Acid/Base Balance Acid/Base Balance

o The body usually produces more acids than bases. Acids enter the body via food ingestion and metabolism of lipids and proteins

o Factors affecting balance: Age Environment GI output Chronic disease(s) Trauma Therapies

o Rates of acid/base correction differ as between the different systems Buffers function almost instantaneously Respiratory mechanisms take several minutes to hours to kick in Renal mechanisms may take up to several days to be effective

pH : the balance between the lung & the kidneys

o Measures acidity/alkalinity based on the presence of hydrogen ions in the blood pH is inversely proportional to the number of hydrogen ions in the blood

The more H+ ions present, the lower the pH o Water has a pH of 7o Normal: 7.35 – 7.45

Death occurs is pH is <6.8 or >8 o < 7.35 = acidosiso > 7.45 = alkalosis

PO2 : indicates partial pressure of oxygen that is dissolved in the arterial blood

o Normal: 80 – 100 o In the elderly, there’s a normal, expected decline in the PaO2 level

HCO3 : bicarbonate

o Normal: 22 - 26o Bicarbonate is a major buffer in the body; level is controlled by the kidneys

Blood pH decreases kidneys compensate by retaining HCO3 to buffer the blood Blood pH increases kidneys compensate by excreting HCO3 \ to help prevent the

blood from becoming too alkaline

CO2 : reflection of respiratory breadth and depth

o Normal: 35 – 45o Carbonic acid is the combination of water & CO2 produced during the breathing process,

i.e., the amount produced during ventilation

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o Imbalance indicates respiratory problem (Lungs are very quick to react/adjust CO2 levels)o RESPIRATORY ALKALOSIS : PaCO2 < 35

Causes: Hyperventilation (blow off CO2) – fear, anxiety, trauma, high respirator setting Hypoxia, Pulmonary embolism Pain Some medications (Doxapran, which is a respiratory stimulant) Anesthetic-induced hypoventilation Other conditions with increased metabolic demands

o Thyroid storm, Fever, Gram-negative sepsis, Pregnancy Clinical manifestations:

Tachypenia, Dysrhythmias possible (with palpations), diaphoresis Dizziness, Light-headedness Numbness, confusion, inability to concentrate and blurred vision Dry mouth Tetany and spasms of the arms and legs

Patient may suffer from a hyperventilation syndrome will have tinnitus (i.e., ringing in the ears), palpitations, diaphoresis, dry mouth, tremors, pre-cordial pain, n/v, epigastric pain, blurred vision, changes in LOC and seizures

Treatment: Resolve the underlying disorder (i.e., if it’s due to anxiety, give patient anti-

anxiety meds and teach the patient proper breathing exercises) Monitor patient for respiratory muscle fatigue and exhaustion Monitor patient for signs of acute respiratory failure SOB, tachycardia,

tachypenia, DOE, fatigue, syncope

o RESPIRATORY ACIDOSIS : PaCO2 > 45; pH <7.35; carbonic acid accumulating in blood Causes: Hypoventilation (holding onto CO2) – can result from anything that

prevents lungs from ventilating properly & allows CO2 build up in lungs Acute: object aspiration, pulmonary edema, pneumothorax, pneumonia, pulmonary

embolism, pain, chest wall injury (flail chest), gross abdominal distentiono CNS related – head trauma, overuse of narcotics/sedatives, anesthesia or

impaired respiratory muscles r/t spinal cord injury Chronic: COPD/emphysema, HF, advanced MS, bronchial asthma

Clinical manifestations: Dyspnea; respiratory distress, Shallow respirations (poor diaphragmatic lift) Headaches, Restlessness, Confusion *If severe, will exhibit: profound CNS depression, drowsiness,

unresponsiveness and cardiac issues (tachycardia & dysrhythmias) Treatment:

