time of
presentation [3]. In hospital, mortality ranged from 8% in
hemodynamic stable patients, to 65% in those warranting
cardiopulmonary resuscitation. In contrast, long-term out-
come of PE was mainly attributed to the underlying dis-
ease such as cancer, congestive heart failure, infection and
chronic lung disease [4].
Therapeutic options in pulmonary embolism include
thrombolysis, which intuitively makes sense, especially
for patients with massive PE and shock [1]. However,
convincing scientific evidence of therapeutic fact is lack-
ing and a large-scale clinical trial is overdue [1]. The
primary endpoint of such clinical trials is usually mortal-
ity. Therefore, to design these clinical studies, distinct
clinical indicators of mortality risks are urgently needed.
In patients with confirmed diagnosis of PE, we studied
several subgroups defined by demographic data, risk fac-
tors of thromboembolic disease, clinical findings as well
as interventions prior and after admission in respect of
their individual mortality rates.
Materials and methods
283 consecutive patients with pulmonary embolism (PE),
who attended the Emergency Department of Vienna General
Hospital (ED) between July 1993 and June 1999, were includ-
ed. Study endpoint was mortality rate on the third day after
admission.
Diagnosis of pulmonary embolism was established by high
clinical suspicion based on history and clinical examination at
time of admission plus one of the following: 1) a Spiral CT
showing partial or complete filling defects of central or seg-
mental pulmonary arteries, 2) a high probability ventilation-
perfusion lung scan, or 3) occluding emboli in the pulmonary
vasculature at necropsy.
All Spiral CT examinations were performed within the
first 24 hours after admission to the ED on a state of the art
Spiral CT scanner conducting 50 rotations at 250 mAS (Philips
Tomosca SR 7000; Philips, Baest, NL). Findings suggestive of
PE were classified as: a) no filling defects, b) filling defects in
central pulmonary arteries and c) segmental filling defects.
Ventilation/Perfusion lung scintigraphy (V/Q-Scan) was per-
formed within the first 24 hours, with techniques and interpre-
tations according to literature [5]. Autopsy was performed
within 24 hours after refractory cardiac arrest.
Blood samples were drawn for arterial blood gas and
lactate analysis (ABL 700, Radiometer Copenhagen, DK) and
for D-dimer determination (Data-Fi Dimertest Latex Assay,
American Dade, Miami, FL, USA).
Electrocardiography (ECG) on admission (12 standard
leads were recorded) and at least three more during the first 24
hours, were studied in respect of heart rate (HR) and ventricular
depolarisation. To eliminate patients presenting depolarisation
abnormalities at baseline, these electrocardiographic criteria
were only considered when they were reversible during follow
up. “S1Q3T3 pattern” was defined as an S wave in lead I and
Q wave in lead III, with an amplitude of more than 0.15 mV
(1.5 mm) associated with inversion of the T wave in lead III.
“Anterior subepicardial ischemia” was defined by the presence
of pointed and symmetrical inverted T waves in lead V1 to V4.
Atrial fibrillation, ST-depression, pulmonary P-wave, complete
or incomplete right bundle branch block were defined accord-
ing to conventional criteria [6].
Echocardiography was performed transthoracically (scan
heads: 2.5/2.0 MHz HP, V4c Acuson) or transesophageal
(Omniplane II TEE probe HP 21367 or biplane TEE probe V
510 B, Acuson) on commercially available units (Sonos 2500
Hewlett Packard, Waltham, MA, USA or 128XP/10M, Acuson,
Mountain View, CA, USA.) according to established guidelines
[7].
PE was treated with unfractionated (UF) heparin, throm-
bolysis and general intensive care (oxygen supplementation,
fluid management, catecholamines, sedoanalgesia, mechanical
ventilation to achieve normoventilation and adequate oxygen-
ation) if indicated. Unless contraindicated, UF heparin was
applied to each patient, dose was adjusted to a target range of
an aPTT of 60–80 sec. According to the discretion of the at-
tending physician (determined by the patients cardio respirato-
ry status and by common contraindications) thrombolysis was
initiated with rt-PA (Actilyse, Boehringer Mannheim, G) in
doses of 100 mg administered over 90 minutes via peripheral
vein access [8] or as bolus treatment with 0,6 mg/kg/2 min [9].
In case of cardiac arrest, cardiopulmonary resuscitation was
performed according to established guidelines [10].
The following criteria were used for definition of sub-
groups:
Demographic data and risk factors: Age, sex, history of
malignant or thromboembolic disease, family history of throm-
boembolic disease, chronic obstructive pulmonary disease, re-
cent (< 4 weeks) operation or trauma, cardiomyopathy, obesity,
recent longer journeys (< 3 days > 4 hours in sitting position).
