Fluid and Electrolyte Balance

Pervin BOZKURTProfessor of Anaesthesiology

Total Body Water (TBW)

Newborn 80%

Aged <50%

50%Male60%

60% TBW

40% TBW

• Semipermeable membranes– Water in and out freely– Acts as barrier to other substances

• Osmosis is movement of water fromless concentrated solution to moreconcentrated solution in semipermeable membranes

• Osmolarity: is amount of solute pervolume of solvent (mosm/L)

• Osmolality ( mosm/kg)

Serum Osmolarity

Normal: 280-300mosm/L

• THIRST• Hormones (affect balance of water and Na)

– ADH: retains or secretes water– Aldosterone:

• ↑causes Na and water retention and K loss• ↓causes Na and water loss and K retention

– ANF• Plasma protein

– Albumin (major plasma protein)– Regulates blood volume– Prevents water in blood from diffusing into interstitial fluid

• Kidneys– Control concentration and volume of blood by removing water and waste

(1 - 2 l urine daily)– Regulate blood pH– Filter 170 l of plasma

What keeps water in balance?

Negative Balance

• volume depletion (hypovolaemia)– total body water ↓, osmolarity normal

• haemorrhage, severe burns, chronic vomiting or diarrhea

• dehydration – total body water ↓, osmolarity rises

• lack of drinking water, diabetes, profuse sweating, diuretics

– infants are more vulnerable– affects all fluid compartments– most serious effects: circulatory shock, neurological

dysfunction, death

Why Hypovolemia is Importantfor Anaesthesiologist

• PTs are more vulnerable to vasodilation– (-) inotropic effect of inhalation agents and

barbiturates

– Histamine release (morphine, meperidin, NMB)

• Dose requirements decrease—volumeof distribution drugs decrease

• Regional anesthesia esp. Centralblocks are contrandicated– Due to extensive sympathetic block

Hypervolemia

• Increased fluid intake• Decreased fluid excretion• Stress—Secretes ADH• Importance for anesthesia

– Main role of anesthesiologist toachieve gas exchange

– Hypervolemia- pulmonary interstitialedema, alveolar edema, pleural fluidand ascitis –cause derangements.

cations anionsNa+ 142 Cl- 100K+ 4.5 HCO3

- 27Ca2+ 2.5 PO4

2- 2Mg2+ 1 SO4

2- 1protein 15organic acids 5

150 150

↑ anion gap:

↑ protein, organic acids, PO42-, SO4

2-

↓ Ca2+, Mg2+

abnormal anion - eg drugs(salicylate, methanol, ethanol etc)

cations anionsNa+ 142 Cl- 100K+ 4.5 HCO3

- 27Ca2+ 2.5 PO4

2- 2Mg2+ 1 SO4

2- 1protein 15organic acids 5

150 150

↓ anion gap (rare):

↓ unmeasured anion (hypoalbuminaemia)

↑ Ca2+, Mg2+

abnormal cation - IgG myeloma

Sodium

• Major extracellular cation• Affects water distribution

– ↓Na level (promotes water excretion)– ↑Na level (promotes water retention)

• Maintains osmotic pressure of ECF• Maintains acid-base balance• Promotes neuromusc. function • Influences Cl and K levels

Na

Na

Na

Na

Na

Na

Hypernatremia

• For elective surgery Na <150mEq/mL• Consequences in anesthesiology practice similar to HYPOVOLEMIA

Treatment according to derangementSLOWLY

Calculation of water deficit in hypernatremia

• Normal TBW X 140= Existing TBW X PlasmaNa

• Example:• 70kg M N a160 mEq/LT. What is the amount of

fluid deficit• (70X0.6)X140= Existing TBW X160• Existing TBW=36.7• Fluid loss = (70X0.6)-36.7)=5.3• Give 5% D in wter in 48 hours

hypernatraemia - management

general principles

correct slowly to avoid cerebral oedema

- 0.5 - 0.7 mmol / l / h

treat underlying cause

Hyponatremia

• For elective surgery Na >135mEq/mL• Consequences in anesthesiology practice

• similar to HYPERVOLEMIA• Special issue : TURP syndrome

Hyponatraemia - emergency treatment

controversial

rapid correction → central pontinemyelinosis

hyponatraemia → encephalopathy( if severe and rapid onset)

Eg. TURP Syndrome

Potassium• Major intracellular cation

– Maintains cellular osmotic equilibrium– Regulates muscular activity (cardiac/skeletal muscles)– Maintains acid-base balance

• Na and K relationship:↑in one will cause↓ in the other– Body usually conserves Na– But has no method to conserve K– Kidneys will excrete K (even in K depletion)

