Fluids And Electrolytes

MEDICAL-SURGICAL NURSING Arni A. Magdamo, MD, MHA, MBA, FPCP Harvard University School of Medicine Massachusetts General Hospital Institute of Health Sciences

Fluids and Electrolytes

Water, water everywhere… but not a drop to drink… WALT WHITMAN

FLUID BALANCE  Water and its electrolytes are distributed in two major compartments:  63% of the total body water is found within cells across the age groups.  37% of the total body water is found outside the cells, mainly in tissue spaces, plasma of blood, and lymph.

 The intracellular and extracellular fluid compartments are maintained in a steady state to ensure proper physiologic functioning.

FLUID BALANCE TOTAL BODY WATER (AS PERCENTAGE OF BODY WEIGHT) IN RELATION TO AGE AND SEX AGE

MALE

FEMALE

UNDER 18

65%

55%

18-40

60%

50%

40-60

50-60%

40-50%

OVER 60

50%

40%

Intracellular Fluid Compartment  Includes all the water and electrolytes inside the cells of the body.  Approximately 63% of the total body water is contained within cell membranes.  Contains high concentrations of potassium, phosphate, magnesium and sulfate ions, along with most of the proteins in the body.

Intracellular Fluid Compartment EXAMPLE: How much water is in the intracellular fluid compartment of a 25-year old male patient who weighs 60 kg? Step #1: Compute the total body water (TBW) based on age and sex. TBW = (60 kg) (0.6) = 36 kg  weight of water = 36 liters  volume of water

Intracellular Fluid Compartment Step #2: Compute for the intracellular fluid volume (usually 63% of the total body water is intracellular fluid) ICF = (36 liters) (0.63) = 22.7 liters

Extracellular Fluid Compartment  Includes all the fluid outside the cells: interstitial fluid, plasma, lymph, secretions of glands, fluid within subcompartments separated by epithelial membranes.  Constitutes approximately 37% of the total body water.  Contains high concentrations of sodium, chloride and bicarbonate.  One-third of the ECF is in plasma.

Extracellular Fluid Compartment EXAMPLE: How much water is in the circulatory system of a 32-year old female patient who weighs 52 kg? Step #1: Compute for the total body water based on age and sex. TBW = (52 kg) (0.5) = 26 kg  weight of water = 26 liters  volume of water

Extracellular Fluid Compartment Step #2: Compute for the extracellular fluid volume (usually 37% of the total body water). ECF = (26 liters) (0.37) = 9.6 liters Step #3: Compute for the plasma volume. Plasma = (9.6 liters)/3 = 3.2 liters

Transcellular Exchange Mechanisms:  ACTIVE TRANSPORT  PASSIVE TRANSPORT    

Diffusion Osmosis Filtration Facilitated diffusion

Serum Osmolality  Reflects the amount of solute particles in a solution and is a measure of the concentration of a given solution.  Can be calculated using the formula: Osmserum = 2 (Na) + BUN + glucose Normal value = 285 – 295 mosm/kg

 Sodium is the most active determinant of serum osmolality and is therefore actively moved across membranes to ensure normal osmolality.

Hence, if too much salt is used in food, the pulse hardens. HUANG TI (THE YELLOW EMPEROR), 2697-2597 B.C.

Ions NORMAL VALUES AND MASS CONVERSION FACTORS Normal Plasma Values

Mass Conversion

Sodium (Na+)

135 – 145 meq/L

23 mg = 1 meq

Potassium (K+)

3.5 – 5.0 meq/L

39 mg = 1 meq

Chloride (Cl-)

98 – 107 meq/L

35 mg = 1 meq

Bicarbonate (HCO3-)

22 – 26 meq/L

61 mg = 1 meq

Calcium (Ca2+)

8.5 – 10.5 mg/dL

40 mg = 1 mmol

Phosphorus

2.5 – 4.5 mg/dL

31 mg = 1 mmol

Magnesium (Mg2+)

1.8 – 3.0 mg/dL

24 mg = 1 mmol

285 – 295 mosm/kg 265 - 305 mosm/kg

-

Osmolality

Sodium  Dominant extracellular ion.  About 90 to 95% of the osmotic pressure of the extracellular fluid results from sodium ions and the negative ions associated with them.  Recommended dietary intake is less than 2.5 grams per day.  Kidneys provide the major route by which the excess sodium ions are excreted.

