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IntraDialytic Hypertension (Basic Science → Evidence → Practice) - Dr. Gawad
The document discusses intra-dialytic hypertension, highlighting its mechanisms, treatment options, and scientific evidence regarding its management. It emphasizes the importance of factors such as volume overload, sympathetic over-activity, and electrolyte imbalances in the condition, along with various treatments like sodium level monitoring, dry weight assessment, and the use of specific medications. The evidence presented is described as weak due to the limited number of studies and conflicting results.
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IntraDialytic Hypertension (Basic Science → Evidence → Practice) - Dr. Gawad
- 1. Intra-Dialytic Hypertension Basic Science→ Evidence → Practice Mohammed Abdel Gawad Nephrologist – Alexandria – Egypt Founder & Chairman of NephroTube [email protected]
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- 3. 2010;115(3):c182-8 A sustained increaseof BP during the dialysis session with BP values during and at the end of the dialysis session exceeding BP values at dialysis onset
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- 6. 2010 Mar;55(3):580-9 Low SaO2 NDT.2018 Jun 1;33(6):1040-1045
- 7. Weak Soft Evidence •Small number of patients were tested by different studies • Conflicting and contradictory results • Study design may not be strong enough
- 8. Mechanism Treatment Volume overload• Bioimpedence dry weight assessment • Extended dialysis session or daily short sessions Net sodium gain • Check predialysis sodium level, minimize NaG Removal of ant-HTN medications • Non Dialyzable drug (Carvedilol) Sympathetic over-activity Activation of the RAAS • Inhibition of RAAS • Adrenergic blockers such as alpha- and beta- blockers (Carvedilol) Endothelial cell dysfunction • Specific ET1 antagonists (such as avosentan) !! • Nonspecific ET1 inhibitors (RAAS-i or carvedilol) High ionized calcium • Avoid high Ca path if available Hypokalemia • Avoid low K path if available ESAs • Avoid ESA administration during HD session Low SaO2 • Monitor SaO2 during HD session Intradialytic HTN
- 9. n = 131MHD 2018 Feb;22(1):22-30
- 12. This may beinterpreted as a greater refilling from the interstitial space in fluid- overloaded patients 2006 May;69(10):1833-8
- 13. The session time variedbetween 4 and 7 h 2002 Jan-Feb;15(1):42-7 Modest ultrafiltration More aggressive ultrafiltration only 1 patient presented with pedal edema
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- 15. Mechanism Treatment Volume overload• Bioimpedence dry weight assessment • Extended dialysis session or daily short sessions Net sodium gain • Check predialysis sodium level, minimize NaG Removal of ant-HTN medications • Non Dialyzable drug (Carvedilol) Sympathetic over-activity Activation of the RAAS • Inhibition of RAAS • Adrenergic blockers such as alpha- and beta- blockers (Carvedilol) Endothelial cell dysfunction • Specific ET1 antagonists (such as avosentan) !! • Nonspecific ET1 inhibitors (RAAS-i or carvedilol) High ionized calcium • Avoid high Ca path if available Hypokalemia • Avoid low K path if available ESAs • Avoid ESA administration during HD session Low SaO2 • Monitor SaO2 during HD session Intradialytic HTN
- 16. Mechanism Treatment Volume overload• Bioimpedence dry weight assessment • Extended dialysis session or daily short sessions Net sodium gain • Check predialysis sodium level, minimize NaG Removal of ant-HTN medications • Non Dialyzable drug (Carvedilol) Sympathetic over-activity Activation of the RAAS • Inhibition of RAAS • Adrenergic blockers such as alpha- and beta- blockers (Carvedilol) Endothelial cell dysfunction • Specific ET1 antagonists (such as avosentan) !! • Nonspecific ET1 inhibitors (RAAS-i or carvedilol) High ionized calcium • Avoid high Ca path if available Hypokalemia • Avoid low K path if available ESAs • Avoid ESA administration during HD session Low SaO2 • Monitor SaO2 during HD session Intradialytic HTN
