Fluids And Electrolytes Handouts

Lecture Notes on Fluids and Electrolytes Prepared By: Mark Fredderick R Abejo R.N, MAN

STI COLLEGE GLOBAL CITY College of Nursing MEDICAL AND SURGICAL NURSING

solute – the substance dissolved solvent – substance in which the solute is dissolved usually water (universal solvent) molar solution (M) - # of gram-molecular weights of solute per liter of solution osmolality – concentration of solute per kg of water normal range = 275-295 mOsm/kg of water osmolarity – concentration of solute per L of solution * since 1kg=1L, & water is the solvent of the human body, osmolarity & osmolality are used interchangeably

Fluids and Electrolytes IV.

Lecturer: Mark Fredderick R. Abejo RN, MAN ________________________________________________ FLUIDS & ELECTROLYTES I. Fluid Status of Human Body A. Homeostasis: state of the body when maintaining a state of balance in the presence of constantly changing conditions B. Includes balance of fluid, electrolytes, and acidbase balance C. Body water intake and output approximately equal (2500 mL/24 hr.)

Adult body: 40L water, 60% body weight 2/3 intracellular 1/3 extracellular (80% interstitial, 20% intravascular) Infant: 70-80% water Elderly: 40-50% water

II. Body Fluid Composition A. Water: 60% of body weight B. Electrolytes: substances that become charged particles in solution 1. Cations: positively charged (e.g. Na+, K+) 2. Anions: negatively charged (e.g. Cl-) 3. Both are measured in milliequivalents per liter (mEq/L) C. Balance of hydrostatic pressure and osmotic pressure regulates movement of water between intravascular and interstitial spaces III. Body Fluid Distribution: A. 2 body compartments: 1. Intracellular fluids (ICF): fluids within cells of body [major intracellular electrolytes: Potassium (K+), Magnesium (Mg +2)] 2. Extracellular fluids (ECF): fluid outside cells; [major extracellular electrolytes: Sodium (Na+), Chloride(Cl-)]; this is where transportation of nutrients, oxygen, and waste products occurs B.

Locations of ECF: 1. Interstitial: fluid between most cells 2. Intravascular: fluid within blood vessels; also called plasma 3. Transcellular: fluids of body including urine, digestive secretion, cerebrospinal, pleural, synovial, intraocular, gonadal, pericardial

MS: Fluids and Electrolyte

Mechanisms of Body Fluid Movement (i.e. movement of solutes, solvents across different extracellular locations) A. Osmosis: water is mover; water moves from lower concentration to higher concentration 1. Normal Osmolality of ICF and ECF: 275 – 295 mOsm/kg 2. Types of solutions according to osmolality Isotonic: all solutions with osmolality same as that of plasma .Body cells placed in isotonic fluid: neither shrink nor swell Hypertonic: fluid with greater concentration of solutes than plasma Cells in hypertonic solution: water in cells moves to outside to equalize concentrations: cells will shrink Hypotonic: fluid with lower concentration of solutes than plasma Cells in hypotonic solution: water outside cells moves to inside of cells: cells will swell and eventually burst (hemolyze) 3. Different intravenous solutions, used to correct some abnormal conditions, categorized according to osmolality: B.

C.

D.

Diffusion: solute molecules move from higher concentration to lower concentration 1. Solute, such as electrolytes, is the mover; not the water 2. Types: simple and facilitated (movement of large water-soluble molecules) Filtration: water and solutes move from area of higher hydrostatic pressure to lower hydrostatic pressure 1. Hydrostatic pressure is created by pumping action of heart and gravity against capillary wall 2. Usually occurs across capillary membranes Active Transport: molecules move across cell membranes against concentration gradient; requires energy, e.g. Na – K pump

Hydrostatic pressure -pushes fluid out of vessels into tissue space; higher to lower pressure – due to water volume in vessels; greater in arterial end – swelling: varicose veins, fluid overload, kidney failure & CHF Osmotic pressure -pulls fluid into vessels; from weaker concentration to stronger concentration - from plasma proteins; greater in venous end - swelling: liver problems, nephrotic syndrome

Abejo

Lecture Notes on Fluids and Electrolytes Prepared By: Mark Fredderick R Abejo R.N, MAN

V.

Mechanisms that Regulate Homeostasis: How the body adapts to fluid and electrolyte changes? A. B.

C.

D.

E.

Thirst: primary regulator of water intake (thirst center in brain) Kidneys: regulator of volume and osmolality by controlling excretion of water and electrolytes Renin-angiotension-aldosterone mechanism: response to a drop in blood pressure; results from vasoconstriction and sodium regulation by aldosterone Antidiuretic hormone: hormone to regulate water excretion; responds to osmolality and blood volume Atrial natriuretic factor: hormone from atrial heart muscle in response to fluid excess; causes increased urine output by blocking aldosterone

Fluid Balance Regulation Thirst reflex triggered by: 1. decreased salivation & dry mouth 2. increased osmotic pressure stimulates osmoreceptors in the hypothalamus 3. decreased blood volume activates the renin/angiontensin pathway, which simulates the thirst center in hypothalamus

ADH – produced by hypothalamus, released by posterior pituitary when osmoreceptor or baroreceptor is triggered in hypothalamus Aldosterone – produced by adrenal cortex; promotes Na & water reabsorption

Sensible & Insensible Fluid Loss Sensible: Insensible:

urine, vomiting, suctioned secretions lungs , skin, GI and evaporation

Normal Fluid Intake and Loss in Adults Intake:  Water in food  Water from oxidation  Water in liquid

Output:    

1,000 mls 300 mls 1,200 mls

TOTAL

2,500 mls

Skin Lungs Feces Kidneys TOTAL

500 mls 300 mls 150 mls 1,500 mls 2,500 mls

Renin-Angiotensin 1. drop in blood volume in kidneys = renin released 2. renin = acts on plasma protein angiotensin (released by the liver) to form angiotensin I 3. ACE = converts Angiotensin I to Angiotensin II in the lungs 4. Angiotensin II = vasoconstriction & aldosterone release MS: Fluids and Electrolyte

Abejo

Lecture Notes on Fluids and Electrolytes Prepared By: Mark Fredderick R Abejo R.N, MAN

IV Fluids Isotonic

Hypotonic

Hypertonic

 LR PNSS (0.9%NSS) NM D5W - isotonic in bag - dextrose=quickly metabolized=hypotonic D2.5W 0.45% NSS 0.3% NSS 0.2% NSS D50W D10W D5NSS D5LR 3%NSS

Colloids (usually CHONs) & Plasma expanders Dextran – synthetic polysaccharide, glucose solution increase concentration of blood, improving blood volume up to 24 hrs contraindicated: heart failure, pulmonary edema, cardiogenic shock, and renal failure Hetastarch – like Dextran, but longer-acting expensive derived from corn starch Composition of Fluids Saline solutions – water, Na, Cl Dextrose solutions – water or saline, calories Lactated Ringer‟s – water, Na, Cl, K, Ca, lactate Plasma expanders – albumin, dextran, plasma protein (plasmanate) - increases oncotic pressure, pulling fluids into circulation Parenteral hyperalimentation – fluid, electrolytes, amino acids, calories A.

