FLUID AND ELECTROLYTES

Water distribution  Water accounts for approximately ;• 60% of body weight in men.• 55% in women,• reflecting the typically greater body fat content in

women.• Reflection of body fat – lean tissues(muscle, solid

organs) have high water content• Highest in newborns ~80%

• Approximately 66% of this water is in the intracellular fluid (ICF)

• While 33% in the extracellular fluid (ECF);

• Only 8% of body water is in the plasma

5

Total body water (TBW)

Fluid Compartments

Intracellular fluid (ICF)

• Fluid inside the cell

• Most (2/3) of the body’s H20 is in the ICF.

Extracellular Fluid (ECF)

• Fluid outside the cell. • 1/3 of body’s H20• More prone to loss• 3 types:Interstitial- fluid

around/between cellsIntravascular- (plasma)

fluid in blood vesselsTranscellular –CSF,

Synovial fluid etc

• Water is not actively transported in the body.

• It is, in general, freely permeable through the ICF and ECF .

• But its distribution is determined by the osmotic contents of these compartments.

• Except in the kidneys, the osmotic concentrations, or osmolalities, of these compartments are always equal: they are isotonic.

• Any change in the solute content of a compartment engenders a shift of water, which restores isotonicity.

• The major contributors to the osmolality of the ECF ;

• sodium and its associated anions, • mainly chloride and• Bicarbonate• The ICF, the predominant cation is potassium. • Other determinants of ECF osmolality include;• glucose • urea.• Protein makes a numerically small contribution of

approximately 0.5%.

• This is because osmolality is dependent on the molar concentrations of solutes: although the total concentration of plasma proteins is approximately 70 g/L, their high molecular weight results in their combined molar concentrations being <1 mmol/L.

• However, since the capillary endothelium is relatively impermeable to protein and since the protein concentration of interstitial fluid is much less than that of plasma,

• Therefore the osmotic effect of proteins is an important factor in determining water distribution between these two compartments.

• The contribution of proteins to the osmotic pressure of plasma is known as the colloid osmotic pressure or oncotic pressure.

• Under normal circumstances,

• the amounts of water taken into the body and

• lost from it are equal over a period of time.

• Water is obtained from the diet oxidative metabolism.

• The minimum volume of urine necessary for normal excretion of waste products is about 500 mL/24 h.

• But, as a result of obligatory losses by other routes, the minimum daily water intake necessary for the maintenance of water balance is approximately 1100 mL.

• This increases if losses are abnormally large e.g excessive sweating diarrhoea.

• Water intake is usually considerably greater than this minimum requirement but the excess is easily excreted through the kidneys.

• Water is lost through the

• kidneys,

• skin,

• lungs

• gut

Mechanisms of Fluid Gain and Loss

Gain• Fluid intake 1500ml• Food intake 1000ml• Oxidation of nutrients

300ml(10ml of H20 per 100 Kcal)

Loss• “Sensible”

Can be seen.Urine 1500mlSweat 100ml

• “Insensible”Not visible.Skin (evaporation) 500mlLungs 400mlFeces 200ml

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Fluid Balance

Daily Water Gain and Loss

Copyright 2009, John Wiley & Sons, Inc.

Sodium distribution

• The body of an adult man contains approximately 4000 mmol of sodium, 70% of which is freely exchangeable.

• The remainder being complexed in bone. • The majority of the exchangeable sodium is

extracellular.• Normal ECF sodium concentration is 135-145

mmol/L, while that of the ICF is only 4-10 mmol/L.

Sodium distribution

• Most cell membranes are relatively impermeable to sodium but some leakage into cells occurs and the gradient is maintained by

• active pumping of sodium from the ICF to the ECF by Na+, K+-ATPase.

• As with water, sodium input and output normally are balanced.

• The normal intake of sodium in the western world is 100-200 mmol/24 h.

• but the obligatory sodium loss, via the kidneys, skin and gut, is <20 mmol/24 h.

• Thus, the sodium intake necessary to maintain sodium balance is much less than the normal intake.

• Excess sodium is excreted in the urine.

• Despite this, excessive sodium intake may be harmful: there is evidence that it is a contributory factor in hypertension.

Potassium distribution • Potassium is the predominant intracellular

cation.

• Some 90% of the total body potassium is free and therefore exchangeable.

• While the remainder is bound in red blood cells, bone and brain tissue.

Potassium distribution• However, only approximately 2% (50-60 mmol)

of the total is located in the extracellular compartment.

• where it is readily accessible for measurement.

• Plasma potassium concentration is not, therefore, an accurate index of total body potassium status, but, because of the effect of potassium on membrane excitability, is important in its own right.

water and Sodium Homoeostasis

• Any loss of water from the ECF, such as occurs with water deprivation,

• will increase its osmolality and

• result in movement of water

• from the ICF to the ECF.

