Electrolyte and Metabolic


A. Salahuddin, M.D
Dept. of Anesthesiologi, ICU and Pain Management
Faculty of Medicine Hasanuddin University


 Common in critically ill & injured patients
 Alter physiologic function and contribute to
morbidity & mortality
 The most common electrolyte disturban-
ce in critically ill patients are: disturbance in
K, Na, Ca, Mg, P levels
 Metabolic disturbance accompany many
systemic disease processes or result of
altered endocrine function


 Review causes and clinical manifestations
of severe electrolyte disturbances
 Outline emergent management of
electrolyte disturbances
 Recognize acute adrenal insufficiency and
appropriate treatment
 Describe management of severe
hyperglycemic syndromes

Principles of Electrolyte Disturbances

 Implies an underlying disease process
 Treat the electrolyte change, but seek the
 Clinical manifestations usually not specific
to a particular electrolyte change, e.g.,
seizures, arrhythmias

Principles of Electrolyte Disturbances

 Clinical manifestations determine urgency
of treatment, not laboratory values
 Speed and magnitude of correction
dependent on clinical circumstances
 Frequent reassessment of electrolytes

& hypernatremia  Others: Calcium : hypo.& hyperkalemia  Sodium : hypo.Electrolyte Disturbances  Potassium: hypo.& hypercalcemia Phosphate : hypo.& hyperphosphatemia Magnesium : hypomagnesemia .

Metabolic Disturbances  Severe hyperglycemic syndromes  Acute adrenal insufficiency .

Potassium (K)  Essential for maintenance of the electrical membrane potential  Alteration of K primarily effect the CV. and GI systems. neuromuscular. .

Overview of Potassium Balance .

5mmol/L) Can occur as a result from: 1.5mEq/L (<3.intercompartmental shift / transcellular shift of K 3.increased K loss (renal or extrarenal losses) 2.inadequate or decreased K intake . Hypokalemia Plasma [K+] <3.

Causes of hypokalemia Transcellular Shifts Renal Losses Extrarenal Decreased Intake Losses Alkalosis Diuresis Diarrhea Malnutrition Hyperventilation Metabolic alkalos Profuse sweating Alcoholism Insulin Renal tub defects Anorexia nervosa β-adrenergic agonists Diabetic ketoacid Drugs (diuretics. aminoglycosides. amphotericin B) Hypomagnesemia Vomiting .

nausea. abdominal cramps. paresthesia.Clinical manifestation:  Cardiac system:  arrhythmias (ventricular. conduction delay. QT prolo- ngation. sinus bradycardia)  ECG abnormalities (U waves. & supraventricular. flat or inverted T waves)  Neuromuscular system: muscle weakness or paralysis. and vomiting . ileus.

fatigue. paralysis.Hypokalemia  Neuromuscular manifestations: weakness. ileus  Nephrogenic DI  ECG changes: U waves. respiratory dysfunction  GI: constipation. flattened T waves  Arrhythmias .

Inc. Mosby items and derived items © 2005. 2002 by Mosby.Box 26-1. .Symptoms of hypokalemia.

Little.Increased ammonia production .Effect of hypokalemia Cardiovaskular: .Tetany .ECG changes/dysrhythmias .Negative nitrogen balance .Ileus Renal: . Brown and Company.Skeletal muscle weakness . 3 rd ed.Myocardial dysfunction Neuromuscular: .Polyuria (nephrogenic DI) .ed: Renal and Electrolyte Disorders. .Encephalopaty in patients with liver disease Adapted from Schrier RE. 1986.Increased bicarbonate reabsorption Hormonal: .Decreased insulin secretion .Rhabdomyolisis .Decreased aldosteron secretion Metabolic: .

 Due to Delayed ventricular repolarization:  T wave flattening and inversion  Prominent U wave  ST segment depression  Increased P wave amplitude  Prolongation of the PR interval .

