FLUID & ELECTROLYTE BALANCE

Prof. M. H. Mumtaz

BALANCE

Water Balance

Elecrolyte Balance

Acidbase Balance

Nutritional Balance

FLUID & ELECTROLYTE BALANCE

Intke & loss routes. Distribution of water and electrolytes. Physiological control of water and

sodium. Assessment of balance. Physiological response to pathological

conditions. Practical approach to therapy.

NORMAL ROUTES

INTAKE

Food Drink Metabolic

OUTPUT

Urine Stool Sweat Respiration

PATHOLOGICAL ROUTES

Intravenous Nasogastric aspiration

Enterostomy Colostomy

RENAL LOSS

FILTERATION

REABSORPTION

FILTERATION

WATER 180L/24h 125mls/min 7.5/hr 4xBW =15xECF

=60xPV

SODIUM 30000mmol/24hr 18125Ueq/min

REABSORPTION

WATER 75%PT 5%L 15%DT 4-4.86%CT Urine 1ml/kg/hr

SODIUM CI 14585Ueq HCO3 3375Ueq PO4 NH3 50Ueq K+ 50Ueq Total – 18060Ueq

24-HRS RENAL DEALING

Mmol Filtered Reabsorbed Secreted Excreted Location

Na+ 26000 25850 150 PLDC

K+ 900 900 100 100 PD

Cl- 18000 17850 150 PLDC

HCO3 4900 4900 PD

Urea 870 460 410 PLDC

Creatinin 12 1 1 12

Uric acid 50 49 4 5 P

Glucose 800 800 P

Total 51532 50810 105 827 PLDC

SECRETION IN GUT

SALIVARY– Quantitiy 1500/24 hrs.

GASTRIC– Quantitiy 3000/24 hrs.

BILIARY– Quantitiy 500/24 hrs.

PANCREATIC– Quantitiy 2000/24 hrs.

TOTAL– Quantitiy 7000mls.

FEACAL LOSS

Na+ & H2O secretion Na+ & H2O absorption– Epithelial cells– Duration of contact

H2O secreted > 7000ml Loss = 100-150mls Na+ secreted.– 1500mmols/24hrs– Loss 15mmol/24hrs

LOSS IN SWEAT & EXPIRED AIR

900mls water 30mmols Na Sweat loss.– Temp.– ADH.– Aldosterone

Respiratory loss.– Respiratory rate.– Hamidification.

DISTRIBUTION OF WATER & ELECTROLYTEwater distribution

Total body water 60% of body wt in male Total body water 52% of body wt in female

2/3rd IC

1/3rd EC

66% extravascular

33% intravascular

ELECTROLYTE DISTRIBUTION mmol/L

Subtance Plasma Interstitial F IC

Na+ 141.00 144.00 10.00

K+ 3.70 3.80 156.00

Cl- 102.00 115.00 3.00

HCO-3 25.00 28.00 10.00

Ca++ 2.5 0.00 0.00

Mg++ 0.80 0.00 11.00

PO4-- 1.10 0.00 31.00

IC EC

Sodium Low 100 time

Potassium 30 time more Less

Magnessium Predominantly more

Less

Phosphates Predominantly more

Less

chlorids less Predominantly

PHYSIOLOGIC CONTROL OF SODIUM

Aldosterone (2nd factor) Non aldosterone (factors)– GFR (1st factor)– Renal blood flow.– Oncotic pressure in tubular blood.– Third factor

ANGIOTENSINOGEN

ANGIOTENSIN I

ANGIOTENSIN II

ANGIOTENSIN III

LIVER 2 GLOBULIN

FROM KIDNEY & ELSEWHERE

DECAPEPTIDE

IN LUNG

OCTAPEPTIDE

INACTIVE METABOLITESINACTIVE METABOLITES

HEPTAPEPTIDE

AMINOPEPTIDE

CONVERTING ENZYME

RENIN

RENIN ANGIOTENSIN SYSTEM

Indomethacin

B. Blocker

Peptostatin

Captopril

Saralasin

PHYSIOLOGIC CONTROL OF WATER

Intake.– Thirst.

Loss.– ADH– Non ADH factors.

