fluid and electrolyte balance lecture

8/20/2019 Fluid and Electrolyte Balance Lecture

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DR MODUPE KUTI

FWACP (Lab Med)


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Water is the most abundant constituent in the body50% of weight in women;60% of weight in menDifference due to adipose tissue composition

Total Body Water divided into 2 compartmentsExtracellular : 25 – 45%

▪ Intravascular – plasma water (25%)▪ Extravascular – interstitial fluid (75%)Intracellular : 55 – 75%


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Interfaces betweenExtracellular and Intracellular fluids – Cell membranesIntravascular and Interstitial – Capillary walls

Movement of fluids betweenExtracellular and Intracellular–

Osmolality (solute or particle concentration of a fluid, expresse

milliosmoles per kilogram of water (mosmol/kg).Water crosses cell membranes to achieve osmotic equilibrium (ECFosmolality = ICF osmolality).normal plasma osmolality is 275 – 290 mosmol/kg

Osmolality can measured or calculated –1.8[Na + Cl] + Urea (mg/dL)/6 + Glucose (mg/dL)/


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Major ECF solutes – Sodium, Chloride, BicarbonateMajor ICF solutes – Potassium, Organic Phosphates (ATP, creatinephosphate, phospholipids)

Differences due to disparities in permeability, and the presence oftransporters and active pumps

Intravascular and InterstitialStarling’s Forces

capillary hydraulic pressure – from blood pressurecolloid osmotic pressure – oncotic pressure (proteins)Occurs across the capillary wall


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For steady state, water intake must equal water excretionPhysiologic influences for both actions

Water intake

Water Ingestion▪ Primary Stimulus is thirst mediated either by an increase in effective osmola

or a decrease in ECF volume or blood pressure.▪ Osmoreceptors, located in the anterolateral hypothalamus, are stimulated by

rise in tonicity.▪ Urea and glucose are ineffective osmoles

Water ExcretionNormal individuals have an obligate water loss consisting of

▪

Urine, Stool, and Evaporation from the skin and respiratory tract.


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Physiologic Regulation▪ principal determinant of water excretion isarginine vasopressin(AVP) synthesize

in the supraoptic and paraventricular nuclei of the hypothalamus and secretthe posterior pituitary gland.

▪ Binding to V2 receptors on the basolateral membrane of principal cells collecting duct leads to the insertion of water channels into the luminal memb

▪ The net effect is passive water reabsorption along an osmotic gradient frolumen of the collecting duct to the hypertonic medullary interstitium.

▪

The major stimulus for AVP secretion is increased osmolality▪ Effective osmolality is primarily determined by the plasma Na concentration

because major ECF solutes are Na salts,▪ Nonosmotic factors that regulate AVP secretion include effective circulating

(arterial) volume, nausea, pain, stress, hypoglycemia, pregnancy, and numerodrugs.


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85 to 90% of all Sodium is extracellular, actively pumped out of the cell by thNa–KATPase pumpECF volume is a reflection of total body Sodium content

Volume regulatory mechanisms ensure that Sodium loss balances Sodium gainNormal Na concentration in plasma : 135 – 145mmol/L

Sodium Intake

Typical western diet consume approximately 150 mmol of NaCl daily.Excess Na in diet ECF expansion increased renal excretion


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Sodium ExcretionRegulation of excretion is main determinant of Na balanceMajor regulatory mechanism is tubular Na reabsorptionMost important determinant of Na reabsorption is renin–angiotensin sacting via aldosteroneFiltered Sodium

▪ About 60% is reabsorbed in PCT▪ 25 to 30% in the thick ascending limb of the loop of Henle(Loop diuretics)▪ 5% in the DCT (thiazide-sensitive)▪ Final Na reabsorption in the cortical and medullary collecting duct (Aldos)


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HYPOVOLEMIA – generally refers to a state of combined salt and water loss exceedingintake leading to ECF volume contraction

CausesRenal

▪ Diuretics – thiazides, loopact on specific parts of the tubules

▪ Osmotic Diuresis – increased filtration ofglucose – poorly controlled diabetesmannitol – tubules are impervious, neurosurgeryprotein – hyperalimentation (high protein)

▪ Hypoaldosteronism – Hypoadrenalism e.g. Addison’s disease▪ Salt Wasting Nephropathies – Tubule and interstitial renal disorders▪ Diabetes Insipidus – Central or Nephrogenic▪ Acute Tubular Necrosis – Diuretic phase, glomerulus recovers before tub