Increase ventilation to help blow off excess carbonic acid build-up First: stabilize patient by possibly providing mechanical ventilation Then: correct underlying cause

o If due to a narcotic od, give a reversal agento If due to gross pain, manage the paino If lung collapse/pneumothorax, a chest tube will be insertedo If due to bronchial spasms, give bronchodilatorso If due to acute infection, give antibiotics as ordered

Give oxygen but O2 on its own won’t completely correct problem

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Ensure adequate hydration, i.e., 2-3 L of fluid over 24 hourso METABOLIC ACIDOSIS : HCO3 < 22 pH < 7.35

There is a deficit of bicarb in blood or an excess of acids other than carbonic acid Causes:

Liver/Kidney failure DKA (diabetic ketoacidosis) Diarrhea, Dehydration Starvation Aspirin poisoning

Clinical manifestations: Low BP, increased RR (deep, labored breathing) Headache, confusion, nausea, vomiting Restlessness - which progresses to lethargy, then stupor or coma Chest pain and dysrhythmias Muscle pain/weakness Warm, flushed skin (due to peripheral vasodilation) * Hyperkalemia is very common in metabolic acidosis

Treatment: Treat underlying cause, which centers on hypoxic tissue anywhere in the

body (hypoxic tissue produces metabolic acidosis) Only treat with bicarbonate if the metabolic acidosis is RENAL in nature

o METABOLIC ALKALOSIS : HCO3 > 26 pH > 7.45 Excess of bicarb or a loss of acid somewhere in the body Causes:

Excess base from ingesting antacids or excessive use of bicarbs to treat reflux disease (i.e., Sodium Bicarbonate)

Acid loss via vomiting, gastric suction or excess use of diuretics * May see HYPOKALEMIA in metabolic acidosis

Clinical manifestations: Dizziness, lethargy, disorientation, seizures and coma Weakness, muscle twitching, muscle cramps and tetany, nausea/vomiting Respiratory depression

Treatment: Most difficult of all of the acid/base imbalances to treat DIAMOX stimulates kidneys to excrete excess bicarb IV infusion of HCl in severe cases

“ROME” Respiratory is Opposite, the Metabolic is Equivalento Respiratory: low is alkaloidic, high is acidic

*pH and PCO2 HAVE AN INVERSE RELATIONSHIP Respiratory alkalosis, the pH will be high and the PCO2 will be low Respiratory acidosis, the pH will be low and the PCO2 will be high

o Metabolic: low is acidic, high is alkaloidic * pH and BICARB WILL ALWAYS MOVE IN THE SAME DIRECTION Metabolic alkalosis, the pH is high and the bicarb is high Metabolic acidosis, the pH is low and the bicarb is low

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Arterial Blood Gasses (ABGs)

Should be put on ice once drawn, and pressure should be maintained for a few minutes after draw

Very important to analyze ABG levels in a step-by-step, sequential process

1. Look at the pH level - is it acidotic or alkalotic?

2. Is it a lung problem or a kidney problem?

o In respiratory disorders, the bicarb will always remain the same

3. So, look at the bicarb level

o If it’s metabolic problem, pH increases (m. alkalosis) and so does the bicarb

*When the pH & bicarb move in the same direction (either up or down), it will always be a

METABOLIC DISORDER, and: the paCO2 will always remain normal. *

Exception: body always tries to compensate re: acid/base balances

o Uncompensated & partially compensated : pH remains outside the normal range by shifting

the H+ ions

o Fully compensated : pH returns to the normal range, but the other values may still be

abnormal

Four Examples Using ABGs .

o 1. pH is 7.22 (low). PaCO2 is high. Bicarb is normal.

This is an example of respiratory acidosis because the pH and the PaCO2 are moving in opposite directions.

Treatment: oxygen, mechanical ventilation, pulmonary toileting and bronchodilators.

o 2. pH is 7.45 (high). PaCO2 is low and the bicarb is 25 (normal).

This is an example of respiratory alkalosis/hyperventilation because, once again, the pH and PaCO2 are moving in opposite directions.

