scholarly journals P1317 Very late onset of platypnoea orthodeoxia syndrome as first clinical scenario of patent foramen ovale

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
S M Binno ◽  
L Moderato ◽  
G Pastorini ◽  
B Matrone ◽  
D Aschieri ◽  
...  

Abstract We report a case of a 83-year-old female, who had an admission for dyspnea. Laboratory showed D-dimer 1000 ng/ml, haemoglobin 12.4 mg/dL, CPR 0.08mg/dl whereas on Arterial Blood Gas test she had hypoxia with respiratory alkalosis. In view of suspected pulmonary embolism, she underwent Thoracic Computed Tomography scan that excluded it. During the stay the patient seemed more symptomatic while in standing position(with SpO2s 89% while supine plunging to 50% while standing): ABGs were performed both standing (reservoir 15 l/min pH 7.50, pO2 37.2 mmHg, pCO2 37.1 mmHg, HCO3 28.9 mmol/l) and recumbent position (reservoir 15 l/min pH 7.47, pO2 65.5 mmHg, pCO2 35.1 mmHg, HCO3 25.6 mmol), showing a difference of 28 mmHg. Subsequently the patient underwent v/p pulmonary scintigraphy: no signs of pulmonary embolism though it revealed a multiple focus of capitation Tc-99m macro aggregated albumin in brain, thyroid and kidneys (IMG top), compatible for veno-arterial shunt. Trans-esophageal echocardiography (TOE) revealed a massive stretched patent foramen ovale (PFO) with continuous right-to-left shunting through the atria. The bubble test (IMG bottom) confirmed the presence of patency along with sudden passage of microbubbles through the foramen. Qp/Qs = 0.8, due to volume overload in the left atrium from the right atrium. The imaging along with clinical scenario confirmed the suspected diagnosis of platypnea-orthodeoxia, finding the patent foramen ovale as the anatomical cause. Platypnea-orthodeoxia syndrome is a clinical condition characterized by dyspnea. Typically blood oxygen saturation declines with standing position while it resolves with recumbent. The classification entails 3 groups: intracardiac shunting (most common presentation), pulmonary shunting, ventilation-perfusion mismatch. Presence of multiple focus of albumin macroaggregates outside the lungs in v/p scintigraphy examination is suggestive for veno-arteriuous shunt: without shunt, normally all the albumin aggregates are hampered in the lungs’ field. Images in bottom are taken in sequence from a single acquisition during the TOE, in one single cardiac beat. Here is depicted the evidence of the PFO, the influx of bubbles in the right atrium and the instantaneous and massive shunt of the bubbles across the interatrial septum, in the left atrium. Usually the diagnosis is performed within 55 years old: it is interesting how late the diagnosis occurred in this patient with such resounding clinical manifestation. Top Scintigraphy with ventilation and perfusion lung scan sequences. Next, scintigraphy with capitation of Tc-99m macro aggregated albumin in brain, thyroid and kidneys. Bottom, Transesophageal echocardiogram: images taken within the same heart beat proving right-to-left passage of bubble across the septum. Abstract P1317 Figure. Scintigraphy and Transesophageal echo

ESC CardioMed ◽  
2018 ◽  
pp. 2756-2758
Author(s):  
Dieuwertje Ruigrok ◽  
Anton Vonk Noordegraaf

Acute right ventricular (RV) failure and impaired gas exchange (mainly hypoxaemia) can be two important issues clinicians are confronted with in patients with acute pulmonary embolism. An acute increase in RV afterload due to mechanical obstruction and vasoconstriction is the crucial factor starting a cascade with compensatory mechanisms, RV dilatation, RV ischaemia, and inflammation ultimately leading to RV dysfunction/failure. On the other hand, vascular occlusion leads to redistribution of pulmonary perfusion to regions with relative overperfusion causing profound hypoxaemia. Less commonly, shunting occurs due to atelectasis or due to opening of a patent foramen ovale, causing refractory hypoxaemia. Understanding these mechanisms is crucial in making the right treatment decisions when faced with a patient with acute pulmonary embolism and haemodynamic or respiratory instability.


2007 ◽  
Vol 25 (3) ◽  
pp. 297-299 ◽  
Author(s):  
Zehra Bugra ◽  
Dilek Hunerel ◽  
Yelda Tayyareci ◽  
Ozcan Ruzgar ◽  
Sabahattin Umman ◽  
...  

2021 ◽  
Vol 28 (2) ◽  
pp. 50-57
Author(s):  
V. I. Tseluyko ◽  
L. M. Yakovleva ◽  
S. M. Sukhova ◽  
O. V. Radchenko ◽  
T. V. Pylova ◽  
...  

