Electrolytes Nsg.ppt

MEDICAL AND SURGICAL NURSING

Fluids and Electrolytes

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 acid- base 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% waterElderly: 40-50% water

II. Body Fluid CompositionA. Water: 60% of body weightB. Electrolytes: substances that become

charged particles in solution1. 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 waterbetween 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 wheretransportation 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

solute – the substance dissolvedsolvent – substance in which the solute is dissolved

- usually water (universal solvent)molar solution (M) - # of gram-molecular weights of

solute per liter of solutionosmolality – concentration of solute per kg of waternormal 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

IV. 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 concentration1. Normal Osmolality of ICF and

ECF: 275 – 295 mOsm/kg2. Types of solutions according to

osmolalityIsotonic: 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 shrinkHypotonic: fluid with lower concentration of solutes than plasma Cells in hypotonicsolution: 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. 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)

C. 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 capillarymembranes

D. 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

MS: Fluids and Electrolyte Abejo

V.


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

A. Thirst: primary regulator of water intake (thirst center in brain)

B. Kidneys: regulator of volume andosmolality by controlling excretion of water and electrolytes

C. Renin-angiotension-aldosterone mechanism: response to a drop in blood pressure; results from vasoconstriction and sodium regulation by aldosterone

D. Antidiuretic hormone: hormone to regulate water excretion; responds to osmolality and blood volume

E. Atrial natriuretic factor: hormone fromatrial heart muscle in response to fluid excess; causes increased urine output by blocking aldosterone

Fluid Balance RegulationThirst reflex triggered by:

1. decreased salivation & dry mouth2. increased osmotic pressure

stimulates osmoreceptors in the hypothalamus

3. decreased blood volume activates the renin/angiontensin pathway, which simulates the thirst center in hypothalamus

Renin-Angiotensin1. drop in blood volume in kidneys = renin released2. renin = acts on plasma protein angiotensin

(released by the liver) to form angiotensin I

3. ACE = converts Angiotensin I to Angiotensin II inthe lungs

4. Angiotensin II = vasoconstriction & aldosterone release

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

TOTAL 2,500 mls

Output: Skin Lungs Feces Kidneys

TOTAL

500 mls300 mls150 mls

1,500 mls2,500 mls

Intake:

Water in foodWater from oxidation Water in liquid

1,000 mls300 mls

1,200 mls

MS: Fluids and Electrolyte

IV FluidsIsotonic LR

PNSS (0.9%NSS) NM

Hypotonic D5W- isotonic in bag- dextrose=quickly

metabolized=hypotonicD2.5W0.45% NSS0.3% NSS0.2% NSS

Hypertonic D50W D10W D5NSS D5LR 3%NSS

Colloids (usually CHONs) & Plasma expandersDextran – 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, ClDextrose 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 circulationParenteral 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, withincreased solutes concentration and sodium concentration

Pathophysiology of Fluid Volume Deficit

Etiologic conditions include:a. Vomitingb. Diarrheac. Prolonged GI suctioningd. Increased sweatinge. Inability to gain access to fluidsf. Inadequate fluid intakeg. Massive third spacing

Risk factors are the following:a. Diabetes Insipidusb. Adrenal insufficiencyc. Osmotic diuresisd. Hemorrhagee. Comaf. 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. Elevated BUN due to depletion of fluids or decreased renal perfusion

2. Hemoconcentration3. Possible Electrolyte imbalances:

Hypokalemia, Hyperkalemia, Hyponatremia, hypernatremia

4. Urine specific gravity is increased (concentrated urine) above 1.020

NURSING MANAGEMENT

1. Assess the ongoing status of the patient by doing an accurate input and output monitoring

2. Monitor daily weights. Approximate weight loss 1 kilogram = 1liter!

3. Monitor Vital signs, skin and tongue turgor, urinary concentration, mental function and peripheral circulation

4. Prevent Fluid Volume Deficit from occurring byidentifying risk patients and implement fluid replacement therapy as needed promptly

5. Correct fluid Volume Deficit by offering fluids orally if tolerated, anti-emetics if with vomiting, and foodswith adequate electrolytes

