fluid pdf - د. بسام

Third stage

Surgery

Lec-1-2

.د

سام

1/1/2014

Fluid & Electrolytes balance

Functions of Fluids



Move electrolytes and oxygen into and out of cells as needed.



Aid digestion.



Cleanse the body of waste.



Regulate body temperature.



Lubricate joints and mucous membranes.

Compartments of Body and Distribution of Water by Weight



60 % Water

o  Plasma 5%
o  Interstitial 15%
o  Intracellular 40%



40% Solids

o fat, protein, carbohydrates, minerals

Total Body Water



Approximately 60% of body weight (males)



Approximately 50% of body weight (females)



Approximately 75% in newborns (less body fat)



Obese/elderly decrease above by 10%



To calculate TBW (L) = Current wt (kg) x 60%

• Fluid compartments are separated by membranes that are freely permeable to water

– but impermeable to solutes.

• Movement of fluids is due to:

– hydrostatic pressure differentials

– osmotic pressure differentials

Fluid Balance

Solute Homeostasis

• Electrolytes – charged particles

– Cations – positively charged ions

• Na

, K

, Ca

, H

– Anions – negatively charged ions

• Cl

, HCO

, PO

• Non-electrolytes - Uncharged particles

• Proteins, urea, glucose, O

, CO

Giving IVF

• Normal body fluid and composition

• Daily requirement of the body

• Changes and losses

•

Fluids to be given

Daily requirement

• Size : 1.5 l H2O/M2 of the surface area24 hours

• Weight : 35ml/Kg/24 hours

Intravenous Fluids

Crystalloids

• Hypertonic

• Isotonic

• Hypotonic

Colloids

• Albumin

• Dextrans

Crystalloids

NS:

154 Na+

154 K+

5% dextrose

278mmol/l dextrose

GS (0.18%saline, 4%dextrose) 30 Na 30Cl- 222 mmol/l dextrose

Hartman’s

131 Na+

5 K+ 29mmol/l HCO3

111 mmol/l CL-

2mmol/l Ca++

Ringer’s

147 Na

4 K+

156 Cl-

2.2 mmol/l Ca++

Colloids

Synthetic, commercially prepared volume expanders containing polysaccharide molecules
(sugar & starch)

Albumin (5% and 25%)

10% Dextran 40 and 6% Dextran 70

Prescribing fluid regime

• It depend on :

• Basal requirements

• Continuous abnormal losses over and above basal requirement

• Pre-existing dehydration and electrolyte loss

1. Basal requirement

• 2000 cc 5% GW + 500 cc 0.9% saline

• 2000 cc 5% GW + 500 cc hartman’s

• 2500( 4% GW 0.18% saline)

• Adding to this K+ 1mmol/kg

• Each 1 cc contains 2 meq of K+

2. Replacing ONGOING LOSS

FROM:

o  Nasogastric tube
o  Drains
o  Evaporation during operation
o  Blood loss
o  Paracentesis
o  Thoracocentesis

3. Pre-existing dehydration

A. Assessment:

o  history:(thirst, intake out put, check the chart)
o  examination: (mucus mm, eye, skin, UOP, HR, BP, capillary refilling, confusion)
o  haematocrit, S.albumin. B. urea, S.electrolyte
o  Central venous pressure(3-8 mmH2O), PCWP (5-12 mmHg)

B. correction:

o identify the compartment the fluid has been lost from(bowel losses come from ECF,

pure water loss from TBW, protein containing fluid from plasma)

o fluid replacement should be similar to that which has been lost

Electrolyte balance

(Sodium)

o  Predominant extracellular cation
o   136 -145 mEq / L
o  Pairs with Cl- , HCO3- to neutralize charge
o  Most important ion in water balance

o Important in nerve and muscle function

• Reabsorption in renal tubule regulated by:

o  Aldosterone
o  Renin/angiotensin
o  Atrial Natriuretic Peptide (ANP)

K + (Potassium)

o  Major intracellular cation
o  150- 160 mEq/ L
o  Regulates resting membrane potential
o  Regulates fluid, ion balance inside cell

• Regulation in kidney through:

o Aldosterone
o Insulin

Cl ˉ (Chloride)

o  Major extracellular anion
o  105 mEq/ L
o  Regulates tonicity
o  Reabsorbed in the kidney with sodium

• Regulation in kidney through:

o Reabsorption with sodium
o Reciprocal relationship with bicarbonate

Hypernatremia

o  Plasma Na+ > 145 mEq / L
o  Due to ↑ Na + or ↓ water
o  Water moves from ICF → ECF
o  Cells dehydrate

