A substance containing H+ that can be liberated or released, such as carbonic acid.

An acid releases H+, as follows:

H2CO3 (Carbonic Acid) releases H+ to form HCO3- (Bicarbonate Base)

A substance that can accept or trap H+ ions, such as the bicarbonate ion.

A base traps H+, as follows:

HCO3- (Bicarbonate Base) traps H+ to form H2CO3 (Carbonic Acid)

• Strong Acid: Dissociates (separates) completely in solution & releases all of its H+ ions
• Weak Acid: Releases only a small number of H+ ions.

• Strong Base: Binds or accepts H+ ions easily.
• Weak Base: Accepts H+ ions less readily.

• Unit of measure used to describe acid-base balance.
• An expression of H+ ion concentration & the resulting acidity or alkalinity of a substance.
• Ranges from 1-14
• Neutral is 7. Ex. water
• Below 7= Acid
• Above 7= Alkaline
• A reflection of the balance b/t CO2 & bicarbonate.
• Homeostasis of pH exists when production of acids & bases equal excretion of acids & bases.

Death occurs when: below 6.8 and above 7.8

Acidosis: 6.80-7.35

Normal: 7.35-7.45

Alkalosis: 7.45-7.80

*Normal value of arterial blood pH: 7.35-7.45

*Normal blood plasma is slightly alkaline and has a normal pH: 7.35-7.45

1. Chemical buffer system
2. Respiratory mechanisms
3. Renal mechanisms

• A substance that prevents body fluids from becoming overly acidic or alkaline. They combine w/ excess acids or bases to prevent major changes in pH, keeping the pH of body fluids as close as possible to normal (7.35-7.45)\
• Can act as a base & bind or soak up H+ ion. Can act as a acid and release H+ ions.

1. The carbonic acid-sodium bicarbonate buffer system
2. The phosphate buffer system
3. The protein buffer system

• The ratio of carbonic acid (H2CO3), the most common acid in human body fluid, to the body's most common base, bicarbonate (HCO3-), is important for acid-base balance & is the most important buffer system of the body.
• 20:1 Ratio- Normal ECF has a ratio of 20 parts bicarbonate to 1 part carbonic acid.

Carbonic Acid-Sodium Bicarbonate Buffer System

(Cont.)

• The lungs, under the control of the medulla, help by regulating the production of carbonic acid resulting from the combination of carbon dioxide and water.
• The kidneys assist the bicarbonate system by regulating the production of bicarbonate.

• 2nd buffer system is active in ICF, especially in the renal tubules.
• Converts alkaline sodium phosphate, a weak base, to acid-sodium phosphate in the kidneys.

• The 3rd buffer system is a mixture of plasma proteins & the globin portion of hemoglobin in RBCs. 
• Because plasma proteins & hemoglobin possess chemical groups that can combine w/ or liberate H+ ions, they tend to maximize changes in pH & serve as buffering agents over a range of pH values working both inside & outside the cell.

its acidic 

High amount of H+ ions

its alkaline

low amount of H+ ions

• Due to the huge surface from which CO2 can readily diffuse, the lungs can bring about rapid changes in H+ when needed
• CO2 is constantly produced by cellular metabolism (H2CO3 yields CO2 & H2O), is excreted by exhalation. When the amt of CO2 in the blood increases, the sensitive chemoreceptors in the respiratory center in the medulla are stimulated to increase the rate & depth of respirations to eliminate more CO2. 
• **Lungs are the primary controller of the body's carbonic acid supply.\
• Respiratory system is able to respond quickly in a healthy individual to restore the normal pH. However, this response is short term, and the response of the kidneys is needed for longterm adjustment.

Respiratory Regualation of H+ ions (Cont.)

What happens as more CO2 is exahaled vs. when the blood level of CO2 decreases:

• As more CO2 is is exhaled, the H2CO3 level in the blood decreases, & the pH of the blood becomes more alkaline. (Decreases CO2-Increases pH-Decreases H+ ions)
• When the blood level of CO2 decreases, the respiratory center decreases the rate & depth of respirations to retain the CO2 so that carbonic acid can be formed, thereby maintaining the delicate balance. (Increases CO2-Decreases pH-Increases H+ ions)

• The kidneys excrete or retain H+ ions and form or excrete bicarbonate ions in response to the pH of the blood.
• In the presence of acidosis, the kidneys excrete H+ ions & form & conserve bicarbonate ions, thus raising the pH to the normal range.
• If alkalosis is present, the kidneys retain H+ ions & excrete bicarbonate ions in an effort to return to a balanced state. 
• **The concentration of bicarbonate in the plasma is regualted by the kidneys.

