Hepatopulmonary syndrome versus portopulmonary hypertension: Distinctions and dilemmas
โ Scribed by M J Krowka
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 196 KB
- Volume
- 25
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
โฆ Synopsis
ter, venous blood bypasses the capillary-alveoli interface via direct arteriovenous channels (dilated compared with capillary diameters รต8 m ), hence never becoming oxygenated; an Cirrhosis, portal hypertension, and even acute liver failure anatomic shunt. 9 If enough partial pressure of inspired oxymay result in a complex change in the pulmonary arterial gen is given (100% O 2 ) to a patient with hepatopulmonary bed. As a result, there are at least two clinically important syndrome and precapillary or capillary dilatation, a dramatic and very distinct pulmonary vascular consequences: hepatorise in PaO 2 can often be realized as oxygen can now thorpulmonary syndrome (HPS) and portopulmonary hypertenoughly diffuse the entire venous blood flow. On the other sion (PPH). These entities are pathophysiologically distinct hand, 100% inspired oxygen has little effect on PaO 2 in the in that hepatopulmonary syndrome is characterized by vasopatient with direct arteriovenous communications. Theredilatation and portopulmonary hypertension results from vafore, the term ''anatomic shunt'' should really be reserved soconstriction. The clinical implications are also quite disfor the situation when a direct arteriovenous communication similar in the most dramatic presentations: gas exchange problem can be shown. impairment in HPS (severe hypoxemia) and hemodynamic An additional and different type of ''shunt'' can occur in compromise in PPH (right heart failure). 3, which the alveoli are completely filled with fluid and exudate Such ''remodeling'' of the pulmonary vascular bed has deor simply not aerated (as in atelectasis). This is considered fied simple cause and effect relationships to date. The balance to be a ''physiological shunt,'' again, no oxygen can reach the between vasoconstrictors and vasodilators, combined with venous blood, response to 100% O 2 is extremely poor, but the the possible effects of growth factors, conjures numerous and process is not associated with direct arteriovenous communicomplicated hypotheses. cations, dilated precapillary or capillary vessels. The prob-Abbreviations: HPS, hepatopulmonary syndrome; PPH, portopulmonary hypertension; 99m TcMAA, technetium macroaggregated albumin lung scanning; OLT, orthotopic liver oxygenation was nicely shown by the reduction in alveolartransplantation.
arterial oxygen gradient or estimated shunt and that is clini-
๐ SIMILAR VOLUMES
Hepatopulmonary syndrome (HPS) and portopulmonary hypertension (PPHTN) are distinct clinical entities that may complicate liver disease. Although HPS and PPHTN are different, several reports describe 6 patients in whom both conditions have occurred, either concurrently or sequentially, sometimes wit