scholarly journals Volume overload in hemodialysis: diagnosis, cardiovascular consequences, and management

2020 ◽  
Author(s):  
Charalampos Loutradis ◽  
Pantelis A Sarafidis ◽  
Charles J Ferro ◽  
Carmine Zoccali
Keyword(s):  
Time Window ◽  
Diastolic Pressure ◽  
Current Knowledge ◽  
Volume Overload ◽  
Dry Weight ◽  
Left Ventricular ◽  
Bioimpedance Spectroscopy ◽  
Fluid Removal ◽  
Clinical Criteria ◽  
Long Time

Abstract Volume overload in haemodialysis (HD) patients associates with hypertension and cardiac dysfunction and is a major risk factor for all-cause and cardiovascular mortality in this population. The diagnosis of volume excess and estimation of dry weight is based largely on clinical criteria and has a notoriously poor diagnostic accuracy. The search for accurate and objective methods to evaluate dry weight and to diagnose subclinical volume overload has been intensively pursued over the last 3 decades. Most methods have not been tested in appropriate clinical trials and their usefulness in clinical practice remains uncertain, except for bioimpedance spectroscopy and lung ultrasound (US). Bioimpedance spectroscopy is possibly the most widely used method to subjectively quantify fluid distributions over body compartments and produces reliable and reproducible results. Lung US provides reliable estimates of extravascular water in the lung, a critical parameter of the central circulation that in large part reflects the left ventricular end-diastolic pressure. To maximize cardiovascular tolerance, fluid removal in volume-expanded HD patients should be gradual and distributed over a sufficiently long time window. This review summarizes current knowledge about the diagnosis, prognosis and treatment of volume overload in HD patients.

Apoptosis in the left ventricle of chronic volume overload causes endocardial endothelial dysfunction in rats

2002 ◽  
Vol 282 (4) ◽  
pp. H1197-H1205 ◽  
Author(s):  
Michael J. Cox ◽  
Harpreet S. Sood ◽  
Matthew J. Hunt ◽  
Derrick Chandler ◽  
Jeffrey R. Henegar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blot Analysis ◽  
Diastolic Pressure ◽  
Volume Overload ◽  
Left Ventricular ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Heart Weight ◽  
Sprague Dawley ◽  
Lung Weight ◽  
Cardiac Relaxation

The hypothesis is that chronic increases in left ventricular (LV) load induce oxidative stress and latent matrix metalloproteinase (MMP) is activated, allowing the heart to dilate in the absence of endothelial nitric oxide (NO) and thereby reduce filling pressure. To create volume overload, an arteriovenous (A-V) fistula was placed in male Sprague-Dawley rats. To decrease oxidative stress and apoptosis, 0.08 mg/ml nicotinamide (Nic) was administered in drinking water 2 days before surgery. The rats were divided into the following groups: 1) A-V fistula, 2) A-V fistula + Nic, 3) sham operated, 4) sham + Nic, and 5) control (unoperated); n = 6 rats/group. After 4 wk, hemodynamic parameters were measured in anesthetized rats. The heart was removed and weighed, and LV tissue homogeneates were prepared. A-V fistula caused an increase in heart weight, lung weight, and end-diastolic pressure compared with the sham group. The levels of malondialdehyde (MDA; a marker of oxidative stress) was 6.60 ± 0.23 ng/mg protein and NO was 6.87 ± 1.21 nmol/l in the LV of A-V fistula rats by spectrophometry. Nic treatment increased NO to 13.88 ± 2.5 nmol/l and decreased MDA to 3.54 ± 0.34 ng/mg protein ( P= 0.005). Zymographic levels of MMP-2 were increased, as were protein levels of nitrotyrosine and collagen fragments by Western blot analysis. The inhibition of oxidative stress by Nic decreased nitrotyrosine content and MMP activity. The levels of tissue inhibitor of metalloproteinase-4 mRNA were decreased in A-V fistula rats and increased in A-V fistula rats treated with Nic by Northern blot analysis. TdT-mediated dUTP nick-end labeling-positive cells were increased in A-V fistula rats and decreased in fistula rats treated with Nic. Acetylcholine and nitroprusside responses in cardiac rings prepared from the above groups of rats suggest impaired endothelial-dependent cardiac relaxation. Treatment with Nic improves cardiac relaxation. The results suggest that an increase in the oxidative stress and generation of nitrotyrosine are, in part, responsible for the activation of metalloproteinase and decreased endocardial endothelial function in chronic LV volume overload.