Sodium  In the presence of aldosterone, the reabsorption of sodium ions in the loop of Henle is very efficient. When aldosterone is absent, the reabsorption of sodium in the nephron is greatly reduced and the amount of sodium lost in the urine increases.  Also excreted from the body through the sweat mechanism.

Sodium  Primary mechanisms that regulate the sodium ion concentration in the extracellular fluid:  Changes in the blood pressure  Changes in the osmolality of the extracellular fluid

Sodium Regulation INCREASED SODIUM

Increased ADH secretion, Decreased urine volume and increased plasma volume

DECREASED SODIUM

Decreased aldosterone secretion, decreased sodium reabsorption

NORMAL Na+

DECREASED SODIUM

Decreased ADH secretion, Increased urine volume and decreased plasma volume

Increased aldosterone secretion, increased sodium reabsorption

INCREASED SODIUM

Potassium  Electrically excitable tissue such as muscle and nerves are highly sensitive to slight changes in extracellular potassium concentration.  The ECF concentration of potassium must be maintained within a narrow range for tissues to function normally.

Potassium  Aldosterone also plays a major role in regulating the concentration of potassium ions in the ECF.  Circulatory system shock resulting from plasma loss, dehydration, and tissue damage causes extracellular potassium ions to become more concentrated than normal. In response, aldosterone secretion increases and causes potassium secretion to increase.

Potassium Regulation INCREASED POTASSIUM

Increased aldosterone secretion with increased potassium secretion by the kidneys and increased potassium in urine

DECREASED POTASSIUM

NORMAL K+

DECREASED POTASSIUM

Decreased aldosterone secretion with decreased potassium secretion by the kidney and decreased potassium in the urine

INCREASED POTASSIUM

Calcium  Extracellular concentration of calcium ions is maintained within a narrow range.  Increases and decreases in ECF concentration of calcium ions have dramatic effects on the electrical properties of excitable tissues.  Parathyroid hormone (PTH) secreted by the parathyroid glands increases extracellular calcium levels.

Calcium  Calcitonin is secreted by the thyroid gland.  It reduces blood levels of calcium when they are too high.

Calcium Regulation Increased Calcitonin secretion with decreased bone resorption INCREASED CALCIUM

Decreased parathyroid hormone secretion with decreased bone resorption, decreased intestinal calcium absorption, and decreased kidney calcium reabsorption

DECREASED CALCIUM

NORMAL Ca++

DECREASED CALCIUM

Increased parathyroid hormone secretion with increased bone resorption, increased intestinal calcium absorption, and increased renal calcium reabsorption

INCREASED CALCIUM

Phosphate and Sulfate  Phosphate and sulfate are reabsorbed by active transport in the kidneys.  Rate of reabsorption is slow, so that if the concentration of these ions in the filtrate exceeds the ability of the nephron to reabsorb them, the excess is excreted in the urine.

Fluid and Electrolyte Management General Management of Fluids

Maintenance Therapy: Minimum Water Requirements  Can be estimated from the sum of the urine output necessary to excrete the daily solute load (500 mL per day if the urine concentrating ability is normal) plus the insensible water losses from the skin and respiratory system (500 to 1000 mL per day), minus the amount of water produced from endogenous metabolism (300 mL per day)  Two to three liters of water are needed to produce a urine volume of 1 to 1.5 liters daily.