Water and Sodium Homoeostasis

• However, a slight increase in ECF osmolality will still occur,

• stimulating the hypothalamic thirst centre, which promotes a desire to drink, and

• the hypothalamic osmoreceptors, which causes the release of vasopressin (antidiuretic hormone or ADH).

• If ECF osmolality falls, there is no sensation of thirst and vasopressin secretion is inhibited.

• A dilute urine is produced, allowing water loss and restoration of ECF osmolality to normal.

• If an increase in ECF osmolality occurs as a result of the presence of a solute such as urea that diffuses readily across cell membranes, ICF osmolality is also increased and osmoreceptors are not stimulated.

• The vasopressin responses to changes in osmolality occur rapidly.

• In health, the ingestion of water surplus to requirements leads to a rapid diuresis.

• And water depletion to a rapid increase in the concentration of the urine.

Role of Aldosterone

• Aldosterone, released from the adrenal cortex in response to activation of the renin-angiotensin system, stimulates

• Sodium reabsorption in the distal parts of the

distal convoluted tubules and collecting ducts

• And is the major factor controlling renal sodium excretion.

Role of Aldosterone

• But in essence, renin secretion is stimulated primarily by

• a decrease in renal perfusion secondary to a decrease in blood volume - specifically by a fall in arterial blood volume

Natriuretic peptide hormones

•Natriuretic peptide hormones also have a role in controlling sodium excretion.

•Atrial natriuretic peptide (ANP) is a 28 amino acid peptide, one of a family of similar peptides, secreted by the cardiac atria in response to atrial stretch following a rise in atrial pressure (e.g. due to ECF volume expansion).

Natriuretic peptide hormones• ANP acts both directly by ;• inhibiting distal tubular sodium reabsorption • And through decreasing renin (and hence

aldosterone) secretion. • It also antagonizes the pressor effects of

noradrenaline (norepinephrine) and angiotensin II (and thus tends to increase GFR) and has a systemic vasodilatory effect.

Natriuretic peptide hormones

• It appears to provide 'fine tuning' of sodium homoeostasis but is probably more important in pathological states than physiologically

Volume Control• Osmoreceptors and Baroreceptors

– Osmoreceptors in paraventricular and supraventricular nuclei in hypothalamus – control thirst and ADH secretion from posterior pituitary• Increased free water or decreased osmolality

= decreased ADH and water reabsorption•Fine tuning day-to-day

Volume Control

– Baroreceptors in cardiac atrium, aortic arch and carotid sinuses•Neural and hormonal feedback.

Volume Control

•Renin-Angiotensin

•Renin: released from juxtaglomerular cells of

afferent arterioles in kidney ( BP, NaCl)

•Cleaves angiotensinogen (α-2 globulin

produced by liver) to angiotensin 1

Volume Control•Angiotensin: cleaved by ACE which is

produced by vascular endothelial cells of pulmonary tissues.

• Increases vascular tone, stimulates catecholamine release from adrenal medulla and sympathetic nerve terminals.

•Decreases RBF and GFR – increases sodium reabsorption by indirect and direct effect (aldosterone release from adrenal cortex)

Volume Control•Aldosterone

•Produced in zona glomerulosa of adrenal cortex

• Increased absorption of sodium in Collecting Duct & Distal Convoluted Tubules– stabilizing Na channel in open state, increases number of channels in apical membrane•Increases Na/K activity•Increases sodium reabsorption and potassium

excretion

Volume Control• Natriuretic Peptide

– Brain and Renal• Released by atrial myocytes from wall

distension• Inhibitory effect on renal sodium absorption• Urodilatin – ANP-like substance, synthesized by

cortical collecting tubule–Released by kidney tubules in response to

atrial distension and sodium loadingTwice as potent as ANP, increases cGMP

= Na, Cl, water diuresis

• Physiological responses to a decrease in plasma volume.

• These involve both responses to restore plasma volume and maintain blood pressure

Water and Sodium Depletion • Water depletion or combined water and sodium

depletion will occur if losses are greater than intake.

• Depletion of water alone is seen much less frequently than depletion of both water and sodium.

• As sodium cannot be excreted from the body without water, sodium loss never occurs alone but is always accompanied by some loss of water

Water and Sodium Depletion • Death: Occurs when water loss amounts

to approx• 15 per cent of body wt. (about 22% of

total body water),• which happens on about the 7th to 10th

day of complete water deprivation , if not treated.

Water excess • This is usually related to an impairment of water

excretion.

• However, the limit to the ability of the healthy kidneys to excrete water is about 20 mL/min and, occasionally, excessive intake is alone sufficient to cause water intoxication.

