Artykuły w Czytelni Medycznej o SARS-CoV-2/Covid-19

Zastanawiasz się, jak wydać pracę doktorską, habilitacyjną lub monografię? Chcesz dokonać zmian w stylistyce i interpunkcji tekstu naukowego? Nic prostszego! Zaufaj Wydawnictwu Borgis – wydawcy renomowanych książek i czasopism medycznych. Zapewniamy przede wszystkim profesjonalne wsparcie w przygotowaniu pracy, opracowanie dokumentacji oraz druk pracy doktorskiej, magisterskiej, habilitacyjnej. Dzięki nam nie będziesz musiał zajmować się projektowaniem okładki oraz typografią książki.

Poniżej zamieściliśmy fragment artykułu. Informacja nt. dostępu do pełnej treści artykułu tutaj
© Borgis - Postępy Nauk Medycznych 6/2011, s. 523-528
*Ryszard Gellert1, Dorota Daniewska1, Danuta Kobus1, Tomasz Żelek1, Ewa Wolska1, Wojciech Drewniak2, Joanna Kotlarska2
Akwafereza w leczeniu zaostrzenia przewlekłej niewydolności serca – uzasadnienie i początkowe doświadczenia kliniczne jednego ośrodka
AQUAPHERESIS for Acute Decompensated Heart Failure in Adults – rationale and initial clinical experience in a single center
1Department of Nephrology, Medical Center for Postgraduate Education, Warsaw
Head of Department: prof. Ryszard Gellert
2Department of Cardiology, Warsaw Medical University, Warsaw
Head of Department: prof. Marek Dąbrowski
Kolejnych 20 pacjentów z opornym na diuretyki zaostrzeniem przewlekłej niewydolności serca poddano 1-11 sesji izolowanej ultrafiltracji. W przypadku, gdy pojawiały się biochemiczne wskazania do lecznia nerkozastępczego, po zakończeniu sesji ultrafiltracji wykonywano hemodializę. Nie stwierdzono istotnych klinicznych ani technicznych problemów w usuwaniu tą metodą 2500-3500 ml wody osocza w czasie pojedynczej sesji i redukowania w ten sposób ciężaru ciała o 12-30 kg. Śmiertelność w całej grupie wyniosła 45%, ale była niższa u osób poniżej 80. roku życia (27,3%). Hemodializ wymagał jeden z 9 pacjentów mających mniej niż 80 lat i wypisanych ze szpitala, a tylko 1 z 5 powyżej 80. roku życia, którzy wymagali hemodializ został wypisany ze szpitala. Wnioskujemy, że izolowana ultrafiltracja jest bezpieczną procedurą leczniczą, która może być oferowana pacjentom z oporną na diuretyki ciężką niewydolnością krążenia, a dołączająca się konieczność leczenia hemodializami jest złym czynnikiem rokowniczym, zwłaszcza u osób po 80. roku życia.
20 consecutive patients presenting with acute decompensated diuretic-resistant heart failure were subjected to 1-11 sessions of isolated ultafiltration, followed by hemodialysis when biochemically indicated. There were no major technical nor clinical problems to remove 2500-3500 ml/session and reduce the body weight by even 12 or 30 kg. The crude mortality rate was 45% for the whole group, but only 27.3% in patients aged less than 80 years. One patient below the age of 80, out of 9 discharged, needed concomitant hemodialysis, but only one of those over 80 out of 5 in need for concomitant hemodialysis survived. We conclude ultrafiltration is a safe procedure that could be offered to diuretic resistant patients with severe congestive heart failure, but the ensuing need for concomitant hemodialysis is a bad prognostic factor, especially in patients over 80 years of age.
Aquapheresis means taking away (aphairesis, gr.) water (aqua, lat.) from the body, with an objective to restore euvolemia in fluid overloaded patients. Fluid overload can be caused by numerous reasons, mainly by heart, liver and kidney diseases. Congestive heart failure (CHF) is the most common reason for severe hypervolemia. Out of 105 388 CHF patients in 274 hospitals, congestion was present in almost 90%. The most common co-morbid conditions were hypertension (73%), coronary artery disease (57%), and diabetes (44%). Interestingly, the evidence of mild or no impairment of systolic function was found in 46% of patients only. In-hospital mortality was 4.0% and the median hospital length of stay was 4.3 days (1). The reduction, or even total removal, of extra body fluid is crucial to the successful therapy of the acute decompensated heart failure (ADHF) in patients with advanced heart failure. This is usually achieved with the use of saluretics, usually furosemide, indapamide, or torasemide, given orally in outpatient settings. If the in-patient treatment for ADHF is needed, furosemide as intravenous bolus or infusion is the therapeutic gold standard.