Fluid / Electrolyte Replacement: Insensible Water Losses  Usually average 500 to 1000 mL daily, and

depend on respiratory rate, ambient temperature, humidity and body temperature.  Water losses increase by 100 ml daily for each degree of body temperature over 37°C.  Fluid losses from sweating can vary enormously and depend on physical activity and body and ambient temperature.  Mechanical ventilation accentuate losses from the respiratory tract.

Fluid / Electrolyte Replacement: Insensible Water Losses A 72-year old female was admitted for pneumonia in the elderly, community-acquired. Previous day’s profile: Total urine output: 1,700 ml 3 episodes of loose stools, approximately 250 per episode Highest temperature: 39.7 degrees Celsius On mechanical ventilator for the past three days

Fluid / Electrolyte Replacement: Insensible Water Losses Today’s Orders: NGT feeding with the following: TCR: 1700 kcal/day 6 equal feedings, 2:1 dilution Flush with 100 ml plain water after every feeding Compute for the IVF rate for today if the patient is to be connected to an adult venoset. What would be your choice of IVF?

Maintenance Therapy: Minimum Water Requirements  Weighing the patient daily is the best means of assessing net gain or loss of fluid, since the gastrointestinal, renal and insensible fluid losses of the hospitalized patient are unpredictable.

ECF Volume Depletion  Occurs with losses of both sodium and water.  The character of the fluid loss will dictate the clinical picture. If the loss is isotonic, the osmolality is unaffected and intracellular volume will change minimally.  Loss of hypotonic fluid will lead to an increase in serum or plasma osmolality.

ECF Volume Depletion  Manifestations of ECF volume depletion depend on the magnitude and on serum osmolality.  Symptoms:       

Anorexia Nausea Vomiting Apathy Weakness Orthostatic lightheadedness Syncope

ECF Volume Depletion  Weight loss is an important sign and provides an estimate of the magnitude of the volume deficit.  Other physical findings:       

Orthostatic hypotension Poor skin turgor Sunken eyes Absence of axillary sweat Oliguria Tachycardia Shock and coma (severe volume depletion)

ECF Volume Depletion  Causes of ECF volume depletion:     

Gastrointestinal losses Diuretics Renal or adrenal disease Blood loss Sequestration of fluid

ECF Volume Depletion: Treatment  Should be directed at restoration of the ECF volume with solutions containing the lost water and electrolytes.  Daily assessment of weight, ongoing fluid losses and serum electrolyte concentrations.  Mild degrees of volume depletion can be corrected orally.

ECF Volume Depletion: Treatment  More severe deficits accompanied by circulatory compromise should be treated initially through intravenous isotonic fluid replacement until hemodynamic stability has been restored. One to two liters of fluid should be given over the first hour.  Further therapy should be guided by the symptoms and signs.

Parenteral Solutions COMMONLY USED PARENTERAL SOLUTIONS IV Solutions

Osmolality (mosm/kg)

Glucose (g/liter)

Sodium (meq/liter)

Chloride (meq/liter)

5% D/W

252

50

-

-

10% D/W

505

100

-

-

50% D/W

2525

500

-

-

0.45% NaCl

154

-

77

77

0.9% NaCl

308

-

154

154

3% NaCl

1026

-

513

513

Ringer’s lactate

282

-

130

109

5% D/NR

294

50

147

147

5% D/NM

290

50

77

77

ECF Volume Excess  Manifestations:  Weight gain is the most sensitive and consistent sign of ECF volume excess.  Edema is usually not apparent until 2 to 4 kg of fluid have been retained.  Dyspnea  Tachycardia  Jugular venous distention  Hepatojugular reflux  Rales on pulmonary auscultation

ECF Volume Excess  Causes:   

Heart, liver or renal failure Excessive renal sodium and water retention Unnecessary salt administration

ECF Volume Excess: Treatment  Must address not only the ECF volume excess but also the underlying pathologic process.  Treatment of the nephrotic syndrome and the cardiovascular volume overload associated with renal failure.  Treatment of heart failure and cirrhosis.

