Fluids and Electrolytes

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Chapter 3

The Cellular Environment: Fluids and Electrolytes, Acids and Bases

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Distribution of Body Fluids

Total body water

Intracellular fluid (ICF): Inside the cell

Extracellular fluid (ECF): Outside the cell

Interstitial fluid

Intravascular fluid

Cerebrospinal fluid (CSF)

Lymphatic, synovial, intestinal, biliary, hepatic, pancreatic, pleural, peritoneal, pericardial, and intraocular fluids

Sweat

Urine

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Aging and Distribution of Body Fluids

Total body water (cont’d)

Newborn: 75% to 90% of body weight

Childhood: 60% to 65% of body weight

Adults: 60% of body weight

Older adults: Percent declines with age

Men have a greater percentage of body water when compared with women

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Water Movement between the ICF and ECF

Osmolality

Osmotic forces

Sodium for the ECF

Potassium for the ICF

Aquaporins

A family of water channel proteins that provide permeability to water

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Water Movement between the ICF and ECF (cont’d)

Osmosis: Is how water moves between the ICF and ECF compartments.

Water moves between the plasma and interstitial fluid through osmosis and hydrostatic pressure, which occur across the capillary membrane.

Net filtration: Is the movement across the capillary wall.

As described according to the Starling law or hypothesis

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Water Movement between Plasma and Interstitial Fluid

Starling hypothesis

Net filtration is equal to the forces favoring filtration minus the forces opposing filtration

Forces favoring filtration

Capillary hydrostatic pressure (blood pressure)

Interstitial oncotic pressure (water pulling)

Forces opposing filtration or forces favoring reabsorption

Plasma oncotic pressure (water pulling)

Interstitial hydrostatic pressure

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Alterations in Water Movement: Edema

Accumulation of fluid in the interstitial spaces

Causes:

Increased capillary hydrostatic pressure (venous obstruction)

Decreased plasma oncotic pressure (losses or diminished production of albumin)

Increased capillary permeability (inflammation and immune response)

Lymph obstruction (lymphedema)

Sodium retention

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Alterations in Water Movement: Edema (cont’d)

Causes

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Alterations in Water Movement: Edema (cont’d)

Clinical Manifestations

Localized vs. generalized

Dependent edema

Pitting edema

“Third space”

Swelling and puffiness

Tighter-fitting clothes and shoes

Weight gain

Treatment

Elevate edematous limbs

Use compression stockings or devices

Avoid prolonged standing

Restrict salt intake

Take diuretic agents

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Alterations in Water Movement: Edema (cont’d) Question 1

A person with heart failure has edema in the lower legs and sacral area. The nurse suspects this condition is due to a(n):

Increase in plasma oncotic pressure

Decrease in capillary hydrostatic pressure

Decrease in lymph obstruction pressure

Increase in capillary hydrostatic pressure

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ANSWER AND RATIONALE: 4. Increase in capillary hydrostatic pressure. Heart failure produces salt and water retention and subsequent volume overload, which increases capillary hydrostatic pressure which leads to edema.

1. An increase in plasma oncotic pressure produces movement of fluid from the interstitial space into the vascular space which would decrease edema.

2. A reduction in capillary hydrostatic pressure decreases the force for filtration of fluid from the capillary which would decrease edema.

3. A decrease in lymph obstruction would not cause edema; an increase in lymph obstruction would lead to edema.

Overview of Electrolytes

Electrolytes are in both ECF and ICF compartments but are in different concentrations.

Some electrolytes are more concentrated in the ICF compartment, as compared with the ECF compartment.

All electrolytes move across compartments but must be in balance for optimal health.

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Overview of Electrolytes

Cation

Potassium (K+)

Anions

Phosphate

Organic ions

Intracellular

Extracellular

Cation

Sodium (Na+)

Anions

Chloride (Cl–)

Bicarbonate (HCO3–)

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Na+ and Cl– Balance

Sodium

Is the primary ECF cation.

Regulates osmotic forces.

Roles include:

Neuromuscular irritability, acid-base balance, cellular reactions, and transport of substances

Is regulated by aldosterone and natriuretic peptides.

Chloride

Is the primary ECF anion.

Provides electroneutrality.

Follows sodium.

