Chapter 16: Acid-Base, Fluids, and Electrolytes

ACID-BASE, FLUIDS, AND ELECTROLYTES jo · ACID-BASE EQUILIBRIUM I. ACID-BASE INTERPRETATION AND TREATMENT (THE BASICS) > Think of the body as a machine that constantly produces acid as a waste product. > Production: We make massive amounts of volatile acid (CO₂, 10,000 - 15,000 mmol/ day) & a small amount of nonvolatile acid (sulfuric/phosphoric acid, ~50-100 mEq/day). > Defense: To keep our pH safe (7.35–7.45), we buffer these acids in the blood and then excrete them: • Lungs: Blow off CO₂ (volatile acid). • Kidneys: Excrete H⁺ and reabsorb HCO₃⁻ (nonvolatile acid). Key Definitions to Memorize: > Acidemia/Alkalemia: Refers strictly to the blood pH (Low or High). > Acidosis/Alkalosis: Refers to the physiologic process causing the change. Note: You can have an acidosis (process) without acidemia (low pH) if your body compensates perfectly! A. INTERPRETATION MODELS 1. Henderson–Hasselbalch: The classic clinical approach. It looks at the relationship between pH, Bicarbonate (HCO₃⁻), and CO₂. II. HOW TO INTERPRET ABGS (SIMPLIFIED) Step 1: Look at pH (NV is 7.35-7.45) is it ACIDOSIS or ALKALOSIS Step 2: Look at PaCO2 (Respiratory or Metabolic) WHERE: ↓ pH,↓PaCO2 = same direction → METABOLIC > 6.1 = pKa of carbonic acid ; 0.3 = blood solubility coefficient of CO₂ at 37°C. ↓pH, ↑PaCO2 = opposite → RESPIRATORY 2. Stewart Approach: A more complex physiochemical model involving "Strong Ions" SMOR = Same Metabolic, Opposite Respiratory (Na, K, Cl, Lactate). It helps explain mechanisms (like why saline causes acidosis) Step 3: Know if compensated or uncompensated, or partially but isn't necessarily better for prognosis. If RESPIRATORY > Three independent variables determine plasma pH and HCO₃⁻ concentration: > Check pH & compensatory HCO3 (metabolic) PaCO2 concentration of weak acids If METABOLIC strong ion difference > Check pH & compensatory PaCO2 (respiratory) COMPENSATORY MECHANISM 1. Respiratory acidosis = Increased HCO3 (↓pH,↑PaCO2,↑HCO3) 2. Respiratory alkalosis = Decreased HCO3 (↑pH, ↓PaCO2,↓HCO3) 3. Metabolic acidosis = Decreased PaCO2 (↓pH,↓PaCO2,↓PaCO2) 4. Metabolic alkalosis = Increased PaCO2 (↑pH,↑PaCO2,↑PaCO2) TIC TAC TOE APPROACH pH = 7.34 (under Acid) PaCO2 = 23 (under Base) HCO3 = 12 (under Acid) Acid pH HCO3 Normal Base CO2 Partially compensated metabolic acidosis Acid Normal Base pH = 7.44 (normal but on the side of Basic) HCO3 pH PaCO2 PaCO2 = 33 (under Base) HCO3 = 17 (under Acid) Fully compensated Respiratory Alkalosis III. METABOLIC ACIDOSIS > Definition: pH < 7.35 + ↓HCO₃⁻ (< 21) + Compensatory ↓PaCO₂(Hyperventilation) > The Big Divide (Anion Gap): We split this into two types based on the "Anion Gap" (AG). IV. METABOLIC ALKALOSIS 1. HAGMA (HIGH ANION GAP ACIDOSIS > 13) > Definition: pH >7.45 + ↑ HCO₃⁻ (>27) + Compensatory ↑PaCO₂(Hypoventilation) > Caused by extra unmeasured acids (e.g., Lactic acid, Ketoacids). > The Big Divide (Chloride): Check the Urine Chloride 2. NAGMA (NON-ANION GAP ACIDOSIS < 13) • Saline Responsive (Urine Cl <20): Often due to "contraction" (dehydration) or > Caused by loss of Bicarbonate (Diarrhea) or too much Chloride (Saline vomiting. The kidneys hold onto bicarb because they are desperate for volume. resuscitation). Give Saline (NaCl) to fix it. > Treatment: Fix the underlying cause. • Saline Resistant: Due to excess mineralocorticoids (aldosterone) or severe Note: Using Bicarbonate to treat the pH is controversial. It generally doesn't improve hypokalemia. Saline won't help. You need Potassium or drugs like mortality unless the patient has Acute Kidney Injury (AKI). Spironolactone/Acetazolamide. V. RESPIRATORY ALKALOSIS > Definition: pH > 7.45 + ↓PaCO₂ (< 36). > Mechanism: Breathing too fast (Hyperventilation) washes out CO₂. > Causes: Pain, Anxiety, Hypoxemia, or Iatrogenic (ventilator set too high). > Brain Effects: ↓CO₂ causes CEREBRAL VASOCONSTRICTION. • Clinical Gem: Neurosurgeons sometimes hyperventilate patients intentionally to shrink brain volume (↓ ICP), but doing it too much causes brain ischemia. > May lead to hypocalcemia, hypokalemia, bronchoconstriction, and cardiac arrhythmias. VI. RESPIRATORY ACIDOSIS > Definition: pH < 7.35 + ↑PaCO₂ (> 44). > Mechanism: Breathing too slow (Hypoventilation) or lung failure. > Causes: Opioids/Sedatives (stops the drive), COPD/Asthma (stops the flow), or Muscle weakness. > Compensation: The kidneys are slow! They take days to retain bicarb to fix the pH. We call this "Chronic Respiratory Acidosis". > Treatment: Fix the ventilation! (Naloxone for opioids, BIPAP/Ventilator for failure). > Benefits of Respiratory acidosis: 1. ↑catecholamine release →↑CO & BP 2. ↑perfusion to vital organs 3. Shifts O2 Hgb curve to the RIGHT leading to ↑O2 unloading to the tissues. VII. CLINICAL GUIDE IN INTERPRETING ACID-BASE DISORDERS AND ABG RESULTS To get the right answer on an exam or in the ICU, follow these steps exactly: 1 Check pH: Acidemia (<7.35) or Alkalemia (>7.45)? 2 Check PaCO₂ & HCO₃⁻: Which one matches the pH direction? (This is your Primary disorder). ◦ Example: Acidemic + High CO₂ = Respiratory Acidosis. 3 Check Chronicity (If Respiratory): Is the bicarb high yet? If yes, it's chronic. If no, it's acute. 4 Calculate Anion Gap (If Metabolic Acidosis): ◦ Even if pH is normal, check this! A high gap means a hidden acidosis. ◦ Correction: Adjust for Albumin (it hides the gap). 5 Check Compensation: Is the body fighting back correctly? ◦ Winter's Formula (for Met. Acidosis): Expected PaCO₂ = (1.5×HCO3 )+8±2. ◦ Result: If measured CO₂ is different from expected, you have a Mixed Disorder. 