• This can sometimes occur in patients with psychiatric disorders.

Water excess

• It has also been described in people drinking large amounts of beer with a low solute content.

• Because this results in a low osmotic load for excretion and there is a minimum osmolality below which the urine can not be diluted further.

Water excess

• Increased thirst can occur in ;

• organic brain disease (particularly trauma, and following surgery).

• Although decreased thirst is more common.

• The clinical features of water overload are related to cerebral over-hydration, the incidence and severity depending upon the extent of the water excess and its time course

Electrolytes of plasma

• Cations mEq/L (a) Plasma

• Na+ = 143 • K+ = 5• Ca++ = 5 • Mg++ = 2 • Total = 155

• Anions mEq/L• Cl– = 103• HCO–

3 = 27

• HPO-4 = 2

• SO-4 = 1

• Proteins– = 16• Organic acids– = 6• Total = 155

Electrolytes• Work with fluids to keep the body healthy and in

balance• They are solutes that are found in various

concentrations and measured in terms of milliequivalent (mEq) units

• Can be negatively charged (anions) or positively charged (cations)

• For homeostasis body needs: Total body ANIONS = Total body CATIONS

Electrolytes

Cations

Positively charged

Sodium Na+ Potassium K+ Calcium Ca++ Magnesium Mg++

Anions

Negatively charged

• Chloride Cl-• Phosphate PO4-• Bicarbonate HCO3-

Electrolyte Functions

• Regulate water distribution• Muscle contraction• Nerve impulse transmission• Blood clotting• Regulate enzyme reactions (ATP)• Regulate acid-base balance

Sodium Na+• 135-145mEq/L• Major Cation• Chief electrolyte of the ECF• Regulates volume of body fluids• Needed for nerve impulse & muscle fiber

transmission (Na/K pump)• Regulated by kidneys/ hormones

Hypernatremia or Sodium excess • Serum Na+ > 145mEq/L • Results from Na+ gained in excess of H2O OR

Water is lost in excess of Na+• Water shifts from cells to ECF• S/S: thirst, • dry mucous membranes & lips,• oliguria, • increased temp & pulse, flushed skin, confusion• Tx: IV therapy/diet

Sodium excess • Sodium excess can result from increased

intake or decreased excretion.

• The clinical features are related primarily to expansion of ECF volume.

• Sodium overload is more usually due to impaired excretion than to excessive intake.

• The most frequent cause is secondary aldosteronism.

Sodium excess • Secondary hyperaldosteronism ,also

known as• hyperreninism, or• hyperreninemic hyperaldosteronism)

• It is due to over-activity of the renin-angiotensin system.

Sodium excess • Secondary refers to an abnormality that indirectly

results in pathology through a predictable physiologic pathway, i.e.,

• a renin-producing tumor leads to increased aldosterone

• As the body's aldosterone production is normally regulated by renin levels

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

Due to:

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

• Long term sweating with chronic fever• Respiratory infection → water vapor loss• Diabetes (mellitus or insipidus) – polyuria

– Insufficient intake of water (hypodipsia)

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Clinical manifestationsof Hypernatremia

• Thirst• Lethargy• Irritability• Seizures• Fever• Oliguria

HypernatremiaEvaluation

• Volume• Serum sodium, osmolality, BUN/Creatinine• Urine sodium, osmolality

Sodium excess • This is seen in patients who, despite clinical

evidence of increased ECF volume (e.g. peripheral oedema), appear to have a decreased effective arterial blood volume,

• Due, for example, to venous pooling or a disturbance in the normal distribution of ECF between the vascular and extravascular compartments.

Sodium excess • This phenomenon is particularly associated with

cardiac failure, hypoalbuminaemia and hepatic cirrhosis.

• Many such patients with sodium excess are, paradoxically, hyponatraemic, implying the coexistence of a defect in free water excretion.

Sodium excess • This is probably in part due to an increase in

vasopressin secretion as a result of the decreased effective blood volume.

• Also, the decrease in GFR and consequent increase in proximal tubular sodium reabsorption decreases the delivery of sodium and chloride to the loops of Henle and distal convoluted tubules.

Sodium excess • This reduces the kidneys' diluting capacity,

thereby compromising water excretion.

• Renal disease is a relatively uncommon cause of sodium excess, as is increased mineralocorticoid secretion due to primary adrenal disease (as in Conn's syndrome).

Let’s think about….Hypernatremia

• What are some medical conditions that may cause elevated serum Na?

• Renal failure

• Diabetes Insipidus

• Diabetes Mellitus ( hyperglycemic dehydration)

• Cushings syndrome (hyperaldosteronism)

Let’s think about….Hypernatremia

• What are some other patient populations at risk for hypernatremia?