FLUID VOLUME DEFICIT or HYPOVOLEMIA 



Definition: This is the loss of extra cellular fluid volume that exceeds the intake of fluid. The loss of water and electrolyte is in equal proportion. It can be called in various terms- vascular, cellular or intracellular dehydration. But the preferred term is hypovolemia. Dehydration refers to loss of WATER alone, with increased solutes concentration and sodium concentration

Pathophysiology of Fluid Volume Deficit 

Etiologic conditions include: a. Vomiting b. Diarrhea c. Prolonged GI suctioning d. Increased sweating e. Inability to gain access to fluids f. Inadequate fluid intake g. Massive third spacing

MS: Fluids and Electrolyte

Risk factors are the following: a. Diabetes Insipidus b. Adrenal insufficiency c. Osmotic diuresis d. Hemorrhage e. Coma f. Third-spacing conditions like ascites, pancreatitis and burns

PATHOPHYSIOLOGY: Risk Factors --- inadequate fluids in the body ---- decreased blood volume ----- decreased cellular hydration ---- cellular shrinkage ---- weight loss, decreased turgor, oliguria, hypotension, weak pulse, etc.

ASSESSMENT: Physical examination      

Weight loss, tented skin turgor, dry mucus membrane Hypotension Tachycardia Cool skin, acute weight loss Flat neck veins Decreased CVP

Subjective cues    

Thirst Nausea, anorexia Muscle weakness and cramps Change in mental state

Laboratory findings 1. 2. 3. 4.

Elevated BUN due to depletion of fluids or decreased renal perfusion Hemoconcentration Possible Electrolyte imbalances: Hypokalemia, Hyperkalemia, Hyponatremia, hypernatremia Urine specific gravity is increased (concentrated urine) above 1.020

NURSING MANAGEMENT 1. 2. 3.

4.

5.

6. 7. 8.

Assess the ongoing status of the patient by doing an accurate input and output monitoring Monitor daily weights. Approximate weight loss 1 kilogram = 1liter! Monitor Vital signs, skin and tongue turgor, urinary concentration, mental function and peripheral circulation Prevent Fluid Volume Deficit from occurring by identifying risk patients and implement fluid replacement therapy as needed promptly Correct fluid Volume Deficit by offering fluids orally if tolerated, anti-emetics if with vomiting, and foods with adequate electrolytes Maintain skin integrity Provide frequent oral care Teach patient to change position slowly to avoid sudden postural hypotension

Abejo

Lecture Notes on Fluids and Electrolytes Prepared By: Mark Fredderick R Abejo R.N, MAN

B.

FLUID VOLUME EXCESS: HYPERVOLEMIA  Definition : Refers to the isotonic expansion of the ECF caused by the abnormal retention of water and sodium  There is excessive retention of water and electrolytes in equal proportion. Serum sodium concentration remains NORMAL

4.

Teach patient about edema, ascites, and fluid therapy. Advise elevation of the extremities, restriction of fluids, necessity of paracentesis, dialysis and diuretic therapy. Instruct patient to avoid over-the-counter medications without first checking with the health care provider because they may contain sodium

5.

Pathophysiology of Fluid Volume Excess 

Etiologic conditions and Risks factors a. Congestive heart failure b. Renal failure c. Excessive fluid intake d. Impaired ability to excrete fluid as in renal disease e. Cirrhosis of the liver f. Consumption of excessive table salts g. Administration of excessive IVF h. Abnormal fluid retention

PATHOPHYSIOLOGY Excessive fluid --- expansion of blood volume ----- edema, increased neck vein distention, tachycardia, hypertension.

The Nursing Process in Fluid Volume Excess ASSESSMENT Physical Examination  Increased weight gain  Increased urine output  Moist crackles in the lungs  Increased CVP  Distended neck veins  Wheezing  Dependent edema

ELECTROLYTES 

Sources of electrolytes 

IMPLEMENTATION ASSIST IN MEDICAL INTERVENTION 1. 2. 3.

Administer diuretics as prescribed Assist in hemodialysis Provide dietary restriction of sodium and water

NURSING MANAGEMENT 1.

2. 3.

Continually assess the patient‟s condition by measuring intake and output, daily weight monitoring, edema assessment and breath sounds Prevent Fluid Volume Excess by adhering to diet prescription of low salt- foods. Detect and Control Fluid Volume Excess by closely monitoring IVF therapy, administering medications, providing rest periods, placing in semi-fowler‟s position for lung expansion and providing frequent skin care for the edema

MS: Fluids and Electrolyte

Foods and ingested fluids, medications; IVF and TPN solutions

Functions of Electrolytes  Maintains fluid balance  Regulates acid-base balance  Needed for enzymatic secretion and activation  Needed for proper metabolism and effective processes of muscular contraction, nerve transmission Types of Electrolytes  CATIONS- positively charged ions; examples are sodium, potassium, calcium  ANIONS- negatively charged ions; examples are chloride and phosphates]  The major ICF cation is potassium (K+); the major ICF anion is Phosphates  The major ECF cation is Sodium (Na+); the major ECF anion is Chloride (Cl-)

ELECTROLYTE IMBALANCES

Subjective cue/s  Shortness of breath  Change in mental state Laboratory findings 1. BUN and Creatinine levels are LOW because of dilution 2. Urine sodium and osmolality decreased (urine becomes diluted) 3. CXR may show pulmonary congestion

Electrolytes are charged ions capable of conducting electricity and are solutes found in all body compartments.

SODIUM   

The most abundant cation in the ECF Normal range in the blood is 135-145 mEq/L A loss or gain of sodium is usually accompanied by a loss or gain of water.  Major contributor of the plasma Osmolality  Sources: Diet, medications, IVF. The minimum daily requirement is 2 grams Functions: 1. 2. 3. 4. 5. 6. 7.

8.

Participates in the Na-K pump Assists in maintaining blood volume Assists in nerve transmission and muscle contraction Primary determinant of ECF concentration. Controls water distribution throughout the body. Primary regulator of ECF volume. Sodium also functions in the establishment of the electrochemical state necessary for muscle contraction and the transmission of nerve impulses. Regulations: skin, GIT, GUT, Aldosterone increases Na retention in the kidney

Abejo

Lecture Notes on Fluids and Electrolytes Prepared By: Mark Fredderick R Abejo R.N, MAN

SODIUM DEFICIT: HYPONATREMIA

In summary:



Physical Examination  Altered mental status  Vomiting  Lethargy  Muscle twitching and convulsions (if sodium level is below 115 mEq/L)  Focal weakness

Definition : Refers to a Sodium serum level of less than 135 mEq/L. This may result from excessive sodium loss or excessive water gain.

