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The susceptible patient

A E Raine1

  • 1Department of Nephrology, St Bartholomew's Hospital, London, UK.

Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association
|January 1, 1996
PubMed
Summary

Acute hypotension during hemodialysis is common. Left ventricular hypertrophy (LVH) and diastolic dysfunction are key factors, impacting cardiac filling and blood pressure regulation in susceptible patients.

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Area of Science:

  • Nephrology
  • Cardiology
  • Physiology

Background:

  • Acute hypotension complicates hemodialysis in 20-33% of patients.
  • While intravascular hypovolemia is the immediate cause, patient susceptibility suggests additional contributing factors.
  • Potential factors include autonomic neuropathy, left ventricular hypertrophy (LVH), diastolic dysfunction, and abnormal vascular compliance.

Purpose of the Study:

  • To investigate the multifactorial nature of intradialytic hypotension.
  • To identify patient-specific factors contributing to hypotension during hemodialysis.
  • To explore the role of cardiac abnormalities in dialysis-induced hypotension.

Main Methods:

  • Review of existing literature on intradialytic hypotension.
  • Analysis of patient data correlating hypotension with cardiac structure and function.
  • Examination of cardiovascular reflex responses and vascular compliance in susceptible individuals.

Main Results:

  • While autonomic neuropathy's role is debated, a strong association exists between LVH and dialysis hypotension.
  • Patients prone to hypotension exhibit LVH and diastolic dysfunction, with impaired ventricular filling.
  • Mechanisms may involve impaired cardiac filling, reduced cardiac output, and paradoxical sympathetic withdrawal.

Conclusions:

  • Left ventricular hypertrophy and diastolic dysfunction are significant contributors to intradialytic hypotension.
  • Understanding these cardiac factors is crucial for managing hypotension in hemodialysis patients.
  • Further research into impaired venous compliance, anemia, and vasodilator pathways may reveal additional therapeutic targets.

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