Fluid and Electrolyte Management Sodium

Sodium  The primary extracellular cation.  Always accompanies water in the extracellular fluid compartment.

Hyponatremia  Defined as serum concentration less than 135 meq/L.  Most common electrolyte abnormality observed in a general hospitalized population.  Initial approach is the determination of serum osmolality.

Hyponatremia SERUM OSMOLALITY

Normal

ISOTONIC Hyponatremia Hyperproteinemia Hyperlipidemia

Low

HYPOTONIC Hyponatremia VOLUME STATUS

High

HYPERTONIC Hyponatremia Hyperglycemia Mannitol, sorbitol, Glycerol, maltose

Hyponatremia VOLUME STATUS

Hypovolemic

Una <10 meq/L Extrarenal salt Dehydration Diarrhea Vomiting

Una >20 meq/L Renal salt loss Diuretics ACE-inhibitors Nephropathies MineraloCorticoid lack

Euvolemic

SIADH Postop HypoNa Hypothyroidism Psychogenic polydipsia Beer potomania Drug reactions

Hypervolemic

Edematous states: Congestive heart failure Hepatic disease Nephrotic syndrome Advanced CHF

Treatment  Hypertonic (3%) saline with furosemide is indicated for symptomatic hyponatremic patients.  For asymptomatic patients, approach includes water restriction, isotonic saline infusion and administration of demeclocycline.

Hypernatremia  Serum sodium > 145 meq/L  Develops from excess water loss, frequently accompanied by an impaired thirst mechanism.

Hypernatremia: Treatment  Directed toward correcting the cause of the fluid loss and replacing water and, as needed, electrolytes.  Calculation of water deficit:  When calculating fluid replacement, both the deficit and the maintenance requirement should be added to each 24-hour replacement regimen.

Hypernatremia: Treatment  Calculation of water deficit (cont’d) Water deficit = current TBW x ([Na] – 140) 140 where [Na] is the measured serum sodium and TBW is the total body water (as percentage of the total body weight based on age and sex.

Hypernatremia: Treatment Given a 38/F with a body weight of 50 kg and a serum sodium level of 160 meq/L: What is the total water deficit? How much water should you give your patient during the first 24 hours?

Hypernatremia: Treatment Water deficit = TBW x ([Na] - 140) 140 = (50 kg)(0.5) (160-140) 140 = 25 liters (20) 140 = 25 liters (0.14) = 3.5 liters

Hypernatremia: Treatment Volume to be replaced in 24 hours = TBW x (160 – 148) 148 = 25 liters (12) 148 = 25 liters (0.08) = 2 liters

Fluid and Electrolyte Management Potassium

Hypokalemia  A total body deficit of about 350 meq occurs for each 1 meq/L decrement in serum potassium concentration.  Changes in blood pH and hormones (insulin, aldosterone, and β-adrenergic agonists) independently affect serum potassium levels.

Hypokalemia: Clinical Findings  Symptoms and Signs:     

Muscular weakness Fatigue Muscle cramps Constipation or ileus Flaccid paralysis, hyporeflexia, and rhabdomyolysis

Hypokalemia: Clinical Findings  Laboratory Findings:      

Decreased amplitude and broadening of the T waves Prominent U waves Depressed ST segments T wave inversion Atrioventricular block (1st, 2nd, 3rd degree AV blocks) Cardiac arrest

Note: Hypokalemia also increases the likelihood of digitalis toxicity

Hypokalemia: Treatment  Safest way is with oral potassium.  Intravenous replacement is indicated for patients with severe hypokalemia.  If serum potassium is > 2.5 meq/L, and there are ECG abnormalities, potassium can be given at a rate of 10 meq/L/hr in concentration that should never exceed 80 meq/L.