• Elderly ( decreased thirst mechanism )

• Patient’s receiving:-tube feedings-corticosteroid drugs-certain diuretic therapies

Let’s think about….Hypernatremia

• Sign & Symptoms

• Seizures, • coma, • death my result if hypernatremia is left untreated. • Why?

• Cells loose fluid into the ECF causing irreversible cell damage.

Sodium measurement

• Sodium concentration used to be measured by flame photometry, which determines the number of sodium atoms in a defined volume of solution.

• Sodium is now usually measured by ion-selective electrodes, which determine the activity of sodium, that is, the number of atoms that act as true ions in a defined volume of water.

Hyponatremia

• Serum Na+ <135mEq/L• Results from excess of water or loss of Na+• Water shifts from ECF into cells• S/S: abd cramps, confusion, • Nausea/Vomiting,• Headach, pitting edema over sternum• Rx: Diet/IV therapy/fluid restrictions

Hyponatraemia • A slightly low plasma sodium concentration is a

frequent finding.

• The mean plasma sodium concentration of hospital inpatients is 5 mmol/L lower than in healthy controls.

• Mild hyponatraemia is seen with a wide variety of illnesses and may be multifactorial in origin.

Hyponatraemia

• It is essentially a secondary phenomenon that merely reflects the presence of disease

• • Treatment should be directed at the underlying

cause and not at the hyponatraemia.

Hyponatraemia

• Hyponatraemia itself may warrant primary treatment

• But usually only when it is severe or associated with clinical features of water intoxication.

Causes• It has been emphasized that plasma sodium

concentration depends upon the• amounts of both sodium and water in the plasma

• Therefore a low sodium concentration does not necessarily imply sodium depletion.

Causes

• Indeed, hyponatraemia is more frequently a result of a defect in water homoeostasis that causes

• water retention and

• hence dilution of plasma sodium.

Causes• One of three mechanisms is usually primarily

responsible for the development and maintenance of hyponatraemia, although in individual patients more than one factor may be involved.

• These are: • 1.Depletion of sodium (hypovolaemic

hyponatraemia)• 2.Excess of water (euvolaemic hyponatraemia)• 3.Excess of water and sodium (hypervolaemic

hyponatraemia).

Hyponatremia• 1.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• 2.Normovolemic hyponatremia

– When hyponatremia is caused by SIADH (syndrome of inappropriate antidiuretic hormone secretion), glucocorticoid deficiency, hypothyroidism, or water intoxication, urine sodium concentration is greater than 20 mEq/L

• Rx: – Fluid restriction– Correct endocrine abnormality

Hyponatremia• 3.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

Causes of Hyponatremia Based on Extracellular Fluid Volume Status• 1. Hypovolemic

• Gastrointestinal solute loss (diarrhea, emesis)• Third-spacing (ileus, pancreatitis)• Diuretic use• Addison's disease• Salt-wasting nephritis

Causes of Hyponatremia Based on Extracellular Fluid Volume Status• 2. Euvolemic• Syndrome of inappropriate antidiuretic hormone

(SIADH)• Diuretic use• Glucocorticoid deficiency• Hypothyroidism• Beer drinker's potomania,• psychogenic polydipsia

Causes of Hyponatremia Based on Extracellular Fluid Volume Status• 3. Hypervolemia with Decreased Effective

Circulating Blood Volume• Decompensated heart failure• Advanced liver cirrhosis• Renal failure with or without nephrosis

93

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

1.Depletion of sodium

• Sodium cannot be lost without water

• And isotonic or hypotonic loss would not be expected to cause a fall in plasma sodium concentration.

1.Depletion of sodium • However, hyponatraemia can occur in sodium-

depleted patients, and is due either to • Inappropriate replacement of fluid (e.g.

containing insufficient sodium) or, • in severe sodium depletion, to the hypotonic

stimulus to vasopressin secretion, which overrides the osmotic control and permits water retention at the expense of a decrease in osmolality.

• It should be noted that, in patients with hyponatraemia due to sodium depletion, clinical signs of sodium depletion may be present.

• Unless the sodium loss is occurring through the kidneys, increased aldosterone secretion should cause maximal renal sodium retention and the urinary sodium concentration will be low (usually <20 mmol/L).

2.Water excess• This gives rise to a dilutional hyponatraemia

with reduced plasma osmolality.

• It can occur acutely purely due to excessive water intake, but this is rare.

• Normal kidneys are capable of excreting 1 L of water per hour.

• Water intoxication and hyponatraemia will thus be seen only

• when very large quantities of fluid are ingested rapidly, as is seen in some patients with psychoses.

• It can also occur in people who drink large quantities of weak beer.