Banana 12.8Dried apricots 5

OJ 11.4Broccoli, carrots

Tomato 5-10

Meats 12Scallops 30

Daily diet - 40mEq of KNormal diet: 60-100

Hypokalemia

Paralytic IleusPostural HypotensionCardiac dysrhythmiasIncreased sensitivity to Digitalis toxicityMuscle cramps and tendernessParalysisConfusionDepressionMetabolic Alkalosis• K- supplements

– Liquid: KCL 10 - 20, 40 mEq/15cc– Tablets: KCL (extended-release)– Slow-K – K-Lyte– Single dose should not exceed 20mEq

• For elective surgery K >3.5mEq/L

• Peaked T waves• Wide QRS complexes• Depressed ST segments

Treatment of Hyperkalemia

• Avoid foods containing K• Avoid drugs

– containing K- crystalized penicillin– increasing K- sucsinilcholine

• Avoid intravenous solutionscontaining K– Ringer’s Lactate– Isolyte ( P, M, S)– Kadalex

Bicarbonate

H+ ions moves oppositely to KNa HCO3

- (50 mmol iv)

(if severe acidosis pH <7.2)

hypokalaemia hyperkalaemia

neuro-muscular

weakness, paralysis weakness, paradepressed tendreflexes

cardiac arrhythmias ECG changes

arrhythmias ECG changes

GI ileus ileus nausea, vomitinpain

renal tubular dysfunction, polyuria

-

metabolic alkalosis acidosis

Clinical effects

Clinical effects

hypokalaemia hyperkalaemia

prolonged PRT-wave flattening/inversionprominent U waves

tall, peaked T waveQRS wideningQRS fusion with T waveproducing sine waveAV dissociation, VT, VF

“Crush Syndrome”

Oda et al, J Trauma March 1997

Criticisms After Marmara Earthquake

• “Crush syndrome was not properly recognized in some cases.”

• “Most of these patients received only 2,000 to 3,000 mL/day of infused fluids during the initial 3 days.”

• “…we need to avoid such failure to recognize crush syndrome and to start infusion without delay.”

Definitions• Direct Mechanical Crush - physical disruption and

immediate death of cells• Crush Injury - interference with normal membrane

function and circulation of blood to an area of tissue which leads to cell death

• Compartment Syndrome - a form of crush injury caused by swelling inside a muscle body surrounded by inelastic fascia

• Crush Syndrome A group of systemic manifestations that occur after crush inhury. Blood then returns to the affected part after the compressive force is removed allowing toxic products to enter the systemic circulation.

Pathophysiology

• Crush injury interrupts the supply of blood which causes cells to function anaerobically

• Integrity of cells breaks down causing them to become leaky which results in swelling, rupturing or otherwise being destroyed

• Extreme force causes immediate muscle cell disruption and death

Pathophysiology

• Mechanisms cause buildup and cellular release of:– Lactic Acids– Potassium– Myoglobin– Uric Acid– Phosphate– Lysozymes– Enzymes (CPK and others)

– Oxygen free radicals

– Superoxides– Histamines– Leukotrienes– Peroxides

Pathophysiology

• As patient is extricated, the compression force is lifted allowing blood to re-perfuse the injured area.

• Patient dies because of one or more of the following primary causes:– Hypovolemia– Dysrhythmia and Cardiotoxicity– Renal Failure

Causes of Death

• Hypovolemia– ruptured blood vessels bleed freely– capillaries leak fluid into tissue (third spacing)

• Dysrhythmia and Cardiotoxicity– high blood toxins return to central circulation – severe acid load causes Ventricular-fib– high K level causes dysrythmias

• Renal failure– enzymes digest cell membranes– myoglobin precipitates in kidney tubules

Post-Extrication Assessment– Symptoms may be subtle and develop gradually

• entrapped limb may appear dusky to black in color– ecchymotic lesions– marked edema/swelling– +/- distal pulses

• watch for symptoms of hypovolemia• arrhythmias - enlarged or “peaked” T waves; prolonged

PR or QRS complex; loss of P wave; PVC, V-tach or V-fib• urine may appear dark reddish-brown like coca-cola

TreatmentI. Patient monitoring: hypovolaemia (arterial pressure, urine

output), electrolyte disorders and serum creatinine kinaselevels

II. Volume replacement: target of 200 ml/h urine output– Physiological serum while muscle remains under pressure– After removal of patient from the subsidence and

haemodynamic stabilisation, give a liquid formula of75–110 mmol/l NaCl in 5% dextrose( 5%dextrose in water+ 40 mEq NaHCO3 ( 4 amp NaHCO3)+ 10g/l mannitol (50ml 20% mannitol)