Due to:

o  Excess Na intake (hypertonic IV solution)
o  Excess Na retention (oversecretion of aldosterone)
o  Loss of pure water



Long term sweating with chronic fever



Respiratory infection → water vapor loss



Diabetes (mellitus or insipidus) – polyuria

o Insufficient intake of water (hypodipsia)

Clinical manifestations of Hypernatremia:

o  Thirst
o  Lethargy
o  Irritability
o  Seizures
o  Fever
o  Oliguria

Treatment of Hypernatremia:

o Calculate the free water deficit:

0.6 x wt (kg) x (patient’s sodium/140 - 1)

o  Correct the free water deficit at a rate of 1mEq/L/hr
o  Check serum Na every 4hr
o  Use isotonic salt-free IV fluid

Hyponatremia

Symptoms and signs

o  Anorexia
o  Headache
o  Nausea
o  Emesis
o  Impaired response to verbal stimuli
o  Impaired response to painful stimuli
o  oliguria
o  Bradycardia
o  Hypertension or hypotension
o  Altered temperature regulation
o  Hypotension
o  Renal failure as consequence of hypotension
o  Tachycardia
o  Weakness
o  Muscular cramps

Hypovolemic hyponatremia

o Renal losses caused by diuretic excess, osmotic diuresis, salt-wasting nephropathy,

adrenal insufficiency, proximal renal tubular acidosis, metabolic alkalosis, and
pseudohypoaldosteronism result in a urine sodium concentration greater than 20
mEq/L

o Extrarenal losses caused by vomiting, diarrhea, sweat, and third spacing result in a

urine sodium concentration less than 20 mEq/L

o Rx: Volume resuscitation with NS

Normovolemic hyponatremia

o When hyponatremia is caused by SIADH, reset osmostat, glucocorticoid deficiency,

hypothyroidism, or water intoxication, urine sodium concentration is greater than 20
mEq/L

o Rx: Fluid restriction, Correct endocrine abnormality

Hypervolemic hyponatremia

o If hyponatremia is caused by an edema-forming state (eg, congestive heart failure,

cirrhosis, nephrotic syndrome), urine sodium concentration is less than 20 mEq/L

o If hyponatremia is caused by acute or chronic renal failure, urine sodium concentration

is greater than 40 mEq/L

o Rx: Correct underlying state

Treatment of Hyponatremia

o  Correct serum Na by 1mEq/L/hr
o  Check serum Na q4hr
o  Use 3% saline in severe hyponatremia
o  Goal is serum Na 130
o  Avoid too rapid correction:

– Central pontine myelinolysis
– Flash pulmonary edema

Acute Hyponatremia

o Na < 120 and duration < 48 hrs
o Etiology:

–  Postoperative
–  Exercise with hypotonic fluid replacement
–  Drugs - Ecstasy

o Treat aggressively using 3% saline to raise Na by 5mm/L in one hour
o Beware rapid drop in vasopressin levels

Hypochloremia

o Most commonly from gastric losses

– Emesis, gastric suctioning, EC fistula

o Often presents as a contraction alkalosis with paradoxical aciduria (Na+ retained and

H+ wasted in the kidney)

o Rx: resuscitation with normal saline

Hyperchloremia

o Most commonly from over-resuscitation with normal saline
o Often presents as a hyperchloremic acidemia with paradoxical alkaluria (H+ retained

and Na+ wasted in the kidney)

o Rx: stop normal saline and replace with hypotonic crystalloid

Hypokalemia

o Serum K+ < 3.5 mEq /L
o Beware if diabetic

– Insulin pushes K+ into cells
– Ketoacidosis – H+ replaces K+, which is lost in urine

o β – adrenergic drugs or epinephrine

Causes of Hypokalemia

o Decreased intake of K+
o Increased K+ loss

–  Chronic diuretics
–  Severe vomiting/diarrhea
–  Acid/base imbalance
–  Trauma and stress
–  Increased aldosterone
–  Redistribution between ICF and ECF

Clinical manifestations of Hypokalemia

o  Neuromuscular disorders
o  Weakness, flaccid paralysis, respiratory arrest, constipation
o  Dysrhythmias, appearance of U wave
o  Postural hypotension
o  Cardiac arrest

Rx- Increase K+ intake, but slowly, preferably by foods

Hyperkalemia

o  Serum K+ > 5.5 mEq / L
o  Check for renal disease
o  Massive cellular trauma
o  Insulin deficiency
o  Addison’s disease
o  Potassium sparing diuretics

o Decreased blood pH
o Exercise pushes K+ out of cells

Clinical manifestations of hyperkalemia:

o  Early – hyperactive muscles , paresthesia
o  Late - muscle weakness, flaccid paralysis
o  Peaked T-waves
o  Dysrhythmias
o  Bradycardia, heart block, cardiac arrest