6. Maintain skin integrity7. Provide frequent oral care8. Teach patient to change position slowly to

avoid sudden postural hypotension


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

Pathophysiology of Fluid Volume Excess

Etiologic conditions and Risks factorsa. Congestive heart failure

b. Renal failurec. Excessive fluid intaked. Impaired ability to excrete fluid as in

renal diseasee. Cirrhosis of the liverf. Consumption of excessive table saltsg. Administration of excessive IVFh. Abnormal fluid retention

PATHOPHYSIOLOGY

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

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

Subjective cue/s Shortness of breath Change in mental state

Laboratory findings1. BUN and Creatinine levels are LOW because

of dilution2. Urine sodium and osmolality decreased (urine

becomes diluted)3. CXR may show pulmonary congestion

IMPLEMENTATION

ASSIST IN MEDICAL INTERVENTION

1. Administer diuretics as prescribed2. Assist in hemodialysis3. Provide dietary restriction of sodium and

waterNURSING MANAGEMENT

1. Continually assess the patient‟s condition by measuring intake and output, daily weight monitoring, edema assessment and breath sounds

2. Prevent Fluid Volume Excess by adhering to diet prescription of low salt- foods.

3. 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

4. Teach patient about edema, ascites, and fluid therapy. Advise elevation of the extremities, restriction of fluids, necessity of paracentesis, dialysis and diuretic therapy.

5. Instruct patient to avoid over-the-counter medications without first checking with the health care provider because they may contain sodium

ELECTROLYTES

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

Sources of electrolytes

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

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 gramsFunctions:

1. Participates in the Na-K pump2. Assists in maintaining blood volume3. Assists in nerve transmission and

muscle contraction4. Primary determinant of ECF

concentration.5. Controls water distribution throughout

the body.6. Primary regulator of ECF volume.7. Sodium also functions in the establishment of

the electrochemical state necessary for muscle contraction and the transmission of nerve impulses.

8. Regulations: skin, GIT, GUT, Aldosterone increases Na retention in the kidney

SODIUM DEFICIT: HYPONATREMIA

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 Factorsa. Fluid loss such as from Vomiting and nasogastric

suctioningb. Diarrheac. Sweatingd. Use of diureticse. Fistula

Other factorsa. Dilutional hyponatremia

Water intoxication, compulsive water drinking where sodium level is diluted with increased water intake

b. SIADHExcessive secretion of ADH causing water retention and dilutional hyponatremia

PATHOPHYSIOLOGYDecrease 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

ASSESSMENTSodium 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 lossand 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 increasingintracranial pressure occurs: lethargy Confusion muscular twitching focal weakness hemiparesis papilledema convulsions

In summary:

Physical Examination Altered mental status Vomiting Lethargy Muscle twitching and convulsions (if sodium level

is below 115 mEq/L) Focal weakness

Subjective Cues Nausea Cramps Anorexia Headache

Laboratory findings1. Serum sodium level is less than 135 mEq/L2. Decreased serum osmolality3. Urine specific gravity is LOW if caused by sodium

loss4. In SIADH, urine sodium is high and specific gravity

is HIGHIMPLEMENTATION

ASSIST IN MEDICAL INTERVENTION1. 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 SIADH3. Provide water restriction if with excess volume

NURSING MANAGEMENT

1. Provide continuous assessment by doing an accurate intake and output, daily weights, mental status examination, urinary sodium levels and GI manifestations. Maintain seizure precaution

2. Detect and control Hyponatremia by encouraging foodintake with high sodium content, monitoring patients on lithium therapy, monitoring input of fluids like IVF, parenteral medication and feedings.

3. Return the Sodium level to Normal by restricting waterintake 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 factorsa. Fluid deprivationb. Water loss from Watery diarrhea, fever,

and hyperventilationc. Administration of hypertonic solutiond. Increased insensible water losse. Inadequate water replacement, inability to

swallowf. Seawater ingestion or excessive oral

ingestion of salts


Other factorsa. Diabetes insipidusb. Heat strokec. Near drowning in oceand. Malfunction of dialysis

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

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, andhallucinations in severe hypernatremia. Dehydration (hypernatremia) is often overlooked as

the primary reason for behavioral changes in the elderly.