Treatment (1) Treatment is aimed: Correcting the underlying cause Administering potassium  Stop offending drugs (if possible)  Correct hypomagnesemia & other electrolyte disturbances  Correct alkalosis .

infusion rate can be slowed after symptoms resolve)  Absence of life-threatening manifestation: KCl 10 mEq/hr IV .Treatment (2)  K <3mEq/L (<3mmol/L) & asymptomatic: K enterally (orally or NGT) (KCl 20-40mEq every 4-6 hrs)  K <2-2.5mEq/L (<3mEq/L if on digoxin) or if symptoms are present: K intravenously  Arrhythmias or paralysis: KCl 20-30mEq via central venous catheter (sequential infusion: 10mEq in 100 mL fluid over 20 mins.

correct the potassium level before correcting pH (K shift intracellularly as the pH increases) .Treatment (3)  Acedemia is present.

8th Ed. The Harriet Lane Handbook. Fluid and electrolyte. Lund GJ.K+ deficit (mEq/L) = fluid deficit (L) x proportion from ICF x K+ concentration (mEq/L) in ICF. 2009 .

Monitoring  Continuous ECG monitoring is necessa- ry (during parenteral administration of high concentration of KCl)  Serum K levels must be monitored at frequent interval during repletion (every 1-2 hrs during initial replacement) .

Blood-Gas Analysis .

Hyperkalemia  Potassium >5. .000/mm3.5 mEq/L (>5.5 mmol/L)  Most often results from renal dysfunction  Pseudohyperkalemia may result from a white blood cell count >100.000/mm3 or platelet count >600.

)  Hemolysis Excessive intake .Causes of hyperkalemia Renal dysfunction Cell death: Acidemia  Rhabdomyolisis  Tumor lysis Hypoaldosteronism  Burns Drugs (potassium-sparing diuretics. ACE inhibitors. etc.

Clinical manifestation  Heart:  arrhythmias (heart block. diminished P waves. paralysis. dimi- nished conduction and contraction)  ECG abnormalities (diffuse peaked T waves. sine waves)  Muscle: muscle weakness. QRS widening. pares- thesias. and hypoactive reflexes . bradycardia. PR prolongation.

 ECG change:  Peaked T-wave  Widening of QRS complex  PR prolongation  Loss of P wave  Loss of R wave amplitude  ST depression (occationally elevation)  Sine wave  Ventricular fibrillation and asystole .

Treatment (1)  Recognition & treatment of underlying diseases  Removal of offending drugs  Limitation of potassium intake  Correction of acidemia or eletrolyte abnorma- lities  Any serum potassium level >6 mEq/L should be addressed. but the urgency of treatment depends on clinical manifestation  The presence of ECG changes mandates immediate therapy .

Treatment (2)  ECG abnormalities present: CaCl 5-10 mL of a 10% solution IV over 5-10 mins (the effect lasts only 30-60 mins & should be followed by additional treatment)  Redistribution of K: ■ Na bicarbonate 1 mEq/kg (1 mmol/kg) IV over 5-10 mins (beware of potential Na overload with Na bicarbonate) ■ 50 g of 50% dextrose over 5-10 mins with 10 U of regular insulin IV ■ Inhaled β2-agonists in high dose (albuterol 10-20 mg)  Removal of K from body: ■ Increase urine output with a loop diuretic ■ Increase GI K loss with Na polystyrene sulfonate 25-50 g in sarbitol. enterally or by enema ■ Dialysis .

Monitoring Should be monitored during evaluation & treatment: ◙ Repeat serum K levels ◙ Continuous cardiac monitoring and serial ECG tracings .

Sodium  Primary functions: ◈ determinant of osmolality in the body ◈ involved in the regulation of extracellular volume  Abnormalities in circulating Na primarily effect neuronal & neuromuscular function. .

Overview of Sodium Balance .

