Download Disturbances of fluid and electrolyte balance

Disturbances of fluid and electrolyte
balance
Csaba Hermann MD
Dept. of Anesthesiology and Intensive Care
Semmelweis University
Homeostasis
• The maintenance of normal volume and normal
composition of the extracellular fluid is vital to life.
• Homeostasis: the various physiologic arrangements
which serve to restore the normal state, once it has been
disturbed
•
•
•
•
Fluid balance
Electrolyte balance
Osmotic balance
Acid-base balance
General principles
• Diffusion: movement of the particles in a solution from
the area of high concentration to the area of lower
concentration
• Electrolyte: inorganic substance that dissociates into
ions
• Osmosis: diffusion of solvent molecules (water) into
region in which there is a higher concentration of a
solute (electrolyte) to which the membrane is
impermeable
• Osmotic pressure: the pressure necessary to prevent
solvent migration
• Osmol: concentration of osmotic active particles
General principles
• Osmolarity : number of osmoles per liter of solution
• Osmolality: number of osmoles per kilogram of solvent
• Measurement: depression of freezing point
• Calculation (plasma): 2x(Na+K)+glucose+BUN
(mmol/l)
• Tonicity: effective osmolality of a solution relative to
plasma
• Colloids: high molecular weight particles (> 20000 D)
• Oncotic pressure (colloid osmotic pressure): the
pressure necessery to prevent diffusion of solvent
molecules (water) into region in which there is a higher
concentration of a colloid to which the membrane is
impermeable
Extracellular space
Intravasal
Intracellular space
Interstitial space
space
Water
Electrolytes
Colloids
Capillary wall
Cell membrane
Oncotic pressure
Osmotic pressure
Body Fluid Volumes
Compartment
Fluid Vol.
(l)
% Body
Fluid
% Body
Wgt.
Total Body
Fluid
Intracellular
Fluid
(ICF)
Extracellular
Fluid (ECF)
42
100
60
28
67
40
14
33
20
Plasma
2.8
6.6
(20% ECF)
26.4
(80% ECF)
4
Interstitial
Fluid
Lymph &
Transcellular
Fluid
11.2
Neg.
Neg.
16
Neg.
Daily Water Balance (liters)
OUTPUT
INPUT
• FLUID INTAKE 1.5
• INSENSIBLE
0.8
• IN FOOD
0,8
• SWEAT
0,1
• METABOLIC
0.3
• FECES
0.2
• Total
2,6
• URINE
1.5
• Total
2.6
Composition of fluids (mmol/l)
Fluid
ICF
Plasma
ISF
Liquor
Verejték
Nyál
Gastric juice
H+: 40-60
Intestinal juice
Na+
12
140
145
147
20-40
10
20-80
K+
140
4-5
4,4
3
5
26
5-20
HCO312
26
27
23
15
-
120-140
5-15 20-40
Cl 4
112
117
113
15-40
10
100-150
10
Fluid replacement
•
•
•
•
0-10 kg: 100 ml/kg/d
11-20 kg: 50 ml/kg/d
> 20 kg: 20 ml/kg/d
4-2-1 (ml/kg/h)
Patient (70 kgs)
• 1-10 kg
• 11-20 kg
• >20 kg
(4-2-1)
4 ml/kg/h
2 ml/kg/h
1 ml/kg/h
Together:
40 ml/h
20 ml/h
50 ml/h
110 ml/h
2640ml/d
Fluid Balance
• The main way to regulate body water gain is by adjusting
the volume of water intake, mainly by drinking more or
less fluid. The thirst center in the hypothalamus governs
the urge to drink.
• Although increased amounts of water and solutes are
lost through sweating and exhalation during exercise,
loss of excess water or excess solutes depends mainly
on regulating excretion in the urine.
• The extent of urinary Na (and Cl) loss is the main
determinant of body fluid volume, whereas the extent of
urinary water loss is the main determinant of body fluid
osmolarity.
Fluid Balance
• Angiotensin II and aldosterone reduce urinary loss of
Na+ and Cl- and thereby increase the volume of body
fluids (baroreceptors: sinus caroticus, kidney)
• Stimulation of ANP production: elevation of atrial wall
tension (Angiotensin)
• ANP promotes natriuresis, elevated excretion of Na+
(and Cl- ), which decreases blood volume.