Pathophysiology Etiologic Factors a. Fluid loss such as from Vomiting and nasogastric suctioning b. Diarrhea c. Sweating d. Use of diuretics e. Fistula Other factors a. Dilutional hyponatremia Water intoxication, compulsive water drinking where sodium level is diluted with increased water intake b. SIADH Excessive secretion of ADH causing water retention and dilutional hyponatremia PATHOPHYSIOLOGY Decrease sodium concentration --- hypotonicity of plasma -- water from the intravascular space will move out and go to the intracellular compartment with a higher concentration --cell swelling --Water is pulled INTO the cell because of decreased extracellular sodium level and increased intracellular concentration The Nursing Process in HYPONATREMIA

Subjective Cues  Nausea  Cramps  Anorexia  Headache Laboratory findings 1. Serum sodium level is less than 135 mEq/L 2. Decreased serum osmolality 3. Urine specific gravity is LOW if caused by sodium loss 4. In SIADH, urine sodium is high and specific gravity is HIGH IMPLEMENTATION ASSIST IN MEDICAL INTERVENTION 1. Provide sodium replacement as ordered. Isotonic saline is usually ordered.. Infuse the solution very cautiously. The serum sodium must NOT be increased by greater than 12 mEq/L because of the danger of pontine osmotic demyelination 2. Administer lithium and demeclocycline in SIADH 3. Provide water restriction if with excess volume NURSING MANAGEMENT 1.

ASSESSMENT Sodium Deficit (Hyponatremia) Clinical Manifestations  Clinical manifestations of hyponatremia depend on the cause, magnitude, and rapidity of onset.  Although nausea and abdominal cramping occur, most of the symptoms are neuropsychiatric and are probably related to the cellular swelling and cerebral edema associated with hyponatremia.  As the extracellular sodium level decreases, the cellular fluid becomes relatively more concentrated and „pulls” water into the cells.  In general, those patients having acute decline in serum sodium levels have more severe symptoms and higher mortality rates than do those with more slowly developing hyponatremia.  Features of hyponatremia associated with sodium loss and water gain include anorexia, muscle cramps, and a feeling of exhaustion.  When the serum sodium level drops below 115 mEq/L (SI: 115 mmol/L), thee ff signs of increasing intracranial pressure occurs:  lethargy  Confusion  muscular twitching  focal weakness  hemiparesis  papilledema  convulsions

MS: Fluids and Electrolyte

2.

3.

Provide continuous assessment by doing an accurate intake and output, daily weights, mental status examination, urinary sodium levels and GI manifestations. Maintain seizure precaution Detect and control Hyponatremia by encouraging food intake with high sodium content, monitoring patients on lithium therapy, monitoring input of fluids like IVF, parenteral medication and feedings. Return the Sodium level to Normal by restricting water intake if the primary problem is water retention. Administer sodium to normovolemic patient and elevate the sodium slowly by using sodium chloride solution

SODIUM EXCESS: HYPERNATREMIA  

Serum Sodium level is higher than 145 mEq/L There is a gain of sodium in excess of water or a loss of water in excess of sodium.

Pathophysiology: Etiologic factors a. Fluid deprivation b. Water loss from Watery diarrhea, fever, and hyperventilation c. Administration of hypertonic solution d. Increased insensible water loss e. Inadequate water replacement, inability to swallow f. Seawater ingestion or excessive oral ingestion of salts

Abejo

Lecture Notes on Fluids and Electrolytes Prepared By: Mark Fredderick R Abejo R.N, MAN

Other factors a. Diabetes insipidus b. Heat stroke c. Near drowning in ocean d. Malfunction of dialysis

IMPLEMENTATION ASSIST IN THE MEDICAL INTERVENTION 1. 2.

PATHOPHYSIOLOGY Increased sodium concentration --- hypertonic plasma ---water will move out form the cell outside to the interstitial space ----- CELLULAR SHRINKAGE ----- then to the blood ---- Water pulled from cells because of increased extracellular sodium level and decreased cellular fluid concentration

The Nursing Process in HYPERNATREMIA

3.

NURSING MANAGEMENT 1.

2.

3.

Sodium Excess (Hypernatremia) Clinical Manifestations  primarily neurologic  Presumably the consequence of cellular dehydration.  Hypernatremia results in a relatively concentrated ECF, causing water to be pulled from the cells.  Clinically, these changes may be manifested by: o restlessness and weakness in moderate hypernatremia o disorientation, delusions, and hallucinations in severe hypernatremia.  Dehydration (hypernatremia) is often overlooked as the primary reason for behavioral changes in the elderly.  If hypernatremia is severe, permanent brain damage can occur (especially in children). Brain damage is apparently due to subarachnoid hemorrhages that result from brain contraction. A primary characteristic of hypernatremia is thirst. Thirst is so strong a defender of serum sodium levels in normal people that hypernatremia never occurs unless the person is unconscious or is denied access to water; unfortunately, ill people may have an impaired thirst mechanism. Other signs include dry, swollen tongue and sticky mucous membranes. A mild elevation in body temperature may occur, but on correction of the hypernatremia the body temperature should return to normal. ASSESSMENT Physical Examination  Restlessness, elevated body temperature  Disorientation  Dry, swollen tongue and sticky mucous membrane, tented skin turgor  Flushed skin, postural hypotension  Increased muscle tone and deep reflexes  Peripheral and pulmonary edema

4. 5. 6.

Laboratory findings 1. Serum sodium level exceeds 145 mEq/L 2. Serum osmolality exceeds 295 mOsm/kg 3. Urine specific gravity and osmolality INCREASED or elevated MS: Fluids and Electrolyte

Continuously monitor the patient by assessing abnormal loses of water, noting for the thirst and elevated body temperature and behavioral changes Prevent hypernatremia by offering fluids regularly and plan with the physician alternative routes if oral route is not possible. Ensure adequate water for patients with DI. Administer IVF therapy cautiously Correct the Hypernatremia by monitoring the patient‟s response to the IVF replacement. Administer the hypotonic solution very slowly to prevent sudden cerebral edema. Monitor serum sodium level. Reposition client regularly, keep side-rails up, the bed in low position and the call bell/light within reach. Provide teaching to avoid over-the counter medications without consultation as they may contain sodium

POTASSIUM      

 

The most abundant cation in the ICF Potassium is the major intracellular electrolyte; in fact, 98% of the body‟s potassium is inside the cells. The remaining 2% is in the ECF; it is this 2% that is all-important in neuromuscular function. Potassium is constantly moving in and out of cells according to the body‟s needs, under the influence of the sodium-potassium pump. Normal range in the blood is 3.5-5 mEq/L Normal renal function is necessary for maintenance of potassium balance, because 80-90% of the potassium is excreted daily from the body by way of the kidneys. The other less than 20% is lost through the bowel and sweat glands. Major electrolyte maintaining ICF balance Sources- Diet, vegetables, fruits, IVF, medications

Functions: 1. 2. 3. 4. 5.

