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 Table of Contents  
ORIGINAL ARTICLE
Year : 2019  |  Volume : 17  |  Issue : 4  |  Page : 349-353

Effect of extracorporeal blood flow on blood pressure, pulse rate, and cardiac output in hemodialysis patients


1 Internal Medicine Department, Assiut University, Assiut, Egypt
2 Internal Medicine Department, Aswan University, Aswan, Egypt
3 Cardiology Department, Aswan University, Aswan, Egypt

Date of Submission28-Apr-2019
Date of Decision21-Jun-2019
Date of Acceptance22-Jul-2019
Date of Web Publication14-Feb-2020

Correspondence Address:
Hala A El-Ebidi
Nephrology Unit, Internal Medicine Department, Aswan University Hospital, Aswan, 81528
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/AZMJ.AZMJ_73_19

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  Abstract 


Background Intradialytic hypotension (IDH) is a common clinical practice to reduce the extracorporeal blood flow rate (EBFR).
Aim The aim of this study is to investigate the effect of changes in EBFR on blood pressure (BP), pulse rate (PR), and cardiac output (COP) in hemodynamically stable patients during hemodialysis (HD).
Patients and methods The population of this study consists of 40 patients who were on RD three session weekly. Patients were investigated before and after one conventional HD session. Before the HD session, an echocardiograph was performed to evaluate left ventricular ejection fraction and establish the degree of potential heart failure. Furthermore, arteriovenous fistula recirculation, a confounder of the measurement of EBFR, was excluded at an EBFR of 400 ml/min.
Result In this study regarding measure of BP, PR, and COP at EBFR 200, 300, and 400 ml/min, there was a significant increase in systolic BP at an EBFR of 200 ml/min as compared with an EBFR of 300 ml/min and an EBFR of 400 ml/min, but there was no significant change in systolic BP at an EBFR of 300 ml/min as compared with an EBFR 400 ml/min. Regarding diastolic BP, mean arterial pressure, PR, and COP at an EBFR of 200, 300, and 400 ml/min, there was no significant change in mean arterial pressure and COP.
Conclusion IDH has been associated with many adverse clinical events including myocardial stunning, cerebral atrophy, and increased mortality. Change of EBFR from 400 ml/min or from 300 ml/min to EBFR 200 ml/min can increase in BP, so it helps in decreased occurrence of complications of IDH, compared with other methods of increasing BP during HD. There is no significant relation between change of EBFR and diastolic BP.

Keywords: blood flow rate, cardiac output, extracorporeal circulation, intradialytic hypotension, renal dialysis


How to cite this article:
Hafez MZ, El-Ebidi HA, Mohammed RG, Ahmed OA. Effect of extracorporeal blood flow on blood pressure, pulse rate, and cardiac output in hemodialysis patients. Al-Azhar Assiut Med J 2019;17:349-53

How to cite this URL:
Hafez MZ, El-Ebidi HA, Mohammed RG, Ahmed OA. Effect of extracorporeal blood flow on blood pressure, pulse rate, and cardiac output in hemodialysis patients. Al-Azhar Assiut Med J [serial online] 2019 [cited 2020 Sep 29];17:349-53. Available from: http://www.azmj.eg.net/text.asp?2019/17/4/349/278399




  Introduction Top


Symptomatic hypotension during hemodialysis (HD) [intradialytic hypotension (IDH)] occurs in 15–30% of HD sessions [1], and it is an independent predictor of cardiovascular morbidity [2] and mortality [3].

IDH events are a common complication of maintenance HD, affecting up to one-third of chronic dialysis treatment sessions [4]. IDH can be defined as an abrupt decline in blood pressure (BP) that causes symptoms and/or requires an intervention [5]. IDH has been associated with many adverse clinical events, including myocardial stunning [6], cerebral atrophy [7] and increased mortality [8].

Predisposing factors include intrinsic patient-related factors such as the presence of autonomic neuropathy [9], abnormal cardiac reserve [10], and reduced venous compliance [11] as well as potentially modifiable treatment-related parameters such as ultrafiltration (UF) profiling [12] and changes in serum calcium concentration [13].

The underlying pathophysiology of IDH seems to be multifactorial. Factors such as inadequate plasma volume during fluid removal [1], rapid reduction in plasma osmolality [14], autonomic dysfunction [15], heart disease [16], impaired baroreflexes [17], release of endotoxins [18], adenosine [19], and increased synthesis of endogenous vasodilators have been suggested [20].