• The major hormone that regulates water loss and thus
body fluid osmolarity is ADH (Hypothalamus)
• The regulation of the volume of body fluids superior to
the regulation of osmolarity
Water Deficit
•
INCREASED OSMOLARITY SENSED BY
HYPOTHALAMIC RECEPTORS
RELIEVES
•
FALL IN ECF VOLUME
•
FALL IN ARTERIAL BLOOD PRESSURE
STIMULATION
OF HYPOTHALAMIC
NEURONS
INCREASED THIRST
RELIEVES
INCREASED VASOPRESSIN
OPEN PORES
IN COLLECTING
DUCT
ARTERIOLAR
VASOCONSTRICTION
MORE WATER REABSORBED
INCREASED WATER INTAKE
FALL IN URINE OUTPUT
DECREASED PLASMA OSMOLARITY
DECREASED PLASMA OSMOLARITY
Blood pressure and renal handling of
sodium
FALL IN SODIUM LOAD
RELIEVES
FALL IN ARTERIAL PRESSURE
INCREASE IN
ALDOSTERONE
SECRETION
FALL IN GFR
FALL IN FILTERED
SODIUM
FALL IN EXCRETION OF
SODIUM, CHLORIDE, AND
FLUID
INCREASED CONSERVATION
OF SODIUM AND FLUID
INCREASE IN
SODIUM
ABSORPTION
Disturbances of fluid homeostasis
• Disturbance of fluid balance (intake≠output)
• Dehydraton, Overhydration (hyperhydration)
• Disturbance of osmolarity (electrolyte intake≠water
intake)
• Isonatremic (isotonic)
• Hyponatremic (hypotonic)
• Hypernatremic (hypertonic)
Disturbances of fluid homeostasis
Diagnosis:
• Physical signs: skin turgor, oedema, mucous
membranes, neck veins, puls, liver, level of
consciousness, capillary refill, fontanel (children)
• Vital sings: blood pressure; heart rate; (respiratory rate);
body temperature; CVP; urine output; serum and urine
Na, osmolarity; Htk; serum total protein
Dehydration
• Signs: increased thirst (except: advanced age, hypotonic
dehydration), weakness, decreased skin turgor, dry
mucous membranes, empty neck veins, decreased urine
output, elevated Htk, fever, tachycardia, hypotension,
decreased CVP,lethargy, stupor, coma
• Mild (loss: 4% of body weight): decresed skin turgor,
sunken eyes, dry mucous membranes
• Moderate (loss: 5-8 % of body weight): + oliguria,
orthostatic hypotension, tachycardia
• Severe (loss: 8-10 % of body weight): + hypotension,
decreased level of consciusness, stupor
Dehydration
Isotonic
Se Na
n
Se osmolarity
n
Hb
+
Htk
+
Blood volume
Thirst
mod. increase
Hypertonic
Hypotonic
+
+
+
+
increased
+
+
no
Isotonic dehydration
• Intracellular fluid volume remains constant
• External loss: vomiting, diarrhoea, haemorrhage, burning
• Internal loss: ileus, ascites, pleural effusion
• Therapy: volume replacement wiht isotonic solution
Hypertonic dehydration
• Extracellular + intracellular fluid loss; elevated osmolarity
• Causes: inadequate replacement of hypotonic fluid loss,
osmotic diuresis (diabetes), decreased ADH secretion,
high fever, heat stroke, massive diarrhoea
• Therapy: slow water replacement, hypotonic solutions
are contraindicated in the first phase of replacement
• Water deficit (l): 0,6*kg*((Nameasured/Nanormal)-1)
Hypotonic dehydration
• Decreased extracellular fluid volumen, elevated
intracellular fluid volume
• Causes: inadequate fluid replacement with hypotonic
solution, elevated ADH secretion + extracellular fluid
loss, Addison’s disease, diuretics, vomiting
• Usually no thirst
• Therapy: Isotonic fluid replacement, Na replacement in
case of severe hyponatraemia
Hyperhydration
• Signs: oedema, increased skin turgor, elevated CVP,
distended neck veins, pulmonary oedema
SeNa
Se osmolarity
Hb
Htk
Blood volume
Isotonic
n
n
+
Hypertonic
+
+
-+
Hypotonic
(-)
+
Isotonic hyperhydration
• Intracellular fluid volume remains constant
• Causes: renal failure, heart failure; decreased oncotic
pressure, increased isotonic fluid intake
• Therapy: decrease intake, diuretics
Hypertonic hyperhydration
• Infrequent
• Causes: renal failure, excessive hypertonic fluid input
• Increased thirst, fever, convulsion, coma
• Therapy: diuretics, dialysis + slow replacement with
hypotonic solutions
Hypotonic hyperhydration
• Intracellular fluid volume is also increased
• Water poisoning
• Causes: heart failure, near drowning (fresh-water),