Mannitol. Urea. Glucose.

ADH

Hypothalmic

Cellular arosmolality

Na+ Concentration (Osmolality)

Water

Renal Blood flow

Aldosterone

Angiotensin

Renin

A

B

CONTROL OF WATER IN COMPARTMENTS

INTRAVASCULAR/INTERSTITIAL Proteins – colloid osmotic pressure. Hydrostatic pressure.

INTERSITITAL/INTRACELULAR Osmolality – predominantly – Na+

CONTRIBUTION OF PLASMA CONSTITUENTS TO PLASMA OSMOLARITY

Electrolyte Concentration Osmolality

Na+ anion 135

135

270

K+ anion 3.5

3.5

7

Ca++ anion 2.5

2.5

5

Mg++ anion 1

1

2

Urea 5 5

Gencose 5 5

Protein 70G/L 1

Total 295

THE KINETICS OF PVE

INTRACELLULAR INTERSTITIAL VASCULAR

HP

CAPILLARY

CELL

EG

OSMILALITY

Na+

COP

BLOOD VOLUME

RENINALDOSTE

Na+

Na+

ADH Osmolality

H2O

ASSESSMENT OF BALANCEassessment of state of hydration

History. Helping Tools

Clinical state. 1,CVP

– Blood pressure. 2,T.E.D.

S,D,M, 3,LIDCO/any?

– Heart rate.

– Temperature.

– Skin texture.

ASSESSMENT OF BALANCEassessment of state of hydration

Lab evidence.– Haemoconcentration.

Proteins. Hb. Haematocrit.

– Hemodilution. Protein. Hb. HCT

ASSESSMENT OF IMBALANCE Hypo-osmolality (hyponatraemia)– Cellular overhydration.– Headache.– Confusion.– Fits.– Coma.

Hyper-osmolality (hypernatraemia)– Cellular dehydration.– Thirst.– Confusion.– Coma.– No fits.

HYPOVOLEMIA (ISOMOLOL) Hypotension. Collapse. Haemoconcentration . Low GFR uremia.

HYPERVOLEMIA (ISOMOLOL) Blood pressure. Oedema. Cardiac failure. Haemodilution. Urea.

CLINICAL PRESENTATIONS

Sodium

Mmol/L

125 141 155 120

Proteins L/L

65 45 65 45

DISTURBANCE OF Na+ & H2O METABOLISM

H2O & Na+ Deficiency

I Predominant H2O

depletion.

With homeostasis

Without homeostatis

II Predominant Na+

depletion.

With homeostasis

Without homeostatis

DISTURBANCE OF Na+ & H2O METABOLISMH2O & Na+ Excess

III Predominant H2O

excess.

With homeostasis

Without homeostatis

IV Predominant Na+

excess.

Without homeostatis

PREDOMINANT H2O DEPLETION

WITH HOMEOSTASIS

Excess fluid loss.– Sweat.– Gastric juice.– Stool.– On respirator.– Extensive burns.

Deficient intake.– Inadequate water supply– Mechanical obstruction to

intake.

WITHOUT HOMEOSTASIS

Comatosed patient response to thirst.

Diabetes inspidus. Osmotic diresis. Nephrogenic diabetes

inspidus.

PREDOMINANT H2O DEPLETION

HOMEOSTASIS? Clinical signs.

– Hypernatraemia.– Dehydration.– Oligurea.

Lab. Findings– Hypernatremia & haemacrit.– Mild uraemia

Urine. volume osmolality. SG– Urea increase

CLINICAL FINDINGS Polyrea. Urine of low osmolality. Low SG. Low urea concentration.

UNCONSCIOUS PATIENT water depletion Na+

CAUSES Over breathing.– Pneumonia.– Acidosis.– Brain stem injury.

Inadequate humidification. Hypertonic infusions. Diabetes inspidus. No response to thirst. Infants with gastroenteritis. Infats with bronchopneumonia.

ADH

Hypothalmic

Cellular arosmolality

Na+ Concentration (Osmolality)

Water

Renal Blood flow

Aldosterone

Angiotensin

Renin

A?

B

PREDOMINANT Na+ DEPLETION

WITH HOMEOSTASIS

Vomiting Diarrhoea. Fistula Sweating

Replacement low Na+ homeostasis?

