Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Pulmonary Veno-Occlusive Disease Workup

  • Author: Hakim Azfar Ali, MD; Chief Editor: Ryland P Byrd, Jr, MD  more...
 
Updated: Apr 01, 2016
 

Approach Considerations

Pulmonary veno-occlusive disease (PVOD) should be suspected in patients who have been diagnosed with pulmonary arterial hypertension (PAH) but who have radiographic findings suggestive of left-sided heart failure. The diagnosis is based on clinical and radiographic findings. Surgical or transbronchial biopsy should not be performed secondary to the very high rate of complications, including death.

Most patients with PVOD present with progressive dyspnea upon exertion.[37] Often, right-sided heart failure is initially suspected (owing to edema, jugular venous distention, a loud P2 sound, and hypoxemia) or left-sided heart failure is considered (secondary to radiographic findings of bilateral pulmonary infiltrates and Kerley B lines).

When these patients are evaluated using echocardiography or right-sided heart catheterization, the diagnosis of pulmonary hypertension is confirmed but their wedge pressure (if the pulmonary artery catheter is properly wedged) is within normal limits. In summary, PVOD is currently recognized based on 1 of 2 sets of findings, as follows (see Table 1, below):

  • The patient is diagnosed with pulmonary arterial hypertension (PAH) but a review of the chest radiograph and CT scan raises the suggestion of pulmonary edema.
  • The patient is diagnosed with suspected pulmonary edema but echocardiography or right-sided heart catheterization reveals pulmonary hypertension.

Table 1. Distinguishing Pulmonary Edema From PVOD Based on Radiographic, Echocardiographic, and Heart Catheterization Data (Open Table in a new window)

Features Pulmonary Edema PVOD
Chest radiograph    
Kerley B lines Present Present
Pleural effusion Usually present May be present
Enlarged cardiac silhouette Present Less prominent
Enlarged pulmonary artery Present Present
Chest CT scan    
Thickened septae Present Present
Pleural effusion Usually present May be present
Enlarged heart Present Less prominent
Enlarged pulmonary artery Present Present
Septal concavity into left ventricle Absent Present
Echocardiogram    
Pulmonary artery systolic pressure Elevated (usually not >80 mm Hg) Elevated (may be >80 mm Hg)
Left atrial enlargement Present Absent
Right atrial enlargement Present Present
Right ventricular hypertrophy Absent Present
Paradoxical septal motion Absent Present
Large pericardial effusion Absent May be present
Right-sided heart catheterization    
Pulmonary vascular resistance Below 3.0 Wood units Above 3.0 Wood units
Pulmonary capillary wedge pressure Above 18 mm Hg Usually below 15 mm Hg



(if catheter is properly wedged)



Mean pulmonary artery pressure Elevated (almost never >50 mm Hg) Elevated (may be >50 mm Hg)
Cardiac output May be normal, low, or high Mostly decreased, may be low normal
Oxyhemoglobin step-up Absent Absent

Lab studies

Laboratory parameters are generally unremarkable and not helpful in the diagnostic workup, although microangiopathic hemolytic anemia, proteinuria, and elevations in serum immunoglobulin G and M concentrations have been reported. Note, however, that laboratory results are more abnormal in cases of PVOD associated with autoimmune disease. The level of brain natriuretic peptide is expected to be high in patients with overt right-sided heart failure.

Pulmonary function tests

The single-breath diffusing capacity for carbon monoxide (DLCO) is usually reduced in persons with PVOD. A restrictive ventilatory defect has also been reported in many cases. However, the decrease in DLCO is usually out of proportion to the degree of restrictive or obstructive abnormality.

Next

Echocardiography

An echocardiogram is an extremely useful initial noninvasive tool to assess right-sided pressures and to rule out left ventricular abnormalities and valvular heart disease.