6 Delta-Delta Ratio (Δ/Δ): (Only if Anion Gap is high). • Compares how much the Gap went up vs. how much Bicarb went down. • Helps find hidden metabolic alkalosis or non-gap acidosis. Formula Name Equation Purpose Anion Gap Na+ - (Cl- + HCO3-) Diagnoses AG Metabolic Acidosis Winter's Formula (1.5 X HCO3-) + 8 + 2 Checks respiratory compensation for Met. Acidosis Corrected AG AG observed + 2.5 X (4.5 - Albumin) Adjusts gap for low albumin (common in sick patients) 🧠 ! FLUID MANAGEMENT I. PHYSIOLOGY A. BODY FLUID COMPARTMENTS > Total Body Water (TBW) makes up 60% of body weight in men and 50% in women. It is divided into two main compartments: Compartment % of TBW Intracellular Fluid (ICF) 2/3 (55-65%) Fluid inside cells. Definition Key Feature Rich in Potassium (K+). Extracellular Fluid (ECF) 1/3 (35-45%) Fluid outside cells. Rich in Sodium (Na+). MNEMONIC: "PISO" Potassium In, Sodium Out The ECF is further divided into: 1. Interstitial Fluid (ISF): ~75% of ECF. This is the fluid between cells. 2. Intravascular Fluid (IVF/Plasma): ~25% of ECF. This is the fluid inside blood vessels. ◦ Note: Red blood cells are technically Intracellular, not Intravascular fluid. Example (70kg Male): • TBW: 42 Liters • ICF: 25.2 Liters (60%) or 40% • ECF: 16.8 Liters (40%) or 20% [ISF: 12.6L (75%) + Plasma: 4.2L (15%)] MNEMONIC: "60-40-20-15-5 Rule" C. DISTRIBUTION OF INFUSED FLUIDS (WHAT HAPPENS WHEN WE GIVE FLUIDS?) > We use mathematical models to predict where fluid goes. 1. STATIC MODEL (THE CLASSIC VIEW) > This assumes body spaces are fixed containers. It helps calculate how much fluid is needed to expand Plasma Volume (PV). > Free Water (D5W): Distributes everywhere (TBW). • To replace 2L blood loss: Need 32 Liters of D5W! (Inefficient). > Crystalloid (Lactated Ringers/Saline): Distributes in ECF (Plasma + Interstitial). • To replace 2L blood loss: Need 12 Liters of LR. (Ratio ~3:1 or 4:1 redistribution). > Colloid (5% Albumin): Stays in Plasma (PV). • Expands volume 1:1 (or slightly more by pulling interstitial fluid in). > Hyperoncotic Colloid (25% Albumin): Powerful pull. • Expands PV by 400mL for every 100mL infused. 2. KINETIC MODEL (THE MODERN VIEW) > The body is dynamic, not static. Factors affecting fluid distribution include: > Anesthesia (Isoflurane): Causes vasodilation → reduced urine output → fluid gets stuck in extravascular tissues (edema). > Vasopressors: ◦ Phenylephrine: Decreases intravascular retention (squeezes fluid out). ◦ Isoproterenol: Increases intravascular retention. > Glycocalyx: Rapid infusions can damage this endothelial lining, releasing "trapped" B. PHYSIOLOGY OF FLUID MOVEMENT non-circulating fluid, making it look like plasma volume increased more than it > There are two different barriers with different rules for movement: actually did. 1. Cell Membrane (Separates ICF ECF) D. REGULATION OF OSMOLARITY AND CIRCULATING VOLUME (HOW DOES THE BODY MAINTAIN BALANCE) > Rule: Water moves by Osmosis (Effective Osmolarity). 1. INTAKE REGULATION > Mechanism: Water flows to the side with ↑solute concentration. > Primary Driver: Thirst. > The Players: > Triggers: ◦ Na+/K+ ATPase pumps keep Na+ high outside (140 mEq/L) and K+ high inside Hypertonicity: ↑ Plasma Osmolarity (detects even a 2% change). (150 mEq/L). Hypovolemia: ↓ Effective Circulating Volume (ECV). ◦ Clinical Pearl: ECF volume is determined by total body Na+. Angiotensin II: Signals the brain to drink. 2. Capillary Membrane (Separates Interstitial Intravascular) 2. OUPUT REGULATION (THE KIDNEY) > The body controls output via four main hormonal systems: > Rule: Water moves by Starling Forces (Hydrostatic vs. Oncotic Pressure). Renin-Angiotensin-Aldosterone System (RAAS): > Mechanism: > Trigger: ↓ BP, ↓ Na+, or Sympathetic tone. • Small ions (Na+, K+) pass freely (no gradient). > Renin: Released by JGA → Converts Angiotensinogen to Ang I. • Large molecules (Albumin) cannot pass. > ACE: Converts Ang I → Ang II. > The Player: Albumin creates Oncotic Pressure, holding water inside the blood vessels. > Angiotensin II (The Workhorse): • Vasoconstriction (↑ BP). • Triggers Aldosterone release. • Stimulates Thirst & ADH. • Constricts Efferent Arteriole (preserves GFR). • Increases Na+ reabsorption in proximal tubule. Aldosterone: > Action: Reabsorbs Sodium (Na+) in the distal tubules. Water follows salt. > Result: Urinary sodium excretion can drop to near zero. Natriuretic Peptides (ANP, BNP, CNP): > Trigger: Stretch (Volume Overload). > Action: Dump fluid. Promotes Diuresis (water loss), Natriuresis (salt loss), and Vasodilation. > Types: ANP (Atrial), BNP (Ventricular - heart failure marker), CNP (Endothelial). Antidiuretic Hormone (ADH/Vasopressin): > Trigger: Hypertonicity (primary) or Severe Hypovolemia (secondary). Also Pain, Nausea, Opiates. > Action: • V1 Receptor: Vasoconstriction. • V2 Receptor: Inserts Aquaporin-2 channels in collecting ducts→Reabsorbs H2O > Result: Concentrates urine (up to 1,200 mOsm/kg) and dilutes plasma. Hormone Trigger Angiotensin II ↓ Volume / Sympathetic Vasoconstrict + Save Salt Primary Action Aldosterone Ang II / ↓ Na+ Effect on Fluid/Salt Retains Na+ & Water Distal Tubule Na+ Reabsorption Retains Na+ (Water follows) ADH (Vasopressin) ↑ Osmolarity / ↓ Volume Collecting Duct Water Channels Retains Free Water Natriuretic Peptides Heart Stretch Diuresis / Vasodilation Excretes Na+ & Water II. FLUID REPLACEMENT THERAPY A. MAINTENANCE OF FLUID REPLACEMENT > Traditional maintenance calculations are useful for stable patients with limited oral intake (e.g., bowel prep) but NOT for acutely ill or surgical patients with altered physiology. Daily Losses to Replace: > Urine: ~1,000 mL/day. > Insensible (Skin/Lungs): 500–1,000 mL/day. > GI Tract: 100–200 mL/day. Electrolyte Requirements: > Sodium (Na+): ~75 mEq/day (Renal handling is efficient). > Potassium (K+): ~40 mEq/day (Renal handling is less efficient; be careful). Dextrose Warning: > Historically: Used to prevent protein breakdown. > Current Practice: AVOID UNLESS the patient is an infant or on insulin. > Why? Surgical stress causes hyperglycemia (Diabetogenic) → Osmotic Diuresis + Worse Neurologic Outcomes (Ischemia/TBI). > Target Glucose: < 180 mg/dL is better than tight control (81-108 mg/dL) for mortality. III. SURGICAL FLUID REQUIREMENT A. WATER AND ELECTROLYTE COMPOSITION OF FLUID LOSSES > We replace obligate losses (urine/insensible) + specific surgical losses. Composition of Losses: > Protein-Rich (Plasma-like): Wound drainage, Burn edema, Ascites. > Variable Composition (GI Fluids): • Gastric (Acidic + High Cl−): Loss causes Hypochloremic Metabolic Alkalosis. • Treatment: 0.9% Saline (NaCl). • Diarrhea (Bicarbonate Rich): Loss causes Hyperchloremic Metabolic Acidosis. • Treatment: Balanced crystalloid (Lactate/Acetate) or Bicarb. B. INFLUENCES OF PERIOPERATIVE AND INTRAOPERATIVE FLUID INFUSION RATES ON CLINICAL OUTCOMES Intraoperative Strategies: Liberal vs. Restrictive > The debate continues, but generally: 1. Minor Surgery (Ambulatory): Liberal is better. 