+

Fluids and ElectrolytesIM 2013 (AVM)

+Outline

Potassium

Calcium

Magnesium

Phosphate

Creatinine and Renal Function

Water and Sodium

Bicarbonate

Inotropes

+

Basic Metabolic Panel

Na + Cl- BUN Ca++

Glu Mg++

K+ CO3-- Cr Phos--

3

+

POTASSIUM

+Potassium (K+)

Normal range: 3.5-4.5

Largely contained intra-cellular SK does not reflect total body K

Important roles: contractility of muscle cells, electrical responsiveness

Principal regulator: kidneys

5

+Potassium (K+)

Daily requirement 1-2 mEq/kg

Complete absorption in the upper GI tract

Kidneys regulate balance 10-15% filtered is excreted

Aldosterone: increase K+ & decrease Na+ excretion

Mineralocorticoid & glucocorticoid increase K+ & decrease Na+ excretion in stool

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+Potassium (K+)

Acidosis Low pH shifts K+ out of cells (into serum) Hi pH shifts K+ into cells 0.3-1.3 mEq/L K+ change / 0.1 unit change in

pH in the opposite direction

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+Hypokalemia

Hypokalemia <2.5: life threatening Common in severe gastroenteritis

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+Causes of Hypokalemia

Distribution from ECF Hypokalemic periodic

paralysis Insulin, Β-agonists,

catecholamines, xanthine

Decrease intake

Extra-renal losses Diarrhea Laxative abuse Perspiration

Excessive colas consumption

Renal losses DKA Diuretics: thiazide, loop

diuretics Drugs: amphotericin B,

Cisplastin Hypomagnesemia Alkalosis Hyperaldosteronism Licorice ingestion Gitelman & Bartter

syndrome

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+Hypokalemia: Presentation

Presentation Usually asymptomatic Skeletal muscle: weakness & cramps; respiratory

failure Flaccid paralysis & hyporeflexia Smooth muscle: constipation, urinary retention

ECG changes Flattened or inverted T-wave U wave: prolonged repolarization of the Purkinje fibers Depressed ST segment and widen PR interval Ventricular fibrillation can happen

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+Hypokalemia: Presentation

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Hypokalemia

- Flattened or inverted T-wave

- U wave: prolonged repolarization of the Purkinje fibers

- Depressed ST segment and widen PR interval

- Ventricular fibrillation can happen

+Hypokalemia: Treatment

Address the causes & underlying condition

Dietary supplements : leafy green vegetables, tomatoes, citrus fruits, oranges or bananas

Oral K replacement preferred

IV: KCl 0.5-1 mEq/kg over 1 hr (rate of 10 mEq/hr)

K Acetate or K Phos as alternative

Add K sparing diuretics

Correct hypomagnesemia

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+Hypokalemia: Treatment

30cc Oral KCl = 40mEqs K

Kalium Durule = 10mEqs K

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+Causes of Hyperkalemia

Hyperkalemia >6.5 – life threatening; Potential lethal

arrhythmias

Causes Spurious

Difficult blood draw hemolysis false reading Increase intake

Iatrogenic: IV or oral Blood transfusions

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+Causes of Hyperkalemia

Decrease excretion Renal failure Adrenal insufficiency or

CAH Hypoaldosteronism Urinary tract

obstruction Renal tubular disease ACE inhibitors Potassium sparing

diuretics

Trans-cellular shifts Acidemia Rhadomyolysis; Tumor

lysis syndrome; Tissue necrosis

Succinylcholine Malignant

hyperthermia

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+Hyperkalemia: Presentation

Neuromuscular effects Delayed repolarization, faster depolarization, slowing

of conduction velocity Paresthesias weakness flaccid paralysis

EKG changes ~6: peak T waves ~7: increased PR interval ~8-9: absent P wave with widening QRS complex Ventricular fibrillation Asystole

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+Hyperkalemia: Presentation

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+Hyperkalemia: Treatment

Lower K+ temporarily Calcium gluconate 100mg/kg IV Bicarb: 1-2 mEq/kg IV Insulin & glucose

Insulin 0.05 u/kg IV + D10W 2ml/kg then

Insulin 0.1 u/kg/hr + D10W 2-4 ml/kg/hr

Salbutamol (β2 selective agonist) nebulizer

Increase elimination Hemodialysis or hemofiltration Kayexalate via feces Furosemide via urine