ADHF is defined as rapid appearance or worsening of clinical symptoms resulting from systolic or diastolic heart dysfunction, cardiac rhythm disturbance, or inadequate pre- or afterload. It can present in patients with or without previous heart dysfunction, and both conditions lead to the impaired blood volume distribution (to the venous compartment – pulmonary or systemic). Typically, the body fluid volume is increased in patients with chronic heart failure, and normal in patients with no underlying heart disease. The use of diuretics, which is obligatory in ADHF and CHF, in patients presenting ADHF and no fluid retention needs very careful, individualized evaluation, to avoid further decrease in effective blood volume.
The most common factors that precipitate hospitalization for decompensated heart failure are (2):
• Noncompliance with medical regimen, sodium and/or fluid restriction.
• Acute myocardial ischemia.
• Uncorrected high blood pressure.
• Atrial fibrillation and other arrhythmias.
• Recent addition of negative inotropic drugs (e.g., verapamil, nifedipine, diltiazem, beta blockers).
• Pulmonary embolus.
• Nonsteroidal anti-inflammatory drugs.
Excessive alcohol or illicit drug use.
• Endocrine abnormalities (e.g., diabetes mellitus, hyperthyroidism, hypothyroidism).
Concurrent infections (e.g., pneumonia, viral illnesses).
The venous blood volume expansion, pulmonary and systemic (both, splanchnic and peripheral), typical of CHF, results from decreased cardiac output, vascular resistance or pathological flow between the cardiac cavities. Even if the effective blood volume (i.e. inside the big arterial vessels) in chronic heart failure has been well preserved, the venous compartment is enlarged, second to sodium and water retention resulting from renal hypoperfusion. The chronic renal hypoperfusion second to heart dysfunction (cardiorenal syndrome type II) triggers many adaptive mechanisms – activation of renin-angiotensin-aldosterone axis, vasopressin release, increased blood natriuretic hormone levels and many others. Fluid retention leads to the increased pre- or afterload, increased cardiac filling pressures, myocardiac distention and remodeling, which close the vicius circle of progressive heart injury (3), and further deteriorate renal filtration (GFR) (4). The last might also result directly from the increased splanchnic venous pressure (5). This remains true for the opposite situation, when the fluid retention is triggered by renal insufficiency.
It is well known the hemoconcentration resulting from intensive diuretic treatment correlates positively with reduction of GFR in CHF and the decreased post-hospital survival (6). The higher the dose of diuretics is needed for reducing hypervolemia the worse is the prognosis (7, 8). The reduction in GFR and the CHF are the well known independent risk factors for death in general population. The coexistence of the two is even more fatal (9), which clearly suggest, aggressive diuretic therapy resulting in worsening renal fuction should be avoided. Renal failure worsens prognosis in both, the systolic and the diastolic CHF, and the impact of renal failure is more visible in patients with preserved ejection fraction (10), and even more in those with coexisting anemia (11). The episode of ADHF further worsens post-hospital CHF patients’ survival, irrespective of renal failure (12). In-hospital mortality is increased and the length of stay prolonged in ADHF patients with renal failure (13). Interestingly, heart failure in patients on chronic hemodialysis is not a frequent cause of death, for it accounts for 7% of death only (14).
Worsening of renal insufficiency leads to less secretion of diuretics into the tubular fluid, so it requires an increase in the total dose of diuretic for an effective amount reaches its site of action (15). However, the diuretic-induced activation of the renin-angiotensin-aldosterone system, results in an increased sodium and water reabsorption through a variety of mechanisms. Hypertrophy of distal tubule epithelial cells results in greater sodium absorption distal to the loop of Henle, the site of action of loop diuretics (16). In patients with decompensated heart failure, venous pressure is also elevated, leading to decreased absorption of oral agents and decreased renal blood flow and consequently, renal sodium excretion (17).
In case the diuretic resistance ensues, due to renal injury or any other cause, the retained fluid can be rapidly removed from the body by inducing massive diarrhea, the use of vasopressin receptor antagonists (vaptans), which is still not well established, or by a well know mechanical, extracorporeal support which enables to control the volume and rate of water removal.