20-30 mL/kg reduces PONV (Nausea/Vomiting) and pain compared to restrictive. 2. Major Surgery (Abdominal/Cardiac): Goal-Directed Therapy (GDT) is best. ◦ Restrictive (<1kg gain): Fewer cardiopulmonary/healing complications but higher AKI (Acute Kidney Injury) risk. ◦ Liberal: Higher risk of Pneumonia and Pulmonary Edema. ◦ Conclusion: Use monitors (GDT) to give just enough fluid to optimize Cardiac Output, avoiding both hypovolemia (renal failure) and hypervolemia (edema). IV. COLLOIDS, CRYSTALLOIDS, AND HYPERTONIC SOLUTIONS A. PHYSIOLOGY AND PHARMACOLOGY > Osmosis: Movement of solvent (e.g., water) across a selectively permeable membrane from low → high solute concentration. > Osmolarity: Concentration of all solutes/liter (Normal: 275 to 290 mmol/kg) Clinical Verdicts: > General Mortality: No difference between Crystalloids and Albumin. > Traumatic Brain Injury (TBI): AVOID Albumin. The SAFE trial showed increased mortality with albumin in TBI (likely due to hypo-osmolar carrier increasing ICP). > Sepsis: Albumin might help in septic shock (ALBIOS trial post-hoc), but HES kills kidneys. > Cirrhosis: Albumin is useful for Spontaneous Bacterial Peritonitis (SBP) and large volume paracentesis (>5L). > Osmolality: Concentration of all solutes/kg > Tonicity: Concentration of solutes that don't cross membranes (Determines cell size). Determined by Na+. > Oncotic Pressure: Pull exerted by proteins (Albumin). Opposes hydrostatic pressure to keep fluid in vessels. • σ of 0 = free permeability; 1 = complete impermeability. • Glycocalyx: A protective lining on vessels that limits fluid leak. Disease/trauma damages it, making vessels "leaky." > Starling Law of Capillary Filtration: Q = fluid filtration, k = capillary filtration coefficient (conductivity of water), A = area of the capillary membrane, Pc = capillary hydrostatic pressure, Pi = interstitial hydrostatic pressure, σ = the reflection coefficient for albumin, πi = interstitial oncotic pressure, and πc = capillary oncotic pressure NOTE: Capillary hydrostatic pressure is the most powerful factor promoting fluid movement into the IFV and is determined by capillary flow, arterial resistance, venous resistance, and venous pressure. B. CLINICAL IMPLICATIONS OF CHOICE BETWEEN ALTERNATIVE FLUIDS Fluid Type Examples Crystall oids Normal Saline Cheap, Available. (NS) Hyperchloremic Acidosis (Large volume). Expands Interstitial space (Edema). Buffered (LR/ PlasmaLyte) Less Acidosis. Slightly hypotonic (Caution in TBI). Albumin (5% or 25%) Stays intravascular longer (70% vs 20% for crystalloid). Less edema? Expensive. No clear mortality benefit in general sepsis/trauma. Hydroxyethyl Starch (HES) Effective volume expander. Avoid in Sepsis. Causes Kidney Failure & Coagulopathy. Colloids Pros Cons/Risks C. CLINICAL IMPLICATIONS OF HYPERTONIC FLUID ADMINISTRATION > Hypertonic solutions (e.g., 3% or 7.5% Saline) pull water out of cells and into the blood. > Mechanism: Increases osmolarity → Draws water from brain/interstitium → Expands intravascular volume rapidly with small volume. > Benefits: • TBI/Neurosurgery: ↓ICP (Intracranial Pressure) effectively. Similar to Mannitol but maintains BP/Volume better (Mannitol causes diuresis/ hypovolemia). • Resuscitation: "Small Volume Resuscitation." Less edema (positive fluid balance is lower). > Risks: • Hypernatremia/Hyperosmolarity: Can theoretically open the Blood-Brain Barrier. • Hyperchloremic Acidosis: Similar to Normal Saline. • Central Pontine Myelinolysis: If chronic hyponatremia is corrected too fast (rare in acute resuscitation). B. > Tilt Test (Orthostatics): ◦ Positive Definition: HR ↑ >20 bpm AND SBP ↓ >20 mmHg upon standing. ◦ Limitations: Young/healthy people can compensate for 20% blood loss with only tachycardia (no BP drop). Elderly may have orthostasis even when euvolemic. Laboratory Markers > BUN/Creatinine Ratio: Ratio > 20:1 suggests dehydration (Prerenal Azotemia). ◦ Creatinine Note: Poor early marker of AKI; depends on muscle mass. > Urinary Electrolytes (Prerenal Signs): ◦ Urine Sodium (Na+) < 20 mEq/L (Kidney is saving salt). ◦ Urine Osmolarity > 400 mOsm/kg (Kidney is concentrating urine). ◦ FENa (Fractional Excretion of Na) < 1%. > Acid-Base: ◦ Mild Hypovolemia: Metabolic Alkalosis (Contraction alkalosis). ◦ Severe Hypovolemia: Metabolic Acidosis (Lactic acidosis from shock). INTRAOPERATIVE MONITORING: STATIC PARAMETERS > These provide a snapshot but generally fail to predict Fluid Responsiveness (i.e., whether giving fluid will actually increase Cardiac Output). Clinical Scenario Recommended Fluid Strategy Avoid / Caution Routine Maintenance Isotonic Crystalloid (LR/ PlasmaLyte) Dextrose (unless insulin/infant). Parameter Limitation Gastric Losses (Vomiting) 0.9% Normal Saline (Corrects alkalosis) Lactated Ringers (contains lactate, acts like bicarb). Blood Pressure (BP) Anesthesia/Vasopressors alter vascular tone independent of volume. Normal BP ≠ Normal Cardiac Output. Traumatic Brain Injury Isotonic or Hypertonic Saline Albumin (↑ Mortality), Hypotonic fluids (D5W, 1/2 NS). Heart Rate (HR) Non-specific. Can be caused by pain, light anesthesia, or drugs. Crystalloids first. Albumin if shock Hydroxyethyl Starch (HES) (Kidney failure). refractory. Urine Output (UOP) Sepsis Stress response (ADH/Aldosterone) causes oliguria during surgery even in euvolemic patients. Poor predictor of AKI. Major Surgery Goal-Directed Therapy (GDT) CVP (Central Venous Pressure) Poor predictor. A normal CVP (6–12 mmHg) does not guarantee adequate preload or fluid responsiveness. Blind fluid restriction (AKI risk) or liberal overload (Pneumonia risk). V. FLUID STATUS: ASSESSMENT AND MONITORING A. PREOPERATIVE & CONVENTIONAL ASSESSMENT History & Risk Factors > Hypovolemia Risks: Bowel prep, diuretics, trauma, burns, sepsis, vomiting/diarrhea. > Hypervolemia Risks: Congestive Heart Failure (CHF), Renal Failure, Liver Disease. Physical Exam Signs > Oliguria: Suggests hypovolemia but is unreliable (confounded by diuretics or renal disease). > Supine Hypotension: Indicates >30% blood volume loss. ◦ Caution: Chronic hypertension or agitation can mask this (false normal). C. INTRAOPERATIVE MONITORING: DYNAMIC PARAMETERS > These methods use heart-lung interactions to predict Fluid Responsiveness. Arterial Waveform Analysis (PPV / SVV) > Mechanism: Mechanical ventilation (positive pressure) squeezes the chest → ↓ Venous Return →↓ Stroke Volume. > Interpretation: If the arterial waveform "swings" significantly with respiration, the heart is volume-dependent. ◦ Pulse Pressure Variation (PPV) > 13% = Fluid Responsive. ◦ Stroke Volume Variation (SVV) > 10–13% = Fluid Responsive. > The "Fine Print" (Must-haves for accuracy): "M T R E" 1. Controlled Ventilation (No spontaneous breathing). 2. Tidal Volume ≥ 8 mL/kg (Need adequate chest pressure). 3. Regular Rhythm (No Atrial Fibrillation). 4. Closed Chest (Open chest loses the pressure effect). Passive Leg Raise (PLR) & Bolus > PLR Maneuver: Lifting legs auto-transfuses ~300mL blood to the heart. ◦ If CO increases >10-15%, the patient needs fluid. ◦ Contraindication: TBI (raises ICP) or abdominal hypertension. > Fluid Challenge: Give 250mL bolus. If CO increases >10-15%, continue fluid. Esophageal Doppler > Measures blood flow velocity in the descending aorta. > Key Metric: Corrected Flow Time (FTc). ◦ FTc < 0.35 sec: Hypovolemic (Needs fluid). ◦ FTc > 0.40 sec: Euvolemic. Echocardiography (TTE / TEE / POCUS) > Hypovolemia Signs: ◦ "Kissing Walls": Small, hyperdynamic Left Ventricle (LV) at end-diastole. ◦ IVC Collapsibility: Inferior Vena Cava collapses with respiration (more reliable in spontaneously breathing patients). Summary Table: Static vs. Dynamic Feature Static Parameters Dynamic Parameters Examples CVP, BP, HR, Urine Output PPV, SVV, Passive Leg Raise Concept "What is the pressure right now?" "Will the heart pump more if I give fluid?" Accuracy for Volume Low High (if requisites met) Clinical Use High-risk / Major surgery (Goal-Directed Therapy) ! Routine cases ELECTROLYTES I. SODIUM A. PHYSIOLOGIC ROLE > Sodium is the primary driver of fluid volume. > Normal Serum Level: 135–145 mEq/L. > Role: ◦ Tonicity Driver: Sodium determines ECF tonicity (effective osmolarity). Where sodium goes, water follows via aquaporins to balance the concentration. ◦ Action Potentials: Essential for nerve signaling (Na-K-ATPase pump maintains the gradient). > Regulation: • (ADH/Vasopressin): The main regulator. Secreted by the posterior pituitary in response to Hypertonicity (primary trigger) or Hypotension/Hypovolemia (secondary trigger). It causes Water Retention in the kidney (collecting ducts). • Aldosterone/ANP: Regulate total body sodium (and thus volume) via excretion/ retention. B. HYPONATREMIA (↓Na+) > Defined as Serum Na < 135 mEq/L. > The Mechanism: Generally caused by excess Total Body Water (TBW) relative to total body sodium. Risk: > Acute (<48h): Brain cells swell (cerebral edema) because they haven't adapted yet. Symptoms: Nausea, headache, confusion, seizures, herniation, death. > Chronic (>48h): Brain cells adapt by dumping internal osmoles. Few symptoms, but high risk if corrected too fast (Osmotic Demyelination). Types of Hyponatremia: 1. Hypotonic (<270 mOsm): True hyponatremia. (Most common). 2. Isotonic/Hypertonic: "False" or dilutional. Caused by Hyperglycemia (Glucose pulls water into ECF, diluting Na) or Mannitol/Glycine (from TURP syndrome). ◦ Correction Factor: Na drops 1.6–2.4 mEq for every 100 mg/dL rise in glucose. 3. Pseudohyponatremia: Lab error due to high lipids/proteins interfering with measurement. Normal osmolarity. Diagnostic Algorithm Step 1: Check Serum Osmolarity > Normal/High: Hyperglycemia, Mannitol, or Pseudohyponatremia. > Low (<270): True Hypotonic Hyponatremia. (Go to Step 2). Step 2: Check Urine Osmolarity (ADH Activity) > Low (<100 mOsm): ADH is suppressed. The kidneys are working correctly to dump water. ‼ > High (>100 mOsm): ADH is active (inappropriately or appropriately). (Go to Step 3) Step 3: Check Urine Sodium (Volume Status) > Low Urine Na (<30 mEq/L): The body is trying to save salt/volume. ◦ Hypervolemic: Heart Failure, Cirrhosis, Nephrosis (ECF is overloaded, but "effective" volume is low). ◦ Hypovolemic: Dehydration, GI Losses (Vomiting/Diarrhea). > High Urine Na (>30 mEq/L): The kidneys are dumping salt. ◦ Euvolemic: SIADH (Syndrome of Inappropriate ADH), Hypothyroidism, Adrenal Insufficiency. ◦ Hypovolemic: Cerebral Salt Wasting (CSW), Diuretics. Clinical Pearl: SIADH vs. Cerebral Salt Wasting (CSW) Both occur in neuro patients (SAH/ TBI). Treatment & Correction Risk > SIADH: Patient is Euvolemic. Treatment = Fluid Restriction (0.5 to 1 L/day). Treatment Strategy: > CSW: Patient is Hypovolemic (dumping salt/water). Treatment = Volume & Salt > Symptomatic/Severe (Seizures/Coma): Treat urgently! Replacement (3% Saline). ◦ Goal: Raise Na by 4–6 mEq/L quickly to