Calcium: increases threshold potential decrease cardiac cell excitability

Bicarb: stimulate an exchange of cellular H+ for Na+, thus stim Na,K ATPase

Insulin: shift K into cells via Na,K-ATPase; last a few hours

Beta agonist: promote K shift into cells

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+

CALCIUM

+Calcium

Normal range: 8.8-10.1 with half bound to albumin

Ionized (free or active)calcium: 4.4-5.4 – relevant for cell function

Majority is stored in bone

Hypoalbuminemia falsely decreased calcium (alb in g/L): Ca measured + [0.8 x (Albn – Alb m)]

(alb in g/dL): Ca measured + [(40 – Alb) x 0.02]

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+Calcium

Roles: Coagulation Cellular signals Muscle contraction Neuromuscular transmission

Controlled by parathyroid hormone and vitamin D

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+Hypocalcemia: Presentation

Neuromuscular irritability

Paresthesias: oral, perioral and acral, tingling or pin & needles

Tetany (Chvostek & Trousseau signs)

Hyperreflexia

Laryngospasm

Jittery, poor feedings or vomiting in newborns

ECG changes: prolonged QT intervals

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+Hypocalcemia: Treatment

Supplements IV: gluconate or chloride with EKG change Oral calcium with vitamin D Calcium gluconate 10ml 10% wt/vol (90mg or

2.2mmol) IV, diluted in 50ml of 5%dextrose or 0.9%NaCl

Infusion: 10amps Ca gluc or 900mg Ca in 1L of D5 or 0.9%NaCl over 24hrs

Treat accompanying hypomagnesemia

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+Hypercalcemia: Presentation

Groans: constipation

Moans: psychic moans (fatigue, lethargy, depression)

Bones: bone pain

Stones: kidney stones

Psychiatric overtones: depression & confusion

Fatigue, anorexia, nausea, vomiting, pancreatitis

ECG: short QT interval, widened T wave

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+Hypercalcemia: Treatment

Fluid & diuretics 4-6L of IV saline may be needed in first 24hrs Forced diuresis with loop diuretic

Oral supplement: biphosphate or calcitonine Zoledronic acid (4mg IV over 30mins) Pamidronate (60-90 IV over 2-4hrs) Etidronate (7.5mg/kg/d for 3-7d) Onset 1-3days

Glucocorticoids IV hydrocortisone 100-300mg daily Oral prednisone (40-60mg daily for 3-7d)

Dialysis

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+

MAGNESIUM

+Magnesium

Normal range: 1.5-2.3

60% stored in bone

1% in extracellular space

Necessary cofactor for many enzymes

Renal excretion is primary regulation

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+Hypomagnesemia: Presentation

Weakness, muscle cramps

Cardiac arrhythmias Prolonged PR, QRS & QT Torsade de pointes Complete heart block & cardiac arrest with level >15

CNS: irritability, tremor, athetosis, jerking, nystagmus

Hallucination, depression, epileptic fits, HTN, tachycardia, tetany

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+Hypomagnesemia: Treatment

Oral or IV supplement Oral MgCl2, MgO, Mg(OH)2: in divided doses

totalling 20-30mmol/d (40-60meq/d) IV MgCl2 as infusion of 50mmol/d (100meq/d) May also give MgSO4 IV

Correct ongoing loss

Correct for calcium, potassium, and phosphate as well

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+Hypermagnesemia Presentation

Weakness, nausea, vomiting

Hypotension, hypocalcemia

Arrhythmia and asystole

4.0 mEq/L hyporeflexia

>5 prolonged AV conduction

>10 complete heart block

>13 cardiac arrest

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+Hypermagnesemia: Treatment

Magnesium-free cathartics or enemas

IV hydration

Calcium infusion IV in doses of 100-200 over 1-2hrs

Diuretics

Dialysis

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+

PHOSPHORUS

+Phosphorus

Normal range: 2.3 - 4.8

Most store in bone or intracellular space

<1% in plasma

Intracellular major anion, most in ATP

Concentration varies with age, higher during early childhood

Necessary for cellular energy metabolism

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+Hypophosphotemia

Presentation: Muscle dysfunction and weakness: diploplia, low CO,

dysphagia, respiratory depression AMS WBC dysfunction Instability of cell membrane rhabdomyolysis

Treatments Supplementation with IV as neutral mixtures of Na and

Phos salts Oral phosphate 750-2000mg in divided doses Necessary to avoid Ca-Phos product >50 Correct hypocalcemia

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+Hyperphosphotemia

Presentation: Tetany, seizures, accelerated nephrocalcinosis,

pulmonary and cardiac calcifications (mainly due to widespread calcium phosphate precipitates)