IDH is usually treated by discontinuation of fluid removal and volume replacement [3]. Reduction in extracorporeal blood flow rate (EBFR) during HD has been suggested as a supplementary treatment modality [21]. However, data on the effect of changes in EBFR on BP during HD are conflicting and very limited. Interestingly, data from Trivedi et al. [22] demonstrated that the systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean BPs were significantly higher during the BFR of 400 ml/min as compared with the blood flow of 200 ml/min; however, data from Philip et al. [23] demonstrated a SBP was significantly higher at an EBFR of 200 ml/min as compared with 300 ml/min, but not as compared with 400 ml/min. At EBFR of 200, 300, and 400 ml/min, DBP, mean arterial pressure (MAP), pulse rate (PR), and cardiac output (COP) remained unchanged.


  Aim Top


The aim of this study is to investigate the effect of changes in EBFR on BP, PR, and COP in hemodynamically stable patients during HD.


  Patients and methods Top


The population of this study consists of 40 patients on RD three session weekly. The study was approved by the ethical committee, and a written consent was taken from all patients involved.

Inclusion criteria

The following were the inclusion criteria:
  1. Patients with an arteriovenous fistula as vascular access.
  2. Age of 18 years or above. Before study examination, the selected patients were not susceptible to symptomatic BP decline during HD.


Exclusion criteria

The following were the exclusion criteria:
  1. Pregnancy
  2. Dementia.
  3. Asymptomatic decline in SBP below 100 mmHg or a symptomatic decline in SBP equal to or above 30 mmHg during study examination.


Methods

Patients were investigated before and after one conventional HD session done by using 4008S hemodialysis machine (Fresenius Medical Care 61346 Bad Homburg v. d. H., Germany). Before the HD session, echocardiography was performed to evaluate left ventricular ejection fraction and establish the degree of potential heart failure. Furthermore, arteriovenous fistula recirculation (15 patients with radiocephalic fistula and 25 patients with brachiocephalic fistula), a confounder of the measurement of EBFR, was excluded at an EBFR of 400 ml/min. Echocardiograph was performed by using ultrasound system (Philips IE 33) using an S5 transducer (manufactured by Philips Ultrasound, 3000 Minuteman Road Andover MA, United States). After the HD session with regular UF of a maximum of 1 l/h for the patients to obtain dry weight, UF was stopped, whereas dialysis was continued, to avoid any influence of fluid removal during the investigation. The patients were examined at EBFR of 200, 300, and 400 ml/min in random order.

Each EBFR was maintained for 15 min to gain steady state before measurements of BP, PR, and COP. BP and PR were measured thrice, and a mean was calculated, whereas COP was measured twice, and a mean was calculated. If there was a difference of more than 15%, a third COP was measured and the mean of the two nearest results was used for calculation. Apart from the assessment of body weight, all measurements were carried out with the patients in the supine position.

All HD sessions were according to the dialysis unit’s standard with a temperature of 37°C and dialysate ion-concentrations consisting of the following: NA+ 140 mmol/l, HCO3− 38 mmol/l, K+ 2.0 mmol/l, and CA2+ 1.25 mmol/l. Filters used were PF 170 or PF 210 from Gambro (Gambro Lundia AB Monitor Division Magistratsvägen, Lund, Sweden).

BP and PR were measured using the dialysis machine, whereas COP was measured using echocardiography.

All statistical studies were done using SPSS version 22 (IBM Software Group ATTN: Licensing 200 W, Madison, St. Chicago, IL, USA) ([Figure 1]).
Figure 1 Chart title shows chronic diseases among patients in the study.

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  Results Top


The demographic data of the patients are illustrated in [Table 1]. The study included 40 patients with end-stage renal disease on regular dialysis.
Table 1 Baseline patient characteristics and clinical data in the study group

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Their ages ranged from 29 to 67 years, with mean±SD of 51.6±9 years. Overall, 20 (50%) patients were males and 20 (50%) were females.

Among these patients, 23 (58%) had hypertension, 13 (32%) had diabetes mellitus, six (15%) had ischemic heart disease, two (4%) had systemic lupus erythematosus, one (2%) had bronchial asthma, one (2%) had rheumatic heart disease, and one (2%) had thyrotoxicosis.

