Reduced baroreflex sensitivity and pulmonary dysfunction in alcoholic cirrhosis: effect of hyperoxia

2010 ◽  
Vol 299 (3) ◽  
pp. G784-G790 ◽  
Author(s):  
Søren Møller ◽  
Jens S. Iversen ◽  
Aleksander Krag ◽  
Peter Bie ◽  
Andreas Kjær ◽  
...  

Patients with cirrhosis exhibit impaired regulation of the arterial blood pressure, reduced baroreflex sensitivity (BRS), and prolonged QT interval. In addition, a considerable number of patients have a pulmonary dysfunction with hypoxemia, impaired lung diffusing capacity (DlCO), and presence of hepatopulmonary syndrome (HPS). BRS is reduced at exposure to chronic hypoxia such as during sojourn in high altitudes. In this study, we assessed the relation of BRS to pulmonary dysfunction and cardiovascular characteristics and the effects of hyperoxia. Forty-three patients with cirrhosis and 12 healthy matched controls underwent hemodynamic and pulmonary investigations. BRS was assessed by cross-spectral analysis of variabilities between blood pressure and heart rate time series. A 100% oxygen test was performed with the assessment of arterial oxygen tensions (PaO2) and alveolar-arterial oxygen gradient. Baseline BRS was significantly reduced in the cirrhotic patients compared with the controls (4.7 ± 0.8 vs. 10.3 ± 2.0 ms/mmHg; P < 0.001). The frequency-corrected QT interval was significantly prolonged in the cirrhotic patients ( P < 0.05). There was no significant difference in BRS according to presence of HPS, PaO2, DlCO, or Child-Turcotte score, but BRS correlated with metabolic and hemodynamic characteristics. After 100% oxygen inhalation, BRS and the QT interval remained unchanged in the cirrhotic patients. In conclusion, BRS is significantly reduced in patients with cirrhosis compared with controls, but it is unrelated to the degree of pulmonary dysfunction and portal hypertension. Acute hyperoxia does not significantly revert the low BRS or the prolonged QT interval in cirrhosis.

2013 ◽  
Vol 60 (2) ◽  
pp. 15-21
Author(s):  
Kráľová E. ◽  
Jankyová S. ◽  
Pekárik A. ◽  
Čuboň J. ◽  
Stankovičová T.

Abstract We observed the changes in electrical activity, biometric and haemodynamic parameters of hearts in animals with experimental diabetes mellitus (DM). As well the effect of carvedilol, PycnogenolR and its combination with carvedilol on DM heart function was tested. DM was induced by streptozotocin over three sequential days at a dose of 25 mg/kg body weight i.p. We started therapy by suspension of carvedilol, PycnogenolR and their combination for six weeks. Blood pressure was measured using tail cuff plethysmography. ECG, haemodynamic and biometric parameters were measured in isolated hearts perfused according to the Langendorff. DM rats had increased systolic arterial blood pressure, thicker free wall of left ventricle but weakened myocardial contractility compared with controls. In contrast to controls, electrophysiological parameters showed prolonged QT interval and increased incidence of dysrhythmias in DM rats. The PycnogenolR administration induced regression of left ventricular hypertrophy, improved left ventriculi contraction and increased coronary flow; however, it did not improve the electrical activity of the myocardium compared with DM ones. Carvedilol also reversed the myocardial remodelling, shortened the duration of QT interval and suppressed the incidence of dysrhythmias. The common combination of drugs improved biometric and haemodynamic parameters compared with DM animals, however, not so significantly as monotherapy. On the other hand, the combination of carvedilol and PycnogenolR significantly reduced the duration of the QT interval and shortened the incidence of dysrhythmias. We can conclude that the administration of PycnogenolR effectively improved haemodynamic parameters, and carvedilol affected biometric parameters and also electrical parameters in DM animals. We observed the marked synergic effect of the combination of both drugs on the electrical activity of myocardium. This combination shortened the most pathologically prolonged QT interval and reduced the number of dysrhythmias.


2019 ◽  
Vol 3 (3) ◽  
pp. 211-214 ◽  
Author(s):  
Elizabeth Schell ◽  
Joshua Pathman ◽  
Richard Pescatore ◽  
Pollianne Bianchi

We describe the case of a patient presenting with odd neurologic symptoms initially thought to represent somatization who was found to have critical hypokalemia manifesting as hypokalemic non-periodic paralysis. It was determined that the patient had baseline hypokalemia as a function of alcohol abuse, exacerbated by self overmedication with hydrochlorothiazide for elevated blood pressure readings at home. The diagnosis was suspected when an electrocardiogram was obtained demonstrating a pseudo-prolonged QT interval with ST depression, consistent with T-U wave fusion and a QU interval with an absent T wave.1 The patient received oral and intravenous potassium and magnesium supplementation with resolution of symptoms.


Author(s):  
Ghariani Rania ◽  
Chrif Yosra ◽  
Samar Derbal ◽  
Rihab Laamouri ◽  
Fatma Ben Dahmene ◽  
...  