Hyponatremia  Sodium <135 mEq/L (>135 mmol/L)  Most common cause: associated with a low serum osmolality is excess secretion of ADH (euvolemic hyponatremia) or associated with hypovolemic and hypervolemic conditions  The presence of a nonsodium solute: glucose and mannitol (characterized by an elevated serum osmolality  Pseudohyponatremia: occurs in the presence of severe hyperlipidemia. or hyperglycemia . hyperproteinemia.

Causes of hyponatremia Euvolemia Hypovolemia Hypervolemia SIADH Diuretic use CHF Psychogenic polydipsia Aldosterone deficiency Cirrhosis Hypothyroidism Renal tubular dysfunction Nephrosis Inappropriate water admi. Diarrhea dren Third-space fluid losses . Vomiting nistration to infanst/chil.

Clinical manifestation  CNS: disorientation. nausea and vomiting  Muscle: weakness & CNS-driven respiratory arrest . decreased mentation. irritability. seizures. coma. lethargy.

Algorithm for treatment of hypernatremia hypernatremia water & Na+ loss water loss increased Na+ content replace isotonic loss replace water deficit loop diuretic replace water deficit replace any water deficit .

Volume is replaced.Treatment (1)  Treating the underlying disease  Removing offending drugs  Improving the circulating Na level  Hypovolemic hyponatremia: usually responds to IV volume repletion (with normal saline).  Hypervolemic hyponatremia: usually not severe & improves with successful treatment of the underlying condition . ADH is suppressed & free water is excreted by the kidneys.

Treatment (2)  Hyponatremia is acute or symptomatic: serum Na level should be increased restricting free-water intake increasing free-water clearence with loop diuretics replacing IV volume with normal saline (154 mEq/L) or hypertonic 3% saline (513 mEq/L)  The goal of therapy: to remove free water & not Na .

the Na+ deficit.6 x BB . can be estimated by the following formula: Na+ deficit=TBW x (desired [Na+]-present [Na+] ) TBW : 0.The amount of NaCl necessary to raise plasma [Na+] to the desired value.

6x 60 ( 130 – 126 ) = 144 meq.Example:  Koreksi Na : 0.5 meq/jam atau 10 meq/ 20 jam Jadi yang dibutuhkan : 280/20 = 14 ml per jam NaCl 3 % .  Koreksi Na 3% : 144/513 = 280 ml syarat 0.

which exceeds Na loss . Hypernatremia Sodium >145 mEq/L (>145 mmol/L) Indicates intracellular volume depletion with a loss of free water.

Causes of hypernatremia Water Loss Reduced Water Excessive Sodium Intake Intake Diarrhea Altered thirst Salt tablets Vomiting Impaired access Hypertonic saline Excessive sweating Sodium bicarbonate Diuresis Diabetes insipidus .

seizures. lethargy. coma  Muscle function: muscle weakness  Polyuria: the presence of diabetes insipidus or excess salt and water intake .Clinical manifestation  CNS: altered mentation.

Treatment (1)  Centers on correcting the underlying cause of hypernatremia  The vast majority of patients require free- water repletion  The water deficit can be calculated using equation: water deficit (L)=0.6 x wt (kg) [(Na2/Na1)-1] Na1 = the normal sodium level Na2 = the measured sodium level .

Example: A 70-kg man is found to have a plasma [Na+] of 160 mEq/L. What is his water deficit? .

6). assuming he had a normal [Na+] 140 mEq/L and a TBW content that is 60% of body weight: Normal TBW x 140 = present TBW x [Na+]plasma (70 x 0.If one assumes that the hypernatremia if from water loss only.7 = 5. then total body osmoles are unchanged.7 ltr Water deficit = normal TBW – present TBW = (70 x 0. Thus.3 L .36.6) x 140 = present TBW x 160 present TBW = 36.

300 mL over 48 hours. 5.To replace this deficit over 48 hours. or 110 mL/hour . one would give 5% Dextrose in water intrave- nously.

keto- acidosis. and osmotic diuresis-induced dehydration  Life-threatening hyperglycemic syndromes: diabetic ketoacidocis (DKA) and hyper- glycemic hyperosmolar nonketotic syndro- me (HHNK) . Hyperglycemic Syndromes  Results from a relative or absolute lack insulin  Characterized by: hyperglycemia.