Treatment: rest, possible intubation, anti-anxiety meds, manage pain, decrease fever, give antibiotics as ordered, avoid stress.

o 3. pH is under 7.30. PaCO2 is 36 (normal) and bicarb is low.

This is an example of metabolic acidosis. Treatment: oxygen. Reverse any diabetic ketoacidotic states by giving

insulin. Give high quality nutrition, prepare patient for dialysis and reverse any aspirin poisoning.

o 4. pH is 7.50 (high), PaCO2 is 42 (normal) and bicarb is 33 (high).

This is an example of metabolic acidosis - can tell because of the bicarb shift. Treatment: IV fluids and measures to reduce the excess base.

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Fluid Volume Regulation

Ways In Which the Body Regulates Fluids:

o Kidneys - the kidneys regulate extracellular fluid volume by selectively retaining or

excreting water and electrolytes. Kidneys also regulate the pH of extracellular fluid by

excretion or retention of Hydrogen ions. Kidneys also regulate fluids by excreting

metabolic wastes

o Heart and Blood Vessels - move fluid via pumping action. This pumping action moves

sufficient volume and also permits the regulation of serum (i.e., water and electrolytes) via

stretch receptors along the atria and blood vessels, both of which respond to either

hypovolemic states or hypervolemic states

o Lungs - alveoli ventilation eliminates approximately 13 mEqs of Hydrogen ions to help

maintain an acid/base balance in order to remove approximately 300 ml of water/day

o Pituitary gland - Excretes hormones to help move fluid, specifically the Antidiuretic

Hormone (ADH) - also known as vasopressin. As ADH secretion increases, water retention

increases. As ADH secretion decreases, water retention decreases

o Adrenal glands - play a significant role. Responsible for secreting Aldosterone, another

hormone, which acts at the distal tubules of the kidneys and helps to regulate how much Na

and K is moved back and forth

o Parathyroid gland - affects regulation of calcium to the kidneys, which in turn affects

absorption of fluids by the kidney tubules.

Normal daily intake for a healthy adult is approximately 2,200 to 2,700 mL/day (output ~ same)

o Remove fluid by:

Kidneys remove fluid through formation of urine

Skin through diaphoresis

Lung through water vapor

GI tract normally lose 100-200ml/day - can greatly increase with diarrhea/vomiting

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Fluid Volume Deficit (Hypovolemia) Loss of water and electrolytes from extracellular fluid increase in hematocrit, blood becomes

thicker/more viscous, increase in serum electrolytes and urine specific gravity (urine becomes more concentrated)

Possible causes: o GI abnormalities, i.e., excessive NG tube suctioning, diarrhea/vomiting.

o Severely diaphretic (via chronic elevated temp due to septic disease process)

o Loss of water renally from diuretic therapy, diabetes insipidus (malformation of ADH),

chronic kidney disease, adrenal insufficiency, osmotic dieresiso 3rd-spacing process, usually seen in burn patients, but only within the first 24 hours of a

burn injury. Can also see 3rd-spacing in peritonitis, with an intestinal obstruction or with ascites

Assess:o Vital signs

o Any type of hypothermia, tachycardia, thready pulse, hypotension (especially orthostatic),

decrease in intravenous pressures, tachypnea or hypoxiao Any dizziness, syncope, confusion, n/v, anorexia, acute weight loss

o Is patient thirsty? Does he have dry mucous membranes? A very dry tongue?

o Look for slow capillary refill, cool/clammy skin, diaphoresis, sunken eyeballs, flattened

neck veins, absence of tears and decreased skin turgor

Labs: o HCT may be increased (due to dehydration)

But HCT could also be low, if the patient is bleeding outo If patient is dehydrated, will see increased:

