Cardiac Dysfunction
Mabrouk Bahloul, Anis N. Chaari, Hatem Kallel, Abdelmajid Khabir, Adnne Ayadi, Hanne
Charfeddine, Leila Hergafi, Adel D. Chaari, Hedi E. Chelly, Chokri Ben Hamida, Noureddine
Rekik and Mounir Bouaziz
Am J Crit Care 2006;15:462-470
2006 American Association of Critical-Care Nurses
Published online http://www.ajcconline.org
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AJCC, the American Journal of Critical Care, is the official peer-reviewed research
journal of the American Association of Critical-Care Nurses (AACN), published
bimonthly by The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656.
Telephone: (800) 899-1712, (949) 362-2050, ext. 532. Fax: (949) 362-2049.
Copyright 2006 by AACN. All rights reserved.
BACKGROUND Acute neurogenic pulmonary edema, a common and underdiagnosed clinical entity, can
occur after virtually any form of injury of the central nervous system and is a potential early contributor
to pulmonary dysfunction in patients with head injuries.
OBJECTIVE To explore myocardial function in patients with evident neurogenic pulmonary edema after
traumatic head injury.
METHODS During a 1-year period in a university hospital in Sfax, Tunisia, information was collected
prospectively on patients admitted to the 22-bed intensive care unit because of isolated traumatic head
injury who had neurogenic pulmonary edema. Data included demographic information, vital signs, neu-
rological status, physiological status, and laboratory findings. All of the patients had computed tomogra-
phy and plain radiography of the neck and determination of cardiac function.
RESULTS All 7 patients in the sample had cardiac dysfunction. Evidence of myocardial damage was
confirmed by echocardiography in 3 patients, pulmonary artery catheterization in 3 patients, and/or
postmortem myocardial biopsy in 4 patients. Echocardiography studies, repeated 7 days after the initial
study in one patient and 90 days afterward in another, showed complete improvement in wall motion,
with a left ventricular ejection fraction of 0.65.
CONCLUSION All patients who had neurogenic pulmonary edema due to traumatic head injury had
myocardial dysfunction. The mechanisms of the dysfunction were multiple. The great improvement in
wall motion seen in 2 patients indicated the presence of a stunned myocardium. Further studies are
needed to understand the mechanisms of this cardiac dysfunction. (American Journal of Critical Care.
2006;15:462-470)
462 AMERICAN JOURNAL OF CRITICAL CARE, September 2006, Volume 15, No. 5 http://ajcc.aacnjournals.org
http://ajcc.aacnjournals.org AMERICAN JOURNAL OF CRITICAL CARE, September 2006, Volume 15, No. 5 463
Patient
Parameter 1 2 3 4 5 6 7
Age, y 23 12 6 14 12 49 38
Sex Male Male Male Male Male Male Male
Simplified Acute
Physiology Score II 31 ND ND ND ND 32 31
Time between accident
and admission to
intensive care unit, h 1 1 1 1 1 1 1
Score on Glasgow
Coma Scale 3 4 7 7 5 8 10
Body temperature, C 35 37.6 37 36.5 ND 37.8 38.2
Heart rate,
beats per minute 112 120 130 84 120 35 123
Blood pressure, mm Hg
Systolic 92 100 100 100 50 200 140
Diastolic 43 60 50 50 20 80 70
Respiratory rate before
mechanical ventilation,
breaths per minute 28 24 27 35 8 33 34
Arterial oxygen saturation
while breathing air, % ND ND ND 75 54 79 ND
Glucose level, mmol/L
(mg/dL) 5.5 (99) 6.5 (117) 8.7 (157) 6.7 (121) ND 7.9 (142) 9.4 (169)
Shock No No No No Yes No No
pH 7.43 7.42 7.11 7.32 ND 7.45 7.27
PaCO2, mm Hg 33 27.7 34.8 35.2 ND 21.8 38.5
Bicarbonate, mmol/L 26 18.1 11.2 18.6 ND 15.4 24.6
PaO2 during mechanical
ventilation, mm Hg 177 153 78 175 ND 251 109
Fraction of inspired oxygen 1.00 0.60 0.50 0.60 ND 1.00 0.60
Creatine phosphokinase,
U/L 695 ND ND ND ND ND 270
Alanine aminotransferase,
U/L ND 32 ND 20 ND ND ND
Aspartate
aminotransferase, U/L ND 77 ND 40 ND ND ND
Mechanical ventilation Yes Yes Yes Yes Yes Yes Yes
Urea, mmol/L (mg/dL) 5.5 (15) 10 (28) 6.2 (17) 3 (8) ND 7.7 (22) 5.3 (15)
Hemoglobin, g/L 106 110 72 94 ND 139 95
Hospital stay, d 7 5 3 4 1 15 5
Use of catecholamines Yes Yes Yes Yes Yes Yes Yes
Type of catecholamine Dobut/epin Dobut Dobut Epin Dobut/norepin Dobut Epin
Outcome Died Survived Survived Died Died Survived Died
Abbreviations: Dobut, dobutamine; Epin, epinephrine; ND, not determined; Norepin, norepinephrine.