Clinical manifestations  Result from hyperglycemia & excess ketone production Hyperglycemia: Hyperosmolality Osmotic diuresis-induced dehydration Fluid & electrolyte loss Dehydration Volume depletion Ketone (DKA): Acidosis Osmotic diuresis .

Clinical features  Weakness  Anorexia  Dehydration  Nausea/vomiting  Polyuria  Ileus  Polydipsia  Abdominal pain  Altered mental status  Hyperpnea  Coma  Fruity odor to the  Tachycardia breath (DKA)  Arrhythmias  Hypotension .

Laboratory investigation  Hyperglycemia  Hyperosmolality (more common in HHNK)  Glukosuria  Ketonemia/Ketonuria (DKA)  Anion gap metabolic acidosis (DKA)  Hypokalemia  Hypophosphatemia  Hypomagnesemia  Leukocytosis  Azotemia  Elevated amylase  Creatine phosphokinase .

& identify precipitating factors (infection. stroke. pancreatitis)  Volume deficits correlate with the severity of hyperglycemia & are usually greater in HHNK  Normal saline: replenish IV volume & restore hemodynamic stability (1 L in the first hour. provide insulin.Treatment (1)  The goal: to restore the fluid & electrolyte balance. 250-500 mL/hr as needed) . MI.

Treatment (2)  After 1-2 L of NS.5 saline) should be used to avoid hyperchloremic metabolic acidosis  Urine output should be maintained at 1-3 mL/kg/hr (ensure adequate tissue perfusion & clearance of glucose)  Invasive hemodynamic monitoring (arterial catheter. fluids with less Cl (0. PA catheter): required in patients with underlying CV disease .

Treatment (3)  DKA:  Loading dose: 5-10 U regular human insulin  IV route is the most reliable & easiest to titrate  Continuous infusion is necessary with serial monitoring of the blood glucose & electrolyte concentration  HHNK:  Smaller doses of insulin are usually adequate (1-2 U) .

switch to glucose-containing fluids to avoid hypoglycemia  10% dextrose may be necessary to maintain glucose levels >150 mg/dL (>8. the patient is stable) . ketonemia has cleared.8 mmol/L).Monitor glucose levels  Frequently  Glucose decreases to >250 mg/dL (<13.3 mmol/L) while continuing insulin infusion  Subcutaneous insulin (BS is controlled.

 Insulin & correction of acidosis shift potassium intracellularly & may lead to precipitous drops in K levels  K deficit range from 3-10 mEq/kg  K should be added to fluid therapy as soon as serum K is recognized or thought to be normal or low and urine output is documented  K levels should be monitored frequently until levels stabilize & acidosis is resolved (DKA) .

0  Look for precipitating of DKA (infection. Administer 10% dextrose if necessary to maintain serum glucose >150 mg/dL  Continue insulin infusion until ketosis is cleared (negative serum ketones with correction of increased anion gap). . and urine output is documented  Add glucose to crystalloid infusion when serum glucose is <250 mg/dL. initially with NS  Institute insulin infusion at 0. Do not decrease insulin infusion rate unless symptomatic hypoglycemia or precipitous drops in serum glucose.1 U/kg/hr  Consider bicarbonate if pH<7. MI.Priorities in initial resuscitation of DKA  Institute crystalloid resuscitation. GI bleed)  Add KCl to fluid resuscitation when serum K is known or expected to be low or normal.

Course Text. 2nd edition. Saunders Company . Lange Medical Books/McGraw-Hill Medical Publishing Division  Physiologic and Pharmacologic Bases of Anesthesia. Society of Critical Care Medicine  Lange Clinical Anesthesiology. 3rd edition. 3rd edition. 3rd edition.References:  Fundamental Critical Care Support.B. Williams and Wilkins  Textbook of Critical Care. W.