Previous
Next

Chest Radiography

The most common chest radiography finding in pulmonary veno-occlusive disease (PVOD) is the presence of interstitial infiltrates. Kerley B lines similar to those associated with pulmonary edema may be seen as a result of interstitial edema and enlargement of pulmonary lymphatic channels. Central pulmonary arteries may be enlarged, as in other causes of pulmonary hypertension, and scattered, patchy opacities may be present. Pleural effusion may be present and is mostly right sided. However, the absence of these radiographic abnormalities does not exclude the condition.[38]

Previous
Next

CT Scanning

CT scanning commonly reveals septal thickening and diffuse or patchy ground-glass opacities.[39] The presence of subpleural septal thickening (observed in 93% of cases) and diffuse, ill-defined, centrilobular ground-glass opacities (observed in 73% of cases) is highly suggestive of PVOD in patients with pulmonary hypertension. Other findings on CT scans include small nodules, dependent areas of consolidation, lymphadenopathy, and pleural effusions. The association of ill-defined nodules, septal thickening, and lymphadenopathy should raise the suggestion of a diagnosis of PVOD. (See the image below.)[40, 41]

Pulmonary veno-occlusive disease in a 43-year-old Pulmonary veno-occlusive disease in a 43-year-old man. An axial computed tomography (CT) scan (lung window level) shows multiple septal lines (arrowhead) and a dilated central pulmonary artery (arrow). Image courtesy of Thoracic Imaging Section, Department of Radiologic Pathology, Armed Forces Institute of Pathology.

The ground-glass attenuation may result from alveolar septal thickening and epithelial hyperplasia. The central pulmonary veins and the left atrium are not enlarged, in contrast to patients with mitral stenosis, cor triatriatum, or left atrial myxoma.[42] Pericardial effusion may be present in patients with advanced right-sided heart failure. Enlarged pulmonary arteries resulting from pulmonary hypertension are almost universal.

Previous
Next

Selective Pulmonary Artery Angiogram

This study may be helpful in ruling out chronic pulmonary thromboembolic disease, but it is rarely needed. A ventilation-perfusion scan is generally sufficient to clinically exclude significant or, more precisely, operable, chronic pulmonary thromboembolic disease.

A selective pulmonary artery angiogram in a patient with suspected pulmonary veno-occlusive disease (PVOD) offers very little additional clinically relevant information when ventilation-perfusion scan findings are normal or show a low probability for chronic pulmonary thromboembolic disease or in patients who are not suitable candidates for pulmonary thromboendarterectomy, even if they were diagnosed with chronic pulmonary thromboembolic disease.[43]

Previous
Next

Ventilation-Perfusion Scanning

In patients with pulmonary veno-occlusive disease (PVOD), abnormal ventilation-perfusion scan findings are not unusual. The scan may reveal focal areas of hypoperfusion, which may lead to a misdiagnosis of chronic thromboembolic pulmonary hypertension. A high-probability ventilation-perfusion scan in a patient with pulmonary hypertension does not always indicate a proximal pulmonary arterial process.

The reported ventilation-perfusion scan findings have also included (1) diffuse, patchy distribution of tracer material without clear segmental or subsegmental defects and (2) a unilateral absence of perfusion due to severe, asymmetrical involvement. The type of defect may vary depending on the size and location of the involved veins.[44]

Previous
Next

Cardiac Catheterization

Interestingly, a clue to the diagnosis of pulmonary veno-occlusive disease (PVOD) is the inability to accurately measure the wedge pressure during cardiac catheterization. Multiple wedge pressure measurements or a distal wedge reading confirmed by a partial pressure of oxygen similar to arterial blood should be performed to determine the correct wedge pressure.

A correctly performed pulmonary capillary wedge pressure measurement generally reveals normal or decreased wedge pressure, despite the fact that the pulmonary capillary pressures (in the absence of a static blood column) are elevated. Occasionally, an elevated wedge pressure may be obtained, depending on the degree of venous occlusion and collaterals. This may occur because of the patency of the larger pulmonary veins.[29]

In PVOD, the use of a short-acting pulmonary arterial vasodilator, such as inhaled nitric oxide or intravenous epoprostenol or adenosine, during acute vasoreactivity testing may precipitate acute pulmonary edema. The edema results from increased transcapillary hydrostatic pressures in the setting of acute arterial vasodilation and preexisting venous occlusion. The development of pulmonary edema in response to a pulmonary vasodilator, therefore, is strongly suggestive of the diagnosis of PVOD.[45] This complication in association with the poor response of PVOD patients to PAH-specific therapy argues against vasodilator testing in patients in whom PVOD is strongly suspected.