Subjective Cues  Delusions and hallucinations  Extreme thirst  Behavioral changes

Administer hypotonic electrolyte solution slowly as ordered Administer diuretics as ordered Loop diuretics (thiazides ok) Desmopressin is prescribed for diabetes insipidus

6.

Maintains ICF Osmolality Important for nerve conduction and muscle contraction Maintains acid-base balance Needed for metabolism of carbohydrates, fats and proteins Potassium influences both skeletal and cardiac muscle activity. ( For example, alterations in its concentration change myocardial irritability and rhythm ) Regulations: renal secretion and excretion, * Aldosterone promotes renal excretion * Acidosis promotes K exchange for hydrogen

Abejo

Lecture Notes on Fluids and Electrolytes Prepared By: Mark Fredderick R Abejo R.N, MAN

POTASSIUM DEFICIT: HYPOKALEMIA 

Condition when the serum concentration of potassium is less than 3.5 mEq/L

Pathophysiology 

Etiologic Factors a. Gastro-intestinal loss of potassium such as diarrhea and fistula b. Vomiting and gastric suctioning c. Metabolic alkalosis d. Diaphoresis and renal disorders e. Ileostomy



Other factor/s a. Hyperaldosteronism b. Heart failure c. Nephrotic syndrome d. Use of potassium-losing diuretics e. Insulin therapy f. Starvation g. Alcoholics and elderly PATHOPHYSIOLOGY

Decreased potassium in the body impaired nerve excitation and transmission signs/symptoms such as weakness, cardiac dysrhythmias etc..

IMPLEMENTATION ASSIST IN THE MEDICAL INTERVENTION 1. 2.

The Nursing Process in Hypokalemia

Clinical Manifestations  Potassium deficiency can result in widespread derangements in physiologic functions and especially nerve conduction.  Most important, severe hypokalemia can result in death through cardiac or respiratory arrest.  Clinical signs rarely develop before the serum potassium level has fallen below 3 mEq/L (51: 3 mmol/L) unless the rate of fall has been rapid.  Manifestations of hypokalemia include fatigue, anorexia, nausea, vomiting, muscle weakness, decreased bowel motility, paresthesias, dysrhythmias, and increased sensitivity to digitalis.  If prolonged, hypokalemia can lead to impaired renal concentrating ability, causing dilute urine, polyuria, nocturia, and polydipsia ASSESSMENT Physical examination  Muscle weakness  Decreased bowel motility and abdominal distention  Paresthesias  Dysrhythmias  Increased sensitivity to digitalis Subjective cues  Nausea , anorexia and vomiting  Fatigue, muscles cramps  Excessive thirst, if severe Laboratory findings 1. Serum potassium is less than 3.5 mEq/L 2. ECG: FLAT “T” waves, or inverted T waves, depressed ST segment and presence of the “U” wave and prolonged PR interval. 3. Metabolic alkalosis MS: Fluids and Electrolyte

3.

Provide oral or IV replacement of potassium Infuse parenteral potassium supplement. Always dilute the K in the IVF solution and administer with a pump. IVF with potassium should be given no faster than 1020-mEq/ hour! NEVER administer K by IV bolus or IM

NURSING MANAGEMENT 1.

2.

3.

4.

5.

Continuously monitor the patient by assessing the cardiac status, ECG monitoring, and digitalis precaution Prevent hypokalemia by encouraging the patient to eat potassium rich foods like orange juice, bananas, cantaloupe, peaches, potatoes, dates and apricots. Correct hypokalemia by administering prescribed IV potassium replacement. The nurse must ensure that the kidney is functioning properly! Administer IV potassium no faster than 20 mEq/hour and hook the patient on a cardiac monitor. To EMPHASIZE: Potassium should NEVER be given IV bolus or IM!! A concentration greater than 60 mEq/L is not advisable for peripheral veins.

POTASSIUM EXCESS: HYPERKALEMIA  Serum potassium greater than 5.5 mEq/L Pathophysiology 

Etiologic factors a. Iatrogenic, excessive intake of potassium b. Renal failure- decreased renal excretion of potassium c. Hypoaldosteronism and Addison‟s disease d. Improper use of potassium supplements



Other factors 1. Pseudohyperkalemia- tight tourniquet and hemolysis of blood sample, marked leukocytosis Abejo

Lecture Notes on Fluids and Electrolytes Prepared By: Mark Fredderick R Abejo R.N, MAN

2. 3. 4.

Transfusion of “old” banked blood Acidosis Severe tissue trauma

PATHOPHYSIOLOGY Increased potassium in the body ---- Causing irritability of the cardiac cells --- Possible arrhythmias!!

The Nursing Process in Hyperkalemia

Clinical Manifestations  By far the most clinically important effect of hyperkalemia is its effect on the myocardium.  Cardiac effects of an elevated serum potassium level are usually not significant below a concentration of 7 mEq/L (SI: 7 mmol/L), but they are almost always present when the level is 8 mEq/L (SI: 8 mmol/L) or greater.  As the plasma potassium concentration is increased, disturbances in cardiac conduction occur.  The earliest changes, often occurring at a serum potassium level greater than 6 mEq/ L (SI: 6 mmol/L), are peaked narrow T waves and a shortened QT interval.  If the serum potassium level continues to rise, the PR interval becomes prolonged and is followed by disappearance of the P waves.  Finally, there is decomposition and prolongation of the QRS complex. Ventricular dysrhythmias and cardiac arrest may occur at any point in this progression.  Note that in Severe hyperkalemia causes muscle weakness and even paralysis, related to a depolarization block in muscle.  Similarly, ventricular conduction is slowed.  Although hyperkalemia has marked effects on the peripheral neuromuscular system, it has little effect on the central nervous system.  Rapidly ascending muscular weakness leading to flaccid quadriplegia has been reported in patients with very high serum potassium levels.  Paralysis of respiratory muscles and those required for phonation can also occur.  Gastrointestinal manifestations, such as nausea, intermit tent intestinal colic, and diarrhea, may occur in hyperkalemic patients. ASSESSMENT Physical Examination  Diarrhea  Skeletal muscle weakness  Abnormal cardiac rate Subjective Cues  Nausea  Intestinal pain/colic  Palpitations Laboratory Findings 1. Peaked and narrow T waves 2. ST segment depression and shortened QT interval 3. Prolonged PR interval 4. Prolonged QRS complex 5. Disappearance of P wave 6. Serum potassium is higher than 5.5 mEq/L 7. Acidosis MS: Fluids and Electrolyte

IMPLEMENTATION ASSIST IN MEDICAL INTERVENTION 1. Monitor the patient‟s cardiac status with cardiac machine 2. Institute emergency therapy to lower potassium level by: a. Administering IV calcium gluconateantagonizes action of K on cardiac conduction b. Administering Insulin with dextrose-causes temporary shift of K into cells c. Administering sodium bicarbonate-alkalinizes plasma to cause temporary shift d. Administering Beta-agonists e. Administering Kayexalate (cation-exchange resin)-draws K+ into the bowel NURSING MANAGEMENT 1. 2. 3. 4. 5.