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Na+ and Cl– Balance (cont’d)

Renin-angiotensin-aldosterone system

Aldosterone

Increases reabsorption of sodium by the distal tubule of the kidney

Natriuretic peptides

Decreases tubular resorption, and promotes urinary excretion of sodium

Atrial natriuretic peptide

Brain natriuretic peptide

Urodilantin (kidney)

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Na+ and Cl– Balance (cont’d)

Renin-Angiotensin-Aldosterone system

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Water Balance

Is regulated by thirst perception and the antidiuretic hormone (ADH)

Thirst perception

Osmolality receptors (osmoreceptors)

Stimulated from hyperosmolality, dry mouth, plasma-volume depletion

Increases water intake

Baroreceptors

Stimulated from depleted plasma volume

Causes release of ADH

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Water Balance (cont’d)

ADH

Is released when there is an increase in plasma osmolality or decrease in circulating blood volume.

Is also called arginine vasopressin.

Increases water reabsorption.

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Water Balance (cont’d)

Antidiuretic hormone

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Water Balance (cont’d) Question 2

A person reports severe diarrhea for 2 days. The nurse understands this stimulates a(n):

Reduction in aldosterone secretion

Reduction in renin secretion

Increase in antidiuretic hormone secretion

Increase in natriuretic peptide secretion

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ANSWER AND RATIONALE: 3. Increase in antidiuretic hormone secretion. Hypovolemia stimulates volume sensitive receptors and baroreceptors and results in secretion of antidiuretic hormone to increase water reabsorption.

1. Volume depletion produces an increase in aldosterone secretion through the activation of the renin angiotensin aldosterone system.

2. Volume depletion produces an increase in renin secretion and initiates the renin angiotensin aldosterone system.

4. Volume depletion results in reduced secretion of natriuretic peptides. Natriutetic peptides are diuretics which would make more loss of fluid.

Alterations in Na+, Cl–, and Water Balance

Isotonic alterations

Total body water change with proportional electrolyte change

Isotonic volume depletion (hypovolemia)

Isotonic volume excess (hypervolemia)

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Alterations in Na+, Cl–, and Water Balance: Hypertonic Alterations

Hypernatremia

Serum sodium >147 mEq/L

Related to sodium gain or water loss

Water movement from the ICF to the ECF

Intracellular dehydration

Manifestations: Intracellular dehydration, convulsions, pulmonary edema, hypotension, tachycardia

Treatment: Isotonic salt-free fluids

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Alterations in Na+, Cl–, and Water Balance: Hypertonic Alterations (cont’d)

Hyperchloremia

Occurs with hypernatremia or a bicarbonate deficit.

Is usually secondary to pathophysiologic processes.

Is managed by treating the underlying disorders.

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Alterations in Na+, Cl–, and Water Balance: Hypertonic Alterations (cont’d)

Water deficit

Dehydration

Pure water deficits

Renal free water clearance

Manifestations

Tachycardia, weak pulse, and postural hypotension

Elevated hematocrit and serum sodium levels

Headache, dry skin, and dry mucous membranes

Treatment: Give water, and stop fluid loss

Hypotonic saline solutions or 5% dextrose in water

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Alterations in Na+, Cl–, and Water Balance: Hypotonic Alterations

Decreased osmolality

Hyponatremia or free water excess

Hyponatremia decreases the ECF osmotic pressure, and water moves into the cell

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Alterations in Na+, Cl–, and Water Balance: Hypotonic Alterations (cont’d)

Hyponatremia

Serum sodium level <135 mEq/L

Sodium deficits cause plasma hypoosmolality and cellular swelling

Pure sodium deficits; low intake; dilutional hyponatremia; hypotonic hyponatremia; hypertonic hyponatremia

Manifestations: Lethargy, headache, confusion, apprehension, seizures, and coma

Treatment:

Depends on underlying disorder

Restrict water intake

Administer intravenous (IV) fluids

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Alterations in Na+, Cl–, and Water Balance: Hypotonic Alterations (cont’d)

Hypochloremia

Is usually the result of hyponatremia or elevated bicarbonate concentration.

Some causes are:

Vomiting

Metabolic alkalosis

Cystic fibrosis

Treat the underlying cause.

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Alterations in Na+, Cl–, and Water Balance: Hypotonic Alterations (cont’d)

Water excess

Compulsive water drinking, causing water intoxication

Decreased urine formation

Syndrome of inappropriate ADH (SIADH)

ADH secretion causes water reabsorption

Manifestations: Cerebral edema, muscle twitching, headache, and weight gain

Treatment: Fluid restriction; may need hypertonic sodium chloride IV solution

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Potassium

Is the major intracellular cation.