Disuse inhibition of newly functional coronary collateral circulation in ponies

1992 ◽  
Vol 262 (2) ◽  
pp. H385-H390
Author(s):  
K. S. Rugh ◽  
C. R. Ross ◽  
R. D. Sarazan ◽  
R. B. Boatwright ◽  
D. O. Williams ◽  
...  
Keyword(s):  
Diastolic Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
Shortening Velocity ◽  
Coronary Collateral ◽  
Work Index ◽  
Percent Recovery ◽  
Velocity Of Shortening ◽  
Stroke Work Index ◽  
Long Time

We evaluated the loss of coronary collateral function in the absence of stimulation (disuse inhibition) by doubling the interval between successive left anterior descending coronary artery (LAD) occlusions in ponies in which collateral function initially had been enhanced by 2-min occlusions at 30-min intervals. Before collateralization, occlusion caused segment systolic shortening, velocity of shortening, and stroke work index in the LAD-dependent left ventricular apex to decrease, whereas heart rate and left ventricular end-diastolic pressure increased. After 476 +/- 102 occlusions, segment function recovered to preocclusion levels and hemodynamics were unchanged during occlusion. Occlusion did not elicit sustained functional deterioration until the occlusion interval was greater than or equal to 32 h. During the occlusion after the 128-h interval, segment systolic shortening, velocity of shortening, and stroke work index were reduced 69 +/- 8, 38 +/- 9, and 46 +/- 13%, respectively. Percent recovery of systolic shortening during successive occlusions declined exponentially (T1/e = 102.0 +/- 17.3 h). Thus, in ponies collateral function progressively declines when the occlusion interval is greater than or equal to 32 h, but complete inhibition does not occur even after 128 h without occlusion. This indicates that collateral function in ponies can be maintained by occlusions that are far less frequent than those needed for initial collateral development. The long time constant of collateral disuse inhibition suggests that equine collaterals are quite resistant to the effects of occlusion cessation and differ from canine collaterals in that respect.

Reduction of Carnitine Content by Inhibition of Its Biosynthesis Results in Protection of Isolated Guinea Pig Hearts against Hypoxic Damage

1996 ◽  
Vol 1 (3) ◽  
pp. 235-242 ◽  
Author(s):  
Pradip K. Dhar ◽  
Ingrid L. Grupp ◽  
Arnold Schwartz ◽  
Gunter Grupp ◽  
Mohammed A. Matlib
Keyword(s):  
Guinea Pigs ◽  
Initial Rate ◽  
Diastolic Pressure ◽  
Contractile Function ◽  
Dry Weight ◽  
Treated Group ◽  
Left Ventricular ◽  
Untreated Group ◽  
Free Carnitine ◽  
Isolated Hearts

Background 3-(2,2,2-trimethylhydrazinium) propionate (THP or mildronate) is an inhibitor of carnitine biosynthesis. This study was carried out to determine whether feeding of guinea pigs with THP results in decreased myocardial-free carnitine content and, as a result, attenuates hypoxic damage in isolated and paced work-performing hearts. Methods and Results Guinea pigs were administered either distilled water or 100 mg THP/kg/day orally for 10 days. The treatment resulted in about a 50% decline in myocardial-free carnitine content, from 11.1 ± 0.2 (n = 5) to 5.6 ± 0.2 (n = 5) μM/g dry weight of the heart. The left ventricular contractile function of the hearts was measured during normoxic perfusion (PO2 = 590 mmHg), hypoxic perfusion (PO2 = 149 mmHg), and reperfusion (PO2 = 590 mmHg). In both untreated and THP-treated groups, the rate of development of intraventricular pressure (+dP/dt) under normoxic perfusion was similar; however, +dP/dt declined to about 10% of the initial rate within 20 minutes of hypoxic perfusion. In the THP-treated group of hearts, the initial decline was slower than that of the untreated animal hearts. After 20 minutes of normoxic reperfusion following 60 minutes of hypoxic perfusion, the recovery of +dP/dt and -dP/dt was greater in the THP-treated group than in the untreated group. The elevation of end-diastolic pressure during hypoxia was completely reversed by normoxic reperfusion of the THP-treated group but not in the untreated group. Mitochondria isolated from hearts from the THP-treated group after normoxic reperfusion following hypoxic perfusion exhibited better respiratory function than those from untreated hearts. Conclusion The data suggest that feeding guinea pigs with THP results in reduced myocardial-free carnitine content and attenuation of hypoxic and reperfusion injury in isolated hearts.

scholarly journals Are high flow arteriovenous accesses associated with worse haemodialysis?

