fluid

Fluid & Electrolytes balancelecture 1

Dr. Bassam K. Al-Hajjar
Specialist Pediatric Surgeon (F.I.B.M.S-ped. surg.)

Functions of Fluids

1. Move electrolytes and oxygen into and out of cells as needed. 2. Aid digestion. 3. Cleanse the body of waste. 4. Regulate body temperature. 5. Lubricate joints and mucous membranes.

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%

* Total body water (TBW)

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 *

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Fluid Balance



Solute Homeostasis
Electrolytes – charged particlesCations – positively charged ionsNa+, K+ , Ca++, H+Anions – negatively charged ionsCl-, HCO3- , PO43-Non-electrolytes - Uncharged particlesProteins, urea, glucose, O2, CO2 *

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

Parentral fluids

CrystalloidsNS: 154 Na+154 K+5% dextrose278mmol/l dextroseGS (0.18%saline, 4%dextrose)30 Na30Cl-222 mmol/l dextroseHartman’s131 Na+5 K+29mmol/l HCO3111 mmol/l CL-2mmol/l Ca++Ringer’s147 Na4 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% saline2000 cc 5% GW + 500 cc hartman’s2500( 4% GW 0.18% saline)Adding to this K+ 1mmol/kgEach 1 cc contains 2 meq of K+

2. Replacing ONGOING LOSS

FROM: Nasogastric tube Drains Evaporation during operation Blood loss Paracentesis Thoracocentesis

3. Pre-existing dehydration

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

B. correction: identify the compartment the fluid has been lost from(bowel losses come from ECF, pure water loss from TBW, protein containing fluid from plasma) fluid replacement should be similar to that which has been lost

Electrolyte balance

Na + (Sodium) Predominant extracellular cation 136 -145 mEq / L Pairs with Cl- , HCO3- to neutralize charge Most important ion in water balance Important in nerve and muscle function Reabsorption in renal tubule regulated by: Aldosterone Renin/angiotensin Atrial Natriuretic Peptide (ANP)

Electrolyte balance

K + (Potassium) Major intracellular cation 150- 160 mEq/ L Regulates resting membrane potential Regulates fluid, ion balance inside cell Regulation in kidney through: Aldosterone Insulin

Electrolyte balance

Cl ˉ (Chloride)Major extracellular anion105 mEq/ LRegulates tonicityReabsorbed in the kidney with sodiumRegulation in kidney through:Reabsorption with sodiumReciprocal relationship with bicarbonate


Hypernatremia Plasma Na+ > 145 mEq / LDue to ↑ Na + or ↓ waterWater moves from ICF → ECFCells dehydrateDue to:Excess Na intake (hypertonic IV solution)Excess Na retention (oversecretion of aldosterone)Loss of pure waterLong term sweating with chronic feverRespiratory infection → water vapor lossDiabetes (mellitus or insipidus) – polyuriaInsufficient intake of water (hypodipsia) *

Clinical manifestationsof Hypernatremia

Thirst Lethargy Irritability Seizures Fever Oliguria
*

Treatment of Hypernatremia

Calculate the free water deficit:0.6 x wt (kg) x (patient’s sodium/140 - 1)Correct the free water deficit at a rate of 1mEq/L/hrCheck serum Na every 4hrUse isotonic salt-free IV fluid *

HyponatremiaSymptoms and signs

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

Hyponatremia

Hypovolemic hyponatremia 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 Extrarenal losses caused by vomiting, diarrhea, sweat, and third spacing result in a urine sodium concentration less than 20 mEq/L Rx: Volume resuscitation with NS

Hyponatremia

Normovolemic hyponatremia When hyponatremia is caused by SIADH, reset osmostat, glucocorticoid deficiency, hypothyroidism, or water intoxication, urine sodium concentration is greater than 20 mEq/L Rx: Fluid restriction Correct endocrine abnormality

Hyponatremia

Hypervolemic hyponatremia 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 If hyponatremia is caused by acute or chronic renal failure, urine sodium concentration is greater than 40 mEq/L Rx: Correct underlying state