The first action on blood taken by the kidney is to separate plasma water in the renal glomerulus. Exactly the same process is mimicked by dialysers and hemofilters in a process driven by exerting the hydraulic pressure difference between blood and the contralateral side of the semipermeable filtration membrane. This convective technique became available to dialysis patients in mid-seventies of the past century. And from the very first moment it was clear the procedure could be usefull in treating decompensated heart failure (18). This convective process has to be individually tailored regarding the volume and rate of fluid removal. If it takes several hours (usually more than 6), and the rate of ultrafiltration is of maximum 0.16 ml/min/kg lean body mass (usually 500 ml/h in adults), the procedure is called slow continuous ultrafiltration (SCCUF). The higher ultrafiltration volumes and higher ultrafiltration rates cause hemoconcentration and call for intravenous infusion of crystalloids to prevent it. In such case the process is called hemofiltration (HF). The infusion of a substitution fluid is the only factor to differentiate SCUF and HF. The last one can last longer than 24 hours, which is known as continuous hemofiltration. It is usually performed on venous blood (continuous veno-veno hemofiltration, CVVH). Quick removal of relatively small amount of plasma water is called isolated ultrafiltration (IUF), to differentiate it from the ultrafiltration (UF) occurring during hemodialysis.
There are three types of engines enabling filtration – hemodialysis monitor to perform isolated ultrafiltration, continuous renal replacement therapy monitors to perform SCUF or CVVHF, and specialized ultrafiltration monitors to perform solely the SCUF. The last technology is currently commercially unavailable in Europe. All three techniques operate on venous blood, which means blood is taken from the splanchnic overloaded compartment and returned to it after the volume has been reduced by ultrafiltration. The access to venous blood to ensure sufficient extracorporeal blood flow is possible by insertion of a central catheter. Typically the 250-500 ml/h of water is removed, the blood flow varies 20-200 ml/min, and systemic coagulation is obtained with heparin infusion (1000 IU/h, adjusted accordingly to ACT). The volume of the In-circuit extracorporeal blood is small – 30-50 ml.
Removig only 2-3 l of plasma water in 4-6 hours promotes relief of dyspnea, reduces the right (-70%) and left (-45%) ventricular filling pressures, the pulmonary arterial pressure and arteriolar resistance, without significant variations in heart rate, aortic pressure, cardiac index, and systemic vascular resistance. The urinary output is substantially enhanced by the procedure (19). Even removing as little as 1.6 l of plasma water by aquapheresis resulted within the first 48 hours in significant, and sustained for at least three month, decrease in plasma renin, norepinephrine, and aldosterone. This was not observed after furosemide (20). Also the removal of more than 4 l of plasma water was safe and resulted in clinical improvement (21).
However, the intention to remove 4 liters of plasma water in 8 hours results, in 45% of patients, in plasma creatinine increase of at least 0.3 mg/dl (22). This means the ultrafiltration rate of 500 ml/min for longer than 6 hours, and decreasing body fluids by 3 liters, results in severe renal hypoperfusion (and even acute renal injury) in 45% of patients, and is similar to that caused by intravenous saluretics (23).
For the aforementioned reasons congestion, the most frequent reason for hospital admission due to heart failure, which is traditionally treated with loop diuretics, should be removed with UF, if resistance to diuretics ensues. Diuretics, particularly in high doses, can be deleterious. In addition, patients with renal hypoperfusion second to advanced heart failure present diminished response to loop diuretics. In such cases, ultrafiltration removes more body fuids as compared to diuretics, while demonstrating no major safety concerns, and decreasing re-hospitalizations within 90 days in selected groups of patients. Generally, ultrafiltration for removing water excess in diuretic resistant patients presenting with ADHF, or severe CHF is considered a safe, well tolerated procedure, which in some cases restores sensitivity to diuretics.
Material and methods