Treatments Limited Volume expansion Aluminum hydroxide antacids or sevelamer for

chelating Hemodialysis

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+Creatinine and Renal Function

+BUN/CREA RATIO

BUN / Crea x 247

> 20:1 prerenal azotemia

10-15:1 oliguric acute renal failure

+Creatinine Clearance Estimation (Cockcroft-Gault)

Female = Male x 0.85

(lower fraction of body weight is muscle the metabolism of which yields creatinine)

+

CKD Stage

Description GFR mL/min/1.73

m2

1 Kidney damage w/ normal / increased

90

2 GFRKidney damage w/ mildly decreased

60-89

3 GFRModerately decreased GFR

30-59

4 Severely decreased GFR 15-29

5 Renal failure < 15 (or dialysis)

+

WATER and SODIUM

+Sodium (Na+)

Bulk cation of extracellular fluid change in SNa reflects change in total body Na+

Principle active solute for the maintenance of intravascular & interstitial volume

Absorption: throughout the GI system via active Na,K-ATPase system

Excretion: urine, sweat & feces

Kidneys are the principal regulator

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+Sodium (Na+)

Kidneys are the principal regulator 2/3 of filtered Na+ is reabsorbed by the proximal

convoluted tubule, increase with contraction of extracellular fluid

Countercurrent system at the Loop of Henle is responsible for Na+ (descending) & water (ascending) balance – active transport with Cl-

Aldosterone stimulates further Na+ re-absorption at the distal convoluted tubules & the collecting ducts

<1% of filtered Na+ is normally excreted but can vary up to 10% if necessary

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+Sodium (Na+)

Normal SNa: 135-145

Major component of serum osmolality Sosm = (2 x Na+) + (BUN / 2.8) + (Glu / 18) Normal: 285-295

Alterations in SNa reflect an abnormal water regulation

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+Sodium (Na+)

Hyponatremia Na+<135 Seizure threshold ~125 <120 life threatening

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+Hyponatremia: Presentation

Cellular swelling due to water shifts into cells

Anorexia, nausea, emesis, malaise, lethargy, confusion, agitation, headache, seizures, coma

Chronic hyponatremia: better tolerated

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+Hyponatremia: Treatment

Rapid correction central pontine myelinolysis

Goal 12 mEq/L/day

Fluid restriction with SIADH

Hyponatremic seizures Poorly responsive to anti-convulsants Hypertonic saline Need to bring Na to above seizure threshold

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+Causes of Hypernatremia

Excessive intake Improperly mixed formula Exogenous: bicarb, hypertonic saline, seawater

Water deficit: Central & nephrogenic DI Increased insensible loss Inadequate intake

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+Causes of Hypernatremia

Water and sodium deficit GI losses Cutaneous losses Renal losses

Osmotic diuresis: mannitol, diabetes mellitus Chronic kidney disease Polyuric ATN Post-obstructive diuresis

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+Hypernatremia: Presentation

Dehydration

“Doughy” feel to skin

Irritability, lethargy, weakness

Intracranial hemorrhage

Thrombosis: renal vein, dura sinus

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+Hypernatremia: Treatment

Rate of correction for Na+ 1-2 mEq/L/hr

Calculate water deficit Water deficit = 0.6 x wt (kg) x [(current Na+/140) – 1]

Rate of correction for calculated water deficit 50% first 12-24 hrs Remaining next 24 hrs

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+Sodium (Na+)

Urine Outpu

t

SerumNa

UrineNa

Serum Osm

UrineOsm

DI

SIADH

CSW

+Serum or Plasma Osmolality

2Na + Glu + BUN

Normal 280-290 mosmol/kg

Use in plasma osmolal gap

+Urine Osmolality (mosmol/kg)

2 (urine Na + urine K) + urine urea +

urine glucose

Use in urine osmolal gap

+Water Deficit

= [(Plasma Na – 140) / 140] x total body water in hypernatremia due to water loss

[(Plasma Na – 140) / 140] x

[(0.5 in men or 0.4 in women)

x lean body weight] Use in hypernatremia due to water loss, but should

be corrected slowly over at least 48-72h, ideally w/ hourly serum Na determination to target 0.5 mmol/L/h but not > 12 mmol/L over the 1st 24h.