• The logical treatment of dilutional hyponatraemia is;

• to restrict the patient's water intake to less than that required to maintain normal water balance, for example to 500-1000 mL/24 h.

• Water restriction is unpleasant and may be impractical in chronic cases.

• Demeclocycline, a drug that antagonizes the action of vasopressin on the renal collecting ducts, has been used for this purpose.

• If patients are symptomatic, urgent correction of the hyponatraemia is required.

• Hypertonic saline (3%) should be infused at a rate sufficient to increase the plasma sodium concentration initially by 1 mmol/L per hour but not by >12 mmol/L over 24 h.

• Regular clinical assessment and measurement of plasma sodium concentration are essential.

• In chronic dilutional hyponatraemia, correcting the sodium concentration too rapidly risks causing central pontine myelinolysis;

• a brain syndrome characterized by • spastic quadriplegia,• pseudobulbar palsy( it is a medical condition

characterised by the inability to control facial movements (such as chewing and speaking)) and

• cognitive changes.

• Hypoxaemia or the presence of chronic liver disease may increase this risk.

• This condition has a poor prognosis

3.Combined water and sodium excess

• This is a frequent cause of hyponatraemia.

• It underlies the hyponatraemia of congestive cardiac failure, hypoproteinaemic states and some patients with liver failure.

• A decrease in the total negative charge on plasma proteins, which contributes to the anion gap, can reduce sodium in plasma.

• This is unusual, but it may contribute to hyponatraemia in severe hypoalbuminaemia.

• The fact that there is sodium excess is indicated by signs of increased ECF volume (e.g. peripheral oedema).

• The logical treatment in these patients involves measures to treat the underlying cause and remove the excess sodium and water (e.g. with diuretics).

• Despite the hyponatraemia, saline should not be given as these patients are already sodium overloaded.

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)

Potassium K+• 3.5-5.0 mEq/L• Chief electrolyte of ICF• Major mineral in all cellular fluids• Aids in muscle contraction, nerve & electrical

impulse conduction, regulates enzyme activity, regulates IC H20 content, assists in acid-base balance

• Regulated by kidneys/ hormones• Inversely proportional to Na

Potassium Homoeostasis• Dietary potassium intake is of the order of 75-150

mmol/day, values higher in the range being associated with a high intake of fruit and vegetables.

• Extracellular potassium balance is controlled primarily by the kidneys and, to a lesser extent, by the gastrointestinal tract.

• In the kidneys, filtered potassium is almost completely reabsorbed in the proximal tubules.

• Some active potassium secretion takes place in the most distal part of the distal convoluted tubules but potassium excretion is primarily a passive process.

• The active reabsorption of sodium generates a membrane potential that is neutralized by the movement of potassium and hydrogen ions from tubular cells into the lumen.

• Thus, urinary potassium excretion depends upon several factors:

• the amount of sodium available for reabsorption in the distal convoluted tubules and the collecting ducts

• the relative availability of hydrogen and potassium ions in the cells of the distal convoluted tubules and the collecting ducts

• the capacity of these cells to secrete hydrogen ions

• the circulating concentration of aldosterone

• the rate of flow of tubular fluid: a high flow rate (e.g. osmotic diuresis, treatment with diuretics) favours the transfer of potassium into the tubular lumen.

• In the distal nephron, potassium is secreted in exchange for either sodium or hydrogen ions: increased delivery of sodium increases the potential secretion of potassium.

• Aldosterone stimulates potassium excretion both;

• indirectly, by increasing the active reabsorption of sodium in the distal convoluted tubules and the collecting ducts, and

• directly, by increasing active potassium secretion in the distal part of the distal convoluted tubules.

• Aldosterone secretion from the adrenal cortex is stimulated indirectly by activation of the renin-angiotensin system in response to hypovolaemia and directly by hyperkalaemia.

• Since both hydrogen and potassium ions can neutralize the membrane potential generated by active sodium reabsorption, there is a close relationship between potassium and hydrogen ion homoeostasis.

• In an acidosis, hydrogen ions will tend to be secreted in preference to potassium; in alkalosis, fewer hydrogen ions will be available for excretion and there will be an increase in potassium excretion.

• Thus, there is a tendency to hyperkalaemia in acidosis and to hypokalaemia in alkalosis.

• An exception to this tendency is renal tubular acidosis caused by defective renal hydrogen ion excretion.

• In this condition, because of the decrease in hydrogen ion excretion, potassium secretion must increase to balance sodium reabsorption.

• The result is the unusual combination of hypokalaemia with acidosis.

• Healthy kidneys are less efficient at conserving potassium than sodium: even on a potassium-free intake, urinary excretion remains at 10-20 mmol/24 h.

• Since there is also an obligatory loss from the skin and gut of approximately 15-20 mmol/24 h, the kidneys cannot compensate if intake falls much below 40 mmol/24 h.