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Extrarenal –▪ Gastrointestinal (vomiting, nasogastric suction, drainage, fistula, diarrhea)

About 9L of fluids enter GIT/24hrs : 2L ingestion, 7L secretionAlmost 98% is reabsorbed, faecal loss is 100 – 200ml/dayEnhanced secretion or impaired reabsorption

▪ Skin/respiratory (insensible losses, sweat, burns)Insensible water loss typically about 500ml/24hrIncreased during febrile illness, prolonged heat exposure,Increased water /salt loss through sweatHyperventilation, mechanically ventilated persons, neonates


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▪ Third space loss (burns, peritonitis, pancreatitis)ECF, but is not in equilibrium with ECF or ICF, effectively lostburns – subcutaneous tissueretroperitoneal space in acute pancreatitisperitoneal cavity in acute peritonitis

▪ Severe Hemorrhage


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PathophysiologyECF volume contraction decreased plasma volume decreased preload decre

cardiac output hypotension triggers baroreceptors in the carotid sinus and aort

arch activation of the sympathetic nervous system and the renin–angiotensin syste

Main CVS goal – maintain mean arterial pressure and cerebral and coronary perfusi

Main Renal goal – restoring ECF volume by decreasing GFR and filtered load of sodby increasing proximal tubular and collecting duct(RAS–Aldo) absorptionof Na


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Clinical Features

History may help define aetiology – vomiting, diarrhoea, polyuria

Other symptoms not specific – fatigue, weakness, cramps, thirst and postural dizzioliguria, cyanosis, diminished skin turgor and dry mucmembranes

Signs – Decreased JVP, Postural hypotension/tacchycardia

Biochemical Changes – Increased Urea, CreatinineUrine Na, Urine Osmolality change depend on aetiology


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HYPONATREMIAPlasma Sodium Concentration – < 130mmol/L

Typically associated with hypoosmolality – < 280 mosmol/kg

Most commonly due to impaired excretion of free water

Impaired filtration and delivery of water to the diluting sites in the nChronic Renal FailureCortisol Deficiency, Hypothyroidism


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Impaired reabsorption of Na and Cl in excess of water in the thickascending limb of the loop of Henle and in the distal nephron

Diuretics, especially thiazideHypoaldosteronismSalt Wasting Nephropathy

Maintenance of a dilute urine due to impermeability of the collecting

water in the absence of AVPSyndrome of inappropriate AVP secretion ( neuropsychaitric diseas

malignant tumours, pulmonary diseases)AVP release due to pain, nausea


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Primary or psychogenic polydipsia:Inability to excrete a free water load because renal excretorycapacity is exceeded; > 12L per day

Primary Sodium Loss, in excess of water GIT loss in vomiting, diarrhea, fistulas

PseudohyponatremiaNormal plasma osmolality

HyperlipidemiaHyperproteinemia


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Clinical FeaturesRelated to osmotic water shift leading to increased ICF volume,specifically brain swelling and edema – mainly neurologic

Headache, lethargy, confusion, obtundation, stupor, seizures, coma

Severity is dependent on the rapidity of the development of thecondition as well as the absolute decrease in plasma [Na]

InvestigationPlasma OsmolalityUrine OsmolalityUrine [Na]Urine [K]


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HYPERNATREMIAis defined as a plasma Na concentration > 145 mmol/Lis a state of hyperosmolalityAssociate ICF volume contraction

Causesdue to primary Na gain orwater loss –––commonest cause

The appropriate response to hypernatremia1. increased water intake stimulated by thirst and2. the excretion of the minimum volume of maximally concentrated

urine reflecting AVP secretion in response to an osmotic stimulus


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Causes of Free Water LossRenal or Extra renal

Renal Causes – most common cause

Diuretics – Loop diuretics interfere with the counter–current mechanismimpairing renal concentrating abilityOsmotic Diuresis– Presence of non–reabsorbed substances, glucose, mannitol

Water is lost in excess of Na Diabetes Insipidus- non–osmotic urinary water loss

Central – characterised by impaired AVP secretion– trauma, neurosurgery, granulomatous disease,

vascular accidents, infection, idiopathicmay also be familial


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Nephrogenic – resulting from end–organ (renal) resistance to actions ocongenital V2 receptor or aquaporin gene defects– acquired drugs (lithium), hypercalcemia, hyperkalem

