NUR631 Week 3: fluid/electrolyte/ABGs

Class II hypovolemic shock is characterized by a. tachycardia. b. hypertension. c. lactic acidosis. d. narrowed pulse pressure.

ANS: A Class II hypovolemic shock is characterized by the patient becoming anxious and restless. Blood pressure is normal with the patient supine but shows orthostatic changes. Lactic acidosis and narrowed pulse pressure are not found in Class II hypovolemic shock.

Administration of which therapy is most appropriate for hypovolemic shock? a. Crystalloids b. Vasoconstrictor agents c. Inotropic agents d. 5% dextrose in water

ANS: A Crystalloids are solutions that contain electrolytes. Isotonic solutions, such as lactated Ringers, are commonly used crystalloid solutions. These solutions are preferred for volume resuscitation, because they remain in the extracellular space and are more effective in increasing blood volume. Vasoconstrictor agents are contraindicated in hypovolemic shock. Isotonic crystalloids are the most appropriate fluid for volume resuscitation and are preferred over glucose or hypotonic electrolyte solutions.

Respiratory alkalosis is caused by a. hyperventilation. b. pneumonia. c. chest muscle weakness. d. pulmonary edema.

ANS: A Hyperventilation causes respiratory alkalosis as a result of loss of carbonic acid. Pneumonia, chest muscle weakness, and pulmonary edema cause carbonic acid to accumulate in the blood and result in respiratory acidosis.

The finding of ketones in the blood suggests that a person may have a. metabolic acidosis. b. metabolic alkalosis. c. respiratory acidosis. d. respiratory alkalosis.

ANS: A Ketones are produced from breakdown of fat in the body as a result of starvation or lack of ability to utilize glucose in diabetes mellitus. Ketoacids in the blood indicate a very high ketone level in the body, which leads to metabolic acidosis. Ketonuria from high ketones in the blood would not indicate metabolic alkalosis. The respiratory system does not influence ketone level.

Uncompensated metabolic alkalosis would result in a. increased pH, increased HCO3 - . b. increased pH, decreased HCO3 - . c. decreased pH, increased HCO3 - . d. decreased pH, decreased HCO3 - .

ANS: A Metabolic alkalosis is characterized by increased HCO3 - and increased pH. HCO3 - is a base and would be increased. Decreased pH indicates an uncompensated or partially compensated acidosis.

The effect of nitric oxide on systemic arterioles is a. vasodilation. b. vasoconstriction. c. not significant. d. opposed by nitrate drugs

ANS: A Nitric oxide causes vasodilation in the systemic arterioles. Vasoconstriction is not associated with nitric oxide. There is a significant effect on the systemic arterioles related to nitric oxide. The effects of nitric oxide are not known to be opposed by nitrate drugs.

A patient in septic shock is getting IV fluids but remains hypotensive and the nurse notes third spacing of fluids. What is the mechanism behind these observations? a. Capillary leaking of fluids b. Inadequate fluid administration c. Ongoing vasoconstriction d. Destruction of CAM molecules

ANS: A The hallmark of septic shock is the development of vasodilation, increased cellular permeability, and hypovolemia. Neutrophil diapedesis between endothelial cells results in increased permeability of the capillary membrane. The patient remains hypotensive but fluid builds up in third spaces. It is not due to inadequate fluid administration, ongoing vasoconstriction, or destruction of CAM (cellular adhesion molecules).

Clinical manifestations of extracellular fluid volume deficit include a. weak pulse, low blood pressure, and increased heart rate. b. thirst, dry mucous membranes, and diarrhea. c. confusion, lethargy, coma, and perhaps seizures. d. cardiac dysrhythmias, paresthesias, and muscle weakness.

ANS: A Clinical manifestations of extracellular fluid volume deficit include weak pulse, low blood pressure, and increased heart rate. Extracellular fluid volume deficit does not cause diarrhea. Confusion, lethargy, coma, and perhaps seizures are associated with osmolality imbalances such as hyponatremia. Cardiac dysrhythmias, paresthesias, and muscle weakness are manifestations of electrolyte imbalances.

The electrolyte that has a higher concentration in the extracellular fluid than in the intracellular fluid is ___ ions. a. sodium b. phosphate c. magnesium d. potassium

ANS: A Extracellular fluid has a higher sodium ion concentration than does intracellular fluid. Intracellular fluid has a higher phosphate, magnesium, and potassium ion concentration than does extracellular fluid.

Decreased neuromuscular excitability is often the result of a. hypercalcemia and hypermagnesemia. b. hypomagnesemia and hyperkalemia. c. hypocalcemia and hypokalemia. d. hypernatremia and hypomagnesemia

ANS: A Hypercalcemia and hypermagnesemia result in decreased neuromuscular excitability. Hypomagnesemia, hypocalcemia, and hypomagnesemia result in increased neuromuscular excitability.

Effects of hypernatremia on the central nervous system typically include a. confusion. b. excitation. c. insomnia. d. hallucinations.

ANS: A Hypernatremia causes osmotic shrinking of brain cells, which manifests as confusion or coma. Hypernatremia does not usually cause central nervous system excitation, insomnia, or hallucinations

Early manifestations of a developing metabolic acidosis include a. coma. b. headache. c. muscle cramps. d. short and shallow respirations.

