ICU Resource

ICU Resource THIS PAGE FOR MY ICU RESOURCES COLLECTION AND UPDATES

22/12/2025

https://zurl.co/4wfZ7 Circulatory shock presents pathophysiological complexity across septic, haemorrhagic and cardiogenic aetiologies. Multimodal assessment uses capillary refill time, lactate, central venous oxygen saturation and the PCO2 gap, with echocardiography and ultrasound to detect venous congestion. Data overload, discordant markers and limited devices can hinder decisions, and over 60% of recommendations rely on expert opinion while artificial intelligence may help.

22/12/2025
22/12/2025

A CHEST How I Do It proposes a standardized approach for high-flow nasal cannula discontinuation focused on liberation, using a stepwise approach guided by physiology.

Read more in the November issue of the journal CHEST®: https://hubs.ly/Q03SgtPN0

22/12/2025
22/12/2025

موضوع مهم جدا عن استخدام الصوديوم بيكربونات
نقلا عن دكتور محمد عامر
مساء الفل 🥲😅.
عمرك قبل كده كنت واقف في arrest ولقيت حد كاريزما كده وانت شغال جه قالك علق ٢٠٠ بيكارب بعذ اذنك.
او مثلاً عمرك كنت واقف مثلاً في الطوارئ ومعاك حالة metabolic acidosis من غير سبب واضح ولقيت حد برده كاريزما جاي كده قالك اديله ٢٠٠ بيكارب شوت بعد اذنك.
او بتمر في الرعاية وعيان shocked وفيه lactic acidosis ولقيت نفس الشخص الكاريزما جاي يقولك اديله ٢٠٠ بيكارب.

دلوقتي جه سؤال حلو اووي ايه البيكارب اللي استاذنا ده ماشي يوزعه في كل ال metabolic acidosis ده وهل فعلاً صح استعماله ولا غلط.

اول حاجة الصوديوم بيكارب هو ايه وتاريخه ايه؟
هو ال baking soda واول من اكتشفه هو المصرين القدماء في وادي النطرون وسموه natron salt وده خليط طبيعي بين كربونات وبيكربونات الصوديوم وكانوا بيستخدموه في التحنيط.

الصوديوم بيكارب هو عبارة عن weak base ال PH ~ 8.3

وظيفته ايه او ايه فايدة البيكارب في الجسم
بيعمل buffer system من خلال المعادلة دي
H+ HCO3 = H2CO3 > CO2+H2O

فبيعمل معادلة للحمض بأنه يطلع ميه وCO2 وخلي بالك من ال CO2 لان الرئة لازم تكون شغالة كويس او مش عيان مثلاً COPD وتديله مش هيعرف يتخلص من ال CO2 وهيتجمع وهيعمل paradoxical respiratory acidosis بالاضافة ان CO2 is shift to intracellular tissue causing intracellular acidosis.

ده يديك سؤال هو انا لما بحقن العيان ب ⲚⲁⲎⲤⲞ3 ايه اللي بيحصل في جسمه؟؟

𝟙. ℂ𝕆₂ ℝ𝕖𝕥𝕖𝕟𝕥𝕚𝕠𝕟 → ℂ𝕖𝕣𝕖𝕓𝕣𝕒𝕝 𝔼𝕕𝕖𝕞𝕒 & ↑ 𝕀ℂℙ

• Mechanism: NaHCO₃ reacts with H⁺ → forms CO₂ + H₂O (buffer reaction).
• Excess CO₂ diffuses into cells → worsens intracellular acidosis.
• In the brain: ↑ CO₂ → cerebral vasodilation → ↑ cerebral blood flow → cerebral edema & ↑ ICP.
• Clinical Note: Lungs must be intact to excrete the extra CO₂; otherwise, brain complications worsen.

