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FLUID AND ELECTROLYTE IMBALANCES

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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 (third space)

 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

Balance
Fluid and electrolyte homeostasis is maintained in the body
Neutral balance: input = output

Positive balance: input > output

Negative balance: input < output

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Solutes dissolved particles

Electrolytes charged particles
Cations positively charged ions

Na+, K+ , Ca++, H+ Anions negatively charged ions Cl-, HCO3- , PO43-

Non-electrolytes - Uncharged
Proteins, urea, glucose, O2, CO2
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 Body fluids are:

Electrically neutral Osmotically maintained

Specific number of particles per volume of fluid

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Homeostasis maintained by:

Ion transport
Water movement Kidney function

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Tonicity
Isotonic Hypertonic Hypotonic

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Cell in a hypertonic solution

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Cell in a hypotonic solution

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Movement of body fluids Where sodium goes, water follows. Diffusion movement of particles down a concentration gradient.
Osmosis diffusion of water across a selectively permeable membrane Active transport movement of particles up a concentration gradient ; requires energy
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ICF to ECF osmolality changes in ICF not rapid

IVF ISF IVF happens constantly due to changes in fluid pressures and osmotic forces at the arterial and venous ends of capillaries

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Makulay ang Buhay sa Sinabawang Gulay

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Regulation of body water

ADH antidiuretic hormone + thirst
Decreased amount of water in body
Increased amount of Na+ in the body Increased blood osmolality

Decreased circulating blood volume

Stimulate osmoreceptors in hypothalamus

ADH released from posterior pituitary Increased thirst

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Result: increased water consumption increased water conservation Increased water in body, increased volume and decreased Na+ concentration

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Dysfunction or trauma can cause: Decreased amount of water in body Increased amount of Na+ in the body Increased blood osmolality Decreased circulating blood volume

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Edema is the accumulation of fluid within the interstitial spaces.

Causes: increased hydrostatic pressure lowered plasma osmotic pressure

increased capillary membrane permeability

lymphatic channel obstruction

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Hydrostatic pressure increases due to: Venous obstruction: thrombophlebitis (inflammation of veins)

hepatic obstruction
tight clothing on extremities

prolonged standing
Salt or water retention congestive heart failure renal failure
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Decreased plasma osmotic pressure:

plasma albumin (liver disease or protein malnutrition) plasma proteins lost in : glomerular diseases of kidney hemorrhage, burns, open wounds and cirrhosis of liver

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Increased capillary permeability:

Inflammation immune responses

Lymphatic channels blocked: surgical removal infection involving lymphatics lymphedema

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Fluid accumulation:
increases distance for diffusion may impair blood flow = slower healing increased risk of infection pressure sores over bony prominences Psychological effects
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Edema of specific organs can be life threatening (larynx, brain, lung)

Water is trapped, unavailable for metabolic processes. Can result in dehydration and shock. (severe burns)

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Electrolyte balance
Na + (Sodium)
90 % of total ECF cations 135 -145 mEq / L

Pairs with Cl- , HCO3- to neutralize charge

Low in ICF Most important ion in regulating water balance

Important in nerve and muscle function

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Regulation of Sodium
Renal tubule reabsorption affected by hormones:

Aldosterone

Renin/angiotensin
Atrial Natriuretic Peptide (ANP)

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Potassium
Major intracellular cation
ICF conc. =3.5-5.5 mEq/L Resting membrane potential Regulates fluid, ion balance inside cell pH balance

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Regulation of Potassium
Through kidney

Aldosterone Insulin

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Isotonic alterations balance

in water

Occur when TBW changes are accompanied by = changes in electrolytes

Loses plasma or ECF

Isotonic fluid loss

ECF volume, weight loss, dry skin and mucous membranes, urine output, and hypovolemia ( rapid heart rate, flattened neck veins, and normal or B.P. shock)

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 Isotonic fluid excess

Excess IV fluids Hypersecretion of aldosterone Effect of drugs cortisone

Get hypervolemia weight gain, decreased hematocrit, diluted plasma proteins, distended neck veins, B.P. Can lead to edema ( capillary hydrostatic pressure) pulmonary edema and heart failure

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No Dandruff,Just Soft Hair

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Electrolyte imbalances: Sodium