• The acid-base regulation by the kidneys occurs more slowly than that which occurs by the carbonic acid-sodium bicarbonate system or by respiratory regulation. 
• It may take up to 3 days for a normal fluid pH to be restored by the kidneys.
• The ph of urine varies, depending on the H+ ions that are being excreted, but its generally b/t 4.5-8.2

Fluid Volume Deficit

Hypovolemia:

(Isotonic fluid loss)

• Fluid volume deficit can be caused by a loss of both water & solutes in the same proportion from the ECF space.
• Both osmotic & hydrostatic pressure changes force the interstitial fluid into the intravascular space in an effort to compensate for the loss of volume in the blood vessels. As the interstitial space is depleted, its fluid becomes hypertonic, & cellular fluid is then drawn into the interstital space, leaving cells without adequate fluid to function properly. Fluid volume deficits result from the loss of body fluids, especially if fluid intake is decreased simultaneously. (Intracellular Fluid loss)

Hypovolemia

S&S:

• Loss of body weight
• Changes in input & output
• changes in vital signs
• skin changes

*A 5% weight loss is considered a pronounced fluid deficit; an 8% loss or more is considered severe. A 15% weight loss is life threatening.

Hypovolemia

Third-Space Fluid Shift:

• Refers to a distributional shift of body fluids into the transcellular compartment, such as the pleural (abdomen), peritoneal (ascites), or pericardial areas; joint cavaties; the bowel; or an excess accumulation of fluid in the interstitial space. The fluid moves out of the intravascular spaces (plasma) to any of these spaces. Once trapped in these space, the fluid is not easily exchanged w/ ECF. A deficit in ECF volume occurs. (ECF fluid loss-Fluid loss can't be measured)

Hypovolemia

Third Space Fluid shift related to:

• Shifts related to a disruption in the colloid osmotic pressure (decreased albumin), increased fluid volume (excess IV fluid replacement, renal dysfunction), increased capillary hydrostatic pressure (hear failure), hyponatremia, or an increase in the permeability of the capillary membrane (gross tissue trauma). A third space fluid shift may occur as a result of a severe burn, a bowel obstruction, or hypoalbuminemia.
• S&S: pailor, cold limbs, weak/rapid pulse, hypotension, LOC

Fluid Volume Deficit

Hypovolemia

(Isotonic Fluid loss)

Risk Factors:

1. GI: vomiting, diarrhea, suction, fistula
2. Excessive sweating
3. Skin trauma, burns, draining wounds
4. Third space fluid shift
5. excessive laxative or diuretic use
6. Polyuria from renal disease or diuretics
7. Hyperglycemia
8. Hemorrhage
9. Change in mental status
10. Liver failure

Fluid Volume Deficit

Hypovolemia

(Isotonic Fluid loss)

1. Thirst
2. Weight loss over short period
3. Weakness, fatigue, anorexia
4. Dry mucous membranes
5. Poor skin & tongue turgor
6. sunken eyes
7. flat neck veins
8. urine output <30 mL/hr
9. Increase urine specific gravity, hematocit, BUN, serum sodium

Fluid Volume Deficit

Hypovolemia

(Isotonic Fluid loss)

1. Assess for presence or worsening of FVD
2. Administer oral fluids if indicated
3. Provide fluids to meet body needs. (oral fluids or IV solutions)
4. Monitor I&O and volumetic solution (VS)
5. Monitor pt's response to fluid intake, either oral or parenteral.
6. Be alert for signs of fluid overload.
7. Provide oral and skin care.

Fluid Volume Excess

Hypervolemia:

(Excess of Isotonic)

• Excessive retention of water & sodium in ECF in equal proportions resulting in fluid volume excess.
• Due to increased extracellular osmotic pressure from the retained sodium & water, fluid is pulled from the cells to equalize the tonicity.
• By the time the intracellular & extracellular spaces are isotonic to each other, an excess of water & sodim is in the ECF, whereas the cells are nearly depleted. The excessive ECF may accumulate in either the intravascular compartments or interstitial spaces. 