𝟚. ℍ𝕪𝕡𝕠𝕜𝕒𝕝𝕖𝕞𝕚𝕒 (𝕧𝕚𝕒 ℍ⁺/𝕂⁺ 𝔼𝕩𝕔𝕙𝕒𝕟𝕘𝕖 – ℍ𝕒𝕞𝕓𝕦𝕣𝕘𝕖𝕣 𝕊𝕙𝕚𝕗𝕥)

• Mechanism:
• Alkalosis (↑ pH) → cells take up H⁺, release K⁺.
• Result: ↓ serum potassium → risk of arrhythmias, muscle weakness.

𝟛. ℍ𝕪𝕡𝕖𝕣𝕟𝕒𝕥𝕣𝕖𝕞𝕚𝕒 & 𝕍𝕠𝕝𝕦𝕞𝕖 𝕆𝕧𝕖𝕣𝕝𝕠𝕒𝕕
• Mechanism:
• 8.4% NaHCO₃ contains 1,436 mEq/L sodium → hypertonic.
• Pulls water into vessels: 150 mL NaHCO₃ ≈ 1 L intravascular expansion.
• Risks: Pulmonary edema, heart failure (esp. in renal/cardiac patients).



𝟜. ℍ𝕪𝕡𝕠𝕔𝕒𝕝𝕔𝕖𝕞𝕚𝕒

• Mechanism:
• Alkalosis increases albumin binding to calcium → ↓ ionized Ca²⁺.
• Symptoms: Tetany, seizures, prolonged QT interval.



𝟝. 𝕃𝕖𝕗𝕥𝕨𝕒𝕣𝕕 𝕊𝕙𝕚𝕗𝕥 𝕠𝕗 𝕆𝕩𝕪𝕙𝕖𝕞𝕠𝕘𝕝𝕠𝕓𝕚𝕟 ℂ𝕦𝕣𝕧𝕖 (𝔹𝕠𝕙𝕣 𝔼𝕗𝕗𝕖𝕔𝕥)

• Mechanism:
• Alkalosis ↑ hemoglobin’s O₂ affinity → less O₂ released to tissues.
• Result: Tissue hypoxia, especially dangerous in shock/sepsis.



𝟞. ↑ 𝔾𝕝𝕪𝕔𝕠𝕝𝕪𝕤𝕚𝕤 → ℍ𝕪𝕡𝕖𝕣𝕘𝕝𝕪𝕔𝕖𝕞𝕚𝕒

• Mechanism:
• NaHCO₃ stimulates glycolysis → ↑ glucose output.
• Risk: Worsens hyperglycemia, particularly in diabetics/ketoacidosis.



𝟟. ↑ 𝟞-ℙ𝕙𝕠𝕤𝕡𝕙𝕠𝕗𝕣𝕦𝕔𝕥𝕠𝕜𝕚𝕟𝕒𝕤𝕖 𝔸𝕔𝕥𝕚𝕧𝕚𝕥𝕪 → ↑ 𝕆𝕣𝕘𝕒𝕟𝕚𝕔 𝔸𝕔𝕚𝕕𝕤

• Mechanism:
• Glycolysis accelerates → ↑ pyruvate → converts to lactate in hypoxic states.
• Paradox: NaHCO₃ can increase lactic acidosis, worsening the very acidosis it aims to treat

لذلك بقا مفروض مندهوش الا لو ال benift > risk وده شئ مهم.

هنا بقا نيجي للنقطة المهمة يعني ايه acidosis and acidemia ؟

1. Aᴄɪᴅᴏsɪs ᴠs. Aᴄɪᴅᴇᴍɪᴀ

Acidosis
• Refers to the pathophysiological process that increases the concentration of hydrogen ions ([H⁺]) in the body.
• Can be:
• Metabolic: due to loss of bicarbonate (e.g. diarrhea) or accumulation of non-volatile acids (e.g. lactic acid, ketoacids).
• Respiratory: due to CO₂ retention (e.g. hypoventilation).
• Acidosis may or may not lead to acidemia if there’s compensation from other systems.

Acidemia
• Refers to an actual decrease in arterial blood pH below 7.35, as measured on arterial blood gas (ABG).
• It is the end result of one or more acidosis processes overwhelming compensatory mechanisms.
• A patient can have both metabolic and respiratory acidosis together (i.e., mixed acid-base disorders).