Symptoms and interventions prior and after admission:
Out of hospital cardiac arrest or syncope, cardiac arrest on
arrival, cardiac arrest and cardiopulmonary resuscitation within
24 hours, need for mechanical ventilation due to respiratory
arrest or insufficiency, initiation of thrombolysis, performance
of lactate, blood gas and D-Dimer determination, V/Q-Scan and
Spiral CT performance.
Electrocardiographic findings: Heart rate >100 beats/min,
atrial fibrillation, pulmonary P wave, incomplete and complete
right bundle branch block, S1Q3T3 pattern, ST-depression and
anterior subepicardial ischemia.
768 Janata et al., Mortality of patients with pulmonary embolism
Echocardiographic findings: no signs of right ventricular
strain, hyperkinetic dilated right ventricle, dilated right ventri-
cle with septum bulging, hypokinetic dilated right ventricle,
visible thrombi in right atrium, right ventricle or pulmonary
artery.
For statistical comparison between survivors and non-sur-
vivors chi-square tests with Yates correction and Fisher’s exact
tests were used. For comparison of non-parametric data, Stu-
dent’s T-tests in SPSS 8.0 program was used. Mortality was
calculated as the percentage of non-survivors of the total num-
ber of patients in each subgroup. The 95% confidence interval
was calculated according to a standard formula [11].
Results
Diagnosis of pulmonary embolism (PE) was estab-
lished in 283 patients based on high clinical suspicion
plus:
a) A positive Spiral CT, and positive V/Q-Scan (n=11)
b) A positive Spiral CT, and positive autopsy finding
(n = 3)
c) A high probability V/Q-Scan, and autopsy finding
(n = 1)
d) A positive Spiral CT (n = 206)
e) A high probability V/Q-Scan (n= 26)
f) Positive autopsy findings (n= 36)
Spiral CT was performed in 226 patients (80%), in
220 cases pulmonary embolism could be documented. The
images showed central thrombi in 97 patients (44%) and
in 123 patients (56%) segmental filling defects were evi-
dent. In six patients, a negative CT was in contrast to a
high probability V/Q-Scan. V/Q-Scans were performed on
74 patients (26%); 37 (50%) showed a high probability
and 37 (50%) an intermediate to low probability of PE
was diagnosed. All 37 patients of the latter group had
positive evidence of pulmonary embolism in Spiral CT.
Autopsy was performed on 40 patients (14%) with clini-
cally suspected PE. In all of these patients, pulmonary
embolism was documented and interpreted as main cause
of death.
Of the 283 patients with PE, 42 died by day 3 (mortal-
ity rate 15%). Survivors did not differ significantly from
non-survivors in respect of demographic data and risk
factors of thromboembolic disease (Table 1). Therefore,
we did not analyse the different subgroups in respect of
mortality. In Table 2, symptoms and interventions at time
of and prior to attendance at the ED are listed. Survivors
differed significantly from non-survivors in respect of:
necessity of CPR within the first 24 hours, need for me-
chanical ventilation, syncope, initiation of thrombolytic
treatment, lactate measurement, feasibility of performance
of a V/Q Scan or Spiral CT. Mortality of these different
subgroups is reported in Table 3, showing that mortality of
patients with PE and cardiac arrest on arrival was 95%
compared to 1% in patients with PE, in whom a V/Q-scan
could be performed. Mortality was 80% in patients with
PE who were mechanically ventilated and was only 8%
patients with PE, who received a complete 12 lead ECG or
a D-dimer determination.
A complete 12 lead ECG was recorded in all patients
after return of spontaneous circulation on admission
(n = 262). Survivors differed significantly from non-survi-
vors in respect of: a pulmonary P wave, presence of
complete right bundle branch block, S1Q3T3 pattern, ST-
depression, and anterior subepicardial ischemia (Table 4).
Mortality of these different subgroups is reported in Table
5, showing that mortality was 38% in patients with PE and
complete RBB compared to 0% in patients with normal
ECG. Patients with ECG pattern of anterior subepicardial
ischemia had a mortality of 18%.
Echocardiography was performed in 195 patients by
transthoracic (n = 168) or transesophageal (n = 27) exami-
nation. Survivors differed significantly from non-survi-
vors with respect to: absence of right ventricular strain,
dilated hyperkinetic right ventricle, dilated hypocentre
right ventricle and visible thrombi (Table 6). Mortality of
these different subgroups is reported in Table 7, showing
that mortality was 66% in patients with a dilated hypoki-
netic right ventricle compared to 2% in patients with no
signs of right ventricular strain and 0% in patients with a
hyperkinetic right ventricle.
