Sunteți pe pagina 1din 3

Canadian Journal of Cardiology 33 (2017) 1336.e1e1336.e3 www.onlinecjc.


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
Department of Cardiology, Hospital de Santa Cruz, Centro Hospitalar de Lisboa Ocidental, Carnaxide, Portugal
Department of Cardiology, Hospital de Faro, Centro Hospitalar do Algarve, Faro, Portugal
Department of Cardiothoracic Surgery, Hospital de Santa Cruz, Centro Hospitalar de Lisboa Ocidental, Carnaxide, Portugal

Hypoxemia after myocardial infarction (MI) is usually explained by L’hypoxemie après un infarctus du myocarde (IM) est en ge  ne
common culprits, including congestive heart failure, pre-existing lung causee par des facteurs courants, notamment l’insuffisance cardiaque
disease, and pulmonary infection. We report a case of a 60-year-old congestive, une maladie pulmonaire pre existante et une infection
woman who experienced severe persistent hypoxemia caused by a pulmonaire. Nous abordons le cas d’une femme de 60 ans qui
patent foramen ovale in the setting of anterior MI complicated by a sente une hypoxe
pre mie grave persistante cause e par un foramen
contained left ventricular rupture. ovale permeable et qui a des ante
cedents d’IM complique
 par un faux
anevrisme du ventricule gauche.

Case Presentation mechanical ventilation. Once again, arterial blood gas de-
A 60-year-old woman without known cardiovascular dis- terminations were noticeable for an unexpectedly low and
ease was admitted to the cardiac intensive care unit after worsening PaO2/FIO2 gradient that did not improve with
successful primary angioplasty (Video 1 ; view video 100% oxygen; the chest radiograph, however, showed a nearly
online) performed for anterior ST-segment elevation normal finding (Fig. 1A), thus ruling out pneumonia and
myocardial infarction (MI). Serial transthoracic echocardiog- acute respiratory distress syndrome. At this stage, we also
raphy prompted by recurrent vomiting and progressive hy- excluded pulmonary thromboembolism, and a cardiac right-
potension revealed a de novo pericardial effusion causing to-left shunt had become the most probable explanation
cardiac tamponade (Video 2 ; view video online). After despite being totally unexpected previously (Video 3 ;
an emergent median sternotomy, a hemorrhagic suffusion view video online). Clinical suspicion was heightened by the
involving the apex became evident, necessitating blood and finding of orthodeoxia during mechanical ventilation. Trans-
clot evacuation, application of a biological glue, and poly- esophageal echocardiography was performed, revealing an
tetrafluoroethylene patch placement. Marked hemodynamic aneurysmal interatrial septum with a large exclusive right-to-
improvement was then observed. The patient’s subsequent left shunt detectable by color Doppler and many bubbles
clinical course was remarkable for dyspnea and severe oscil- traversing from the right to left atrium after intravenous
lating hypoxemia (nadir of partial pressure of oxygen to agitated saline administration (Videos 4 and 5 ; view
inspired oxygen fraction ratio [PaO2/FIO2 < 100]), which videos online). An unremarkable pulmonary angiogram was
persisted after intravenous furosemide administration, left- seen during cardiac catheterization (Video 6 ; view video
sided thoracentesis, and noninvasive positive pressure venti- online), as were nearly normal pulmonary pressures. The right
lation, ultimately requiring endotracheal intubation and atrial venous wave denoted a constrictive morphologic con-
dition, and an underlying right-to-left pressure gradient was
Received for publication May 2, 2017. Accepted July 12, 2017. detected (Fig. 1C). The cause had apparently been found, and
Corresponding author: Dr António Tralhão, Department of Cardiology, the patient was scheduled for patent foramen ovale (PFO)
Hospital de Santa Cruz, Centro Hospitalar de Lisboa Ocidental, Av. Prof. closure. Under transesophageal echocardiographic guidance, a
Reinaldo dos Santos, 2790-134 Carnaxide, Portugal. Tel.: 00351210431000; size 23 Amplatzer occluder (St Jude Medical, St Paul, MN)
fax: 00351214188095.
E-mail: was placed through the defect (Fig. 1D and Video 7 ;
See page 1336.e2 for disclosure information. view video online). Blood gas measurements taken from the
0828-282X/Ó 2017 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.
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 measurement, ie, larger pressure in the right atrium than in
improvement in PaO2, allowing extubation in 48 hours and the left atrium. Although difficult to confirm, it seems
discharge after 1 week. 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
Discussion pressure gradient that favoured the shunting of blood
Right-to-left atrial shunting leading to hypoxemia after through the PFO. Even though it was clinically required,
MI has seldom been reported in the literature. In all these invasive positive pressure mechanical ventilation further
cases, the mechanism depended on increased right atrial promoted the shunt by increasing right ventricular after-
pressure from an inferior MI with right ventricular load. To the best of our knowledge, this is the first case of
involvement, causing a shunting of blood through either an right-to-left shunting caused by an anterior MI. Despite this
atrial septal defect or a PFO.1-4 Intuitively, we suspect that condition’s rarity, physicians should include the possibility
other factors may play a role, because the incidence of both of an intracardiac shunt through a PFO as a possible and
PFO and inferior MI is far larger than the occurrence of potentially remediable cause of severe persistent hypoxemia
hypoxemia attributable to this single mechanism. At first after acute MI with any localization.
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 Disclosures
mechanism. Surprisingly, we found an inverted pressure The authors have no conflicts of interest to disclose.
Tralhão et al. 1336.e3
Right-to-Left Shunt After MI

References 4. Franco T, Melández J, Malkin R, Schulman P. Acute right to left shunt

through patent foramen ovale presenting as hypoxemia after myocardial
1. Bassi S, Amersey R, Andrews R. Right ventricular infarction complicated infarction: a case report. Cases J 2009;2:8878.
by right to left shunting through an atrial septal defect: successful treat-
ment with an Amplatzer septal occluder. Heart 2005:94-6.
2. Scheinman MM, Evans GT. Right to left shunt in patients with acute Supplementary Material
myocardial infarction. A proposed mechanism. Am J Cardiol 1972;29:757-66. To access the supplementary material accompanying this
3. Silver T, Lieberman EH, Thibault GE. Refractory hypoxemia in inferior article, visit the online version of the Canadian Journal of
myocardial infarction from right-to-left shunting through a patent foramen Cardiology at and at
ovale: a case report and review of the literature. Clin Cardiol 1994;17:627-30. 1016/j.cjca.2017.07.014.