Fluid & Electrolyte Balance, Transfusion Therapy and Acid–Base Review

Magnesium: Physiology & Sources

• Second-most abundant intracellular cation after potassium.
• 50\text{–}60\% of total body Mg is stored in bone; remainder in muscle & soft tissue.
• Core functions
  • Regulates nerve impulse transmission & skeletal/ smooth/ cardiac muscle contraction.
  • Stabilises blood pressure & modulates vascular tone.
  • Participates in carbohydrate metabolism → maintains serum glucose.
  • Structural support for bone & teeth (with Ca & P).
  • Essential co-factor in >300 enzymatic reactions: protein, DNA & RNA synthesis.
• Dietary acquisition
  • Whole foods: leafy greens (spinach, kale), nuts/seeds (almonds, cashews, pumpkin seeds), legumes (black beans, chick-peas, lentils), whole grains (quinoa, brown rice, oats, whole-wheat bread), fatty fish (salmon, mackerel), avocado, banana, dark chocolate \ge 70\% cocoa.
  • Fortified products: breakfast cereals, plant milks (almond, soy), selected breads & snack bars.
  • Supplements (Mg oxide, citrate, glycinate, etc.) if ordered.

Normal & Critical Serum Mg Values

• Reference laboratory range (adult): 1.6\text{–}2.6\,\text{mg·dL}^{-1} (facility specific).
• Critical
  • Severe hypomagnesaemia < 0.5\,\text{mg·dL}^{-1}.
  • Severe hypermagnesaemia > 3.0\,\text{mg·dL}^{-1} (life-threatening threshold rises to >12\,\text{mg·dL}^{-1}).

Hypomagnesaemia

• Aetiology
  • Medication losses: loop & thiazide diuretics, certain aminoglycosides, proton-pump inhibitors.
  • ↓ Intake: poor diet, general under-nutrition.
  • ↓ GI absorption: Crohn’s, coeliac disease.
  • ↑ GI losses: severe diarrhoea, pancreatitis.
  • ↑ Renal excretion: uncontrolled T2DM (osmotic diuresis), alcohol use disorder, post-burn diuresis.
  • Associated electrolyte shifts: hypokalaemia, hypocalcaemia.
• Clinical presentation (usually at <1.2\,\text{mg·dL}^{-1})
  • Mild–moderate: nausea, vomiting, anorexia, fatigue, generalised weakness.
  • Severe: neuromuscular irritability (tetany, cramps, spasticity), paraesthesias, seizures, personality/ mood change, arrhythmias & coronary/ peripheral vasospasm— potentiated when combined with other dyselectrolytaemias.
• Diagnostics
  • Serum Mg on BMP/CMP; always assess concurrent K^+ & Ca^{2+}.
  • 12-lead ECG for dysrhythmia.
• Management
  • Oral Mg salts for mild–moderate deficit (observe for diarrhoea).
  • IV Mg sulfate for severe or symptomatic cases (telemetry required).
  • Correct underlying cause; reinforce Mg-rich diet.

Hypermagnesaemia

• Criticality scale
  • Moderate symptoms above 7\,\text{mg·dL}^{-1}.
  • Severe/ life-threatening at >12\,\text{mg·dL}^{-1}.
• Causes
  • Renal insufficiency/ failure (most common: impaired excretion).
  • Excess intake: Mg-containing laxatives, antacids, over-supplementation.
  • Drug-induced: lithium, chronic opioids.
  • Massive tissue injury/ trauma (cellular release).
• Symptom progression
  1. Mild – nausea, dizziness, lethargy, confusion.
  2. Moderate – worsening confusion, somnolence, blurred vision, headache, flushing, constipation.
  3. Severe – flaccid paralysis, respiratory depression, profound hypotension, bradycardia → AV block, seizure, coma, cardiac arrest.
• Work-up mirrors hypomagnesaemia (BMP/CMP ± ECG).
• Treatment
  • Mild: discontinue Mg sources (OTC antacids/ laxatives/supplements).
  • Moderate: IV Ca^{2+} (gluconate or chloride) as physiological antagonist; IV loop diuretics + isotonic saline to enhance renal excretion.
  • Severe/ anuric renal failure: emergent haemodialysis.
  • Continuous monitoring of cardiac rhythm, BP, neuromuscular status; serial Mg labs.

