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Learning Station 2 Electrolyte Abnormalities

1999 American Heart Association

Acknowledgments
Terry Mengert, MD, University of Washington, has graciously donated the instructor materials for electrolyte abnormalities to the AHA. He was the original author, designer, and developer of these materials. Mary Fran Hazinski, RN, MSN, refined the material and wrote the instructors notes. Deems Okamoto, MD, contributed extensively to the background science and pathophysiology.
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Learning Objectives
After completing this learning station you should be able to List causes, clinical effects, and management of major electrolyte imbalances Describe prearrest approach to major electrolyte imbalances Describe resuscitation of patients with major electrolyte imbalances
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Abnormalities to Review
Potassium Magnesium Sodium (hyponatremia) Acid-base imbalances

Electrolyte Abnormalities
Potential Consequences
May produce critical illness May lead to arrhythmias: VT/VF from hyper- or hypokalemia, hypomagnesemia, acidosis Asystole from hyper- or hypokalemia, acidosis PEA from hyperkalemia, acidosis Resuscitation can be impossible unless specific treatment provided
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Red Flags and Risk Factors for Electrolyte Abnormalities


Abnormal vital signs Altered mental status History of Prolonged, chronic disease Gastrointestinal or renal disease; malnutrition Diabetes, other endocrinopathies Cancer Alcohol or drug abuse

Diagnosis and Therapy


General Guidelines
Suspect problems: maintain high level of suspicion, order indicated lab studies early Primary ABCD Survey: support if needed O2IVmonitorfluids: provide a safety net Fluid resuscitation often indicated (caution when CHF present) Caution: Avoid rapid correction of electrolyte abnormalities (consider patient acuity)

Prehospital Diagnosis and Therapy


General ACLS guidelines apply Action often needed before lab results available Empiric therapy often justified Dialysis patient with VT: hyperkalemia TCA OD with arrhythmias: give sodium bicarbonate Alcoholic patient with arrhythmias: give Mg and K Drug OD with torsades de pointes: give Mg
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Case 1
59-year-old patient with dialysis-dependent end-stage renal disease Presents with weakness, nausea, vomiting, dyspnea, malaise Vital signs: HR = 100 bpm, BP = 170/110 mm Hg, RR = 26/min, temp = 35C

Case 1
Clinical exam Rales over lower third of chest Gallop heart sounds Abdomen benign Patient uncomfortable but awake

How would you manage this patient now?


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Hyperkalemia
Diagnosis
Causes Inadequate excretion (eg, renal failure) Excessive intake Shift from tissues (eg, crush injury, hemolysis)

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Hyperkalemia
Diagnosis
ECG changes: peaked T waves, flattened or absent P waves, prolonged PR interval, prolonged QRS, sine-wave pattern, arrhythmias Laboratory exam: stat K+, electrolyte panel

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Case 1: Progression
At 8:23 AM the nurse states, Youd better look at this rhythm strip. Patient alert, talking; weak, BP = 80/55 mm Hg, RR 24/min What is your first action? What medications were given by 8:27?

08:23 AM

Rx??

08:27 AM

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Case 1 Progression: 4 minutes later (8:27 AM)


What medications should be administered at this time?

08:27 AM

(continuous strip)

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Case 1 Progression: 8:31 AM (final strip 8 min from start)


What is the full regimen for this problem?

08:31 AM

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Hyperkalemia
Therapy
Stabilize excitable tissues: calcium chloride or calcium gluconate (Note: Do not use in digoxin poisoning!) Produce K+ intracellular shift: sodium bicarbonate, glucose and insulin, -agonist (albuterol) Remove K+ from body: furosemide, cation exchange resins, dialysis
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Case 2
20-year-old college student brought to ED by paramedics after syncopal episode History of bulimia but otherwise healthy Vital signs: HR = 100 bpm, BP = 100/61 mm Hg, RR = 16/min, afebrile

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Case 2
Clinical: eroded teeth, prominent parotid glands, thin Laboratory exam: Hct = 47, WBC = 5.1, preg (), Na+ = 136, K+ = 3.0, Cl = 86, bicarb = 41, BUN = 14, creat = 1, glu = 90, anion gap = 9

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Case 2
Estimate patients K+ deficit Outline your therapy for this patient Fluid therapy Electrolyte therapy Psychosocial intervention and follow-up

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Hypokalemia
Causes Redistribution Extrarenal loss (vomiting, diarrhea, nasogastric suction, poor intake, sweat) Renal losses (metabolic alkalosis, renal tubular acidosis, diuretics, etc)

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Hypokalemia
Symptoms: neuromuscular (weakness, paralysis), gastrointestinal (ileus), renal (polyuria, increased BP) ECG changes: T-wave flattening and inversion, U wave, ST depression, arrhythmias, digoxin toxicity