• Potassium is secreted in gastric juice (5-10 mmol/L) and much of this, along with dietary potassium, is reabsorbed in the small intestine.

• In the colon and rectum, potassium is secreted in exchange for sodium, partly under the control of aldosterone.

• Stools normally contain some potassium, but considerable amounts can be lost in patients with

• fistulae or • chronic diarrhoea (up to 30 mmol/L), or • in patients who are losing gastric secretions

through persistent vomiting or• nasogastric aspiration. • Movement of potassium between the

intracellular and extracellular compartments can have a profound effect on plasma potassium concentration.

• The cellular uptake of potassium is stimulated by insulin.

• Potassium ions move passively into cells from the ECF in exchange for sodium, which is actively excluded by a membrane-bound, energy-dependent sodium pump.

• Hyperkalaemia can result if the activity of this sodium pump is impaired or if there is damage to cell membranes.

• Potassium uptake into cells is stimulated by • insulin and β-adrenergic stimulation;• α-adrenergic stimulation has the opposite effect.

• Transcellular shifts of hydrogen ions can cause reciprocal shifts in potassium and vice versa.

• In a systemic acidosis;• intracellular buffering of hydrogen ions results in

the displacement of potassium into the ECF.

• In alkalosis, there is a shift of hydrogen ions from the ICF to the ECF, and a net movement of potassium ions in the opposite direction, which tends to produce hypokalaemia.

• Similarly, potassium depletion can lead to systemic alkalosis.

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

Hypokalemia• Serum level < 3.5mEq/L• Results from decreased intake, loss via GI/Renal

& potassium depleting diuretics• Life threatening-all body systems affected• S/S muscle weakness & leg cramps, decreased GI

motility, cardiac arrhythmias • Rx: diet/supplements/IV therapy

Lets think about …Hypokalemia• What are some medical conditions that may cause

a hypokalemia?Renal Disease / CHF (dilutional)Metabolic AlkalosisCushings Disease ( Na retention leads to K loss

• What are some conditions that might cause actual loss of potassium from the body?GI losses – nasogastric suctioning, vomiting, diarrheaCertain diuretic therapies Inadequate intake – ( body cannot conserve K, need PO intake)

• Cardiac arrest may occur when serum K levels fall below 2.5 mEq/L. Why?

• Increased cardiac muscle irritability leads to PACs and PVCs, then AF

Potassium Depletion and Hypokalaemia

• Potassium depletion occurs when output exceeds intake.

• Except in patients who are fasting, inadequate intake is rarely the sole cause of potassium depletion.

• However, increased loss of potassium, either from the gut or (more often) through the kidneys, is a frequent occurrence.

• If renal potassium excretion is <40 mmol/L in a patient with hypokalaemia, excessive renal excretion is unlikely to be the cause.

• Drug therapy is often implicated in the pathogenesis of potassium depletion.

• When hypokalaemia is a result of potassium depletion, it usually develops slowly and is only corrected slowly when the cause is effectively treated.

• In contrast, hypokalaemia as a result of redistribution of potassium from the extra- to the intracellular compartment usually develops acutely, and can normalize rapidly.

Clinical features • Even severe hypokalaemia may be

asymptomatic. Hypokalaemia causes hyperpolarization of excitable membranes, thus decreasing their excitability.

• When symptoms are present, they are related primarily to disturbances of neuromuscular function: muscular weakness, constipation and paralytic ileus are common problems.

Management• Although the plasma potassium concentration is a

poor guide to total body potassium, a plasma concentration of 3.0 mmol/L generally implies a deficit of the order of 300 mmol.

• The first step in the management of hypokalaemia should be to identify and treat the causative condition, but potassium replacement is frequently required.

• Since any potassium deficit will be almost entirely from the ICF but administered potassium first enters the ECF, replacement must be undertaken with care, particularly when the intravenous route is used.

• As a guide, the following potassium dosages should not be exceeded without good reason: a rate of 20 mmol/h, a concentration of 40 mmol/L in intravenous fluid or a total of 140 mmol/24 h.

• Thorough mixing with the bulk of the fluid to be infused is vital.

Hyperkalemia• Serum level >5 mEq/L

• Results from excessive intake, trauma, crush injuries, burns, renal failure

• S/S muscle weakness, cardiac changes, N/V, parathesias of face/fingers/tongue

• Rx:diet/meds/IV therapy/ possible dialysis.

Lets think about …Hyperkalemia• What are some medical conditions that may cause

hyperkalemia?Renal Disease=most common causeBurns and other major tissue traumaMetabolic Acidosis Addison’s Disease ( Na loss leads to K retention )

• What are some conditions that might cause potassium levels to rise in the body?Certain diuretic therapies Excessive intake – ( inappropriate supplements)

Lets think about …Hyperkalemia

• Cardiac arrest may occur when serum K levels rise above 7mEq/L. Why?