Extra–renal▪ Increased insensible water loss – Sweating, Fever, Hyperventilation

▪ Osmotic diarrheas – lactulose, sorbitol, viral gastroenteritis


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Clinical Features – ICF volume contraction – decreased brain cell volume

– typically neurologic: altered mental status, weakness,neuromuscular irritability, focal neurologic deficits, coma, seiz

symptoms of underlying disease

Investigations

Urine volumeUrine OsmolalityUrine [Na]


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Potassium is the major intracellular cation

Normal plasma K concentration is 3.5 to 5.0 mmol/L; ICF is about 150 mm

The ratio of ICF to ECF K concentration (normally 38:1) is crucial for norneuromuscular function (gradient maintained by the basolateral Na, K-ATPpump actively transports K in and Na out of the cell in a 2:3 ratio)

The K intake of individuals on an average western diet is 40 – 120 mmol/

Following a meal, absorbed K enters facilitated by insulin release and bascatecholamine levels.

Eventually, however, the excess K is excreted in the urine


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Potassium Excretion – Renal Excretion is the major route of elimination ofdietary and other sources of [K]

Some 90% of filtered K is reabsorbed by the proximal convoluted tubuleloop of Henle

K delivery to the DCT and CCD roughly equals the dietary intake▪ Net excretion depends on K status: excess or depletion, regulates total

balance▪ Principal cell is responsible for K secretion in the DCT and CCD

Regulationa) Aldosterone – secreted in response to renin and angiotensin or hyperkale

exchanges Na for either K or Hydrogen.b) Hyperkalemia – increases K secretion


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Hypokalemia – defined


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Renal LossCauses most cases of chronic hyperkalemia

Primary hyperaldosteronism (Mineralocorticoid excess states) – Connsyndrome, Adrenal hyperplasia, Adrenal carcinoma, Renin secretingtumors, Renovascular hypertension

Non– aldosterone mineralocorticoid excess states – Congenital adrenhyperplasia, Cushing’s syndrome

Non Renal Loss

Every body fluid has a higher [K] than plasmaLoss of ANY body fluid in amounts above physiologic will cause hypokalaemSaliva, Large bowel secretions,Vom iting Nasogastric secretions


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Clinical Features – Fatigue, myalgia, Muscular weakness of the extremities due to lowresting membrane potential

– Respiratory muscle weakness, paralysis– Inversion of the T wave, prominent U wave– prolonged PR interval, increased risk of ventricular arrhythmias

Investigation24 hr Urine [K]

PSEUDOHYPOKALEMIAPatients with marked leucocytosis and normokalemia may have a low measurplasma [K] concentration due to white blood cell uptake of K at room temperature.Avoid by storing blood sample on ice or rapidly separating plasma/serum from cells


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Hyperkalemia defined as [K] > 5.0mmol/L

Pseudohyperkalemiaartificial elevated plasma [K] due to movement out of the cells immediately p

or following venepunctureContributory factorsprolonged use of torniquetRepeated fist clenchingHemolysisMarked leucocytosisThrombosis

Repeat with proper venepuncture, use plasma (not serum),


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1. Increased intake – rarely the sole cause, overzealous parenteral replacement

2. Release from cells1. Intravascular hemolysis

2. Tumor lysis syndrome3. Rhabdomyolysis4. Metabolic Acidosis – result of intracellular buffering of [H]5. Insulin deficiency – promotes movement of K out of the cells


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3. Decreased renal loss – Cause of most chronic hyperkalemia

Renal Failure – Acute (increased release from cells – acidosis and catabolismChronic – when GFR falls below 10 – 15ml/min

– oliguric

Decreased K secretionPrimary hypoaldosteronism – adrenal insufficiencyimpaired Na reabsorption

Secondary hypoaldosteronism – heparin, ACEi, NSAID

Pseudohypoaldosteronism – resistance to aldosteronismtubuloinsterstitial disease, K sparingdiuretics


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Clinical Features

Partial depolarisation of the membrane with impaired excitabilityMuscle weakness, Flaccid paralysis

Cardiac toxicity – increased T wave amplitude (peaked T waves)ventricular arrhythmias, asystole

fluid and electrolyte balance lecture

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