stop brain swelling. Danger: If you restrict fluid in CSW (thinking it's SIADH), you can cause cerebral ◦ Dose: 100 mL of 3% Hypertonic Saline over 10 mins. ischemia! > Asymptomatic/Chronic: Correct slowly. ◦ Limit: < 8-10 mEq/L increase in 24 hours. ◦ SIADH: Fluid restriction, Salt tablets, Vaptans (ADH antagonists). The Major Risk: Osmotic Demyelination Syndrome (ODS) > Mechanism: If chronic hyponatremia is corrected too fast, water rushes out of brain cells too quickly, causing cell shrinkage and myelin destruction (Central Pontine Myelinolysis). > Symptoms: Pseudobulbar palsy, quadriparesis, "Locked-in" syndrome. Occurs days after correction. > Rescue: If you overshoot, STOP correction. Give DDAVP (Desmopressin) or D5W to relower sodium. Summary Table: Differential Diagnosis Condition Serum Osm Urine Osm Urine Na Volume Status Treatment Polydipsia Low Low Variable Euvolemic GI Loss / Dehydration Low High Low (<30) Hypovolemic Heart Failure Low High Low (<30) Hypervolemic Diuretics / Restriction SIADH Low High High (>30) Euvolemic Fluid Restriction / Vaptans Cerebral Salt Wasting Low High High (>30) Hypovolemic Volume + Hypertonic Saline Stop drinking water Isotonic Fluids (0.9% NS) C. HYPERNATREMIA (↑Na+) > Definition: Serum Sodium > 145 mEq/L. > Pathophysiology: Usually due to water depletion (Impaired thirst or restricted access). > Mortality: High (40–60% increase) in ICU patients. Severity matters more than duration. > CNS Effects: Hypertonic serum pulls water out of brain cells → Cellular Shrinkage. • Symptoms: Lethargy, irritability, hyperreflexia, seizures, intracranial hemorrhage, coma. THREE MAJOR MECHANISMS: 1. Increased Renal Losses (Diabetes Insipidus - DI): > Central DI: Brain doesn't make/release ADH (Trauma, Pituitary surgery, Tumors). > Nephrogenic DI: Kidneys ignore ADH (Lithium toxicity, Hypokalemia, Hypercalcemia). > Osmotic Diuresis: Mannitol, Glucose (DKA). 2. Extrarenal Losses (Most Common in ICU): > Insensible: Fever, sweating, burns, tachypnea (Respiratory loss). > GI Tract: Vomiting, diarrhea, NG suction. > Impaired Thirst: Altered mental status, sepsis, elderly (decreased osmoreceptor sensitivity). 3. Excessive Sodium Intake (Iatrogenic): > Hypertonic saline, Sodium Bicarbonate ampules (very concentrated!), TPN errors. Diagnostic Approach: 1. Check Urine Osmolarity: > Low (< 300 mOsm): Kidneys aren't concentrating urine = Diabetes Insipidus. ▪ Test: Give Desmopressin (DDAVP). ▪ Response: Urine concentrates = Central DI. No change = Nephrogenic DI. > High (> 600 mOsm): Kidneys are working properly (saving water) = Extrarenal Loss or Salt Overload. Treatment: > Calculate Water Deficit: Formula based on weight and current Na⁺. > Correction Speed: Slowly! Reduce Na⁺ by < 10 mEq/L per 24 hours. ◦ Risk: Rapid correction causes cerebral edema. > Fluids: D5W (Free water) or Enteral water. If hypovolemic, restore volume with Isotonic Saline first. II. POTASSIUM A. PHYSIOLOGIC ROLE > The master of membrane potential. > Distribution: 98% Intracellular (150 mEq/L) vs. 2% Extracellular (3.5–5.0 mEq/L). > Role: Resting membrane potential, action potentials (Cardiac/Muscle). > Regulation (The Kidney is King): ◦ Excretion: Occurs in the Distal Convoluted Tubule and Collecting Duct. (90% K+ ingested are renally excreted). ◦ Aldosterone: The main driver. Resorbs Na⁺ → Secretes K⁺ (dumps it in urine). ◦ Flow Rate: High urine flow washes K⁺ away, encouraging more secretion. > Shifts: ◦ Acidosis: H⁺ enters cell, K⁺ leaves → Hyperkalemia. ◦ Alkalosis: K⁺ enters cell → Hypokalemia. ◦ Insulin/β2 -Agonists: Drive K⁺ into cells (Hypokalemia). B. HYPOKALEMIA (↓K+) Etiology: 1. Abnormal Losses (Most Common): ◦ GI: Vomiting, Diarrhea. ◦ Renal: Diuretics (Loop/Thiazide), Hyperaldosteronism. 2. Transcellular Shifts: Alkalosis, Insulin, Albuterol. 3. Magnesium Deficiency: Hypomagnesemia causes renal K⁺ wasting. You cannot fix the K⁺ until you fix the Mg²⁺. Clinical Features: > Cardiac: Arrhythmias, U-waves, flattened T-waves. > Neuromuscular: Weakness, ileus, paralysis. Treatment: > Mild: Oral replacement (Safer). > Severe/Symptomatic: IV replacement. ◦ Peripheral Line: Max 10–20 mEq/hr (burns veins). ◦ Central Line: Max 40 mEq/hr (watch ECG). > Correction: 1 mEq/L drop in serum ≈ 300 mEq total body deficit. [Target K (usually 4) - actual K] x weight x 0.4 = mEqs needed to be replaced > Dilute K+ and give as infusion. Diluted volume is arbitrary, usually 50-100cc. Adjust accordingly to avoid excessive loading if patient has CKD, HF, etc. > There is also a daily requirement of 2-4 mEqs/kg/day. Include this when correcting intraop (can be divided per hour). Example: 41/M for colonoscopy, weight = 45 kg, K+ = 2.8 Calculating deficit: (4 - 2.8) x 45 x 0.4 = 21.6 mEqs Calculating daily requirement: 2 - 3 mEqs x 45 = 135 mEqs/24 hrs = 5.625 mEqs/hr Total Correction per hour: 21.6 + 5.625 =27.225 27.225 mEqs/hour > Since we can only give 10 mEqs per hour, order will be: KCl 10 mEqs (2 mEqs/mL) diluted in enough PNSS to make 50 cc, to run for 1 hr x 3 cycles Emergency Treatment ("C-BIG-K"): 1. Stabilize Membrane (Immediate): > Calcium Gluconate/Chloride: Protects the heart. Does not lower K⁺ levels. Effect lasts 30–60 mins. 2. Shift K⁺ Into Cells (Temporary): > Insulin + Glucose: Drives K⁺ in. > β2 -Agonists (Albuterol): Drives K⁺ in. > Bicarbonate: Only effective if patient is acidotic. 3. Eliminate K⁺ from Body (Definitive): > Diuretics: Furosemide (Lasix). > Binders: Patiromer, Zirconium Cyclosilicate (Lokelma). Note: Kayexalate is no longer recommended due to bowel necrosis risk. > Dialysis: The ultimate fix for renal failure patients. C. HYPERKALEMIA (↑K+) Etiology: 1. Impaired Excretion: Renal Failure (GFR < 15), Medications (ACE Inhibitors, ARBs, Spironolactone, NSAIDs). 2. Shifts: Acidosis, Tissue damage (Rhabdomyolysis, Tumor Lysis, Hemolysis), Succinylcholine (causes K⁺ efflux). 