What’s the meaning of strong acids

2. Sᴛʀᴏɴɢ Aᴄɪᴅs (ᴠs. Wᴇᴀᴋ Aᴄɪᴅs)

Definition
• A strong acid is one that completely dissociates in aqueous solution, releasing all its H⁺ ions.

In the context of metabolic acidosis, “strong acids” are often organic or exogenous acids:
• Lactic acid → from anaerobic metabolism or sepsis.
• Ketoacids → from uncontrolled diabetes (DKA) or starvation.
• Toxic alcohol metabolites:
• Formic acid (methanol)
• Glycolic/Oxalic acid (ethylene glycol)
• These acids increase unmeasured anions, leading to high anion gap acidosis.



3. Aɴɪᴏɴ Gᴀᴘ (AG)

Definition & Formula
• AG = Na⁺ – (Cl⁻ + HCO₃⁻)
Normal AG ≈ 8–12 mEq/L
• It represents unmeasured anions in plasma (e.g., lactate, ketones, phosphates, sulfates, toxins).

Clinical Use
• Helps classify metabolic acidosis:
• High AG Metabolic Acidosis (HAGMA) = accumulation of non-volatile acids.
• Normal AG (NAGMA) = loss of bicarbonate with compensatory ↑ Cl⁻ (see next section)

4. Hɪɢʜ Aɴɪᴏɴ Gᴀᴘ ᴠs. Nᴏɴ-Aɴɪᴏɴ Gᴀᴘ Mᴇᴛᴀʙᴏʟɪᴄ Aᴄɪᴅᴏsɪs

ℍ𝕚𝕘𝕙 𝔸𝕟𝕚𝕠𝕟 𝔾𝕒𝕡 𝕄𝕖𝕥𝕒𝕓𝕠𝕝𝕚𝕔 𝔸𝕔𝕚𝕕𝕠𝕤𝕚𝕤 (ℍ𝔸𝔾𝕄𝔸)

Causes:

Mnemonic: MUDPILES

• Methanol → formic acid
• Uremia → sulfuric/phosphoric acid retention
• Diabetic ketoacidosis → β-hydroxybutyric/acetoacetic acid
• Paraldehyde or Propylene glycol
• Isoniazid/Iron overdose
• Lactic acidosis
• Ethylene glycol → glycolic/oxalic acid
• Salicylates (late)

Mechanism:
• Accumulation of non-volatile acids leads to consumption of HCO₃⁻, and rise in unmeasured anions.



ℕ𝕠𝕣𝕞𝕒𝕝 𝔸𝕟𝕚𝕠𝕟 𝔾𝕒𝕡 𝕄𝕖𝕥𝕒𝕓𝕠𝕝𝕚𝕔 𝔸𝕔𝕚𝕕𝕠𝕤𝕚𝕤 (ℕ𝔸𝔾𝕄𝔸)

Causes:

Mnemonic: HARD-ASS

• Hyperalimentation (TPN)
• Acetazolamide (CA inhibitor)
• Renal tubular acidosis
• Diarrhea
• Adrenal insufficiency
• Saline infusion (0.9% NaCl)
• Spironolactone

Mechanism:
• Direct loss of bicarbonate (via kidneys or gut).
• To maintain electroneutrality, Cl⁻ increases, keeping the AG normal.
• Associated with volume expansion and hyperchloremia.

ليه انا جبتلك سيرة الacidosis علشان اقولك اسبابها زي ما هيا فوق كده ،، طيب ماذا بعد بقا امتي استعمل وامتي مستعملش البيكارب في كل واخد من دول بالدليل العلمي ،، مليش دعوة باي حاجة بره ده ولو فيه دليل علمي معاك قوله في الكومنتات هرحب بيه جدًا