The development of acute fulminant pulmonary edema, and even death, has been reported with infusion of even a very low dose of intravenous epoprostenol. Hence, great caution should be used in patients with suspected PVOD while administering intravenous epoprostenol.[46]

Previous
Next

Bronchoscopic Examination

Bronchoscopy does not have a major role in the management of PVOD but it may be performed to rule out other lung diseases in cases of an atypical presentation. Hyperemia of the small airway mucosa with vascular engorgement in the form of bright red, longitudinal streaks has been reported. The trachea and main bronchi may be spared because the venous drainage of the central airways is into bronchial veins, which are not involved. Bronchoalveolar lavage may suggest chronic alveolar hemorrhage.

Transbronchial lung biopsy is contraindicated because of the presence of pulmonary hypertension and the risk of excessive bleeding.

Previous
Next

Surgical Lung Biopsy

Surgical lung biopsy in the presence of moderate or severe pulmonary arterial hypertension (PAH) is associated with a significant risk of morbidity and mortality. Although this is a somewhat controversial issue, a surgical lung biopsy in patients with suspected pulmonary veno-occlusive disease (PVOD) also carries a serious risk of morbidity and mortality, particularly in the setting of high pulmonary vascular pressure.[47] Moreover, the results of the biopsy rarely affect PVOD treatment.

Some experts who favor biopsy argue that it provides prognostic information that facilitates decision making with regard to the timing of lung transplantation listing. In the authors’ opinion, however, the risk of surgical lung biopsy outweighs the value and usefulness of the information obtained. Alternative means of assessment, such as CT scan findings and observation of the patient (to determine whether there has been a lack of improvement or continued clinical worsening despite specific PAH therapies), may be used to make decisions about the listing for and timing of lung transplantation.

Previous
 
 
Contributor Information and Disclosures
Author

Hakim Azfar Ali, MD Consultant in Pulmonary and Critical Care Medicine, Christiana Care Hospital

Hakim Azfar Ali, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Thoracic Society, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Shoaib Alam, MD Staff Clinician, Pulmonary and Vascular Medicine, National Heart, Lung, and Blood Institute, National Institutes of Health

Shoaib Alam, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society, Society of Critical Care Medicine, International Society for Magnetic Resonance in Medicine, European Respiratory Society, Pennsylvania Thoracic Society

Disclosure: Nothing to disclose.

Chief Editor

Ryland P Byrd, Jr, MD Professor of Medicine, Division of Pulmonary Disease and Critical Care Medicine, James H Quillen College of Medicine, East Tennessee State University

Ryland P Byrd, Jr, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Acknowledgements

Stephen P Peters, MD, PhD, FACP, FAAAAI, FCCP, FCPP Professor of Genomics and Personalized Medicine Research, Internal Medicine, and Pediatrics, Associate Director, Center for Genomics and Personalized Medicine Research, Director of Research, Section on Pulmonary, Critical Care, Allergy and Immunologic Diseases, Wake Forest University School of Medicine

Stephen P Peters, MD, PhD, FACP, FAAAAI, FCCP, FCPP is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Association of Immunologists, American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Thoracic Society, and Sigma Xi

Disclosure: See below for list of all activities None None

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
  1. Rounds S, Cutaia MV. Pulmonary hypertension: Pathophysiology and clinical disorders. Baum GL, Crapo JD, Celli BR, Karlinsky JB, eds. Textbook of Pulmonary Diseases. Philadelphia, Pa: Lippincott-Raven; 1998. 1273-95.

  2. Wagenvoort CA. Lung biopsy specimens in the evaluation of pulmonary vascular disease. Chest. 1980 May. 77(5):614-25. [Medline].

  3. Thadani U, Burrow C, Whitaker W, et al. Pulmonary veno-occlusive disease. Q J Med. 1975 Jan. 44(173):133-59. [Medline].

  4. Wagenvoort CA. Pulmonary veno-occlusive disease. Entity or syndrome?. Chest. 1976 Jan. 69(1):82-6. [Medline].

  5. Hora J. Zur Histologie der klinischen "primaren Pulmonalsklerose". Frankfurt Z Pathol. 1934. 47:100-08.

  6. Shackelford GD, Sacks EJ, Mullins JD, et al. Pulmonary venoocclusive disease: case report and review of the literature. AJR Am J Roentgenol. 1977 Apr. 128(4):643-8. [Medline].