3. Pseudohyperkalemia: Lab error due to hemolysis during blood draw (tourniquet too III. CALCIUM A. PHYSIOLOGIC ROLE tight, fist clenching). Distribution: ECG Progression (Memorize This): > Storage: 99% in Bone (Hydroxyapatite). 1. 5.5–6.5 mEq/L: Peaked T-Waves (Earliest sign). > Serum: 1% in ECF. Divided into: 2. > 6.5 mEq/L: Prolonged PR, flattened P-waves. ◦ Protein Bound (45%): Mostly to albumin. Biologically inactive. 3. > 7.0–8.0 mEq/L: QRS Widening → Sine Wave → VFib/Asystole. ◦ Ionized Ca2+ (50%): Biologically Active. ◦ Complexed (5%): Bound to phosphate/citrate. > Normal Levels: ◦ Total Calcium: 8.5–10.5 mg/dL. ◦ Ionized Calcium: 1.0–1.25 mmol/L (The clinically relevant value). Hormonal Regulation (The Three Players): 1. Parathyroid Hormone (PTH): Increases Calcium. ◦ Bone: Resorption (releases Ca). ◦ Kidney: Reabsorption of Ca. 2. Vitamin D (Calcitriol): ↑ Ca2+. ◦ Gut: Increases absorption. 3. Calcitonin: ↓ Ca2+. ◦ Kidney: Promotes excretion. ◦ Bone: Inhibits osteoclasts. > Cardiac: Essential for contractility (Calcium-Induced Calcium Release) and Pacemaking (SA/AV nodes). Note: Calcium channel blockers (Diltiazem/Verapamil) slow HR by blocking these channels. Treatment: > Vascular: Maintains smooth muscle tone (BP). > Intravenous Replacement: > Coagulation: Factor IV! Essential for the Clotting Cascade (Factors II, VII, IX, X) and ◦ Calcium Chloride (10%): 272 mg elemental Ca/10mL. Potent. Use central line Platelet activation. (sclerosis risk). Good for codes/OR. B. HYPOCALCEMIA (↓Ca2+) ◦ Calcium Gluconate (10%): 90 mg elemental Ca/10mL. Gentler. Peripheral line > Low calcium = High excitability. safe. Etiology: > Electrolyte Partners: Must correct Magnesium (cofactor for PTH) and Phosphate > Vitamin D Deficiency: Most common cause. (binds calcium) for successful repletion. > Hypoparathyroidism: Usually post-thyroidectomy (transient or permanent). > Massive Transfusion (The "Diamond of Death"): ◦ Mechanism: Blood products contain Citrate (anticoagulant). Citrate binds ionized calcium. ◦ Risk: Liver normally metabolizes citrate, but shock/hypothermia impairs this. ◦ Result: Severe hypocalcemia + Coagulopathy + Cardiac depression. > Other: Sepsis, Pancreatitis (saponification), Tumor Lysis Syndrome (high phosphate binds calcium). Clinical Presentation: > Neuromuscular Irritability: Paresthesias, Tetany, Laryngospasm (Stridor). > Signs: ◦ Chvostek Sign: Facial spasm upon tapping the facial nerve. ◦ Trousseau Sign: Carpal spasm upon inflating BP cuff (more specific). > Cardiac: Prolonged QT interval, Hypotension, Heart Failure. C. HYPERCALCEMIA (↑Ca2+) > High calcium = "Bones, Stones, Groans, and Psychiatric Overtones". Etiology: > Primary Hyperparathyroidism: Usually a parathyroid adenoma (80%). > Malignancy: PTH-related peptide (PTHrp) secretion or bone metastasis. > Granulomatous Disease: Sarcoidosis/TB (Macrophages activate Vitamin D). > Drugs: Thiazides (retain Ca), Lithium, Vitamin D toxicity. IV. MAGNESIUM Clinical Presentation: > Neurologic: Lethargy, Confusion, Coma. A. PHYSIOLOGIC ROLE > Renal: Polyuria (Nephrogenic DI), Stones (Nephrolithiasis). > Storage: 50–65% in Bone, ~30% in Muscle/Soft Tissue. > GI: Nausea, Vomiting, Pancreatitis. > Serum: <1% of total body Mg. > Cardiac: Short QT interval, Arrhythmias. • Ionized (Free): 70% (Biologically active). Management Strategy: • Bound: 30% (mostly to Albumin). 1. Volume Expansion (First Line): > 0.9% Normal Saline: Promotes calcium excretion in the kidney (Sodium and Calcium > Normal Range: 1.7–2.1 mg/dL. are handled similarly). Key Roles: > Note: Loop diuretics (Lasix) are no longer routine unless volume overload exists. > Cofactor: Needed for >600 enzymes (ATP metabolism, DNA/RNA synthesis). 2. Inhibit Bone Resorption: > Calcium Antagonist: > Bisphosphonates (Pamidronate): Inhibit osteoclast. Mainstay for malignancy. ◦ Neurons: Blocks NMDA receptors (stops excitotoxicity). > Calcitonin: Fast onset but short duration (tachyphylaxis after 48h). ◦ Heart: Blocks L-type Ca channels (slows conduction, stabilizes membrane). > Denosumab: Monoclonal antibody (RANK-L inhibitor) for refractory cases. ◦ Vessels: Vasodilation (Smooth muscle relaxation). 3. Dialysis: For life-threatening, refractory hypercalcemia. > Potassium Regulation: Necessary for the Na-K-ATPase pump. You cannot fix Hypokalemia without fixing Hypomagnesemia first. Summary Table: Calcium Disorders Regulation: Feature Hypocalcemia Hypercalcemia > Intake: Leafy greens, nuts (often low in processed diets). Ionized Ca > Excretion (Kidney): < 1.0 mmol/L > 1.5 mmol/L Level ◦ Filtered at glomerulus. Vit D deficiency, Hypoparathyroidism, Massive Major Causes Hyperparathyroidism, Malignancy ◦ Loop of Henle (Thick Ascending Limb): Major site of reabsorption (and where Transfusion loop diuretics cause loss). Symptoms Tetany, Seizures, Long QT, Hypotension Lethargy, Polyuria, Short QT, Stones Treatment IV Calcium (Chloride/Gluconate), Magnesium repletion Hydration (Saline), Bisphosphonates, Calcitonin Clinical Uses of Magnesium Sulfate (MgSO4 ) System Clinical Use Cardiac Torsades de Pointes (First-line) Stabilizes membrane. Mechanism Atrial Fibrillation / Digoxin Toxicity Slows AV node conduction (Ca-antagonist). Obstetrics Preeclampsia / Eclampsia Tocolysis (Preterm labor) Seizure prophylaxis / Vasodilation. Relaxes uterine smooth muscle. Pulmonary Severe Asthma / COPD Bronchodilation (inhibits Ca-mediated constriction). Anesthesi a NMDA receptor antagonism (reduces pain/tolerance). Analgesia adjunct Endocrine Pheochromocytoma Vasodilation & inhibits catecholamine release. B. HYPOMAGNESEMIA (↓Mg2+) > Very common in ICU (up to 65%) and alcoholics. Etiology: > GI Loss: Diarrhea, PPIs (block absorption channels), Alcoholism. > Renal Loss: Loop diuretics, Alcoholism. Symptoms: > Neuromuscular: Tremors, Tetany, Seizures, Chvostek/Trousseau signs (mimics hypocalcemia). > Cardiac: Torsades de Pointes, Digoxin toxicity worsening. > Electrolyte Triad: Often causes refractory Hypokalemia and Hypocalcemia. Treatment: > Oral: Magnesium Oxide (60-90 mEq/day) (causes diarrhea). > IV: 1–2 g over hours (3-6 hours). Rapid push causes hypotension/flushing. C. HYPERMAGNESEMIA (↑Mg2+) > Etiology: Renal failure + Magnesium-containing laxatives/antacids or overtreatment for preeclampsia. Clinical Progression: 1. Mild: Flushing, Nausea, Loss of Deep Tendon Reflexes (DTRs). 