I. Eᴠɪᴅᴇɴᴄᴇ-Bᴀsᴇᴅ Cʟɪɴɪᴄᴀʟ Usᴇs ᴏғ Sᴏᴅɪᴜᴍ Bɪᴄᴀʀʙᴏɴᴀᴛᴇ ٥ مواقف هستعمله فيهم

𝟙. 𝕊𝕖𝕧𝕖𝕣𝕖 𝕄𝕖𝕥𝕒𝕓𝕠𝕝𝕚𝕔 𝔸𝕔𝕚𝕕𝕠𝕤𝕚𝕤 𝕨𝕚𝕥𝕙 𝕡ℍ < 𝟟.𝟙 (𝕖𝕤𝕡𝕖𝕔𝕚𝕒𝕝𝕝𝕪 𝕨𝕚𝕥𝕙 𝔸𝕂𝕀)

• Use: IV NaHCO₃ can raise serum pH temporarily.
• Indication: Severe acidemia impairs myocardial contractility and vasopressor response.
• Evidence: BICAR-ICU trial showed mortality benefit in AKI subgroup .
• Goal: Raise pH to > 7.2 while treating the cause (e.g., sepsis, hypoperfusion).
يعني بستعمله ك bridge therapy طيب ليه هنا؟ لان في ال AKI الكلي هيا المسؤلة عن طرد الهيدروجين وتديك بيكارب مسئوله عن التظبيط هنا الكلي سابت الراية وقالتلك باي باي كمبورا لحد ما تصلح السبب اللي زعلها علشان كده انت بتدي علشان تساعد الكلي وعلي ما تصلح السبب وعلي ما تشوف هتغسل ولا لاءه وده اللي البيكار ترايل لقيته

BICAR-ICU Trial
• In the BICAR-ICU trial (Jaber et al., 2018):
• Overall, NaHCO₃ did not improve 28-day survival in the whole cohort. للاسف
• But in the pre-specified AKI subgroup:
• Mortality reduced: 63% (NaHCO₃ group) vs 46% (control), p = 0.028
• More ventilator-free and dialysis-free days
• Suggests that selective use of bicarbonate in severe acidemia + AKI may:
• Delay or reduce need for RRT
• Improve hemodynamics without harm
• Enhance survival when kidneys cannot clear acid

𝟚. 𝔸𝕔𝕦𝕥𝕖 ℍ𝕪𝕡𝕖𝕣𝕜𝕒𝕝𝕖𝕞𝕚𝕒 (𝕂⁺ > 𝟞.𝟝 𝕠𝕣 𝔼ℂ𝔾 𝕔𝕙𝕒𝕟𝕘𝕖𝕤)

• Use: NaHCO₃ shifts K⁺ into cells via H⁺/K⁺ exchange.
• Adjunctive therapy with insulin + glucose, β2-agonists, calcium gluconate.
• Best for: Hyperkalemia + acidosis.



𝟛. 𝕋𝕣𝕚𝕔𝕪𝕔𝕝𝕚𝕔 𝔸𝕟𝕥𝕚𝕕𝕖𝕡𝕣𝕖𝕤𝕤𝕒𝕟𝕥 (𝕋ℂ𝔸) 𝕆𝕧𝕖𝕣𝕕𝕠𝕤𝕖 / 𝕊𝕠𝕕𝕚𝕦𝕞 ℂ𝕙𝕒𝕟𝕟𝕖𝕝 𝔹𝕝𝕠𝕔𝕜𝕖𝕣 𝕋𝕠𝕩𝕚𝕔𝕚𝕥𝕪

• Mechanism: Alkalinization of plasma (↑ pH > 7.45) stabilizes myocardium and reduces TCA binding to sodium channels.
• Use: IV boluses of 1–2 mEq/kg NaHCO₃; repeat to maintain QRS < 100 ms.
• Guideline-based indication (ACLS).



𝟜. 𝕋𝕠𝕩𝕚𝕔 𝔸𝕝𝕔𝕠𝕙𝕠𝕝 𝕀𝕟𝕘𝕖𝕤𝕥𝕚𝕠𝕟 (𝕄𝕖𝕥𝕙𝕒𝕟𝕠𝕝, 𝔼𝕥𝕙𝕪𝕝𝕖𝕟𝕖 𝔾𝕝𝕪𝕔𝕠𝕝)

• Use: NaHCO₃ treats associated high AG acidosis by buffering formic/glycolic acids.
• Adjunct to: fomepizole or dialysis.



