Canadian Journal of Cardiology 33 (2017) 1336.e1e1336.e3 www.onlinecjc.
ca
Case Report
Persistent Hypoxemia After Acute Myocardial Infarction:
An Unexpected Culprit
António Tralhão, MD,a Pedro Freitas, MD,a Gustavo Rodrigues, MD,a Hugo Cafe, MD,b
António Miguel Ferreira, MD,a Henrique Mesquita Gabriel, MD,a Luís Bruges, MD,c
Carlos Aguiar, MD,a and Jorge Ferreira, MDa
a
Department of Cardiology, Hospital de Santa Cruz, Centro Hospitalar de Lisboa Ocidental, Carnaxide, Portugal
b
Department of Cardiology, Hospital de Faro, Centro Hospitalar do Algarve, Faro, Portugal
c
Department of Cardiothoracic Surgery, Hospital de Santa Cruz, Centro Hospitalar de Lisboa Ocidental, Carnaxide, Portugal
ABSTRACT
Hypoxemia after myocardial infarction (MI) is usually explained by
common culprits, including congestive heart failure, pre-existing lung
disease, and pulmonary infection. We report a case of a 60-year-old
woman who experienced severe persistent hypoxemia caused by a
patent foramen ovale in the setting of anterior MI complicated by a
contained left ventricular rupture.
Case Presentation
A 60-year-old woman without known cardiovascular dis-
ease was admitted to the cardiac intensive care unit after
successful primary angioplasty (Video 1 ; view video
online) performed for anterior ST-segment elevation
myocardial infarction (MI). Serial transthoracic echocardiog-
raphy prompted by recurrent vomiting and progressive hy-
potension revealed a de novo pericardial effusion causing
cardiac tamponade (Video 2 ; view video online). After
an emergent median sternotomy, a hemorrhagic suffusion
involving the apex became evident, necessitating blood and
clot evacuation, application of a biological glue, and poly-
tetrafluoroethylene patch placement. Marked hemodynamic
improvement was then observed. The patient’s subsequent
clinical course was remarkable for dyspnea and severe oscil-
lating hypoxemia (nadir of partial pressure of oxygen to
inspired oxygen fraction ratio [PaO2/FIO2 < 100]), which
persisted after intravenous furosemide administration, left-
sided thoracentesis, and noninvasive positive pressure venti-
lation, ultimately requiring endotracheal intubation and
Received for publication May 2, 2017. Accepted July 12, 2017.
Corresponding author: Dr António Tralhão, Department of Cardiology,
Hospital de Santa Cruz, Centro Hospitalar de Lisboa Ocidental, Av. Prof.
Reinaldo dos Santos, 2790-134 Carnaxide, Portugal. Tel.: 00351210431000;
fax: 00351214188095.
E-mail: atralhao@gmail.com
See page 1336.e2 for disclosure information.
http://dx.doi.org/10.1016/j.cjca.2017.07.014
0828-282X/Ó 2017 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.

RESUM 
E
L’hypoxemie après un infarctus du myocarde (IM) est en ge  ne
ral
causee par des facteurs courants, notamment l’insuffisance cardiaque
congestive, une maladie pulmonaire pre existante et une infection
pulmonaire. Nous abordons le cas d’une femme de 60 ans qui
sente une hypoxe
pre mie grave persistante cause e par un foramen
ovale permeable et qui a des ante
cedents d’IM complique
 par un faux
anevrisme du ventricule gauche.
mechanical ventilation. Once again, arterial blood gas de-
terminations were noticeable for an unexpectedly low and
worsening PaO2/FIO2 gradient that did not improve with
100% oxygen; the chest radiograph, however, showed a nearly
normal finding (Fig. 1A), thus ruling out pneumonia and
acute respiratory distress syndrome. At this stage, we also
excluded pulmonary thromboembolism, and a cardiac right-
to-left shunt had become the most probable explanation
despite being totally unexpected previously (Video 3 ;
view video online). Clinical suspicion was heightened by the
finding of orthodeoxia during mechanical ventilation. Trans-
esophageal echocardiography was performed, revealing an
aneurysmal interatrial septum with a large exclusive right-to-
left shunt detectable by color Doppler and many bubbles
traversing from the right to left atrium after intravenous
agitated saline administration (Videos 4 and 5 ; view
videos online). An unremarkable pulmonary angiogram was
seen during cardiac catheterization (Video 6 ; view video
online), as were nearly normal pulmonary pressures. The right
atrial venous wave denoted a constrictive morphologic con-
dition, and an underlying right-to-left pressure gradient was
detected (Fig. 1C). The cause had apparently been found, and
the patient was scheduled for patent foramen ovale (PFO)
closure. Under transesophageal echocardiographic guidance, a
size 23 Amplatzer occluder (St Jude Medical, St Paul, MN)
was placed through the defect (Fig. 1D and Video 7 ;
view video online). Blood gas measurements taken from the
1336.e2 Canadian Journal of Cardiology
Volume 33 2017

