FLUIDS AND ELECTROLYTES MALIK ALQUB MD. PhD.. The Cell Has a Limited Repetoire K+140 meq/L 280 milliosmoles/L H 2 0 moves passively Across cell membrane.

FLUIDS ANDELECTROLYTES

MALIK ALQUB MD. PhD.

The Cell Has a Limited Repetoire

K+140 meq/L280 milliosmoles/L

H20 moves passivelyAcross cell membraneAccording to the osmotic gradient

Na+140 meq/L280 milliosmoles/L

High Osmolality Outside The Cell=Shrinkage

Na+150 meq/L300 milliosmoles/L

K+140 meq/L280 milliosmoles/L

H2O

Low Osmolality Outside The Cell=Swelling

K+140 meq/L280 milliosmoles/L

H20

Na+120 meq/L240 milliosmoles/L

RUPTURE

Body Fluid Compartments

2/3 (65%) of TBW is intracellular (ICF) 1/3 extracellular water

25 % interstitial fluid (ISF) 5- 8 % in plasma (IVF intravascular fluid) 1- 2 % in transcellular fluids – CSF,

intraocular fluids, serous membranes, and in GI, respiratory and urinary tracts;

Body Fluids

•Water is most abundant body compound“Average” body water volume in reference tables based on healthy, nonobese 70-kg male• Volume averages 42 L in a 70-kg male• Plasma (3.5 L)• Interstitial fluid (10.5 L)• Intracellular fluid (28 L)

•Water is about 80% of body weight in newborn; about 60% in adult males; and about 50% in adult females

7

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

Movement of fluids due to: hydrostatic pressure osmotic pressure

Capillary filtration (hydrostatic) pressure Capillary colloid osmotic pressure Interstitial hydrostatic pressure Tissue colloid osmotic pressure

Movement of fluids

Osmotic Pressure When a solution containing non-penetrating solutes is

separated from pure water by a membrane, the pressure that must be applied to the solution to prevent the net flow of water into the solution (prevent osmosis) is termed the osmotic pressure of the solution.

The greater the osmolarity, the greater its osmotic pressure.

The lower the water concentration, the higher the osmotic pressure.

Osmotic pressure of a solution is directly proportional to the concentration of osmotically active particles in that solution

OSMOSIS

Movement of the solvent or water across a membrane

Involves solution or water Equalizes the concentration of ions

on each side of membrane Movement of solvent molecules

across a membrane to an area where there is a higher concentration of solute that cannot pass through the membrane

OSMOLALITY

Measure of solution’s ability to create osmotic pressure & thus affect movement of water

Number of osmotically active particles per kilogram of water

Plasma osmolality is 280-300* mOsm/ kg

ECF osmolality is determined by sodium MEASURE used in clinical practice to

evaluate serum & urine

Osmolality In Clinical Practice

Serum 280-300mOsm/kg; Urine 50-1400mOsm/kg

Serum osmolality can be estimated by doubling serum sodium More prescisely 2X Na + urea + glucose

Values are in mmol/L

Osmolarity Regulation

ICF Osm. = ECF Osm. Interstitial Osm = Serum Osm. Hypothalamus is the serum osmostat. It

stimulates thirst and ADH secretion. Primary Defense for Osmolarity =

Thirst Primary Defense for Osmolarity =

Renal excretion of water via ADH effect

Osmolarity Regulation

Maximum concentrating ability of kidney is approximately 800-1600mOsm/kg H20

Max. ADH effect decreases urine output to approximately 500 cc/day

No ADH release increases urine output to 15-20 Liters per day. Uosm = 40 – 80 mOsm/kg H20

Fluid Balance

Fluid Balance

Water circulates freely in ECF compartment

ECF and ICF are normally in osmotic equilibrium and no large-scale circulation occurs between compartments

If abnormal amounts of water move from plasma into interstitial fluid called?