Hypernatremia (high levels of sodium)
Plasma Na+ > 145 mEq / L Due to Na + or water Water moves from ICF ECF Cells dehydrate

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 Hypernatremia Due to:

Hypertonic IV soln. Oversecretion of aldosterone

Loss of pure water

Long term sweating with chronic fever Respiratory infection water vapor loss Diabetes polyuria Insufficient intake of water (hypodipsia)

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Clinical manifestations of Hypernatremia

Thirst
Lethargy Neurological dysfunction due to dehydration

of brain cells Decreased vascular volume

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Treatment of Hypernatremia
Lower serum Na+

Isotonic salt-free IV fluid Oral solutions preferable

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Hyponatremia
Overall decrease in Na+ in ECF Two types: depletional and dilutional

Depletional Hyponatremia
Na+ loss: diuretics, chronic vomiting Chronic diarrhea Decreased aldosterone Decreased Na+ intake

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 Dilutional Hyponatremia:
Renal dysfunction with intake of hypotonic fluids Excessive sweating increased thirst intake of

excessive amounts of pure water Syndrome of Inappropriate ADH (SIADH) or oliguric renal failure, severe congestive heart failure, cirrhosis all lead to:

Impaired renal excretion of water

Hyperglycemia attracts water

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 Neurological symptoms

Clinical manifestations of Hyponatremia

Lethargy, headache, confusion, apprehension, depressed

reflexes, seizures and coma

Muscle symptoms
Cramps, weakness, fatigue

Gastrointestinal symptoms
Nausea, vomiting, abdominal cramps, and diarrhea

Tx limit water intake or discontinue meds

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Hypokalemia
Serum K+ < 3.5 mEq /L
Beware if diabetic

Insulin gets K+ into cell Ketoacidosis H+ replaces K+, which is

lost in urine

adrenergic drugs or epinephrine

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Causes of Hypokalemia
Decreased intake of K+
Increased K+ loss

Chronic diuretics Acid/base imbalance Trauma and stress

Increased aldosterone
Redistribution between ICF and ECF
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Clinical manifestations of Hypokalemia

Neuromuscular disorders Weakness, flaccid paralysis, respiratory

arrest, constipation

Dysrhythmias, appearance of U wave Postural hypotension Cardiac arrest Others table 6-5 Treatment Increase K+ intake, but slowly, preferably by foods

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Hyperkalemia
Serum K+ > 5.5 mEq / L
Check for renal disease Massive cellular trauma Insulin deficiency Addisons disease Potassium sparing diuretics Decreased blood pH Exercise causes K+ to move out of cells
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Clinical manifestations of Hyperkalemia

Early hyperactive muscles , paresthesia
Late - Muscle weakness, flaccid paralysis Change in ECG pattern Dysrhythmias Bradycardia , heart block, cardiac arrest

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Treatment of Hyperkalemia
If time, decrease intake and increase renal excretion
Insulin + glucose

Bicarbonate
Ca++ counters effect on heart

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Calcium Imbalances
Most in ECF Regulated by: Parathyroid hormone

Blood Ca++ by stimulating osteoclasts GI absorption and renal retention Calcitonin from the thyroid gland Promotes bone formation renal excretion

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Love ko toh!

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Hypercalcemia
Results from:
Hyperparathyroidism Hypothyroid states Renal disease Excessive intake of vitamin D Milk-alkali syndrome Certain drugs Malignant tumors hypercalcemia of malignancy

Tumor products promote bone breakdown Tumor growth in bone causing Ca++ release

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Hypercalcemia
Usually also see hypophosphatemia Effects:
Many nonspecific fatigue, weakness, lethargy Increases formation of kidney stones and pancreatic stones Muscle cramps Bradycardia, cardiac arrest Pain GI activity also common

Nausea, abdominal cramps Diarrhea / constipation

Metastatic calcification
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Hypocalcemia
Hyperactive neuromuscular reflexes and tetany

differentiate it from hypercalcemia Convulsions in severe cases Caused by:

Renal failure Lack of vitamin D Suppression of parathyroid function Hypersecretion of calcitonin Malabsorption states Abnormal intestinal acidity and acid/ base bal. Widespread infection or peritoneal inflammation
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Hypocalcemia
Diagnosis:
Chvosteks sign