6. 7.

8.

Provide continuous monitoring of cardiac status, dysrhythmias, and potassium levels. Assess for signs of muscular weakness, paresthesias, nausea Evaluate and verify all HIGH serum K levels Prevent hyperkalemia by encouraging high risk patient to adhere to proper potassium restriction Correct hyperkalemia by administering carefully prescribed drugs. Nurses must ensure that clients receiving IVF with potassium must be always monitored and that the potassium supplement is given correctly Assist in hemodialysis if hyperkalemia cannot be corrected. Provide client teaching. Advise patients at risk to avoid eating potassium rich foods, and to use potassium salts sparingly. Monitor patients for hypokalemia who are receiving potassium-sparing diuretic CALCIUM

   

Majority of calcium is in the bones and teeth Small amount may be found in the ECF and ICF Normal serum range is 8.5 – 10.5 mg/dL Sources: milk and milk products; diet; IVF and medications Abejo

Lecture Notes on Fluids and Electrolytes Prepared By: Mark Fredderick R Abejo R.N, MAN

Functions: 1. 2. 3. 4. 5.

Needed for formation of bones and teeth For muscular contraction and relaxation For neuronal and cardiac function For enzymatic activation For normal blood clotting

HYPOCALCEMIA  Low levels of calcium in the blood 

Risk Factors a. Hypoparathyroidism (idiopathic or postsurgical) b. Alkalosis (Ca binds to albumin) c. Corticosteroids (antagonize Vit D) d. Hyperphosphatemia e. Vit D deficiency f. Renal failure (vit D deficiency)



Clinical Manifestation  Decreased cardiac contractility  Arrhythmia  ECG: prolonged QT interval, lengthened ST segment  Trousseau’s sign (inflate BP cuff 20mm above systole for 3 min = carpopedal spasm)

Regulations: 1. 2. 3.

GIT- absorbs Ca+ in the intestine; Vitamin D helps to increase absorption Renal regulation- Ca+ is filtered in the glomerulus and reabsorbed in the tubules: Endocrine regulation: 



Parathyroid hormone from the parathyroid glands is released when Ca+ level is low. PTH causes release of calcium from bones and increased retention of calcium by the kidney but PO4 is excreted Calcitonin from the thyroid gland is released when the calcium level is high. This causes excretion of both calcium and PO4 in the kidney and promoted deposition of calcium in the bones.

 Chvostek’s sign (tap facial nerve anterior to the ear = ipsilateral muscle twitching)

    

Tetany Hyperreflexia, seizures Laryngeal spasms/stridor Diarrhea, hyperactive bowel sounds Bleeding

Collaborative Management 1. Calcium gluconate 10% IV 2. Calcium chloride 10% IV 3. both usually given by Dr, very slowly; venous irritant; cardiac probs 4. Oral: calcium citrate, lactate, carbonate; Vit D supplements 5. Diet: high calcium 6. Watch out for tetany, seizures, laryngospasm, resp & cardiac arrest 7. Seizure precautions Sources: milk, yogurt, cheese, sardines, broccoli, tofu, green leafy vegetables

MS: Fluids and Electrolyte

Abejo

Lecture Notes on Fluids and Electrolytes Prepared By: Mark Fredderick R Abejo R.N, MAN

HYPERCALCEMIA

HYPOMAGNESEMIA

 

is an elevated calcium level in the blood usually from bone resorption



is an electrolyte disturbance in which there is an abnormally low level of magnesium in the blood.



Risk Factors / Causes a. Hyperparathyroidism (eg adenoma) b. Metastatic cancer (bone resorption as tumor‟s ectopic PTH effect) – eg. Multiple myeloma c. Thiazide diuretics (potentiate PTH effect) d. Immobility e. Milk-alkali syndrome (too much milk or antacids in aegs with peptic ulcer)





Clinical Manifestation  groans (constipation)  moans (psychotic noise)  bones (bone pain, especially if PTH is elevated)  stones (kidney stones)  psychiatric overtones (including depression and confusion)

Risk Factors and Cause a. Chronic alcoholism (most common), Alcohol stimulates renal excretion of magnesium, b. Inflammatory bowel disease c. Small bowel resection d. GI cancer e. chronic pancreatitis (poor absorption) f. Loop and thiazide diuretic use (the most common cause of hypomagnesemia) g. Antibiotics (i.e. aminoglycoside, amphotericin, pentamidine, gentamicin, tobramycin, viomycin) block resorption in the loop of Henle. h. Excess calcium i. Excess saturated fats j. Excess coffee or tea intake k. Excess phosphoric or carbonic acids (soda pop) l. Insufficient water consumption m. Excess salt or sugar intake n. Insufficient selenium,vitamin D, sunlight exposure or vitamin B6 o. Increased levels of stress

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Clinical Manifestation  Weakness  muscle cramps  cardiac arrhythmia  increased irritability of the nervous system with tremors, athetosis, jerking, nystagmus and an extensor plantar reflex. Confusion  disorientation  hallucinations  depression  epileptic fits  hypertension, tachycardia and tetany.

