Transcript MAINTAINENCE THERAPY

Osmolality
Goldman
A mole of a substance is the mol wt of that substance in grams
E.g. the mol wt of NaCl is 23+35.5= 58.5
Therefore 1mole NaCl = 58.5 g.
1 millimole is 1/1000 of a mole
Therefore 1millimole of NaCl is 58.5 mg.
The weight of a salt in mg can be converted into millimoles by dividing the weight in mg
by the mol.wt
e.g 1g (1000mg) NaCl = 17.1 millimoles
Mol wt of NaCl =58.5 Therefore 1000/58.5= 17.1
Mol wt of glucose C6H12O6 = 12x6 +1x12 +16x6 = 72+12+96=180
Osmolality – a Molal solution contains a gram mol wt of the substance dissolved in 1000g
of the solvent
(A Molar solution contains a gram mol wt of the substance dissolved in 1 Liter of solvent)
It is determined by measuring the depression of the freezing point of a solution,
compared to water,using an osmometer and expressing the value in *C below 0*C
The value can also be expressed in milliosmoles ,using the factor 1000Osm=186*C or
1*C=538mOsm
The normal range of serum osmolality is 275-290mOsm/kg of serum
NORMAL BODY COMP
WashMan
Total Body Water- Water makes up
60% of body wt in males (42l in 70kg male)
50%
in females
80%
in newborns
2/3 is ICF – Intracellular Fluid ( 40%-28L in 70kg male)
1/3 is ECF-Extracellular (20% body wt-14I) of which1/4 is Intravascular (plasma 5% body
wt-3.5L) and 3/4 Interstitial(10.5L)
Total body water is controlled by ADH
SODIUM-85-90% is in ECF
Change in serum Na (i.e. Intravascular Na) indicates disturbed water homeostasis and
ICF volume
Change in sodium content ( total body Na) are manifest as ECF expansion (edema) or
contraction
Osmolality or tonicity is the solute or particle concentration of a fluid.
Solutes that are restricted to the ICF ( K & organic phosphate esters) or
ECF(Na & accompanying anions) determine the effective tonicity or osmolality
Rule of thumb -Extracellular osmolality = 2x serum Na + 10
Normal body fluid vol and osmolality is maintained by kidneys despite wide variations in
salt and water intake
NORMAL ELECTROLYTE COMP
OF IV &IC mmol/L
Schwartz
ELECTROLYTE
Intravascular
(SERUM)
ICF
Sodium (Na)
135-145
10
Potassium (K)
3.5-4.5
150
Chloride (Cl)
85-115
HPO4+SO4
150
10
Bicarbonate(HCO3) 22-29
Calcium (Ca)
2-2.5
Magnesium (Mg)
0.75-1.25
20
GI –NORMAL VALUES
Secretion
VOL
ml/d
Saliva
1000
Na
mmol/l
Cl
mmol/l
Condon /ACS Manual
K
mmol/l
HCO3
mmol/l
100
75
5
25-30
Gastric Juice pH <4 2500
60
100
10
Gastric Juice pH >4 2000
100
100
10
Bile
1500
140
100
10
35
Pancreatic Juice
1000
140
75
10
100
Succus Entericus
3500
100
100
20
35
Diarrhoea
10004000
60
45
20
35
Average Electrolyte Composition
Na+
(mmol/L)
K+
(mmol/
L)
Cl–
(mmol/
L)
Sweat
30–50
5
Gastric
secretions
20
Pancreatic
juice
Replacement Guidelines per Liter Lost
HCO3–
(mmolL)
0.9%
Saline (mL)
Current diagnosis
0.45%
Saline (mL)
D5 W
(mL)
KCl
(mmol/L
)
50
500
500
5
10
10
300
700
20
130
5
35
115
400
600
5
2 amps
Bile
145
5
100
25
400
5
0.5 amp
Duodenal
fluid
60
15
100
10
1000
15
0.25 amp
Ileal fluid
100
10
60
60
600
10
1 amp
Colonic
diarrhea
1401