Increases in plasma osmolality trigger thirst and release of antidiuretic hormone (ADH)

Primary Regulatory Hormones Affect fluid and electrolyte balance:

1. antidiuretic hormone (ADH)

2. aldosterone 3. natriuretic peptides

Antidiuretic Hormone (ADH)

Stimulates water conservation at kidneys: reducing urinary water loss concentrating urine

Stimulates thirst center: promoting fluid intake

ADH Production

Osmoreceptors in hypothalamus monitor osmotic concentration of ECF (plasma, CSF)

Change in osmotic concentration in plasma and CSF alters osmoreceptor activity

Osmoreceptor neurons secrete ADH in proportion to osmotic concentraiton via the posterior pituitary

Aldosterone

Is secreted by adrenal cortex in response to: rising K+ (sensed at the adrenal cortex) or falling

Na+ levels in blood activation of renin–angiotensin system (usually

due to changes in blood volume) Determines rate of Na+ absorption and K+

loss along DCT and collecting system “Water Follows Salt”

High plasma aldosterone concentration causes kidneys to conserve salt

Conservation of Na+ by aldosterone also stimulates water retention

Aldosterone

Figure 26.8

Natriuretic Peptides

ANP and BNP are released by cardiac muscle cells in response to abnormal stretching of heart walls due to elevated blood pressure or volume Reduce thirst Block release of ADH and aldosterone Cause diuresis Lower blood pressure and plasma volume

Fluid Shifts

Rapid water movements between ECF and ICF in response to an osmotic gradient

If ECF osmotic concentration increases: ECF becomes hypertonic to ICF water moves from inside cells to ECF

If ECF osmotic concentration decreases: ECF becomes hypotonic to ICF water moves from ECF into cells

Water Losses

Dehydration develops when water losses exceed water gains

If water is lost, but electrolytes retained: ECF osmotic concentration rises water moves from ICF to ECF in a fluid shift Both ECF and ICF will be slightly more

concentrated than before but they will be osmotically balanced

net change in ECF is small homeostatic responses will occur to replace

lost water

Water Losses

If water is lost, but electrolytes retained, ECF (and ICF) have higher concentrations, lower volumes

hypothalamus senses elevated ECF osmolarity this and releases ADH to restore fluid balance

New water in the ECF will shift into ICF and restore volumes and concentrations

Severe Water Loss

Causes: excessive perspiration inadequate water consumption repeated vomiting diarrhea

Water Gains If water is gained, but electrolytes are

not: ECF volume increases ECF becomes hypotonic to ICF fluid shifts from ECF to ICF Basically the opposite of water loss:

Reach osmotic balance but at lower concentrations, higher volumes

may result in overrhydration: distorts cells changes solute concentrations around enzymes disrupts normal cell functions

Water Gains

If water is gained, but electrolytes are not:

ECF is at lower concentration, higher volume

This triggers decrease in ADH release, fluid is lost and ICF will lose some water back to ECF, restoring both volume and concentration balance

Causes of Overhydration

Ingestion of large volume of fresh water Injection into bloodstream of hypotonic

solution Endocrine disorders like excessive ADH

production Inability to eliminate excess water in

urine: chronic renal failure heart failure cirrhosis

Disorders of Water Balance:

Figure 26.7a

Hypervolemia Hypovolemia

peripheral and presacral edema pulmonary edema jugular venous distension hypertension Decreased hematocrit decr. serum protein

poor skin turgor dry mucous membranes flat neck veins hypotension increased hematocrit Increased serum prot.

pitting edema

jugular venous distension

Electrolyte Balance

Electrolyte Balance

Requires equal rates of gain and loss for each electrolyte in the body

Electrolyte concentration directly affects water balance

Concentrations of individual electrolytes affect cell functions

37

Solutes – dissolved particles

Electrolytes – charged particles Cations – positively charged ions

Na+, K+ , Ca++, H+

Anions – negatively charged ionsCl-, HCO3

- , PO43-

Non-electrolytes .Proteins, urea, glucose, O2, CO2

Rules of Electrolyte Balance

• Most common problems with electrolyte balance are caused by imbalance between gains and losses of sodium ions

• Problems with potassium balance are less common, but more dangerous than sodium imbalance

• Changes in plasma sodium levels affect: Plasma volume, blood pressure ICF and interstitial fluid volumes

Na+, K+

Sodium holds a central position in fluid and electrolyte balance

Sodium is the dominant cation in ECF Sodium salts provide 90-95% of ECF

osmolarity (concentration): sodium chloride (NaCl) sodium bicarbonate

Sodium concentration in the ECF normally remains stable

Potassium Is the dominant cation in ICF

SODIUM (NA)

Main extracellular fluid (ECF) cation Helps govern normal ECF osmolality Helps maintain acid-base balance Activates nerve & muscle cells Influences water distribution (with

chloride)

