Bienvenidos!

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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)

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 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

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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 water balance
 Occur when TBW changes are

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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

 β – 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  Addison’s 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:
 Chvostek’s sign  Trousseau’s sign

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

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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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•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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+ 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 (Addison’s) •Severe Dehydration with Oliguria

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+ •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  Doesn’t 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  Restlessness

Signs and Symptoms of Respiratory Acidosis

 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 can’t 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 doesn’t 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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