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Hypokalemia
Therapy
Oral: gradual oral replacement (10 to 30 mEq/d) preferable to IV replacement if possible Intravenous: more rapid replacement indicated for Severe deficit (<2.5 mEq/L) Severe symptoms Moderate deficit (3.0 to 3.5) during digoxin therapy Moderate deficit (3.0 to 3.5) in patient who cannot take orally
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Hypokalemia
Therapy
Intravenous Maximum IV replacement: 10 to 20 mEq/h; central or peripheral; label tubing Continuously monitor ECG Check K+ levels frequently during IV replacement

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Severe Hypokalemia
Emergency Therapy During Cardiac Arrest
Often can see the arrest coming Have impending PEA If cardiac arrest imminent or present: Initial infusion: 2 mEq/min, then 10 mEq IV over 5 to 10 min Document in chart that rapid infusion rate is intentional
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Case 3
28-year-old AIDS patient taking daily IV pentamidine for pneumocystis carinii pneumonia Clinical exam: altered mental status, hyperreflexia Lab exam: critically low potassium (2.9 mEq/L) and low calcium (6.5 mEq/L) What electrolyte disorders are present? How will you manage this patient?

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Hypomagnesemia
Causes Inadequate diet (malnutrition, IV feeding) Malabsorption, GI loss (diarrhea) Diuretics, alcohol, drugs (gentamicin, pentamidine, cyclosporin, cisplatin) Hyperparathyroidism, lactation

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Hypomagnesemia
Symptoms/signs: anorexia, nausea, lethargy, personality changes, altered mentation (if severe), neuromuscular abnormalities, seizures, hypokalemia, hypocalcemia ECG changes: arrhythmias (QT prolongation)

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Hypomagnesemia
Therapy
Mild or chronic: oral replacement (eg, Mg sulfate 400 mg PO q day or bid) Severe, symptomatic: 1 to 2 g (8 mEq/g) IV over 15 min, followed by 6 g in IV fluid per day (may require 3 to 7 days). Check levels daily and monitor DTRs closely.

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Hypomagnesemia
Therapy
Seizures: 2 g (16 mEq = 4 mL of 50% MgSO4) IV over 10 min; consider calcium gluconate Torsades de pointes: 2 g IV over 1 to 2 min Caution: Monitor for hypermagnesemia if renal failure present

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Case 4
65-year-old woman with known lung cancer Presents at home with 1-week history of declining mental status at home, including confusion, disorientation, and lethargy Clinical exam: unremarkable except for changed mentation What is your differential diagnosis? What is your initial approach?
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Case 4
Patient Progression: The patient suffers a grand mal seizure. STAT serum sodium is 108 mEq/L. What now?

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Hyponatremia
Causes (consider volume status) Volume depletion: GI, renal loss, 3rd spacing Euvolemia: SIADH, hypothyroidism, adrenal insufficiency Volume overload: CHF, liver disease, nephrotic syndrome
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Hyponatremia
Symptoms Asymptomatic unless acute or severe (Na <120 mEq/L) Abrupt fall in sodium produces extravascular fluid shift that may result in CNS edema with nausea, vomiting, headache, irritability, lethargy, seizures, coma, and even death
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Hyponatremia
Diagnosis
Assess volume status Evaluate kidney function (consider thiazide diuretics) Rule out congestive heart failure or liver failure Consider thyroid or adrenal disease In elderly consider poor solute intake
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Hyponatremia
Diagnosis
Rule out SIADH: causes = CONDM CNS disease Other (pain, postoperative, hypothyroidism) Nonmalignant pulmonary disease (COPD, pneumonia) Drugs Malignancy
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Hyponatremia
Therapy
Limit free water intake Treat underlying condition Correct volume deficit with 0.9% sodium chloride Correct hyponatremia gradually: increase by 0.5 mEq/L per hour, to a maximum of 10 to 12 mEq/L in the first 24 hours
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Hyponatremia
Therapy
Administer 3% NaCl for severe symptoms Correct at 1 mEq/L per hour until symptoms controlled, then Raise by 0.5 mEq/L per hour

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Case 4: Patient Progression


1. Calculate sodium deficit plan to increase sodium by 1 mEq/L per hour over 4 hours
Deficit = (Desired [Na+] Current [Na+]) 0.6 Body Weight (In women, use 0.5 Body Weight in calculation.)

2. Calculate volume of 3% NaCl (513 mEq Na+/L) required to correct deficit 3. Infuse 3% NaCl to increase serum sodium 1 mEq/h

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Case 4: Patient Progression


1. Calculate sodium deficit plan to increase sodium 4 mEq/L in 4 hours, current Na+ 108 mEq/L
Deficit = (112 mEq/L 108 mEq/L) 0.5 70 kg = 140 mEq

2. Determine volume of 3% NaCl to be administered


Volume = 140 mEq 513 mEq/L = 0.27 L (270 mL) of 3% NaCl

3. Administer solution over 4 hours (67 mL/h) to increase serum sodium 4 mEq over 4 hours
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Case 5
36-year-old with type I diabetes mellitus presents with 36-hour history of nausea, vomiting, low-grade fever, and malaise Vital signs: HR = 130 bpm, BP = 95/60 mm Hg, RR = 32/min, temp = 38.4C

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Case 5
Clinical exam: HEENT normal, neck supple, lungs clear, heart and abdomen unremarkable, mental status clear

How would you manage this patient?