  

Arrhythmia ECG: shortened QT interval, decreased ST segment Hyporeflexia, lethargy, coma

Collaborative Management 1. If parathyroid tumor = surgery 2. Diet: low Ca, stop taking Ca Carbonate antacids, increase fluids 3. IV flushing (usually NaCl) 4. Loop diuretics 5. Corticosteroids 6. Biphosphonates, like etidronate (Calcitonin) & alendronate (Fosamax) 7. Plicamycin (Mithracin) – inhibits bone resorption 8. Calcitonin – IM or intranasal 9. Dialysis (severe case) 10. Watch out for digitalis toxicity 11. Prevent fractures, handle gently

MAGNESIUM      

2nd most abundant intracellular cation 50% found in bone, 45% is intracellular ATP (adenosine triphosphate), the main source of energy in cells, must be bound to a magnesium ion in order to be biologically active. competes with Ca & P absorption in the GI inhibits PTH Normal value : 1.5-2.5 mEq/L

Functions: 1. important in maintaining intracellular activity 2. affects muscle contraction, & especially relaxation 3. maintains normal heart rhythm 4. promotes vasodilation of peripheral arterioles Sources: green leafy vegetables, nuts, legumes, seafood, whole grains, bananas, oranges, cocoa, chocolate

MS: Fluids and Electrolyte

* Like hypocalcemia, hypokalemia Potentiates digitalis toxicity Collaborative Management 1. Magnesium sulfate IV, IM (make sure renal function is ok) – may cause flushing 2. Oral: Magnesium oxide 300mg/day, 3. Mg-containing antacids (SE diarrhea) 4. Diet: high magnesium (fruits,green vegetables, whole grains cereals, milk, meat, nuts and sea foods ) 5. Promotion of safety, protect from injury

HYPERMAGNESEMIA 

Etiologic Factors a. Magnesium treatment for pre-eclampsia b. Renal failure c. Diabetic Ketoacidosis d. Excessive use of Mg antacids/laxatives

PATHOPHYSIOLOGY Increase Mg. ----- Blocks acetylcholine release ---- decrease excitability of muscle

Abejo

Lecture Notes on Fluids and Electrolytes Prepared By: Mark Fredderick R Abejo R.N, MAN

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Clinical Manifestation  Hyporeflexia  Hypotension, bradycardia, arrhythmia  Flushing  Weakness, lethargy, coma  Decreased RR & respiratory paralysis  Loss of DTR‟s

HYPERPHOSPHATEMIA 

Risk Factors a. Acidosis (Ph moves out of cell) b. Cytotoxic agents/chemotherapy in cancer c. Renal failure d. Hypocalcemia e. Massive BT (P leaks out of cells during storage of blood) f. Hyperthyroidism

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Clinical Manifestation  Calcification of kidney, cornea, heart  Muscle spasms, tetany, hyperreflexia

*like hypercalcemia Collaborative Management 1. Diuretics 2. Stop Mg-containing antacids & enemas 3. IV fluids rehydration 4. Calcium gluconate – (antidote, antagonizes cardiac & respiratory effects of Mg) 5. Dialysis – if RF

PHOSPHORUS      

primary intracellular anion part of ATP – energy 85% bound with Ca in teeth/bones, skeletal muscle reciprocal balance with Ca absorption affected by Vit D, regulation affected by PTH (lowers P level) Normal value : 2.5-4.5 mg/dL

Functions: 1. bone/teeth formation & strength 2. phospholipids (make up cell membrane integrity) 3. part of ATP 4. affects metabolism, Ca levels Sources: red & organ meats (brain, liver, kidney), poultry, fish, eggs, milk, legumes, whole grains, nuts, carbonated drinks

HYPOPHOSPHATEMIA 



Risk Factors a. Decreased Vit D absorption, sunlight exposure b. Hyperparathyroidism (increased PTH) c. Aluminum & Mg-containing antacids (bind P) d. Severe vomiting & diarrhea Clinical Manifestation  Anemia, bruising (weak blood cell membrane)  Seizures, coma  Muscle weakness, paresthesias  Constipation, hypoactive bowel sounds

*like hypocalcemia

Collaborative ManagementM 1. Aluminum antacids as phosphate binders: Al carbonate (Basaljel), Al hydroxide (Amphojel) 2. Ca carbonate for hypocalcemia 3. Avoid phosphate laxatives/enemas 4. Increase fluid intake 5. Diet: low Phos, no carbonated drinks

CHLORIDE    

Functions: 1. helps regulate BP, serum osmolarity 2. part of HCl 3. acid/base balance (exchanges with HCO3)

Sources: salt, canned food, cheese, milk, eggs, crab, olives

HYPOCHLOREMIA 

Risk Factors a. Diuresis b. Metabolic alkalosis c. Hyponatremia, prolonged D5W IV d. Addison‟s

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Clinical Manifestation  Slow, shallow respirations (met. Alkalosis)  Hypotension (Na & water loss)

*Like hypercalcemia Collaborative Management 1. Sodium phosphate or potassium phosphate IV (give slowly, no faster than 10 mEq/hr) 2. Sodium & potassium phosphate orally (NeutraPhos, K-Phos) – give with meals to prevent gastric irritation 3. Avoid Phos-binding antacids 4. Diet: high Mg, milk 5. Monitor joint stiffness, arthralgia, fractures, bleeding

MS: Fluids and Electrolyte

extracellular anion, part of salt binds with Na, H (also K, Ca, etc) exchanges with HCO3 in the kidneys (& in RBCs) Normal value: 95 -108 mEq/L

Collaborative Management 1. Administer IV or Oral : KCl, NaCl 2. Diet: high Cl (& usually Na)

HYPERCHLOREMIA 

Risk Factors / Cause a. Metabolic acidosis b. Usually noted in hyperNa, hyperK

Abejo

Lecture Notes on Fluids and Electrolytes Prepared By: Mark Fredderick R Abejo R.N, MAN

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Clinical Manifestation  Deep, rapid respirations (met. Acidosis)  hyperK, hyperNa S/S  Increased Cl sweat levels in cystic fibrosis

Collaborative Management 1. Diuretics 2. Hypotonic solutions, D5W to restore balance 3. Diet: low Cl (& usually Na) 4. Treat acidosis

Acid-Base Balance Mechanisms Buffer - prevents major changes in ECF by releasing or accepting H ions Buffer mechanism: first line (takes seconds) 1. combine with very strong acids or bases to convert them into weaker acids or bases 2. Bicarbonate Buffer System - most important - uses HCO3 & carbonic acid/H2CO3 - (20:1) - closely linked with respiratory & renal mechanisms 3. Phosphate Buffer System - more important in intracellular fluids, where concentration is higher - similar to bicarbonate buffer system, only uses phosphate 4. Protein Buffer System - hemoglobin, a protein buffer, promotes movement of chloride across RBC membrane in exchange for HCO3 Respiratory mechanism: 2nd line (takes minutes) 1. increased respirations liberates more CO2 = increase pH 2. decreased respirations conserve more CO2 = decrease pH carbonic acid (H2CO3) = CO2 + water Renal mechanism: 3rd line (takes hours-days) 1. kidneys secrete H ions & reabsorb bicarbonate ions = increase blood pH 2. kidneys form ammonia that combines with H ions to form ammonium ions, which are excreted in the urine in exchange for sodium ions Review: Acid-Base Imbalance pH – 7.35-7.45 pCO2 – measurement of the CO2 pressure that is being exerted on the plasma 35-45mmHg PaO2- amount of pressure exerted by O2 on the plasma 80-100mmHg SaO2- percent of hemoglobin saturated with O2 Base excess – amount of HCO3 available in the ECF -3 to +3

