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Department of Geriatric Medicine, Tokyo University Hospital, Japan
Correspondence to: Shinji Teramoto, MD, FCCP, Department of Geriatric Medicine, Tokyo University Hospital, 7-3-1 Hongo Bunkyo-ku, Tokyo, Japan 113-8655
To the Editor:
In a recent issue of CHEST (June 1999), Schott and coworkers1 reported that orthotopic liver transplantation (OLT) could be performed successfully, even though pulmonary hypertension (PH) is severe. They proposed that severe PH (mean pulmonary artery pressure > 40 mmHg) should not be automatically considered as a contraindication to OLT.
Concerning the arterial blood gas analyses, the authors stated that the important increase in the alveolar-arterial oxygen pressure difference (P [A-a] O2) before OLT was due to a ventilation/perfusion mismatch because an intracardiac or intrapulmonary shunt was excluded. They speculated that the increase in the P(A-a)O2 was in part the consequence of a very high blood flow in the pulmonary circulation due to the very high cardiac output. Because the contrast-enhanced echocardiographic study is a sensitive method to detect intrapulmonary right-to-left shunt, their speculation may be true in part. However, the other possibilities are also considered. Hypoxemia is often observed in patients with chronic liver diseases in the absence of intrinsic lung disease. Recent evidences suggested that nitric oxide (NO) is an important mediator of impaired oxygenation in patients with cirrhosis.2 3 4 NO is a vasodilating substance, which can abolish the local vasoconstrictive reflex to alveolar hypoxia, increasing the ventilation/perfusion mismatch, which is one of the mechanisms of oxygenation abnormalities in cirrhosis. Rolla and coworkers2 reported that the exhaled NO output is well correlated with P(A-a)O2 in patients with liver cirrhosis. Matsumoto et al3 also reported that increased NO levels in exhaled air in patients with decompensated, but not in patients with compensated cirrhosis. Furthermore, the increase in NO concentration after liver transplantation is reported to be correlated with the improvement in oxygenation.4 There is a possibility that the increased production of NO in the lung may be the other cause of vasodilation and intrapulmonary shunting responsible for hypoxemia in the patient. However, the mechanism of hypoxemia in liver disease may not be simple. Inhaled NO might worsen hypoxemia in cases where the ventilation/perfusion mismatching is the prominent mechanism, but may benefit patients with increased shunt flow in the better ventilated lung. Several investigators have reported that NO inhalation improved postoperative hypoxemia in patients following liver transplantation for hepatic dysfunction.5 6 Thus, the effects of NO inhalation before and after liver transplantation may have some clinical merit for the study of the pathophysiology of hypoxemia. In addition, delivering 100% oxygen by a nonrebreathing mask may have a diagnostic value of functional right-to-left shunting.7 Because the improvement of oxygenation in liver disease after live transplantation is considered to be complicated,8 9 10 11 the simple explanation may not solely be true. It may depend on the degree of intrapulmonary shunt, portal hypertension, increased cardiac output, and increased NO production in lungs.8 9 10 11
Although severe pulmonary hypertension should not automatically be considered as a contraindication to OLT, as stated by others, the other exclusion criteria may be necessary for the indication of OLT in liver diseases with pulmonary hypertension.
References
Strasbourg, France
Correspondence to: Ari Chaouat, MD, Service de Pneumologie, Hopital de Hautepierre, Avenue Moliere, Strasbourg 67098, France
To the Editor:
Teramoto et al have discussed the possible mechanisms of gas exchange impairment in patients with end-stage chronic liver disease. In our case report (June 1999)1 , in fact, we did not discuss these mechanisms in detail. We rather focused on a more practical message: which patients should be scheduled for liver transplantation when they suffer from portopulmonary hypertension? In particular, the mechanism of pulmonary hypertension must be considered: a patient having severe pulmonary hypertension but without signs of right ventricular failure and mild to moderate increase in pulmonary vascular resistance should not be systematically excluded from the liver transplantation list. However, as stated by Teramoto et al, the pulmonary hemodynamic measurements are not the sole criteria.
With regard to the mechanism of hypoxemia, we have stated in our report1 that it was the consequence of ventilation/perfusion mismatch. Since hypoventilation and intracardiac or intrapulmonary shunts were excluded, and since limitation in diffusion of oxygen cannot induce a marked resting hypoxemia, the ventilation/perfusion mismatch was the only possibility left. The question is, what explains such a ventilation/perfusion mismatch? Teramoto et al raise the interesting point that an increase in nitric oxide is responsible for a poor or absent hypoxic pressor response as a cause of hypoxemia. This was established in the hepatopulmonary syndrome,2 but to our knowledge never explored in portopulmonary hypertension. The increase in nitric oxide production in the lung is an interesting hypothesis; this increase could be due to (1) the stimulation of type II nitric oxide synthase (NOS) by proinflammatory cytokines or endotoxin, or (2) an increase activation of type III NOS.3 The latter could be due in our patient to the very high increase in cardiac output, since shear stress is a well-known stimulus of type III NOS. In fact, arterial blood gas abnormalities in our patient were similar to those usually observed in primary pulmonary hypertension. Perhaps it was the decrease of alveolar-arterial oxygen gradient observed after liver transplantation due to the disappearance of NOS II and NOS III stimuli. The fact that alveolar-arterial oxygen gradient was still elevated after that procedure could be secondary to irreversible small artery lesions.
Pulmonary hemodynamics and gas exchange in patients with chronic liver failure are an interesting area. Understanding their mechanisms in hepatopulmonary syndrome and portopulmonary hypertension could give clues on the hypoxic pulmonary vasoconstriction and the development of pulmonary vascular diseases.
References
This article has been cited by other articles:
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  K. L. Swanson and M. J. Krowka Arterial Oxygenation Associated With Portopulmonary Hypertension* Chest, June 1, 2002; 121(6): 1869 - 1875. [Abstract] [Full Text] [PDF]
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