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- 21. Mechanism Treatment Volume overload• Bioimpedence dry weight assessment • Extended dialysis session or daily short sessions Net sodium gain • Check predialysis sodium level, minimize NaG Removal of ant-HTN medications • Non Dialyzable drug (Carvedilol) Sympathetic over-activity Activation of the RAAS • Inhibition of RAAS • Adrenergic blockers such as alpha- and beta- blockers (Carvedilol) Endothelial cell dysfunction • Specific ET1 antagonists (such as avosentan) !! • Nonspecific ET1 inhibitors (RAAS-i or carvedilol) High ionized calcium • Avoid high Ca path if available Hypokalemia • Avoid low K path if available ESAs • Avoid ESA administration during HD session Low SaO2 • Monitor SaO2 during HD session Intradialytic HTN
- 22. Mechanism Treatment Volume overload• Bioimpedence dry weight assessment • Extended dialysis session or daily short sessions Net sodium gain • Check predialysis sodium level, minimize NaG Removal of ant-HTN medications • Non Dialyzable drug (Carvedilol) Sympathetic over-activity Activation of the RAAS • Inhibition of RAAS • Adrenergic blockers such as alpha- and beta- blockers (Carvedilol) Endothelial cell dysfunction • Specific ET1 antagonists (such as avosentan) !! • Nonspecific ET1 inhibitors (RAAS-i or carvedilol) High ionized calcium • Avoid high Ca path if available Hypokalemia • Avoid low K path if available ESAs • Avoid ESA administration during HD session Low SaO2 • Monitor SaO2 during HD session Intradialytic HTN
- 23. 2005 Apr;45(4 Suppl3):S1-153
- 24. 2005 Apr;45(4 Suppl3):S1-153
- 25. 2012 Aug;7(8):1300-9 Carvedilol among25 participants with intradialytic hypertension
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- 27. Mechanism Treatment Volume overload• Bioimpedence dry weight assessment • Extended dialysis session or daily short sessions Net sodium gain • Check predialysis sodium level, minimize NaG Removal of ant-HTN medications • Non Dialyzable drug (Carvedilol) Sympathetic over-activity Activation of the RAAS • Inhibition of RAAS • Adrenergic blockers such as alpha- and beta- blockers (Carvedilol) Endothelial cell dysfunction • Specific ET1 antagonists (such as avosentan) !! • Nonspecific ET1 inhibitors (RAAS-i or carvedilol) High ionized calcium • Avoid high Ca path if available Hypokalemia • Avoid low K path if available ESAs • Avoid ESA administration during HD session Low SaO2 • Monitor SaO2 during HD session Intradialytic HTN
- 28. Mechanism Treatment Volume overload• Bioimpedence dry weight assessment • Extended dialysis session or daily short sessions Net sodium gain • Check predialysis sodium level, minimize NaG Removal of ant-HTN medications • Non Dialyzable drug (Carvedilol) Sympathetic over-activity Activation of the RAAS • Inhibition of RAAS • Adrenergic blockers such as alpha- and beta- blockers (Carvedilol) Endothelial cell dysfunction • Specific ET1 antagonists (such as avosentan) !! • Nonspecific ET1 inhibitors (RAAS-i or carvedilol) High ionized calcium • Avoid high Ca path if available Hypokalemia • Avoid low K path if available ESAs • Avoid ESA administration during HD session Low SaO2 • Monitor SaO2 during HD session Intradialytic HTN
- 29. 2010 Mar;55(3):580-9 N EnglJ Med 1992;327:1912–1918 J Appl Physiol 2008;105:1873–1876 Contrib Nephrol 1984;41:292–298
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- 32. Mechanism Treatment Volume overload• Bioimpedence dry weight assessment • Extended dialysis session or daily short sessions Net sodium gain • Check predialysis sodium level, minimize NaG Removal of ant-HTN medications • Non Dialyzable drug (Carvedilol) Sympathetic over-activity Activation of the RAAS • Inhibition of RAAS • Adrenergic blockers such as alpha- and beta- blockers (Carvedilol) Endothelial cell dysfunction • Specific ET1 antagonists (such as avosentan) !! • Nonspecific ET1 inhibitors (RAAS-i or carvedilol) High ionized calcium • Avoid high Ca path if available Hypokalemia • Avoid low K path if available ESAs • Avoid ESA administration during HD session Low SaO2 • Monitor SaO2 during HD session Intradialytic HTN
- 33. Mechanism Treatment Volume overload• Bioimpedence dry weight assessment • Extended dialysis session or daily short sessions Net sodium gain • Check predialysis sodium level, minimize NaG Removal of ant-HTN medications • Non Dialyzable drug (Carvedilol) Sympathetic over-activity Activation of the RAAS • Inhibition of RAAS • Adrenergic blockers such as alpha- and beta- blockers (Carvedilol) Endothelial cell dysfunction • Specific ET1 antagonists (such as avosentan) !! • Nonspecific ET1 inhibitors (RAAS-i or carvedilol) High ionized calcium • Avoid high Ca path if available Hypokalemia • Avoid low K path if available ESAs • Avoid ESA administration during HD session Low SaO2 • Monitor SaO2 during HD session Intradialytic HTN