[Table 2] shows that mean±SD SBP (130±14) at EBFR 200 was significantly higher (P<0.05) compared with mean±SD SBP (127±14) at EBFR of 300. However, the table shows that there was no significant change in mean±SD DBP (65.7±9.1) (P=0.16), mean±SD mean BP (84.7±9) (P=0.2), and mean±SD PR (76.8±6.9) (P=0.2) at EBFR 200 compared with mean±SD DBP (65.6±9), mean±SD mean BP (84.7±9.4), mean±SD PR (76.7±7), and mean±SD COP (4.92±0.6) (P=0.5) at EBFR 300.
Table 2 Blood pressure, pulse rate, and cardiac output at extracorporeal blood flow rates of 200 and 300

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[Table 3] shows that mean±SD SBP (130±14) at EBFR 200 was significantly higher (P<0.05) compared with mean±SD SBP (126±14) at EBFR 400. However, the table shows that there was no significant change in mean±SD DBP (65.7±9.1) (P=0.1), mean±SD mean BP (84.7±9) (P=0.8), mean±SD PR (76.8±6.9) (P=0.2), and mean±SD COP (4.91±0.7) (P=0.9) at EBFR 200 compared with mean±SD DBP (65.5±91), mean±SD mean BP (84.6±9), mean±SD PR (76.7±6.8), and mean±SD COP (4.89±0.6) at EBFR 400.
Table 3 Blood pressure, pulse, rate and cardiac output at extracorporeal blood flow rates of 200 and 400

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[Table 4] shows that there was no significant change in mean±SD SBP (126±14) (P=0.08), mean±SD DBP (65.6±9) (P=0.5), mean±SD mean BP (84.7±9.4) (P=0.6), mean±SD PR (76.7±7) (P=0.5), and mean±SD COP (4.92±0.6) (P=0.1) at EBFR 300 compared with mean±SD SBP (126±14), mean±SD DBP (65.5±9.1), mean±SD mean BP (84.6±9), mean±SD PR (76.7±6.8), and mean±SD COP (4.89±0.6) at EBFR 400.
Table 4 Blood pressure, pulse rate and cardiac output at of extracorporeal blood flow rates 300 and extracorporeal blood flow rates 400

Click here to view



  Discussion Top


In this study regarding measure of BP, PR, and COP at EBFR 200, 300, and 400 ml/min, there was a significant increase in SBP at an EBFR 200 ml/min as compared with an EBFR 300 ml/min and EBFR 400 ml/min, but there was no significant change in SBP at an EBFR 300 ml/min as compared with an EBFR 400 ml/min.

At EBFR 200, 300, and 400 ml/min, DBP, MAP, PR and COP showed no significant changes.

These results are similar to the results of Philip et al. [23], which found an increase in SBP at an EBFR 200 ml/min compared with that at EBFR 300 ml/min, but in the study by Philip et al., there was no significant change between SBP at EBFR 400 ml/min compared with EBFR 200 ml/min.

Against our study, Trivedi et al. [22] demonstrated an increase in SBP (4.1 mmHg) and DBP (3.0 mmHg) during an increase in EBFR from 200 to 400 ml/min.

A randomized study by Alfurayh et al. [24] examined the effect of randomly chosen EBFR of 250, 350, and 450 ml/min in 10 young, stable chronic HD patients free of antihypertensive treatment during three HD sessions a week apart. They found no changes in left ventricular ejection fraction or CO nor in PR or BP.

In a prospective, observational study of 218 prevalent HD patients, Flythe et al. [25] did not find any association between changes in EBFR and SBP variability (EBFR >400 vs. ≥400 ml/min). In contrast, data from the HEMO study [26] suggested a lower incidence of IDH with increasing EBFR.

Comparable to previous studies, there are several limitations of this study. None of the patients experienced any IDH during the investigation. Whether a reduction in EBFR during IDH will affect systemic BP is still not established.

All patients in this study were examined at the end of a conventional dialysis. Previous data by Bergström et al. [14] have demonstrated that a rapid reduction in plasma osmolarity (removal of urea and other solutes) initiated at the onset of HD contributes to IDH, owing to osmotic removal of fluid into the cells depleting the extracellular volume and interference with sympathetic responsiveness to volume depletion (UF).


  Conclusion Top


  1. IDH is a common complication in a HD patient, affecting up to one-third of chronic HD patients.
  2. IDH is an independent predictor of cardiovascular morbidity and mortality.
  3. IDH has been associated with many adverse clinical events including myocardial stunning, cerebral atrophy, and increased mortality.
  4. Change of EBFR from 400 ml/min or from 300 ml/min to EBFR 200 ml/min can increase BP, so it can help in decreased occurrence of complications of IDH, compared with other methods of increasing BP during HD.
  5. There is no significant relation between change of EBFR and DBP, MAP and COP.


Recommendation

  1. Decrease in EBFR to 200 ml/min will help us in prevention of IDH.
  2. Further studies are needed to evaluate the relation between EBFR and change in BP.
  3. Other studies needed to be done during HD without stopping UF.


Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

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    Figures

  [Figure 1]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

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