MS: Fluids and Electrolyte

Interpretation Arterial Blood Gases     Step 1     Step 2    

Step 3    

If acidosis the pH is down If alkalosis the pH is up The respiratory function indicator is the PCO2 The metabolic function indicator is the HCO3

Look at the pH Is it up or down? If it is up - it reflects alkalosis If it is down - it reflects acidosis

Look at the PCO2 Is it up or down? If it reflects an opposite response as the pH,  then you know that the condition is a respiratory imbalance If it does not reflect an opposite response as the pH - move to step III

Look at the HCO3 Does the HCO3 reflect a corresponding response with the pH If it does then the condition is a metabolic imbalance

FACTORS AFFECTING BODY FLUIDS, ELECTROLYTES AND ACID-BASE BALANCE AGE   

Infants have higher proportion of body water than adults Water content of the body decreases with age Infants have higher fluid turn-over due to immature kidney and rapid respiratory rate

GENDER AND BODY SIZE  Women have higher body fat content but lesser water content  Lean body has higher water content ENVIRONMENT AND TEMPERATURE  Climate and heat and humidity affect fluid balance DIET AND LIFESTYLE  Anorexia nervosa will lead to nutritional depletion  Stressful situations will increase metabolism, increase ADH causing water retention and increased blood volume  Chronic Alcohol consumption causes malnutrition ILLNESS  Trauma and burns release K+ in the blood  Cardiac dysfunction will lead to edema and congestion MEDICAL TREATMENT, MEDICATIONS AND SURGERY  Suctioning, diuretics and laxatives may cause imbalances Abejo

Lecture Notes on Fluids and Electrolytes Prepared By: Mark Fredderick R Abejo R.N, MAN

ACID-BASE BALANCE PROBLEMS

RESPIRATORY ACIDOSIS  pH < 7.35  pCO2 > 45 mm Hg (excess carbon dioxide in the blood)  Respiratory system impaired and retaining CO2; causing acidosis Common Stimuli a. Acute respiratory failure from airway obstruction b. Over-sedation from anesthesia or narcotics c. Some neuromuscular diseases that affect ability to use chest muscles d. Chronic respiratory problems, such as Chronic Obstructive Lung Disease Signs and Symptoms  Compensation: kidneys respond by generating and reabsorbing bicarbonate ions, so HCO3 >26 mm Hg  Respiratory: hypoventilation, slow or shallow respirations  Neuro: headache, blurred vision, irritability, confusion  Respiratory collapse leads to unconsciousness and cardiovascular collapse Collaborative Management 1. Early recognition of respiratory status and treat cause 2. Restore ventilation and gas exchange; CPR for respiratory failure with oxygen supplementation; intubation and ventilator support if indicated 3. Treatment of respiratory infections with bronchodilators, antibiotic therapy 4. Reverse excess anesthetics and narcotics with medications such as naloxone (Narcan) 5. Chronic respiratory conditions  Breathe in response to low oxygen levels  Adjusted to high carbon dioxide level through metabolic compensation (therefore, high CO2 not a breathing trigger)  Cannot receive high levels of oxygen, or will have no trigger to breathe; will develop carbon dioxide narcosis  Treat with no higher than 2 liters O2 per cannula 6. Continue respiratory assessments, monitor further arterial blood gas results

RESPIRATORY ALKALOSIS  pH < 7.35  pCO2 < 35 mm Hg.  Carbon dioxide deficit, secondary to hyperventilation Common Stimuli a. Hyperventilation with anxiety from uncontrolled fear, pain, stress (e.g. women in labor, trauma victims) b. High fever c. Mechanical ventilation, during anesthesia

MS: Fluids and Electrolyte

Signs and Symptoms  Compensation: kidneys compensate by eliminating bicarbonate ions; decrease in bicarbonate HCO3 < 22 mm Hg.  Respiratory: hyperventilating: shallow, rapid breathing  Neuro: panicked, light-headed, tremors, may develop tetany, numb hands and feet (related to symptoms of hypocalcemia; with elevated pH more Ca ions are bound to serum albumin and less ionized “active” calcium available for nerve and muscle conduction)  May progress to seizures, loss of consciousness (when normal breathing pattern returns)  Cardiac: palpitations, sensation of chest tightness Collaborative Management 1. 2.

3. 4.

Treatment: encourage client to breathe slowly in a paper bag to rebreathe CO2 Breathe with the patient; provide emotional support and reassurance, anti-anxiety agents, sedation On ventilator, adjustment of ventilation settings (decrease rate and tidal volume) Prevention: pre-procedure teaching, preventative emotional support, monitor blood gases as indicated

METABOLIC ACIDOSIS  pH <7.35  Deficit of bicarbonate in the blood NaHCO3 <22 mEq/L  Caused by an excess of acid, or loss of bicarbonate from the body Common Stimuli a. Acute lactic acidosis from tissue hypoxia (lactic acid produced from anaerobic metabolism with shock, cardiac arrest) b. Ketoacidosis (fatty acids are released and converted to ketones when fat is used to supply glucose needs as in uncontrolled Type 1 diabetes or starvation) c. Acute or chronic renal failure (kidneys unable to regulate electrolytes) d. Excessive bicarbonate loss (severe diarrhea, intestinal suction, bowel fistulas) e. Usually results from some other disease and is often accompanied by electrolyte and fluid imbalances f. Hyperkalemia often occurs as the hydrogen ions enter cells to lower the pH displacing the intracellular potassium; hypercalcemia and hypomagnesemia may occur Signs and Symptoms  Compensation: respiratory system begins to compensate by increasing the depth and rate of respiration in an effort to lower the CO2 in the blood; this causes a decreased level of carbon dioxide: pCO2 <35 mm HG.  Neuro changes: headache, weakness, fatigue progressing to confusion, stupor, and coma  Cardiac: dysrhythmias and possibly cardiac arrest from hyperkalemia  GI: anorexia, nausea, vomiting  Skin: warm and flushed Abejo

Lecture Notes on Fluids and Electrolytes Prepared By: Mark Fredderick R Abejo R.N, MAN

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Respiratory: tries to compensate by hyperventilation: deep and rapid respirations known as Kussmaul‟s respirations

Diagnostic test findings: 1. ABG: pH < 7.35, HCO3 < 22 2. Electrolytes: Serum K+ >5.0 mEq/L 3. Serum Ca+2 > 10.0 mg/dL 4. Serum Mg+2 < 1.6 mg/dL Collaborative Management 1. Medications: Correcting underlying cause will often improve acidosis 2. Restore fluid balance, prevent dehydration with IV fluids 3. Correct electrolyte imbalances 4. Administer Sodium Bicarbonate IV, if acidosis is severe and does not respond rapidly enough to treatment of primary cause. (Oral bicarbonate is sometimes given to clients with chronic metabolic acidosis) Be careful not to overtreat and put client into alkalosis 5. As acidosis improves, hydrogen ions shift out of cells and potassium moves intracellularly. Hyperkalemia may become hypokalemia and potassium replacement will be needed. 6. Assessment  Vital signs  Intake and output  Neuro, GI, and respiratory status;  Cardiac monitoring  Reassess repeated arterial blood gases and electrolytes

METABOLIC ALKALOSIS  pH >7.45  HCO3 > 26 mEq/L  Caused by a bicarbonate excess, due to loss of acid, or a bicarbonate excess in the body

1. 2. 3. 4.