Fluid Volume Excess

Hypervolemia

Causes:

Fluid Volume Excess

Hypervolemia

Edema:

• Accumulation of fluid in the interstitial space. Can be observed around the eyes, fingers, ankles, & sacral space, & can also accumulate in or around body organs. 
• Accumulation of fluid may result in weight gain in excess of 5%. The amt or severity of edema is typically graded.

Fluid Volume Excess

Hypervolemia

Risk Factors:

1. Comprised regulatory mechanisms: renal failure, CHF, cirrhosis of liver, Cushing's syndrome.
2. GI irrigation w/ hypotonic fluid.
3. Excess IV fluids w/ sodium
4. Excessive ingestion of sodium-containing substances in diet or sodium-containing medications
5. Corticosteroid therapy

1. Weight gain over short period.
2. Shortness of breath
3. crackles & wheezes in lungs
4. Pulmonary edema
5. Decreased BUN, hematocrit, serum sodium, urine specific gravity
6. Increase BP

Fluid Volume Excess

Hypervolemia

Nursing Interventions:

1. Assess for presence or worsening of FVE.
2. Avoid OTC drugs or check w/ physician or pharmacist about sodium content.
3. Administration of diuretics & monitor response.
4. Promote rest.
5. Use semi-Fowler's position for orthopnea.
6. Promote adherence to fluid restrictions & pt teaching related to sodium & fluid restrictions.

• Refers to a sodium deficit in ECF caused by a loss of sodium or gain of water.
• Serum Sodium <135 mEq/L
• Sodium may be lost through vomiting, diarrhea, fistulas, sweating, or the use of diuretics.

• Decrease in Na causes fluid to move by osmosis from the less concentrated ECF compartment to the ICF space.
• This shift of fluid leads to swelling of cells, w/ resulting confusion, hypotension (low bp), edema, muscle cramps, weakness, dry skin.

Hyponatremia

Risk Factors:

1. Loss of sodium, as in: loss of GI fluids, use of diuretics, adrenal insufficiency.
2. Gains of H2O, as in: Excessive administration of D5W, H2O intoxication
3. Disease states associated w/ SIADH (a form of hyponatremia)
4. Pharmocologic agents that may impair H2O excretion

Hyponatremia

Assessments:

• Anorexia
• Nausea & vomiting
• Lethargy
• confusion
• muscle cramps
• coma
• seizures
• Poor skin turgor

Hyponatremia

Nursing Interventions:

• Monitor fluid losses & gains
• Monitor of dietary sodium & fluid intake
• identification and monitoring of at-risk patients 
• the effects of medications (diuretics and lithium)
• Check urine specific gravity

• Refers to a surplus of sodium in ECF caused by excess water loss or an overall excess of sodium.
• Serum sodium >145mEq/L)
• Causes: excess water loss, excess sodium administration, diabetes insipidus, heat stroke, hypertonic IV solutions, diarrhea 

• Fluids move from the cells because of the increased extracellular osmotic presssure, causing them to shrink & leaving them without sufficient fluid.
• The cells of the CNS are affected, resulting in signs of neurological impairment, including restlessness, weakness, disorientation, delusion, & hallucinations. Brain damage can occur.

Hypernatremia

Risk Factors:

1. Water deprivation
2. Increased sensible & insensible water loss
3. ingestion of large amts of salt
4. excessive parenteral administration of Na-containing solutions
5. Profuse sweating
6. diabetes insipidus

Hypernatremia

Assessments:

1. Thirst
2. Elevated body temp
3. tongue dry & swollen, stiky mucous membranes
4. Disorientation & hallucinations
5. Restlessness & weakness

Hypernatremia

Nursing Interventions:

• Monitor fluid losses & gains.
• Oberve for excessive intake of high Na foods
• Monitor for changes in behavior such as restlessness, lethargy, & disorientation
• Look for excessive thirst & elevated body temp.
• assess for over-the-counter (OTC) sources of sodium
• offer and encourage fluids to meet patient needs, and provide sufficient water with tube feedings

• Refers to a potassium deficit in ECF & is a common electrolyte abnormality.
• Serum potassium <3.5 mEq/L
• Causes: vomiting, gastric suction, alkalosis, diarrhes, use of diuretics

• When the extracellular k level falls, k moves from the cell, creating an intracellular k deficiency
• Na & H ions are then retained by the cells to maintain isotonic fluids.
• These electrolyte shifts influence normal cellular functioning, the pH of ECF, & the functions of most body systems, including the cardiovascular system.

