BODY WATER & SODIUMDr Nagy Abdel-Hady

Sayed-Ahmed

Total Body Water

Intracellular fluid (ICF): 40%

Extracellular fluid (ICF): 20%

a- Insterstitial: 15%

b- Intravascular: 5%

____

Subtotal 20%

____

Total Body Water (TBW): 60%

Total Body Water 60% BW

ICF= 40% BW ECF= 20% BW

Pla

sma=

5%

ISF=

15%

Primary Cations & Anions of ICF & ECF

Cations (mEq/L)

Anions (mEq/L)

ICF K = 135 Mg = 43

PO4 = 90 Protein = 70

SO4 = 18

ECF Na = 140 K = 4.5

Cl = 103 HCO3 = 26

Proteins = 16

Data from Serum Electrolytes

Serum levelElectrolyte At Wt Val Equiv

Wt mg/dl mEq/L

Sodium (Na) 23 1 23 322 140

Potassium (K) 39 1 39 17.5 4.5

Calcuim (Ca) 40 2 20 10 5

Magnessium (Mg) 24 2 12 2.4 2

Chloride (Cl) 35.5 1 35.5 35.7 102

Phosphorus (P) 31 1.8 17.2 3.4 2.0

OsmosisOsmosisThe movement of water across a The movement of water across a membrane from a solution of membrane from a solution of lower conc. to a solution of higher lower conc. to a solution of higher conc.conc.

Osmotic activity depends on the Osmotic activity depends on the number of particles in the number of particles in the solution.solution.

For a compound that does not For a compound that does not dissociate 1 mmol = 1 mosmol. For a dissociate 1 mmol = 1 mosmol. For a compound that dissociates 1 mmol= compound that dissociates 1 mmol= more than 1 mosmolmore than 1 mosmol

18)/()/(cos dlmgglucLmmoleglu

18)/(2 dlmgglucNatonicity

8.2182 BUNglucNatoncitiy

Natonicity 2

Tonicity=2 x Na (mmol/L) + glucose (mmol/L)

Tonicity=2 x Na (mmol/L)

Plasma Oncotic Pressure•Determine movement of water between intravascular compartment and the rest of ISF.

•It depends largely on serum albumin conc.

Extracellular Tonicity & Plasma Oncotic Pressure

K Na Pr

Pla

sma

ISFICF

Glu

K

K

K

KK

K

KK

K

Na

Na

NaNa

Na

NaGluGlu

GluNa

GluPr

Diagnoses for Water & Soduim

A- Water Diagnoses

1- Water Deficit = Hypernatremia

2- Water Excess = Hyponatremia

3- Normal Water = Normal S.Na

B- Sodium Diagnoses

1- Sodium Deficit = Decr. ECF & hypotension

2- Sodium Excess = Incr. ECF & hypertension

3- Sodium WNL = No hypotension or edema

Water Losses in NPO Adult PatientsDaily Average

(ml)Range(ml) Medium Maximum

A- Sensible losses Urine 500-1500 1200 1500 Feces 100-200 100 100B- Insensible losses Lung 600-800 600 800 Sweat 100-300 200 300 Total Water Losses 2100 2700C- Catabolism = Water gain -300 -300Overall Water Losses per day 1800 2400

For FEVER: 200 ml for every 1°C above 37 or 100 ml for every 1°F above 99 per day

SWEATING: -mild 300 -moderate 600 -severe 1000 ml

Source Na K Cl HCO3 H+

A- Stomach 40 10 130 - 60

B- 1. Duodenum 140 5 80 65 -

2. Jujenum/ileum 130 5 105 30 -

3. Bile 140 5 110 35 -

4. Pancreas 140 5 55 90 -

C- Colon 50 20 40 30 -

Average Electrolyte Content of GI Secretion (mEq/L)

SWEAT electrolyte: Na = 50 K = 5 Cl = 55

Volume overload (Na Excess)