Selected Water and Electrolyte Solutions Isotonic Solutions A. 0.9% NaCl (isotonic, also called NSS) Na+ 154 mEq/L Cl- 154 mEq/L (308 mOsm/L) Also available with varying concentrations of dextrose (the most frequent used is a 5% dextrose concentration 



 

Common Stimuli a. Loss of hydrogen and chloride ions through excessive vomiting, gastric suctioning, or excessive diuretic therapy Response to hypokalemia b. Excess ingestion of bicarbonate rich antacids or excessive treatment of acidosis with Sodium Bicarbonate Signs and Symptoms  Compensation: Lungs respond by decreasing the depth and rate of respiration in effort to retain carbon dioxide and lower pH  Neuro: altered mental status, numbness and tingling around mouth, fingers, toes, dizziness, muscle spasms (similar to hypocalcemia due to less ionized calcium levels)  Respiratory: shallow, slow breathing Diagnostic test findings 1. ABG‟s: pH> 7.45, HCO3 >26 2. Electrolytes: Serum K+ < 3.5 mEq/L 3. Electrocardiogram: as with hypokalemia

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MS: Fluids and Electrolyte

An isotonic solution that expands the ECF volume, used in hypovolemic states, resuscitative efforts, shock, diabetic ketoacidosis, metabolic alkalosis, hypercalcemia, mild Na deficit Supplies an excess of Na and Cl; can cause fluid volume excess and hyperchloremic acidosis if used in excessive volumes, particularly in patients with compromised renal function, heart failure or edema Not desirable as a routine maintenance solution, as it provides only Na and Cl (and these are provided in excessive amounts) When mixed with 5% dextrose, the resulting solution becomes hypertonic in relation to plasma, and in addition to the above described electrolytes, provides 170cal/L Only solution that may be administered with blood products

B. Lactated Ringer’s solution (Hartmann’s solution) Na+ 130 mEq/L K+ 4 mEq/L Ca++ 3 mEq/L Cl- 109 mEq/L Lactate (metabolized to bicarbonate) 28 mEq/L (274 mOsm/L) Also available with varying concentration of dextrose (the most common is 5% dextrose) 

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Collaborative Management

Correcting underlying cause will often improve alkalosis Restore fluid volume and correct electrolyte imbalances (usually IV NaCl with KCL). With severe cases, acidifying solution may be administered. Assessment  Vital signs  Neuro, cardiac, respiratory assessment  Repeat arterial blood gases and electrolytes

An isotonic solution that contains multiple electrolytes in roughly the same concentration as found in plasma (note that solution is lacking in Mg++) provides 9 cal/L Used in the tx of hypovolemia, burns, fluid lost as bile or diarrhea, and for acute blood loss replacement Lactate is rapidly metabolized into HCO3- in the body. Lactated Ringer‟s solution should not be used in lactic acidosis because the ability to convert lactate into HCO3- is impaired in this disorder. Abejo

Lecture Notes on Fluids and Electrolytes Prepared By: Mark Fredderick R Abejo R.N, MAN

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Not to be given with a pH > 7.5 because bicarbonates is formed as lactate breaks down causing alkalosis Should not be used in renal failure because it contains potassium and can cause hyperkalemia Similar to plasma

C. 5% Dextrose in Water (D5W) No electrolytes 50 g of glucose         

An isotonic solution that supplies 170 cal/L and free water to aid in renal excretion of solutes Used in treatment of hypernatremia, fluid loss and dehydration Should not be used in excessive volumes in the early post-op period (when ADH secretion is increased due to stress reaction) Should not be used solely in tx of fluid volume deficit, because it dilutes plasma electrolyte concentrations Contraindicated in head injury because it may cause increased intracranial pressure Should not be used for fluid resuscitation because it can cause hyperglycemia Should be used with caution in patients with renal or cardiac dse because of risk of fluid overload Electrolyte-free solutions may cause peripheral circulatory collapse, anuria in pt. with sodium deficiency and increased body fluid loss Converts to hypotonic solution as dextrose is metabolized by body. Overtime D5W without NaCl can cause water intoxication (ICF vol. excess bec. solution is hypotonic)

Hypotonic Solutions

Hypertonic Solutions E. 3% NaCl (hypertonic saline) Na+ 513 mEq/L Cl- 513 mEq/L (1026 mOsm/L)     

F. 5% NaCl (hypertonic solution) Na+ 855 mEq/L Cl- 855 mEq/L (1710 mOsm/L)   

   

  

Provides Na, Cl and free water Free water is desirable to aid the kidneys in elimination of solute Lacking in electrolytes other than Na and Cl When mixed with 5% dextrose, the solution becomes slightly hypertonic to plasma and in addition to the above-described electrolytes provides 170 cal/L Used in the tx of hypertonic dehydration, Na and Cl depletion and gastric fluid loss Not indicated for third-space fluid shifts or increased intracranial pressure Administer cautiously, because it can cause fluid shifts from vascular system into cells, resulting in cardiovascular collapse and increased intracranial pressure

MS: Fluids and Electrolyte

Highly hypertonic solution used to treat symptomatic hyponatremia Administered slowly and cautiously, because it can cause intravascular volume overload and pulmonary edema Supplies no calories

Colloid Solutions G. Dextran in NS or 5% D5W Available in low-molecular-weight (Dextran 40) and highmolecular-weight (Dextran 70) forms  

D. 0.45% NaCl half-strength saline) Na+ 77 mEq/L Cl- 77 mEq/L (154 mOsm/L) Also available with varying concentration of dextrose (the most common is 5% dextrose)

Used to increase ECF volume, decrease cellular swelling Highly hypertonic solution used only in critical situations to treat hyponatremia Must be administered slowly and cautiously, because it can cause intravascular volume overload and pulmonary edema Supplies no calories Assists in removing ICF excess

    

Colloid solution used as volume/plasma expander for intravascular part of ECF Affects clotting by coating platelets and decreasing ability to clot Remains in circulatory system up to 24 hours Used to treat hypovolemia in early shock to increase pulse pressure, CO, and arterial BP Improves microcirculation by decreasing RBC aggregation Contraindicated in hemorrhage, thrombocytopenia, renal dse and severe dehydration Not a substitute for blood or blood products

Abejo