Dehydration (Water Loss > Sodium Loss)

• Definition: Pure H₂O deficit → hypernatraemia & ↑ plasma osmolality.
• Contributing factors
  • GI fluid loss (vomiting, diarrhoea).
  • Excessive perspiration (fever, heat exposure).
  • Polyuria (e.g., uncontrolled DM, diuretics).
  • Fever, ↓ fluid intake, impaired thirst (elderly, infants, benzodiazepines, SSRIs).
• Manifestations
  • Mild–moderate: thirst, dry mucosa, lethargy, cognitive slowing, ↓ skin turgor, oliguria (concentrated urine).
  • Severe: tachycardia, hypotension (↓ preload), shock, coma → multi-organ failure if uncorrected.
• Diagnostics: BMP/CMP (hypernatraemia), ↑ serum osmolality, urine specific gravity >1.030.
• Therapy
  • Oral rehydration solutions if alert.
  • IV hypotonic: D5W or 0.45\% NS, infused slowly to prevent cerebral oedema.

Fluid Volume Deficit: Hypovolaemia

• Loss of both water & electrolytes → ↓ circulating volume.
• Aetiology: haemorrhage, diarrhoea/ vomiting, severe burns (capillary leak), third-spacing (ascites, pancreatitis), excessive sweating, over-diuresis, major trauma.
• S/S (progressive)
  • Early: thirst, dry mucous membranes, tenting skin (unreliable in elderly), ↓ urine output.
  • Progression: lethargy, muscle weakness, orthostatic hypotension, tachycardia (compensatory).
  • Severe: confusion, tachypnoea, chest pain, palpitations, oliguria, hypovolaemic shock (>20\% blood volume loss) → MODS.
• Diagnostics
  • BMP/CMP: dyselectrolytaemias.
  • ↑ BUN/Cr (prerenal); CBC may show ↑ haemato­crit (hemoconcentration) or ↓ if haemorrhage.
  • Urine specific gravity high.
• Treatment
  • Mild: oral fluids/electrolytes.
  • Moderate–severe: isotonic IV 0.9\% NS or Lactated Ringer’s; PRBC transfusion if haemorrhagic.

Fluid Volume Excess: Hypervolaemia

• Excess Na^+ & H₂O in ECF.
• Common causes: CHF (↓ cardiac output → RAAS activation), CKD (↓ urine output), cirrhosis/ ESLD (portal HTN, ↓ albumin → ascites), drugs (vasodilators, CCBs).
• Hallmark findings
  • Rapid weight gain, peripheral/ sacral oedema.
  • Cardiopulmonary: JVD, bounding pulse, hypertension, crackles/ rales, dyspnoea; severe → pulmonary oedema & respiratory distress.
• Work-up: Daily weights, oedema grading, BMP/CMP (variable Na^+), urine Na^+ to assess renal handling.
• Management
  • Loop diuretics (furosemide); thiazides if mild.
  • Fluid & sodium restriction.
  • Daily weights, I&O charting.
  • Haemodialysis in refractory CKD; paracentesis for tense ascites.

Blood Components & Their Uses

• Whole blood seldom transfused—components are targeted via centrifugation (≈60\% plasma / 40\% cells).
• Red Blood Cells (PRBC)
  • Carry O2 & remove CO2; lifespan 120 days; production \approx2\times10^6 cells·s^{-1}.
  • 1 unit PRBC raises Hb by \approx1\,\text{g·dL}^{-1} & Hct by 3\%.
  • Typical trigger: Hb < 7\text{–}8\,\text{g·dL}^{-1} (patient/context dependent).
  • Rough rule: Hct \approx Hb \times 3 (e.g., Hb 10\Rightarrow Hct\sim30\%).
• Platelets
  • Indicated when count < 20{,}000\,\text{µL}^{-1} or active bleeding.
  • Single transfusion may pool platelets from up to 10 donors.
• Plasma (FFP)
  • Contains clotting factors, proteins, electrolytes; stored frozen & thawed → Fresh Frozen Plasma.
  • Utilised for coagulopathy, massive transfusion, liver failure, burns.
  • Fractionation yields derivatives (albumin, factor VIII, immunoglobulin, etc.).
• Cryoprecipitate: rich in fibrinogen, factor VIII, XIII & vWF.
• Granulocytes (WBC) rarely transfused—reserved for severe neutropenia unresponsive to G-CSF.
• Autologous donation: patient pre-donates own blood for elective surgery; NOT acceptable to most Jehovah’s Witnesses.