■Manifestations:– Edema Congested neck veins Basal

pulmonary rales Hypertension Puffy eyes Dyspnea

■Causes– Decreased excretion of Na & H2O: Acute renal

failure, CRF, – Na & H2O retention: Congestive heart failure,

nephrotic syndrome, nephritic syndrome, liver cell failure, hypercortisolism or hyperaldosteronism, excess sex hormones, drugs, ….etc.,

– Excess intake of salt, hyperinfusion, hypertransfusion

Volume Contraction (Na Deficit)■Manifestations:– Dry skin + loss of turgor, Sunken eyes– Empty neck veins rapid pulse– Hypotension Decrease consciousness– Oliguria

■Causes:– Decreased intake– Increased loss: GIT (vomiting/diarrhea), skin

(sweating, burn, wounds), urinary (salt loosing nephropathy), whole blood, third space (sequestration)

Hypovolemia

Mild: 4% loss TBW or < 15% blood volume Moderate: 6% TBW or 15-30% BV Severe: 8% TBW or 30-40% BV Shock: >8% TBW or > 40% BV S/Sx:

MS changes, sleepy, apathy, coma orthostatic, tachy, decreased pulse pressure,

low CVP, low PCWP Poor turgor, hypothermia, dry membranes Oliguria, ileus, weakness

Hypovolemia, continued

Lab: BUN:Cr ratio greater than 20Inc. hematocrit, 3% per liter

deficitFeNa < 1%, increased urine

spec. gravity and osmolality

Hypovolemia, continued

Treatment:Acute: 2L LR via large bore IV then

bloodSubacute:

Isotonic or hypotonic deficits give isotonic NS or hypotonic 1/2NS or LR (e.g. vomiting = NS, diarrhea = LR)

Hypertonic deficits (e.g. dehydration with jejunal feedings) give D5W. Seen in fever, ventilator, or diaphoresis

Hypervolemia

Etiology: Cardiac failure, Renal failure, mobilization of fluid, iatrogenic, psychologic or Ecstasy

S/Sx: Wt gain over baseline. (Fasting

losses are 0.25-0.5 kg/day) JVD, rales or wheezing, pedal/sacral

edema elevated CVP or PCWP Pulmonary edema on CXR

Hypervolemia, continued

Lab: Decreased Hct and albumin Na may be low, normal or

increased but total body Na is usually increased

Treatment: Water restrict to 1500 cc/day +/- Diuretics Sodium restrict to 0.5 gm/day (Albumin followed by diuretics)

HYPONATREMIA

= WATER EXCESS

Hyponatremia: Definition & Clinical Settings

•Plasma Na <135

•Frequent in hospitalized pts (10-15%)

•Less common in ambulatory pts and usually assoc. with a chronic disease state

•It may be a finding that leads to diagnosis of a specific disease state e.g. overt heart failure, liver disease, or undiagnosed Addison’s disease, hypopituitarism, hypothyroidism.

•It may be a harbinger of excessive diuretic use or may present as a complication of other drugs use e.g. cyclophosphamide or vincristine

•It may be an early feature of oat cell carcinoma of the lung

Sings & Symptoms of Hyponatremia

The development and severity of signs & symptoms of hyponatremia depend on:

*Severity *Rate of decline *Age of pt

Brain requires time to extrude osmoles

AnorexiaNauseaVomiting* muscle cramps * lethargy

* disorientation * agitation* level of conc. * D.T.reflexes* path. reflexes * C.S. respiration* hypothermia * pseudobulbar palsy* seizures * coma

• Based on biochemical severity:– Mild: 130-135– Moderate: 125-129– Severe: <125

• Based on time of development: Acute or chronic

Classification of hyponatremia

Classification of hyponatremia

Hyponatremia

True Hyponatremia

Total Body Water > T.B.Na

T.B. Water < T.B. Na

i.e. no change in ratio between TBW & TB Na

Pseudohyponatremia

or

Hyponatremia

True Hyponatremia

ECF Water > ECF Na

ECF Water < ECF Na

i.e. no change in ratio between ECF-Water & ECF Na

Pseudohyponatremia

orHyperosmolar Hyponatremia

Hyponatremia

True Hyponatremia

Pseudohyponatremia

HypoosmolarHyperosmolar Hyponatremia

Normosmolar

Hyperosmolar

Hyperosmolar HyponatremiaDistributional

Osmotic-related

Osmotically-active material in plasma e.g.

glucose, mannitol, methanol etc...