Hypokalemia

Risk Factors:

1. Diarrhea
2. Vomiting or gastic secretions
3. K-wasting diuretics
4. Poor intake as in anorexia nervosa, alcoholism, k-free parenteral fluids

Hypokalemia

Assessment:

• Fatigue
• Anorexia, nausea, vomiting
• Muscle weakness
• Decreased bowel motility
• cardiac arrhythmias
• Postural hypotension
• Paresthesias or tender muscles

Hypokalemia

Nursing Interventions:

1. Encourage extra k intake if possible.
2. Educate about abuse of laxatives & diuretics.
3. Be knowledgeable about danger of IV k administration 
4. Monitor k level.

• Refers to an excess of k in ECF.
• Serum potassium >5 mEq/L
• Causes: renal failure, hypoaldosteronism, use of certain medications (Potassium chloride, heparin, ACE inhibitors, NSAIDS & k-sparing diuretics)
• Nerve conduction & muscle contractility can be affected. Skeletal muscle weakness & paralysis may occur. Cardiac irregularities (cardiac arrest)

Hyperkalemia

Risk Factors:

1. Decreased k excretion: renal failure, k-sparing diuretics
2. hypoaldosteronism
3. high k intake, especially in presence of renal insufficency
4. Shift of k out of cells (acidos, tissue trauma, malignant cell lysis)

Hyperkalemia

Assessment:

1. Vague muscle weakness
2. Cardiac arrhythmias
3. GI symptoms: nausea, intermittent intestinal colic, diarrhea
4. Problems w/ breathing (respiratory impairment)
5. Anxiety

Hyperkalemia

Nursing Interventions:

1. Follow rules for safe administration of k
2. Avoid giving pts w/ renal insufficency k-saving diuretics, k supplements, or salt substitutes.
3. Caution about foods high in k content
4. Monitor medication effects and k levels
5. Na and medications may contain k

• Refers to a calcium deficit in ECF
• Serum level less than 8.5 mg/dL
• Causes: inadequate calcium intake, impaired calcium absorption, & excessive calcium loss.

Hypocalcemia

Risk Factors:

1. Surgical hypoparathyroidism
2. malabsorption
3. Vit D deficiency
4. Acute pancreatitis
5. Excessive administration of citrated blood
6. Alkalotic states

Hypocalcemia

Assessment:

1. Trousseau's & chvostek's signs
2. Numbness & tingling of fingers & toes.
3. mental changes
4. seizures
5. spasm of laryngeal muscles
6. ECG changes
7. Cramps in muscles of extremities

Hypocalcemia

Nursing Interventions:

1. IV of calcium gluconate
2. calcium and vitamin D supplements
3. weight-bearing exercises to decrease bone calcium loss
4. patient teaching related to diet and medications
5. nursing care related to IV calcium administration

• Refers to an excess of calcium in ECF.
• Serum level >10.5 mg/dL
• Causes: cancer & hyperparathyroidism

Hypercalcemia

Risk Factors:

1. Hyperparathyroidism
2. Malignant neoplastic disease
3. large doses of vit D
4. overuse of calcium supplements
5. prolonged immobilization-bone loss

Hypercalcemia

Assessment:

1. Muscular weakness
2. tiredness, lethargy
3. constipation
4. anorexia, nausea, vomiting
5. Decrease memory & attention span
6. Renal stones
7. cardiac arrest

Hypercalcemia

Nursing interventions:

1. administer fluids
2. encourage ambulation
3. fluids of 3 to 4 L/d
4. provide fluids containing sodium unless contraindicated and fiber for constipation
5. Safety precautions
6. Force fluids to prevent renal stones

• Refers to a magnesium deficit in the ECF
• Serum level < 1.8 mg/dL
• Causes: nasogastic suction, diarrhea, withdrawal from alcohol, administration of tube feedings or parenteral nutrition, sepsis, or burns.