• Decreased electrical impulse conduction leads to bradycardia and eventually asystole.

Potassium Excess and Hyperkalaemia • Potassium excess can be due to excessive intake

or decreased excretion.

• A normal intake may be excessive if excretion is decreased (e.g. in renal failure).

• Excessive intake is otherwise virtually always iatrogenic (induced inadvertently by medical treatment) and the result of parenteral administration.

• Hyperkalaemia can result from potassium excess but can also be a result of redistribution of potassium from the intra- to the extracellular compartment.

• This mechanism can sometimes give rise to hyperkalaemia even in a patient who is potassium depleted (e.g. in diabetic ketoacidosis).

• As with hypokalaemia, more than one cause of hyperkalaemia may be present.

• Spurious hyperkalaemia, due to the leakage of potassium from blood

Clinical features• Hyperkalaemia is less common than hypokalaemia

but is more dangerous: through its effect on the heart, it can kill without warning.

• It lowers the resting membrane potential, shortens the cardiac action potential and increases the speed of repolarization.

• Cardiac arrest in asystole or slow ventricular fibrillation may be the first sign of hyperkalaemia.

• The risk increases significantly with potassium concentrations;

• exceeding 6.5 mmol/L (particularly if the increase has occurred rapidly);

• a true potassium concentration of >7.0 mmol/L is a medical emergency.

• It is therefore necessary to be alert for this disorder in appropriate circumstances,

• for instance in acute renal failure, to ensure that effective early management is instituted.

• Characteristic ECG changes may precede cardiac arrest.

Management• Intravenous calcium gluconate (10 mL of a 10%

solution given over 1 min and repeated as necessary) affords some degree of immediate protection to the myocardium by antagonizing the effect of hyperkalaemia on myocardial excitability.

• Intravenous glucose and insulin, for example 500 mL of 20% dextrose with 20 units of soluble insulin given over 30 min, promotes intracellular potassium uptake.

• Salbutamol, which activates Na+,K+-ATPase, has a similar effect.

• If insulin is used, blood glucose must be monitored for the subsequent 6 h because of the risk of hypoglycaemia.

• In an acidotic patient, hyperkalaemia can be controlled temporarily by bicarbonate infusion (using a 1.26% solution, not 8.4%, which risks causing ECF volume expansion because of the high sodium concentration).

• In acute renal failure and in other circumstances where the hyperkalaemia is uncontrollable, dialysis will be required.

• In chronic renal failure, restriction of potassium intake and the administration of oral ion-exchange resins are often successful in preventing dangerous hyperkalaemia until such time as dialysis becomes necessary for other reasons.

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Calcium • Normal 4.5-5.5 mEq/L

• 99% of Ca in bones, other 1% in ECF and soft tissues

• Total Calcium – bound to protein – levels influenced by nutritional state

• Ionized Calcium – used in physiologic activities – crucial for neuromuscular activity

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Calcium• Required for blood coagulation, neuromuscular

contraction, enzymatic activity, and strength and durability of bones and teeth

• Nerve cell membranes less excitable with enough calcium

• Ca absorption and concentration influenced by Vit D, calcitriol (active form of Vitamin D), PTH, calcitonin, serum concentration of Ca and Phos

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Causes of Hypocalcemia • Most common – depressed function or surgical

removal of the parathyroid gland• Hypomagnesemia• Hyperphosphatemia• Administration of large quantities of stored blood

(preserved with citrate)• Renal insufficiency• ↓ absorption of Vitamin D from intestines

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Signs/Symptoms• Abdominal and/or extremity cramping• Tingling and numbness• Positive Chvostek or Trousseau signs• Tetany; hyperactive reflexes• Irritability, reduced cognitive ability, seizures• Prolonged QT on ECG, hypotension, decreased

myocardial contractility• Abnormal clotting

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Treatment• High calcium diet or oral calcium salts (mild) - √

formulas for calcium content • IV calcium as 10% calcium chloride or 10%

calcium gluconate – give with caution• Close monitoring of serum Ca and digitalis levels• ↓ Phosphorus levels ↑ Magnesium levels • Vitamin D therapy

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Hypercalcemia• Causes

– Mobilization of Ca from bone– Malignancy– Hyperparathyroidism– Immobilization – causes bone loss– Thiazide diuretics– Thyrotoxicosis– Excessive ingestion of Ca or Vit D

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Signs/Symptoms• Anorexia, constipation• Generalized muscle weakness, lethargy, loss of

muscle tone, ataxia• Depression, fatigue, confusion, coma• Dysrhythmias and heart block• Deep bone pain and demineralization• Polyuria & predisposes to renal calculi• Pathologic bone fractures

