What causes hypotension in patients with end-stage renal disease (ESRD) during hemodialysis?

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Causes of Low Arterial Pressure During Hemodialysis

Intradialytic hypotension results from two fundamental mechanisms: insufficient intravascular volume to support the ultrafiltration rate and inadequate cardiovascular compensatory responses to volume removal. 1

Primary Pathophysiologic Mechanisms

Volume-Related Causes

  • Excessive ultrafiltration is the most common cause, occurring when fluid removal exceeds the rate of vascular refilling from the interstitial compartment. 2
  • Ultrafiltration rates as low as 6 mL/h/kg can be associated with higher mortality risk, indicating that even modest rates can overwhelm compensatory mechanisms in vulnerable patients. 1
  • Inadequate dry weight assessment leads to chronic hypovolemia, triggering compensatory mechanisms including increased thirst and paradoxically higher interdialytic weight gains. 1

Impaired Cardiovascular Compensation

  • Autonomic dysfunction is particularly prevalent in diabetic patients and those with long-standing ESRD, resulting in blunted sympathetic responses to volume depletion. 2, 1
  • Impaired neurohormonal responses include blunted activation of the renin-angiotensin-aldosterone system and sympathetic nervous system during intravascular volume loss. 1
  • Defective vascular reactivity affects both resistance and capacitance vessels during hemodialysis sessions, preventing adequate compensatory vasoconstriction. 2

Dialysis Treatment-Related Factors

Dialysate Composition and Temperature

  • Acetate-containing dialysate contributes to hypotension by decreasing total vascular resistance, increasing venous pooling, and increasing myocardial oxygen consumption. 1
  • Elevated dialysate temperature (37°C) promotes peripheral vasodilation and reduces sympathetic tone, whereas the optimal temperature of 34-35°C increases peripheral vasoconstriction through enhanced sympathetic activity. 1, 3
  • Bicarbonate-buffered dialysate should replace acetate-based solutions to minimize hypotensive episodes. 2, 3

Rapid Solute and Thermal Shifts

  • Increased core body temperature during standard dialysis is related to heat load from the extracorporeal system or secondary to volume removal, increasing the risk for hypotension. 2
  • Urea and osmotic shifts can contribute to hemodynamic instability, with protracted hypotension exaggerating urea rebound and compromising dialysis adequacy. 2, 1

Patient-Specific Risk Factors

High-Risk Populations

  • Diabetic patients with autonomic neuropathy show exaggerated drops in systolic and diastolic blood pressures compared to those without autonomic dysfunction. 2
  • Elderly patients (≥65 years) have increased susceptibility to intradialytic hypotension. 2
  • Patients with pre-dialysis systolic blood pressure <100 mmHg, including anephric patients and those on long-term dialysis. 2
  • Patients with cardiovascular disease, including left ventricular hypertrophy with diastolic dysfunction, systolic dysfunction with heart failure, valvular disease, or pericardial disease. 2

Cardiac Dysfunction

  • Left ventricular dysfunction (both systolic and diastolic) impairs the heart's ability to maintain cardiac output during volume removal. 2
  • Endothelial dysfunction assessed by flow-mediated dilation is independently associated with intradialytic hypotension, with every 5% decrease in flow-mediated dilation associated with a 7.5 mmHg decrease in systolic blood pressure. 4

Medication-Induced Hypotension

  • Antihypertensive medications taken before dialysis prevent compensatory vasoconstriction and cardiac responses, exacerbating hypotension. 1, 3
  • Dialyzable antihypertensive agents including enalapril, ramipril, methyldopa, atenolol, acebutolol, nadolol, minoxidil, and nitroprusside are removed during hemodialysis, potentially causing paradoxical blood pressure changes. 2
  • Nitrates used before dialysis sessions increase the risk of hypotension in patients with coronary artery disease. 2

Nutritional and Metabolic Factors

  • Food intake immediately before or during hemodialysis causes splanchnic vasodilation and decreased peripheral vascular resistance, redirecting blood flow away from the peripheral circulation. 1
  • Severe anemia reduces oxygen-carrying capacity and impairs cardiovascular compensation, though correction to hemoglobin ≥11 g/dL can reduce hypotension incidence. 1, 3
  • Hypoalbuminemia and poor nutritional status are associated with increased risk of intradialytic hypotension. 2

Critical Clinical Pitfalls

  • Intradialytic hypotension occurs in 25% to 50% of all hemodialysis treatments, making it the most common acute complication. 2, 5
  • Recurrent hypotension creates a cascade of end-organ ischemia affecting the heart, brain, liver, gut, and kidneys, contributing to increased morbidity and mortality. 1
  • Premature termination of dialysis due to hypotension results in inadequate dialysis dose (suboptimal Kt/V) and failure to meet ultrafiltration goals. 2
  • Long-term consequences include volume overload from suboptimal ultrafiltration, left ventricular hypertrophy with associated morbidity and mortality, and interdialytic hypertension. 2

References

Guideline

Pathogenesis of Hemodialysis-Associated Hypotension

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Guideline

Management of Hemodialysis Complications

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Research

Associations of endothelial dysfunction and arterial stiffness with intradialytic hypotension and hypertension.

Hemodialysis international. International Symposium on Home Hemodialysis, 2011

Research

Setting the stage.

American journal of kidney diseases : the official journal of the National Kidney Foundation, 2001

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This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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