Table 1. Demographic data and risk factors for thromboembolic disease of survivors and non-survivors with pulmonary
embolism
All Survivors Non-survivors p
283 (100%) 241 (85%) 42 (15%)
Mean age (years + SD) 55 +17 54+17 59+ 18 0.131
Male n (%) 135 (48%) 117 (49%) 18 (43%) 0.607
Malignant disease 29 (10%) 25 (10%) 4 (10%) 1.000
Recent thrombosis 98 (35%) 84 (35%) 14 (33%) 0.998
Family history of TE disease 26 (9%) 25 (10%) 1 (2%) 0.173
Chronic lung disease 28 (10%) 24 (10%) 4 (10%) 1.000
Recent surgery 37 (13%) 30 (12%) 7 (17%) 0.617
Recent trauma 21 (7%) 17 (7%) 4 (10%) 0.812
Cardiomyopathy 27 (10%) 22 (9%) 5 (12%) 0.779
Obesity 144 (51%) 123 (51%) 21 (50%) 1.000
Recent longer journey 16 (6%) 14 (6%) 2 (5%) 1.000
TE disease Thromboembolic disease; p* survivors versus non-survivors.
769Janata et al., Mortality of patients with pulmonary embolism
Table 3. Mortality of patients with pulmonary embolism in respect of clinical signs and interventions prior to and after admission
All Mortality
n = 283 % n % 95% CI
Cardiac arrest on arrival 22 8 21 95 86 to 100
Out of hospital cardiac arrest 33 12 28 85 73 to 97
CPR within the first 24 hours 48 17 37 77 65 to 89
Mechanical ventilation 50 18 40 80 69 to 91
Syncope 49 17 18 37 23 to 51
Thrombolysis 84 30 25 30 20 to 40
Lactate measured 139 49 36 26 19 to 33
BGA performed 197 70 35 18 13 to 23
Echo performed 195 69 34 17 12 to 22
ECG performed 262 93 21 8 5 to 11
D-dimer determined 148 52 12 8 4 to 12
Spiral CT performed 226 80 5 2 0 to 4
V/Q-scan performed 74 26 1 1 0 to 3
CPR Cardiopulmonary resuscitation; BGA blood gas analysis; V/Q-scan ventilation/perfusion lung scintigraphy; CT computer
tomography.
Table 4. ECG findings at admission to the emergency department of survivors and non-survivors with pulmonary embolism
All Survivors Non-survivors p*
n = 262 n = 241 n = 21
Normal ECG 36 (14%) 36 (15%) 0
Heart rate > 100 bpm 139 (53%) 128 (53%) 11 (52%) 0.870
Atrial fibrillation 28 (11%) 23 (10%) 5 (24%) 0.096
Pulmonary P wave 23 (9%) 16 (7%) 7 (33%) < 0.001
Incomplete RBB 75 (29%) 68 (28%) 7 (33%) 0.805
Complete RBB 52 (20%) 32 (13%) 20 (95%) < 0.001
S1Q3T3 pattern 75 (29%) 59 (24%) 16 (76%) < 0.001
ST-Depression 53 (20%) 40 (17%) 13 (61%) < 0.001
Anterior subepicardial ischemia 79 (30%) 65 (27%) 14 (67%) < 0.001
ECG Electrocardiogram; RBB right bundle branch block; p* survivors versus non-survivors.
Table 2. Clinical signs and interventions prior and after admission to the emergency department of survivors and non-survivors
with pulmonary embolism
All patients Survivors Non-survivors p*
n = 283 n = 241 n = 42
Cardiac arrest on arrival 22 (8%) 1 (0.4%) 21 (50%) < 0.001
Out of hospital cardiac arrest 33 (12%) 5 (2%) 28 (67%) < 0.001
CPR within the first 24 hours 48 (17%) 11 (5%) 37 (88%) < 0.001
Mechanical ventilation 50 (18%) 10 (4%) 40 (95%) < 0.001
Syncope 49 (17%) 31 (13%) 18 (43%) < 0.001
Thrombolysis 84 (30%) 59 (25%) 25 (60%) < 0.001
Lactate measured 139 (49%) 103 (43%) 36 (86%) < 0.001
BGA performed 197 (70%) 162 (67%) 35 (83%) 0.055
Echocardiography performed 195 (69%) 161 (67%) 34 (81%) 0.099
Electrocardiography performed 262 (93%) 241 (100%) 21 (50%) < 0.001
D-dimer determined 148 (52%) 136 (56%) 12 (29%) < 0.001
Spiral CT performed 226 (80%) 221 (92%) 5 (12%) < 0.001
V/Q-scan performed 74 (26%) 73 (30%) 1 (2%) < 0.001
CPR Cardiopulmonary resuscitation; BGA blood gas analysis; V/Q-scan ventilation/perfusion lung scintigraphy; CT computer
tomography; p* survivors versus non-survivors.