  7. De Vries TW, Weening JJ, Roorda RJ. Pulmonary veno-occlusive disease: a case report and a review of therapeutic possibilities. Eur Respir J. 1991 Sep. 4(8):1029-32. [Medline].

  8. Chazova I, Robbins I, Loyd J, et al. Venous and arterial changes in pulmonary veno-occlusive disease, mitral stenosis and fibrosing mediastinitis. Eur Respir J. 2000 Jan. 15(1):116-22. [Medline].

  9. Wagenvoort CA, Wagenvoort N, Takahashi T. Pulmonary veno-occlusive disease: involvement of pulmonary arteries and review of the literature. Hum Pathol. 1985 Oct. 16(10):1033-41. [Medline].

  10. Lathen C, Zhang Y, Chow J, Singh M, Lin G, Nigam V, et al. ERG-APLNR axis controls pulmonary venule endothelial proliferation in pulmonary veno-occlusive disease. Circulation. 2014 Sep 30. 130(14):1179-91. [Medline]. [Full Text].

  11. Dai Z, Matsui Y. Pulmonary veno-occlusive disease: an 80-year-old mystery. Respiration. 2014. 88(2):148-57. [Medline].

  12. Sanderson JE, Spiro SG, Hendry AT, et al. A case of pulmonary veno-occlusive disease respondong to treatment with azathioprine. Thorax. 1977 Apr. 32(2):140-8. [Medline].

  13. Kishida Y, Kanai Y, Kuramochi S, et al. Pulmonary venoocclusive disease in a patient with systemic lupus erythematosus. J Rheumatol. 1993 Dec. 20(12):2161-2. [Medline].

  14. Zhang L, Visscher D, Rihal C, et al. Pulmonary veno-occlusive disease as a primary cause of pulmonary hypertension in a patient with mixed connective tissue disease. Rheumatol Int. 2007 Oct. 27(12):1163-5. [Medline].

  15. Morassut PA, Walley VM, Smith CD. Pulmonary veno-occlusive disease and the CREST variant of scleroderma. Can J Cardiol. 1992 Dec. 8(10):1055-8. [Medline].

  16. Johnson SR, Patsios D, Hwang DM, et al. Pulmonary veno-occlusive disease and scleroderma associated pulmonary hypertension. J Rheumatol. 2006 Nov. 33(11):2347-50. [Medline].

  17. McDonnell PJ, Summer WR, Hutchins GM. Pulmonary veno-occlusive disease. Morphological changes suggesting a viral cause. JAMA. 1981 Aug 7. 246(6):667-71. [Medline].

  18. Escamilla R, Hermant C, Berjaud J, et al. Pulmonary veno-occlusive disease in a HIV-infected intravenous drug abuser. Eur Respir J. 1995 Nov. 8(11):1982-4. [Medline].

  19. Davies P, Reid L. Pulmonary veno-occlusive disease in siblings: case reports and morphometric study. Hum Pathol. 1982 Oct. 13(10):911-5. [Medline].

  20. Voordes CG, Kuipers JR, Elema JD. Familial pulmonary veno-occlusive disease: a case report. Thorax. 1977 Dec. 32(6):763-6. [Medline].

  21. Runo JR, Vnencak-Jones CL, Prince M, et al. Pulmonary veno-occlusive disease caused by an inherited mutation in bone morphogenetic protein receptor II. Am J Respir Crit Care Med. 2003 Mar 15. 167(6):889-94. [Medline].

  22. Joselson R, Warnock M. Pulmonary veno-occlusive disease after chemotherapy. Hum Pathol. 1983 Jan. 14(1):88-91. [Medline].

  23. Knight BK, Rose AG. Pulmonary veno-occlusive disease after chemotherapy. Thorax. 1985 Nov. 40(11):874-5. [Medline].

  24. Liu L, Sackler JP. A case of pulmonary veno-occlusive disease: Etiological and therapeutic appraisal. Angiology. 1973. 23:299-304.

  25. Williams LM, Fussell S, Veith RW, et al. Pulmonary veno-occlusive disease in an adult following bone marrow transplantation. Case report and review of the literature. Chest. 1996 May. 109(5):1388-91. [Medline].

  26. Hosokawa K, Yamazaki H, Nishitsuji M, Kobayashi S, Takami A, Fujimura M, et al. Pulmonary Veno-occlusive Disease Following Reduced-intensity Allogeneic Bone Marrow Transplantation for Acute Myeloid Leukemia. Intern Med. 2012. 51(2):195-8. [Medline].

