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* From the Departments of Pulmonary and Critical Care Medicine (Drs. Ghamande and Stoller) and Pediatric Cardiology (Dr. Rhodes), the Division of Medicine (Dr. Ramsey), the Cleveland Clinic Foundation, Cleveland, OH.
Correspondence to: James K. Stoller, MD, FCCP, Department of Pulmonary and Critical Care Medicine, A90, The Cleveland Clinic Foundation, 9500 Euclid Ave, Cleveland, OH 44195; e-mail: stollej{at}ccf.org
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Abstract |
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Key Words: diaphragm dysfunction • hypoxemia • patent foramen ovale
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Introduction |
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TOPAbstractIntroductionCase ReportDiscussionReferences |
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Far less commonly, PFO can be associated with clinical sequelae of hypoxia due to a right-to-left anatomic shunt or with the paradoxic embolization of either a clot or gas.3 When a right-to-left shunt (RLS) does occur, excessive right-sided pressures often are implicated, although RLS also may occur in the absence of a pressure gradient as a result of streaming that accompanies anatomic changes (eg, postpneumonectomy).4 To our knowledge, only two earlier reports5 6 have described the development of an intracardiac RLS through a PFO associated with hemidiaphragmatic paralysis.
To extend the spectrum of PFO sequelae in patients with hemidiaphragm elevation and to describe the utility of catheter closure of the PFO to improve oxygenation, the current report presents a third patient with hemidiaphragm elevation who experienced severe hypoxemia from a RLS through a PFO. In our patient, the severity of hypoxemia prompted the closure of the PFO by a catheter-deployed double-umbrella device, causing marked and immediate improvement in the patient’s oxygenation.
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Case Report |
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On the patient’s arrival at our hospital, marked hypoxemia was noted, with the following arterial blood gas levels: fraction of inspired oxygen, 1.0; PaO2, 55 mm Hg; PCO2, 25 mm Hg; and pH, 7.50. The initial workup included a CT scan of the chest confirming the presence of right middle and right lower lobe atelectasis with an elevated right hemidiaphragm but no mediastinal mass to explain phrenic nerve dysfunction. An incidental note was made of the presence of calcified subcarinal and hilar nodes, which was consistent with her history of Histoplasma infection. A transesophageal echocardiogram confirmed the presence of a bidirectional shunt on the basis of a PFO. Duplex studies showed deep venous thrombosis below the knee, and a pulmonary arteriogram was performed showing no evidence of pulmonary embolism and normal pulmonary arterial pressures (30/15 mm Hg; mean pulmonary arterial pressure, 21 mm Hg; pulmonary artery occlusion pressure, 10 mm Hg). Because of concerns about an endobronchial lesion, bronchoscopy was performed, which showed some scant secretions in the left lung but no endobronchial lesions. A sniff test was performed that showed paradoxic cephalad motion of the right hemidiaphragm, which was consistent with the presence of a paralyzed right hemidiaphragm.
In the absence of a pulmonary embolism, the patient’s hypoxemia was
deemed disproportionate to the atelectasis, and an anatomic shunt was
considered likely. This assessment prompted the reconsideration of a
PFO as being a probable source of the RLS. As a result, cardiac
catheterization was undertaken with the intention of deploying an
umbrella device (CardioSEAL atrial septal double umbrella; Nitinol
Medical Technologies, Inc; Boston, MA) to close the PFO. The
catheterization confirmed the presence of a PFO with no evidence of a
right-to-left pressure gradient. Specifically, the mean left atrial
pressure was 7 mm Hg (A-wave pressure, 11 mm Hg; V-wave pressure, 8 mm
Hg), and the mean right atrial pressure was 7 mm Hg (A-wave pressure, 9
mm Hg; V-wave pressure, 7 mm Hg). Transient closure of the PFO with a
balloon was associated with immediately improved oxygen saturation.
Based on this finding, the double-umbrella device was deployed using a
standard technique to permanently occlude the foramen ovale, causing
marked and immediate improvement in the patient’s oxygenation
(ie, her fraction of inspired oxygen requirement to maintain
saturation at 
90% fell from 0.9 L before closure of the PFO to 3.5
L while using a nasal cannula to receive oxygen immediately following
the closure of the PFO). When seen as an outpatient 1 month after the
placement of the umbrella device, the patient felt well and had good
functional status. A repeat surface echocardiogram showed no evidence
of a shunt, and she no longer required supplemental oxygen (resting
room air pulse oximetry saturation, 94%).
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Discussion |
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1. As in the postpneumonectomy setting and in the previously reported patients with an elevated right hemidiaphragm, an RLS through a PFO can occur without a right-to-left pressure gradient and can be associated with significant venous admixture and hypoxemia.7
2. In the absence of a pressure gradient favoring right-to-left blood flow, the presumed mechanism of the shunt is the streaming of blood through the PFO as it enters the right atrium. As has been suggested by Swan et al,8 and as was observed intraoperatively by Murray et al,5 when a shunt follows a pneumonectomy, we can speculate that a shift in the anatomic relation of the vena cavae to the interatrial septum caused by the hemidiaphragm paralysis encourages this streaming of blood.
3. In the face of a relatively clear lung parenchyma and in the absence of pulmonary vascular disease, clinicians should suspect an anatomic shunt when assessing patients with high supplemental oxygen requirements.
Although the available evidence in this case fails to prove that hemidiaphragm elevation caused the shunt to occur, several observations strongly support this suspicion. First, our patient was known to have symmetric diaphragms, as seen on a chest radiograph 5 months before her admission to the referring hospital. Similarly, given her current profound hypoxemia, her evident intolerance of low arterial oxygen tensions, and her not requiring oxygen before the current hospitalizations, it seems likely that the hypoxemia and the elevated hemidiaphragm were temporally associated. In one patient previously reported by Cordero et al,6 the normalization of PaO2 (to 78 mm Hg on room air) and the shunt fraction (to 6%) when the hemidiaphragm paralysis was resolved established that the elevated hemidiaphragm encouraged the RLS through the PFO. In the second patient reported,5 intraoperative findings suggested "an anatomical displacement allowing the inferior vena cava to streamline through this septal opening." In our patient, although the hemidiaphragmatic dysfunction persisted, prompting the closure of the PFO as a strategy to improve oxygenation, we suspect that the same mechanism of the streaming of blood through a PFO induced by hemidiaphragm paralysis was at play.
As with the case of right-to-left shunting through a PFO following pneumonectomy, we are struck by the disproportionate association of the RLS with right-sided pathology. In the setting of pneumonectomy, our prior review7 showed that 16 of 17 reported cases of RLS with platypnea were associated with right pneumonectomy. In the setting of hemidiaphragm dysfunction, all three available reports (present case included) have involved dysfunction of the right hemidiaphragm. Given the proposed mechanism that shunting without a pressure gradient is due to the streaming of inferior vena caval blood that is encouraged by a shift of the interatrial septum,8 the right-sided predilection seems logical.
While our report extends the spectrum of causes for RLS through a PFO, it is important to recognize other settings in which such anatomic shunting has been described. Specifically, as presented in Table 1 , described causes include, for instance, right atrial myxoma, right ventricular infarction, and the effects of positive-pressure ventilation. Our experience reminds clinicians of yet another possible cause that should be considered when profound hypoxemia can be explained neither by vascular disease nor parenchymal lung disease.
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Footnotes |
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Received for publication January 26, 2001. Accepted for publication May 15, 2001.
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