Trousseaus sign

Treatment
IV calcium for acute Oral calcium and vitamin D for chronic

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DEFINITION : Phosphorus Deficit (Serum Phosphate levels less than 1.7 mEq/L or less than 2.5 mg/dl or less than 0.8 mmol/L) ETIOLOGY : 1. Decreased PO4 = Intake/Absorption: A. Excessive or prolonged antacid use (Antacids absorbs PO4) B. Chronic LEM, Alcoholism C. Malnutrition D. Increased Vitamin D (increased Ca++, decreased PO4)

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.Nursing Goals :

Prevent Hypophosphatemia 2. Restore normal PO4 levels Nursing Actions : 1. For mild PO4 = decreased a. remove precipitated functions b. give adequate PO4 in diet 2. For severe PO4 = decreased a. PO4 = replacement IV - - - - K+ PO4 tablets b. Watch out for PO4 toxicity c. High PO4 = diet - - - - - carbonated drinks, processed foods, milk, eggs, meats
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H Y P E R P H O S P H A TE M I A DEFINITION : Phosphate Excess (Serum PO4 = greater than 4.5 mg/dl or Greater than 2.6 mEq/L or Greater than 1.5 mmol/L ETIOLOGY : 1. Increased PO4 = Intake/Absorption : A. Excessive PO4 = therapy especially IV B. Excessive Fleets enema (Phospho Soda and Neutra Phosphate) 2. Incresaed PO4 = Release from cells

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Decreased PO4 Intake 1. Low PO4 diet * Avoid : milk, eggs, liver, nuts, kidney, sardines any food with milk, poultry, legumes, hard cheese, creams, whole grain cereals, dried fruits, dried vegetables, sweetbreads. 2. Avoid PO4 continuing enemas, laxatives 3. Hydrate with Ca++ continuing IV solutions. Diurese to eliminate excess PO4 = 4. Administer ALOH - gel in the form of antacids (via GIT) called PO4 = binding agents 5. Dialysis for Renal failure

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HYPOMAGNESEMIA DEFINITION : Magnesium Deficit (Serum Mg++ less than 1.5 mEq/L) ETIOLOGY : Decrease Mg++ Intake/Absorption A. Prolonged malnutrition - Anorexis nervosa,Bulimia B. Starvation C. IV therapy without Mg++ D. Malabsorption syndromes E. Steatorrhea, Pancreatitis F. Ileal resection G. Chronic Alcoholism H. Hypercalcemia

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Nursing Actions : I. For Mild Mg++ Deficit : * Dietary replacement of Mg++ - green vegetables - nuts, legumes, peanuts - chocolate , cocoa, tea and coffee - fruits, bananas, grape fruits, orange II. For Severe Mg++ Deficit : * Mg++ SO4 = IV Magnesium SO4 (Epson salt, Mg++SO4=) Dose : 15 gms. in1 glass H2O or other liquid. 1 - 5 gms. (25-50 % solution) up to 6x Daily 1 - 4 gms. (10-20% solution)IV Toxicity : : drowsiness : tetany : decreased or (-) deep tendon reflexes : decreased BP, decreased RR, decreased HR : Flushing, sweating
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HYPERMAGNESEMIA DEFINITION : Magnesium Excess (Serum Mg++ greater than 2.5 mEq/L Or greater than 3.0 mg% Or greater than 1.25 mmol/L Or S.I.U.) ETIOLOGY : 1. Increase Mg++ Intake or Absorption 1.Increase use Mg++ spontiniung antacids, cathartics irrigating solutions 2.Increase IV infusion of MG++ 3.Increase treatment with MgSO4 4.Aspiration of sea water (near drowning) 2. Increased Mg++ Retention Oliguria Renal Failure Adrenal Insufficiency (Addisons) Severe Dehydration with Oliguria