Hypomagnesemia

Risk Factors:

1. Chronic alcoholism
2. intestinal malabsorption
3. diarrhea
4. enteral or parenteral feeding deficient in magnesium

Hypomagnesemia

Assessment:

1. Neuromuscular irritability (Twitch): increased reflexes, coarse reflexes, seizures
2. cardiac manifestations: increased susceptibility to digitalis, toxicity
3. disorientation, mood changes

Hypomagnesemia

Nursing Interventions:

1. Assess for magnesium deficit because it predisposes pt to digitalis toxicity
2. take seizure precautions if needed
3. educate pt if abuse of diuretics or laxatives is a problem
4. If you have hypomagnesemia; you will have hypocalcemia.
5. nursing care related to IV magnesium sulfate

• Refers to a magnesium excess in the ECF.
• Serum level > 2.7 mg/dL
• Causes:Occurs w/ renal failure when the kidneys fail to excrete magnesium or from excessive magnesium intake

Hypermagnesemia

Risk Factors:

1. renal failure
2. adrenal insufficiency
3. excessive mag administration during treatment of eclampsia
4. Hemodialysis w/ hard water or dialysate high in mag content

Hypermagnesemia

Assessment:

1. Flushing & sense of skin warmth
2. hypotension
3. depressed respirations
4. drowsiness; hypoactive reflexes, muscular weakness
5. cardiac abnormalities
6. ECG changes

Hypermagnesemia

Nursing Interventions:

1. Be alert for bp & shallow respirations, lethargy, drowsiness, & coma
2. Dont give mag-containing meds to pt w/ renal failure or compromised renal function
3. Be cautious of OTC drugs
4. check deep tendon reflexes frequently
5. IV calcium gluconate

• Refers to a below normal concentration of phosphorus in the ECF,
• Serum level <2.5 mg/dL
• Causes: administration of calories to malnourished pts, alcohol withdrawal, diabetic ketoacidosis, hyperventilation, insulin release, absorption problems,diuretic use.

Hypophosphatemia

Risk Factors:

1. Glucose administration
2. refeeding after starvation
3. hyperalimentation
4. alcohol withdrawal
5. diabetic ketoacidosis
6. respiratory alkalosis

Hypophosphatemia

Assessments:

1. Cardiomyopathy
2. acute resp failure
3. seizures
4. decrease tissue oxygenation
5. joint stiffness
6. increased susceptibility to infection 

Hypophosphatemia

Nursing Interventions:

1. aware of greater risk for infection
2. Administer IV phosphate products cautiously
3. Introduce hyperalignmentation cautiously in pts who are malnourished
4. sudden increase in serum phosphate level can cause hypocalcemia.
5. encourage foods high in phosphorus
6. introduce calories for malnourished patients receiving parenteral nutrition

• Refers to above-normal concentrations of phosphorus in the ECF.
• Serum level >4.5 mg/dL
• Causes: impaired kiney excretion & hypoparathyroidism

Hyperphosphatemia

Risk Factors:

1. Renal failure
2. chemotherapy
3. large intake of milk
4. excessive intake of phosphate containing laxatives
5. large vit D intake
6. Hyperthyroidism
7. Chemotherapy

Hyperphosphatemia

Assessment:

1. Short term consequences: symptoms of tetany, such as tingling of fingertips & ard the mouth, numbness, & muscles spasms
2. Long term consequences: precipitation of calcium phosphate in nonosseous sites such as the kidneys, joints, arteries, skin, or cornea.

Hyperphosphatemia

Nursing Interventions:

1. Monitor for signs of tetany.
2. Signs of hypocalcemia
3. Instruct pt that use of phosphate-containing laxatives can result in hyperphosphatemia
4. Avoid foods high in phosphorus content.

