FLIUD VOLUME IMBALANCES

":~jnay reflect-an increase a decrease in total body fluid or an altered distribution of ~4Y:fluids. There are two major alterations in extacellular fluid (ECF) balance: fluid ~i\Jme deficit and fluid volume excess.

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"ciacellular fluid volume deficit reflects a contracted vascular compartment due either ;lgnificant ECF loss or to an accumulation of fluid in the interstitial soace. 'trointestinal dysfuntion is the most common cause ofECF deficit. "Fluid volume itoccurs when there is an excessive loss of body water or an inadequate , nsatory intake. THE ECF consists predominantly of the electrolytes, sodium and' elide, both of whichtend to attract water; these electrolytes also leads to loss of water. ,,', Clinically, ECF deficit is characterized by acute weight loss, altered '>;;~?c3.rdiovascular function that reflects the underling ECF volume deficit, and complaints of ,._t~~Il.~ea and vomiting. Symptomatology reflects a dehydrated state with sunken eyeballs, ::;~~'.poor skin turgor, and oliguria. , ,.si,s. "Laboratory findings in fluid volume deficit reflects hemoconcentration; the serum ';'f"hemoglobin, hematocrit, and proteins are increased. Blood urea nitrogen elevated above' -1-~"20'mg/I 00 ml. The urine specific gravity reflects high solute concentration of more than
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ireatment,for ECF volume deficit entails fluid replacement (orally or intravenously) until the oliguria is relived and the cardiovascular and neurologic systems , stabilize. Isotonic electrolyte solutions such as 0.9% NaCI or lactated Ringer's solution are used to treat the hypotensive patient in fluid volume deficit. A hypotonic electrolyte solution (0.45% NaCl) often used to provide electolyte and free water for renal excretion of metabolic wastes. .
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FLUID VOLUME EXCESS Extracellur fluid volume excess causes an expansion of the ECF compartment. The

pri,tnary cause ofECF excess is cardiovascular dysfunction. Fluid volume_excess,is

.~},Vays secondary to increase in total body sodium cont~\vhich ~~(tOta1 body ,~ter increase. Normally, the posterior pituitary deceases secretion of the antidiuretic hormone (ADH) when excess water moves into the cells. This causes the kidney to eliminate excess fluid. However, if the patient has an excessive secretion of ADH, the water will be retained, placing the patient at risk for fluid volume excess. Excessive secretion of ADH can be caused by fear, pain, postoperative reaction 12 t024 hours after surgery, and acute infections. Clinically, ECF volume excess has distinct signs and symptoms, the most prominent being weight gain. Oedema is usually not apparent until 2 to 4 kg of fluid have been retain. Alteration in respiratory and cardiovascular function are present include hypertension and tachycardia.

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In fluid volume excess, the hematocit may be decreases because of'hemodilution. The serum sodium osmolarity will be decreased if hypervolernia occurs as a result of excess retention of water. Treatment ofECF volume excess is directed toward sodium and fluid restriction, administration of diuretics and the treatment of the underling cause

MAJORE-IGTR()tYTE

IMBALANCES

There are two types of major electrolyte imbalances: (1) Metabolic (base bicarbonate deficit and excess) acidosis and alkalosis (2) Respiratory (carbonic acid deficit and excess) acidosis. ~etabolic Acid-Base Imbalance Normal ref Value: 22-26rnEq/l Base Bicarbonate Deficit: Metabolic Acidosis
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Metabolic acidosis is a clinical disturbance characterised by a low pH and a low plasma IlCa level. Thiscondition can occur by a gain of hydrogen (H+) iconior a loss ofHCQ3 r_,'c-<.:.,-,-, ~,--;, \....--:::. \ .""'-".." \,;;""6,,,E.._~\ c.:::,,,,- .._,~,, 'y-, . ;:y\. :';'1 <, .",<-. ~ U\. 2. A.- '- ;.;.,'~'", c.':...~"_ ~< ~ . \..-'\. '. Etiology . ,)~. Metabolic .:. .:. .:.
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acidosis occurs with a loss ofHCqp-om Diarrhoea Draining fistulas Administration of TPN

Ketoacidosis from: .:. Diabetes mellitus .:. Alcoholism .:. Starvation Lactk~acidosis from .:. Respiratory failure .:. Circulatory failure .:. Ingestion of certain drugs or toxins .:. Some hereditary disorders .:. Septic shock .:. Renal failure in excess retention of hydrogen ions .:. Ingestion of aspirin .:. Ethylene alcohol .:. Ammonium chloride

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Signs and symptoms .:. Headache .:. Confusion .:. Drowsiness .:. Increased respiratory rate kussmaul breathing .:. Nausea .:. Vomiting ~:. Decreased cardiac output '.:. Bradycardia

.. Base Bicarbonate Excess: Metabolic Alkalosis tj\\ ::-,'':;;oe"::, '" ';:c, \, Is a clinical disturbance characterized by a high pH and a high plasma HC~ concentrtion. It can be p~.9duced by a gain ofHC~or a loss of hydrogen ion. Etiology >- Gastrointestinalloss of hydrogen ions from gastric suctiosing and vomiting >- Renal loss of hydrogen ions occurs from potassium losing diuretics >- Excess of mineralocorticoid ~ Hypercalcemia >- Hypoparathyroidism Signs and Symptoms >- Dizziness >- Depressed respirations >- Tingling of fingers and toes )- Circumoral paresthesia ,, >- Hypertonic reflexes >- Hypotention >- Cardiac dysrhytbmias , >- Hyperventilation .: I1 Hypokalemia ~ : }>' Decreased ionized calcium
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RESPIRATORY ACID-BASE IMBALANCE