Management:

o  10% Calcium Gluconate or Calcium Chloride
o  Insulin (0.1U/kg/hr) and IV Glucose
o  Frusemide 1mg/kg (if renal function is normal)
o  Hemodialysis

Calcium Imbalances

o Most in ECF
o Regulated by:

– Parathyroid hormone

 ↑Blood Ca

by stimulating osteoclasts

 ↑GI absorption and renal retention

– Calcitonin from the thyroid gland

 Promotes bone formation
 ↑ renal excretion

Hypercalcemia

Results from:

o  Hyperparathyroidism
o  Hypothyroid states
o  Renal disease
o  Excessive intake of vitamin D
o  Milk-alkali syndrome
o  Certain drugs
o  Malignant tumors – hypercalcemia of malignancy

– Tumor products promote bone breakdown
– Tumor growth in bone causing Ca++ release

Effects:

o  Many nonspecific – fatigue, weakness, lethargy
o  Increases formation of kidney stones and pancreatic stones
o  Muscle cramps
o  Bradycardia, cardiac arrest
o  GI activity also common

– Nausea, abdominal cramps
– Diarrhea / constipation

Treatment:

o  Duiresis
o  Calcitonin , mithramycine and corticosteroid.
o  Specific treatment of parathormone producing focus.

Hypocalcemia

o Hyperactive neuromuscular reflexes and tetany differentiate it from hypercalcemia
o Convulsions in severe cases

Caused by:

o  Renal failure
o  Lack of vitamin D
o  Suppression of parathyroid function
o  Hypersecretion of calcitonin
o  Malabsorption states
o  Abnormal intestinal acidity and acid/ base bal.
o  Widespread infection or peritoneal inflammation

Diagnosis:

o Chvostek’s sign
o Trousseau’s sign

Treatment

o IV calcium for acute
o Oral calcium and vitamin D for chronic

Water homeostasis

acid and base regulation

Regulation of body water

Any of the following:

• Decreased amount of water in body

• Increased amount of Na+ in the body

• Increased blood osmolality

• Decreased circulating blood volume

Results in:

• Stimulation of osmoreceptors in hypothalamus

• Release of ADH from the posterior pituitary

• Increased thirst

And thus: water consumption and conservation

Transport of Water and Fluids



Osmolality: concentration of a solution determined by the number of dissolved
particles per kilogram of water. Osmolality controls water movement and distribution
in body fluid compartments



Diffusion: the random movement of particles in all directions through a solution



Active transport: movement of solutes across membranes; requires expenditure of
energy



Filtration: transfer of water and solutes through a membrane from a region of high
pressure to a region of low pressure



Osmosis: movement of water across a membrane from a less concentrated solution to
a more concentrated solution

Fluid shifting:



1st space shifting- normal distribution of fluid in both the ECF compartment and ICF
compartment.



2nd space shifting- excess accumulation of interstitial fluid (edema)



3rd space shifting- fluid accumulation in areas that are normally have no or little
amounts of fluids (ascites)

Water depletion

This occur due to:

Insufficient intake of water and electrolytes:



Impaired thirst mechanism



Inability to swallow fluids

Excessive fluid loss through secretions or excretions:



Potent diuretic therapy



Diabetes insipidus



Fluid losses from GI tract



Excessive sweating

Clinical signs and symptoms:



Intense thirst



Acute weight loss



Decreased skin turgor, Dry mucous membranes, Rough, dry tongue



Changes in behavior :agitation, restlessness, weakness



Flat neck veins in supine position



Weak thready pulse



Orthostatic hypotension



oliguria

Treatment:



Since a fluid volume deficit decreases blood flow to kidneys, treatment must begin
promptly to prevent damage to kidneys.