2. Moderate: Hypotension, Bradycardia, Somnolence. 3. Severe (>10 mg/dL): Respiratory depression, Heart Block, Cardiac Arrest. Treatment: > Antidote: IV Calcium (Gluconate or Chloride) – directly antagonizes Mg effects on the heart/nerves. > Clearance: Fluids + Loop Diuretics (if renal function intact) or Dialysis. V. PHOSPHORUS A. PHYSIOLOGIC ROLE > Energy: Backbone of ATP. > Oxygen Transport: Vital for 2,3-DPG (regulates Oxygen-Hemoglobin dissociation). • Low Phos → Low 2,3-DPG → Left Shift (O2 stuck to Hgb). > Structure: Bone (Hydroxyapatite), DNA/RNA backbone, Cell membranes (Phospholipids). Regulation: > Kidney: Main regulator. ◦ PTH: Dumps Phosphate (Phosphaturic). ◦ FGF-23: Dumps Phosphate. ◦ Vitamin D: Increases absorption. B. HYPOPHOSPHATEMIA (↓) > Common in refeeding and respiratory alkalosis. Etiology: > Redistribution (Most Common): ▪ Refeeding Syndrome: Insulin drives Phos into cells. ▪ Respiratory Alkalosis: Drives Phos into cells. > Poor Absorption: Vitamin D deficiency, Antacids (bind Phos). Symptoms: > Muscle: Weakness (Failure to wean from ventilator), Rhabdomyolysis. > Cardiac: Heart failure. > Neuro: Encephalopathy, Seizures. > Heme: Hemolysis (Red cell fragility). Treatment: > Oral: Preferred (Safer). > IV: Sodium or Potassium Phosphate. > Caution: Run slowly. Fast infusion precipitates with Calcium → Severe ↓Ca2+. C. HYPERPHOSPHATEMIA (↑) > The hallmark of Renal Failure. Etiology: > Renal Failure (CKD): Cannot excrete load. > Cell Lysis: Tumor Lysis Syndrome, Rhabdomyolysis (Massive release of intracellular Phos). Consequences: > Precipitates with Calcium → Hypocalcemia (Tetany). > Calciphylaxis: Calcium-Phosphate crystals deposit in vessels/skin (painful necrosis). Treatment (The "3 D's"): 1. Diet: Restrict phosphate intake. 2. Drugs: Phosphate Binders (Sevelamer, Calcium Acetate) – take with meals. 3. Dialysis: Definitive removal. Electrolyte Interactions Cheat Sheet Primary Issue Effect on Other Electrolytes Mechanism Hypomagnesemia Causes Hypokalemia Mg is needed for renal K retention. Causes Hypocalcemia Mg is needed for PTH secretion/action. Hyperphosphatemia Causes Hypocalcemia Phos binds Ca in blood (precipitation). Acidosis Causes Hyperkalemia H+ enters cell / K+ leaves. Alkalosis Causes Hypokalemia H+ leaves cell / K+ enters. # Question Answer & High-Yield Fact 1 What is the Glycocalyx, and why is it What are the three components of the pH = 6.1 + log([HCO3-] / 0.03 x PaCO2). Relates pH to the 7 important in fluid therapy? 1 Henderson-Hasselbalch equation for blood ratio of metabolic (HCO3) to respiratory (CO2) components. pH? 1 Hypertonic Saline (3%) is primarily 8 used for what two indications? PaCO2 = (1.5 x [HCO3-]) + 8 (+/- 2). Used to check for What is Winter's Formula, and when do you 2 appropriate respiratory compensation in metabolic 1 Why should Hetastarch (HES) colloids use it? acidosis. 9 be avoided in sepsis and renal failure? In Acute Respiratory Acidosis, for every 10 3 mmHg increase in PaCO2, how much does [HCO3-] increase? 1 mEq/L. (Acute compensation is minimal; renal compensation takes days). Dynamic vs. Static fluid indices: 2 Which is better for predicting fluid 0 responsiveness? In Chronic Respiratory Acidosis, for every 4 10 mmHg increase in PaCO2, how much does [HCO3-] increase? 2 For PPV/SVV to be accurate, what 4 mEq/L. (The kidneys have had time to retain bicarbonate). 1 conditions must be met? 5 How do you calculate the Anion Gap (AG)? AG = [Na+] - ([Cl-] + [HCO3-]). Normal is ~8-12 mEq/L. 6 What is the mnemonic for High Anion Gap Metabolic Acidosis? "MUDPILES": Methanol, Uremia, DKA, Paraldehyde/ Propylene glycol, Isoniazid/Iron, Lactic acidosis, Ethylene glycol, Salicylates. 7 If a patient has hypoalbuminemia, how must you correct the Anion Gap? For every 1 g/dL drop in Albumin, add 2.5 to the calculated Anion Gap. (Albumin is a major unmeasured anion). A protective layer on the endothelium. Damage (e.g., from sepsis or hypervolemia) increases capillary permeability, leading to edema ("Capillary Leak"). 1. Severe Symptomatic Hyponatremia. 2. Reducing Intracranial Pressure (ICP) (draws water out of brain cells). They are associated with increased risk of Acute Kidney Injury (AKI)and Coagulopathy (impairs Factor VIII/vWF). Dynamic indices (e.g., Pulse Pressure Variation [PPV], Stroke Volume Variation [SVV]) are superior to static ones (CVP). 1. Controlled mechanical ventilation. 2. Regular sinus rhythm. 3. Closed chest. 4. Tidal volume > 8 mL/kg. A Passive Leg Raise (PLR) maneuver 2 Approximately 300 mL of venous blood from the legs/splanchnic effectively gives a "fluid bolus" of how 2 bed. much volume? 2 What is the most common cause of 3 Hypertonic Hyponatremia? Hyperglycemia. (Glucose draws water into ECF, diluting Sodium). Correction factor: Na drops 1.6 mEq for every 100 mg/dL glucose rise. Osmotic Demyelination Syndrome (ODS) 2 Chronic Hyponatremia. (Correcting > 10-12 mEq/L in 24h A co-existing Non-Gap Metabolic Acidosis (hyperchloremic 4 is caused by correcting which electrolyte shrinks neurons). "From Low to High, your Pons will Die." abnormality too quickly? acidosis) is present along with the gap acidosis. Chronic Hypernatremia. (Correcting too fast causes water Loss of Bicarbonate via Diarrhea (GI loss) or Renal Tubular 2 Cerebral Edema is a risk of correcting What is the primary cause of Non-Anion Gap to rush into adapted brain cells). "From High to Low, your 9 Acidosis (Renal loss). Also excessive Saline (NaCl) 5 which electrolyte abnormality too quickly? Metabolic Acidosis (Normal AG)? Brain will Blow." infusion. What does a Delta-Delta (Δ/Δ) ratio < 1.0 8 indicate in high anion gap acidosis? 