WITHOUT HOMEOSTASIS

Addison disease. Psaudo-addison disease. Renal tubular failure.

PREDOMINANT Na+ DEPLETION

WITH

HOMEOSTASIS Clinical signs.– Hypernatraemia.

Lab. Findings– Hypernatremia vol. of urine

– Haemodilution plasone urea.

– Urinary Na+ excretion.

WITHOUT HOMEOSTASIS

Clinical signs.– Fluid depletion

– Hypo-osmolality.

Lab. Finding Haemo-concentration Renal circulatory

insufficiency uraemia.

ADH

Hypothalmic

Cellular arosmolality

Na+ Concentration (Osmolality)

Water

Renal Blood flow

Aldosterone

Angiotensin

Renin

A

B?

PREDOMINANT H2O EXCESScommonly associated with failure of homeostasis

WITH HOMEOSTASIS

Fluid with low Na+ Homeostasis? Clinical signs.– Hypo-osmolality.

Lab. Findings.– Haemodilution.– Hyponatraemia.

FAILURE OF HOMEOSTASIS

Renal failure. Anappropriate ADH

secretion. Oxytocin drip in 5%

glucose.

PREDOMINANT H2O DEPLETION

Clinical signs.– Hypernatraemia.

Lab. Findings– Hypernatremia vol. of urine

– Haemodilution plasone urea.

– Urinary Na+ excretion.

Clinical signs.– Fluid depletion

– Hypo-osmolality.

Lab. Finding Haemo-concentration Renal circulatory

insufficiency uraemia.

ADH

Hypothalmic

Cellular arosmolality

Na+ Concentration (Osmolality)

Water

Renal Blood flow

Aldosterone

Angiotensin

Renin

A?

B

PREDOMINANT Na+ EXCESSALWAYS FAILURE OF HOMEOSTASIS

Primary aldosteronism (conn’s syndrome).– Cushings syndrome.– Secondary aldosteronism.

Clinical finding (conn’s syndrome)– Volume excess.– Hypertension rarely oedema.– Those of hypokalaemia.

PREDOMINANT Na+ EXCESSALWAYS FAILURE OF HOMEOSTASIS

Lab. Findings.– Hypokaelemia. HCO3. Na+. Urinary Na+ (Hypokalaemia a

lkalosis + BP

Aldo + Renin.

PREDOMINANT Na+ EXCESSALWAYS FAILURE OF HOMEOSTASIS

2ndary aldosteronism. Clinical finding (conn’s syndrome)– As in primary.

Lab. Findings.– Normal Na+ Urinary Na+.– Findings of primary abnormality.– Hypokalaemia – Uraemia.

THERAPYWaterNeonate – 1 month

1st wk 110mls/kg/24hrs.

2nd 3rd wk 120-130mls/kg/24hrs.

1month – 1yr 100mls/kg/24hrs

1yr – 3yrs 90mls/kg/24hrs

3yrs – 7yrs 80mls/kg/24hrs

7yrs – 13yrs 70mls/kg/24hrs

13yrs onwards like adulsts 40-60mls/kg/24hrs

Calculate/hour then/min then drops/min

ELECTROLYTE Na+ 1.5 - 2mmol/kg/24hrs K+ 1 - 1.52mmol/kg/24hrs Ca++ as requried Mg 0.5mmol/GN2 loss PO4 0.5mmol/kg/24hrs Na+ 1.5 - 2mmol/kg/24hrsDAILY CALCULATIONS1st day – Per kg wtSubsequent days = weighting

= previous Out P+500mls

THERAPY DURING OPERATION Daily fluid requirement. Hb correction. Blood loss.– Newborn >10% of blood volume.

– Adults >15% of blood volume.

HB correctionNormal Hb of that age – Hb of patient x blood volume.

Blood volume– Premature 85-90mls/kg.

– Newborn 80-85mls/kg.

– Adults 75-80mls/kg.

THERAPY DURING OPERATION

CONTROVERSIAL?

Benefit No renal failure.