770 Janata et al., Mortality of patients with pulmonary embolism
Table 5. Mortality of patients with pulmonary embolism and different ECG findings
All Mortality
n = 262 (100%) n % 95% CI
Normal ECG 36 (14%) 0 0 0 to 3
Heart rate > 100 bpm 139 (53%) 11 8 3 to 13
Atrial fibrillation 28 (11%) 5 18 4 to 32
Pulmonary P wave 23 (9%) 7 30 11 to 49
Incomplete RBB 75 (29%) 7 9 3 to 15
Complete RBB 52 (20%) 20 38 25 to 51
S1Q3T3 pattern 75 (29%) 16 21 12 to 30
ST-Depression 53 (20%) 13 25 13 to 37
Anterior subepicardial ischemia 79 (30%) 14 18 10 to 26
ECG Electrocardiogram; RBB right bundle branch block.
Table 6. Echocardiographic findings of survivors and non-survivors with pulmonary embolism
All Survivors Non-survivors p*
n = 195 n = 161 n = 34
No signs of right ventricular strain 51 (26%) 50 (31%) 1 (3%) < 0.001
Hyperkinetic right ventricle 42 (22%) 42 (26%) 0 0.002
Bulging of septum 73 (37%) 59 (37%) 14 (41%) 0.763
Hypokinetic right ventricle 29 (15%) 10 (6%) 19 (56%) < 0.001
– Thrombi in RA / RV/ PA 21 (7%) 9 (4%) 12 (35%) < 0.001
RA Right atrium; RV right ventricle; PA pulmonary artery; p* survivors versus non-survivors.
Discussion
Diagnosis of PE depends on clinical suspicion and the
availability of diagnostic imaging procedures such as Spi-
ral CT, V/Q-scanning or pulmonary angiography. These
days, Spiral CT is widely accepted and often employed as
it offers a non-invasive accurate diagnosis of PE [12].
Although the negative predictive value of Spiral CT is still
under debate [13, 14], we used it in most of our patients to
confirm the diagnosis of PE. However, in the presence of
severe hemodynamic instability, we had to rely on the
findings of ECG, and bedside echocardiography and to
proceed to thrombolytic treatment without seeking further
diagnostic workup by imaging methods [3]. Diagnosis of
PE was confirmed at autopsy if our therapeutic interven-
tions at last were unsuccessful. This approach enabled us
to define 283 patients who we studied for both overall
mortality and mortality within individual clinically de-
fined subgroups.
Overall, mortality of our patients with PE was 15%,
which compares favourably to recently published data [3].
Looking for particular high or low mortality subgroups
among different demographic characteristics and risk fac-
tors for thromboembolic disease, we were not able to
detect significant differences between survivors and non-
survivors, which contrasts to published literature [2] and
may be due to our study population or our relatively small
sample size.
In patients with cardiac arrest on arrival, out of hospi-
tal cardiac arrest and cardiac arrest within the first 24
hours, we found mortality rates ranging between 65 and
100%, which agree with the data reported by Kasper et al.
[3]. Moreover, we found that patients requiring mechani-
cal ventilation had mortality rates of 80% and those with
Table 7. Mortality of patients with pulmonary embolism and different echocardiographic findings
All Mortality
n = 195 n % 95% CI
No signs of right ventricular strain 51 (26%) 1 2 0 to 6
Hyperkinetic right ventricle 42 (22%) 0 0 0 to 3
Bulging of septum 73 (37%) 14 19 10 to 28
Hypokinetic right ventricle 29 (15%) 19 66 37 to 73
– Thrombi in RA / RV/PA 21 (7%) 12 57 36 to 78
RA Right atrium; RV right ventricle; PA pulmonary artery.
771Janata et al., Mortality of patients with pulmonary embolism
syncope as a sign of moderate cardiovascular instability,
had mortality rates of 37%.
Thrombolytic therapy should promote rapid resolu-
tion of pulmonary emboli and has been recommended for
treatment of major pulmonary embolism [8]. However,
these recommendations are based retrospective data or
small prospective trials [1, 8]. Our data shows that our
patients who received thrombolytic treatment had a mor-
tality of 30%, which reflects the heterogeneity of the
population we treated, but does not allow any conclusion
about the efficiency of that treatment. Recently we have
shown, that only two of twenty-one patients with PE and
cardiac arrest, who received thrombolytic treatment sur-
vived to be dismissed from hospital [15]. As mentioned
earlier, convincing scientific evidence on the value of
thrombolytic therapy in patients with PE, is still lacking
[1].
Although we realize, that blood gas levels are of
insufficient value to exclude PE [16], we used blood gas
analysis and lactate determination to estimate the amount
of cardio respiratory compromise [17]. Mortality of pa-
tients with PE in whom blood gas and lactate determina-
tions were performed ranged between 13 and 33%.
