Middle cerebral artery blood flow velocity in patients with cirrhosis

Dillon, John; Plevris, JN; Chan, Kwan-Leung; Lo, Nordesjö; Miller, Jeffrey D.; Bouchier, I. A. D.; Hayes, PC

doi:10.1097/00042737-199511000-00012

Cited by 31 publications

(20 citation statements)

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“…Patients with decompensated cirrhosis showed significant higher resistive index in the middle cerebral artery than those without ascites. This was also the experience of Dillon et al 12 who assessed intracranial blood flow in 37 cirrhotic patients without clinically evident hepatic encephalopathy. Although the presence of ascites was not indicated in the article, Child A cirrhotic patients, who usually have no ascites, showed normal peak systolic, end diastolic, and mean blood flow velocities in the middle cerebral artery.…”

Section: Discussionmentioning

confidence: 71%

“…Measurement of PRA, norepinephrine concentration, and inulin were performed with methods described in detail elsewhere. 12,13 Arterial pressure and pulse rate were measured in conditions of bed rest by sphygmomanometry using the automatic device Omega 1400 (In Vivo Research Laboratories, Broken Arrow, OK).…”

Section: Methodsmentioning

confidence: 99%

“…Using transcranial Doppler ultrasonography in the middle cerebral artery, Larsen et al 10 and Lagi et al 11 have recently reported that cerebral autoregulation is impaired in some patients with cirrhosis. On the other hand, Dillon et al 12 have reported that cerebral flow in the middle cerebral artery is reduced in Child B and C cirrhotic patients. These results prompted us to investigate the cerebral vascular resistance, as estimated by the resistive index in the middle cerebral artery, in patients with compensated and decompensated cirrhosis without encephalopathy.…”

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confidence: 97%

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Increased cerebrovascular resistance in cirrhotic patients with ascites

et al. 1998

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Studies assessing regional hemodynamics in patients with cirrhosis and ascites have shown vasodilation in the splanchnic circulation and vasoconstriction in the renal circulation and in the brachial and femoral artery vascular territories. The aim of this study was to assess the cerebral vascular resistance in cirrhotic patients with ascites. The resistive index in the middle cerebral artery (an index of the cerebral vascular resistance) and in a renal interlobar artery were measured by Doppler ultrasonography in 7 healthy subjects: 13 patients with compensated cirrhosis and 24 patients with ascites (13 with renal failure). The arterial blood pressure and the activity of the renin-angiotensin and sympathetic nervous systems, as estimated by plasma renin activity and plasma norepinephrine concentration, respectively, were also measured. The resistive index in the middle cerebral artery was significantly increased in patients with ascites (0.68 ؎ 0.05, mean ؎ SD) as compared with patients without ascites (0.60 ؎ 0.01, P F .05) and with healthy patients (0.52 ؎ 0.01, P F .01). Renal resistive index was also increased in patients with ascites (0.77 ؎ 0.01) compared with the other two groups (0.68 ؎ 0.02 and 0.62 ؎ 0.00, respectively; P F .001). The resistive index in the middle cerebral artery showed a direct correlation with renal resistive index (r ‫؍‬ .73, P F .01), plasma renin activity (r ‫؍‬ .61, P F .01), and norepinephrine (r ‫؍‬ .53, P F .01). The resistive index in the middle cerebral artery showed an inverse correlation with mean arterial pressure (r ‫,54.؊؍‬ P F .01). These results indicate that in patients with cirrhosis and ascites there is a cerebral vasoconstriction which is probably related with the arterial hypotension and the overactivity of vasoconstrictor systems. (HEPATOL-OGY 1998;28:39-44.)Portal hypertension in cirrhosis is associated with a hyperdynamic circulation, which is characterized by hypervolemia, high cardiac output, arterial hypotension, and low peripheral vascular resistance. 1 These circulatory abnormalities are thought to be secondary to a splanchnic arteriolar vasodilation related to the increase in portal pressure. Portal hypertension in experimental animals is associated with a generalized splanchnic arteriolar vasodilation. 2,3 There is indirect evidence that this also occurs in human cirrhosis, as hepatic blood flow is usually normal or increased in these patients, even though 60% to 80% of portal flow is shunted through the collateral circulation. 4 In addition, the mean transit time in the splanchnic vascular bed is substantially reduced in alcoholic cirrhotic patients, which indicates a hyperkinetic splanchnic circulation in these patients. 5 Finally, studies using echo-Doppler have documented increased splenic and mesenteric blood flow in patients with cirrhosis. 6,7 Investigations assessing regional circulations in human cirrhosis are also consistent with that concept. Renal blood flow is reduced and renal vascular resistance is increased in most patients with cirrhosi...