Powyżej zamieściliśmy fragment artykułu, do którego możesz uzyskać pełny dostęp.

Płatny dostęp do wszystkich zasobów Czytelni Medycznej

Aby uzyskać płatny dostęp do pełnej treści powyższego artykułu oraz WSZYSTKICH około 7000 artykułów Czytelni, należy wprowadzić kod:

Kod (cena 30 zł za 30 dni dostępu) mogą Państwo uzyskać, przechodząc na tę stronę.
Wprowadzając kod, akceptują Państwo treść Regulaminu oraz potwierdzają zapoznanie się z nim.

1. Adams KF Jr, Fonarow GC, Emerman CL et al.: ADHERE Scientific Advisory Committee and Investigators. Characteristics and outcomes of patients hospitalized for heart failure in the United States: rationale, design, and preliminary observations from the first 100,000 cases in the Acute Decompensated Heart Failure National Registry (ADHERE). Am Heart J 2005; 149: 209-16.
2. Jessup M, Abraham WT, Casey DE et al.: 2009 focused update: ACCF/AHA Guidelines for the Diagnosis and Management of Heart Failure in Adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: developed in collaboration with the International Society for Heart and Lung Transplantation. Circulation 2009; 119: 1977-2016.
3. Bart BA: Treatment of congestion in congestive heart failure: ultrafiltration is the only rational initial treatment of volume overload in decompensated heart failure. Circ Heart Fail 2009; 2: 499-504.
4. Damman K, van Deursen VM, Navis G et al.: The Increased Central Venous Pressure Is Associated With Impaired Renal Function and increased Mortality in a Broad Spectrum of Patients With Cardiovascular Disease. J Am Coll Cardiol 2009; 53: 597-9.
5. Mullens W, Abrahams Z, Skouri HN et al.: Elevated Intra-Abdominal Pressure in Acute Decompensated Heart Failure A Potential Contributor to Worsening Renal Function? J Am Coll Cardiol 2008; 51: 300-6.
6. Testani JM, Chen J, McCauley BD et al.: Potential Effects of Aggressive Decongestion During the Treatment of Decompensated Heart Failure on Renal Function and Survival. Circulation 2010; 122: 265-72.
7. Mielniczuk LM, Tsang SW, Desai AS et al.: The Association Between High-Dose Diuretics and Clinical Stability in Ambulatory Chronic Heart Failure Patients. J Card Fail 2008; 14: 388-93.
8. Peacock WF, Costanzo MR, De Marco T et al.: ADHERE Scientific Advisory Committee and Investigators. Impact of intravenous loop diuretics on outcomes of patients hospitalized with acute decompensated heart failure: insights from the ADHERE registry. Cardiology 2009; 113 (1): 12- 9.
9. Sandhu A, Soman S, Hudson M, Besarab A: Managing anemia in patients with chronic heart failure: what do we know? Vasc Health Risk Manag 2010; 6: 237-52.
10. Ahmed A, Rich MW, Sanders PW et al.: Chronic kidney disease associated mortality in diastolic versus systolic heart failure: a propensity matched study. Am J Cardiol 2007 Feb 1; 99 (3): 393-8.
11. Al-Ahmad A, Rand WM, Manjunath G et al.: Reduced kidney function and anemia as risk factors for mortality in patients with left ventricular dysfunction.J Am Coll Cardiol 2001; 38: 955-62.
12. Ahmed A, Allman RM, Fonarow GC et al.: Incident heart failure hospitalization and subsequent mortality in chronic heart failure: a propensity-matched study. J Card Fail 2008; 14: 211-218.
13. Fonarow GC, Adams KF, Abraham WT: ADHERE Investigators. Risk stratification for in-hospital mortality in heart failure using classification and regression tree (CART) methodology: analysis of 33,046 patients in the ADHERE registry. J Cardiac Fail 2003; 9: S79.
14. Drechsler C, Pilz S, Obermayer-Pietsch B et al.: Vitamin D deficiency is associated with sudden cardiac death, combined cardiovascular events, and mortality in haemodialysis patients. Eur Heart J 2010; 31: 2253-2261.
15. Brater DC: Diuretic therapy. N Engl J Med 1998; 339: 387-395.
16. Sarraf M, Masoumi A, Schrier RW: Cardiorenal syndrome in acute decompensated heart failure. Clin J Am Soc Nephrol 2009; 4: 2013-26.
17. Mullens W, Abrahams Z, Francis GS et al.: Importance of venous congestion for worsening of renal function in advanced decompensated heart failure. J Am Coll Cardiol 2009; 53: 589-96.
18. Silverstein ME, Ford CA, Lysaght MJ, Henderson LW: Treatment of Severe Fluid Overload by Ultrafiltration N Engl J Med 1974; 291: 747-751.