If hypernatremia is severe, permanent brain damagecan 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.

ASSESSMENTPhysical 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

Subjective Cues Delusions and hallucinations Extreme thirst Behavioral changes

Laboratory findings1. Serum sodium level exceeds 145 mEq/L2. Serum osmolality exceeds 295 mOsm/kg3. Urine specific gravity and osmolality

INCREASED or elevated

IMPLEMENTATION

ASSIST IN THE MEDICAL INTERVENTION

1. Administer hypotonic electrolyte solution slowly as ordered

2. Administer diuretics as orderedLoop diuretics (thiazides ok)

3. Desmopressin is prescribed for diabetes insipidus

NURSING MANAGEMENT

1. Continuously monitor the patient by assessing abnormal loses of water, noting for the thirst and elevated body temperature and behavioral changes

2. 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

3. Correct the Hypernatremia by monitoring the patient‟s response to the IVF replacement. Administerthe hypotonic solution very slowly to prevent sudden cerebral edema.

4. Monitor serum sodium level.5. Reposition client regularly, keep side-rails up, the

bed in low position and the call bell/light within reach.

6. Provide teaching to avoid over-the countermedications 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 ofthe 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, medicationsFunctions:

1. Maintains ICF Osmolality2. Important for nerve conduction and

muscle contraction3. Maintains acid-base balance4. Needed for metabolism of carbohydrates, fats

and proteins5. Potassium influences both skeletal and cardiac

muscle activity.( For example, alterations in its concentration changemyocardial irritability and rhythm )

6. Regulations: renal secretion and excretion,* Aldosterone promotes renal excretion* Acidosis promotes K exchange for hydrogen

POTASSIUM DEFICIT: HYPOKALEMIA

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

Pathophysiology

Etiologic Factorsa. Gastro-intestinal loss of potassium such

as diarrhea and fistulab. Vomiting and gastric suctioningc. Metabolic alkalosisd. Diaphoresis and renal disorderse. Ileostomy

Other factor/sa. Hyperaldosteronismb. Heart failurec. Nephrotic syndromed. Use of potassium-losing diureticse. Insulin therapyf. Starvationg. Alcoholics and elderly

PATHOPHYSIOLOGY

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

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: 3mmol/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

ASSESSMENTPhysical 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 findings1. Serum potassium is less than 3.5 mEq/L2. ECG: FLAT “T” waves, or inverted T waves,

depressed ST segment and presence of the “U” wave and prolonged PR interval.

3. Metabolic alkalosis

IMPLEMENTATION

ASSIST IN THE MEDICAL INTERVENTION


1. Provide oral or IV replacement of potassium2. 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 10- 20-mEq/ hour!

3. NEVER administer K by IV bolus or IM

NURSING MANAGEMENT

1. Continuously monitor the patient by assessing the cardiac status, ECG monitoring, and digitalis precaution

2. Prevent hypokalemia by encouraging the patient to eat potassium rich foods like orange juice, bananas,cantaloupe, peaches, potatoes, dates and apricots.

3. Correct hypokalemia by administering prescribed IV potassium replacement. The nurse must ensure that the kidney is functioning properly!

4. Administer IV potassium no faster than 20 mEq/hourand hook the patient on a cardiac monitor. To EMPHASIZE: Potassium should NEVER be given IV bolus or IM!!

5. A concentration greater than 60 mEq/L is not advisablefor peripheral veins.

POTASSIUM EXCESS: HYPERKALEMIA

Serum potassium greater than 5.5 mEq/LPathophysiology

Etiologic factorsa. Iatrogenic, excessive intake of potassiumb. Renal failure- decreased renal excretion

of potassiumc. Hypoaldosteronism and Addison‟s

diseased. Improper use of potassium supplements

Other factors1. Pseudohyperkalemia- tight tourniquet and

hemolysis of blood sample, marked leukocytosis

2. Transfusion of “old” banked blood

3. Acidosis4. Severe tissue trauma

PATHOPHYSIOLOGYIncreased 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 7mEq/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 muscleweakness 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 withvery 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.

