Managing HBOT Safely in Dialysis Patients: What You Should Know
- mdavis107
- Oct 8, 2020
- 6 min read
Updated: 2 days ago
Understanding the Overlap Between Kidney Disease and Cardiac Risk
More than 15 million Americans live with chronic kidney disease—nearly 500,000 of whom require dialysis.¹ Unfortunately, dialysis patients face significantly elevated cardiovascular risks. Cardiac disease is the leading cause of death in this population, accounting for up to 60% of cardiac-related deaths due to arrhythmias or sudden cardiac arrest.¹–³
The long-term prognosis after a cardiac event is grim. One study noted a two-year mortality rate of 74% for dialysis patients following cardiac arrest.⁴ In-hospital CPR offers little hope—multiple studies report six-month mortality rates as high as 97%.⁵–⁷
One such study reviewed 24 patients who had CPR during dialysis in a small medical center over a 3-year period and reported a mortality rate of 100%.⁷

Understanding the Primary Risk Factors in Dialysis Patients
Cardiac disease remains the number one cause of death among both hemodialysis and peritoneal dialysis patients.¹ This includes sudden cardiac arrest, arrhythmias such as ventricular fibrillation, and complications related to underlying structural heart disease.¹–³ Other contributing factors include chronic fluid overload, severe hypertension, and electrolyte imbalances—particularly involving potassium.⁹–¹⁰
Because these risks are so prevalent, even stable-seeming dialysis patients may be one misstep away from decompensation. For hyperbaric medicine teams, this reality underscores the need for heightened caution, close coordination with nephrology teams, and thoughtful scheduling aligned with dialysis sessions.
Why Dialysis Patients Face Such High Cardiac Risks in HBOT
Nearly all dialysis patients have some degree of cardiac disease, making them uniquely vulnerable.⁸–⁹ Several cardiac conditions are highly prevalent in the dialysis population and contribute significantly to sudden cardiac risk, including:
Hypertension, affecting over 90% of dialysis patients¹⁰
Left ventricular hypertrophy (present in 75%)¹¹
Coronary artery disease and congestive heart failure¹²
Prolonged QT intervals and increased QT dispersion, both predictive of sudden death¹³–¹⁵
These structural and electrical abnormalities worsen over time, particularly as years on dialysis increase.¹⁵ While these risk factors are significant on their own, it's often difficult to attribute sudden cardiac death to a single mechanism. Most dialysis patients have overlapping conditions—such as ischemic heart disease, structural changes, and arrhythmic instability—making precise attribution challenging.¹,⁸
Added Stressors of Hemodialysis
End-stage kidney disease with dialysis introduces physiological stressors not typically seen in the general population with heart disease. These include predialysis volume overloading and intra- or postdialysis hypotension:
Rapid fluid shifts may lead to volume overload or hypotension
Potassium and other electrolytes undergo large fluxes with hemodialysis, and both hyperkalemia and hypokalemia are known to precipitate sudden death or cardiac arrhythmias
Based on these facts, researchers have conducted extensive retrospective studies and reported nearly a 50% increased frequency of sudden cardiac death on Mondays for patients dialyzing Monday, Wednesday, and Friday.⁵ Cardiac arrests have also been shown to cluster around dialysis sessions on Mondays and Tuesdays, depending on a patient’s schedule.⁵,¹⁶,²² A 14-year retrospective review identified 102 cardiac arrests at outpatient centers—nearly 70% occurred during dialysis. All were related to ventricular fibrillation or tachycardia, although the overwhelming majority of sudden deaths occur outside of dialysis centers.¹⁸ Combined, these risks require HBOT providers and technicians to exercise extra caution—especially on high-risk days like Mondays or Tuesdays, when patients may not have completed their first dialysis session of the week.
Best Practices for Managing HBOT in Dialysis Patients
Given these risks, dialysis patients should be classified as high-risk when planning for hyperbaric oxygen therapy.¹²,¹⁹–²¹ Extra precautions are necessary:
Pre-Treatment Assessment
Conduct a 12-lead EKG and chest X-ray
Because dialysis alters lab values significantly—sometimes within hours—those labs may not reflect a patient’s current clinical status. In contrast, pre-treatment weight can help identify fluid overload, a key red flag for instability.
In-Treatment Considerations
Never take vitals or blood draws from an arm with an arteriovenous (AV) fistula or shunt. Because blood-borne infections are the second leading cause of death in dialysis patients, maintaining strict precautions around AV access is critical during HBOT.
Use manual blood pressure cuffs to assess for irregular pulse
Observe the patient continuously throughout treatment. Any observed or patient-centered concerns should be promptly discussed with the supervising provider, who will determine whether HBOT should be paused or discontinued
Post-Treatment Monitoring
Ensure post-HBOT evaluation by the supervising physician to confirm that the patient is stable prior to discharge
Monitor closely for delayed cardiac symptoms, including changes in heart rhythm, blood pressure, or consciousness
Ideally, HBOT should be scheduled after dialysis sessions when the patient is most hemodynamically stable. Avoid Monday and Tuesday morning sessions for patients whose dialysis occurs on adjacent days. Coordinating with local dialysis centers may also be necessary to adjust treatment schedules and promote safer patient timing. Such coordination not only improves patient timing—it fosters stronger collaboration between wound care, nephrology, and nursing teams.