  27. Kramer MR, Estenne M, Berkman N, et al. Radiation-induced pulmonary veno-occlusive disease. Chest. 1993 Oct. 104(4):1282-4. [Medline].

  28. Cassart M, Gevenois PA, Kramer M, et al. Pulmonary venoocclusive disease: CT findings before and after single-lung transplantation. AJR Am J Roentgenol. 1993 Apr. 160(4):759-60. [Medline].

  29. Mandel J, Mark EJ, Hales CA. Pulmonary veno-occlusive disease. Am J Respir Crit Care Med. 2000 Nov. 162(5):1964-73. [Medline].

  30. Wagenvoort CA, Losekoot G, Mulder E. Pulmonary veno-occlusive disease of presumably intrauterine origin. Thorax. 1971 Jul. 26(4):429-34. [Medline].

  31. Cohn RC, Wong R, Spohn WA, et al. Death due to diffuse alveolar hemorrhage in a child with pulmonary veno-occlusive disease. Chest. 1991 Nov. 100(5):1456-8. [Medline].

  32. Rabiller A, Jais X, Hamid A, et al. Occult alveolar haemorrhage in pulmonary veno-occlusive disease. Eur Respir J. 2006 Jan. 27(1):108-13. [Medline].

  33. Rosenthal A, Vawter G, Wagenvoort CA. Intrapulmonary veno-occlusive disease. Am J Cardiol. 1973 Jan. 31(1):78-83. [Medline].

  34. Glassroth J, Woodford DW, Carrington CB, et al. Pulmonary veno-occlusive disease in the middle-aged. Respiration. 1985. 47(4):309-21. [Medline].

  35. Bolster MA, Hogan J, Bredin CP. Pulmonary vascular occlusive disease presenting as sudden death. Med Sci Law. 1990 Jan. 30(1):26-8. [Medline].

  36. Swensen SJ, Tashjian JH, Myers JL, et al. Pulmonary venoocclusive disease: CT findings in eight patients. AJR Am J Roentgenol. 1996 Oct. 167(4):937-40. [Medline].

  37. Laveneziana P, Montani D, Dorfmuller P, Girerd B, Sitbon O, Jais X, et al. Mechanisms of exertional dyspnoea in pulmonary veno-occlusive disease with EIF2AK4 mutations. Eur Respir J. 2014 Oct. 44(4):1069-72. [Medline].

  38. Holcomb BW Jr, Loyd JE, Ely EW, et al. Pulmonary veno-occlusive disease: a case series and new observations. Chest. 2000 Dec. 118(6):1671-9. [Medline].

  39. Maltby JD, Gouverne ML. CT findings in pulmonary venoocclusive disease. J Comput Assist Tomogr. 1984 Aug. 8(4):758-61. [Medline].

  40. Resten A, Maitre S, Capron F, et al. [Pulmonary hypertension: CT findings in pulmonary veno-occlusive disease]. J Radiol. 2003 Nov. 84(11 Pt 1):1739-45. [Medline].

  41. Gunther S, Jais X, Maitre S, Berezne A, Dorfmuller P, Seferian A, et al. Computed tomography findings of pulmonary veno-occlusive disease in scleroderma patients presenting with precapillary pulmonary hypertension. Arthritis Rheum. 2012 May 1. [Medline].

  42. Dufour B, Maitre S, Humbert M, et al. High-resolution CT of the chest in four patients with pulmonary capillary hemangiomatosis or pulmonary venoocclusive disease. AJR Am J Roentgenol. 1998 Nov. 171(5):1321-4. [Medline].

  43. Seferian A, Helal B, Jais X, Girerd B, Price LC, Gunther S, et al. Ventilation perfusion lung scan in pulmonary veno-occlusive disease. Eur Respir J. 2011 Nov 16. [Medline].

  44. Bailey CL, Channick RN, Auger WR, et al. "High probability" perfusion lung scans in pulmonary venoocclusive disease. Am J Respir Crit Care Med. 2000 Nov. 162(5):1974-8. [Medline].