Aldosterone, insulin, epinephrine, and alkalosis facilitate K+ into the cells.

Insulin deficiency, aldosterone deficiency, acidosis, and strenuous exercise facilitate K + out of the cells.

The sodium-potassium (Na + /K +) pump maintains concentration.

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Potassium (cont’d)

Is essential for the transmission and conduction of nerve impulses, normal cardiac rhythms, and skeletal and smooth muscle contraction.

Regulates ICF osmolality and deposits glycogen in liver and skeletal muscle cells.

Kidneys, aldosterone and insulin secretion, and changes in pH regulate K+ balance.

K+ adaptation allows the body to accommodate slowly to increased levels of K+ intake.

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Hypokalemia

Potassium level <3.5 mEq/L

Causes:

Reduced potassium intake

Increased potassium entry into cell

Increased potassium loss

Treatment:

Replace potassium orally and/or intravenously

Manifestations:

Membrane hyperpolarization causes:

Decreased neuromuscular excitability

Skeletal muscle weakness

Smooth muscle atony

Cardiac dysrhythmias

U wave on electrocardiogram (ECG)

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Hyperkalemia

Potassium level >5.5 mEq/L

Rare as a result of efficient renal excretion

Causes:

Increased intake

Shift of K+ from ICF to ECF

Decreased renal excretion

Hypoxia

Acidosis

Insulin deficiency

Cell trauma

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Hyperkalemia (cont’d)

Mild attacks

Tingling of lips and fingers, restlessness, intestinal cramping and diarrhea, T waves on the ECG

Severe attacks

Muscle weakness, loss of muscle tone, flaccid paralysis, cardiac arrest

Treatment

Calcium gluconate, insulin and/or glucose, Na+ bicarbonate, cation exchange resins, dialysis

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Calcium

Most calcium is located in the bone as hydroxyapatite

99% in bone

1% in plasma and body cells

Is necessary for:

Structure of bones and teeth

Blood clotting

Hormone secretion

Cell receptor function

Muscle contractions

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Phosphate

Similar to calcium, most phosphate (85%) is also located in the bone.

Is necessary for high-energy bonds located in creatine phosphate and adenosine triphosphate (ATP) and acts as an anion buffer and needed for muscle contraction energy.

Calcium and phosphate concentrations are rigidly controlled.

Ca++ x HPO4= = K (K is a constant)

If the concentration of one increases, the concentration of the other decreases.

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Calcium and Phosphate

Regulated by three hormones:

Parathyroid hormone (PTH)

Increases plasma calcium levels via kidney reabsorption.

Vitamin D

Is a fat-soluble steroid; increases calcium absorption from the gastrointestinal (GI) tract.

Calcitonin

Decreases plasma calcium levels.

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Hypocalcemia

Calcium levels <8.5 mg/dl

Causes:

Inadequate intake or absorption

Decreases in PTH and vitamin D

Blood transfusions

Treatment:

Calcium gluconate, calcium replacement, decrease phosphate intake

Manifestations:

Increased neuromuscular excitability (partial depolarization)

Muscle spasms

Chvostek and Trousseau signs

Convulsions

Tetany

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Hypercalcemia

Calcium levels >12 mg/dl

Causes:

Hyperparathyroidism

Bone metastasis

Excess vitamin D

Immobilization

Acidosis

Manifestations:

Decreased neuromuscular excitability

Muscle weakness

Manifestations (cont’d):

Kidney stones

Constipation

Heart block

Treatment:

Oral phosphate

IV normal saline

Bisphosphonates

Calcitonin

Corticosteroids

Mithramycin

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Hypophosphatemia

Causes: Intestinal malabsorption and renal excretion, vitamin D deficiency, antacid use, alcohol abuse

Manifestations: Diminished release of oxygen, osteomalacia (soft bones), muscle weakness, bleeding disorders (platelet impairment), leukocyte alterations

Treatment: Treat underlying condition such as respiratory alkalosis and hyperparathyroidism

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Hyperphosphatemia

Causes: Exogenous or endogenous addition of phosphate to ECF, long-term use of phosphate enemas or laxatives, renal failure

High phosphate levels, related to low calcium levels

Manifestations: Same as hypocalcemia with possible calcification of soft tissue

Treatment: Treat underlying condition, aluminum hydroxide, and dialysis

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Magnesium

Is an intracellular cation.