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Section: Discussionmentioning

confidence: 71%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 97%

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Increased cerebrovascular resistance in cirrhotic patients with ascites

et al. 1998

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“…Studies on cerebral blood flow in cirrhosis have found that cerebral blood flow is normal in patients without HE, low or normal in those with subclinical encephalopathy, and markedly reduced in those with encephalopathy [48]. Dillon et al measured the middle cerebral artery velocity with transcranial Doppler, an indirect estimate of cerebral blood flow, in 37 non-encephalopathic cirrhotic patients with varying degrees of liver dysfunction [49].…”

Section: Hepatic Encephalopathymentioning

confidence: 99%

Clinical implications of the hyperdynamic syndrome in cirrhosis

Licata

Mazzola

Ingrassia

et al. 2014

European Journal of Internal Medicine

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The hyperdynamic syndrome is a late consequence of portal hypertension in cirrhosis. The principal hemodynamic manifestations of the hyperdynamic syndrome are high cardiac output, and increased heart rate and total blood volume, accompanied by reduced total systemic vascular resistance. Pathophysiology involves a complex of humoral and neural mechanisms that can determine hemodynamic changes, and lead to hyperdynamic circulation. In this review we focus our attention on the manifestations of the hyperdynamic syndrome. Some of these are well described and directly related to portal hypertension (varices, ascites, hepatic encephalopathy, and hepatorenal syndrome), while others, such as hepatopulmonary syndrome, portopulmonary hypertension, and cirrhotic cardiomyopathy, are less known as clinical manifestations related to cirrhosis and, therefore, merit further investigation.

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“…These studies consistently demonstrated that arterial vasodilation occurs in the splanchnic circulation in patients with cirrhosis, while arterial vasoconstriction occurs in other vascular beds, including renal, brachial, femoral, and cerebral beds [21][22][23][24][25][26][27][28]. At the same time, clinical studies directed to assess tissue-related blood flows, such as cutaneous and muscular blood flows, gave contrasting results, ranging from low to normal or even increased values [29].…”

Section: Pathophysiology Of Hrsmentioning

confidence: 99%

Pathogenesis and management of hepatorenal syndrome in patients with cirrhosis

Angeli¹,

Merkel²

2008

Journal of Hepatology

106

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Hepatorenal syndrome is a severe complication of advanced liver cirrhosis, in patients with ascites and marked circulatory dysfunction. It is clearly established that it has a functional nature, and that it is related to intense renal vasoconstriction. Despite its functional origin, the prognosis is very poor. In the present review, the most recent advances in diagnosis, pathophysiology, and treatment are discussed. Recent developments in pathophysiology are the basis of the new therapeutic strategies, which are currently under evaluation in randomised clinical trials.

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Middle cerebral artery blood flow velocity in patients with cirrhosis

Cited by 31 publications

References 0 publications

Increased cerebrovascular resistance in cirrhotic patients with ascites

Increased cerebrovascular resistance in cirrhotic patients with ascites

Clinical implications of the hyperdynamic syndrome in cirrhosis

Pathogenesis and management of hepatorenal syndrome in patients with cirrhosis

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