10
85
60
1000
10
1 amp
600
400
7.5% NaHCO3 (45 mmol
HCO3–/amp)
ELECTROLYTES/DAY
•
Wash Man
Na- usually 50-150mmols provided. Renal excretion
can fall to < 5mmols/d in absence of intake
•
K –usually 20-60 mmols when renal function
normal
Rule of thumb - Na/K 1mmol/kg/day
•
CHO- 100-150 g in the form of dextrose to
minimise- protein catabolism& ketoacidosis
•
2-3 l of 1/2N Dextrose Saline (90-125ml/hr)
with 20mmols K/ l
MAINTAINENCE THERAPY
Wash Man
500ml - min amount of water req to excrete daily
solute load
Solute load of 600mOsm is produced daily by the
body. Healthy people can concentrate urine to a
max of 1200mOsm/L
• +500ml - insensible loss thru skin, lungs & feces
• -300ml- water prod from endogenous met
Min water required/day=1000-300ml =700ml
Rule of thumb (ROT)- 30 ml/kg/d normal water
reqd
Normally 2-3l water/day to prod 1-1.5L urine
Check daily weight
COMP OF COMMONLY USED IV
FLUIDS
Condon
IV
Osmolality Glucos
mOsm/Kg) e
(Gm/l)
Na
K
mmol/L mmol/l
Cl
mmol/L
HCO3
mmol/l
5%D/W
278
50
0
0
0
0
10%D/W
586
100
0
0
0
0
50%D/W
2778
500
0
0
0
0
0.9%NaCl 308
0
154
0
154
0
DNS
586
50
154
0
154
0
Ringers
lactate
274
130
4
109
28
Kidral
368
26
19
22
24
50
ABNORMAL FLUID &
ELECTROLYTE LOSSES
Wash Manual
1.
2.
3.
4.
5.
INSENSIBLE WATER
GI
RENAL
RAPID INTERNAL SHIFTS
BLOOD
INSENSIBLE WATER LOSS
Wash Manual
From skin and lungs –very variable Inc with
inc resp rate,ambient temp and humidity.
Inc by 100-150 ml/*C>37* body
temp(2ml/kg/*C)
• Sweating- variable 100-2000ml/hr dep on
physical activity and ambient temp
Replacement with 5% dextrose or ¼ NS
RENAL LOSSES
Wash Manual
• Na losses significant in diuretic phase of ATN, diuretic
use,GI losses and catabolic states
• Na retention sig in postop state, dehydration, steroid use
• K loss sig in diuretic use, steroid use, GI losses esp
diarrhoea, ( intracellular shift with Beta agonists like
salbutamol)
• K retention sig in high output renal failure, post trauma,
blood transfusion
RAPID INTERNAL FLUID
SHIFTS
Wash Man
• Occurs with peritonitis, burns, intestinal
obstruction, sepsis, crush injury
• Need to replace sequestered fluid with
normal saline
RENAL FUNCTION
Condon
Assessed by
Urine sp.gr, pH & osmolality of 1st voided urine in the morning• sp.gr should be or > 1.016 and pH 5.8 or lower
• and urine osmolality should be 850mOsmol/Kg water and ratio of
urine to serum osmolality should be at least 3
Tubular Activity Na mmol/L K mmol/L
Normal
>40
>40
Conserving
10-30
20-30
Max retention
<5
15-25
ANION GAP
• Determination of the anion gap is useful in assessing the
etiology of metabolic acidosis.
Mmol Na = mmol Cl- + mmol HCO3- +
Metabolic acidosis can be divided into 2 groups
1- with inc Cl ( as in diarrhoea with loss of HCO3)
2 with inc of unknown anion as in renal failure where there
is inc sulphate and phosphate,
Diabetes ketoacidosis where there is increased ketocacids,
Salicylate poisoning where there is inc salicylate
Lactic acidosis where there is inc lactic acid
Na+140mmol / l= Cl 100mmol + HCO3 10mmol + ?