Is stored most in the muscle and bones.

Interacts with calcium.

Has a plasma concentration of 1.8 to 2.4 mg/dl.

Is a co-factor in intracellular reactions, protein synthesis, nucleic acid stability, and neuromuscular excitability.

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Hypomagnesemia and Hypermagnesemia

Hypomagnesemia

From malabsorption

Associated with hypocalcemia and hypokalemia

Neuromuscular irritability

Tetany, convulsions

Increased reflexes

Treatment: Magnesium sulfate

Hypermagnesemia

From renal failure

Skeletal muscle depression

Muscle weakness

Hypotension

Respiratory depression

Bradycardia

Treatment: Avoid magnesium; dialysis

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Acid-Base Balance

Increasing H+ pH scale Decreasing H+

pH—What is it?

Negative logarithm of the H+ concentration

0 7 14

Very acidic Neutral Very alkaline

Each number represents a factor of 10.

If the solution moves from a pH of 7 to a pH of 6, then the H+ ions have increased tenfold.

If H+ is high in number, pH is low (acidic).

If H+ is low in number, pH is high (alkaline).

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Acid-Base Balance (cont’d)

Acids are formed as end-products of protein, carbohydrate, and fat metabolism.

To maintain the body’s normal pH (7.35-7.45) the H+ must be neutralized by the retention of bicarbonate or excreted.

Bones, lungs, and kidneys are major organs involved in the regulation of acid-base balance.

pH below 6.8 = death.

pH above 7.8 = death.

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Acid-Base Balance (cont’d)

Acid-base balance is mainly concerned with two ions:

Hydrogen (H+)

Bicarbonate (HCO3–)

Alterations of hydrogen and bicarbonate concentrations in body fluids are common in disease processes.

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Acid-Base Balance (cont’d)

Carbonic acid (H2CO3)

Can be eliminated as carbon dioxide (CO2) gas via the lungs

Volatile Acids in the Body

Nonvolatile Acids in the Body

Sulfuric, phosphoric, and other metabolic acids

Is eliminated by the renal tubules with the regulation of HCO3–

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Acid-Base Balance (cont’d)

Sources of H+ ions

CO2 diffuses into the bloodstream where the following reaction occurs:

Regulated by the Lung Regulated by the Kidney

CO2 + H2O  H2CO3  HCO3–+ H+

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Acid-Base Balance (cont’d)

pH control mechanisms

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Buffering Systems

Buffer: Chemical that can bind excessive H+ or OH– without a significant change in pH

Located in the ICF and ECF

Consist of a buffering pair: weak acid and its conjugate base

Most important plasma buffering systems: carbonic acid–bicarbonate system and hemoglobin

Associate and dissociate very quickly (instantaneous)

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Carbonic Acid– Bicarbonate Buffering

Operates in the lung and the kidney.

The greater the partial pressure of carbon dioxide (pCO2), the more carbonic acid is formed.

At a pH of 7.4, the ratio of bicarbonate to carbonic acid is 20:1.

Bicarbonate and carbonic acid can increase or decrease, but the ratio must be maintained.

Lungs can decrease carbonic acid.

Kidneys can reabsorb or regenerate bicarbonate but do not act as fast as the lungs.

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Carbonic Acid– Bicarbonate Buffering (cont’d)

If bicarbonate decreases, then the pH decreases and can cause acidosis.

pH can be returned to normal if carbonic acid also decreases.

This type of pH adjustment is called compensation.

The respiratory system compensates by increasing or decreasing ventilation.

The renal system compensates by producing acidic or alkaline urine.