Urine specific gravity BUN Hypernatremia and hyperglycemia

Further assessment for hypovolemia: o Monitor oxygen stats, heart rhythm, urine output & weight

o Watch for changes in neuro status due to potential changes in sodium levels

Watch for dyspnea on exertiono Maintain IV access; replace fluids/blood

o Provide oral care

o Prevent skin breakdown

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Fluid Volume Excess (Hypervolemia) Happens when the isotonic retention of water and sodium are in abnormally high proportions Causes:

o Over-hydration (excess water replacement without electrolytes)

o Hyperosmotic fluid imbalance (gain more water than the electrolytes needed to move water)

o NA excess from Iv fluid, diet, or meds (anti acid)

Potential complications:o Pulmonary edema

o Heart failure

Compensatory measures: o Increased release of naturetic peptides increased excretion of sodium & water by

kidneys (because the kidneys are trying to flush out the excess fluid) *Kidneys won’t be able to do this effectively if pt has underlying kidney disease.*

Patients at risk: o Heart failure, cirrhosis, increased release/ingestion of steroids, abnormal kidney function

o Has excessive sodium intake from IV fluids, diet or meds (particularly anti-acid meds)

o Overhydrated from water replacement without corresponding electrolyte replacement

o SIADH, an ADH disorder caused by the pituitary gland excreting inappropriate amounts of

ADH, which causes water to be reabsorbed back into the body in disproportionate amountso Head injury, because a head injury can affect pituitary gland function therefore, also

affecting multiple organ systems Labs:

o Decreased HCT, BUN and Creatinine

o Effusions may be seen on chest x-ray

Assess: o Respiratory status – listen for crackles

o Orthopnea/dyspnea on exertion (DOE)

o Vitals – may be tachy with a bounding pulse

o May be hypertensive, tachypnic and may have increased venous pressures

Distended neck veins (i.e., jugular vein distention - JVD)o Confusion

o Muscle weakness

Nursing interventions: o ABGs because patient could be in respiratory alkalosis

o Give oxygen PRN

o Reposition patient every 2 hours

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o Weigh patient daily; monitor/document edema and circulation; closely monitor input/output

Equal amount of I&O is goalo Implement possible fluid restriction; decrease IV flow rate

o Monitor for skin breakdown, especially due to edema

Electrolytes

SODIUM

Normal values: 135-145 mEq/Lo Most plentiful electrolyte in extracellular (95% of body’s sodium); small amounts in intracellular

Hyponatremia : Na < 135o Results from a loss of Na (body has a higher concentration of sodium than water)o Causes:

Diuretic use, Vomiting, diarrhea, Diaphoresis, Adrenal Insufficiencyo Clinical manifestations:

Abdominal cramping; Anorexia; nausea Muscular weakness; Gait disturbance; stupor Irritability/personality changes; Seizures

o If sodium drops < 125, will see profound malaise and nausea If drops between 110-115, may see profound CNS changes, seizures & coma states

o Can also occur in the presence of excess water, which pushes sodium back into the cell Causes of excess water:

Certain oncology meds Other meds, including Elavil (antidepressant) or Tegratol Excessive use of NSAIDs (pt w/ RA, OA or musculoskeletal problems) Certain disease processes (Hodgkin’s Lymphoma, TB, pneumonia, asthma, ARDS) Brain tumors (tend to excrete version of ADH, which causes water imbalances)

o Treatment: Na replacement (PO, NG tube or parenterally) IV fluid will contain Ringer’s Lactate or just normal saline

Hypernatremia : sodium > 145o Due to not enough water intake - almost never see this in patients that are alert and oriented

because their thirst mechanism is intact and if they feel thirsty, they drinko Body will attempt to correct by stimulating release of ADH and thirst mechanismo Causes:

Watery diarrhea, Excessive salt intake, Diabetes insipidus, Side effect of dialysiso Clinical indications:

Thirst; Dry, swollen tongue Increased body temp Restlessness, weakness, lethargy, stupor and coma

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Muscle irritability and seizureso Treatment:

Correct the situation but not too rapidly (can lead to cerebral edema) If condition is due to diabetes insipidus, ADH may be given Monitor I&O, manage fluids Continually monitor Na serum levels, BUN and creatinine

POTASSIUM

Normal values: 3.5 – 5.0 mEq/Lo 98% of K+ in the body is contained within cells - moves in & out of cells freely. The 2%

outside cells contributes to neuromuscular functions within the bodyo Influences skeletal & cardiac muscle activity; major role in acid/base balanceo Must be replaced every day

Dietary average of approximately 50 - 100 mEq/day required The body needs a minimum of 40-60 mEq/day to function

Adosterone Depolarization Dialysate Dialysis Dysrhythmia Hemolysis Hyperpolarization

Hypokalemia : o Causes:

Losses in GI tract (diarrhea/excessive laxative abuse, gastric suctioning or vomiting) Renal loss via diuretics or high-dose steroids Meds such as Penicillin or Amphoceterecin B Extreme diaphoresis, abnormal cell shifting (seen with alkalosis) or with poor

nutritional intake (anorexia nervosa, alcoholics)o Clinical manifestations:

Weakness, flacidity, cramping, restless legs, rhabdomyelosis (muscle breakdown) V-tach, V-fib or Toursades de Pointe (form of V-tach) EKG changes with long Q-T segments Hypotension Dilute urine; polyuria and nocturia Nausea/vomiting with anorexia s/s Hyperglycemia (because the hypokalemic state helps to suppress endogenous

insulin production)o Treatment:

Prevention is best. Diet should include bananas, apricots, avocado, orange juice, guava, passion fruit, papaya, milk, carrots and potatoes.

Supplements (20-40 mEq/day) May need K-riders (IV solutions of pure potassium)

o Nursing interventions:

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Monitor potassium levels very carefully and detect changes early because they could be life-threatening, due to K+ impact on the cardiac system

Patient education: teach patients not to overuse laxatives Monitor for Dig toxicity - hypokalemia can push a patient into Dig toxicity Usually if a patient is on Lasix, he will also be on a potassium supplement Give patient potassium supplement as prescribed

Hyperkalemia : o Causes:

Renal insufficiency secondary to decreased excretion of K+ (because kidney is major route of potassium excretion)

Metabolic acidosis (K+ shifts out of the cell and into the extracellular fluid) Hyperglycemia Beta-blocker medication (these interfere with K+ re-entry into the cell) Chronic Heparin use

o Clinical manifestations: Cardiac changes possible if K > 7 (definitely see if K > 8) EKG: peaked, narrow T-waves, short Q-T segments, long P-R intervals (which

cause A-V blocks) May see loss of a P-wave, V-tach, bradycardia or cardiac arrest

Rapidly ascending muscular weakness, possibly leading to flaccid quadriplegia Resulting paralysis of respiratory muscles can lead to respiratory arrest and

death Nausea, diarrhea and intestinal colic

o Treatment: depends on whether presentation is acute or non-acute Non-acute treatment:

Limit potassium intake Give non-potassium sparing diuretics May give Kayexalate orally or rectally

Acute treatment: order in which you give them doesn’t matter Give calcium gluconate Give hypertonic dextrose and insulin, or sodium bicarbonate Use salt sparingly and avoid potassium-rich foods

CALCIUM

Normal values: 8.6 – 10.2 mg/dL (2.2 – 2.6 mmol/L)o 99% of body’s calcium contained within skeletal system. 1% is between bone & bloodo Major role in holding the body’s cells together and in nerve transmission; activates

enzymes that are essential to many chemical reactions in the bodyo *CALCIUM AND PHOSPHORUS ALWAYS HAVE AN INVERSE RELATIONSHIP*

Extravasation Hypoparathyroidism Hyperphostemia

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Osteomalacia Osteoporosis Rickets Tetany

Hypocalcemia : o Causes:

Acute pancreatitis (the inflamed pancreas releases enzymes that combine with calcium and move the calcium out of the blood)

