Fluids & Electrolytes Janeen Jordan, MD TACS Fellow In General… • 60% of total body weight is water – 40% (2/3) is intracellular (ICF) – 20% (1/3) is extracellular (ECF) • 5% in intravascular • 15% is interstitial • Blood Volume (rbc’s + plasma) = 7% TBW • ECF vs ICF cations – – – – Na+: 142 mEq/L vs 10 mEq/L K+: 4 vs 150 Ca++: 5 Mg++: 3 vs 40 • ECF anions – Cl-: 103 – HCO3: 27 • ICF anions – Phosphates 107 – Proteins 40 – Sulfates 43 In General… • Starling forces control net fluid flux • Q = Kf(Pc-Pi) – σ(πc-πi) – Q net fluid flux (mL/min) – (Pc –Pi) hydrostatic pressure difference between the capillary and interstium – (πc-πi) oncotic pressure difference – Kf filtration coefficient for membrane – σ the permeability factor σ the permeability factor… • In shock states is increased • Colloids cannot maintain oncotic pressure • Replaced with isotonic fluid (3:1) – Hypotonic will distribute to all compartments – Isotonic solutions: 9%NS and LR • Surrogate measures of adequate volume – Blood pressure, heart rate, uop, cardiac/cerebral perfusion Hyponatremia • Defined as <135 mEq/L • Renal defense (can excrete massive load 15L/d) • FW intake with impaired FW excretion – Pathologic release of ADH (stress, pain, n/v, narcotics, hypovolemia) – Thiazide diuretics – anticonvulsants Hyponatremia • When is aggressive tx indicated? • What are the sxs? • What causes these sxs? • What group of patients are at risk? • What is the appropriate emergent tx? • What risk is associated with tx? • Whick patients are at risk for CPM? • What is the most common cause of postop hyponatremia? • Na <120meq/L & low plasma osm • Nausea, malaise, lethargy, seizures, MS changes, coma • Cerebral edema • Women w/ postop low Na – Pt w/ psychogenic polydipsia – Elderly women on thiazide or loop diuretics – Postop pts who are over resuscitated (premenopausal) • Lasix in conjunction with NS or hypertonic saline to increase Na 1meq/hr, then fluid restriction • If tx too rapid, CPM or osmotic cerebral demyelinating syndrome • Pt with preexisting alcoholism or malnutrition Pts with a rate of correction >2.5meq/l/hr or >20meq/day • Fluid overload Assessment of Hyponatremia Serum Osmolality Normal (280-285mOsm) Isoosmotic hyponatremia Pseudohyponatremia hyperlipidemia hyperprotenemia Isotonic infusions glucose, mannitol, glycine, ethanol. glycerol Hypovolemic, hyposmotic Hyponatremia Isovolemic, hypoosmotic Hyponatremia Renal Losses Extrarenal Losses GI loss Diuretic Renal injury Obstruction Adrenal Insuff Skin loss RTA Lung loss Salt wasting Nephritis Isotonic Saline Hypervolemic hypoosmotic Hyponatremia Urine Na (meq/L) <10 <10 Hyperosmotic hyponatremia Hyperglycemia Hypertonic infusions glucose, mannitol, glycine, ethanol, glycerol Assess clinical extracellular fluid volume Urine Na (meq/L) >20 Elevated (>285mOsm) Low (<280mOsm) Water Intoxication vomiting diarrhea pancreatitis >20 Renal failure SIADH Hypothyroidism Pain Emotion Drugs Adrenal Insuff Water Restrict Calulate the Na deficit = 0.6(kg)x(140-Na)+(140xVol deficit in L) <10 >20 Nephrosis Cirrhosis CHF Acute/chronic renal failure Water Restrict Corrected Na = 0.016(measured glucose – 100)+measured Na Hyponatremia summary…. • High-risk groups for poor outcome – Menstruant females – Children – Hypoxic patient • Asymptomatic hyponatremia – Fluid restriction unless hypovolemia is suspected – Demeclocycline – Vasopressin V2 receptor antagonist (Vaptans) • Hyponatremic encephalopathy (seizures, AMS, HA, n/v) – Infuse 3% NaCl at a rate of 1mL/kg/h. ICU setting using an infusion pump. – Check serum Na every 2hrs until sxs free – Stop HTS when asymptomatic OR Na has increased by 15-20meq in initial 48hrs • Hyponatremic encephalopathy with evidence of severe cerebral edema (active seizures, respiratory arrest) – Bolus 100mL of 3% NaCl over 10min – Can repeat bolus 1-2times with the goal of increasing Na 2-4meq/L or until clinical improvement – Begin infusion as for hyponatremic encephalopathy Ayus, JC, et al. N Engl J Med. 1987; 317(19): 1190-95. Hypernatremia • What sxs are present when Na >160meq/L? • What sxs are present when Na >180meq/L? • What is the appropriate tx? • What is the rate of correction? • What is the risk of overly rapid correction? • Irritability, ataxia, anorexia and cramping • Confusion, stupor, seizure, coma • Correction of volume deficit, if present – Replacement of water deficit with D5W – Tx of underlying cause • ½ water deficit in the 1st 24hrs, with a rate of Na decrease not >1meq/hr; correction of the remaining deficit over the next 2448hrs • Cerebral edema and resultant neurologic dysfunction (lethargy, seizures) Assessment