Hypokalemia: Treatment  For severe deficiency, potassium may be given through a intravenous cutdown.  Occasionally, hypokalemia may be refractory to potassium replacement. Magnesium deficiency may make potassium correction more difficult. Concomitant magnesium repletion avoids this problem.

Hypokalemia: Treatment ORAL POTASSIUM REPLACEMENTS LIQUIDS

POWDERS

TABLETS

AMOUNT

meq OF K

ANION

NAMES

15 ml

10

Cl

5% Potassium chloride

15 ml

20

Cl

10% Potassium chloride

15 ml

40

Cl

20% Potassium chloride

15 ml

20

Gluconate

Potassium gluconate

Packet

15

Cl

K-lor

Packet

20

Cl

Potassium chloride

Packet

25

Cl

K-lyte

1

8

Cl

Slow-K

1

8

Cl

Micro-K extencaps

1

10

Cl

K-dur 10

1

20

Cl

K-dur 20

Hypokalemia: Treatment POTASSIUM CONTENT OF FOODS VERY HIGH (12-20 meq)

HIGH (5-12 meq)

BEANS

Garbanzo beans Soy beans

Kidney beans Lima beans

Navy beans Pinto beans

FRUIT (1/2 cup or as stated)

Papaya (one medium)

Apricots (3 halves) Banana (6”) Cantaloupe (1/4”) Honeydew melon (1/4”) Orange (3”) and orange juice Pear (one large) Prunes (4) and prune juice Rhubarb

Hypokalemia: Treatment POTASSIUM CONTENT OF FOODS VERY HIGH (12-20 meq) VEGETABLES (1/2 cup or as stated)

HIGH (5-12 meq) Artichoke (one) Avocado (1/4) Brussel sprouts Carrot (7 ½”) and chard Ketchup (1 tbsp) Potato (one baked, one broiled, 10 fries, ½ cup mashed) Pumpkin and spinach Tomato (one) and tomato juice

Hyperkalemia  Many are spurious or associated with acidosis  Common practice of repeatedly clenching and unclenching the fist during venipuncture may raise the potassium concentration by 1-2 meq/L by causing local release of potassium from forearm muscles.

Hyperkalemia CAUSES OF HYPERKALEMIA SPURIOUS

Leakage from erythrocytes if separation of serum from clot is delayed. Thrombocytosis Marked leukocytosis Repeated fist clenching during phlebotomy Specimen drawn from arm with infusion

DECREASED EXCRETION

Renal failure, acute and chronic Severe oliguria Renal secretory defects Adrenocortical insufficiency Hyporeninemic hypoaldosteronism Spironolactone, triamterene, ACE-I, trimethoprim, NSAIDs

Hyperkalemia CAUSES OF HYPERKALEMIA SHIFT FROM TISSUES

Burns, rhabdomyolysis, hemolysis Metabolic acidosis Hyperosmolality Insulin deficiency Hyperkalemic periodic paralysis Succinylcholine, arginine, digitalis toxicity, beta-adrenergic blockers

EXCESSIVE INTAKE

Over treatment, orally or parenterally

Hyperkalemia: Clinical Findings   

Weakness and flaccid paralysis Abdominal distention and diarrhea ECG is not a sensitive method, but if abnormalities are present, the most common findings are:      

Peaked T waves ST segment elevation Tachyarrhythmia / supraventricular tachycardia Ventricular tachycardia Ventricular fibrillation Cardiac arrest

Hyperkalemia: Treatment  Confirm that the elevated level of serum potassium is genuine.  Measure plasma potassium.  Withholding of potassium.  Giving cation exchange resins by mouth or enema: polystyrene sulfate, 40-80 g/day in divided doses.

Hyperkalemia: Treatment  Emergent treatment is indicated if cardiac toxicity or muscular paralysis is present, or if hyperkalemia is severe (> 6.5-7 meq/L) even in the absence of ECG changes.  Insulin plus 10-50% glucose may be employed to deposit potassium with glycogen in the liver.  Calcium may be given intravenously as an antagonist ion.