+Ideal Body Weight

For men = (106 lb for the first 5 ft + 6 lb for each inch above 5 ft) / 2.2 lb/kg

For women = (100 lb for the first 5 ft + 5 lb for each additional inch) / 2.2 lb/kg

+24-hr Urine Collection Adequacy Creatinine is produced at a constant rate & in

an amount directly proportional to skeletal muscle mass

Creatinine coefficient = 23 mg/kg of ideal body weight in men & 18 mg/kg of IBW in women

If 24 h urine creatinine < IBW x creatinine coefficient inadequately collected specimen

Unpredictable when serum crea > 530 umol/L

+

FLUIDS

+Crystalloids

SOLUTIONS pH Osm

Kcal

Na K Cl Ca

Mg

Lactate

Acetate

(A) ISOTONIC

1. PNSS 5.7 308 - 154

- 154

- - - -

2. D5NSS 4.2 560 200 154

- 154

- - - -

3.D5NR 5.4 552 200 140

5 98 - 3 - 27

4. D5 Eurosol-R 4.6-6.5

552 200 140

5 98 - 3 - 50

5. D5LR 5.3 527 200 130

4 109

3 - 28 -

6. D5 Euromed LR

3.5-6.5

525 200 130

4 109

2.7

- 28 -

7.D5 LVP LR 3.5-5.0

586 200 147

4 158

2.2

- 28 -

8.Plasmasol 148 4-6 547 200 140

5 98 - 3 - 27

+

SOLUTIONS pH Osm

Kcal

Na

K Cl Ca

Mg

Lactate

Acetate

(B) HYPOTONIC

1.D5NM 5.2 368 200 40 13

40

- 3 - 16

2. D5 Eurosol 4.5-6.5

368 200 40 13

40

- 3 - 16

3.D5 Ionosol MB 4.7 350 200 25 20

22

- 3 23 -

4.D5 Eurolon 4.6-6.5

350 200 25 20

22

- 3 23 -

5. Plasmasol 48 4-6 348 200 25 20

24

- 3 23 -

6. D50 .45 Euromed

3.5-6.5

408 200 77 - 77

- - - -

+

BICARBONATE

+Bicarbonate

Normal range: 25-35

Important buffer system in acid-base homeostasis

Increased in metabolic alkalosis or compensated respiratory acidosis

Decreased in metabolic acidosis or compensated respiratory alkalosis

0.15 pH change/10 change in bicarb in uncompensated conditions

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+Indications for HCO3 Therapy

pH < 7.2 and HCO3 < 5 – 10 mmHg

When there is inadequate ventilatory compensation

Elderly on beta blockers in severe acidosis with compromised cardiac function

Concurrent severe AG and NAGMA

Severe acidosis with renal failure or intoxication

+Complications of HCO3 Therapy

Volume overload

Hypernatremia

Hyperosmolarity

Hypokalemia

Intracellular acidosis

Causes overshoot alkalosis

Stimulates organic acid production

tissue O2 delivery

NaHCO3 50 ml = 45 mEq Na

NaHCO3 gr X tab = 7 mEq Na

+Bicarbonate Deficit

= HCO3 space x (desired HCO3 – measured HCO3)

(0.5-0.8* x body weight in kg) x (24** – measured HCO3)

* increases w/ increasing severity of the acidosis, normally 50% of body weight but increases to 80% in severe acidosis as a reflection of the total body buffering capacity.

** For severe acidosis < pH 7.20 in pure HAGMA, goal is to increase HCO3 to 10 mEq/L & pH to 7.15.

+

Goal is to increase plasma HCO3 slowly to 20-22 mEq/L. Notice that the formula uses 24 as the normal bicarbonate.

It tells us what the deficit is, but not what we should give the patient.

We still follow the targets for the above conditions (i.e., use them instead of 24). HCO3 therapy does not come without complications.

+

SHOCK and INOTROPES

+Dobutamine (ugtts/min)

desired dose x body weight in kg / (16.6 *

strength)

Desired dose 2-20 mcg/kg/min

For dobutamine 250 mg/amp 1 amp in 250 mL D5W, strength is 1 (if 2 amps for CHF, 2 and so on)

+Dopamine (ugtts/min)

desired dose x body weight in kg / (13.3 *

strength)

Desired dose 5-15 mcg/kg/min

For dopamine 200 mg/amp 1 amp in 250 mL D5W, strength is 1 (if 2 amps for CHF, 2 and so on)

+Norepinephrine (ugtts/min)

desired dose x body weight in kg / (0.133 *

strength)

Desired dose 0.5-30 mcg/kg/min

For norepinephrine 2 mg/amp 1 amp in 250 mL D5W, strength is 1 (if 2 amps for CHF, 2 and so on)

+

END.