– An average of 12 litres per day should be given for 3 days– Na HCO3 stopped at 36 hIII. If the systemic pH >7.5, then acetazolamide is administeredIV. If diuresis has still not been achieved, CVP monitoring should

be institutedV. If no response occurs, furosemide is used (40 mg, up to a

maximum of 200 mg)VI. Haemodialysis

Management:Hypovolemia

• Large bore I.V.s (NS preferred); Fluid replacement prior to extrication. – consider all injuries including possible

ICP and cardiac overload– consider high volumes of NS may lead

to chemical imbalance

Management:Renal Failure

• Increase urine output – fluid replacement– alkaline diuresis– catheterize patient ASAP to monitor

output• Consider availability of dialysis

equipment

Additional Considerations

• Immobilization of crushed parts• Dress wounds meticulously to

prevent infection; consider I.V. antibiotics

• It is imperative that the rescue team be made aware of the importance of treating the patient PRIOR to extrication

Calcium

• Daily amount needed: 1gram– 98% (bone & teeth, small amount in

ECF)– Ca able to shift in & out of these

structure• Needed for:

– Neuromusc. & enzyme activity– Skeletal development– Blood coagulation

• Body absorbs Ca from GI tract• Vit. D needed• Excreted in urine & feces

Causes, Signs & symptoms

Hypercalcemia Hypocalcemia

Diet DietRenal failure Renal failureLoss of Ca from bone Mg deficitS/S S/SCardiac arrest (↑ST segment)

Depressed ST segment

Deep bone pain, flank pain Tetany, tingling

Trousseau’s, Chvostek’s signs

Magnesium “ forgotten electrolyte” (ICF)

Signs & symptoms

Hypermagnesemia (Hypermagnesemia (↑↑4mEq/L)4mEq/L)CNS: insomnia

Hypomagnesemia (NIDDM,ETOH)Hypomagnesemia (NIDDM,ETOH)

Drowsy, lethargic, coma

CV: ↓P, BP, cardiac arrest Arrhythmias

Neuromusc: ↓reflexes, weakness Weakness, seizures, tremors

Resp. depression

1ml/kg/hr30-35ml/kg

What happens to fluidsgiven İV?

IV therapy• Goals

Maintain hydrationReplace fluids (water, calories, protein, vitamins/minerals, electrolytes)

Restore acid-base balanceRestore blood volumeProvide access for medications

IV fluids• Isotonic

– Osmotic pressure same as body fluid• Expands & stays in intravasc. space

• Uses: bloodloss, hypotensionNormal saline (NS) 0.9%LR (lactated Ringer’s): Na, K, Cl, Ca, lactateD5W (fluids, calories) acts as hypotonic

– Hydrates cells, depletes circ. System• Hypotonic

– Less osmotic pressure than ICF (cell swells)• Hydrates cells but depletes circ. System

• Hypertonic– Expands intravascular space,depletes intracellular

compartments (cell shrinks)

Isolyte-M Hyper (400) 40 40 35Isolyte Iso (294) 140 98 10 5 50

Isolyte-P Hyper(350) 25 22 20 50 23

Isolyte-S Iso (295) 141 98 5

Colloid Solutions

AlbuminDextran-

40 Rheomacrodex ( microcirculation)

70 MacrodexHydroxyethystarch

IsohesExpahesVarihes

GelatineGelofuscine

İsotonicContain

Na and Cl154 mEq/L

Catheter types• Peripheral• Central

– Short term• Cvp• Swan• Dialysis

– Long term• Ports

Catheter infections:sources

Peripheral IV insertion

Peripheral IV insertion

Peripheral IV insertion

IV Complications• Infiltration

– Fluid outside vessel causing swelling, pain, little or no IV flow

• Catheter shear– Piece of catheter separates

• Air embolism– Air enters blood stream (10-100 cc have

been fatal)• Infection

– Localized or systemic

Home

Temporary central venous catheters

Seldinger technique

• Trendelenburgposition

• Stiff,soft tipped guide wire

• Flouroscopy• CXR

Catheter Complications : early• Infections• Injury

– Cardiac,lymphatic,• Malposition• Air embolism

– Insertion and removal– Cardiovascular collapse, wheel mill murmur– Left lateral decubitus positioning, air

aspiration if possible, thoracotomy if necessary

Arterial access

• Hemodynamic monitoring• Frequent blood gas evaluations• Chemotherapy infusion

– Limb perfusion– Hepatic arterial infusions

Arterial access:site selection