Can persist with HYPOmagnesium and HYPERphosphatemia (renal patients) Insufficient blood levels of Vitamin D and malabsorption syndromes (Crohn’s

Disease, IBS, small bowel resection patients) Loop diuretics; Dilantin Alcoholics

o Clinical manifestations: Tetany Circumoral paresthesia (i.e., mouth tingling) Spasms in the face/extremities Carpal spasms (i.e., + trousseau’s sign) + Chvostek’s sign Seizures, depression, memory problems, delusions and hallucinations V-tach or v-fib or prolonged q-t intervals Dry, scaly skin Alopecia

o Treatment: Treat underlying cause PO oral calcium supplements Will see HYPOmagnesium also - Low Mg levels also need to be corrected

o Emergent Hypocalcemia : If calcium levels are very, very low, this is considered a medical emergency Patient will need IV calcium in a slow, controlled infusion EKG must be monitored very closely

Hypercalcemia : o Causes:

Malignancyo Clinical manifestations:

Very depressed reflexes, muscle weakness Constipation, anorexia, n/v Behavioral/personality changes Possible acute psychosis/confusion (because the CSF might now have calcium in it) Polyuria, polydyspnea

Can ultimately lead to nephrogenic diabetes insipidus, which is reversible Possible renal stones or renal colic Changes in heart rhythm and contraction

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o Interventions: Institute seizure precautions if profound CNS changes are present Monitor patient’s airway & cardiac function very carefully Educate patient re: diet Hydrate well to prevent kidney stones Discontinue any calcium supplements

MAGNESIUM

Normal values: 1.3 – 2.3 mEq/L (1.8 – 3.0 mg/dL; 0.8 – 1.2 mmol/L)o Most abundantly available electrolyte after potassium; mostly concentrated in the boneso Major role in the CV system, i.e., in vasodilation, BP and heart rhythmo Mg levels closely affected by the Ca/phosphorus balance; mostly excreted in loop of henle

Hypomagnesemia : o Causes:

Critically ill patients Profound GI losses (consistent NG tube suction, diarrhea or fistulas) Any changes in the small bowel [small bowel is primary site for Mg absorption] Alcoholics, secondary to decreased dietary intake, vomiting & diarrhea

Alcohol also causes an increase in Mg secretion in urine Certain meds, including loop diuretics, Gentamycin, Tobramycin and Kinamycin Cysplotin (a chemo drug)

o Clinical manifestations: Weakness and tremors; Tetany Tonic/clonic or focal seizures + Trousseau’s sign Premature ventricular contraction (pvc), dysthythmias, v-tach and v-fib Disorientation, vertigo, depression and psychosis *IF A PATIENT HAS HYPOMAGNESIUM, THAT PATIENT WILL ALSO

HAVE HYPOKALEMIA*o Treatment:

Green vegetables, meat, seafood, dairy and Mg supplements (PO, IV or IM) The ideal Mg value for a cardiac patient is 2.0

o Nursing interventions: Monitor for Digoxin toxicity Institute seizure precautions

Hypermagnesemia : very uncommono Causes:

Advanced renal failure, especially in patients with GFRs below 30 Most likely receiving dialysis & will get Mg in either water or dialysis fluid

Advancing age (older patients might have kidney problems) Overuse of Mg-containing antacids (Milk of Magnesia, Citrate Magnesia, Maalox)

o Clinical manifestations: Facial flushing

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Drowsiness; Headache; nausea/vomiting Hypoactive reflexes Depressed respirations, coma & respiratory arrest if hypermagnesium state is severe

o Treatment: prevention is best Avoid Mg in the presence of any renal insufficiency If any respiratory complications occur, give IV Calcium to help decrease Mg If the patient is on dialysis, make sure that the dialysis fluid is Mg-free