2018 ◽  
Vol 40 (2) ◽  
pp. 136-142 ◽  
Author(s):  
Ivo Laranjinha ◽  
Patrícia Matias ◽  
Ana Azevedo ◽  
David Navarro ◽  
Carina Ferreira ◽  
...  
Keyword(s):  
Multivariate Analysis ◽  
Cardiac Output ◽  
Retrospective Study ◽  
Randomized Controlled Trials ◽  
Volume Overload ◽  
Dry Weight ◽  
High Flow ◽  
Controlled Trials ◽  
Bioimpedance Spectroscopy ◽  
Randomized Controlled

ABSTRACT Introduction: An arteriovenous (AV) access flow (Qa) of 400 mL/min is usually sufficient for an effective hemodialysis (HD), but some accesses continue developing and become high flow accesses (HFA). Some authors postulated that an HFA might shift a significant portion of dialyzed blood from the cardiac output, which could decrease HD efficiency and lead to volume overload. Objective: The aim of our study was to evaluate if HFA is associated with reduced HD efficiency and/or volume overload in prevalent HD patients. Methods: We performed a 1-year retrospective study and assessed HD efficiency by the percentage of sessions in which the Kt/V > 1.4 and volume overload by bioimpedance spectroscopy. Results: The study included 304 prevalent HD patients with a mean age of 67.5 years; 62.5% were males, 36.2% were diabetics, with a median HD vintage of 48 months. Sixteen percent of the patients had a HFA (defined as Qa > 2 L/min). In multivariate analysis, patients with HFA presented higher risk of volume overload (OR = 2.67, 95%CI = 1.06-6.71) and severe volume overload (OR = 4.06, 95%CI = 1.01-16.39) and attained dry weight less frequently (OR = 0.37, 95%CI = 0.14-0.94). However, HFA was not associated with lower Kt/V. Conclusion: Our results suggest that patients with HFA have higher risk of volume overload. However, contrarily to what has been postulated, HFA was not associated with less efficient dialysis, measured by Kt/V. Randomized controlled trials are needed to clarify these questions.

Influence of the pericardium on left ventricular diastolic pressure-volume curves in dogs with sustained volume overload

1983 ◽  
Vol 105 (6) ◽  
pp. 995-1001 ◽  
Author(s):  
Valmik Bhargava ◽  
Ralph Shabetai ◽  
John Ross ◽  
Kunio Shirato ◽  
Richard S. Pavelec ◽  
...  
Keyword(s):  
Diastolic Pressure ◽  
Volume Overload ◽  
Left Ventricular

scholarly journals Modification of a Volume-Overload Heart Failure Model to Track Myocardial Remodeling and Device-Related Reverse Remodeling

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Egemen Tuzun ◽  
Roger Bick ◽  
Cihan Kadipasaoglu ◽  
Jeffrey L. Conger ◽  
Brian J. Poindexter ◽  
...  
Keyword(s):  
Heart Failure ◽  
Wall Thickness ◽  
Ventricular Remodeling ◽  
Diastolic Pressure ◽  
Volume Overload ◽  
Left Ventricular ◽  
Reverse Remodeling ◽  
Sheep Model ◽  
Dystrophin Expression ◽  
Cellular Markers

Purpose. To provide an ovine model of ventricular remodeling and reverse remodeling by creating congestive heart failure (CHF) and then treating it by implanting a left ventricular assist device (LVAD). Methods. We induced volume-overload heart failure in 2 sheep; 20 weeks later, we implanted an LVAD and assessed recovery 11 weeks thereafter. We examined changes in histologic and hemodynamic data and levels of cellular markers of CHF. Results. After CHF induction, we found increases in LV end-diastolic pressure, LV systolic and diastolic dimensions, wall thickness, left atrial diameter, and atrial natriuretic protein (ANP) and endothelin-1 (ET-1) levels; β-adrenergic receptor (BAR) and dystrophin expression decreased markedly. Biopsies confirmed LV remodeling. After LVAD support, LV systolic and diastolic dimensions, wall thickness, and mass, and ANP and ET-1 levels decreased. Histopathologic and hemodynamic markers improved, and BAR and dystrophin expression normalized. Conclusions. We describe a successful sheep model for ventricular and reverse remodeling.