Why This Matters
With a 20-fold higher cardiovascular mortality risk than the general population, dialysis patients require heightened vigilance during HBOT. Careful coordination with local dialysis centers is essential—not only to prevent complications, but to strengthen interdisciplinary relationships that enhance patient care and operational alignment.
Shared Health Services supports hospitals and physician practices in navigating the challenges of complex patient populations—like those on dialysis—through safe, compliant HBOT program design. Whether it’s refining protocols or adjusting treatment workflows, we provide practical, experience-based guidance to help your team provide confident, well-supported care for high-risk patients.
References
US Renal Data System: USRDS 2009 Annual Data Report. Bethesda, Maryland, National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Disease, 2009.
Herzog CA. Cardiac arrest in dialysis patients: Approaches to alter an abysmal outcome. Kidney International. 2003; 63 (Suppl 84): S197-S200.
US Renal Data System: USRDS 2001 Annual Data Report. Bethesda, Maryland, National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Disease, 2001.
Herzog CA, Ma JZ, Collins AJ. Poor long-term survival after acute myocardial infarction among patients on long term dialysis. New England Journal of Medicine. 1998; 339: 799-805.
Karnik JA, Young BS, Lew NL, et al. Cardiac arrest and sudden death in dialysis units. Kidney International. 2001; 60: 350-357.
Moss AH, Holley JL, Upton MB. Outcomes of cardiopulmonary resuscitation in dialysis patients. Journal of the American Society of Nephrology. 1992; 3: 1238-1243.
Lai M, Hung K, Huang J, et al. Clinical findings and outcomes of intra hemodialysis cardiopulmonary resuscitation. American Journal of Nephrology. 1999; 19: 468-473.
Cheung AK, Sarnak MJ, Yan G, et al. Cardiac disease in maintenance hemodialysis patients: results of the HEMO study. Kidney International. 2004; 65: 2380-2389.
Bleyer AJ, Hartman J, Brannon PC, et al. Characteristics of sudden death in hemodialysis patients. Kidney International. 2006; 69: 2268-2273.
Siscovick DS, Raghunathan TE, Psaty BN, et al. Diuretic therapy for hypertension and the risk of primary cardiac arrest. New England Journal of Medicine. 1994; 330: 1852-1857.
Amann K, Rychlik I, Miltenberger-Miltenyi G, Ritz E. Left ventricular hypertrophy in renal failure. Kidney International. 1998; 54 (Suppl 68): S78-S85.
Foley R, Parfrey P, Sarnak M. Clinical epidemiology of cardiovascular disease in chronic renal disease. American Journal of Kidney Disease. 1998; (5 Suppl 3): S112-S119.
Raizada V, Skipper B, Luo W, Garza L, et al. Renin-angiotensin polymorphisms and QTc interval prolongation in end-stage renal disease. Kidney International. 2005; 68: 1186-1189.
Cupisti A, Galetta F, Caprioli R, et al. Potassium removal increases the QTc interval dispersion during hemodialysis. Nephron. 1999; 82: 122-126.
Bleyer AJ. Clues at the scene of the crime: sudden death in dialysis patients. Peritoneal Dialysis International. 2009; 29: 23–25.
Bleyer AJ, Russell GB, Satko SG. Sudden and cardiac death rates in hemodialysis patients. Kidney International. 1999; 55: 1553-1559.
Davis TR, Young BA, Eisenberg MS, et al. Outcome of cardiac arrests attended by emergency medical services staff at community outpatient dialysis centers: cardiac arrest in dialysis facilities. Kidney International. 2008; 73: 933-939.
Herzog CA, Mangrum JM, Passman R. Non-coronary heart disease in dialysis patients: Sudden cardiac death in dialysis patients. Seminars in Dialysis. 2008; 21 (4): 300-307.
Gilbertson DT, Liu J, Xue JL, et al. Projecting the number of patients with end stage renal disease in the United States to the year 2015. Journal of the American Society of Nephrology. 2005; 16: 3736-3741.
Culleton BF, Larson MG, Wilson PW, et al. Cardiovascular disease and mortality in a community-based cohort with mild renal insufficiency. Kidney International. 1999; 56: 2214-2219.
Henry RM, Kostense PJ, Bos G, et al. Mild renal insufficiency is associated with increased cardiovascular mortality: the Hoorn study. Kidney International. 2002; 62: 1402-1407.
Lafrance JP, Nolin L, Senecal L, et al. Predictors and outcome of cardiopulmonary resuscitation (CPR) calls in a large hemodialysis unit over a seven-year period. NDT. 2006; 21: 1006-1012.
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