Recent studies confirm the increasing value of
echocardiography in the diagnosis of PE [7, 18]. Echocar-
diography can be performed at the bedside and therefore
even in hemodynamically unstable patients. In agreement
with recently published data [7] we found significant dif-
ferences between survivors and non-survivors in respect
of signs of right ventricular strain, dilated hyperkinetic
and hypokinetic right ventricle and even visible thrombi.
Mortality rates of patients who received echocardiograph-
ic evaluation were as high as 17%. Depending on the
echocardiographic findings, mortality increased to 57%
when thrombi were visible in the right atrium, right ventri-
cle, or pulmonary artery.
Occurrence of the “anterior subepicardial ischemic
pattern” in the ECG may serve as indicator of major PE
[19]. In our patient’s ECGs, we found significant differ-
ences between survivors and non-survivors regarding the
presence of complete right bundle branch block, S1Q3T3
pattern, ST-depression and anterior subepicardial is-
chemia. Mortality of the patients who received a 12 lead
ECG was 8% and increased to 18% in patients with “an-
terior subepicardial ischemic pattern” and to 38% when a
right bundle brunch block was visible. However, in pa-
tients with normal ECGs mortality was zero.
D-dimer determinations retain a high negative predic-
tive value and therefore are recommended for use in emer-
gency wards, mainly to rule out thromboembolic disease
[20, 21]. Therefore, it is not surprising that the D-dimer
test was used only in 52% of our patients, which had a
mortality rate of 8%.
Patients who were stable enough to undergo spiral CT
and V/Q scan examinations had lowest mortality ranges of
0–4%, indicating that the feasibility of these diagnostic
procedures itself predicts a better outcome a priori. In
these subgroups, difference in mortality caused by any
intervention will be very difficult to prove.
Although we know that the retrospective design of our
study may limit our findings and conclusions, we believe
that it adds further information to knowledge and under-
standing of the inhomogeneous clinical picture of PE.
Planning of interventional studies should consider these
observations and limit the interventions to study to a
precisely defined homogeneous subgroup. If mortality is a
desired endpoint, these studies will have to be conducted
in subgroups with higher mortality rates in order to find
significant differences.
Very high mortality rates have to be expected in pa-
tients with PE who require cardiopulmonary resuscitation
and mechanical ventilation. When the patients status al-
lows diagnostic procedures such as Spiral CT and V/Q-
Scan, mortality of PE is as low as 1 to 2%. These facts
have to be considered, when clinical intervention trials in
pulmonary embolism with mortality as endpoint are being
planned.
References
1. Goldhaber SZ (2001) Thrombolysis in pulmonary embo-
lism. A large-scale clinical trial is overdue. Circulation
104: 2876–2878
2. Heit J, Silverstein M, Mohr D, Petterson T, O’Fallon W,
Melton III L (1999) Predictors of survival after deep vein
thrombosis and pulmonary embolism. Arch Intern Med
159: 445–453
3. Kasper W, Konstantinides S, Geibel A, Olschewski M,
Heinrich F, Grosser K, et al (1997) Management strategies
and Determinants of outcome in acute major pulmonary
embolism: results of a multi-centre registry. J Am Coll
Cardiol 30: 1165–1171
4. Carson J, Kelley M, Duff A, Weg J, Fulkerson W, Palevsky
H, et al (1992) The clinical course of pulmonary embo-
lism. N Engl J Med 326: 1240–1245
5. The PIOPED Investigators (1990) Value of the ventilation/
perfusion scan in acute pulmonary embolism: results of the
prospective investigation of pulmonary embolism diagno-
sis (PIOPED). JAMA 263: 2753–2759
6. Stein P, Dalen J, Mc Intyre K, Sasahara A, Wenger N,
Willis P (1975) The electrocardiogram in acute pulmonary
embolism. Progr Cardiovasc Dis 17: 247–257
7. Kasper W, Meinertz T, Henkel B, Eissner D, Hahn K,
Hoffmann T, et al (1986) Echocardiographic findings in
patients with proved pulmonary embolism. Am Heart J
112: 284–290
8. Goldhaber SZ (1995) Contemporary pulmonary embolism
thrombolysis. Chest 107 [Suppl]: 45–51
9. Diehl J, Meyer G, Igual J, Collignon M, Gieselbrecht M,
Even P, Sors H (1992) Effectiveness and safety of bolus
