Effect of Liver Failure on the Response of Ventilation and Cerebral Circulation to Carbon Dioxide in Man and in the Goat

Stanley, N. N.; Salisbury, B. G.; McHenry, Lawrence C.; Cherniack, Neil S.

doi:10.1042/cs0490157

Cited by 12 publications

(10 citation statements)

References 49 publications

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“…Chronic hyperventilation with a resulting compensated respiratory alkalosis is a common observation in patients with cirrhosis [20][21][22]. The present data confirm this observation, the increase in V 'E being due to an increase both of tidal volume and respiratory frequency.…”

Section: Breathing Pattern and Arterial Blood Gas Valuessupporting

confidence: 80%

“…The present data confirm this observation, the increase in V 'E being due to an increase both of tidal volume and respiratory frequency. Several mechanisms have been proposed to explain hyperventilation in cirrhotic patients [20,21], but the real reason is still obscure. No change in V 'E was observed after LVP, and this suggests that ascites was probably not implicated in this abnormality.…”

Section: Breathing Pattern and Arterial Blood Gas Valuesmentioning

confidence: 99%

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Respiratory mechanics in patients with tense cirrhotic ascites

Duranti

Laffi²,

Misuri³

et al. 1997

Eur Respir J

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Lung volumes are decreased by tense ascites and increase after large volume paracentesis (LVP). The overall effect of ascites and LVP on the respiratory function is poorly understood.We studied eight cirrhotic patients with tense ascites before and after LVP. Inspiratory muscle force (maximal transdiaphragmatic pressure (Pdi,max), and the lowest pleural pressure (Ppl,min)) was assessed while the patients were seated. Rib cage and abdominal volume displacements, as well as pleural and gastric pressures were measured during quiet breathing while the patients were supine.Pdi,max and Ppl,min were normal and did not change after LVP (from 84.2±19.7 to 85.2±17.0 cmH 2 O and from 68.3±19.7 to 74±15.9 cmH 2 O, respectively). The abdominal contribution to the generation of tidal volume was greater than that of the rib cage (79 vs 21%), a pattern which did not change after LVP (73 and 27%). We conclude that the strength of the inspiratory muscles is normal or reduced in seated cirrhotic patients. In the supine position, tense ascites results in an increase in lung elastic load and development of positive end-expiratory pressure, with a consequent overload and increased activation of inspiratory muscles. Large volume paracentesis decreases overloading and activation, but does not change the strength of the inspiratory muscles. Eur Respir J 1997; 10: 1622-1630

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Section: Breathing Pattern and Arterial Blood Gas Valuessupporting

confidence: 80%

Section: Breathing Pattern and Arterial Blood Gas Valuesmentioning

confidence: 99%

Respiratory mechanics in patients with tense cirrhotic ascites

Duranti

Laffi²,

Misuri³

et al. 1997

Eur Respir J

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“…The experiments utilized six goats (A-F) and were performed in conjunction with a previously reported study of the effects of liver failure on the CO, responsiveness of the cerebral circulation and metabolism (Stanley et al, 1975). We chose to study the goat because each internal maxillary artery, a branch of the external carotid artery, provides the total blood flow to each cerebral hemisphere via the rete mirabile (Andersson & Jewel], 1956) and this favourable anatomical arrangement allows the easy measurement of CBF at frequent intervals with a technique described by Edelman, Epstein, Cherniack & Fishman (1972).…”

Section: Animalsmentioning

confidence: 99%

“…In patients with liver cirrhosis there is a reduction in CBF'') and CMRo2, which is related to the severity of hepatic encephalopathy (Fazekas, Ticktin, Ehrentraut & Alman, 1956;Posner & Plum, 1960;James, Nashat, Sampson, Williams & Garassini, 1969b). The response of CBF to an increase in arterial C 0 2 tension is also depressed in liver failure, and a further reduction in CMRo2 occurs during hypercapnia (Stanley, Salisbury, McHenry & Cherniack, 1975). Since arterial hypoxaemia is a frequent complication of liver disease (Stanley, Ackrill & Wood, 19721, the present study Mas undertaken to determine whether there might also be an alteration of CBF responsiveness and the stability of CMRo2 in hypoxia during liver failure.…”

Section: Introductionmentioning

confidence: 95%

Effect of Liver Failure on the Cerebral Circulatory and Metabolic Responses to Hypoxia in the Goat