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. Prevent onset of Mg++ Excess : Prevent administration of MG++ to patient with Renal Failure Check urine output For seriously ill patients, check for Mg++ toxicity when administering MgSO4 C. Avoid Mg++ rich foods : Whole grain cereals Dark green vegetables Dried peas and beans Soy products Nuts especially cashews and almonds Peanut butter Cocoa, chocolates Bananas, sea salt Egg yolk 2. Restore Mg++ at normal Hydrate with D5W Diureses with loop diuretics Avoid Mg++ containing antacids Administer I.V. Ca++ Gluconate 10 cc slow IV as antidote to Mg++ * Increase Ca++ - - - Decrease Mg++ Dialysis for Renal Failure
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3. Prevent Complications : Be alert for s/s of respiratory difficulty related to respiratory paralysis or laryngospasm Monitor for Cardiac Dysrythmias and abnormal vital signs (decreased BP, decreased HR, decreased RR) EKG change : Increased T wave : Increased PR interval : Increased QRS complex

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No SUGAR

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By: Franco R. Ganacias

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SLUMDOG MILLIONAIRE

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Acid and Base Balance and Imbalance

by: Franco R. Ganacias

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pH Review
pH = - log [H+]
H+ is really a proton Range is from 0 - 14 If [H+] is high, the solution is acidic; pH < 7 If [H+] is low, the solution is basic or alkaline ;

pH > 7

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Normal Blood Gas

Partial pressure of oxygen (PaO2) - 75 - 100 mmHg
Partial pressure of carbon dioxide (PaCO2) -

35 - 45 mmHg A pH of 7.35 - 7.45 Oxygen saturation (SaO2) - 94 - 100% Bicarbonate - (HCO3) - 22 - 26 mEq/L

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Arterial Blood Gas

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 Acids are H+ donors. Bases are H+ acceptors, or give up OH- in

solution. Acids and bases can be:

Strong dissociate completely in solution

HCl, NaOH Weak dissociate only partially in solution Lactic acid, carbonic acid

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The Body and pH

Homeostasis of pH is tightly controlled
Extracellular fluid = 7.4 Blood = 7.35 7.45 < 6.8 or > 8.0 death occurs Acidosis (acidemia) below 7.35 Alkalosis (alkalemia) above 7.45

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Small changes in pH can produce major disturbances

Most enzymes function only with narrow pH ranges
Acid-base balance can also affect electrolytes

(Na+, K+, Cl-) Can also affect hormones

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The body produces more acids than bases

Acids take in with foods
Acids produced by metabolism of lipids and

proteins Cellular metabolism produces CO2. CO2 + H20 H2CO3 H+ + HCO3-

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Control of Acids
1. Buffer systems

Take up H+ or release H+ as conditions change Buffer pairs weak acid and a base Exchange a strong acid or base for a weak one Results in a much smaller pH change
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Bicarbonate buffer
Sodium Bicarbonate (NaHCO3) and carbonic acid (H2CO3)
Maintain a 20:1 ratio : HCO3- : H2CO3

HCl + NaHCO3 H2CO3 + NaCl

NaOH + H2CO3 NaHCO3 + H2O

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Phosphate buffer
Major intracellular buffer
H+ + HPO42- H2PO4-

OH- + H2PO4- H2O + H2PO42-

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Protein Buffers
Includes hemoglobin, work in blood and ISF

Carboxyl group gives up H+

Amino Group accepts H+ Side chains that can buffer H+ are present on 27 amino

acids.

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2. Respiratory mechanisms
Exhalation of carbon dioxide
Powerful, but only works with volatile acids Doesnt affect fixed acids like lactic acid CO2 + H20 H2CO3 H+ + HCO3 Body pH can be adjusted by changing rate

and depth of breathing

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3. Kidney excretion
Can eliminate large amounts of acid
Can also excrete base Can conserve and produce bicarb ions Most effective regulator of pH If kidneys fail, pH balance fails

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Rates of correction
Buffers function almost instantaneously
Respiratory mechanisms take several minutes

to hours Renal mechanisms may take several hours to days

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Acid-Base Imbalances
pH< 7.35 acidosis
pH > 7.45 alkalosis The body response to acid-base imbalance is

called compensation May be complete if brought back within normal limits Partial compensation if range is still outside norms.
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Compensation
If underlying problem is metabolic, hyperventilation or hypoventilation can help : respiratory compensation. If problem is respiratory, renal mechanisms can bring about metabolic compensation.