Left ventricular failure induced by myocardial infarction. I. Myocyte hypertrophy

1985 ◽  
Vol 248 (6) ◽  
pp. H876-H882 ◽  
Author(s):  
P. Anversa ◽  
A. V. Loud ◽  
V. Levicky ◽  
G. Guideri
Keyword(s):  
Myocardial Infarction ◽  
Diastolic Pressure ◽  
Pressure Overload ◽  
Volume Overload ◽  
Left Ventricular Pressure ◽  
Systolic Arterial Pressure ◽  
Left Ventricular ◽  
Cellular Growth ◽  
Left Ventricular Failure ◽  
Ventricular Failure

To determine whether left ventricular failure after acute myocardial infarction is associated with a growth response of the myocytes that tends to compensate for the loss of muscle mass and function, the left coronary artery in rats was ligated near its origin, and the animals were killed 3 days later. Elevated left ventricular end-diastolic pressure and decreased first derivative of left ventricular pressure and systolic arterial pressure indicated significant impairment of ventricular function. Absolute infarct size, determined morphometrically by measurement of the fraction of myocyte nuclei lost, averaged 57%. Hypertrophy of surviving left ventricular myocytes was 28%, involving a 14% increase in cell length and a 6% increase in diameter. Right ventricular myocyte volume per nucleus increased 21% by a 10% enlargement of cellular diameter with no change in length. These results show on a cellular basis that myocardial hypertrophy in the left ventricle is accomplished by cellular shape changes characteristic of a combination of pressure and volume overload hypertrophy, whereas cellular growth in the right ventricle is consistent with pressure overload hypertrophy.

Captopril reduces left ventricular enlargement induced by chronic volume overload

1990 ◽  
Vol 259 (3) ◽  
pp. H796-H803
Author(s):  
R. G. Gay
Keyword(s):  
Pulse Pressure ◽  
Diastolic Pressure ◽  
Ex Vivo ◽  
Volume Overload ◽  
Wall Stress ◽  
Left Ventricular ◽  
Aortic Occlusion ◽  
End Diastolic Volume ◽  
Volume Relation ◽  
Captopril Treatment

The effect of captopril treatment on left ventricular (LV) function, mass, and volume during chronic volume overload induced by production of aortic insufficiency (AI) was studied. AI was caused by mechanical disruption of the aortic valve in 175- to 225-g male Sprague-Dawley rats. At 24 h after surgery, AI and sham-operated rats were divided into control and captopril treatment (2 g/l drinking water) groups. After 2 mo of treatment, hemodynamics were measured in open-chest rats, and the LV pressure-volume relation was determined ex vivo. Compared with sham-operated rats, in the untreated AI rats, aortic pulse pressure was increased nearly 100%, LV end-diastolic pressure was 10 +/- 1 vs 3 +/- 1 mmHg, and LV end-diastolic volume was 1.25 +/- 0.07 vs 0.36 +/- 0.03 ml. LV weight was increased 43% and the LV pressure-volume relation was shifted rightward by AI. LV systolic and diastolic wall stress were increased in rats with AI. Peak LV pressure during aortic occlusion was decreased in AI rats, however, peak wall stress during aortic occlusion was not different compared with sham-operated rats. Captopril treatment decreased aortic pulse pressure and LV systolic pressure. Both LV weight and LV end-diastolic volume measured from the ex vivo pressure-volume relation at LV end-diastolic pressure were increased by 33% in untreated AI rats compared with captopril-treated AI rats. Captopril treatment of AI rats shifted the LV pressure-volume to the left compared with untreated rats. LV pressure and wall stress during aortic occlusion were not changed in captopril-treated AI rats.(ABSTRACT TRUNCATED AT 250 WORDS)

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