.'-~ormal reference value: Partial pressure of carbon dioxide (Pacoz) 38-42 mm Hg

.):'Carbonic Acid Excess: Respiratory

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Acidosis
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'!;;~~espiratory acidosis is due to inadequate excretion of carbon dioxide and inadequate ;;~y~ntilation resulting in all increase of serum levels or carbon dioxide and H2 C03. Acute i;~fJspiratoryacidosis is usually associated with emergency situations.
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Etiology . AcuteJespiratory acidosis-can result from pulmonary, neurologic, and cardiac ;;t~;c~i.ises such as: pulmonary edema, aspiration of a foreign body, pneumothorax, severe ,c;;;ii,};\; eumonia, and severe, prolonged exacerbation of acute asthma, overdose of sedatives, . diac arrest, and massive pulmonary embolism. " .Qu:o.ni_c respiratory acidosis results from emphysema, bronchial asthma .;:~tbronchiectasis,postoperative pain, obesity, and tight abdominal binders
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-:'}~ignsand Symptoms Tachynea Dyspnea .Dizziness .Seizures .Warm Flushed skin Vectricularfibrillation

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\bonic"Acid Deficit: Respiratory

Alkalosis

. spiratory alkalosis is usually due to hyperventilation, which causes "blowing off" of :"~- on dioxide and 'a: decrease in H2C03 content. Respiratory alkalosis can be acute or ~.;~;~hro~c ..~ . "-'-', C:3
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Acuteacloosi-s- results from pulmonary disorders that produce hypoxemia or :. ';V,~~ulation of the respiratory ceaters. Underling causes ofhypoxernia include: high fever, 'I,~"pneumonia, congestive heart failure, pulmonary emboli, hypotension, asthma, and .'.}i~a1ation of ih-ita.nts. Caus~s of sti~ul~tion of respi:ato~ cent~rs include ~ety (most
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mecharncal ventllatlO.h, CNS lesions involving the respiratory '.>H;c~nter, asd salicylate overdose (an early SIgn).

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Signs and Symptoms ~ Light-headedness >- Inability to concentrate >- Numbness and tingling of extremities > Tinnitus >- - Palpitation > Epigastric pain > Blurred visioe-percordial pain > Sweating > Drymouth >- Tremulousness. >- Seizures and l~onicionsr'3

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Pa02 ,Oxygen saturation Base excess6hteficit

7.35':'7.45 35-45mmHg80-100 mmHg 95o/tr-IOO% +or-2 22-26 mEq/L

7.3_2~T3 pC0242 pOi40 mm 75%

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-' Acid-Base Disturbances and Compensation

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Respiratory acidosis Resplr~tory alkalosis Metabolicacidosis Metabolic alkalosis

} PaCOz' 1 or:n~r~alhC03'~ ,!pH ,Kidneys eliminate H+ and retainHC03:J;. PaCOz'1 or normal HC03 ~,tpHKid~y~'conserve H+and excrete HC03.J.. ornormalPaC02,:J;HC03~,tpH:_ Lungs:eliminate CO2, conserve HC03tor normalPaC02, l' flC03-,t pH Lungsi ventilation to t PC02,kfdneys , conserve H+to excrete HC03-

ASSESSlVIENT

In determining the problem and mode of correction offluid and electrolyte, in balance the first step is assessing the clients need. Assessment must be approached subjectively and objectively.

ASSESSMENT
SUBJECTIVE: In this approach the client is assessed in a head to toe fashion. Eyes: sunken or periorbital odema, absence of tears when crying Mouth- dry lips! cracked, dry mucus membrane. N e~: flattened or distorted neck vein. Skin- dry inelastic skin or cool and clammy/scaly/crack, ascites, hot to touch. Feet- swollen, pitting or non pitting OBJECTIVE: Here a are more detailed invasive account is taken CNS- muscle twitching, hyperactive tendon raflses convulsion, restlessness, weakness, delirium, coma, increased intracramed pressure, fatigue, apathy, confusion and anorascie. Renal- oliguria Cardiovascularincreased BP and pulse tachycardia, hypotension, irregular pulse rythmn. Pulmonary coughing changes in reperative rales or rhonchi in the lungs. Renal- oliguria, metabolism, elevated temperature DIAGNOSIS (1) Aeleration in fluid and electrolytes: excess related to disease process evidenced by ,\ periorbital odema hypertension, distorted neck, veins and irregular pulse rate, cold clamming skin. (2) :')Alterationand F ~d E deficit related to disease process evidenced by sunken eyes, dry !! scaly skin, flattened-neck ve~~, hyperthermia, oliguria.

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The aim is to restore homeostasis. rationale. (1) Take blood sample for U + and check for IV therapy order. Rationale to determine patient fluid electrolytes status and need for correction. (2) (3) (4) Establish I\! access for IVF therapy as replacement and maintenance in fluid balance. Ascertain the need for (from U+ E) and initiate electrolyte replacement therapy as ordered .. Maintain intake and output to..determine retention or depletion offluid

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Monitor vis to determine electrolyte and fluid levels ( fluid level- fever, respiration and pulse). Daily or alternate days weight to determine or loss, therefore the need for change in IV therapy. IV drug as indicated or prescribed in managing fluid excess or deficit e.g antidiuretics.

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Monitor for side effects of electrolytes and fluid replacement therapy. Record and report Monitor for unexpected outcome/ complication e.g infultration

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E~ALUATION Reassess client to determine response to therapy Repeat U+ E to ascertain return of normal valves
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Check and other physical assessment parameters. Check FBC.

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