Hyperkalemia: Treatment  Stimulate transcellular shifts by giving betaadrenergic agonist drugs.  Sodium bicarbonate as an emergency measure.  Hemodialysis or peritoneal dialysis.

Hyperkalemia: Treatment EMERGENCY TREATMENT OF HYPERKALEMIA MODALITY

MECHANISM OF ACTION

ONSET

DURATION

PRESCRIPTION

K REMOVED FROM BODY

Calcium

Antagonizes cardiac conduction abnormalities

0-5 min

1 hour

Ca gluconate 10%, 5-30 ml IV; CaCl 5%, 5-30 ml IV

None

Bicarbonate

Shifts K into cells

15-30 min

1-2 hours

None

Insulin

Shifts K into cells

15-60 min

4-6 hours

NaHCO3 44-88 meq IV SAI, 5-10 u IV, plus glucose 50%, 25 g IV

Albuterol

Shifts K into cells

15-30 min

2-4 hours

Nebulized albuterol, 10-20 mg in 4 ml saline

None

None

Hyperkalemia: Treatment NON-EMERGENCY TREATMENT OF HYPERKALEMIA MODALITY

MECHANISM OF ACTION

DURATION OF TREATMENT

PRESCRIPTION

K REMOVED FROM BODY

0.5-2 hours

Furosemide 40-160 mg IV or orally with or without NaHCO3, 0.5-3 meq/kg daily Oral: 15-30 g in 20% sorbitol (50-100 ml) Rectal: 50 g in 20% sorbitol

Variable

Loop diuretic

Increased renal K excretion

Sodium polystyrene sulfonate (Kayexalate

Ion exchange resin binds K

1-3 hours

Hemodialysis

Extracorporeal K removal

48 hours

Blood flow > 200-300 ml/min; Dialysate K = 0

200-300 meq

Peritoneal dialysis

Peritoneal K removal

48 hours

Fast exchange, 3-4 L/hr

200-300 meq

0.5-1 meq/g

Fluid and Electrolyte Management Calcium

Calcium  Constitute 2% of body weight, but only 1% of the total body calcium is in solution in body fluid.  In plasma, calcium is present as a non-diffusible complex with protein (33%); as a diffusible but undissociated complex with anions like citrate, bicarbonate, and phosphate (12%); and as ionized calcium (55%).

Calcium  Normal total plasma (or serum) calcium concentration is 8.5 to 10.5 mg/dL.  It is the ionized calcium that is necessary for muscle contraction and nerve function (normal: 4.7 to 5.3 mg/dL).

Hypocalcemia  Seen commonly in critically ill patients due to acquired defects in parathyroid-vitamin D axis.  Results occasionally in hypotension which responds to calcium replacement therapy.

Hypocalcemia CAUSES OF HYPOCALCEMIA DECREASED INTAKE OR ABSORPTION

Malabsorption Small bowel bypass, short bowel Vitamin D deficit

INCREASED IONS

Alcoholism Chronic renal insufficiency Diuretic therapy (furosemide or bumetanide)

ENDOCRINE DISEASES

True and pseudohypoparathyroidism Calcitonin hypersecretion

PHYSIOLOGIC CAUSES

Alkalosis and decreased response to vit. D Decreased serum albumin Hyperphosphatemia Aminoglycosides, loop diuretics, foscarnet

Hypocalcemia: Clinical Findings  Symptoms and Signs:  Extensive spasm of skeletal muscle causing cramps and tetany  Laryngospasm with stridor  Convulsions with paresthesias of the lips and extremities  Abdominal pain  Chvostek’s sign  Trousseau’s sign

Hypocalcemia: Clinical Findings  Laboratory Findings:    

Low serum calcium Elevated serum phosphorus Low serum magnesium Prolonged QT interval on the ECG

Hypocalcemia: Treatment  Severe symptomatic hypocalcemia:  In the presence of tetany, arrhythmias or seizures, calcium gluconate 10% is administered intravenously for 10-15 minutes or via calcium infusion.  10-15 mg of calcium per kilogram body weight, or 6-8 10-ml vials of 10% calcium gluconate (558-744 mg of calcium) is added to 1 liter of D5W and infused over 4 to 6 hours.