The aim – to study the relationship between the level of NT-proBNP, clinical-anamnestic and echocardiographic parameters in patients with pulmonary embolism (PE).Materials and methods. The study was carried out on 45 patients with PE, which was confirmed by computed tomo­­graphy. An echocardiographic study was carried out during hospitalization of patients according to the standard protocol. The examination plan of patients, along with standard laboratory tests, included the determination of the level of highly sensitive troponin I, C-reactive peptide (CRP) and NT-proBNP.Results and discussion. The level of NT-proBNP is increased in patients with PE, even in the absence of heart failure (2932±266 pg/ml). There were no significant differences in the level of the indicator depending on the gender of patients (p=0.3), on the presence of arterial hypertension (p=0.92) and the concomitant oncological process (p=0.88). A correlation was found between NT-proBNP level and the size of the right and left atrium: right atrium (p=0.014), left atrium (p=0.025). The relationship between the level of NT-proBNP and the pressure in the pulmonary artery according to ultrasound data was proved (in patients with PE without signs of pulmonary hypertension, the level of NT-proBNP is 405 pg/ml, versus 4067 pg/ml in the group of patients with increased pressure in the pulmonary artery (p=0.0047). A correlation was found between the levels of NT-proBNP and CRP.Conclusions. There is a significant increase in the level of NT-proBNP in patients with PE, the degree of which correlates with an increase in the size of the right atrium and pressure in the pulmonary artery (p=0.0047).


Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 3673-3673
Author(s):  
Payal C. Desai ◽  
Nicole Kendel ◽  
Melanie Heinlein ◽  
Ying Huang ◽  
Eric H. Kraut ◽  
...  

Abstract Introduction: During an episode of vaso-occlusive crisis, some patients with sickle cell disease may develop a transient hypoxemia. While frequently attributed to acute chest syndrome or pulmonary embolism, clinically a portion of patients develop hypoxemia without a clear etiology. On echocardiography, some patients were noted to have Patent Foramen Ovale (PFO) and others were noted to have intrapulmonary shunting. We sought to further characterize this clinical finding in sickle cell patients. Methods: We conducted a single institution retrospective chart review from 2008 through 2015 to evaluate the incidence of pulmonary shunting and PFOs in patients with SCD, as demonstrated on an echocardiography. We further characterize each of these episodes with clinical and laboratory findings at the time of the event. The presence of absence of shunting and type of shunting was further verified by a single cardiologist reviewing all episodes. Kruskal-Wallis test or Fisher's exact test was used to compare characteristics between patients with intracardiac or intrapulmonary shunting. Results: A total of 36 (18 female (F), 18 male (M)) of the 352 (10%) patients seen at the Ohio State Comprehensive Sickle Cell Center were noted to have shunting on their echocardiogram reported over the 7 year time period. Independent review by cardiology confirmed the presence of a shunt in 32 patients (9%, 95% CI: 6-13%) (15F, 17M). The median age at the time of reporting was 29 (range: 18-51 yrs). Shunting was observed in patients of all genotypes (94% SS/SB0; 6% SC/SBeta+). Fourteen (6 F, 8 M) of the thirty-two (44%, 95% CI: 26-62%) patients under study were noted to have cardiac shunting and eighteen (9 F, 9 M) (56%, 95% CI: 38-74%) were noted to have pulmonary shunting. In the patients with cardiac shunting, all 14/14 were confirmed to have a PFO by independent cardiac review. At the time of echo, 27/32 (87%) were hospitalized and 19/32 (59%) had clinical hypoxia on the day of the echocardiography. Patients with cardiac shunting tended to have higher proportion of hypoxia compared with patients with pulmonary shunting (71% vs. 50%). 19/32 (59%) had concurrent CT angiography and 1/32 (5%) patients was confirmed to have a pulmonary embolism. This patient demonstrated a concurrent PFO. 9 (28%) had a concurrent diagnosis of acute chest syndrome (4 with cardiac shunting and 5 with pulmonary shunting). The median value of TR jet velocity at baseline was 2.64 (range: 2.0-4.0) (n=18) and the median TR jet velocity at the time of event was 2.67 m/s (range: 2.0-3.8 m/s) (n=27). In the cardiac shunting group, the TR jet velocity was 2.85 m/s (range: 2.0 -3.27m/s) and in the pulmonary shunting group, the TR jet velocity was 2.6 m/s (range: 2.2-3.8 m/s). Conclusion: Patients with SCD presenting with increasing hypoxia may have intracardiac or intrapulmonary shunting. A patent foramen ovale that opens during vaso-ossclusive crisis may cause transient hypoxemia. This opening is thought to be due to increasing pulmonary pressures. While the long term implications of this finding are currently being studied, intracardiac shunting should be considered in the differential of patients with SCD presenting with increasing hypoxia of unclear etiology. Disclosures No relevant conflicts of interest to declare.


2000 ◽  
Vol 26 (9) ◽  
pp. 1401-1402 ◽  
Author(s):  
D. Matamis ◽  
A. Karasakalides ◽  
A. Vakalos ◽  
M. Rali ◽  
D. Riggos

Author(s):  
Chadi Allam ◽  
Zeina Kadri ◽  
Rabih Azar

An 86-year-old man with end-stage renal disease on hemodialysis with an arteriovenous fistula in his left upper extremity presented to his hemodialysis session with thrombosis of his arteriovenous fistula. The patient underwent surgical thrombectomy. The patient later showed evidence of peripheral embolization and livedo reticularis. Transthoracic and transesophageal echocardiograms revealed a large thrombus (5x2 cm) in the left atrium prolapsing to the right atrium via a patent foramen ovale and another thrombus (white arrow) adherent to the apical wall of the right ventricle. The thrombus in the left atrium was intermittently crossing the mitral valve and entering the left ventricle.


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