Figure 1. (A) Nearly normal chest radiograph, excluding infectious disease, significant pleural effusion, or acute respiratory distress syn-
drome while the patient remained hypoxemic. (B) Transesophageal echocardiogram depicting a large right-to-left shunt through a patent
foramen ovale. (C) Venous waveform obtained through catheterization of the right atrium (RA), revealing a clear prominent descent and a right-
to-left mean pressure gradient of 3 mm Hg between the right and left atria and accompanying pulmonary capillary wedge pressure (PCWP)
measurement. (D) Successful Amplatzer occluder placement through the defect illustrated by 2- and 3-dimensional transesophageal echo-
cardiographic imaging.

radial artery before and after PFO closure showed a dramatic
improvement in PaO2, allowing extubation in 48 hours and
discharge after 1 week.
Discussion
Right-to-left atrial shunting leading to hypoxemia after
MI has seldom been reported in the literature. In all these
cases, the mechanism depended on increased right atrial
pressure from an inferior MI with right ventricular
involvement, causing a shunting of blood through either an
atrial septal defect or a PFO.1-4 Intuitively, we suspect that
other factors may play a role, because the incidence of both
PFO and inferior MI is far larger than the occurrence of
hypoxemia attributable to this single mechanism. At first
glance, one would expect pulmonary hypertension second-
ary to left ventricular dysfunction or a superimposed lung
(vascular or parenchymal) disorder, or both, to be a key
mechanism. Surprisingly, we found an inverted pressure
measurement, ie, larger pressure in the right atrium than in
the left atrium. Although difficult to confirm, it seems
plausible from hemodynamic data that a localized
constriction encircling the right atrial wall resulting from
remnant clots in the pericardial space might have created a
pressure gradient that favoured the shunting of blood
through the PFO. Even though it was clinically required,
invasive positive pressure mechanical ventilation further
promoted the shunt by increasing right ventricular after-
load. To the best of our knowledge, this is the first case of
right-to-left shunting caused by an anterior MI. Despite this
condition’s rarity, physicians should include the possibility
of an intracardiac shunt through a PFO as a possible and
potentially remediable cause of severe persistent hypoxemia
after acute MI with any localization.
Disclosures
The authors have no conflicts of interest to disclose.
Tralhão et al.
Right-to-Left Shunt After MI
References
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by right to left shunting through an atrial septal defect: successful treat-
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2. Scheinman MM, Evans GT. Right to left shunt in patients with acute
myocardial infarction. A proposed mechanism. Am J Cardiol 1972;29:757-66.
3. Silver T, Lieberman EH, Thibault GE. Refractory hypoxemia in inferior
myocardial infarction from right-to-left shunting through a patent foramen
ovale: a case report and review of the literature. Clin Cardiol 1994;17:627-30.
1336.e3
4. Franco T, Melández J, Malkin R, Schulman P. Acute right to left shunt
through patent foramen ovale presenting as hypoxemia after myocardial
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Supplementary Material
To access the supplementary material accompanying this
article, visit the online version of the Canadian Journal of
Cardiology at www.onlinecjc.ca and at http://dx.doi.org/10.
1016/j.cjca.2017.07.014.