 Asymptomatic hypocalcemia:  Oral calcium and vitamin D preparations  Calcium carbonate is well tolerated and inexpensive.

Hypocalcemia: Treatment TREATMENT OF HYPOCALCEMIA MODALITY

AMOUNT OF CALCIUM

ONSET

Intravenous calcium (Calcium gluconate)

93 mg (4.7 meq) per 10 ml

Immediate

Oral calcium (calcium carbonate)

40% elemental calcium; 250 mg/624 mg tablet or 500 mg/1250 mg tablet or 500 mg/1500 mg tablet

< 1 hour

DOSE 93-186 mg over 10-15 mins; then 10-15 mg/kg over 4-6 hours. 250-500 mg calcium 3 to 5 times a day.

Hypercalcemia CAUSES OF HYPERCALCEMIA INCREASED INTAKE OR ABSORPTION

Milk-alkali syndrome

ENDOCRINE DISORDERS

Primary and secondary hyperparathyroidism

Vitamin D or vitamin A excess Acromegaly Adrenal insufficiency

NEOPLASTIC DISEASES

Tumors producing PTH-related proteins Metastases to bone Lymphoproliferative disease Secretion of prostaglandins and osteolytic factors

MISCELLANEOUS CAUSES

Thiazide diuretics and renal transplant complications Sarcoidosis and Paget’s disease of the bone Hypophosphatasia, immobilization, iatrogenic

Hypercalcemia: Clinical Findings  Symptoms and Signs:   

Polyuria and constipation Stupor, coma and azotemia Ventricular extrasystoles and idioventricular rhythm

 Laboratory Findings:   

Significant elevation of serum calcium Serum phosphorus may or may not be elevated Shortened QT interval on the ECG

Hypercalcemia: Treatment  Renal excretion of calcium is promoted by giving saline with furosemide.  Treatment of underlying condition.

Fluid and Electrolyte Management Magnesium

Magnesium  About 50% of total body magnesium exists in the insoluble state in bone.  Only 5% is present as extracellular cation; the remaining 45% is contained in cells as intracellular cation.  Normal plasma concentration is 1.5-2.5 meq/L, with about one-third bound to protein and twothirds existing as free cation.  Excretion is via the kidney.

Hypomagnesemia  Nearly half of hospitalized patients have unrecognized hypomagnesemia.  In critically ill patients, arrhythmias and sudden death may be complications.

Hypomagnesemia CAUSES OF HYPOMAGNESEMIA DIMINISHED ABSORPTION OR INTAKE

Malabsorption, chronic diarrhea, laxative abuse Prolonged gastrointestinal suction Small bowel bypass, malnutrition Alcoholism, parenteral alimentation

INCREASED LOSS

DKA, diuretic therapy, diarrhea Hyperaldosteronism, Bartter’s syndrome Hypercalciuria Renal magnesium wasting

UNEXPLAINED

Hyperparathyroidism Postparathyroidectomy Vitamin D therapy Aminoglycoside antibiotics, cisplatin, amphotericin B

Hypomagnesemia: Clinical Findings  Symptoms and Signs:        

Weakness Muscle cramps CNS hyperexcitability with tremors Athetoid movements Jerking, nystagmus Positive Babinski response Hypertension, tachycardia and ventricular arrhythmias Confusion and disorientation

Hypomagnesemia: Clinical Findings  Laboratory Findings:    

Decreased serum magnesium levels Hypocalcemia and hypokalemia Prolonged QT interval on the ECG Lengthening of the ST segment on the ECG

Hypomagnesemia: Treatment  Use of IVF containing magnesium as chloride or sulfate, 240-1200 mg/day (10-50 mmol/day) during the period of severe deficit, followed by 120 mg/day (5 mmol/day) for maintenance.  MgSO4 may also be given intramuscularly in a dosage of 200-800 mg/day (8-33 mmol/day) in four divided doses.  Serum levels must be monitored.