ASSESSMENTPhysical Examination Diarrhea Skeletal muscle weakness Abnormal cardiac rate

Subjective Cues Nausea Intestinal pain/colic Palpitations

Laboratory Findings1. Peaked and narrow T waves2. ST segment depression and shortened QT

interval3. Prolonged PR interval4. Prolonged QRS complex5. Disappearance of P wave6. Serum potassium is higher than 5.5 mEq/L7. Acidosis

IMPLEMENTATION


ASSIST IN MEDICAL INTERVENTION1. Monitor the patient‟s cardiac status with cardiac

machine2. Institute emergency therapy to lower potassium

level by:a. Administering IV calcium gluconate-

antagonizes action of K on cardiac conduction

b. Administering Insulin with dextrose-causestemporary shift of K into cells

c. Administering sodium bicarbonate-alkalinizes plasma to cause temporary shift

d. Administering Beta-agonistse. Administering Kayexalate (cation-

exchange resin)-draws K+ into the bowelNURSING MANAGEMENT

1. Provide continuous monitoring of cardiac status, dysrhythmias, and potassium levels.

2. Assess for signs of muscular weakness, paresthesias, nausea

3. Evaluate and verify all HIGH serum K levels4. Prevent hyperkalemia by encouraging high risk

patient to adhere to proper potassium restriction5. 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

6. Assist in hemodialysis if hyperkalemia cannot be corrected.

7. Provide client teaching. Advise patients at risk to avoideating potassium rich foods, and to use potassium salts sparingly.

8. Monitor patients for hypokalemia who are receivingpotassium-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

Functions:

1. Needed for formation of bones and teeth

2. For muscular contraction and relaxation3. For neuronal and cardiac function4. For enzymatic activation5. For normal blood clotting

Regulations:

1. GIT- absorbs Ca+ in the intestine; Vitamin D helps to increase absorption

2. Renal regulation- Ca+ is filtered in the glomerulusandreabsorbed in the tubules:

3. 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 ofboth calcium and PO4 in the kidney and promoted deposition of calcium in the bones.

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

Collaborative Management1. Calcium gluconate 10% IV2. Calcium chloride 10% IV3. both usually given by Dr, very slowly; venous

irritant; cardiac probs4. Oral: calcium citrate, lactate, carbonate; Vit D

supplements5. Diet: high calcium6. Watch out for tetany, seizures, laryngospasm, resp

& cardiac arrest7. Seizure precautions

Sources:milk, yogurt, cheese, sardines, broccoli, tofu, green leafy vegetables

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. Hyperphosphatemiae. Vit D deficiencyf. 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

abovesystole for 3 min = carpopedal spasm)

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



HYPERCALCEMIA

is an elevated calcium level in the blood

usually from bone resorption Risk Factors / Causes

a. Hyperparathyroidism (eg adenoma)b. Metastatic cancer (bone resorption as tumor‟s

ectopic PTH effect) – eg. Multiple myelomac. Thiazide diuretics (potentiate PTH effect)d. Immobilitye. 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) Arrhythmia ECG: shortened QT interval, decreased ST

segment Hyporeflexia, lethargy, coma

Collaborative Management1. If parathyroid tumor = surgery2. Diet: low Ca, stop taking Ca Carbonate

antacids, increase fluids3. IV flushing (usually NaCl)4. Loop diuretics5. Corticosteroids6. Biphosphonates, like etidronate (Calcitonin)

& alendronate (Fosamax)7. Plicamycin (Mithracin) – inhibits bone

resorption8. Calcitonin – IM or intranasal9. Dialysis (severe case)10. Watch out for digitalis toxicity11. 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 activity2. affects muscle contraction, & especially relaxation3. maintains normal heart rhythm4. promotes vasodilation of peripheral arterioles

Sources:green leafy vegetables, nuts, legumes, seafood, whole grains, bananas, oranges, cocoa, chocolate

HYPOMAGNESEMIA

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

Risk Factors and Causea. Chronic alcoholism (most common),

Alcohol stimulates renal excretion of magnesium,

b. Inflammatory bowel diseasec. Small bowel resectiond. GI cancere. 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 calciumi. Excess saturated fatsj. Excess coffee or tea intakek. Excess phosphoric or carbonic acids (soda pop)l. Insufficient water consumptionm. Excess salt or sugar intaken. Insufficient selenium,vitamin D,

sunlight exposure or vitamin B6o. Increased levels of stress

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.