administration of alteplase in massive pulmonary embo-
lism. Am J Cardiol 70: 1477–1480
10. Emergency Cardiac Care Committee and subcommittees
of the American Heart Association (1992) Guidelines for
cardiopulmonary resuscitation and emergency cardiac
care. J Am Med Assoc 268: 2171–2302
11. Gardner M, Altman DG (1989) Statistics with confidence,
1st edn. BMJ Books, pp 28–33
12. Bankier A, Janata K, Fleischmann F, Kreuzer S, Mallek R,
Frossard M, et al (1997) Severity assessment of acute
pulmonary embolism with spiral CT: evaluation of two
modified angiographic scores and comparison with clinical
data. J Thorac Imaging 12: 150–158
13. Rathbun S, Raskob G, Whitsett T (2000) Sensitivity and
specificity of helical computed tomography in the diagno-
sis of pulmonary embolism: a systematic review. Ann In-
tern Med 132: 227–232
772 Janata et al., Mortality of patients with pulmonary embolism
14. Baile E, King G, Mueller N, D’Yachochova Y, Coche E,
Pare P, et al (2000) Spiral computed tomography is com-
parable to angiography for the diagnosis of acute pulmo-
nary embolism. Am J Respir Crit Care Med 161: 1010–
1015
15. Kürkciyan I, Meron G, Sterz F, Janata K, Domanovits H,
Holzer M, et al (2000) Pulmonary embolism as cause of
cardiac arrest. Presentation and outcome. Arch Intern Med
160: 1529–1535
16. Stein P, Goldhaber SZ, Henry J, Miller A (1996) Arterial
blood gas analysis in the assessment of suspected acute
pulmonary embolism. Chest 109: 78–81
17. Dantzker DR, Bower JS (1981) Alterations in gas ex-
change following pulmonary thromboembolism. Chest 81:
495–501
18. Pruszczyk P, Torbicki A, Pacho R, Chlebus M, Kuch-
Wocial A, Pruszynski B, et al (1997) Non-invasive diag-
nosis of suspected severe pulmonary embolism. Trans-
esophageal echocardiography vs. spiral CT. Chest 112:
722–728
19. Ferrari E, Imbert A, Chevalier T, Mihoubi A, Morand P,
Baudouy M (1997) The ECG in pulmonary embolism.
Predictive value of negative T waves in precordial leads –
80 case reports. Chest 11: 5375–5343
20. Task force report (2000) Guidelines on diagnosis and man-
agement of acute pulmonary embolism. Eur Heart J 21:
1301–1336
21. Lenzhofer R, Wimmer F, Haydl H, Kardeis J, Gruber G,
Ganzinger U, et al (1993) Prospective study of determin-
ing the value of D-dimer in diagnosing pulmonary embo-
lism. Wien Klin Wochenschr 105: 492–496
Correspondence: Dr. Karin Janata, Department of Emer-
gency Medicine, University of Vienna, Vienna General Hospi-
tal, Währinger Gürtel 18–20, A-1090 Vienna, Austria,
E-mail: karin.janata@akh-wien.ac.at
(Received October 22, 2001, accepted after revision January 14, 2002)
ResearchGate has not been able to resolve any citations for this publication.
Article
Full-text available
Background Pulmonary embolism (PE) is a possible noncardiac cause of cardiac arrest. Mortality is very high, and often diagnosis is established only by autopsy. Methods In a retrospective study, we analyzed clinical presentation, diagnosis, therapy, and outcome of patients with cardiac arrest after PE admitted to the emergency department of an urban tertiary care hospital. Results Within 8 years, PE was found as the cause in 60 (4.8%) of 1246 cardiac arrest victims. The initial rhythm diagnosis was pulseless electrical activity in 38 (63%), asystole in 19 (32%), and ventricular fibrillation in 3 (5%) of the patients. Pronounced metabolic acidosis (median pH, 6.95, and lactate level, 16 mmol/L) was found in most patients. In 18 patients (30%), the diagnosis of PE was established only postmortem. In 42 (70%) it was diagnosed clinically, in 24 of them the diagnosis of PE was confirmed by echocardiography. In 21 patients, 100 mg of recombinant tissue-type plasminogen activator was administered as thrombolytic treatment, and 2 (10%) of these patients survived to hospital discharge. Comparison of patients of the thrombolysis group (n=21) with those of the nonthrombolysis group (n=21) showed a significantly higher rate of return of spontaneous circulation (81% vs 43%) in the thrombolysis group (P=.03). Conclusions Mortality related to cardiac arrest caused by PE is high. Echocardiography is supportive in determining PE as the cause of cardiac arrest. In view of the poor prognosis, thrombolysis should be attempted to achieve return of spontaneous circulation and probably better outcome.
