1. Intradialytic Hypotension
Hank Park

2. Hypotension is a big problem!
• Hypotension during dialysis treatment is an unresolved
issue.
• Delivery of an adequate dose of dialysis is essential to
improve the prognosis of dialysis patients
• Low blood pressure during the hemodialysis procedure is
expected to occur more frequently in patients with
comorbidities because it compels a limit to dialysis time
and dialysis efficacy.
- van der Zee S, Thompson A, Zimmerman R, et al: Vasopressin administration facilitates fluid removal during hemodialysis.
- Davenport A: Intradialytic complications during hemodialysis.
- Imai E, Fujii M, KohnoY, et al: Adenosine A1 receptor antagonist improves intradialytic hypotension.

3. IDH (Intradialytic Hypotension)
• Definition
: A fall in SBP by at least 20mmHg or SBP < 100mmHG
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Cause
Decline Cardiac Function and Systemic Vascular Resistance (SVR) during removed solute
A rapid reduction in Plasma osmolality
High Interdialytic weight gain
Anemia
Autonomic neuropathy
Decrease pressor response to Vasopressor agents
LV Hypertrophy & Decrease cardiac preload
Decrease cardiac reserve
Increase arterial stiffness
Impaired venous compliance
Meal
Use of low sodium/ Increase magnesium dialysate
Anti-hypertension medication before HD
Excessive release of vasodilators (Not Adrenomedullin and Adenosine)
Imbalance in the synthesis of vasoconstrictors (Endothelin & Vasopressin)

4. Intradialytic Hypotension (IDH)
mechanism?
Patient factors
 Cardiac disease
- Systolic dysfunction
- Diastolic dysfunction
 Arrhythmias
 Pericardial disease
 Autonomic neuropathy
 Dietary excess
 Interdialytic weight gain
 Food ingestion in dialysis
 Antihypertensive agents
 Anemia (< Hb 7.0g/dL)
Dialysis procedure factors
 Ultrafiltration, solute removal
 Thermal amplication
 Sympathetic failure
- Increased adenosine
- Increased nitric oxide
 Dialysate composition
 Low sodium (<138mEq/L)
 Low calcium
 High magnesium
 Acetate

5. Brandon’s talk with Dr. Aviram
• Primary concerns
: Hypotension
: Efficiency

6. IDH ---> Hypertension
• Mechanism of therapy for intradialytic hypotension are
of great interest (van der Zee. S et al.)
• Increase in adenosine generation during hemodialysis
may cause vasodilation and decrease in cardiac
output, which results in systemic hypotension (Imai. E et al.)
• Removal of excess extracellular fluid -> symptomatic
decreases in arterial pressure -> intradialytic
hypotension -> chronically volume-expanded ->
Chronic Hypertension (van der Zee. S et al.)

7. Solution?
Routine management
of IDH
 Target dry weight
 Diet fluid counseling
 Medication adjustment
 Correct anemia
 High sodium dialysate
 Sodium modeling
Individualized therapy
of IDH
 High calcium dialysate
 Low-magenesium dialysate
 Carnitine
 Sertraline
 Cool dialysate
 Midodrine (A vasopressor /
antihypotensive agent)

8. How to increase BP?
Farese S. et al. Am J Kidney Dis. 2008.
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TEMS : Transcutaneous muscle simulation , PCMs : Passive cycling movement
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For each patient, each procedure was performed only once weekly and never on
the same weekday.

9. Patient Characteristics

10. TEMS & PCMs during dialysis show
significant results in raising BP

11. Increased Cardiac Output!
• Heart rate was unchanged during both treatment (TEMS &
PCM) modalities.
• Therefore, the observed increase in blood pressure can
only be explained by an increase in either peripheral
resistance or cardiac output.
• For TEMS and active exercise, decreased vascular resistance
has been described. Miller BF et al. Phys Ther 80:53-60, 2000
• Thus, increased cardiac output is a more likely explanation
for the increase in blood pressure, a contention supported
because increased central blood and preload volume
positively alter cardiac output. Hanft LM et al. Cardiovasc Res 77:627-636, 2008
• There is an evidence that electrical muscle stimulation
increases venous backflow from the musculature. Clarke Moloney M
et al. Eur J Vasc Endovasc Surg 31:300-305, 2006

12. Efficiency? Urea & Phosphate!
• Longer observation periods with more patients are needed to
assess potential benefits of TEMS and PCMs on hypotensive
episodes during dialysis sessions

13. Several Studies about Passive Training
• Passive movement of the lower leg has been found to result in an
approximate three-fold increase in muscle blood flow, and stretch
of the muscle tissue without an alteration in either EMG activity or
muscle oxygen uptake. (Krustrup et al. 2004)
• Vascular endothelial growth factor (VEGF) is probably one of the
most important factor for endothelial activation, proliferation and
migration.
• The passive movement model induced an enhanced level of muscle
interstitial VEGF protein and an increased endothelial cell
proliferative effect of muscle interstitial fluid from the muscle as
well as a higher expression of endothelial nitric oxide synthase
(eNOS) mRNA in the muscle. (Hellsten et al. 2008, Am J Physiol
Regul Integr Comp Physiol)

14. Capillarization and presence of proliferating endothelial cells in
skeletal muscle before and after passive training of the leg
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B. Hoier et al. J Physiol 588.19 (2010) pp 3833–3845

15. Relationship with CVD ?
• Farese et al. (Am J Kidney Dis)
: Blood flow in the Femoral Artery increased up to 40% with TEMS
and PCMs (unpublished)
: Increased Cardiac Output by electrical muscle stimulation increases
venous backflow from the musculature (Increased venous return)
• Future direction
: ABI (Ankle Brachial Index) : BP Function between Ankle and Brachial
: FMD : specific to Femoral Arterial function
: Heart Rate Variability : Autonomic dysfunction
: Cardiac Function : Mitral Inflow Conventional Doppler, Mitral
Annular Velocity Tissue Doppler

16. Thank you