HYPONATREMIA
ACS
Caused by
• replacing body loss by water alone or 5% dextrose eg diarrhoea
• Head injury with inappropriate secretion of ADH
• Renal disease with inappropriate loss of Na in the urine
• Starvation where there is breakdown of muscle with production of salt free
water
• Diuretic use especially thiazides
Pseudohyponatremia- The serum Na is falsely low because of
1. High serum lipids or protein – Na falls but osmolality stays the same
2. If plasma glucose is > 20mmol/L,make a correction
3. Blood is drawn from an arm with a dextrose drip
The decreased serum Na causes a fall in the osmolallity of extracelluar comp
and there is movement of water intracellularly causing swelling of cells. This
can cause brain edema with inc intracranial pressure
This causes edema, inc in weight, confusion, apathy, weakness, nausea and
vomiting.
If not corrected the water excess will progress to muscle twitching, convulsions,
stupor and even death as serum Na falls < 120mmol/l
HYPONATREMIA - TREATMENT
• Dont base treatment on serum Na conc
alone
• Correct the underlying cause if possible
• With urine omolality and sodium conc it is
possible to come to a diagnosis
HYPERNATREMIA
Much rarer. Caused by
• Fever in septic patients
• Tube feeding when not diluted with adequate water
• Renal disease with loss of solute poor water as in high output renal failure
where there is dec tubular response to ADH
• Tracheostomy patients
• Nonketotic hyperosmolar dehydration in diabetics secondary to severe
dehydration caused by diuresis and glcosuria
• Clinical manifestations is caused by intracellular dehydration. Pt is thirsty,
irritable, restless,disoriented eventually leading to coma,convulsions, and
even death as serum Na rises to 160mmol/l
• Brain dehydration leads to dec intracranial pressure causing headache, and
when severe can lead to dilatation of intracerebral vessels and eventual
tear/ rupture- cerebral hg is frequent finding in pts dying of hypernatremia
• Treatment is giving adequate volumes of water by mouth or as IV 5%
dextrose. Correction takes 1-2 days
HYPOKALEMIA
The kidney does not conserve K like Na
There is a constant urinary loss of 40-60 mmol K / day
Normal serum K of 4mmol/l is needed for proper function of muscle- skeletal,
cardiac and smooth
Skeletal- muscle weakness, paresthesia, flaccid paralysis when K<3
Cardiac- hypotension, bradycardia, arrythmias, ECG- flat / inverted T waves,
prominent U waves, dep S-T segment
Smooth- decreased intestinal motlity, paralytic ileus, abd distention
Hypokalemic periodic paralysis- after exercise, heavy CHO meal
A deficit of 4-5mmol/l /kg exists for each 1mmol decrease in serum K
Only an emergency when K<2
Can be corrected over 1-2 days If oral is tolerated this is safest – diet rich in
fruits.
Check if renal function is normal
IV K should not exceed 20mmol/hr in thru a peripheral line at a concentration
not greater than 40mmol/L of normal or ½ normal saline with ecg monitering
HYPERKALEMIA
ACS/WASH MAN/Currentdiag07
Usually ass with renal impairment
Caused by
•
Metabolic acidosis
•
Overaggressive K replacement
•
Transcellular shift- tumour lysis, rhabdomyolysis
•
Pseudohyperkalemia- due to lysis of RBCs during venepuncture / transport
Affects cardiac function- bradycardia, hypotension, vent fibrillation, cardiac arrest as K reaches
7mmol/l
ECG changes- peaked T waves, prolonged PR interval and widening of QRS complex, loss of P
waves,
Emergency which needs rapid treatmentStop all K
Give IV
cal gluconate-10ml of 10% soln over 2 min. Immediate, effect lasts1hr
50ml of 50% dextrose + 10 units insulin over 30min K will drop by1mmol/l in 15min and effect lasts
sev hrs
HCO3- 3 ampoules in 1litre 5%dextrose if pt not overhydrated
Frusemide
Salbutamol nebuliser-beta2 agonist therapy. Lowers K by 1mmol in 30min and lasts3 hrs
Cation exchange resins- retention enema- 50gm in150 ml tapwater or 50gm in 100ml of 20% sorbitol
orally. Lowers K by 1mol in 1hr and lasts 6hrs
Anion Gap
ACS
• In any biological system in which ions are
present , electrical neutrality is maintained by the
total # of cations with the total # of anions
• This principal is utilised clinically in patients with
suspected acid base disorders by measuring the
serum sodium, chloride and bicarbonate
concentrations.