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- 38. Mechanism Treatment Volume overload• Bioimpedence dry weight assessment • Extended dialysis session or daily short sessions Net sodium gain • Check predialysis sodium level, minimize NaG Removal of ant-HTN medications • Non Dialyzable drug (Carvedilol) Sympathetic over-activity Activation of the RAAS • Inhibition of RAAS • Adrenergic blockers such as alpha- and beta- blockers (Carvedilol) Endothelial cell dysfunction • Specific ET1 antagonists (such as avosentan) !! • Nonspecific ET1 inhibitors (RAAS-i or carvedilol) High ionized calcium • Avoid high Ca path if available Hypokalemia • Avoid low K path if available ESAs • Avoid ESA administration during HD session Low SaO2 • Monitor SaO2 during HD session Intradialytic HTN
- 39. Mechanism Treatment Volume overload• Bioimpedence dry weight assessment • Extended dialysis session or daily short sessions Net sodium gain • Check predialysis sodium level, minimize NaG Removal of ant-HTN medications • Non Dialyzable drug (Carvedilol) Sympathetic over-activity Activation of the RAAS • Inhibition of RAAS • Adrenergic blockers such as alpha- and beta- blockers (Carvedilol) Endothelial cell dysfunction • Specific ET1 antagonists (such as avosentan) !! • Nonspecific ET1 inhibitors (RAAS-i or carvedilol) High ionized calcium • Avoid high Ca path if available Hypokalemia • Avoid low K path if available ESAs • Avoid ESA administration during HD session Low SaO2 • Monitor SaO2 during HD session Intradialytic HTN
- 40. 2010 Mar;55(3):580-9 Theoretical basedon that high calcium dialysate has been used to improve hemodynamic instability in hypotensive prone patients and/or patients with impaired cardiac function
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- 42. Mechanism Treatment Volume overload• Bioimpedence dry weight assessment • Extended dialysis session or daily short sessions Net sodium gain • Check predialysis sodium level, minimize NaG Removal of ant-HTN medications • Non Dialyzable drug (Carvedilol) Sympathetic over-activity Activation of the RAAS • Inhibition of RAAS • Adrenergic blockers such as alpha- and beta- blockers (Carvedilol) Endothelial cell dysfunction • Specific ET1 antagonists (such as avosentan) !! • Nonspecific ET1 inhibitors (RAAS-i or carvedilol) High ionized calcium • Avoid high Ca path if available Hypokalemia • Avoid low K path if available ESAs • Avoid ESA administration during HD session Low SaO2 • Monitor SaO2 during HD session Intradialytic HTN
- 43. Mechanism Treatment Volume overload• Bioimpedence dry weight assessment • Extended dialysis session or daily short sessions Net sodium gain • Check predialysis sodium level, minimize NaG Removal of ant-HTN medications • Non Dialyzable drug (Carvedilol) Sympathetic over-activity Activation of the RAAS • Inhibition of RAAS • Adrenergic blockers such as alpha- and beta- blockers (Carvedilol) Endothelial cell dysfunction • Specific ET1 antagonists (such as avosentan) !! • Nonspecific ET1 inhibitors (RAAS-i or carvedilol) High ionized calcium • Avoid high Ca path if available Hypokalemia • Avoid low K path if available ESAs • Avoid ESA administration during HD session Low SaO2 • Monitor SaO2 during HD session Intradialytic HTN
- 44. 2010 Mar;55(3):580-9 Low Kpath (Am J Kidney Dis 1995;26:321–326)
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- 46. Mechanism Treatment Volume overload• Bioimpedence dry weight assessment • Extended dialysis session or daily short sessions Net sodium gain • Check predialysis sodium level, minimize NaG Removal of ant-HTN medications • Non Dialyzable drug (Carvedilol) Sympathetic over-activity Activation of the RAAS • Inhibition of RAAS • Adrenergic blockers such as alpha- and beta- blockers (Carvedilol) Endothelial cell dysfunction • Specific ET1 antagonists (such as avosentan) !! • Nonspecific ET1 inhibitors (RAAS-i or carvedilol) High ionized calcium • Avoid high Ca path if available Hypokalemia • Avoid low K path if available ESAs • Avoid ESA administration during HD session Low SaO2 • Monitor SaO2 during HD session Intradialytic HTN