Drawback Blood coaguability

PHYSIOLOGICAL RESPONSE

TO

Stress – Surgery

Stress – Anaesthesia

ADH

Aldosterone

Renin

Retention of

H2O + Na+

Loss of K+

2 – 4 days

MANAGEMENT GUIDELINES

Intr-operative– Hartmann’s solution

or

Ringolact solution– Blood to maintain Hb>10g/dl

Exceptions– Septicaemia.– Lung trauma. PAWP

15ml/kg/hr

POSTOPERATIVE PERIOD

24 – 48 HRS.

dextrose/ saline = 30ml/kg/day

+

30mmol K+/L

– Replace specific losses.

– Maintain urine output>0.5ml/kg/hr.

POSTOPERATIVE PERIOD AFTER 48 HRS– Add Na+– 4% D/W 0.18% saline 30ml/kg/day.

or

5% D/W 7ml/kg/day

+

Normal aline 23ml/kg/day.– Assess serum K+ level.– Consider parentral nutrition.

CHOICE OF FLUIDS

COLLOIDS

Blood in different forms.

Plasma. Plasma substitutes.

CRYSTALLOIDS

Na+ containing fluids.

Na+ free fluids. Hyper-osmolar

solution.

PLASMA

Dried plasma.

FFP.

Plasma protein fraction.

Albumin.

Drid fibrinogen.

Cryoprecipitate.

PLASMA SUBSTITUTES

Dextran.

Gelatin preparations

Polyvinyl pyrolidone

HES

MONITORING

CVS.

Respiratory System.

Renal System.

CNS.

Lab Results.

Helping tools for assessment

1, CVP

2, TED

3, LIDCO

HYPERNATRAEMIA

MANAGEMENT

Definition

Na > 145 mmol/L

Clinical presentation

Na 158—160 mmol/L

Acute /chronic onset

CAUSES

1,Associated with hypovolaemia

2,Associated with hypervolaemia

3,Associated with euvolaemia

CAUSES

Associated with hypovolaemia &

dehydration

1,Dermal loss

2,GI loss

3,Urine loss,diuretics

4,Post obstriction

5,Hyperosmolar- non ketotic coma

CAUSES

Associated with hypervolaemia

Iatrogenic

Hyperaldosteronism

Excess salt ingesation

CAUSES

Associated with euvolaemia

Diabetes inspidus

Hypodipsia

Fever

Hyperventilation

Mechanical ventilation

Clinical presentation

Hyper-osmolarity leads to;

Confusion

Somnolence

Coma

Death

MANAGEMENT

AIMS

Diagnose & treat underlying cause

Correct Hyper-tonicity

MANAGEMENT

INITIAL assessment &investigation

1,Hydration status

2,Consider causes

3,Cause unclear, measure

Urine osmolality

Urine Na concentration

Correction of Hypernatraemia

1, If rapid development in hours ,rapid

correction ie reduce 1 mmol/L/ hour

2,If slow development ie in days, slow

correction, target 10 mmol/L/day

3,Only hypotonic fluids used

4.Correct shock with 0.9% saline

5,Where hypertonic Na gain with overload ,use diuretics +5% Dext.

CORRECTION

6,Determine,

Fluid requirement-water deficit

Required Na fall

Appropriate infusate

Rate of infusion

7,Recheck electrolytes frequently

WATER DEFICIT

Water deficit=

total body water *(1-(140/serumNa) )

Effect of 1L of infusate on serum Na =

;Change in serum Na mmol/L =

(infusate Na-Serum Na/ TBW)

How to drop Na 1 mmol/L/H

Total body water= Body Wt.*60/100

= 70Kg * 60/100= 42 L

ECF = 1/3 rd of 42L = 14 L

EC Na Excess = 14 L (Na excess/L)

= 14 L ( 160-140)

= 14*20 = 280 mmol

How to drop Na 1mmol/L/H

Total Na Excess in ECF=160-140=20*14=280 Total amount of fluid required to lower Na =280/140=2L Rate 1mmol/L/H=14mmol/H in ECF Time required to lower 280 mmol=280/14 =20 hours Rate of fluids to lower 280 mmol Na in 20 hours at the rate of 1mmol/h =2L/20 h =100 mls/hour Type of fluid=5% dextrose in water