• Normally the extracellular conc of Na+ = the
extracellular conc of Cl- + HCO3- + a constant
designated as delta
Mmol Na = mmol Cl- + mmol HCO3- +
Where delta
= 8 +/- 4 mmol/l
ACID BASE BALANCE ACS
• Enormous amount of acid is produced everyday
from daily metabolism
• Oxidation of CHO and fats produce 15,00020,000 mmols of volatile acid as CO2
• Breakdown of sulphur containing aminoacids
and incomplete oxidation of CHO & fats produce
60-70 mmols of fixed acid
• Normally this H+ produced does not change in
extracellular pH from its normal value of 7.4(+/0.2) because of intracellular buffers, pulmonary
and renal mechanisms
• Intracellular buffers are phosphates and proteins
• Extracellular buffers are haemoglobin, proteins
and the bicarbonate- carbonic acid system
ACID BASE BALANCE ACS
• Normally the body keeps the ph at 7.4 by
maintaining the bicarbonate(HCO3) to carbonic
acid (H2CO3) ratio at 20 to 1
HCO3 = 20
H2CO3
1
Increase in the ratio will produce alkalosis ( inc pH)
and decrease will produce acidosis ( dec pH)
Carbonic acid behaves as an acid or as the
neutral gas carbon dioxide and is expressed by
the following equation:
CO2+H2O<->H2CO3 <-> H +HCO3Where formation of carbonic acid from carbon
dioxide or reversion of carbonic acid to water
and carbon dioxide will depend on the acid-base
status
+
ACID BASE BALANCE
H +HCO3- <->H2CO3 <-> CO2+H2O
When acid is added to the system bicarbonate conc will
decrease with a corresponding drop in the
HCO3/H2CO3 ratio <20/1
To combat this ventilation is increased and the newly
formed carbonic acid is quickly converted to CO2 and
blown off by the lungs, thereby reestablishing the ratio.
If alkali is added to the system the HCO3 increases and the
reverse occurs and CO2( and hence carbonid acid) is
retained by the lungs through a decrease in ventilation
and an increased excretion of HCO3 by the kidneys
+
ACID BASE BALANCE-ACIDOSIS
ACS
Respiratory Acidosis- When normal resp is
depressed as in airway obstruction,
hypoventilation, pneumonia, pneumothorax,
asthma, heavy sedation, emphysema, pleural
effusion CO2 is retained increasing Pco2 >
45mmHg, pH decreases. The kidney attempts to
compensate by increasing HCO3 absorption and
H+ excretion
Patient needs ventilatory assistance- intubation
and ventilation to blow off the CO2
Metabolic Acidosis
Metabolic Acidosis- Here there is a deficit of HCO3 due to excessive
acid production eg diabetes with excessive ketone formation or
• renal disease ( inadequate excretion of inorganic acids like
phosphate and sulphate) or
• when there excessive loss of bicarbonate as in diarrhoea,
pancreatic or enterocutaneous fistula or
• Lactic acidosis secondary to shock when anaerobic glycolysis
results in accumulation of lactic acid
Acidosis is dangerous as it
1. decreases myocardial contractility causes a reduction in cardiac
output,
2. decreases responsiveness of peripheral vessels to circulating
cathecholamines causing hypotension and
3. increases refractoriness of the fibrillating heart to defibrillation
making cardiac resuscitation difficult
ACID BASE BALANCE-ALKALOSIS
Alkalosis is better tolerated than acidosis and is fact the most common
acid base abnormality seen in the early postop period.
This is due to post traumatic aldosteronism stimulated by volume
reduction causing retention of Na and HCO3 and secretion of K,
hyperventilation secondary to pain and anxiety and nasogastric
suction causing loss of acid.
Respiratory Alkalosis- Secondary to hyperventilation usually abates when
pain and anxiety subsides. When secondary to hypoxemia it may need
ventilatory support. It results in hypokalemia as extracellular K moves
intracellularly. Hypocapnea results in cerebral vasoconstriction
Metabolic Alkalosis – results from nasogastric suction with loss of H+.(
hypocholeremic, hypokalemic alkalosis) As a result of hypovolemia
the kidney reabsorbs Na exchanging it for K and H – thus resulting in
acid urine – paradoxical aciduria