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Acidosis
Principal effect of acidosis is depression of the CNS

through in synaptic transmission. Generalized weakness Deranged CNS function the greatest threat Severe acidosis causes Disorientation coma death

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Alkalosis
Alkalosis causes over excitability of the central and peripheral nervous systems. Numbness Lightheadedness It can cause : Nervousness muscle spasms or tetany Convulsions Loss of consciousness Death

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Respiratory Acidosis
Carbonic acid excess caused by blood levels of CO2 above 45 mm Hg. Hypercapnia high levels of CO2 in blood Chronic conditions:
Depression of respiratory center in brain that

controls breathing rate drugs or head trauma Paralysis of respiratory or chest muscles Emphysema

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Respiratory Acidosis
Acute conditons:
Adult Respiratory Distress Syndrome Pulmonary edema

Pneumothorax

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Compensation for Respiratory Acidosis

Kidneys eliminate hydrogen ion and retain bicarbonate ion

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 Breathlessness

Signs and Symptoms of Respiratory Acidosis

Restlessness
Lethargy and disorientation Tremors, convulsions, coma Respiratory rate rapid, then gradually depressed Skin warm and flushed due to vasodilation

caused by excess CO2

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Treatment of Respiratory Acidosis

Restore ventilation
IV lactate solution Treat underlying dysfunction or disease

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Respiratory Alkalosis
Carbonic acid deficit
pCO2 less than 35 mm Hg (hypocapnea) Most common acid-base imbalance Primary cause is hyperventilation

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Respiratory Alkalosis
Conditions that stimulate respiratory center:
Oxygen deficiency at high altitudes
Pulmonary disease and Congestive heart failure

caused by hypoxia Acute anxiety Fever, anemia Early salicylate intoxication Cirrhosis Gram-negative sepsis

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Compensation of Respiratory Alkalosis

Kidneys conserve hydrogen ion
Excrete bicarbonate ion

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Treatment of Respiratory Alkalosis

Treat underlying cause
Breathe into a paper bag IV Chloride containing solution Cl- ions

replace lost bicarbonate ions

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Metabolic Acidosis
Bicarbonate deficit - blood concentrations of bicarb

drop below 22mEq/L Causes:

Loss of bicarbonate through diarrhea or renal dysfunction

Accumulation of acids (lactic acid or ketones)

Failure of kidneys to excrete H+

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Symptoms of Metabolic Acidosis

Headache, lethargy
Nausea, vomiting, diarrhea Coma Death

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Compensation for Metabolic Acidosis

Increased ventilation
Renal excretion of hydrogen ions if possible K+ exchanges with excess H+ in ECF ( H+ into cells, K+ out of cells)

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Treatment of Metabolic Acidosis

IV lactate solution

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Metabolic Alkalosis
Bicarbonate excess - concentration in blood is greater than 26 mEq/L Causes:

Excess vomiting = loss of stomach acid Excessive use of alkaline drugs Certain diuretics Endocrine disorders Heavy ingestion of antacids Severe dehydration
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Compensation for Metabolic Alkalosis

Alkalosis most commonly occurs with renal dysfunction, so cant count on kidneys
Respiratory compensation difficult

hypoventilation limited by hypoxia

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Symptoms of Metabolic Alkalosis

Respiration slow and shallow
Hyperactive reflexes ; tetany Often related to depletion of electrolytes Atrial tachycardia Dysrhythmias

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Treatment of Metabolic Alkalosis

Electrolytes to replace those lost
IV chloride containing solution Treat underlying disorder

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Diagnosis of Acid-Base Imbalances

1. Note whether the pH is low (acidosis) or high (alkalosis)
2. Decide which value, pCO2 or HCO3- , is

outside the normal range and could be the cause of the problem. If the cause is a change in pCO2, the problem is respiratory. If the cause is HCO3- the problem is metabolic.

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3. Look at the value that doesnt correspond to the observed pH change. If it is inside the normal range, there is no compensation occurring. If it is outside the normal range, the body is partially compensating for the problem.

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Example
A patient is in intensive care because he suffered a severe myocardial infarction 3 days ago. The lab reports the following values from

an arterial blood sample:

pH 7.3 HCO3- = 20 mEq / L ( 22 - 26)

pCO2 = 32 mm Hg (35 - 45)

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Diagnosis
Metabolic acidosis
With compensation

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