1944 ◽  
Vol 79 (1) ◽  
pp. 9-22 ◽  
Author(s):  
Frank L. Engel ◽  
Helen C. Harrison ◽  
C. N. H. Long

1. In a series of rats subjected to hemorrhage and shock a high negative correlation was found between the portal and peripheral venous oxygen saturations and the arterial blood pressure on the one hand, and the blood amino nitrogen levels on the other, and a high positive correlation between the portal and the peripheral oxygen saturations and between each of these and the blood pressure. 2. In five cats subjected to hemorrhage and shock the rise in plasma amino nitrogen and the fall in peripheral and portal venous oxygen saturations were confirmed. Further it was shown that the hepatic vein oxygen saturation falls early in shock while the arterial oxygen saturation showed no alteration except terminally, when it may fall also. 3. Ligation of the hepatic artery in rats did not affect the liver's ability to deaminate amino acids. Hemorrhage in a series of hepatic artery ligated rats did not produce any greater rise in the blood amino nitrogen than a similar hemorrhage in normal rats. The hepatic artery probably cannot compensate to any degree for the decrease in portal blood flow in shock. 4. An operation was devised whereby the viscera and portal circulation of the rat were eliminated and the liver maintained only on its arterial circulation. The ability of such a liver to metabolize amino acids was found to be less than either the normal or the hepatic artery ligated liver and to have very little reserve. 5. On complete occlusion of the circulation to the rat liver this organ was found to resist anoxia up to 45 minutes. With further anoxia irreversible damage to this organ's ability to handle amino acids occurred. 6. It is concluded that the blood amino nitrogen rise during shock results from an increased breakdown of protein in the peripheral tissues, the products of which accumulate either because they do not circulate through the liver at a sufficiently rapid rate or because with continued anoxia intrinsic damage may occur to the hepatic parenchyma so that it cannot dispose of amino acids.


2008 ◽  
Vol 1 (1) ◽  
pp. 35-41 ◽  
Author(s):  
Amanda S. Y. Chan ◽  
Geoffrey K. Isbister ◽  
Carl M. J. Kirkpatrick ◽  
Stephen B. Duffull

2002 ◽  
Vol 62 (2) ◽  
pp. 580-584 ◽  
Author(s):  
Alberto Bettinelli ◽  
Camillo Tosetto ◽  
Giacomo Colussi ◽  
Ginaluca Tommasini ◽  
Alberto Edefonti ◽  
...  

1997 ◽  
Vol 30 (4) ◽  
pp. 337-339 ◽  
Author(s):  
Rohan Perera ◽  
Andreas Kraebber ◽  
Miles J. Schwartz

2014 ◽  
Vol 2 (1) ◽  
pp. 44-45
Author(s):  
Ahmad Mursel Anam ◽  
Raihan Rabbani ◽  
Farzana Shumy ◽  
M Mufizul Islam Polash ◽  
M Motiul Islam ◽  
...  

We report a case of drug induced torsades de pointes, following acquired long QT syndrome. The patient got admitted for shock with acute abdomen. The initial prolonged QT-interval was missed, and a torsadogenic drug was introduced post-operatively. Patient developed torsades de pointes followed by cardiac arrest. She was managed well and discharged without complications. The clinical manifestations of long QT syndromes, syncope or cardiac arrest, result from torsades de pointes. As syncope or cardiac arrest have more common differential diagnoses, even the symptomatic long QT syndrome are commonly missed or misdiagnosed. In acquired long QT syndrome with no prior suggestive feature, it is not impossible to miss the prolonged QT-interval on the ECG tracing. We share our experience so that the clinicians, especially the junior doctors, will be more alert on checking the QT-interval even in asymptomatic patients. DOI: http://dx.doi.org/10.3329/bccj.v2i1.19970 Bangladesh Crit Care J March 2014; 2 (1): 44-45


2021 ◽  
Vol 14 (1) ◽  
pp. 01-05
Author(s):  
Putu Dyah Widyaningsih ◽  
Putu Gita Pranata Putra ◽  
DG Wedha Asmara ◽  
Erna Bagiari ◽  
Agus Santosa ◽  
...  

The treatment of corona virus disease 2019 (COVID-19)remains in debate, and the use of chloroquine has not been validated by accurate clinical trials.The aim of this study was to provide the possible cardiotoxicity effect of chloroquine in patients with COVID-19. This study was a case-series of prolonged QT interval of COVID-19 patients treated with chloroquine in a hospital in Bali, Indonesia. There were two cases of COVID-19 with exhibited a prolonged QT interval after being administrated of chloroquine. The prolonged QT interval returned to normal after chloroquine was stopped.These cases alert us the cardiotoxicity effect of chloroquine and the need for serial electro-cardiography monitoring before and during therapy. In conclusion, although antiviral and anti-inflammation properties of chloroquine on COVID-19 are promising, its cardiotoxicity effects should be monitored closely for less harm to the patients.


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