1 How does Hypokalemia contribute to 0 Metabolic Alkalosis? It causes intracellular shift of H+ (to balance K+ efflux) and increases renal H+ excretion and bicarbonate reabsorption ("Contraction Alkalosis"). The high Chloride load (154 mEq/L) displaces Bicarbonate 1 Why is Saline (0.9% NaCl) administration a to maintain electroneutrality (strong ion difference 1 cause of Hyperchloremic Metabolic Acidosis? decreases). 1 Mnemonic: Causes of Respiratory 2 Alkalosis? "CHAMPS": CNS disease, Hypoxia, Anxiety/Pain, Mechanical ventilation, Progesterone (Pregnancy), Salicylates/Sepsis. 2 What is the first-line treatment for SIADH? 6 Free Water Restriction. (Vaptans are second line). 2 How do you differentiate Central vs. 7 Nephrogenic Diabetes Insipidus (DI)? Give Desmopressin (DDAVP). If urine osmolality increases, it's Central. If no response, it's Nephrogenic. 2 What is the classic ECG progression of 8 Hyperkalemia? Peaked T waves → Prolonged PR → Loss of P wave → Widened QRS → Sine Wave → VFib/Asystole. 2 What is the immediate treatment for 9 Hyperkalemia with ECG changes? Calcium Gluconate/Chloride (stabilizes cardiac membrane). Then shift K+ (Insulin/Glucose, Bicarb, Albuterol). Succinylcholine. It causes massive K+ efflux from upregulated extrajunctional receptors. What percentage of Total Body 1 Weight is water in an average adult 3 male? 60%. (ICF is ~40%, ECF is ~20%). Which muscle relaxant is contraindicated in 3 patients with burns, denervation, or crush 0 injury due to hyperkalemia risk? How is Extracellular Fluid (ECF) 1 divided between Interstitial and 4 Intravascular spaces? 3:1 ratio. (75% Interstitial, 25% Intravascular). This is why you need ~3-4x volume of crystalloid to replace blood loss. Hypokalemia is often refractory to 3 replacement if which other electrolyte is 1 low? Magnesium. (Mg is required for Na/K ATPase function and renal K retention). 1 Which fluid compartment does 0.9% 5 Normal Saline primarily expand? The entire ECF (Intravascular + Interstitial). Only ~20-25% stays intravascularly after redistribution. 3 Does ** acidosis** cause Hyperkalemia or 2 Hypokalemia? Hyperkalemia. H+ enters cells to be buffered, pushing K+ out to maintain electroneutrality. 1 Which fluid compartment does D5W 6 (5% Dextrose) primarily expand? 3 What are the classic signs of Total Body Water (TBW). Once glucose is metabolized, it acts as 3 Hypocalcemia? free water and distributes to ICF (2/3) and ECF (1/3). Poor volume expander. Chvostek's sign (facial twitch) and Trousseau's sign (carpal spasm with BP cuff). Also QTc prolongation. 3 Why does Massive Transfusion cause 4 Hypocalcemia? The Citrate anticoagulant in blood products chelates serum Calcium. (Worse if liver function is poor/hypothermia slows citrate metabolism). 3 What is the "Diamond of Death" in trauma 5 resuscitation? Hypothermia, Acidosis, Coagulopathy, AND Hypocalcemia. (Hypocalcemia is the new 4th component). 3 Which electrolyte abnormality shortens the 6 QT interval? Hypercalcemia. (Hypocalcemia prolongs it). 3 What is the primary treatment for severe 7 Hypercalcemia? Volume Expansion (Saline) followed by Loop Diuretics. (Bisphosphonates for long-term). 3 Magnesium acts as a physiological 8 antagonist to which ion? Calcium. (It blocks Ca channels). This explains why Hypermagnesemia causes muscle weakness/loss of reflexes. 3 What is the first clinical sign of 9 Hypermagnesemia (Levels 4-6 mg/dL)? Loss of Deep Tendon Reflexes (DTRs). Followed by hypotension, then respiratory arrest/heart block. 4 What is the antidote for 0 Hypermagnesemia? IV Calcium (Calcium Gluconate or Chloride). Hypophosphatemia shifts the 4 Left. (Decreased 2,3-DPG production → hemoglobin holds Oxyhemoglobin Dissociation Curve in which 1 onto oxygen tighter). direction? What syndrome is associated with rapid 4 feeding of malnourished patients, causing 2 Hypophosphatemia? Refeeding Syndrome. (Insulin surge drives Phos into cells). A patient with Pyloric Stenosis (vomiting) 4 presents with what classic acid-base 3 disturbance? Hypochloremic Metabolic Alkalosis. (Loss of H+ and Clfrom stomach). 4 How do you treat a Saline-Responsive 4 Metabolic Alkalosis (Urine Cl < 10)? 0.9% Normal Saline. (Restores volume and Chloride, allowing kidney to excrete Bicarbonate). 4 Why does Acute Salicylate Toxicity cause a 5 mixed acid-base disorder? It causes Respiratory Alkalosis (direct respiratory center stimulation) AND Metabolic Acidosis (uncoupling oxidative phosphorylation). In a patient with COPD (chronic respiratory 4 acidosis), what is the risk of "normalizing" 6 PaCO2 on a ventilator? Severe Metabolic Alkalosis. (The kidneys have retained Bicarbonate; removing the high CO2 leaves unbuffered base). 4 Why is Lactated Ringer's considered a 7 "balanced" salt solution compared to Saline? Its chloride content (109 mEq/L) is closer to plasma (100 mEq/L) than Saline (154 mEq/L), reducing risk of acidosis. 4 What happens to the pH of stored blood 8 (pRBCs) over time? It becomes Acidic (accumulation of lactate and CO2). 4 A trauma patient has a pH of 7.2, PaCO2 30, 9 HCO3 14. What is the primary disorder? Metabolic Acidosis (low pH, low Bicarb). The low PaCO2 is compensatory respiratory alkalosis. 5 Why does Hypoalbuminemia cause 0 "Pseudohypocalcemia"? Total calcium drops because less is protein-bound, but Ionized Calcium (the active form) remains normal. Always check Ionized Ca. Reference: Cullen, B. Fbookid=3285§ionidga, R., Sharar, S. R., Holt, N. F., Connor, C. W., & Nathan, N. (2024). Sharar9. Lippincott Williams & Wilkins, a Wolters Kluwer business. https://anesthesiology.lwwhealthlibrary.com/book.aspx? bookid=3285§ionid=0