𝟝. ℝ𝕖𝕟𝕒𝕝 𝕋𝕦𝕓𝕦𝕝𝕒𝕣 𝔸𝕔𝕚𝕕𝕠𝕤𝕚𝕤 (𝕋𝕪𝕡𝕖 𝕀 𝕒𝕟𝕕 𝕀𝕀)

• Use: Chronic oral bicarbonate therapy replaces lost HCO₃⁻.
• Goal: Prevent nephrocalcinosis and growth retardation (especially in children).
بس عوض العيان بوتاسيوم الاول يا صديقي

Lactic Acidosis and Sodium Bicarbonate: Why Use Is Limited

What Is Lactic Acidosis?
• Occurs when lactate builds up due to hypoxia or impaired metabolism (e.g., in shock, sepsis, hypoperfusion).
• This produces H⁺ ions, leading to metabolic acidosis with low pH and high anion gap.



II. Cᴏɴᴛʀᴏᴠᴇʀsɪᴀʟ / Cᴏɴᴅɪᴛɪᴏɴᴀʟ Usᴇs (Lɪᴍɪᴛᴇᴅ Bᴇɴᴇғɪᴛ ᴏʀ Sᴘᴇᴄɪғɪᴄ Sᴜʙɢʀᴏᴜᴘs)

𝟞. 𝕃𝕒𝕔𝕥𝕚𝕔 𝔸𝕔𝕚𝕕𝕠𝕤𝕚𝕤

• Not routinely recommended
• Use only if:
• pH < 7.1 and associated AKI or vasopressor-resistant shock.
• Why limited?

1. Generates CO₂ → May Worsen Intracellular Acidosis
• Sodium bicarbonate works by buffering H⁺:
H⁺ + HCO₃⁻ → H₂CO₃ → H₂O + CO₂
• CO₂ easily crosses cell membranes, enters cells and reacts with water:
→ CO₂ + H₂O → H⁺ + HCO₃⁻ (inside the cell)
• Result: pH in plasma may rise, but intracellular pH may fall further → worsening cellular acidosis, especially in brain and heart.



2. No Mortality Benefit in General Population
• Large studies (including BICAR-ICU) show no significant survival improvement in patients with lactic acidosis who receive bicarbonate—unless they have severe AKI .
• Treating the underlying cause (e.g., perfusion, infection, hypoxia) is more important.



3. May Increase Lactate Production
• Giving bicarbonate can stimulate glycolysis and shift pyruvate toward lactate in hypoxic tissues → paradoxical lactate rise.
• This worsens the underlying problem instead of solving it.



When Might Bicarbonate Be Justified in Lactic Acidosis?

Use bicarbonate only if:
1. pH < 7.1 (severe acidemia impairs cardiac function).
2. AND patient has:
• Acute kidney injury (AKI) (unable to clear acid), or
• Vasopressor-resistant hypotension (acidosis blunts vasopressor response).

Goal in this setting:
• Temporarily improve cardiac function, perfusion, and responsiveness to vasopressors, while definitive treatment (e.g., fluids, antibiotics, oxygen) is underway

𝟟. 𝔻𝕚𝕒𝕓𝕖𝕥𝕚𝕔 𝕂𝕖𝕥𝕠𝕒𝕔𝕚𝕕𝕠𝕤𝕚𝕤 (𝔻𝕂𝔸)

• Avoid unless pH < 6.9
• Risks: cerebral edema (especially in children), hypokalemia.
• Use cautiously in:
• Severe acidosis with hemodynamic instability
• Refractory hyperkalemia

𝟠. ℂ𝕒𝕣𝕕𝕚𝕒𝕔 𝔸𝕣𝕣𝕖𝕤𝕥

• Not recommended routinely
• Use only in:
• Hyperkalemia
• TCA overdose
• Prolonged arrest (>15 min) (low evidence)
• ACLS removed routine bicarb from arrest algorithm due to lack of outcome improvement.