If fluids cannot be ingested, isotonic IV fluids (.9% NaCL and D5W) are given
initially. Electrolytes are added to IV solution if adequate renal function is present
(Lactated Ringer solution)

Water excess (intoxication)

Overloading body with sodium:

Excessive administration of IV fluids, especially hypertonic solutions

Altered homeostatic regulation of sodium and water:



Chronic renal failure



Congestive heart failure



Excessive corticosteroid therapy



Syndrome of inappropriate secretion of ADH (SIADH)

Clinical signs and symptoms:



Acute weight gain



Peripheral edema



Shortness of breath ( rales in lungs)



Changes in behavior : confusion, lethargy, weakness



Distended neck veins



Full, bounding pulse



Elevated BP

Treatment:



Fluid restriction



Dietary Na+ restriction



Diuretic therapy

Volume Abnormalities

Edema

The accumulation of fluid within the interstitial space

Results in:



increased distance for diffusion



impaired blood flow



slower healing



increased risk of infection



pressure sores over bony prominences



impaired organ function (brain, liver, gut, kidney)

Causes:



increased hydrostatic pressure  venous obstruction, lymphedema, CHF, renal
failure



lowered plasma osmotic pressure (protein loss)  liver failure, malnutrition, burns



increased capillary membrane permeability  Inflammation, SIRS, sepsis

Acid–Base Balance



Body produces large amounts of acid from normal metabolic processes, such as
breakdown of proteins and glucose or oxidation of fat



Body fluids remain slightly alkaline



pH is maintained within a narrow range: 7.38 to 7.42



Regulatory mechanisms maintain pH



Neutralize and eliminate the acids as soon as they are produced to maintain normal
pH

– Blood buffers: resist pH change
– Lungs: control carbonic acid (H

)concentration

– Kidneys: control bicarbonate concentration

“Board-and-fulcrum” concept of normal
bicarbonate-carbonic acid relationships

Blood Buffer System



Respiratory control of carbonic acid

–  Carbonic acid (H2CO3): dissolved as CO2 in plasma
–  Hyperventilation: lowers CO2 and H2CO3 in plasma
–  Decreased or inadequate ventilation: raises CO2 and H2CO3 in plasma



Renal control of bicarbonate concentration

– Kidneys selectively reabsorb filtered bicarbonate
– Kidneys can manufacture bicarbonate to replace amounts lost in buffering acids

from metabolic processes



In any buffer system

– pH depends on ratio of bicarbonate to H2CO3
– Normal ratio: 20 parts Na bicarbonate: 1 part H2CO3

Classification of Acid–Base Disturbances



Metabolic acidosis: increased endogenous acid generated

–  Amount of acid generated exceeds body’s buffering capacity
–  Excess acid is neutralized by bicarbonate
–  Bicarbonate in plasma falls from being consumed in neutralizing excess acid
–  Uremia, ketosis, lactic acidosis



Compensation: by hyperventilation to lower PCO2 and increased bicarbonate
production in kidneys

Metabolic acidosis



Result from primary disturbance of a decreased HCO3 or increased H+ leading to
decrease in pH and a compensatory decrease in PaCO2



Causes:

–  renal glomerular failure
–  salicylate overdose
–  Ketoacidosis (diabetic or alcoholic)
–  renal tubular acidosis
–  ureterosigmoidostomy
–  excess acid intake (TPN)
–  bicarbonate loss(diarrhea, fistula, proximal renal tubular acidosis)

Metabolic alkalosis



Result from primary disturbance of an increase in HCO3 or decrease in H+ leading to
increase in pH and a compensatory increase in PaCO2



Causes:

– excess alkaline intake

• alkali abuse
• over treatment of acidosis

– excessive loss of acid

• vomiting in pyloric stenosis

– increase urinary acidification

•  diuretics
•  excess aldosterone
•  hypokalaemia

Respiratory acidosis



Primary disturbance of increase PCO2 leading to decrease pH and compensatory
increase in HCO3



causes:

– depression of respiratory centre

•  CVA
•  tumors
•  drugs(narcotic,sedative)
•  encephalitis

– decreased chest wall movement

•  neuromuscular disorder(MG)
•  trauma, surgery
•  ankylosing spondylitis

– pulmonary disease(type 2 respiratory failure)

• COAD
• pneumonia

Respiratory alkalosis



Primary disturbance of a decreased PaCO2 leading to an increase in pH and a
compensatory decrease in HCO3



causes:

– stimulation of respiratory centre

•  CVA,encephalitis
•  htpermetabolic state(fever, sepsis, thyrotoxicosis)
•  excersize
•  hypoxia

– exess mechanical ventilation(by patient or ventilator)

• anxiety
• drug(aspirin)

Treatment of acid base disturbances



Treat the underlying cause



Give sodium bicarbonate(8.4%) in metabolic acidosis due to uraemia, diarrhea and
renal tubular acidosis but in other conditions is controversial.

Diagnostic Evaluation of Acid–Base Balance



Clinical evaluation: determination of concentration of bicarbonate in plasma as an
index of patient’s overall status



Laboratory studies
– Blood pH
– PCO

– Bicarbonate