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A 42-Year-Old Man Presenting With Progressive Shortness of Breath and Severe HypoxemiaMan With Shortness of Breath and Severe Hypoxemia FREE TO VIEW

Sameer Khanijo, MD; Seth Koenig, MD, FCCP
Author and Funding Information

From the Division of Pulmonary, Critical Care and Sleep Medicine, Hofstra North Shore-LIJ, New Hyde Park, NY.

CORRESPONDENCE TO: Sameer Khanijo, MD, Division of Pulmonary, Critical Care and Sleep Medicine, Hofstra North Shore-LIJ, New Hyde Park, NY; e-mail: khanijo2@nshs.edu


Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2015;147(3):e83-e85. doi:10.1378/chest.14-1416
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Published online

A 42-year-old man presented to the ED complaining of progressive shortness of breath over a few weeks and malaise, fatigue, nonproductive cough, and bilateral lower-extremity edema. His medical history included HIV (CD4 count, 302/mL), congestive heart failure, and pulmonary fibrosis. He denied fever, chills, sick contacts, and recent travel. The patient admitted to stopping his antiretroviral and diuretic medications approximately 1 month prior to presentation but was still taking warfarin, although he was unclear about why.

Physical examination revealed no signs of respiratory distress despite an oxygen saturation of 76% on room air, which increased to 84% on nonrebreather mask. The patient was afebrile, BP was 117/99 mm Hg, and heart rate was 87 beats/min. Jugular venous distension was present, and bilateral inspiratory crackles were heard on lung auscultation. Generalized edema was present, but clubbing of the fingers was absent. Arterial blood gas results on 100% oxygen revealed a pH of 7.30, Po2 of 53 mm Hg, and bicarbonate level of 26 mEq/L. The remainder of the patient’s laboratory results were significant for an elevated pro-brain natriuretic peptide level, an international normalized ratio of 2.4, and acute kidney injury. Chest radiography showed cardiomegaly and increased interstitial markings. The patient was placed on noninvasive positive pressure ventilation; however, his oxygen saturation worsened slightly. The medical ICU team evaluated the patient for severe hypoxemia and after a history and physical examination, performed a focused, goal-directed ultrasound study (Videos 1-6).

Videos 1-6.

Case Patient

Based upon the patient’s history, clinical exam thus far, and ultrasound images, what would be the best next bedside ultrasound procedure to perform to evaluate the cause of this patient’s hypoxemia?
Next steps: The best test would be a bubble study with echocardiography. This patient demonstrated a significant right to left shunt, after the administration of 10 mL of agitated saline, demonstrating a patent foramen ovale.

Videos 1-7.

Case Patient Discussion

The patient had severe hypoxemic respiratory failure and a history of both congestive heart failure and interstitial pulmonary fibrosis. However, specifics on the type of these conditions were lacking. Video 1 is a thoracic ultrasound revealing a bilateral B-line pattern without evidence of alveolar consolidation or pleural effusion,1 which was representative of both lungs. The lung sliding throughout the lung fields ruled out pneumothorax as the cause of the hypoxemia, and the B-lines appeared “lumpy-bumpy.”2 Copetti et al3 described these pleural line abnormalities as representative of noncardiogenic lung water. It was unclear whether these B-lines represented the patient’s known pulmonary fibrosis or another process, such as early ARDS; pneumonia; an inflammatory process; or simply cardiogenic pulmonary edema superimposed on the interstitial fibrosis. An infection seemed unlikely because the patient was not in respiratory distress, was afebrile, and had a normal WBC count without a left shift.