- 47. Mechanism Treatment Volume overload• Bioimpedence dry weight assessment • Extended dialysis session or daily short sessions Net sodium gain • Check predialysis sodium level, minimize NaG Removal of ant-HTN medications • Non Dialyzable drug (Carvedilol) Sympathetic over-activity Activation of the RAAS • Inhibition of RAAS • Adrenergic blockers such as alpha- and beta- blockers (Carvedilol) Endothelial cell dysfunction • Specific ET1 antagonists (such as avosentan) !! • Nonspecific ET1 inhibitors (RAAS-i or carvedilol) High ionized calcium • Avoid high Ca path if available Hypokalemia • Avoid low K path if available ESAs • Avoid ESA administration during HD session Low SaO2 • Monitor SaO2 during HD session Intradialytic HTN
- 48. If ESA isgiven IV prior to the end of hemodialysis → significant increase in ET1 J Am Soc Nephrol 1991;2:927–936
- 49. Mechanism Treatment Volume overload• Bioimpedence dry weight assessment • Extended dialysis session or daily short sessions Net sodium gain • Check predialysis sodium level, minimize NaG Removal of ant-HTN medications • Non Dialyzable drug (Carvedilol) Sympathetic over-activity Activation of the RAAS • Inhibition of RAAS • Adrenergic blockers such as alpha- and beta- blockers (Carvedilol) Endothelial cell dysfunction • Specific ET1 antagonists (such as avosentan) !! • Nonspecific ET1 inhibitors (RAAS-i or carvedilol) High ionized calcium • Avoid high Ca path if available Hypokalemia • Avoid low K path if available ESAs • Avoid ESA administration during HD session Low SaO2 • Monitor SaO2 during HD session Intradialytic HTN
- 50. Mechanism Treatment Volume overload• Bioimpedence dry weight assessment • Extended dialysis session or daily short sessions Net sodium gain • Check predialysis sodium level, minimize NaG Removal of ant-HTN medications • Non Dialyzable drug (Carvedilol) Sympathetic over-activity Activation of the RAAS • Inhibition of RAAS • Adrenergic blockers such as alpha- and beta- blockers (Carvedilol) Endothelial cell dysfunction • Specific ET1 antagonists (such as avosentan) !! • Nonspecific ET1 inhibitors (RAAS-i or carvedilol) High ionized calcium • Avoid high Ca path if available Hypokalemia • Avoid low K path if available ESAs • Avoid ESA administration during HD session Low SaO2 • Monitor SaO2 during HD session Intradialytic HTN
- 51. 2018 Jun 1;33(6):1040-1045 Withevery percentage point lower mean SaO2, the peridialytic SBP change increased by 0.46mmHg n = 982
- 52. Mechanism Treatment Volume overload• Bioimpedence dry weight assessment • Extended dialysis session or daily short sessions Net sodium gain • Check predialysis sodium level, minimize NaG Removal of ant-HTN medications • Non Dialyzable drug (Carvedilol) Sympathetic over-activity Activation of the RAAS • Inhibition of RAAS • Adrenergic blockers such as alpha- and beta- blockers (Carvedilol) Endothelial cell dysfunction • Specific ET1 antagonists (such as avosentan) !! • Nonspecific ET1 inhibitors (RAAS-i or carvedilol) High ionized calcium • Avoid high Ca path if available Hypokalemia • Avoid low K path if available ESAs • Avoid ESA administration during HD session Low SaO2 • Monitor SaO2 during HD session Intradialytic HTN
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- 55. Mechanism Treatment Volume overload• Bioimpedence dry weight assessment • Extended dialysis session or daily short sessions Net sodium gain • Check predialysis sodium level, minimize NaG Removal of ant-HTN medications • Non Dialyzable drug (Carvedilol) Sympathetic over-activity Activation of the RAAS • Inhibition of RAAS • Adrenergic blockers such as alpha- and beta- blockers (Carvedilol) Endothelial cell dysfunction • Specific ET1 antagonists (such as avosentan) !! • Nonspecific ET1 inhibitors (RAAS-i or carvedilol) High ionized calcium • Avoid high Ca path if available Hypokalemia • Avoid low K path if available ESAs • Avoid ESA administration during HD session Low SaO2 • Monitor SaO2 during HD session Intradialytic HTN