* Like hypocalcemia, hypokalemiaPotentiates digitalis toxicity

Collaborative Management1. Magnesium sulfate IV, IM (make sure

renal function is ok) – may cause flushing2. 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 Factorsa. Magnesium treatment for pre-eclampsiab. Renal failurec. Diabetic Ketoacidosisd. Excessive use of Mg antacids/laxatives

PATHOPHYSIOLOGYIncrease Mg. ----- Blocks acetylcholine release ---- decrease excitability of muscle

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Clinical Manifestation Hyporeflexia Hypotension, bradycardia,

arrhythmia Flushing Weakness, lethargy, coma Decreased RR & respiratory paralysis Loss of DTR‟s

*like hypercalcemia

Collaborative Management1. Diuretics

2. Stop Mg-containing antacids & enemas3. IV fluids rehydration4. 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 & strength2. phospholipids (make up cell membrane

integrity)3. part of ATP4. affects metabolism, Ca levelsSources:red & organ meats (brain, liver, kidney), poultry, fish, eggs, milk, legumes, whole grains, nuts, carbonated drinks

HYPOPHOSPHATEMIA

Risk Factorsa. Decreased Vit D absorption, sunlight exposureb. 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 hypercalcemia

Collaborative Management1. Sodium phosphate or potassium phosphate

IV (give slowly, no faster than 10 mEq/hr)2. Sodium & potassium phosphate orally

(Neutra-Phos, K-Phos) – give with meals to prevent gastric irritation

3. Avoid Phos-binding antacids4. Diet: high Mg, milk5. Monitor joint stiffness, arthralgia,

fractures, bleeding

HYPERPHOSPHATEMIA

Risk Factorsa. Acidosis (Ph moves out of cell)b. Cytotoxic agents/chemotherapy in cancerc. Renal failured. Hypocalcemiae. Massive BT (P leaks out of cells during storage

of blood)f. Hyperthyroidism

Clinical Manifestation Calcification of kidney, cornea,

heart Muscle spasms, tetany, hyperreflexia

*like hypocalcemia

Collaborative ManagementM1. Aluminum antacids as phosphate binders: Al

carbonate (Basaljel), Al hydroxide (Amphojel)

2. Ca carbonate for hypocalcemia3. Avoid phosphate laxatives/enemas4. Increase fluid intake5. Diet: low Phos, no carbonated drinks

CHLORIDE

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/LFunctions:1. helps regulate BP, serum osmolarity2. part of HCl3. acid/base balance (exchanges with HCO3)

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

HYPOCHLOREMIA

Risk Factorsa. Diuresisb. Metabolic alkalosisc. Hyponatremia, prolonged D5W

IVd. Addison‟s

Clinical Manifestation Slow, shallow respirations (met.

Alkalosis) Hypotension (Na & water loss)

Collaborative Management1. Administer IV or Oral : KCl, NaCl2. Diet: high Cl (& usually Na)

HYPERCHLOREMIA

Risk Factors / Causea. Metabolic acidosisb. Usually noted in hyperNa,

hyperK

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

Collaborative Management1. 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 bases2. Bicarbonate Buffer System- most important

- uses HCO3 & carbonic acid/H2CO3 - (20:1)- closely linked with respiratory & renal

mechanisms3. 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

increase pHCO2 =

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 pH2. kidneys form ammonia that combines with H ions

to form ammonium ions, which are excreted in the urinein exchange for sodium ions

Review: Acid-Base Imbalance

pH – 7.35-7.45pCO2 – measurement of the CO2 pressure that is

being exerted on the plasma- 35-45mmHgPaO2- amount of pressure exerted by O2 on the

plasma- 80-100mmHgSaO2- percent of hemoglobin saturated with O2

Base excess – amount of HCO3 available in the ECF - -3 to

+3

Interpretation Arterial Blood Gases

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

Step 1 Look at the pH Is it up or down? If it is up - it reflects alkalosis If it is down - it reflects acidosis