Standard goal-directed echocardiography (Videos 2-6) showed normal left ventricular contractility with a large right atrium and a right ventricle that was thickened, suggesting long-standing pulmonary hypertension. Video 2 is the parasternal long-axis view of the heart. Cardiac contractility appears normal without an obvious valvular abnormality. The right ventricular outflow tract is dilated, and the coronary sinus is quite enlarged. The coronary sinus is normally not visible or very small and drains blood from the thebesian veins into the right atrium. Although there are some rare causes of a visible coronary sinus, elevation of right atrial pressures is most common. No pericardial effusion is seen. Video 3 is the parasternal short-axis view of the heart at the level of the papillary muscles. This view shows flattening of the interventricular septum (IVS), mostly during diastole, and suggests an enlarged right ventricle. Flattening of the IVS mostly during diastole is a sign of volume overload of the right ventricle. Bowing of the IVS predominately in systole is due to pressure overload imposed on the left ventricle. As pulmonary hypertension worsens and progressive remodeling of the right ventricle ensues, contraction of the right ventricle shifts the IVS to move toward the left ventricle and creates the D sign. In this patient, we would have expected a D sign in systole. It is possible that the opening of the PFO decreased the systolic overload enough to remove the flattening of the IVS. The parasternal short-axis view also allows for estimation of overall contractility and observation of whether segmental wall motion abnormalities are present. Here, cardiac contractility is normal without wall motion abnormalities, and there is a small pericardial effusion. Videos 4 and 5 are the apical four-chamber views and demonstrate a significantly enlarged right atrium and a thickened right ventricle causing compression of the left-sided chambers. These echocardiographic images visually define acute to subacute cor pulmonale, which is produced by a sudden or subacute increase in the resistance to blood flow in the pulmonary circulation. Color Doppler echocardiography over the tricuspid valve revealed a large tricuspid regurgitation jet. Although Doppler is not a part of basic goal-directed echocardiography, its use to detect significant regurgitation is helpful and is an easily obtainable skill. A good subcostal image was unobtainable. Video 6 shows an enlarged inferior vena cava (IVC) without changes in size during respiratory variation. Although this patient was not in shock, IVC size often is used to estimate right atrial pressures.4 The patient’s IVC was > 2.5 cm in diameter and without respiratory variation, estimating his right atrial pressure to be 15 to 20 mm Hg.5

Because of the patient’s severe pulmonary hypertension, massively dilated right atrium, severe hypoxemia, and minimal respiratory symptoms, a right-to-left shunt due to PFO was suspected.6 Therefore, a bedside bubble study was performed. Video 7 is the apical four-chamber view after an injection of 10 mL agitated saline into a peripheral IV. Bubbles are visualized entering the right atrium. In a heart without a shunt, all the bubbles would enter the right ventricle and then be directed to the pulmonary circulation where they would dissipate without entering the pulmonary veins. However, in the present patient, bubbles are seen crossing from the right atrium into the left atrium and then through the mitral valve into the left ventricle, indicating the presence of a right-to-left shunt.

Transthoracic echocardiography with the injection of agitated saline is the gold standard for the detection of both intracardiac and intrapulmonary shunts.7 The bubble study is a quick bedside screening tool to aid in the evaluation of shunt and to help to differentiate intracardiac from intrapulmonary shunt. Intracardiac shunts will demonstrate almost immediate crossing of bubbles from the right side to the left side of the heart, whereas an intrapulmonary shunt will show a time delay of the bubbles in the right side of the heart until visualization in the left side of the heart. This is because of the time it takes the bubbles to traverse the pulmonary circulation, which is usually more than three heart beats.8 The present bubble study revealed an intracardiac shunt with almost immediate movement of bubbles from the right atrium to the left atrium, thereby demonstrating that blood flow was bypassing pulmonary circulation and oxygenation. Noninvasive positive pressure ventilation may worsen or even create an intracardiac shunt (ie, opening up a patent foramen) by increasing the afterload on the right ventricle, thereby increasing right atrial pressure and its driving force across the intraatrial septum.9 We believe that the use of noninvasive ventilation in this patient caused the worsening of his hypoxemia because of the increased shunt across the PFO, which was reversed when the nonrebreather mask was used.

Other causes of increased right ventricular afterload were sought. The patient was on warfarin, which was subsequently confirmed to be for known severe pulmonary hypertension secondary to HIV. He had a normal lower-extremity compression study with a therapeutic international normalized ratio, making a pulmonary embolism unlikely. Worsening of his underlying interstitial fibrosis or an infection was possible, but no respiratory distress was present, and the patient admitted to noncompliance with most of his medications, including furosemide. The patient was started on aggressive diuresis with subsequent improvement in both renal function and hypoxemia. He was ultimately titrated from 100% nonrebreather mask to nasal cannula with preservation of oxygen saturation. We believe that the patient’s nonadherence to diuretics led to volume overload, which caused significant right atrial enlargement that worsened his PFO, thereby increasing his hypoxemia.

  • 1. Integrating both lung ultrasound and goal-directed echocardiography allows for rapid evaluation of hypoxemia.

  • 2. When signs of right ventricle pressure, volume overload, or both are present, a bubble study may identify an intracardiac or intrapulmonary shunt as the primary etiology of hypoxemia or, more commonly, in concert with other pulmonary processes.