100 mg/dl in plasma glucose 1.6 mmol/L

in plasma Na

Na+

G

G

G

GG

G

G

H2O

Na+Na+

Na+

Na+

Na+

Na+

PseudohyponatremiaDisplacement

HyperlipidemiaHyperproteinemiaSolids

Water

7% 20%

93% 80%Na

140

mm

ol/L

Na

150

mm

ol/L

Na

150

mm

ol/L

Na

120

mm

ol/L

PseudohyponatremiaDisplacement 2

S. Water = 99.1 - 0.1(S.L.) - 0.07(S.P.)S.L. 1g/L S.Na 1mmol/L

Measuring S Na

Flame emission spectrometer

Ion selective electrodeDirect

Indirect

Potentiometery

Normal HighDisplacement Osmotic

Approach to Hyponatremia

Psudohyponatremia

Low

ECF Volume

Decreased Normal Expanded

Heart FailureLiver cirrhosis

Nephrotic syndrome

Renal failure

measure P. osmolality

True Hyponatremia

Decreased

Approach to Hyponatremia 2

ExpandedNormal

ECF Volume

Urinary Na

Ur Na<10mEq/L Ur Na>20mEq/L

*Diarrhea *Vomiting*Ileus *Cathartics

*Peritonitis *Pancreatitis*Muscle damage *Burn

*Diuretics*Osmotic diuretics*Addison's disease

*Salt-loosing nephropathy

Normal

Approach to Hyponatremia 3

ExpandedDecreased

ECF Volume

Hypothyroidism

Hypopituitrism

Acute pain Psychosis

SIADH

DrugsGlucocorticoid

deficiency

Ur. Na >10mmol/L

SIADH

Pulmonary Disorders

CNS Disorders

*Encephalitis *Meningitis*Brain abscess *A. psychosis*Head trauma *Stroke*S.dural & s.arachnoid hrrge*Guillian-Barre syndrome*A. intermittent porphyria

LungPancreasDuodenum

Pneumonia: viral or bacterialAbcessTBAspergellosis

Carcinoma

Syndrome of Inappropriate Antidiuretic Hormone Secretion

AIDS

*Nicotine *Chlorpropamide *Tolbutamide *Clofibrate *Cyclophosphamide *Morphine *Barbiturates *Vincristine *Tegretol*Acetaminophen *Indomethacine *Isoproterenol

Drugs & Hyponatremia

When to Treat:* When there is s&s of hyponatremia* Energetic treatment if ther is s&s of herniation

HerniationDilated fixed pupils, unilat. dil. pupils, CVS instability, hypoventillation, impaired temp.

regulationRate of Correction:Not > 10 mmol/L 1st day then < 8 mmol/L/day to <130 mmol/L to avoid:

Central pontine

myelinolysis

Fluct. conscious., dysarthria, dysphonia, para- & quadripresis, seizures & coma

Management of Hyponatremia

Osmotic Demy-elination Synd.

Treatment of the Cause

Management of Hyponatremia

Decr. ECF vol

Norm. ECF vol

Incr. ECF vol

Add Sodium

Remove Excess Water

Furosemide + Hypertonic NaCl

ADH antagonists

Management of Hyponatremia -1Remove Excess Water

1- Water restriction:* Slow correction* < 1000 ml/day* Difficulty with nutrition & therapies

2- Osmotic diuresis:* Mannitol 25-100 g/day Hypotonic urine with > 50% free water* Dextrose 25%

For P. Na 10mmol/L, water=0.04 x B.Wt.