Article
Full-text available
Pulmonary embolism is a potentially fatal disorder. Information about the outcome of clinically recognized pulmonary embolism is sparse, particularly given that new treatments for more seriously ill patients are now available. We prospectively followed 399 patients with pulmonary embolism diagnosed by lung scanning and pulmonary angiography, who were enrolled in a multicenter diagnostic trial. We reviewed all hospitalizations, all new investigations of pulmonary embolism, and all deaths among the patients within one year of diagnosis. Of the 399 patients, 375 (94 percent) received treatment for pulmonary embolism, usually conventional anticoagulation. Only 10 patients (2.5 percent) died of pulmonary embolism; 9 of them had clinically suspected recurrent pulmonary embolism. Clinically apparent pulmonary embolism recurred in 33 patients (8.3 percent), of whom 45 percent died during follow-up. Ninety-five patients with pulmonary embolism (23.8 percent) died within one year. The conditions associated with these deaths were cancer (relative risk, 3.8; 95 percent confidence interval, 2.3 to 6.4), left-sided congestive heart failure (relative risk, 2.7; 95 percent confidence interval, 1.5 to 4.6), and chronic lung disease (relative risk, 2.2; 95 percent confidence interval, 1.2 to 4.0). The most frequent causes of death in patients with pulmonary embolism were cancer (in 34.7 percent), infection (22.1 percent), and cardiac disease (16.8 percent). When properly diagnosed and treated, clinically apparent pulmonary embolism was an uncommon cause of death, and it recurred in only a small minority of patients. Most deaths were due to underlying diseases. Patients with pulmonary embolism who had cancer, congestive heart failure, or chronic lung disease had a higher risk of dying within one year than did other patients with pulmonary embolism.
Article
Objectives: The present study investigated current management strategies as well as the clinical course of acute major pulmonary embolism. Background: The clinical outcome of patients with acute pulmonary embolism who present with overt or impending right heart failure has not yet been adequately elucidated. Methods: The 204 participating centers enrolled a total of 1,001 consecutive patients. The inclusion criteria were based on the clinical findings at presentation and the results of electrocardiographic, echocardiographic, nuclear imaging and cardiac catheterization studies. Results: Echocardiography was the most frequently performed diagnostic procedure (74%). Lung scan or pulmonary angiography were performed in 79% of clinically stable patients but much less frequently in those with circulatory collapse at presentation (32%, p < 0.001). Thrombolytic agents were given to 478 patients (48%), often despite the presence of contraindications (193 [40%] of 478). The frequency of initial thrombolysis was significantly higher in clinically unstable than in normotensive patients (57% vs. 22%, p < 0.001). Overall in-hospital mortality rate ranged from 8.1% in the group of stable patients to 25% in those presenting with cardiogenic shock and to 65% in patients necessitating cardiopulmonary resuscitation. Major bleeding was reported in 92 patients (9.2%), but cerebral bleeding was uncommon (0.5%). Finally, recurrent pulmonary embolism occurred in 172 patients (17%). Conclusions: Current management strategies of acute major pulmonary embolism are largely dependent on the degree of hemodynamic instability at presentation. In the presence of severe hemodynamic compromise, physicians often rely on the findings of bedside echocardiography and proceed to thrombolytic treatment without seeking further diagnostic certainty in nuclear imaging or angiographic studies.
Article
Animal studies have demonstrated that thrombolysis with recombinant tissue-type plasminogen activator (rt-PA) is accelerated and that bleeding is reduced when rt-PA is infused over a short period. Previous clinical studies in patients with venous thromboembolism have shown that rt-PA is an effective thrombolytic agent when administered by continuous infusion over 2 to 24 hours. Clinical experience of bolus rt-PA administration in patients with massive acute pulmonary embolism (PE) is, however, limited. A prospective open study was conducted in which 54 patients with massive PE (Miller index > or = 20 of 34) received a 10-minute infusion of rt-PA at a dose of 1 mg/kg. Perfusion lung scanning was used to assess the change in pulmonary perfusion after drug administration. At 48 hours and 10 days, the mean absolute improvements in the perfusion defect were 11 and 31%, respectively. In addition, a significant clinical improvement occurred within 2 hours in 11 of the 15 shocked patients. Five patients died (9%) as a result of persistent shock (3 patients), neurologic damage (1 patient) or intracranial bleeding (1 patient). Major bleeding occurred in 8 patients (15%). Long-term follow-up information was available for 44 of the 49 discharged patients: 2 had died and 12 (27%) complained of persistent exertional dyspnea, 7 of whom had an associated heart or lung disease or chronic thromboembolism at admission. These results suggest that a bolus regimen of rt-PA could provide a convenient approach to thrombolytic therapy in patients with massive PE.(ABSTRACT TRUNCATED AT 250 WORDS)
Article
There is a broad spectrum of gas exchange abnormalities that result from pulmonary thromboembolism. The severity and mechanism of these abnormalities are likely to depend upon the size and location of emboli, the presence or absence of preexisting cardiopulmonary disease, and the time elapsed since embolization. Arterial blood gas alterations and changes in expired gas composition reflected in the Bohr dead space and arterial to end-tidal VO2 gradient are neither sufficiently sensitive nor specific to be of great use in the differential diagnosis of pulmonary thromboembolism.