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Case 5: Lab Results


Glucose: 580 mg/dL Arterial blood gases: pH = 7.00, PO2 = 115, PCO2 = 18, bicarb = 4 What initial fluids are appropriate? How much insulin should be administered? Is bicarbonate therapy appropriate?
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Case 5: Serum Electrolytes


Sodium: 130 mEq/L Potassium: 2.8 mEq/L Chloride: 95 mEq/L Bicarbonate: 5 mEq/L BUN: 28/Creatinine: 2.0 Anion gap: 130 (95 + 5) = 30

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Diabetic Ketoacidosis
Therapy
Evaluate and support ABCDs (including fluid resuscitation) Monitor and manage electrolyte balance: K+, phosphate, magnesium Administer continuous IV insulin Bicarbonate: controversial Identify the cause: the 5 Is
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Acid-Base Imbalance
Diagnosis
Obtain history, assess and support ABCDs Provide O2, establish IV and monitoring, obtain ABG and electrolytes Assess pH: Normal: 7.35 to 7.45 (may use 7.4) Acidotic: < 7.35 (may use 7.4) Alkalotic: >7.45
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Acid-Base Imbalance
Diagnosis
Evaluate pH in light of PCO2 (normal 35 to 45 mm Hg): Subtract PCO2 from 40 Multiply difference (+ or number) by 0.008 Add number to 7.4 to identify pH predicted from PCO2 Identify compensation
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Acid-Base Imbalance
Diagnosis
Calculate change in bicarbonate (normal: 22-26 mEq/L) and PCO2 (normal: 35-45 mm Hg) to identify primary, secondary problems: Metabolic acidosis: decrease in PCO2 from normal = (1.2 change in serum bicarbonate) 2 Metabolic alkalosis: increase in PCO2 from normal = (0.7 change in serum bicarbonate) 5

Acute respiratory acidosis: increase in serum bicarbonate from normal = 0.1 change in PCO2
Chronic respiratory acidosis: increase in serum bicarbonate from normal = 0.3 change in PCO2

Evaluate base excess or deficit (normal 2 to +2)

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Acid-Base Imbalance
Diagnosis
Calculate anion gap (normal: 12 to 15 mEq/L) Anion gap = Na+ (Cl + HCO3) Acidosis with anion gap >16 suggests accumulation of unmeasured anions such as DKA, lactic acidosis (change in bicarb should equal change in anion gap/1-1.5) Acidosis with normal anion gap results from loss of bicarbonate or gain of chloride such as diarrhea (change in bicarb is < change in anion gap/1-1.5) Determine if change in bicarbonate from normal is proportional to change in anion gap; if not, third disturbance likely
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Acid-Base Imbalance
Therapy
Identify and treat the primary process Support ABCDs and provide safety net (oxygen, IV access, ECG monitoring, and fluid therapy) Consider sodium bicarbonate to correct pH to 7.1 to 7.2 if metabolic acidosis is severe (eg, bicarbonate <10 mEq/L and pH <7.0 to 7.1)

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Acid-Base Imbalance
Therapy
Consider bicarbonate (contd) Infusion preferred over bolus therapy Do not normalize pH; correct to 7.1 to 7.2

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Electrolyte Abnormalities
Summary
Electrolyte abnormalities may contribute to arrest or prearrest conditions Suspect abnormalities from history and clinical presentation (empiric treatment may be needed in prehospital setting) Begin all treatment with support of ABCDs

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Electrolyte Abnormalities
Summary
Management of electrolyte abnormalities (eg, hyperkalemia) may be required for successful resuscitation Treatment of diabetic ketoacidosis requires monitoring of glucose, electrolytes, and acid-base balance

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Questions? Comments?

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Stump the Stars!

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Clinical Examples
Predict Electrolyte Abnormalities
24-year-old with 2 days of protracted vomiting: presents with tachycardia and orthostatic hypotension 58-year-old with 3 days of severe diarrhea: presents with tachycardia and orthostatic hypotension 62-year-old with known lung cancer: presents with altered mental status
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Clinical Examples
Predict Electrolyte Abnormalities
30-year-old with type I diabetes mellitus and 2 days of nausea, vomiting, and fever: presents with tachycardia and borderline hypotension 69-year-old with end-stage renal failure: presents with weakness, nausea, slight confusion, tachycardia with widened QRS complexes, and hypertension
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Clinical Examples
Predict Electrolyte Abnormalities
48-year-old alcoholic (binge drinker): presents with tremors, vomiting, slight confusion, and tachycardia 25-year-old injection drug user who passed out after using heroin last night: presents with leg pain and hard buttock, tachycardia, and tachypnea 20-year-old college freshman with known eating disorder: suffered syncopal spell at the dormitory and presents with weakness and tachycardia
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