Figure 27–4

Na+ Regulation

So changes in sodium concentration are corrected by ADH (not aldosterone)

Abnormal Na+ Concentrations in ECF

Hyponatremia: usu. body water content rises (overhydration)

Hypernatremia: usu. body water content declines

(dehydration)

Severe problems with electrolyte concentrations almost always occur secondary to fluid balance problems

HYPERNATREMIA

Serum Na + level > 148 mEq/L serum osmolality > 295 mOsm/kg

Etiologies of Hypernatremia

Primary Sodium Excess

Excess Intake of Sodium

Decreased Urinary Excretion of SodiumHyperaldosteronism

Primary Water LossPoor Intake of Water

Impaired access to water (i.e. infants, elderly patients with dementia or whom are bedbound)

Impaired thirst sensation

Hypothalamic lesions

Increased Urinary Loss of Water

ADH deficiency (Central Diabetes Isipidus DI)

ADH resistance (Nephrogenic DI)

Increased GI Loss of Water

Increased Transcutaneous Loss of Water

Transmembrane Shift of Water (most often due to rapid production of intracellular lactate)

HYPONATREMIA

Serum Na+ < 135 mEq/L (patient may be asymptomatic until level drops below 125)

Etiologies of Hyponatremia

Poor Intake of Sodium

Increased Urinary Loss of Sodium

Diuretics

Proximal RTA

Aldosterone deficiency/resistance

Increased GI Loss of Sodium (Fluid loss must be followed by repletion with free water).

Vomitting

Diarrhea

Increased Transcutaneous Loss of Sodium (Fluid loss must be followed by repletion with free water).

Excessive Intake of Water (1° polydipsia)

Psychosis

Decreased Urinary Excretion of Water

Decreased GFR

Increased ADH

Heart failure

Cirrhosis

SIADH

Transmembrane Shift of Water

Hyperglycemia

Primary Sodium Loss Primary Water Excess

Potassium Balance

98% of potassium in the human body is in ICF

Cells expend energy to recover potassium ions diffused from cytoplasm into ECF

Factors Rate of gain across digestive epithelium Rate of loss into urine, regulated along

distal portions of nephron and collecting system as Na+ from tubular fluid is exchanged for K+ in peritubular fluid

Mechanisms of regulation

Renal regulation

Transcellular shift between the intracellular and extracellular compartments

Factors in Tubular Secretion of K+

1. Changes in concentration of ECF: higher ECF concentration increases rate of

secretion (just because there’s more of it)2. Aldosterone levels affect K+ loss in urine

ion pumps reabsorb Na+ from filtrate in exchange for K+ from peritubular fluid

High K+ plasma concentrations stimulate aldosterone release, lower K+ but Na+ stays

3. Changes in pH: low ECF pH lowers peritubular fluid pH H+ rather than K+ is exchanged for Na+

in tubular fluid so ECF K+ increases

Transcellular shifts

Sodium-potassium ATPase Both insulin and epinephrine increase the

activity of sodium-potassium pump. (An increase in potassium level stimulates

insulin release. --- a feedback mechanism)

Potassium-hydrogen exchange to maintain electrical neutrality In acidosis In alkalosis

POTASSIUM (K+)

DOMINANT INTRACELLULAR ELECTROLYTE

NL SERUM LEVEL 3.5-5.5 *mEq/L

POTASSIUM (K)

Dominant cation in intracellular fluid (ICF)

Regulates cell excitability Permeates cell membranes, thereby

affecting cell’s electrical status Helps control ICF osmolality & ICF

osmotic pressure

HYPERKALEMIA

K+ > 5.5 mEq/L Dangerous due to potential for fatal

dysrhythmias, cardiac arrest Major cause is renal disease Beware of pseudohyperkalemia due