شايف الكاريزما اللي كان بيديه علي الفاضي والمليان

𝟡. ℝ𝕙𝕒𝕓𝕕𝕠𝕞𝕪𝕠𝕝𝕪𝕤𝕚𝕤

• Goal: Alkalinize urine to prevent myoglobin-induced AKI.
• Evidence: No clear benefit over volume resuscitation alone.
• Use only if: Metabolic acidosis is severe.



𝟙𝟘. ℕ𝕠𝕟-𝔸𝕟𝕚𝕠𝕟 𝔾𝕒𝕡 𝕄𝕖𝕥𝕒𝕓𝕠𝕝𝕚𝕔 𝔸𝕔𝕚𝕕𝕠𝕤𝕚𝕤 (ℍ𝕪𝕡𝕖𝕣𝕔𝕙𝕝𝕠𝕣𝕖𝕞𝕚𝕔)

• Use: Oral or IV bicarbonate corrects lost HCO₃⁻.
• Common in: Diarrhea, ureterosigmoidostomy, post-saline infusion acidosis.



III. Non-Critical Uses

11. Urinary Alkalinization
• Used in:
• Salicylate toxicity (↑ renal excretion)
• Tumor lysis syndrome (prevent uric acid crystallization)
• Cystinuria (prevent stone formation)
• Target urine pH: > 7.0–7.5



12. CKD with Chronic Metabolic Acidosis
• Oral bicarbonate may:
• Slow CKD progression
• Improve bone mineral metabolism
• Recommended when serum bicarbonate < 22 mEq/L

اخر حاجة يا عزيزي ان البيكارب مش بيتاخد shot لانه في معظم الحالات. والجرعةبتتحسب بكذا طريقة بس دي احسن .

Formula-based (Base Deficit):

HCO₃⁻ needed (mEq) = 0.5 × body weight (kg) × base deficit

Then give half of that dose IV over 1–2 hours, reassess ABG
Example: 70 kg patient, HCO₃⁻ = 12 → deficit = 12
0.5 × 70 × 12 = 420 mEq total, give ~200 mEq initially

ده خلاصة موضوع فيه جدال كتير.
الأرقام مهمة ولو لاحظ احنا بندي علي PH في معظم الحالات .

- عامر .

02/12/2025

HYPOTENSION DURING DIALYSIS

Hypotension during intermittent hemodialysis is common, and has been attributed to acute volume shifts, shifts in osmolarity, electrolyte imbalance, temperature changes, altered vasoregulation, and sheer hypovolemia. Intradialytic hypotension (IDH) remains to be a major complication of hemodialysis. It occurs in nearly 25% of dialysis sessions and often requires aggressive resuscitative measures and sometimes premature termination of hemodialysis. It is also a significant independent factor affecting mortality in hemodialysis patients.

Definition:
There is no generally accepted definition of intradialytic hypotension. Kidney Disease Outcomes Quality Initiative (K/DOQI) and European Best Practice Guidelines define intradialytic hypotension as the presence of a decrease in systolic blood pressure > 20mm of Hg or a decrease in mean arterial pressure by 10mm of Hg, which is associated with clinical events and need for nursing interventions.

Pathophysiology:
• Among other factors, the major pathophysiology of these episodes is the removal of large volume of blood water and solutes over a short period of time, overwhelming normal compensatory mechanisms, which include plasma refilling and reduction of venous capacity (due to reduction of pressure transmission to veins). In some patients, a seemingly paradoxical and inappropriate reduction of sympathetic tone may occur, causing reduction of arteriolar resistance, decreased transmission of pressure to veins with corresponding increase in venous capacity. Increased sequestration of blood in veins under conditions of hypovolemia reduces cardiac filling, cardiac output and ultimately blood pressure.
• Hypotensive episodes during hemodialysis in patients with end stage renal disease in absence of inadequate maintenance of the plasma volume, pre-existence of cardiovascular disease, or autonomic nervous system dysfunction are accompanied by increased plasma concentrations of the end-products of nitric oxide metabolism (above the expected levels, based on the reduction of urea).