(hyponatremia and hypernatremia)

Sodium:

• controls and regulates volume of body fluids
• Aldosterone secretion & dietary intake control Na levels
• Normal concentration:135 – 145 mEq/l
• Provides nerve impulse transmission
• Regulation of acid-base balance
• Participates in cellular reactions

(hypokalemia and hyperkalemia)

Potassium:

• chief regulator of cellular enzyme activity and water content
• Renal excretion and dietary intake regulate K
• Normal concentration: 3.5 – 5 mEq/l
• Regulates metabolic activities
• Transmission & conduction of nerve impulses
• Smooth muscle contraction (cardiac muscle)

(hypocalcemia and hypercalcemia)

Calcium:

• nerve impulse, blood clotting, muscle contraction, B12 absorption
• Dietary intake primarily regulates Ca
• Normal concentration found in the bone
• Bone and teeth formation
• Cell membrane integrity
• Cardiac and nerve impulse transmission

(hypomagnesemia and hypermagnesemia)

Magnesium:

• metabolism of carbohydrates and proteins,vital actions involving enzymes
• Dietary intake, parathyroid secretions and renal function maintain Mg level
• Provides cardiac and muscle excitability
• Provides neuro-chemical activities
• Provides enzyme activities

(hypophosphatemia and hyperphosphatemia)

Phosphorus:

• involved in important chemical reactions in body, cell division, and hereditary traits
• Dietary intake, renal excretion, intestinal absorption and parathyroid hormone control phosphate.
• Provides buffer in the ICF, assists w/ acid-base balance
• Promotes neuromuscular action and carbohydrate metabolism
• Calcium and Phosphorous are inversely related

• pH: Normal=7.35-7.45/ Acid= <7.35/ Base= >7.45

• PaCO2: Normal=35-45mm Hg/ Acid= >45mm Hg/ Base= <35mm Hg 

• HCO3: Normal=22-26mEq/L/ Acid= <22mEq/L/ Base= >26mEq/L

• pH <7.35=Respiratory acidosis/ Metabolic acidosis
• pH >7.45=Respiratory alkalosis/Metabolic alkalosis
• PaCO2 >45=Respiratory acidosis
• PaCO2 <35=Respiratory alkalosis
• HCO3 <22=Metabolic acidosis
• HCO3 >28=Metabolic alkalosis

PaCO2

-Reflects depth of respiratory ventilation

Normal Range: 35 to 45 mm Hg

• < 35 hyperventilation (Base)
• > 45 hypoventilation (Acid)
• Rate and depth of respiration determines how much CO2 is retained or lost
• Hyperventilation – rate & depth increases, PaCO2 decreases
• Hypoventilation – rate & depth decreases, PaCO2 increases

• < 60 mm Hg leads to anaerobic (living w/out air) metabolism = lactic acid production
• Hypoxemia -> hyperventilation -> Respiratory alkalosis
• Normal range 80 to 100 mm Hg

• Point at which hemoglobin is saturated with O2
• Saturation level drops when < 60 mm Hg PaO2
• Normal range 95 to 99 %

• The amount of blood buffer that exists
• Normal range:  +2
• Alkalosis can occur by ingesting large amounts of antacids

• The major renal component of acid-base balance
• The principal buffer of the ECF
• Normal range:  22 to 26 mEq/l
• < 22 Metabolic acidosis
• >28 Metabolic alkalosis

Acid-Base Imbalance

Homeostasis:

• Low pH (increase H+ concentration) & a low plasma bicarbonate concentration due to gain of H or loss of bicarbonate.
• A proportionate deficit of bicarbonate in ECF. Can occur in the results of an increase in acid components or an excessive loss of bicarbonate. 
• Can be produced by a gain of H+ ions or loss of bicarbonate.
• Lungs – increase rate and depth of respirations = decreased PaCO2
• Kidneys – retain bicarb and excrete hydrogen ions

Metabolic Acidosis

Hyperkalemia:

• With metabolic acidosis, hyperkalemia may occur as potassium shifts out of the cell
• As acidosis is corrected, potassium shifts back into the cell and potassium levels decrease
• Monitor potassium levels, for hyperkalemia
• Serum calcium levels may be low with chronic metabolic acidosis and must be corrected before treating the acidosis

Metabolic Acidosis (Base bicarbonate Deficit)

Risk Factors:

• Diarrhea
• Intestinal Fistulas
• Renal Failure

Metabolic Acidosis

Assessments:

• Headache
• Confusion
• Drowsiness
• Increase respiratory rate & depth
• Nausea & vomiting

Metabolic Acidosis

Nursing Interventions

• Treatment is directed toward correcting the metabolic deficit. If the cause of the problem is excessive intake of chloride, treatment obviously focuses on eliminating the source. 
• When necessary, bicarbonate is administered.
• Check pt pH level.