Hypermagnesemia  Almost always the result of renal insufficiency and the inability to excrete what has been taken in from food or drugs, especially antacids and laxatives.  Potentially life-threatening as it impairs both central nervous system and muscular function.

Hypermagnesemia: Clinical Findings  Symptoms and Signs:    

Muscle weakness Mental obtundation and confusion Hypotension Respiratory muscle paralysis or cardiac arrest

 Laboratory Findings:    

Elevated serum magnesium, BUN, creatinine, K Decreased serum calcium Increased PR interval on the ECG Broadened QRS complex with elevated T waves

Hypermagnesemia: Treatment  Alleviating renal insufficiency  Administration of calcium  Hemodialysis or peritoneal dialysis

In all things, you shall find everywhere the Acid and the Alcaly. OTTO TACHENIUS (1620)

Fluid and Electrolyte Management Acid-Base Disturbances

Arterial Blood Gases  Regulation of pH is accomplished by:   

Kidneys Lungs Buffer systems

 Information obtained from the arterial blood gas measurements:  pH  Partial pressure of carbon dioxide (pCO2)  Partial pressure of oxygen (pO2)  HCO3 level  Oxygen saturation (O2Sat)

Arterial Blood Gases  Normal values:  pH = 7.35 – 7.45  pCO2 = 35 – 45 mmHg  pO2 = 80 – 100 mmHg  HCO3 = 22 – 26 meqs/L  O2Sat > 95%

Arterial Blood Gases  Steps in obtaining an ABG specimen:  Check the bleeding parameters of the patient.  Prepare the following:  Glass syringe  Heparin (1,000 units/mL)  Alcohol  Cotton balls (soaked with alcohol AND dry)  Container with ice water  Aspirate 1 mL of heparin using a glass syringe

Arterial Blood Gases  Steps in obtaining an ABG specimen (cont’d):  Coat the inner surface of the syringe with heparin, taking care to pull and push the plunger to make sure heparin evenly coats the syringe.  Expel the excess heparin from the syringe.  Palpate for the radial pulse.  With the needle directed at a slight angle from the vertical, and pointed cephalad, gradually puncture the site and wait for arterial blood to rush in.

Arterial Blood Gases  Steps in obtaining an ABG specimen (cont’d):  After obtaining the specimen, secure the needle and place the syringe with the specimen in ice water.  Apply direct pressure on the puncture site for at least one minute, or until bleeding stops using a dry sterile cotton ball.  Send the specimen directly to the laboratory.  A sample is allowed to stand for a maximum of two hours only.

ABG Interpretation SUMMARY OF EXPECTED COMPENSATION FOR SIMPLE ACID-BASE DISORDERS DISORDER Metabolic Acidosis

INITIAL CHANGE Decrease in HCO3-

COMPENSATORY RESPONSE Decrease in pCO2: Δ pCO2 = 1.1 – 1.3 (ΔHCO3-)

Metabolic Alkalosis

Increase in HCO3-

Increase in pCO2: Δ pCO2 = 0.6 – 0.7 (ΔHCO3-)

Respiratory Acidosis

Increase in pCO2

Increase in HCO3ACUTE: ΔHCO3-= 0.1 Δ pCO2 + 2

Respiratory Alkalosis

Decrease in pCO2

CHRONIC: ΔHCO3-= 0.3 – 0.35 Δ pCO2 Decrease in HCO3ACUTE: ΔHCO3-= 0.2 – 0.25 Δ pCO2 CHRONIC: ΔHCO3-= 0.4 – 0.5 Δ pCO2