Calculations for Water Deficit or Excess

140mmol/L in ??? L

120 mmol/L in 49 L

168mmol/L in 35 L

140 mmol/L in ??? L

[Na]1 x Water1 = [Na]2 x Water2

Water2 =[Na]1

[Na]2

Water1 x

Water for 10mmol/L [Na]= 0.04 x BWt

140mmol/L in ??? L

120 mmol/L in 49 L

168mmol/L in 35 L

140 mmol/L in ??? L

= 49 x (120/140)= 42 L W = -7 L

= 35 x 168/140= 42 L W = +7 L

W1 = 49 L, Na1 = 120W2 = ???, Na2= 140

W1 = 35 L, Na1 = 168W2 = ???, Na2= 140

Calculations for Water Deficit or Excess

Add Sodium -1Management of Hyponatremia -2

120 mmol/L Na1 in 42 L TBWAdd ??? mmol Na to make it

140 mmol/L Na2 in the 42 L TBW

Added Na = (Na2 - Na1) X TBWTBW = 60% of B.Wt

Added Na = (Na2 - Na1) X 0.6 B.Wt = 20 X 0.6 X 70= 840 mmol free Sodium

Add Sodium -2

1 Litre

The mmol of Na to P. Na 1mmol/L = 0.6 x B.Wt.

The mmol of Na to P. Na 10 mmol/L = 6 x B.Wt.

0.9% NaCl 0.15 mmol/ml2.7% NaCl 0.46 mmol/ml3.0% NaCl 0.50 mmol/ml5.0% NaCl 0.85 mmol/ml6.0% NaCl 1.00 mmol/ml

To incrase S.Na 10 mmol/L in a 80 kg man give 500 ml NaCl 3% over 8 hs.

then 500 ml over 16 hs.

Management of Hyponatremia -3

1 Litre NaCl

1 Litre 0.9% NaCl

Isotonic = No extra water & No extra Na

1 Litre N Saline

=

1 Litre 3.0% NaCl

1 Litre N Saline +

450 mmol NaCl=

Hypertonic = No extra water But Extra Na

1 Litre NaCl

1 Litre 0.45% NaCl

0.5 Litre N Saline + 500 ml Water

=

Hypotonic = Extra water & No Extra Na

1 Litre G. 5%

1 Litre Excess Water

Non Na Soln = Extra water & No any Na

=

Frusemide + Hypertonic Saline

Indications: Acute or severe hyponatremia with CNS s&s

Method:

ADH AntagonistsDemeclocycline 300-600mg BID. Hepatic & renal toxocity!

Lithium:

ADH Receptor antagonist (Vaptans)!!!Less effective!

Management of Hyponatremia -4

1mg/kg furosemide iv infusion 1Litre of urine (75mmol Na): Subst. by 150ml 3% NaCl iv

HYPERNATREMIA

= WATER Deficit

Hypernatremia: Definition & Clinical Settings

• Plasma Na > 150 mEq/L• Less frequent than hyponatremia. • Because thirst obligates patients to drink water that relieves the hypernatremia with only a 1 to 2% rise in plasma osmolality.

• Thus patients with water losses generally do not develop hypernatremia unless there is a defect in thirst mechanism or the patient is unable to get his needs of water

• The very young, the very old and the very sick are those who may be liable

Sings & Symptoms of Hypernatremia -1• Polyuria and polydipsia may be due the underlying urinary concentrating defect rather than the hypernatremia itself

• Cellular dehydration due to ECF hyperosmolality affects mainly the CNS

Rate of Development: Acute is more serious than chronic;

Age of Patients: Old pts are more vulnerable than young

Acute + Adult = 75% mortalilty Acute + Children = 45% mortality

Sings & Symptoms of Hypernatremia -2

• CNS dysfunction correlats with degree of hyperosmolality

• Restlessness, increased irritability, lethargy• Muscle twitches, hyperflexia, tremulousness & ataxia• Above 375 mosm/Kg: tonic muscular spasticity, focal