ABO & Rh Blood Grouping

• Four ABO phenotypes: A, B, AB, O — determined by surface antigens.
• Rh factor: D antigen present (Rh+) or absent (Rh-).
• Incompatible transfusion → immune-mediated haemolysis (life-threatening).
• Compatibility ensured by:
  • Type & screen (ABO/Rh).
  • Cross-match: recipient plasma + donor RBC; agglutination = incompatible.
  • Plasma & platelets require ABO/Rh typing but not formal cross-match.

Transfusion Procedure & Safety Checklist

1. Obtain informed consent & baseline vitals.
2. Large-bore IV (18\text{–}20 G) patent; gather Y-tubing, 0.9\% NS only.
3. Retrieve blood—must begin within 30 min & complete within \le4 h.
4. Two RNs verify at bedside: patient ID, unit number, ABO/Rh, expiration.
5. Remain with patient first 15 min; repeat vitals at 15 min, facility protocol, end of transfusion & +1 h.

Acute Transfusion Reactions (within 24 h)

• Acute haemolytic (ABO incompatible): fever, chills, flank pain, haemoglobinuria → DIC, renal failure.
• Febrile non-haemolytic: temp rise >1\,^{\circ}\text{C} from donor WBC cytokines.
• Allergic: urticaria → anaphylaxis.
• TRALI: non-cardiogenic pulmonary oedema.
• TACO: circulatory overload from rapid infusion.

Immediate Nursing Actions

• STOP transfusion, keep IV line with 0.9\% NS.
• Re-check identifiers, notify provider & blood bank.
• Send blood bag, tubing, patient blood & urine to lab.
• Supportive care: O₂, fluids, meds as ordered.

Delayed Transfusion Reactions ( >24 h – weeks)

• Delayed haemolytic TR: mild, often unnoticed.
• TA-GVHD: donor T-cells attack host; usually fatal.

Acid–Base Balance Essentials

• pH = “power of H^+”.
  • Normal arterial range 7.35\text{–}7.45.
• Homeostatic controls
  1. Chemical buffers (instant): bicarbonate, phosphate, proteins.
  2. Respiratory (minutes, transient): adjust CO_2 via rate/depth.
  • ↑ RR → ↓ CO_2 → ↓ H^+ (alkalinises).
  • ↓ RR → ↑ CO_2 → ↑ H^+ (acidifies).
  1. Renal (hours–days, powerful): reabsorb/ excrete HCO_3^- & H^+.
• Renal impairment => high risk of uncorrected acidosis/ alkalosis.

Arterial Blood Gas (ABG) Parameters

• pH : acid–base status.
• PaCO_2 (35–45 mmHg): respiratory component.
• HCO_3^- (22–26 mEq·L^{-1}): metabolic component.
• PaO2 (80–100 mmHg) & SaO2 (95–100 %) assess oxygenation.
• Disorders named by primary cause
  • Respiratory acidosis/ alkalosis \Rightarrow driven by PaCO_2.
  • Metabolic acidosis/ alkalosis \Rightarrow driven by HCO_3^-.

(NB: Full ABG interpretation is mastered in Med-Surg.)

Self-Study — Intravenous Therapy (Required Reading)

• Calculate IV flow rates & titration.
• Principles of rehydration therapy.
• Selecting, initiating & maintaining IV tubing/ infusion pumps.
• Peripheral vs central venous access devices.
• Recognition & management of IV-related complications (infiltration, phlebitis, CLABSI, air embolus, catheter occlusion).