ICU Resource

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

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).

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𝟜. ℍ𝕪𝕡𝕠𝕔𝕒𝕝𝕔𝕖𝕞𝕚𝕒

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

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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.

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𝟞. ↑ 𝔾𝕝𝕪𝕔𝕠𝕝𝕪𝕤𝕚𝕤 → ℍ𝕪𝕡𝕖𝕣𝕘𝕝𝕪𝕔𝕖𝕞𝕚𝕒

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

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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).

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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.

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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.

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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.

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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).

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𝟜. 𝕋𝕠𝕩𝕚𝕔 𝔸𝕝𝕔𝕠𝕙𝕠𝕝 𝕀𝕟𝕘𝕖𝕤𝕥𝕚𝕠𝕟 (𝕄𝕖𝕥𝕙𝕒𝕟𝕠𝕝, 𝔼𝕥𝕙𝕪𝕝𝕖𝕟𝕖 𝔾𝕝𝕪𝕔𝕠𝕝)

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

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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.

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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.

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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.

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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.

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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.

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𝟙𝟘. ℕ𝕠𝕟-𝔸𝕟𝕚𝕠𝕟 𝔾𝕒𝕡 𝕄𝕖𝕥𝕒𝕓𝕠𝕝𝕚𝕔 𝔸𝕔𝕚𝕕𝕠𝕤𝕚𝕤 (ℍ𝕪𝕡𝕖𝕣𝕔𝕙𝕝𝕠𝕣𝕖𝕞𝕚𝕔)

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

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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

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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 .