increased input of hypotonic solutions (TUR syndrome)
• Symptomes: weakness, nausea, vomiting,altered mental
status
• Therapy: diuretics + fluid replacement with isotonic
solution (+ Natrium)
Hyponatraemia
• Serum Na < 135 mmol/l
• Causes:
• Water problem (excess of water relative to sodium)
• Water excretion by the kidney is impaired
• Pseudohyponatraemia (hyperlipidaemia, hyperproteinaemia)
• Symptoms:
• Cerebral oedema
• Nausea, vomiting, lethargy, confusion, seizures, coma
• Therapy:
• Hypertonic saline (Se Na < 125 mmol/l)
• Isotonic saline (se na > 125 mmol/l)
• Increase rate of se Na level should be less than 2 mmol/h (cave:
Central pontin myelinolysis)
Hypernatraemia
• Se Na > 145 mmol/l
• Causes: inadequate water intake and increased free
water loss; intake of hypertonic sodium solution
• Symptoms:
• Increased thirst
• Central nervous system abnormalities (confusion,
weakness, lethargy, seizures, coma)
• Therapy: water repletion, correction rate of Na level
should be no greater than 2 mmol/h (cave: cerebral
oedema)
ADH
• SIADH (syndrome of inappropriate ADH secretion)
• Ectopic production
• Brain diseases
• Lung diseases
• Therapy: decrease of water intake
• Diabetes insipidus
• Decreased ADH secretion (central), decreased ADH
effect in the kidneys (renal)
• Therapy: ADH (central), hydrochlorothiazide,
indomethacine (renal)
Potassium
• Most abundant cation of ICF, helps maintain ICF volume
• Key role in the resting membrane potential and action
potential of neurons and muscle fibers
• K+ level is controlled by aldosterone
• Hydrogen-potassium exchange in cell membrane
• Minimal potassium intake: 1 mmol/kg
Hyperkalaemia
• Se K > 5 mmmol/l
• Causes
• Impaired excretion
• Renal failure, mineralocorticoid deficiency,
pseudohypoaldosteronism, drugs (potassium
sparing diuretics, ACE-inhibitors NSAID,
cyclosporin)
• Shifts of K out of cells
• Tissue breakdown, acidosis, insulin deficiency
Hyperkalaemia
• Symptoms:
• Cardiac (peaked T waves, loss of P waves, heart blocks,
ventricular arrhytmias, widening of QRS complexes,
asystole)
• Paresthesias, weakness, paralysis
• Acidosis
• Therapy
• Direct antagonism of hyperkalemic effect on cell membrane
polarization
• Calcium gluconate
• Movement of extracellular K into intracellular compartment
• Insulin (+glucose)
• Sodium bicarbonate
• β2-adrenergic agonists
Hyperkalaemia
• Therapy
• Removal K from the body
• Loop diuretics
• Sodium polystyrene sulfonate
• Dialysis
Hypokalaemia
• Se K < 3,5 mmmol/l
• Causes:
• Increased excretion: diarrhoea, renal losses, mineralocorticoid
excess, magnesium depletion
• Shifts of K into cells: drugs (insulin, β2-adrenergic agonists,
theophylline, caffeine), alkalosis, hyperthyreoidism
• Symptoms:
• Cardiac: flat t waves, ST depression, U wave, QT interval
prolongation, arrhytmias
• Muscle paralysis, rhabdomyolysis
• Coma
• Metabolic alkalosis
Hypokalaemia
• Therapy
• Supplementation of K
• (Knormal-Kmeasured) * ttkg * 0.2 + daily need
• Infusion rate: no more, than 20 (30) mmol/h
• Oral supplementation
• 1 gr potassium-chloride containes 13,4 potassium, 1
gr potassium-citrate containes 9,2 mmol/l potassium
Acid-base disorders
Acid-base balance
• H2O  H+ + OH- (steady state: pH 7 (6,8))
• A Henderson-Hasselbach Equation
pH = - log [H+]= pK+log [anion/undissociated acid]
• Extracellular space: 7.38pH  7.42
• Intracellular space: pH ~ 6.8
• Source of H+: intake, metabolism (50 mmol/d), CO2:
12500 ,mmol/d)
• Elimination of H+: kidney, lung (CO2), gastrointestinal
tract, liver
Analysis of acid-base balance
• Respiratory
• Metabolic
• Buffer system (HCO3-, BE)
• Strong ion difference (Na+, K+, Cl-, lactate-) – Stewart
method
Buffers
• A buffer is a substance, that has the ability to bind or release H+ in
solution, thus keeping the pH of the solution relatevily constant
despite of considerable quantities of acid or base
• The important buffer systems in blood include proteins, carbonic
acid-bicarbonate buffers and phosphates.