- 56. Mechanism Treatment Volume overload• Bioimpedence dry weight assessment • Extended dialysis session or daily short sessions Net sodium gain • Check predialysis sodium level, minimize NaG Removal of ant-HTN medications • Non Dialyzable drug (Carvedilol) Sympathetic over-activity Activation of the RAAS • Inhibition of RAAS • Adrenergic blockers such as alpha- and beta- blockers (Carvedilol) Endothelial cell dysfunction • Specific ET1 antagonists (such as avosentan) !! • Nonspecific ET1 inhibitors (RAAS-i or carvedilol) High ionized calcium • Avoid high Ca path if available Hypokalemia • Avoid low K path if available ESAs • Avoid ESA administration during HD session Low SaO2 • Monitor SaO2 during HD session Intradialytic HTN
- 57. Mechanism Treatment Volume overload• Bioimpedence dry weight assessment • Extended dialysis session or daily short sessions Net sodium gain • Check predialysis sodium level, minimize NaG Removal of ant-HTN medications • Non Dialyzable drug (Carvedilol) Sympathetic over-activity Activation of the RAAS • Inhibition of RAAS • Adrenergic blockers such as alpha- and beta- blockers (Carvedilol) Endothelial cell dysfunction • Specific ET1 antagonists (such as avosentan) !! • Nonspecific ET1 inhibitors (RAAS-i or carvedilol) High ionized calcium • Avoid high Ca path if available Hypokalemia • Avoid low K path if available ESAs • Avoid ESA administration during HD session Low SaO2 • Monitor SaO2 during HD session Intradialytic HTN
- 58. Mechanism Treatment Volume overload• Bioimpedence dry weight assessment • Extended dialysis session or daily short sessions Net sodium gain • Check predialysis sodium level, minimize NaG Removal of ant-HTN medications • Non Dialyzable drug (Carvedilol) Sympathetic over-activity Activation of the RAAS • Inhibition of RAAS • Adrenergic blockers such as alpha- and beta- blockers (Carvedilol) Endothelial cell dysfunction • Specific ET1 antagonists (such as avosentan) !! • Nonspecific ET1 inhibitors (RAAS-i or carvedilol) High ionized calcium • Avoid high Ca path if available Hypokalemia • Avoid low K path if available ESAs • Avoid ESA administration during HD session Low SaO2 • Monitor SaO2 during HD session Intradialytic HTN
- 59. Mechanism Treatment Volume overload• Bioimpedence dry weight assessment • Extended dialysis session or daily short sessions Net sodium gain • Check predialysis sodium level, minimize NaG Removal of ant-HTN medications • Non Dialyzable drug (Carvedilol) Sympathetic over-activity Activation of the RAAS • Inhibition of RAAS • Adrenergic blockers such as alpha- and beta- blockers (Carvedilol) Endothelial cell dysfunction • Specific ET1 antagonists (such as avosentan) !! • Nonspecific ET1 inhibitors (RAAS-i or carvedilol) High ionized calcium • Avoid high Ca path if available Hypokalemia • Avoid low K path if available ESAs • Avoid ESA administration during HD session Low SaO2 • Monitor SaO2 during HD session Intradialytic HTN
- 60. Mechanism Treatment Volume overload• Bioimpedence dry weight assessment • Extended dialysis session or daily short sessions Net sodium gain • Check predialysis sodium level, minimize NaG Removal of ant-HTN medications • Non Dialyzable drug (Carvedilol) Sympathetic over-activity Activation of the RAAS • Inhibition of RAAS • Adrenergic blockers such as alpha- and beta- blockers (Carvedilol) Endothelial cell dysfunction • Specific ET1 antagonists (such as avosentan) !! • Nonspecific ET1 inhibitors (RAAS-i or carvedilol) High ionized calcium • Avoid high Ca path if available Hypokalemia • Avoid low K path if available ESAs • Avoid ESA administration during HD session Low SaO2 • Monitor SaO2 during HD session Intradialytic HTN
- 61. Home Messages First lineof management of Intra-dialytic HTN is: 1- Dry weight assessment and removal of excess fluid 2- Dry weight assessment and removal of excess fluid 3- Dry weight assessment and removal of excess fluid 4- Dry weight assessment and removal of excess fluid 5- Dry weight assessment and removal of excess fluid
- 62. Home Messages First lineof management of Intra-dialytic HTN is: 1- Dry weight assessment and removal of excess fluid 2- Dry weight assessment and removal of excess fluid 3- Dry weight assessment and removal of excess fluid 4- Dry weight assessment and removal of excess fluid 5- Dry weight assessment and removal of excess fluid
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