464 AMERICAN JOURNAL OF CRITICAL CARE, September 2006, Volume 15, No. 5 http://ajcc.aacnjournals.org
Patient
Parameter 1 2 3 4 5 6 7
Extradural hematoma No No No Yes No No Yes
Subdural hematoma No Yes Yes No No Yes No
Intracerebral hematoma No No No No No No No
Meningeal hemorrhage No No No Yes Yes Yes No
Cerebral edema Yes No No No Yes Yes No
Cerebral contusion No No No Yes No Yes No
Pneumocephalus No No No Yes No Yes No
Mass lesion No Yes Yes No No No Yes
Herniation No Yes No No No No Yes
Clinical Information
All 7 patients had hyperpnea and tachycardia at
the time of hospital admission. Cardiogenic shock
developed in 1 patient (patient 5, treated with dobu-
tamine and norepinephrine) on hospital admission.
The mean GCS score was 6 (range 3-10). All patients
had already received mechanical ventilation before the
ICU admission. All 7 patients had clinical manifesta-
tions of respiratory distress at the scene of the acci-
dent. The demographic and clinical parameters of the
sample at admission are shown in Table 1. All patients
had received catecholamines on ICU admission to
treat the pulmonary edema (dobutamine at a mean dose
of 10 g/kg per minute plus or minus epinephrine or
norepinephrine).
Brain CT
All patients had brain CT upon admission. The
most common abnormalities were meningeal hemor-
rhage, subdural hematoma, and mass lesion, observed
in 3 patients each (Table 2). Figure 1 shows the cere-
Figure 1 Computed tomography scan of cerebrum of patient bral CT scan for patient 6.
6 shows a subdural hematoma, meningeal hemorrhage, cere-
bral edema, cerebral contusion, and a pneumocephalus. Chest Radiography
The chest radiographs obtained upon admission
showed signs of alveolar pulmonary edema in all
ICU. In 2 patients, myocardial echocardiography was cases (eg, patient 2, Figure 2). In addition, a chest CT
repeated. Finally, a myocardial biopsy and/or pul- scan obtained on ICU admission in patient 5 (Figure 3)
monary biopsy was done for all patients who died. clearly shows signs of alveolar pulmonary edema.
Results Echocardiography
During the study period, 202 patients were admit- Echocardiographic studies in 3 patients showed
ted with traumatic head injury. Only 7 patients were global hypokinesia with a decrease in LVEF (to 0.40)
finally included in this study. The mean time between in 2 patients (patients 2 and 6). In 1 patient (patient 4),
traumatic head injury and ICU admission was 1 hour. however, a diastolic dysfunction with a reduced veloc-
The traumatic head injury was caused by a traffic acci- ity of early filling (E wave), an increase in the velocity
dent in all cases. associated with atrial contraction (A wave), and a ratio
http://ajcc.aacnjournals.org AMERICAN JOURNAL OF CRITICAL CARE, September 2006, Volume 15, No. 5 465
of E to A of less than 1 was observed. For 2 patients Figure 3 Computed tomography scan of the chest of
(patients 2 and 6), echocardiography performed 7 and patient 5 obtained on admission to the intensive care unit
shows alveolar pulmonary edema.
90 days after the initial study showed complete recov-
ery, with an LVEF of 0.65.
Summary
Electrocardiography In all patients included in the study, the diagnosis
The electrocardiograms showed some abnormali- of cardiac dysfunction was suspected because of the
ties in all patients. The most common abnormality signs of acute respiratory distress (cyanosis, inspiratory
was tachycardia, with heart rates exceeding 122/min. retraction of intercostal spaces), the presence of crack-
Other abnormalities also were observed, including ST- les on auscultation of one or both lungs, and the evi-
segment depression in 1 patient and right bundle branch dence of pulmonary edema on the chest radiograph. In
block in 2 patients. Table 3 shows the changes observed patients who underwent echocardiography, the cardio-
for each patient on admission. genic part was confirmed by a low LVEF (at 0.40 with
catecholamine) in 2 patients and by a reduced velocity
Pulmonary Artery Catheterization of early filling (E wave), an increase in the velocity
Pulmonary artery catheterization was done for 3 associated with atrial contraction (A wave), and a ratio
patients (patients 1, 3, and 7). The findings indicated a of E to A of less than 1 in 1 patient (patient 4).
low stroke volume index in all 3 patients. Pulmonary In patients who underwent pulmonary artery
artery wedge pressure was higher in all patients except catheterization, cardiac dysfunction was indicated by a
patient 3. In patient 3, who had pulmonary edema evi- pulmonary artery wedge pressure greater than 18 mm
dent on a chest radiograph, the mixed venous oxygen Hg in 2 patients, and in another patient cardiac dys-
saturation was low (<70%), and the arteriovenous dif- function was indicated by the low mixed venous oxy-
ference in oxygen content was higher than in the other gen saturation (<70%) and the low stroke volume index
patients (Table 4). when treated with catecholamines.
Finally, in patient 5, who was admitted for isolated
Histological Findings traumatic head injury with acute respiratory distress
Postmortem myocardial biopsies were done in 4 associated with a refractory shock, the diagnosis of
cases (patients 1, 4, 5, and 7), and a pulmonary biopsy NPE was made by the medical committee on the basis
was done in 1 case (patient 5). Myocardial biopsy of clinical manifestations (respiratory distress), findings
showed an interstitial edema in all cases without a on chest radiographs, and postmortem biopsy findings.
focus of necrotic muscle fiber or myocardial infiltra-
tion by inflammatory cells. Figure 4 shows the histo-
logical findings on myocardial biopsy specimen for
patient 5. Examination of the pulmonary biopsy speci- All subjects with neurogenic pulmonary
men from patient 5 showed marked alveolar edema edema had cardiac dysfunction.
without signs of inflammatory lesions (Figure 5).
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