Step 2 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 thepH - move to step III

Step 3 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 causeimbalances


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 Stimulia. Acute respiratory failure from airway obstructionb. Over-sedation from anesthesia or narcoticsc. Some neuromuscular diseases that affect ability

to use chest musclesd. 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 shallowrespirations

Neuro: headache, blurred vision, irritability, confusion

Respiratory collapse leads to unconsciousness andcardiovascular collapseCollaborative

Management1. Early recognition of respiratory status and treat cause

2. Restore ventilation and gas exchange; CPR forrespiratory failure with oxygen supplementation; intubation and ventilator support if indicated

3. Treatment of respiratory infections withbronchodilators, 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 percannula6. 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 Stimulia. Hyperventilation with anxiety from

uncontrolled fear, pain, stress (e.g. women in labor, trauma victims)

b. High feverc. Mechanical ventilation, during anesthesia

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, maydevelop 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. Treatment: encourage client to breathe slowly in a paper bag to rebreathe CO2

2. Breathe with the patient; provide emotionalsupport and reassurance, anti-anxiety agents, sedation

3. On ventilator, adjustment of ventilation settings (decrease rate and tidal volume)

4. Prevention: pre-procedure teaching, preventative emotional support, monitor blood gases asindicated

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 Stimulia. 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 diabetesor 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 theintracellular 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 fromhyperkalemia

GI: anorexia, nausea, vomiting Skin: warm and flushed


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

Diagnostic test findings:1. ABG: pH < 7.35, HCO3 < 222. Electrolytes: Serum K+ >5.0 mEq/L3. Serum Ca+2 > 10.0 mg/dL4. Serum Mg+2 < 1.6 mg/dL

Collaborative Management1. Medications: Correcting underlying cause

will often improve acidosis2. Restore fluid balance, prevent dehydration

with IV fluids3. Correct electrolyte imbalances4. 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 ofcells 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

Common Stimulia. 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 SodiumBicarbonate

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 breathingDiagnostic test findings

1. ABG‟s: pH> 7.45, HCO3

>262.3.

Electrolytes: Serum K+ < 3.5 mEq/LElectrocardiogram: as with hypokalemia

Collaborative Management

1. Correcting underlying cause will often improve alkalosis

2. Restore fluid volume and correct electrolyteimbalances (usually IV NaCl with KCL).

3. With severe cases, acidifying solution may be administered.

4. Assessment Vital signs Neuro, cardiac, respiratory assessment Repeat arterial blood gases and electrolytes

Selected Water and Electrolyte Solutions

Isotonic Solutions

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

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 fluidvolume 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 resultingsolution becomes hypertonic in relation to plasma, and in addition to the above described electrolytes, provides 170cal/L

Only solution that may be administered withblood products

B. Lactated Ringer’s solution (Hartmann’s solution)Na+ 130 mEq/LK+ 4 mEq/LCa++ 3 mEq/LCl- 109 mEq/LLactate (metabolized to bicarbonate) 28 mEq/L (274 mOsm/L)Also available with varying concentration of dextrose (themost common is 5% dextrose)

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 thebody. Lactated Ringer‟s solution should not be used in lactic acidosis because the ability to convert lactate into HCO3- is impaired in this disorder.

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 anddehydration

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 maycause increased intracranial pressure

Should not be used for fluid resuscitation because it can cause hyperglycemia

Should be used with caution in patients with renalor 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

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

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 orincreased intracranial pressure

Administer cautiously, because it can cause fluid shifts from vascular system into cells, resulting in cardiovascular collapse and increased intracranial pressure

Hypertonic Solutions

E. 3% NaCl (hypertonic saline)Na+ 513 mEq/LCl- 513 mEq/L(1026 mOsm/L)

Used to increase ECF volume, decrease cellular swelling

Highly hypertonic solution used only in criticalsituations 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

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


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% D5WAvailable in low-molecular-weight (Dextran 40) and high- molecular-weight (Dextran 70) forms

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 RBCaggregation

Contraindicated in hemorrhage, thrombocytopenia, renal dse and severe dehydration

Not a substitute for blood or blood products

Electrolytes Nsg.ppt

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