  • 3. Positive pressure ventilation may worsen hypoxemia due to intracardiac shunt.

Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Other contributions: CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met.

Additional information: To analyze this case with the videos, see the online version of this article.

Lichtenstein D, Mézière G, Biderman P, Gepner A, Barré O. The comet-tail artifact. An ultrasound sign of alveolar-interstitial syndrome. Am J Respir Crit Care Med. 1997;156(5):1640-1646. [CrossRef] [PubMed]
 
Lichtenstein DA, Menu Y. A bedside ultrasound sign ruling out pneumothorax in the critically ill. Lung sliding. Chest. 1995;108(5):1345-1348. [CrossRef] [PubMed]
 
Copetti R, Soldati G, Copetti P. Chest sonography: a useful tool to differentiate acute cardiogenic pulmonary edema from acute respiratory distress syndrome. Cardiovasc Ultrasound. 2008;6(4):16. [CrossRef] [PubMed]
 
Schmidt GA, Koenig S, Mayo PH. Shock: ultrasound to guide diagnosis and therapy. Chest. 2012;142(4):1042-1048. [CrossRef] [PubMed]
 
Kircher BJ, Himelman RB, Schiller NB. Noninvasive estimation of right atrial pressure from the inspiratory collapse of the inferior vena cava. Am J Cardiol. 1990;66(4):493-496. [CrossRef] [PubMed]
 
Gomperts N, Fowler R, Horlick E, McLaughlin P. A broken heart: right-to-left shunt in the setting of normal cardiac pressures. Can J Cardiol. 2008;24(3):227-229. [CrossRef] [PubMed]
 
Gill EA Jr, Quaife RA. The echocardiographer and the diagnosis of patent foramen ovale. Cardiol Clin. 2005;23(1):47-52. [CrossRef] [PubMed]
 
Woods TD, Patel A. A critical review of patent foramen ovale detection using saline contrast echocardiography: when bubbles lie. J Am Soc Echocardiogr. 2006;19(2):215-222. [CrossRef] [PubMed]
 
Ravenscraft SA, Marinelli WA, Johnson T, Henke CA. Profound hypoxemia precipitated by positive end-expiratory pressure: induction of an intracardiac shunt. Crit Care Med. 1992;20(3):434-436. [CrossRef] [PubMed]
 

Figures

Tables

Videos 1-6.

Case Patient

Videos 1-7.

Case Patient Discussion

References

Lichtenstein D, Mézière G, Biderman P, Gepner A, Barré O. The comet-tail artifact. An ultrasound sign of alveolar-interstitial syndrome. Am J Respir Crit Care Med. 1997;156(5):1640-1646. [CrossRef] [PubMed]
 
Lichtenstein DA, Menu Y. A bedside ultrasound sign ruling out pneumothorax in the critically ill. Lung sliding. Chest. 1995;108(5):1345-1348. [CrossRef] [PubMed]
 
Copetti R, Soldati G, Copetti P. Chest sonography: a useful tool to differentiate acute cardiogenic pulmonary edema from acute respiratory distress syndrome. Cardiovasc Ultrasound. 2008;6(4):16. [CrossRef] [PubMed]
 
Schmidt GA, Koenig S, Mayo PH. Shock: ultrasound to guide diagnosis and therapy. Chest. 2012;142(4):1042-1048. [CrossRef] [PubMed]
 
Kircher BJ, Himelman RB, Schiller NB. Noninvasive estimation of right atrial pressure from the inspiratory collapse of the inferior vena cava. Am J Cardiol. 1990;66(4):493-496. [CrossRef] [PubMed]
 
Gomperts N, Fowler R, Horlick E, McLaughlin P. A broken heart: right-to-left shunt in the setting of normal cardiac pressures. Can J Cardiol. 2008;24(3):227-229. [CrossRef] [PubMed]
 
Gill EA Jr, Quaife RA. The echocardiographer and the diagnosis of patent foramen ovale. Cardiol Clin. 2005;23(1):47-52. [CrossRef] [PubMed]
 
Woods TD, Patel A. A critical review of patent foramen ovale detection using saline contrast echocardiography: when bubbles lie. J Am Soc Echocardiogr. 2006;19(2):215-222. [CrossRef] [PubMed]
 
Ravenscraft SA, Marinelli WA, Johnson T, Henke CA. Profound hypoxemia precipitated by positive end-expiratory pressure: induction of an intracardiac shunt. Crit Care Med. 1992;20(3):434-436. [CrossRef] [PubMed]
 
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