Stanley

Cherniack

1976

Clinical Science

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1. Six unanaesthetized goats were used to evaluate the effect of liver failure on the hypoxic responsiveness of cerebral blood flow. The animals breathed air and several different hypoxic gas mixtures enriched with sufficient CO2 to maintain an isocapnic state. The cerebral metabolic rate for O2 (CMRo2) was also measured in four of these goats. 2. In baseline studies there was a linear relationship between cerebral blood flow and arterial O2 saturation (Sa,o2) measured at different levels of isocapnic hypoxia. The slopes of the cerebral blood flow/Sa,o2 response lines were used to quantify the response of cerebral blood flow to hypoxia. In the healthy goat, CMRo2 was not depressed by hypoxia until the O2 tension (Po2) in arterial and cerebral venous blood had fallen below critical threshold values of approximately 3-2 and 2-2 kPa (24 and 16 mmHg) respectively. 3. Liver failure was accompanied by a fall in cerebral blood flow and CMRo2. There was also a depression in the response of cerebral blood flow to hypoxia and a disproportionate reduction of cerebral O2 delivery in hypoxia. CMRo2 was further reduced at arterial and cerebral venous Po2 values, which were much higher than the critical threshold values for producing hypoxic CMRo2 depression in health. 4. It is concluded that the brain becomes more vulnerable to the adverse effects of hypoxia during liver failure. This may be of practical importance in the management of patients with arterial hypoxaemia or other complications (e.g. anaemia or shock), which may reduce cerebral oxygen delivery.

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“…Nur die 3 Patienten mit ausgeprägtem Aszites zeigten dieses Verhalten lediglich in der Mundok klusionsmethode, die ventilatorische Atem antwort war durch den Aszites deutlich ge dämpft. Stanley et al [34] haben beschrie ben, dass Normokapnie bzw. Hyperkapnie bei Patienten mit portokavaler Enzephalo pathie zu einer Verminderung der zerebra len Durchblutung führt.…”

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Lungenfunktion, Gasaustausch und Atemregulation bei Patienten mit portokavaler Enzephalopathie

Sybrecht¹,

Koch²,

Tepe³

et al. 1980

Respiration

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In 17 patients, breathing room air and pure oxygen, with histologically proven cirrhosis of the liver and portocaval encephalopathy grade I, static and dynamic lung volumes, closing capacity and arterial blood gases were determined. Furthermore, CO₂response curves were provided and mouth occlusion pressure measurements were carried out. The residual volume was found to be increased (130 ± 8% of predicted) which resulted in decreased vital capacity (79 ± 2% of predicted) with total lung capacity being normal (94 ± 2% of predicted). Closing capacity was increased to 134 ± 5% of the predicted value. Gas exchange for oxygen was impaired (AaDO₂= 262 ± 30% of predicted). Arterial Po₂, however, was within normal range Pao₂ = 84 ± 3.6 mm Hg) due to hyperventilation (Paco₂= 28.1 ± 0.8 mmHg). Hypoxic ventilatory stimulation could be excluded because inspiration of pure oxygen caused no change of Paco₂ (Paco₂ = 27.3 -f 0.7 mm Hg and Pao₂ = 465 + 16.9 mm Hg with Fιo₂ = 1.0). The slope of the CO₂ response curves was normal, the mouth occlusion pressures, however, were higher than the predicted value: up to Paco₂ of 55 mm Hg. The slope of these curves being smaller than predicted. The results show that in patients with portocaval encephalopathy the lung function is disturbed due to premature airway closure with consequently decreased regional ventilation: perfusion ratios and that regulation of ventilation is impaired by a loss of sensitivity for CO, with high basal output of the respiratory centers not related to CO₂

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Effect of Liver Failure on the Response of Ventilation and Cerebral Circulation to Carbon Dioxide in Man and in the Goat

Cited by 12 publications

References 49 publications

Respiratory mechanics in patients with tense cirrhotic ascites

Respiratory mechanics in patients with tense cirrhotic ascites

Effect of Liver Failure on the Cerebral Circulatory and Metabolic Responses to Hypoxia in the Goat

Lungenfunktion, Gasaustausch und Atemregulation bei Patienten mit portokavaler Enzephalopathie

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