& gand mal seizures

•Plasma osmolality > 325 mosm/Kg•Shrinkage of brain cell•Tearing of cereb vessels•Capillary & venous congestion•Subcortical & subarach. Bleeding•Venous sinus thrombosis

Causes of Hypernatremia -1

With Disturbed Thirst or Drinking

Loss of water or hypotonic soln

Hormonal salt retention

Administration of hypertonic soln

NaCl tab; NaHCO3 tab; NaHCO3 amp;

conc. NaCl soln

Cushing’s syn; Conn’s syn

Extrarenal loss

Excess sweat; diarrhea; vomiting

Renal Losses

Central DI Nephrogenic DI

DI due to Vasopressinase

Osmotic Diuresis

Causes of Hypernatremia -2

With Disturbed Thirst or Drinking

Hormonal salt retention

Administration of hypertonic soln

Renal Losses

Central DI Nephrogenic DI DI due to Vasopressinase:

pregnancy

Osmotic Diuresis: mannitol,

glucose, urea

Loss of water or hypotonic soln

Extrarenal loss

•Idiopathic •Truama •Surgery •Neoplasm: 1ry, 2ry Ca esp breast •Encephalitis •Sarcoidosis •Eosin. granuloma

Renal disease

Systemic diseases affecting kidneys

Diets & Drugs

•Hypokalemia •hypercalcemia

Nephrogenic DIPrimary Renal

disease

Systemic diseases affecting kidneysDiet Drugs

•Medul cyst dis; •CIN; •PCK; •Part. Obstr.; •CRF; •Polyuric ARF

•Multiple myeloma; •Amyloidosis; •Sarcoidosis; •Sjogren’s disease

•Lithium; •Democlocyclin; •Acetohexamide; •Glyburide; •Colchicin; •Tolazamide; •Propoxyphene

•Very low Salt; •Very low protein

Hypovolemia; TBW ; TBNa

Euvolemia; TBW ;

TBNa

Hypervolemia; TBW ; TBNa

U.Na variable

U.Osmo:

U.Na variable U.Osmo: variable

U.Na < 10; U.Osmo:

U.Na >20; U.Osmo:

or

Na gain: •1ry Hi-Ald; •Cushing’s •Hi-tonic Dx •Hi-ton. NaCl •NaHCO3 tab

Extrarenal losses: •Insens. loss: respirat., dermal losses

Ren. losses: •DI: central, nephro., partial, gestational •Hypodipsia

Extra-renal losses: •Insens. losses; •GIT losses

Ren. losses: •Osm. Or loop diuret, •post-obstruction; •Intrin. renal disease

U.Na >20; U.Osmo:

or

Diagnostic Approach to Hypernatremia

Treatment of the Cause

Management of Hypernatremia

Hypovolemia Euvolemia Hypervolemia

•Treat hypovolemia first by N saline

•Treat hypervolemia first by diuretics ± dialysis if RF

•Correct hypernatremia by Water replacement: oral water or IV 5% Dextrose.• Amount to be replaced to incr. Na 10 mmol/L = 0.04 X BWt

Rate of Correction: In acute cases: rapid correction, while in Chronic cases < 2.0 mosm/h or 1/2 correctn over 24 hs & 1/2 correction over next 24 hs

168mmol/L in 35 L

140 mmol/L in ??? L

= 35 x 168/140= 42 L W = +7 L

W1 = 35 L, Na1 = 168W2 = ???, Na2= 140

Correction of Water Deficir

W1 X Na1 = W2 X Na2

Serum Potassium Disorders

Dr Nagy Abdel-Hady Sayed-Ahmed

• Average diet contains~100 mEq daily; 90% of which is excreted by the kidney. Normal serum K+:3.5-5.5 mEq/L

• Hypokalemia and hyperkalemia are Common in the practice of medicine

• K+ is present in the body in a larger IC (90%) and a smaller EC (10%) pools that are in series with each other

• In potassium-depleted states with normal acid-base status, a 1 mEq/liter fall in the S.K+ level reflects the loss of about 300 mEq of K+.