  45. Rubin LJ. Primary pulmonary hypertension. N Engl J Med. 1997 Jan 9. 336(2):111-7. [Medline].

  46. Ogawa A, Miyaji K, Yamadori I, Shinno Y, Miura A, Kusano KF, et al. Safety and Efficacy of Epoprostenol Therapy in Pulmonary Veno-Occlusive Disease and Pulmonary Capillary Hemangiomatosis. Circ J. 2012 Apr 5. [Medline].

  47. Nicod P, Moser KM. Primary pulmonary hypertension. The risk and benefit of lung biopsy. Circulation. 1989 Nov. 80(5):1486-8. [Medline].

  48. Izbicki G, Shitrit D, Schechtman I, et al. Recurrence of pulmonary veno-occlusive disease after heart-lung transplantation. J Heart Lung Transplant. 2005 May. 24(5):635-7. [Medline].

  49. Palmer SM, Robinson LJ, Wang A, et al. Massive pulmonary edema and death after prostacyclin infusion in a patient with pulmonary veno-occlusive disease. Chest. 1998 Jan. 113(1):237-40. [Medline].

  50. Montani D, Achouh L, Dorfmuller P, et al. Pulmonary veno-occlusive disease: clinical, functional, radiologic, and hemodynamic characteristics and outcome of 24 cases confirmed by histology. Medicine (Baltimore). 2008 Jul. 87(4):220-33. [Medline].

  51. Davis LL, deBoisblanc BP, Glynn CE, et al. Effect of prostacyclin on microvascular pressures in a patient with pulmonary veno-occlusive disease. Chest. 1995 Dec. 108(6):1754-6. [Medline].

  52. Badesch DB, Abman SH, Ahearn GS, Barst RJ, McCrory DC, Simonneau G, et al. Medical therapy for pulmonary arterial hypertension: ACCP evidence-based clinical practice guidelines. Chest. 2004 Jul. 126(1 Suppl):35S-62S. [Medline].

  53. Gilroy RJ Jr, Teague MW, Loyd JE. Pulmonary veno-occlusive disease. Fatal progression of pulmonary hypertension despite steroid-induced remission of interstitial pneumonitis. Am Rev Respir Dis. 1991 May. 143(5 Pt 1):1130-3. [Medline].

 
Previous
Next
 
Medium-power photomicrograph (original magnification, X10; hematoxylin and eosin stain) demonstrates a fibrotic interlobular septum containing a vein with an occluded lumen (arrowhead). The occlusion is composed of dense, collagen-rich, fibrous tissue. Image courtesy of Thoracic Imaging Section, Department of Radiologic Pathology, Armed Forces Institute of Pathology.
Pulmonary veno-occlusive disease in a 43-year-old man. An axial computed tomography (CT) scan (lung window level) shows multiple septal lines (arrowhead) and a dilated central pulmonary artery (arrow). Image courtesy of Thoracic Imaging Section, Department of Radiologic Pathology, Armed Forces Institute of Pathology.
Table 1. Distinguishing Pulmonary Edema From PVOD Based on Radiographic, Echocardiographic, and Heart Catheterization Data
Features Pulmonary Edema PVOD
Chest radiograph    
Kerley B lines Present Present
Pleural effusion Usually present May be present
Enlarged cardiac silhouette Present Less prominent
Enlarged pulmonary artery Present Present
Chest CT scan    
Thickened septae Present Present
Pleural effusion Usually present May be present
Enlarged heart Present Less prominent
Enlarged pulmonary artery Present Present
Septal concavity into left ventricle Absent Present
Echocardiogram    
Pulmonary artery systolic pressure Elevated (usually not >80 mm Hg) Elevated (may be >80 mm Hg)
Left atrial enlargement Present Absent
Right atrial enlargement Present Present
Right ventricular hypertrophy Absent Present
Paradoxical septal motion Absent Present
Large pericardial effusion Absent May be present
Right-sided heart catheterization    
Pulmonary vascular resistance Below 3.0 Wood units Above 3.0 Wood units
Pulmonary capillary wedge pressure Above 18 mm Hg Usually below 15 mm Hg



(if catheter is properly wedged)



Mean pulmonary artery pressure Elevated (almost never >50 mm Hg) Elevated (may be >50 mm Hg)
Cardiac output May be normal, low, or high Mostly decreased, may be low normal
Oxyhemoglobin step-up Absent Absent
Previous
Next
 
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.