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Other Buffering Systems

Protein buffering

Proteins have negative charges; as a result, they can serve as buffers for H+; mainly intracellular buffer with hemoglobin

Respiratory and renal buffering

Respiratory: Acidemia causes increased ventilation; alkalosis slows respirations

Renal: Secretion of H+ in urine and reabsorption of HCO3–; dibasic phosphate and ammonia

Cellular ion exchange

Exchanges of K+ for H+ in acidosis and alkalosis

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Acid-Base Imbalances

Normal arterial blood pH

7.35 to 7.45

Obtained by arterial blood gas (ABG) sampling

Acidosis

pH is less than 7.35

Systemic increase in H+ concentration

Alkalosis

pH is greater than 7.45

Systemic decrease in H+ concentration or excess of base

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Acid-Base Imbalances (cont’d)

Four categories

Respiratory acidosis—Elevation of pCO2 as a result of ventilation depression

Respiratory alkalosis—Depression of pCO2 as a result of hyperventilation

Metabolic acidosis—Depression of HCO3– or an increase in noncarbonic acids

Metabolic alkalosis—Elevation of HCO3–, usually as a result of an excessive loss of metabolic acids

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Metabolic Acidosis

Causes

Lactic acidosis

Renal failure

Diabetic ketoacidosis

Diarrhea

Starvation

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Metabolic Acidosis (cont’d)

Noncarbonic acids increase or bicarbonate (base) is lost from ECF or cannot be regenerated by the kidney.

pH drops below 7.35

HCO3– drops: less than 24 mEq/L

Compensation: Hyperventilation and renal excretion of excess acid

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Metabolic Acidosis (cont’d)

Manifestations:

Headache

Lethargy

Kussmaul respirations

Treatment:

Bicarbonate

Lactate-containing solutions: Lactate converted into bicarbonate in the liver

Treat the underlying cause(s)

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Metabolic Acidosis (cont’d)

Anion gap

Used cautiously to distinguish different types of metabolic acidosis.

By rule, anions (–) should equal cations (+).

Not all normal anions are routinely measured.

Represents unmeasured negative ions.

Normal anion gap is 10 to 12 mEq/L.

Normal anion gap or elevated anion gap with metabolic acidosis may help determine the cause.

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Metabolic Alkalosis

Causes

Prolonged vomiting

Gastric suctioning

Excessive bicarbonate intake

Hyperaldosteronism with hypokalemia

Diuretic therapy

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Metabolic Alkalosis (cont’d)

Bicarbonate concentration is increased, usually from excessive loss of metabolic acids (Cl –)

pH is elevated above 7.45.

HCO3– is elevated above 26 mEq/L.

Compensation: Hypoventilation; kidneys conserve H+ and eliminate bicarbonate.

Manifestations: Weakness, muscle cramps, and hyperactive reflexes with signs of hypocalcemia

Treatment: Sodium chloride, potassium, chloride IV (chloride replaces HCO3-)

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Respiratory Acidosis

Causes

Depression of the respiratory center (brainstem trauma, oversedation)

Respiratory muscle paralysis

Disorders of the chest wall (kyphoscoliosis, pickwickian syndrome, flail chest)

Disorders of the lung parenchyma (pneumonitis, pulmonary edema, emphysema, asthma, bronchitis)

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Respiratory Acidosis (cont’d)

Occurs with alveolar hypoventilation

pH is below 7.35.

CO2 elevates from hypercapnia

Compensation: Is not as effective since kidneys take time but conserve bicarbonate and eliminate H+

Manifestations: Headache, restlessness, blurred vision, apprehension, lethargy, muscle twitching, tremors, convulsions, coma

Treatment: Restore adequate ventilation; may need mechanical ventilation; administer IV lactate fluids

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Respiratory Alkalosis

Causes

High altitudes

Hypermetabolic states, such as fever, anemia, and thyrotoxicosis

Early salicylate intoxication

Anxiety or panic disorder

Improper use of mechanical ventilators

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Respiratory Alkalosis (cont’d)

Occurs with hyperventilation and decreased plasma CO2 (hypocapnia)

pH above 7.45

CO2 is decreased below 38 mm Hg

Compensation: Kidneys decrease H+ excretion and bicarbonate absorption

Manifestations: Dizziness, confusion, tingling of extremities (paresthesias), convulsions, and coma with signs of hypocalcemia

Treatment: Paper bag; treat hypoxemia and hypermetabolic states; administer IV chloride fluids

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Summary

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Summary (cont’d) Question 3

A person arrives in the emergency department after a loss of consciousness and the develop-ment of Kussmaul respirations. The individual has a history of diabetes and 2 days of vomiting and diarrhea. The nurse suspects the person has:

Respiratory alkalosis

Respiratory acidosis

Metabolic alkalosis

Metabolic acidosis

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ANSWER AND RATIONALE: 4. Metabolic acidosis. Diabetic ketoacidosis results in an increase in noncarbonic acids and a decrease in bicarbonate ion which produces metabolic acidosis.