• High pH & a high plasma bicarbonate concentration due to a gain of bicarbonate or a loss of H.
• Associated w/ excess of HCO3, a decrease in H+ions, or both, in the ECF. Result of excessive acid losses or increased base ingestion or retention.
• Lungs – retain CO2 by decreasing resp/rate
• Respirations become slow & shallow, & periods of no breathing may occur. 
• Kidneys attempt to excrete excess H2O & NA ions w/ the excessive bicarbonate & retain H+ ions.

Metabolic Alkalosis

Risk Factors:

• Vomiting or gastric secretion
• Hypokalemia
• Renal loss of H+

Metabolic Alkalosis

Asessments:

• Dizziness
• Tingling of fingers & toes
• Hypertonic muscles
• Hypokalemia may be present.
• Decreased respirations

Metabolic Alkalosis

Nursing Interventions

• Treatment is aimed at reversal of the underlying disorder. Sufficient chloride must be supplie for the kidney to absorb Na w/ chloide (allowing the excretion of excess bicarbonate).
• Treatment alos includes administration of NaCl fluids to restore normal fluid volume.

• High PaCO2 due to alveolar hypoventilation.
• Excess of carbonic acid in the ECF. Produced by inadequate excretion of CO2 w/ inadequate ventilation, resulting in elevated plasma CO2 & increased levels of carbonic acid.
• Decrease in alveolar ventilation results in retention of CO2. 
• Increased CO2 stimulates the medulla in the resp center to increase the resp rate. 
• Increased resp rate, CO2 is expelled & the CO2 level of the blood is reduced.
• NaHCO3: buffers the free acids & reduces CO2 levels.

Respiratory Acidosis

Risk Factors:

• Acute Respiratory disease: pulmonary edema, cardiac arrest
• Chronic Respiratory Disease: Emphysema, bronchial asthma, cystic fibrosis

Respiratory Acidosis

Assessments:

• Acute resp acidosis: mental cloudiness, dizziness, muscular twitching, unconsciousness
• Chronic resp acidosis: weakness, dull headache

Respiratory Acidosis

Nursing Interventions:

• Treatment is directed at improving ventilation; pharmocologic measures, pulmonary hygiene measures, adequate hydration, supplemental O2
• Mechanical ventilation may be necessary to correct disorder but must be used cautiously to decrease PaCO2 slowly.

• Low PaCO2, due to alveolar hypertension.
• A primary deficit of carbonic acid in the ECF. Result of hyperventilation breathing that's faster & deeper, & the consequent increase in the elimination of CO2. Loss of CO2 leads to a decrease in the carbonic acid level in the plasma & an increase in the pH.
• Chemoreceptors in the medulla sense the increase in pH & the presence of less carbonic acid & stimulate the body to breath either more slowly or less deeply. 
• Kidney attempt to alleviate the imbalance by increasing the bicarbonate excretion & by retaining more H to correct the imbalance.

Respiratory Alkalosis

Risk Factors:

• Hyperventilation
• Extreme anxiety (most common cause)
• Hypoxemia (decrease O2 & CO2 exchange)

Respiratory Alkalosis

Assessments:

• Lightheadedness
• Hyperventilation syndrome: Tinnitus, palpitations, sweating, dry mouth, tremulousness, convulsions & loss of consciousness

Respiratory Alkalosis

Nursing Interventions

• If anxiety is the cause, encourage pt to breathe more slowly (causes accumulation of CO2) or breathe into a closed system (paper bag). Sedative may also be necessary in extreme anxiety.
• Treatment of other causes is directed at correcting the underlying problem.

decrease pH, decrease HCO3-, Normal PaCO2,

(Acidic)

Increased H+ ions

Increase pH, Increase HCO3-, Normal PaCO2

(Base)

Decrease H+ ions

Decreased pH, Inceased PaCO2, Normal HCO3-

(Acidic)

H+ ions increased

Incrased pH, Decreased PaCO2, Normal HCO3-

(base)

H+ ions decreased