Treatment of Hyponatremia

Correct serum Na by 1mEq/L/hr Check serum Na q4hr Use 3% saline in severe hyponatremia Goal is serum Na 130 Avoid too rapid correction: Central pontine myelinolysis Flash pulmonary edema
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Acute Hyponatremia

Na < 120 and duration < 48 hrs Etiology: Postoperative Exercise with hypotonic fluid replacement Drugs - Ecstasy Treat aggressively using 3% saline to raise Na by 5mm/L in one hour Beware rapid drop in vasopressin levels
*

Hypochloremia

Most commonly from gastric losses Emesis, gastric suctioning, EC fistula Often presents as a contraction alkalosis with paradoxical aciduria (Na+ retained and H+ wasted in the kidney) Rx: resuscitation with normal saline

Hyperchloremia

Most commonly from over-resuscitation with normal saline Often presents as a hyperchloremic acidemia with paradoxical alkaluria (H+ retained and Na+ wasted in the kidney) Rx: stop normal saline and replace with hypotonic crystalloid

Hypokalemia

Serum K+ < 3.5 mEq /LBeware if diabeticInsulin pushes K+ into cellsKetoacidosis – H+ replaces K+, which is lost in urineβ – adrenergic drugs or epinephrine *


Causes of Hypokalemia
Decreased intake of K+ 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

Neuromuscular disorders Weakness, flaccid paralysis, respiratory arrest, constipation Dysrhythmias, appearance of U wave Postural hypotension Cardiac arrest Rx- Increase K+ intake, but slowly, preferably by foods
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Hyperkalemia

Serum K+ > 5.5 mEq / LCheck for renal diseaseMassive cellular traumaInsulin deficiencyAddison’s disease Potassium sparing diureticsDecreased blood pHExercise pushes K+ out of cells *

Clinical manifestations of hyperkalemia

Early – hyperactive muscles , paresthesiaLate - muscle weakness, flaccid paralysisPeaked T-wavesDysrhythmiasBradycardia, heart block, cardiac arrest *

HyperkalemiaManagement

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

* Calcium Imbalances

Most in ECFRegulated by:Parathyroid hormone↑Blood Ca++ by stimulating osteoclasts↑GI absorption and renal retentionCalcitonin from the thyroid glandPromotes bone formation↑ renal excretion


* Hypercalcemia
Results from:Hyperparathyroidism Hypothyroid statesRenal diseaseExcessive intake of vitamin DMilk-alkali syndromeCertain drugsMalignant tumors – hypercalcemia of malignancyTumor products promote bone breakdownTumor growth in bone causing Ca++ release

* Hypercalcemia

Effects:Many nonspecific – fatigue, weakness, lethargyIncreases formation of kidney stones and pancreatic stonesMuscle crampsBradycardia, cardiac arrestGI activity also commonNausea, abdominal crampsDiarrhea / constipation

Treatment

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

* Hypocalcemia

Hyperactive neuromuscular reflexes and tetany differentiate it from hypercalcemia Convulsions in severe cases Caused by: Renal failure Lack of vitamin D Suppression of parathyroid function Hypersecretion of calcitonin Malabsorption states Abnormal intestinal acidity and acid/ base bal. Widespread infection or peritoneal inflammation

Hypocalcemia

Diagnosis:Chvostek’s signTrousseau’s signTreatmentIV calcium for acuteOral calcium and vitamin D for chronic *

Lecture 2 Water homeostasisacid 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

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

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)


* Volume Abnormalities Edema the accumulation of fluid within the interstitial space 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 (H2CO3)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

Blood Buffer System

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 generatedAmount of acid generated exceeds body’s buffering capacityExcess acid is neutralized by bicarbonateBicarbonate in plasma falls from being consumed in neutralizing excess acidUremia, ketosis, lactic acidosisCompensation: 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 statusLaboratory studiesBlood pHPCO2Bicarbonate