Risk factors:
• Older age
• Longer dialysis vintage
• Diabetes
• Lower predialysis blood pressure
• Lower albumin
• Female s*x
• Hispanic ethnicity
• Higher body mass index

Causes of intra-dialytic hypotension:

• Major factors that contribute to intradialytic hypotension include:
o Rapid or excessive ultrafiltration
o A rapid reduction in plasma osmolality
o Incorrectly low prescribed target weight
o Autonomic neuropathy
o Diminished cardiac reserve.
• Other contributors to intradialytic hypotension include the intake of antihypertensive medications or the ingestion of a meal immediately before or during dialysis.
• The composition and temperature of the dialysate fluid may contribute to intradialytic hypotension.
o Hypotension has been associated with the use of dialysate acetate, low sodium, high magnesium, and low calcium.
o Dialysate temperature that is higher than body temperature has also been associated with hypotension.
• Other suggested contributors include the release of adenosine during organ ischemia, the increased synthesis of endogenous vasodilators (such as nitric oxide), and inappropriately low plasma vasopressin levels.

Clinical Presentation:
• Occasionally asymptomatic
• Lightheadedness
• Muscle cramps
• Nausea
• Vomiting
• Dyspnea
• Vagal symptoms, including yawning, sighing, and hoarseness, may be observed before the drop in blood pressure is detected.

Acute management:
• Ultrafiltration rate should be decreased or stopped, depending upon the severity of hypotension.
• The patient should be placed in the Trendelenburg position, where the body is laid flat on the back (supine position), with the feet higher than the head by 15 to 30 degrees.
• Intravascular volume should be replaced in cases when blood pressure is not restored after stopping ultrafiltration and repositioning the patient. We give an intravenous fluid bolus of 250 to 500 mL. Intravenous fluid is effective in restoring blood pressure.
• Oxygen should be administered. There is evidence that intradialytic blood oxygen saturation and its variability are associated with intradialytic hypotension. A decrease in central venous oxygen saturation most likely indicates a decline in cardiac output.
• Patients with persistent hypotension despite measures above should be evaluated for evidence of an underlying serious cause.
o This assessment primarily includes a physical examination, including auscultation of heart and lungs, palpation of the abdomen, and examination of the hemodialysis access for evidence of infection.
o An electrocardiogram should be performed.
o Particular concerns include occult sepsis, previously unrecognized cardiac and/or pericardial disease, and gastrointestinal bleeding.
o Rare, serious causes of hypotension on dialysis include hemolysis, reaction to dialyzer, or air embolus. Hemolysis may be suggested by the simultaneous occurrence of symptoms in multiple patients and occasionally port-wine appearance of blood in the venous line. Air embolus may be accompanied by distinctive clinical findings, including characteristic heart sounds.
o Reactions to the dialyzer or machine tubing may be manifested by chest and back pain and by signs of allergic reaction (urticaria, flushing, coughing, sneezing), in addition to hypotension.
• Hypotension that does not respond to saline bolus or is accompanied by symptoms such as fever, chills, chest and/or abdominal pain, or dyspnea suggests a serious cause. Such patients are generally referred to a hospital for more extensive evaluation. Once serious causes have been excluded, further evaluation is directed to the prevention of future episodes.