1. Respiratory alkalosis is produced by alveolar hyperventilation and reduction in carbon dioxide concentration.

2. Respiratory acidosis is produced by alveolar hypoventilation and increase in carbon dioxide concentration.

3. Metabolic alkalosis is produced by an excess of bicarbonate ion.

Summary (cont’d) Question 4

A person with a history of chronic lung disease arrives in the clinic with a 1-week history of a productive cough, hypoventilation, headache, and muscle twitching. The nurse suspects the person is experiencing:

Respiratory acidosis

Respiratory alkalosis

Metabolic acidosis

Metabolic alkalosis

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ANSWER AND RATIONALE: 1. Respiratory acidosis. Respiratory acidosis is produced by alveolar hypoventilation, which is commonly found in individuals with chronic obstructive pulmonary disease. Headache and muscle twitching are symptoms of elevated carbon dioxide levels produced by hypoventilation.

2. Respiratory alkalosis is produced by alveolar hyperventilation and reduction in carbon dioxide concentration. Symptoms of respiratory alkalosis include dizziness, confusion, paresthesia, convulsions, and coma.

3. Metabolic acidosis is produced by an increase in noncarbonic acids and/or a decrease in bicarbonate ion. Symptoms of metabolic acidosis include headache, lethargy, Kussmaul respirations, anorexia, nausea and vomiting, dysrhythmias, and coma.

4. Metabolic alkalosis is produced by an excess of bicarbonate ion. Symptoms of metabolic alkalosis include muscle weakness, muscle cramps, hyperreflexia, paresthesias, tetany, and seizures.

A 17-year-old boy is admitted to the pediatric intensive care unit after surgery. The teen requires débridement of a wound on his sacrum (triangular bone at the base of the spine). His mother attributes this to difficulty in repositioning him because of his size. He has been in a persistent vegetative state for almost 4 years after suffering a traumatic brain injury as a result of a self-inflicted gunshot to his head.

Unit I: The Cell Case Study 1

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Unit I: The Cell

Case Study 1 (cont’d) Discussion Questions

The sacral area is covered with which type of tissue?

Muscle

Neural

Epithelial

Connective

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ANS: C

Epithelial tissue covers most internal and external surfaces of the body. Muscle tissue is responsible for movement. Neural tissue is composed of highly specialized cells that receive and transmit electric impulses. Connective tissue binds various tissues and organ together, supporting them in their location.

A large portion of the area is removed because of ischemia and cell death. The teen suffers from tissue:

Apoptosis

Necrosis

Catabolism

Metabolism

Unit I: The Cell

Case Study 1 (cont’d) Discussion Questions

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ANS: B

Necrosis is a form of traumatic cell death that results from acute cellular injury. This may be caused by several types of cell injury, such as from repetitive movements against a surface or not being moved from a particular position over a long period of time. Apoptosis is the process of programmed cell death. Biochemical changes occur within a cell leading to characteristic cell changes and death. Catabolism involves the metabolic breakdown of complex molecules into simpler ones, often resulting in a release of energy. Metabolism is the set of life-sustaining transformations within cells of living organisms.

While recuperating, the teen has generalized and dependent swelling. His wound is healing well with no noted redness or drainage.

Unit I: The Cell Case Study 2

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The pathophysiologic process of edema is related to an increase in the forces favoring fluid filtration into tissues. This is caused by:

Lymphatic obstruction

Decreased plasma oncotic pressure

Venous obstruction

Increased capillary permeability

Unit I: The Cell

Case Study 2 (cont’d) Discussion Questions

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ANS: D

Increased capillary permeability is associated with inflammation and the immune response. This is a result of trauma such as burns, allergic reactions and infection. The teen’s body’s natural responses will have responded to the initial inflammation at the site of the resultant wound. Lymphatic obstruction occurs when the lymphatic channels are blocked due to infection or tumor. Decreased plasma oncotic pressure results from losses or diminished production of plasma albumin. This is most commonly associated with liver disease, glomerular disease, hemorrhage, and protein malnutrition. While this may occur due to serous drainage from open wounds or burns, the teen’s wound is healing well and this is not contributing to his edema. Venous obstruction causes an increase in hydrostatic pressure behind an obstruction, such as a venous blood clot, right heart failure, tight clothing and prolonged standing.

Fluids and Electrolytes

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