intradialytic hypotension [투석 중 저혈압]
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Hank Park
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.
IDH (Intradialytic Hypotension)• Definition: A fall in SBP by at least 20mmHg or SBP < 100mmHG
• 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)
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
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 -> intradialytichypotension -> chronically volume-expanded -> Chronic Hypertension (van der Zee. S et al.)
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)
How to increase BP?Farese S. et al. Am J Kidney Dis. 2008.
• TEMS : Transcutaneous muscle simulation , PCMs : Passive cycling movement
• For each patient, each procedure was performed only once weekly and never on the same weekday.
Patient Characteristics
TEMS & PCMs during dialysis show significant results in raising BP
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
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
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 PhysiolRegul Integr Comp Physiol)
Capillarization and presence of proliferating endothelial cells in skeletal muscle before and after passive training of the leg
• B. Hoier et al. J Physiol 588.19 (2010) pp 3833–3845
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
Thank you