Prevention of recurrent episodes:
• Patients who have recurrent episodes of intradialytic hypotension should be carefully evaluated and preventive strategies put in place. Subsequent evaluation and intervention depend upon patient response to initial measures.
• First-line approach: The first-line approach includes reassessing the target weight, avoiding food intake during dialysis, withholding antihypertensive agents prior to dialysis, and limiting interdialytic sodium intake to reduce ultrafiltration requirements.
o Reassess target weight – We reassess the prescription target weight. The optimal target weight is often determined empirically by trial and error ("probing"). Using a trial-and-error approach, the target weight is set just above the weight at which unacceptable symptoms, such as cramping, nausea, and vomiting, or hypotension occur. Future episodes of intradialytic hypotension may be prevented in some patients by increasing the target weight.
o Avoid food during dialysis – We ask patients who are prone to intradialytic hypotension to avoid food during dialysis. Peripheral vascular resistance generally drops 20 to 120 minutes after the ingestion of food, which may cause a decrease in blood pressure.
o Withhold antihypertensive agents – Patients who are prone to intradialytic hypotension should withhold antihypertensive agents prior to dialysis. Among such patients, we avoid prescribing blood pressure medications that need to be taken twice (or more) daily. Whenever possible, we prefer medications that can be given once daily and then ask patients to take the dose at night.
o Limit interdialytic sodium intake – We ask patients who are prone to intradialytic hypotension to limit sodium (salt) intake, which results in a reduction in fluid intake. Excessive sodium intake results in thirst and larger extracellular volume gain that must be removed by ultrafiltration. Since the dialysis time for each session is generally fixed, the ultrafiltration rate must be increased to attain target weight by the end of the individual session. We generally ask patients to limit sodium intake to 1 to 2 grams per day; this amount of sodium is equivalent to 2.5 and 5 grams of salt, respectively, or roughly one-half and one teaspoon of salt, respectively.
o Review dialysate composition – We generally make sure that dialysate calcium and magnesium are ≥2.25 mEq/L and ≥1.0 mEq/L, respectively. Low-dialysate calcium and magnesium have been associated with intradialytic hypotension.
o Increase urine output – Among patients with residual urine output, we attempt to augment urine output with oral diuretic administration. Use of loop diuretics has been associated with lower interdialytic weight gain and lower rates of intradialytic hypotension among hemodialysis patients.
• Second-line approach: The second-line approach includes a cardiac evaluation, the use of cool dialysate, and an increase in dialysis time and/or frequency.
o Assess primary cardiac factors – We perform a careful assessment for primary cardiac factors that may promote the development of intradialytic hypotension. The risk of intradialytic hypotension is increased in patients with heart failure, cardiomegaly, or ischemic heart disease. A pericardial effusion should be excluded with an echocardiogram.
o Use of cool dialysate – If primary cardiac factors are not present on evaluation, we use cool-temperature dialysis. Cool-temperature dialysis has been shown to increase hemodynamic stability. If employing a fixed reduction, we reduce the dialysate temperature to 0.5 to 1.0o C below the patient’s body temperature (as monitored by tympanic thermometer). This may lower the body temperature up to approximately 1ºC. This change is generally well tolerated, although some patients develop unacceptable side effects such as chilling or cramping.
o Increasing dialysis time – If the above measures fail to sufficiently decrease the frequency of intradialytic hypotension, we increase the dialysis time. This may be done by increasing the time per session or by adding an additional treatment per week. Increasing the time and/or frequency of hemodialysis may be effective in preventing or reducing intradialytic hypotension.
• Third-line approach: If other treatment options fail to prevent intradialytic hypotension, we use a third-line approach, which includes giving midodrine and/or switching the patient to other forms of dialysis.
o Midodrine – If all other measures fail to decrease the frequency of intradialytic hypotension, we use the selective alpha-1 adrenergic agonist, midodrine. Among patients with autonomic neuropathy and possibly other patients with severe hemodialysis hypotension not responsive to the above measures, midodrine may be effective and well tolerated. We generally give 2.5 to 5 mg, 15 to 30 minutes prior to dialysis. In cases where hypotension occurs later in the hemodialysis treatment, we utilize split dosing, with an initial dose given 30 minutes prior to dialysis and a second dose given halfway through treatment (at least three hours after the first dose).
o Change to other modes of dialysis – Changing from standard, thrice-weekly, in-center hemodialysis to other modes of dialysis, such as peritoneal dialysis, daily dialysis, hemodiafiltration (HDF; if available), or nocturnal hemodialysis, may be an option for patients who have chronic, debilitating intradialytic hypotension. HDF may mitigate intradialytic hypotension.
• Other treatments — In addition to the measures listed above, the correction of anemia to target levels with erythropoiesis-stimulating agents may decrease the frequency of intradialytic hypotension by improving cardiac function.
(Ref: uptodate.com+ncbi.nlm.nih.gov/books)

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