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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:
Capillary filtration (hydrostatic) pressure Capillary colloid osmotic pressure Interstitial hydrostatic pressure
Balance
Fluid and electrolyte homeostasis is maintained in the body
Neutral balance: input = output
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Non-electrolytes - Uncharged
Proteins, urea, glucose, O2, CO2
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Tonicity
Isotonic Hypertonic Hypotonic
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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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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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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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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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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
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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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in water
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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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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Long term sweating with chronic fever Respiratory infection water vapor loss Diabetes polyuria Insufficient intake of water (hypodipsia)
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Treatment of Hypernatremia
Lower serum Na+
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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:
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Neurological symptoms
Muscle symptoms
Cramps, weakness, fatigue
Gastrointestinal symptoms
Nausea, vomiting, abdominal cramps, and diarrhea
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Hypokalemia
Serum K+ < 3.5 mEq /L
Beware if diabetic
lost in urine
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Causes of Hypokalemia
Decreased intake of K+
Increased K+ loss
Increased aldosterone
Redistribution between ICF and ECF
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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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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
Hypocalcemia
Hyperactive neuromuscular reflexes and tetany
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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SLUMDOG MILLIONAIRE
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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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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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HCl, NaOH Weak dissociate only partially in solution Lactic acid, carbonic acid
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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
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Phosphate buffer
Major intracellular buffer
H+ + HPO42- H2PO4-
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Protein Buffers
Includes hemoglobin, work in blood and ISF
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
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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
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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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Breathlessness
Restlessness
Lethargy and disorientation Tremors, convulsions, coma Respiratory rate rapid, then gradually depressed Skin warm and flushed due to vasodilation
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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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Metabolic Acidosis
Bicarbonate deficit - blood concentrations of bicarb
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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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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
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Diagnosis
Metabolic acidosis
With compensation
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