PHOSPHORUS

Normal values: 2.5 – 4.5 mg/dL (0.8 – 1.45 mmol/L) Hypophosphatemia :

o Causes:

o Clinical manifestations:

o Treatment:

Hyperphosphatemia : o Causes:

o Clinical manifestations:

o Treatment:

CHLORIDE

Normal values: 97 – 107 mEq/L (96 – 106 mmol/L)

Hypochloremia : o Causes:

o Clinical manifestations:

o Treatment:

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Hyperchloremia : o Causes:

o Clinical manifestations:

o Treatment:

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Type Description Osmolality Use Miscellaneous

Normal Saline (NS)

0.9% NaCl in WaterCrystalloid Solution

Isotonic(308 mOsm)

Increases circulating plasma volume when red cells are adequate

Replaces losses without altering fluid concentrations.

Helpful for Na+ replacement

1/2 Normal Saline (1/2

NS)

0.45% NaCl in WaterCrystalloid Solution

Hypotonic(154 mOsm)

Raises total fluid volume

Useful for daily maintenance of body fluid, but is of less value for replacement of NaCl deficit.

Helpful for establishing renal function.

Fluid replacement for clients who don’t need extra glucose (diabetics)

Lactated Ringer’s (LR)

Normal saline with electrolytes and buffer

Isotonic(275 mOsm)

Replaces fluid and buffers pH

Normal saline with K+, Ca++, and lactate (buffer)

Often seen with surgery

D5W

Dextrose 5% in water Crystalloid solution

Isotonic (in the bag)

*Physiologically

hypotonic(260 mOsm)

Raises total fluid volume.Helpful in rehydrating and excretory purposes.

Provides 170-200 calories/1,000cc for energy.

Physiologically hypotonic -the dextrose is metabolized quickly so that only water remains - a hypotonic fluid

D5NS

Dextrose 5% in 0.9% saline

Hypertonic(560 mOsm)

Replaces fluid sodium, chloride, and calories.

Watch for fluid volume overload

D5 1/2 NS

Dextrose 5% in 0.45% saline

Hypertonic(406 mOsm)

Useful for daily maintenance of body fluids and nutrition, and for rehydration.

Most common postoperative fluid

D5LR

Dextrose 5% in Lactated Ringer’s

Hypertonic(575 mOsm)

Same as LR plus provides about 180 calories per 1000cc’s.

Watch for fluid volume overload

Normosol-R

Normosol Isotonic(295 mOsm)

Replaces fluid and buffers pH

pH 7.4 Contains sodium, chloride,

calcium, potassium and magnesium

Common fluid for OR and PACU

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Type Solution Uses Special Considerations

IsotonicDextrose 5% in water

(D5W)

Fluid loss Dehydration Hypernatremia

Use cautiously in renal and cardiac patients

Can cause fluid overload

Isotonic0.9% sodium chloride

(Normal Saline)(NaCl)

Shock Hyponatremia Blood transfusions Resuscitation Fluid challenges DKA

Can lead to overload Use with caution in patients with

heart failure or edema

IsotonicLactated Ringer’s

(LR)

Dehydration Burns Lower GI fluid loss Acute blood loss Hypovolemia due to third spacing

Contains potassium, don’t use with renal failure patients

Don’t use with liver disease, can’t metabolize lactate

Hypotonic0.45% sodium

chloride (1/2 normal saline)

Water replacement DKA Gastric fluid loss from NG or

vomiting

Use with caution May cause cardiovascular collapse

or increased intracranial pressure Don’t use with liver disease,

trauma, or burnsHypertoni

cDextrose 5% in ½

normal saline Later in DKA treatment

Use only when blood sugar falls below 250 mg/dL

Hypertonic

Dextrose 5% in normal saline

Temporary treatment for shock if plasma expanders aren’t available

Addison’s crisis

Don’t use n cardiac or renal patients

Hypertonic

Dextrose 10% in water

Water replacement Conditions where some nutrition

with glucose is required Monitor blood sugar levels

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