• Conversely, if large amounts of K+ are administered acutely, the rise in S.K+ level is less than would be expected if the administered K+ were distributed solely in the ECF.

Physiological Considerations-1

Physiological Considerations-2

Factors Affecting Transcellular Shift of K+

Active transport processes:

•Na+-K+-ATPase: actively transport K+ into cell

•Insulin: promotes K+ transport into cell-adrenergic agents: promotes K+ transport into cell

•Mineralocorticoids: promotes K+ transport into cell

Passive transport processes:

•pH of ECF: alkalosis intracellular K+ shift, while acidosis extracellular K+ shift

•Increased ECF osmolality extracellular K+ shift

Physiological Considerations-3

Effect of pH changes on transcellular shift of K+

As a general rule, a reduction in plasma pH of 0.1 unit in metabolic acidosis raises the serum potassium level by ~0.5 mEq per liter, whereas a plasma pH increase of 0.1 unit produces a similar reduction in serum potassium.

0.1 unit of pH 0.5 mEq/L inverse of S.K+

Physiological Considerations-4Renal Handling of K+

• ~90% of dietary K+ is excreted by the kidney, while <10% is excreted by the GIT

• Almost all the K+ excreted in urine gains access to the urinary space by secretory mechanisms located across distal convoluted and collecting duct segments.

• Factors causing increased urinary loss of K+ are: mineralocorticoids delivery of Na+ to collecting ducts fluid flow to distal tubules Metabolic and respiratory alkalosis excretion of nonreabsorbable solutes

HYPOKALEMIA

Hypokalemia:Causes

Spurious total body potassium

Intracellular shift

Extreme leukocytosis

Hormonal: 2 adrenergic agonists

Drugs: 2 agonists, theophylline, Barium,

Digibind ttt, exog. Glucose & or insulin

Others: Refeeding, periodic

paralysis, ttt of megaloblastic

anemia

Inadequate intake

Renal loss

GIT loss

Decreased Total Body K+

Extrarenal Loss

• Overt diarrhea

• Copious drainage from a fistula

• Villous adenoma

• Intractable vomiting

• ? Loss in perspiration

• Anorexia nervosa or tea & toast diet

• Mineralocorticoid or glucocorticoid excess

• Bartter’s syndome

• Thiazide, loop, & osmotic diuretics

• Renal tubular acidosis

• Chronic metabolic alkalosis

• Liddle’s syndrome, acute leukemia, uretrosigmoidostomy

Renal Loss

Clinical Manifestation of Hypokalemia

Cardiac:•Abnormal ECG

•Atrial & ventricular arrhythmias

•Predispose to digitalis toxicity

Hemodynamic:•Variable BP

•Decr. pressor response to Ang.II

Neuromuscular:•GIT: constipation, ileus

•Skeletal ms: weakness, paralysis, rhabdomyolysis, respiratory paralysis

Endocrinal:•Decr. Renin & Aldosterone

•Decr. Insulin secretion diabetes

•Incr. Prostaglandin?

Kidney:•Decr. GFR & RBF

•Polyuria & polydypsia: conc. defect + stimulate thirst

•Incr. Renal NH3 production: Hep. enceph

•Na+ retention

•Cl- wasting • Metabolic alkalosis

Hypokalemia and Acid Base Disturbance

Hypokalemia + Metabolic Alkalosis:• Alkalosis as a cause of hypokalemia

• Thiazide or loop diuretics

• Mineralocoriticoid or GC excess

• Excess vomiting

• Bartter’s syndrome

• Mg depletion

Hypokalemia + Metabolic Acidosis:• Diarrhea • Diuresis with CA inhibitors

•Renal tubular acidosis type 1 and 2

•Ureterosigmoidostomy

Hypokalemia, continued

• ECG changes in hypokalemia

Management of Hypokalemia - 1Estimation of K+ Deficit

S. K+

3.5 - 3.0

3.0 - 2.5

2..5 - 2.0

Level

mild

moderate

severe

K+ deficit

100-200

200-400

400-800

ECG changes

No

variable

dangerous

Management of Hypokalemia - 2Route of K+ Administration:

• Oral route is preferred

• I.V. route is used in severe conditions

Rate of K+ Administration: • 100 - 250 mEq/day :

•in mild cases: 100

•in moderate cases: 200

•in severe cases: 400 mEq/day

• For parenteral route 10-30 mEq/hour: regular, slow and steady to allow equilibrium across cell membrane

Drugs for hypokalemia:• Potassium sparing diuretics: spironolactone,

ameloride and triametrene

• ACE inhibitors

• Angiotensin receptor blockers

• Beta adrenergic blockers

• Cyclsporine & Trimethoprim

Management of Hypokalemia - 3

Type of K+ salt:

• KCl for alkalosis; K gluconate, acetate or citrate for acidosis; K phosphate for DKA

HYPERKALEMIAHYPERKALEMIA

Hyperkalemia:Causes

Increased total body K+

Pseudo-hyperkalemia

• Hemolysis

• Leukocytosis

• Thrombocytosis

• Exercise + ischemia of z limb

• Acidosis esp. hyperchloremic

• Insulin deficiency

• Hypertonicity e.g. glucose or mannitol

• Drugs: - beta blockers - cationic a.a. - Succinyl choline - Digoxine

• Hyperkalemic periodic paralysis

E.C. Redistribution

of K+

Increased total body K+

Hyperkalemia:Causes-2

Pseudo-hyperkalemia

E.C. Redistribution

of K+

• Penicillin K: 1.7 mmol

• Light salt: 1g ~14 mmol

• Stored blood

Increased Intake

Mineralocorticoid deficiency

Renal Failure;

esp. GFR <5 ml/min

Decreased Excretion

Intrinsic Renal tubular defect in K secretion (pseudohypoaldosteronism)

Pseudo-hyperkalemia Increased

total body K+

E.C. Redistribution of K+

Hyperkalemia:Causes-3

Increased Intake

Decreased Excretion

Mineralocorticoid deficiency

Hypoaldosteronism:• Hyporeninemic: DN, CIN

• Hyperreninemic: resistance to aldosterone

Drugs:• ACEIs • NSAIDs

• Heparin • Cyclosporin

Addison’s disease

Pseudo-hyperkalemia Increased

total body K+

E.C. Redistribution of K+

Hyperkalemia:Causes-4

Increased Intake

Decreased Excretion

Intrinsic Renal tubular defect in K secretion

(pseudohypo-aldosteronism)

Renal Tx rejection

Multiple myeloma Amyloidosis

LE nephritis Sickle cell disease

Obstructive uropathy

Signs & Symptoms of Hyperkalemia

• Cardiac conduction effects with potential cardiac arrest

• ECG changes correlate to some extent with the degree of hyperkalemia

• Neuromuscular symptoms include tingling, parathesia, weakness and even flaccid paralysis

• Cardiac toxicity usually precedes other manifestations

• Hyperkalemia stimulates aldosterone, insulin, and glucagon secretion and suppresses plasma renin

Hyperkalemia – ECG ChangesHyperkalemia – ECG Changes

Management of Hyperkalemia - 1

Urgent ttt

Accord. to presence ECG changes or paralysis

• Decr. Diet K

• withdraw offending drugs

• Drugs that incr. K excretion: lasix, NaCl, K-exchange resins

• Treatment of cause

• Dialysis or Tx if RF

Immediate onset 1-3 min:

10-30 ml 10% Ca-Gluconate IV

Conservative ttt

Quick onset 5-10 min:

25g IV glucose + 5-10 U sol insulin

Quick onset 15-30 min:

50-150 mEq NaHCO3 IV

Quick onset 15-30 min:

Albuterol 20 mg in 4 ml nebulizer