Article
Pulmonary embolism (PE) is still misdiagnosed in a high proportion of cases. 107 patients admitted for suspected pulmonary embolism were studied prospectively to shed light on the value of ELISA-D-dimer and Latex-D-dimer. Pulmonary embolism was ruled out by negative perfusion scans in 66 patients (61.7%) and by angiography in 24 patients. 58% of the scans suggesting a high probability of PE were confirmed by angiography, but only 18% of the scans suggesting a low or intermediate probability of PE. Sensitivity and specificity were 88% and 79%, respectively for the D-dimer ELISA, versus 94% and 90% for the Latex agglutination test. The Latex test increased the positive predictive value of lung scanning suggesting low to intermediate probability of PE (group B) from 18% to 75% and that of lung scanning suggesting high probability of PE (group C) from 58% to 93%. The positive predictive value was improved by ELISA-D-dimer in both groups to 75%. In order to augment the diagnostic efficacy in clinical practice the determination of Latex-D-dimer simultaneously with lung scanning is recommended.
Article
The utility of arterial blood gas levels in excluding the diagnosis of acute pulmonary embolism (PE) was evaluated. Data are from the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED). PE was diagnosed or excluded by pulmonary angiography. Among 330 patients with no prior cardiopulmonary disease, 130 patients had PE and 200 did not. Among 438 patients with prior cardiopulmonary disease, 147 had PE and 291 did not. Definitions were low PaO2 (< 80 mm Hg), low PaCO2 (< 35 mm Hg), and high alveolar-arterial oxygen gradient (P(A-a)O2 [> 20 mm Hg]). Among patients with no prior cardiopulmonary disease who had values of the PaO2 and PaCO2 that were not low and a P(A-a)O2 that was normal, 16 of 42 or 38% (95% confidence interval [CI] = 24 to 54%) had PE. Among patients with prior cardiopulmonary disease who had PaO2 and PaCO2 values that were not low and a P(A-a)O2 that was normal, 4 of 28 or 14% (95% CI = 4 to 33%) had PE. Other combinations of blood gas levels and the P(A-a)O2 gradient, failed to exclude PE in larger percentages of patients. With various combinations of the PaO2 of 80 mm Hg or more, the PaCO2 of 35 mm Hg or higher, and the P(A-a)O2 gradient of 20 mm Hg or less, PE could not be excluded in more than 30% of patients with no prior cardiopulmonary disease and PE could not be excluded in more than 14% of patients with prior cardiopulmonary disease. Blood gas levels, therefore, are of insufficient discriminant value to permit exclusion of the diagnosis of PE.
Article
The value of the ECG for the diagnosis of pulmonary embolism (PE) is debatable. Once the diagnosis of PE has been established, however, the ECG could allow the massive forms to be distinguished. The purpose of our study was to analyze the ECG signs in patients hospitalized for PE in a cardiology unit. Taking a series of 80 consecutive patients hospitalized for PE, we analyzed the ECGs on admission and then during hospitalization. We sought to evaluate changes in ECG signs compared with angiographic and hemodynamic changes in PE. T-wave inversion in the precordial leads is the most common abnormality (68%), and represents the ECG sign best correlated to the severity of the PE. Among those patients with anterior T-wave inversion, 90% had a Miller index over 50% (mean, 60 +/- 8%). Eighty-one percent had a mean pulmonary arterial pressure (PAP) over 30 mm Hg (mean, 37 +/- 8%). This subepicardial ischemic pattern is an even stronger marker of severity when it appears as early as the first day (p < 0.01). Its reversibility is correlated to the changes in PE. After thrombolysis in particular, normalization of repolarization systematically indicates mean Miller and PAP indexes of < 20% and < 20 mm Hg, respectively. The anterior subepicardial ischemic pattern is the most frequent ECG sign of massive PE. This parameter is easy to obtain and reflects the severity of PE. Its reversibility before the sixth day points to a good outcome or high level of therapeutic efficacy.
Article
Thrombolysis debulks clot and provides primary treatment of pulmonary embolism, whereas intensive anticoagulation is critical for secondary prevention of recurrent pulmonary embolism. The decision to use primary therapy or secondary prevention depends upon the patient's risk of suffering an adverse clinical outcome. We utilize echocardiography to help risk-stratify our patients. The presence of normal right ventricular function portends an excellent prognosis with anticoagulation alone. In contrast, the presence of right ventricular hypokinesis or dilatation may indicate a high likelihood of recurrent pulmonary embolism despite adequate anticoagulation. Among high risk patients, thrombolysis can usually rapidly reverse right heart failure and be life-saving. The procedure for administering thrombolytic therapy has been streamlined to improve efficacy, enhance safety, and reduce costs.