to prolonged tourniquet, hemolysis of blood, sampling above KCl infusion

Etiologies of Hyperkalemia

Excessive Dietary Intake

Decreased Urinary Excretion

Decreased GFR

Aldosterone deficiency

Adrenal insufficiency

ACE inhibitors

Aldosterone resistance

Potassium sparing diuretics

Internal Redistribution

Transmembrane Shift

Acidosis

Exercise

Cell Lysis

Rhabdomyolysis

Tumor lysis syndrome

HYPOKALEMIA

K+ < 3.5mEq/L Most common type of electrolyte

imbalance Major cause is increase renal loss

most often associated with diuretics

Can increase the action of digitalis

Etiologies of Hypokalemia

Poor Intake

Increased Urinary Excretion

Decreased reabsorption in loop of Henle

Furosemide

Hyperaldosteronism

Primary hyperaldosteronism

Adrenal adenoma

Adrenal hyperplasia

Secondary hyperaldosteronism

Renovascular hypertension

Renin-secreting tumor

Increased GI Losses

Diarrhea

Laxative abuse

Vomiting / NG drainage

Increased Transcutaneous Losses

sweating

Transmembrane ShiftAlkalosis

Insulin treatment for DKA

High catecholamine states

FLIUD IMBALANCES

The five types of fluid imbalances that may occur are:

Extracellular fluid imbalances(ECFVD) Extracellular fluid volume excess(ECFVE) Extracellular fluid volume shift Intracellular fluid vloume excess(ICFVE) Intrcellular fluid volume deficit(ICFVD)

EXTRACELULLAR FLUID VOLUME DEFICIT

An ECFVD, commonly called as dehydration , is a decrease in intravascular and interstitial fluids

An ECFVD can result in cellular fluid loss if it is sudden or severe

ETIOLOGY AND RISK FACTORS Severe vomiting Diaphoresis Traumatic injuries Third space fluid shifts [percardial, pleural,

pertonial and joint cavities] Fever Gatrointestinal suction Burns

Hyperventilation Decresed ADH secretions Diabetes insipidus Diuretic phase of acute renal failure Use of diuretics

ELDERLY ARE HIGH RISK OF ECFVD DUE TO Decreased thirst response Decreased renal concentration of urine Altered ADH response Increased drug – drug interaction Multiple chronic diseases Decreased access to fluids due to financial

or transportation barriers Chemical or physical restraint Changes in mental status

CLINICAL MANIFESTATION

In Mild ECFVD, 1to 2 L of water or 2% of the body weight is lost

In Moderate ECFVD, 3 to 5L of water loss or 5%weight loss

IN Severe ECFVD , 5 to 10 L of water loss or 8% of weight loss

CLINICAL MANIFESTATION

Thirst Muscle weakness Dry mucus

membrane;dry cracked lips or furrowed tongue

Eyeballs soft and sunken (severe deficit)

Apprehension , restlessness, headache , confusion, coma in severe deficit

Elevated temperature Tachycardia, weak

thready pulse

Postural systolic BP falls >25mm Hg and diastolic fall > 20 mm Hg , with pulse increases > 30

Narrowed pulse pressure, decreased

Flattened neck veins in supine position

Weight loss Oliguria(< 30 mlper

hour) Decreased number and

moisture in stools

LABORATORY FINDINGS

Increased osmolality(> 295 mOsm/ kg) Increased or normal serum sodium level

(> 145mEq/ L ) Increase BUN (>25 mg / L ) Hyperglycemia ( >120 mg /dl ) Elevated hematocrit (> 55%)

MANAGEMENT

Mild fluid volume loss can be corrected with oral fluid replacement

-if client tolerates solid foods advice to take 1200 ml to 1500ml of oral fluids

-if client takes only fluids, increase the total intake to 2500 ml in 24 hours

EXTRACELLULAR FLUID VOLUME EXCESS

ECFVE is increased fluid retention in the intravasular and interstitial spaces

ETIOLOGY AND RISK FACTORS

Heart failure Renal disorders Cirrhosis of liver Increased ingestion of high sodium foods Excessive amount of IV fluids containing

sodium Electrolyte free IV fluids SIADH,Sepsis decreased colloid osmotic pressure lymphatic and venous obstruction

CLINICAL MANIFESTATION

Constant irritating cough Dyspnea & crackles in lungs Cyanosis, pleural fffusion Neck vein obstruction Bounding pulse &elevated BP Pitting & sacral edema Weight gain Change in level of consiousness

LAB INVESTIGATION

serum osmolality <275mOsm/ kg Low , normal or high sodium Decreased hematocrit [ < 45%] Specific gravity below 1.010 Decreased BUN [< 8mg/ dl]

MANAGEMENT

Diuretics [combination of potassium sparing and potassium depleting diuretics]

In people with CHF, ACE inhibitors and low dose of beta blockers are used

A low sodium diet