19. Rimondini A, Cipolla CM, Della Bella P et al.: Hemofiltration as short-term treatment for refractory congestive heart failure. Am J Med 1987; 83: 43-8.
20. Agostoni P, Marenzi G, Lauri G et al.: Sustained improvement in functional capacity after removal of body fluid with isolated ultrafiltration in chronic cardiac insufficiency: failure of furosemide to provide the same result. Am J Med 1994; 96: 191-9.
21. Marenzi G, Lauri G, Grazi M et al.: Circulatory response to fluid overload removal by extracorporeal ultrafiltration in refractory congestive heart failure. J Am Coll Cardiol 2001; 38: 963-8.
22. Liang KV, Hiniker AR, Williams AW et al.: Use of a novel ultrafiltration device as a treatment strategy for diuretic resistant, refractory heart failure: initial clinical experience in a single center. J Card Fail 2006; 12: 707-14.
23. Rogers HL, Marshall J, Bock J et al.: A Randomized, Controlled Trial of the Renal Effects of Ultrafiltration as Compared to Furosemide in Patients With Acute Decompensated Heart Failure, Journal of Cardiac Failure 2008; 14: 1-5.
24. Snopek G, Kotlarska J, Daniewska D et al.: Zastosowanie ultrafiltracji żylnej w leczeniu chorych z ciężką, oporną na leczenie zastoinową niewydolnością serca – opis sześciu przypadków. Kardiol Pol 2008; 66: 1202-1204.
25. Giglioli C, Landi D, Cecchi E et al.: Effects of ULTRAfiltration vs. DIureticS on clinical, biohumoral and haemodynamic variables in patients with deCOmpensated heart failure: the ULTRADISCO study Eur J Heart Fail 2011; 13: 337-346.
26. Costanzo MR, Guglin ME, Saltzberg MT et al.: UNLOAD Trial Investigators. Ultrafiltration versus intravenous diuretics for patients hospitalized for acute decompensated heart failure. J Am Coll Cardiol 2007; 49: 675-83.
27. Costanzo MR, Saltzberg MT, Jessup M et al.: Ultrafiltration Versus Intravenous Diuretics for Patients Hospitalized for Acute Decompensated Heart Failure (UNLOAD) Investigators. Ultrafiltration is Associated With Fewer Rehospitalizations than Continuous Diuretic Infusion in Patients With Decompensated Heart Failure: Results From UNLOAD. Journal of Cardiac Failure 2010; 16: 277-284.
28. Kamath SA: The role of ultrafiltration in patients with decompensated heart failure. Int J Nephrol. 2011 (2011), 190230, 6 pages, doi:10.4061/2011/190230.
29 Costanzo MR, Saltzberg M, O’Sullivan J, Sobotka P: Early ultrafiltration in patients with decompensated heart failure and diuretic resistance. J Am Coll Cardiol 2005; 46: 2047-51.
30. Bart BA, Boyle A, Bank AJ et al.: Ultrafiltration versus usual care for hospitalized patients with heart failure: the Relief for Acutely Fluid-Overloaded Patients With Decompensated Congestive Heart Failure (RAPID-CHF) trial. J Am Coll Cardiol 2005 Dec 6; 46 (11): 2043-2046.
31. Mitra S, Chamney P, Greenwood R, Farrington K: The relationship between systemic and whole-body hematocrit is not constant during ultrafiltration on hemodialysis. J Am Soc Nephrol 2004 Feb; 15 (2): 463-469.
32. Shimazaki M: Is estimation of laser Doppler skin perfusion pressure appropriate during hemodialysis enforcement? The Internet Journal of Cardiovascular Research 2009; 6: 2.
33. Schneditz D, Roob J, Oswald M et al.: Nature and rate of vascular refilling during hemodialysis and ultrafiltration. Kidney Int 1992; 42: 1425-1433.
34. Marenzi G, Lauri G, Grazi M et al.: Circulatory response to fluid overload removal by extracorporeal ultrafiltration in refractory congestive heart failure. J Am Coll Cardiol 2001; 38: 963-968.
35. Jessup M, Abraham WT, Casey DE et al.: 2009 Focused Update: ACCF/AHA Guidelines for the Diagnosis and Management of Heart Failure in Adults: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines Developed in Collaboration With the International Society for Heart and Lung Transplantation. J Am Coll Cardiol 2009; 53: 1343-1382.
otrzymano: 2011-03-01
zaakceptowano do druku: 2011-05-04

Adres do korespondencji:
*Ryszard Gellert
Department of Nephrology Medical Center for Postgraduate Education
Bielański Hospital
Cegłowska Street 80, 01-809 Warsaw
phone: +48 (22) 569-02-06

Postępy Nauk Medycznych 6/2011
Strona internetowa czasopisma Postępy Nauk Medycznych