Download Fluid and Electrolyte Balance

Fluid and Electrolyte Balance
Pervin BOZKURT
Professor of Anaesthesiology
Total Body Water (TBW)
Male
60%
50%
Newborn 80%
Aged <50%
40% TBW
60% TBW
• Semipermeable membranes
– Water in and out freely
– Acts as barrier to other substances
• Osmosis is movement of water from
less concentrated solution to more
concentrated solution in
semipermeable membranes
• Osmolarity: is amount of solute per
volume of solvent (mosm/L)
• Osmolality ( mosm/kg)
Serum Osmolarity
Normal: 280-300mosm/L
What keeps water in balance?
•
•
•
•
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
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 Important
for Anaesthesiologist
• PTs are more vulnerable to vasodilation
– (-) inotropic effect of inhalation agents and
barbiturates
– Histamine release (morphine, meperidin,
NMB)
• Dose requirements decrease—volume
of distribution drugs decrease
• Regional anesthesia esp. Central
blocks are contrandicated
– Due to extensive sympathetic block
Hypervolemia
•
•
•
•
Increased fluid intake
Decreased fluid excretion
Stress—Secretes ADH
Importance for anesthesia
– Main role of anesthesiologist to
achieve gas exchange
– Hypervolemia- pulmonary interstitial
edema, alveolar edema, pleural fluid
and ascitis –cause derangements.
cations
Na+
K+
Ca2+
Mg2+
anions
142
4.5
2.5
1
ClHCO3PO42SO42protein
organic acids
150
100
27
2
1
15
5
150
↑ anion gap:
↑ protein, organic acids, PO42-, SO42↓ Ca2+, Mg2+
abnormal anion
- eg drugs
(salicylate, methanol, ethanol etc)
cations
Na+
K+
Ca2+
Mg2+
anions
142
4.5
2.5
1
ClHCO3PO42SO42protein
organic acids
150
100
27
2
1
15
5
150
↓ anion gap (rare):
↓ unmeasured anion (hypoalbuminaemia)
↑ Ca2+, Mg2+
abnormal cation
- IgG myeloma
Sodium
Na
• Major extracellular cation
• Affects water distribution
– ↓Na level (promotes water excretion)
– ↑Na level (promotes water retention) Na
• Maintains osmotic pressure of ECF
• Maintains acid-base balance
• Promotes neuromusc. function
• Influences Cl and K levels
Na
Na
Na
Na
Hypernatremia
• For elective surgery Na <150mEq/mL
• Consequences in anesthesiology practice similar to HYPOVOLEMIA
Treatment according to derangement
SLOWLY
Calculation of water deficit in
hypernatremia
• Normal TBW X 140= Existing TBW X Plasma
Na
• 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 pontine
myelinosis
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)
Daily diet - 40mEq of K
Normal diet: 60-100
Banana 12.8
Dried apricots 5
OJ 11.4
Broccoli, carrots
Tomato 5-10
Meats 12
Scallops 30
Hypokalemia
Paralytic Ileus
Postural Hypotension
Cardiac dysrhythmias
Increased sensitivity to Digitalis toxicity
Muscle cramps and tenderness
Paralysis
Confusion
Depression
• For elective surgery K >3.5mEq/L
Metabolic Alkalosis
• K–
–
–
–
–
supplements
Liquid: KCL 10 - 20, 40 mEq/15cc
Tablets: KCL (extended-release)
Slow-K
K-Lyte
Single dose should not exceed 20mEq
•
•
•
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 solutions
containing K
– Ringer’s Lactate
– Isolyte ( P, M, S)
– Kadalex
Bicarbonate
ƒ H+ ions moves oppositely to K
ƒ Na HCO3- (50 mmol iv)
(if severe acidosis pH <7.2)
Clinical effects
hypokalaemia
hyperkalaemia
neuro-muscular
weakness, paralysis weakness, para
depressed tend
reflexes
cardiac
arrhythmias
ECG changes
arrhythmias
ECG changes
GI
ileus
ileus
nausea, vomitin
pain
renal
tubular dysfunction,
polyuria
-
metabolic
alkalosis
acidosis
Clinical effects
hypokalaemia
prolonged PR
T-wave
flattening/inversion
prominent U waves
hyperkalaemia
tall, peaked T wave
QRS widening
QRS fusion with T wave
producing sine wave
AV dissociation, VT, VF
“Crush Syndrome”
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
Oda et al, J Trauma
March 1997 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
– Oxygen free
radicals
Potassium
– Superoxides
Myoglobin
– Histamines
Uric Acid
– Leukotrienes
Phosphate
– Peroxides
Lysozymes
Enzymes (CPK and others)
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
Treatment
I. Patient monitoring: hypovolaemia (arterial pressure, urine
output), electrolyte disorders and serum creatinine kinase
levels
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 of
75–110 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 h
III. If the systemic pH >7.5, then acetazolamide is administered
IV. If diuresis has still not been achieved, CVP monitoring should
be instituted
V. 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
Renal failure
Loss of Ca from bone
S/S
Cardiac arrest (↑ST
segment)
Deep bone pain, flank pain
Diet
Renal failure
Mg deficit
S/S
Depressed ST segment
Tetany, tingling
Trousseau’s, Chvostek’s
signs
Magnesium
“ forgotten electrolyte” (ICF)
Signs & symptoms
Hypermagnesemia (↑4mEq/L)
CNS: insomnia
Hypomagnesemia (NIDDM,ETOH)
Drowsy, lethargic, coma
CV: ↓P, BP, cardiac arrest
Arrhythmias
Neuromusc: ↓reflexes, weakness
Weakness, seizures, tremors
Resp. depression
30-35ml/kg
1ml/kg/hr
What happens to fluids
given İV?
IV therapy
• Goals
¾Maintain hydration
¾Replace fluids (water, calories,
protein, vitamins/minerals, electrolytes)
¾Restore acid-base balance
¾Restore blood volume
¾Provide access for medications
IV fluids
• Isotonic
– Osmotic pressure same as body fluid
• Expands & stays in intravasc. space
• Uses: bloodloss, hypotension
¾ Normal saline (NS) 0.9%
¾ LR (lactated Ringer’s): Na, K, Cl, Ca, lactate
¾ D5W (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
Iso (294)
140
Isolyte-M
Hyper (400)
40
Isolyte-P
Hyper(350)
25
Isolyte-S
Iso (295)
141
98
40
22
98
10
5
50
35
20
5
50
23
Colloid Solutions
Albumin
Dextran40 Rheomacrodex ( microcirculation)
70 Macrodex
Hydroxyethystarch
Isohes
Expahes
Varihes
Gelatine
Gelofuscine
İsotonic
Contain
Na and Cl
154 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
• Trendelenburg
position
• 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