of Hypernatremia Assess clinical extracellular fluid volume Hypovolemic Hypernatremia Loss of water+ Na Isovolemic Hypernatremia Low TB Na >20 <10 Urine Na (meq/L) Renal Losses Extrarenal Losses Diuretic GI loss Glycosuria Skin loss Mannitol Lung loss Urea diuresis Acute & chronic RF Loss of water Gain of water+ Na (>) Normal TB Na HighTB Na variable Renal loss DI Central nephrogenic Hypotonic Saline Calulate water deficit = 0.6(kg)x(Na/140-1) Hypervolemic Hypernatremia Urine Na (meq/L) Extrarenal loss skin respiratory insensible Water Replacement >20 Iatrogenic hypertonic NaHCO NaCl tablets hypertonic ivf Mineralocorticoid primary aldo cushing’s Cong adrenal hyperplasia Hypertonic hemodialysis/peritoneal dialysis Diuretics & water replacement Hypernatremia summary… 1. Replete intravascular volume with colloid solution, isotonic saline or plasma. 2. Estimate water deficit. Deficit should be replaced over 48-72 hrs, aiming for a correctionof 1mOsm/L/hr. In severe hypernatremia (>170), do not correct below 150meq in first 48-72 hrs. 3. Hypotonic fluid should be used. Usual replacement fluid is ½ NS. Glucose-containing solutions should be avoided, an oral route should be used if available. 4. Monitor plasma electrolytes every 2hrs until stable If something‘s rotating – go home, you need a break! *g* Hypokalemia • What is the normal daily K+ requirement? • Why is the serum K+ level important in patients taking digoxin? • What are the most common causes of low K+ in the surgical pt? • What acid-base disturbances cause decreased serum K+ levels? • What sxs are associated with hypokalemia? • What EKG changes occur with hypokalemia? • What other electrolyte imbalances often occur with hypokalemia? • How is potassium replaced emergently? • 40-60meq/day • Digoxin and K+ compete for the same receptors, pts are susceptible to digoxin toxicity when K+ is low • Vomiting, diarrhea, NG suction, loop diuretics, deficient oral intake • Alkalosis. H+/K+ pump. • Ileus, weakness, nausea, vomiting • U-waves >1mm in ht and larger than T-waves S-T depression T-wave flattening and inversion • Hypocalcemia, hypomagnemesia • Suggested maximum infusion rate is 20meq/hr via CVL, 10meq/hr peripherally Hyperkalemia What situations call for emergent reduction of serum K+ levels? What is the most serious complication of hyperkalemia? What EKG changes are associated with the disorder? • • In addition to vital signs, which bedside parameter should immediately checked? • • What is pseudohyperkalemia? • • How is K+ emergently reduced? • • • • • • Pt with serum K+ >7mmol/L or EKG changes Life-threatening arrhythmia Peaked T-waves Flat P-waves Increased PR-interval Widened QRS interval with eventual progression to sine wave pattern Urine output, b/c renal failure results in rapid increase in K+ Artificially elevated K+ levels caused by hemolysis or by a tourniquet left in place too long on the arm before collection Hypertonic glucose infusion and insulin Administration of kayexalate 20g QID Hemodialysis HCO3 C BIG K DDi Calcium Lasix Hypocalcemia • What is the most dangerous consequence of severe hypocalcemia? • What are the sxs? • What is the formula for corrected total Ca++? • What is the most accurate measure of Ca++? • How is severe hypocalcemia treated? • What is the most dreaded complication of peripheral IV infusion of calcium? • Laryngeal spasm may occur at very low Ca++ levels • Peripheral paresthesias, Chvostek sign, Trousseau sign, tetany, seizures, MS changes • 0.8(Normal albuminmeasured albumin)+observed Ca++ • Ionized calcium • Administration of 200mg elemental Ca++ • Infiltration causes skin necrosis (CaCl) Hypercalcemia • What levels of serum calcium warrant emergent therapy? • What are the symptoms? • What is the appropriate tx for severe (symptomatic) hypercalcemia? • 13-15mmol/L or w/ sxs • Nausea, vomiting, MS changes, delirium, polyuria, polydipsia and constipation • Increase IV fluids to maintain UOP 80100mL/hr. Lasix for diuresis Scenario • • • • • • 32yo F with no PMHx, elective BTL 0800 D5 ¼ NS at 125mL/hr Po intolerance, ivf continues 0245 c/o HA given vicodin Am labs Na+ 129mEq Generalized seizure and respiratory failure References • Gabrielli, A., et al. Civetta, Taylor & Kirby’s Critical Care, 4th ed. 2009. • Grenvik, A. et al. Textbook of Critical Care, 4th ed. 2000. • Marino, PL. The ICU Book, 3rd ed. 2007 • Rollings, RC., et al. Facts and Formulas. 1984. • Blackbourne, LH., et al. Advanced Surgical Recall, 3rd ed. • DuBose, JJ., et al. Clinical experience using 5% hypertonic saline as a safe alternative fluid for use in trauma. J Trauma. 2010 May;68(5):1172-7