Ventilation-perfusion relationships and central haemodynamics in patients with cirrhosis. Effects of a somatostatin analogue

doi:10.1016/S0168-8278(94)80136-3

Journal of Hepatology

Volume 21, Issue 1, 1994, Pages 52-57

https://doi.org/10.1016/S0168-8278(94)80136-3 Get rights and content

The ventilation-perfusion relationships of the lung (V_A/Q) and central haemodynamics were studied in seven patients with cirrhosis before and 30 min after a bolus injection of a somatostatin analogue, octreotide (Sandostatin, 50 μg i.v.), to elucidate the role of this substance in the hepatopulmonary syndrome. In the basal state all patients had normal spirometry but reduced diffusing capacity. Three patients had various degrees of hypoxaemia (6.9–8.3 kPa) and three had clubbing of the fingers. In the basal state V_A/Q distributions, determined by inert gas elimination technique, showed an intrapulmonary shunt of 7.9±2.2% of cardiac output (range 1.5 to 17.1) and perfusion of lung regions with “low V_A/Q” of 4.4±2.2% of cardiac output (range 0 to 15.4). After octreotide, the amount of shunting increased (10.9±4.4% of cardiac output; non-significant), while “low V_AQ” was unchanged (3.7±1.3% of cardiac output). Arterial oxygen tension decreased from 10.2±1.1 to 9.7±1.1 kPa (non-significant). The mean pulmonary arterial pressure increased from 14.5±1.9 to 16.3±1.8 mmHg (p<0.01). No alterations were seen in heart rate, stroke volume, cardiac output, central pressures or vascular resistances. The results of the present study do not support the hypothesis that octreotide improves hypoxaemia and ventilation-perfusion relationships in patients with hepatopulmonary syndrome.

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Hepatopulmonary syndrome is characterized by the presence of portal hypertension with or without cirrhosis, an increased alveolar-arterial oxygen partial pressure difference greater than or equal to 15 mmHg, and dilated pulmonary capillaries. Hepatopulmonary syndrome is found in up to 20% of patients with cirrhosis and should be considered in any patient who develops dyspnea or hypoxemia. Contrast echocardiography is enough to make the diagnosis of hepatopulmonary syndrome. The exact pathophysiology of hepatopulmonary syndrome remains unknown but nitric oxide is an important factor underlying hepatopulmonary syndrome. Hypoxemia progressively deteriorates and worsens the prognosis of cirrhotic patients. Hypoxemic patients must be controlled regularly to optimise the timing of liver transplantation. Indeed, a preoperative PaO₂ of less than or equal to 50 mmHg alone or in combination with an isotopic shunt fraction greater than or equal to 20% are the strongest predictors of postoperative mortality. There are currently no effective medical therapies for hepatopulmonary syndrome but garlic powder and iloprost inhalation demonstrate clinical improvements in the pre- and in the post-transplant period.
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Citation Excerpt :
Torrecillas et al9 showed the vasoconstrictive effect of somatostatin mediated by the somatostatin SRIF receptor-4.10 Octreotide administration elicits a biphasic response wherein there is an initial transiently induced vasoconstriction of the pulmonary arterial vasculature with a subsequent fall to baseline pressure.11 Such a biphasic response may not be present in these 2 premature infants because their vascular smooth muscles have increased vascular resistance while recovering from hyaline membrane disease.12
The authors report 2 cases of premature neonates who had enterocutaneous fistula complicating necrotizing enterocolitis. Pulmonary hypertension developed after administration of a somatostatin analogue, octreotide, to enhance resolution of the fistula. The authors discuss the mechanism of the occurrence of this complication and recommend caution of its use in high-risk premature neonates. J Pediatr Surg 38:251-253. Copyright 2003, Elsevier Science (USA). All rights reserved.

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Regular PaperVentilation-perfusion relationships and central haemodynamics in patients with cirrhosis. Effects of a somatostatin analogue

Am J Med Sci

Chest

Am J Med

Am J Med

Pulmonary haemodynamics in liver cirrhosis

Semin Respir Med

Ventilation-perfusion inequality in patients with non-alcoholic liver cirrhosis

Eur Respir J

Normalization of ventilation/perfusion relationships after liver transplantation in patients with decompensated cirrhosis: evidence for a hepatopulmonary syndrome

Hepatology

Characterization of hepatic hemodynamics in cirrhotics and non-cirrhotics

Scand J Gastroenterol

Biological actions of vasoactive intestinal peptide in man

Hepatic inactivation of VIP in man and dog

Ann Surg

Influence of VIP on splanchnic and central hemodynamics in healthy subjects

Peptides

Insulin and glucagon levels in liver cirrhosis. Relationship with plasma amino acid imbalance of chronic hepatic encephalopathy

Dig Dis Sci

VIP in cirrhosis: arteriovenous extraction in different vascular beds

Scand J Gastroenterol

Regulation of somatostatin secretion and its biological actions

Somatostatin — physiological and pathophysiological aspects

Scand J Gastroenterol

Regular Paper
Ventilation-perfusion relationships and central haemodynamics in patients with cirrhosis. Effects of a somatostatin analogue