A 26-year-old man with a history of tibial fracture (b)
10 days ago presented to emergency department
with acute respiratory failure and cardiogenic shock.
Initial systolic blood pressure was 80/40 mmHg and
the heart rate was 126 bpm. Blood gas analysis
showed hypoxia, hypocarbia, and lactic acidosis.
Electrocardiography revealed sinus tachycardia along
with S wave in lead I and Q wave and inverted T wave
in lead III (Figure
1a). During diagnostic work-up,
cardiopulmonary arrest occurred and the patient was
intubated and cardiopulmonary resuscitation (CPR)
was initiated. As the patient was unresponsive to the
initial CPR with intravenous (IV) vasopressor therapy,
point-of-care transthoracic cardiac ultrasonography
was performed concurrently with CPR which revealed
severe right ventricular dilatation with poor systolic
function, moderate tricuspid regurgitation (TR),
and a systolic pulmonary artery pressure (sPAP) of
50 mmHg (Figure
1b). Point-of-care lower extremity
venous Duplex ultrasound also showed deep venous
thrombosis in the left lower extremity. Based on
these findings, acute pulmonary embolism (PE) was
suspected and IV unfractionated heparin plus systemic
thrombolytic therapy (TT) with infusion of tissue
plasminogen activator at a rate of 50 mg/h for two hours
were started immediately. At 60 min of CPR, TT
was discontinued and the patient transferred to the operating room under CPR and femoro-femoral venoarterial
extracorporeal membrane oxygenation (ECMO)
(Medos Medizintechnik AG, Stolberg, Germany)
was initiated with a 23-Fr venous and 17-Fr arterial
cannula with restoration of systemic blood flow and
oxygen delivery (4.5 L/min, 3,600 rpm). After ECMO
insertion, IV unfractionated heparin infusion therapy
was started with activated partial thromboplastin time
monitoring. The next day, pulmonary angiography was
performed under ECMO support in the catheterization
laboratory which demonstrated filling defects of the
left lobar arteries, compatible with acute PE. After
24 hours, bedside transthoracic echocardiography
showed complete recovery of the right ventricular
function with a tricuspid annular plane systolic
excursion 24 mm and mild TR with a sPAP of
35 mmHg (Figure
1c, d). The hemodynamically stable
patient was weaned from ECMO after 32 hours.
After weaning from mechanical ventilation and deep
sedation, the patient woke up with right hemiparesis.
Cranial computed tomography demonstrated left
middle cerebral artery territory infarction due to
possible ECMO-related thromboembolism. During the
hospital stay, the patient was followed with rivaroxaban
20 mg/day and stroke rehabilitation program. At
the end of 20 days, the patient was discharged from
hospital with mild neurological sequela. A written
informed consent was obtained from the patient.
Figure 1: On admission, (a) 12-lead-electrocardiography showing
sinus tachycardia along with S wave in lead I, Q wave and
inverted T wave in lead III, (b) point-of-care transthoracic cardiac
ultrasound during cardiopulmonary resuscitation showing severe
right ventricular dilatation, (c) after 24 hours bedside transthoracic
echocardiography showing complete recovery of right ventricular
chamber size and (d) right ventricular systolic function with a
tricuspid annular plane systolic excursion of 22 mm.
RV: Right ventricle; RA: Right atrium; LV: Left ventricle; LA: Left atrium.
Point-of-care ultrasonography including
transthoracic cardiac ultrasound and lower extremity
venous Duplex ultrasound in the emergency department
are helpful imaging methods to urgently diagnose
acute PE. The presence of right heart dilatation,
right ventricle systolic dysfunction with TR, and
elevated sPAP on point-of-care transthoracic cardiac ultrasound and deep venous thrombosis on point-ofcare
lower extremity venous Duplex ultrasound allow
to start emergency treatment in case of suspected
of PE with cardiogenic shock.[1] Management of
PE guidelines recommends TT in patients with
massive PE complicated by cardiopulmonary
shock.[2] On the other hand, ECMO is suggested
to provide cardiopulmonary circulatory support in
patients with high-risk PE complicated with sustained
hemodynamic and respiratory failure, despite initial
TT and vasopressor therapy.[3]
In conclusion, combined use of point-ofcare
ultrasonography, thrombolytic therapy, and
extracorporeal membrane oxygenation are important
diagnostic and therapeutic strategies in acute massive
PE complicated with cardiopulmonary shock.
Declaration of conflicting interests
The authors declared no conflicts of interest with respect to
the authorship and/or publication of this article.
Funding
The authors received no financial support for the research
and/or authorship of this article.