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Hypercalcemic Crisis• Emergency – level of 8-9 mEq/L

• Intractable nausea, dehydration, stupor, coma, azotemia, hypokalemia, hypomagnesemia, hypernatremia

• High mortality rate from cardiac arrest

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Treatment • NS IV – match infusion rate to amount of UOP• I&O hourly• Loop diuretics• Corticosteroids and Mithramycin in cancer clients• Phosphorus and/or calcitonin• Encourage fluids• Keep urine acid

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Evaluation

• Normal serum calcium levels

• Improvement of signs and symptoms

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Magnesium

• Normal 1.5 to 2.5 mEq/L• Ensures K and Na transport across cell membrane• Important in CHO and protein metabolism• Plays significant role in nerve cell conduction• Important in transmitting CNS messages and

maintaining neuromuscular activity

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Magnesium• Causes vasodilatation • Decreases peripheral vascular resistance • Balance - closely related to K and Ca balance• Intracellular compartment electrolyte• Hypomagnesemia - < 1.5 mEq/L• Hypermagnesemia - > 2.5 mEq/L

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Hypomagnesemia• Causes

– Decreased intake or decreased absorption or excessive loss through urinary or bowel elimination

– Acute pancreatitis, starvation, malabsorption syndrome, chronic alcoholism, burns, prolonged hyperalimentation without adequate Mg

– Hypoparathyroidism with hypocalcemia– Diuretic therapy

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Signs/Symptoms • Tremors, tetany, ↑ reflexes, paresthesias of feet

and legs, convulsions• Positive Babinski, Chvostek and Trousseau signs• Personality changes with agitation, depression or

confusion, hallucinations• ECG changes (PVC’S, V-tach and V-fib)

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Treatment• Mild

– Diet – Best sources are unprocessed cereal grains, nuts, legumes, green leafy vegetables, dairy products, dried fruits, meat, fish

– Magnesium salts• More severe

– MgSO4 IM – MgSO4 IV slowly

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Treatment• Monitor Mg q 12 hr

• Monitor VS, knee reflexes

• Precautions for seizures/confusion

• Check swallow reflex

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Hypermagnesemia• Most common cause is renal failure, especially if

taking large amounts of Mg-containing antacids or cathartics; DKA with severe water loss

• Signs and symptoms– Hypotension, drowsiness, absent DTRs,

respiratory depression, coma, cardiac arrest– ECG – Bradycardia, CHB, cardiac arrest, tall T

waves

Treatment • Withhold Mg-containing products

• Calcium chloride or gluconate IV for acute symptoms

• IV hydration and diuretics

• Monitor VS, LOC

• Check patellar reflexes

Evaluation• Serum magnesium levels WNL

• Improvement of symptoms

Phosphorous• Normal 2.5-4.5 mg/dL • Intracellular mineral• Essential to tissue oxygenation, normal CNS

function and movement of glucose into cells, assists in regulation of Ca and maintenance of acid-base balance

• Influenced by parathyroid hormone and has inverse relationship to Calcium

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Hypophosphotemia• Causes

– Malnutrition– Hyperparathyroidism– Certain renal tubular defects– Metabolic acidosis (esp. DKA)– Disorders causing hypercalcemia

Signs/Symptoms• Impaired cardiac function

• Poor tissue oxygenation

• Muscle fatigue and weakness

• N/V, anorexia

• Disorientation, seizures, coma

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Treatment • Closely monitor and correct imbalances

– Adequate amounts of Phos – Recommended dietary allowance for formula-

fed infants 300 mg Phos/day for 1st 6 mos. and 500 mg per day for latter ½ of first year

– 1:1 ratio Phos and Ca recommended dietary allowance. Exception is infants, whose Ca requirements is 400 mg/day for 1st 6 mos and 500 mg/day for next 6 months

Treatment• Treatment of moderate to severe deficiency

– Oral or IV phosphate (do not exceed rate of 10 mEq/h)

– Identify clients at risk for disorder and monitor– Prevent infections– Monitor levels during treatment

Hyperphosphatemia• Causes

– Chronic renal failure (most common)– Hyperthyroidism, hypoparathyroidism– Severe catabolic states– Conditions causing hypocalcemia

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Signs/Symptoms

• Muscle cramping and weakness

• ↑ HR

• Diarrhea, abdominal cramping, and nausea

Treatment• Prevention is the goal • Restrict phosphate-containing foods• Administer phosphate-binding agents • Diuretics• Treat cause• Treatment may need to focus on correcting

calcium levels

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Evaluation

• Lab values within normal limits

• Improvement of symptoms