Buffer
pK
Concentration
Buffer capacity
Bicarbonate
6,1
24 mmol/l
75 %
Hgb
8,25
oxyHgb
6,95
24 mmol/l
25 %
Proteins
-
Phosphates
6,8
Buffers
• Carbonic acid – bicarbonate system:
• H2CO3  H+ + HCO3-  H2O + CO2
• A Henderson-Hasselbach Equation
pH = - log [H+]= pK+log [anion/undissociated acid]
• pH= 6.1 + log[HCO3/0.03xPaCO2 (amount of carbonic acid)]
• Plasma proteins
• Dissociation of their carboxyl or free amino groups
• Hemoglobin
• Dissociation of imidazole groups
• Phosphates : low plasma concentration
Acid-base disorders
• Acidosis: pH<7.35
• Alkalosis: pH>7.45
• Metabolic disturbance: addition of acid or alkali (stronger,
than the buffers) or removal of acid or alkali
• Respiratory disturbance: rise or decline in arterial pCO2
• Compensation:
• Kidneys
• Lung
BGA
pH
arterial
7.37-7.45
mixed venous
7.35-7,43
pCO2 Hgmm(kPa) 35-46(4,6-6,1)
37-50 (4,9-6,6)
actual/standard
21-26/21-26
bicarbonate (mmol/l)
21-26/21-26
BE (mmol/l)
-2,5 - +2,5
-2,5 - +2,5
Anion gap (mmol/l) 10-14
(Siggaard-Andersen Curve Nomogram)
10-14
Metabolic acid-base disorders
• Dysfunction of the primary regulating organs
• Renal failure
• Exogenous administration of drugs or fluids that alter the
body’s ability to maintain normal acid-base balance
• Methanol, ethylene glycol, salicylates
• Abnormal metabolism that overwhelms the normal
defense mechanisms
• Ketoacidosis (diabetic, alcoholic, starvation, metabolic
error)
• Lactic acidosis
Practical classification of
metabolic acid-base disorders
• Iatrogenic
• Fixed
• Symptom of an ongoing acute illness
• Only metabolic acidosis has real clinical importance
Metabolic acidosis
pH<7.35, HCO3<20 mmol/l, BE<-3 mmol/l
Anion gap
(Na++K+) - (Cl-+HCO3-)
normal range: 10-15 mmol/l
• Elevated anion gap: lactic acidosis, ketoacidosis, renal
failure, exogenous administration of acids
• Non-anion gap acidosis: renal tubular acidosis,
gastrointestinal acidosis, Iatrogenic acidosis
(administration of Cl, dilutional acidosis)
Metabolic acidosis
• Symptoms:
• Increased sympathetic activity
• Decreased inotropy, arterial vasodilatation – critical
pH (7,2)
• Decreased oxy-Hgb binding
• Hyperkalaemia
• Insulin resistance
• Free radical formation
• Bone demineralization
• Emesis
• Decreased sensorium
• Hyperventilation
Metabolic acidosis
• Therapy
• Therapy of underlying disease
• Maximizing respiratory compensation
• NaHCO3 mmol = -BE* 0,3 * kg
• Maximal rate of infusion: 1.5 mmol/kg/h
• Adverse effects: hypernatraemia, increased CO2
production, intracellular acidosis
• Tromethamin (Tris-buffer, Tham)
• Penetrates cells
• Maximal daily dose: 5 mmol/kg
• Adverse effect: hypoglycaemia, respiratory
depression, fatal hepatic necrosis
Metabolic alkalosis
pH>7.45, HCO3>26 mmol/l, BE>3 mmol/l
Causes:
• Chloride responsive
• Vomiting, gastric drainage
• Chloride wasting diarrhea (villous adenoma)
• Diuretics
• Post-hyperpnoe
• Chloride-unresponsive
• Mineralocorticoid excess
• Cushing’s syndrome
• Bartter’s syndrome
• Hypokalaemia
• Sodium salt administration (acetate, citrate)
• Massive blood transfusion
• Sodium-lactate (Ringer’s solution)
• Parenteral nutrition
Metabolic alkalosis
• Symptoms
•
•
•
•
•
•
•
Hypoventilation, repiratory depression
Neuromuscular excitability
Hypokalaemia
Seizures
Increased oxy-Hgb affinity
Altered coronary blood flow, vasoconstriction
Decreased cerebral blood flow
Metabolic alkalosis
Therapy
• Therapy of underlying disease
• Chloride responsive alkalosis: NaCl
• Chloride-unresponsive alkalosis: HCl, KCl
• Mineralocorticoid excess: Spironolactone
Respiratory alkalosis
pH>7.45, pCO2<35 Hgmm
• Causes:
• Hypoxic respiratory failure
• Salicylate intoxication
• Early sepsis
• Hepatic failure
• Arteficial hyperventilation
• Symptomes
• Decreased cerebral or coronary blood flow
• Neuromuscular excitability
• Therapy:
• Therapy of underlying disease
• Increasing the dead space
Respiratory acidosis
pH<7.35, pCO2>45 Hgmm
• Cause:
• Respiratory failure
• Symptoms:
• Symptoms of metabolic acidosis + coma
• Therapy:
• Therapy of underlying disease
• Mechanical ventilation