ANS: B Headache is an early manifestation of a developing metabolic acidosis. Coma is a very late symptom of metabolic acidosis. Muscle cramps are not characteristic of metabolic acidosis. Deep rapid respirations are the compensatory mechanism for metabolic acidosis.

A person with acute hypoxemia may hyperventilate and develop a. respiratory acidosis. b. respiratory alkalosis. c. metabolic alkalosis. d. metabolic acidosis

ANS: B Hyperventilation causes much carbonic acid to be blown off, resulting in respiratory alkalosis. Respiratory acidosis is caused by hypoventilation and retention of carbonic acid. Hyperventilation does not cause metabolic acid or base disturbances.

Low cardiac output in association with high preload is characteristic of _____shock. a. hypovolemic b. cardiogenic c. anaphylactic d. septic

ANS: B In cardiogenic shock, preload is high and cardiac output is low. In hypovolemic shock, preload and cardiac outputs are both low. In anaphylactic shock, blood volume may be normal. Septic shock is associated with infections.

In which stage of shock is a patient who has lost 1200 mL of blood, who has normal blood pressure when supine, but who experiences orthostatic hypotension upon standing? a. Class I, Initial Stage b. Class II, Compensated Stage c. Class III, Progressive Stage d. Class IV, Refractory Stage

ANS: B In compensated stage hemorrhage (Class II), the blood loss is between 750 and 1500 mL. Blood pressure remains normal when the patient is supine but decreases upon standing. In initial stage hemorrhage (Class I) blood loss is up to 750 mL, and the patient's vital signs remain normal. Class III hemorrhage (progressive stage) is blood loss of 1500 and 2000 mL. Vital signs are changing. Severe Class IV hemorrhage (refractory stage) occurs when more than 2000 mL is lost. The patient is lethargic, with severe hypotension.

The arterial blood gas pH = 7.52, PaCO2 = 30 mm Hg, HCO3 - = 24 mEq/L demonstrates a. metabolic acidosis. b. respiratory acidosis. c. respiratory alkalosis. d. mixed alkalosis.

ANS: C The high pH, low PaCO2, and normal HCO3 indicate respiratory alkalosis. Metabolic and respiratory acidosis would decrease the pH. The HCO3 - is normal, so no metabolic imbalance is indicated.

A patient presenting with fever, hypotension, and lactic acidosis is most likely to be experiencing what type of shock? a. Cardiogenic b. Septic c. Anaphylactic d. Neurogenic

ANS: B Patients presenting with septic shock may have fever and hypotension. In addition, lactic acidosis may be present because of tissue hypoxemia. Presentation of cardiogenic shock is not inclusive of fever or lactic acidosis. Patients in anaphylactic shock do not have fever or lactic acidosis, and may have normal vital signs initially. Neurogenic shock may result from depression of the vasomotor center in the medulla or spinal cord injury and would not present with fever.

Vomiting of stomach contents or continuous nasogastric suctioning may predispose to development of a. carbonic acid deficit. b. metabolic acid deficit. c. metabolic acidosis. d. carbonic acid excess.

ANS: B Gastric contents are rich in hydrochloric acid; loss of this through suctioning or vomiting leads to a metabolic acid deficit and alkalosis. Carbonic acid is related to the respiratory system. Vomiting produces metabolic alkalosis as a result of loss of acid-rich gastric contents, it does not increase carbonic acid.

Hyperaldosteronism causes a. ECV deficit and hyperkalemia. b. ECV excess and hypokalemia. c. hyponatremia and hyperkalemia. d. excessive water reabsorption without affecting sodium concentration

ANS: B Hyperaldosteronism causes excessive renal retention of sodium and water and excessive potassium excretion, which lead to ECV excess and hypokalemia. Hyperaldosteronism does not cause ECV deficit, hyperkalemia, hyponatremia, or excessive water reabsorption without affecting sodium concentration.

Clinical manifestations of moderate to severe hypokalemia include a. muscle spasms and rapid respirations. b. muscle weakness and cardiac dysrhythmias. c. confusion and irritability. d. vomiting and diarrhea.

ANS: B Hypokalemia causes muscle weakness (or paralysis) and cardiac dysrhythmias. Hypokalemia does not cause muscle spasms and rapid respirations or confusion and irritability. Vomiting and diarrhea can cause hypokalemia, but they are not signs and symptoms of it.

Causes of hypomagnesemia include a. hyperphosphatemia. b. chronic alcoholism. c. oliguric renal failure. d. clinical dehydration.

ANS: B Hypomagnesemia is common with chronic alcoholism. Hyperphosphatemia causes hypocalcemia. Oliguric renal failure and clinical dehydration reduce magnesium excretion.

Tachycardia is an early sign of low cardiac output that occurs because of a. tissue hypoxia. b. anxiety. c. baroreceptor activity. d. acidosis.

ANS: C A number of compensatory responses are set in motion to restore tissue perfusion and oxygenation in the early stage of shock. Baroreceptors located in the aorta and carotid arteries quickly sense the decrease in pressure and transmit signals to the vasomotor center in the brainstem medulla. The sympathetic nervous system stimulates 1 receptors, which respond by increasing the heart rate in an attempt to increase cardiac output. Tachycardia is not caused initially by tissue hypoxia. An early sign of low cardiac output is not anxiety. Tachycardia does not occur because of acidosis.

The major buffer in the extracellular fluid is a. hemoglobin. b. albumin. c. bicarbonate. d. phosphate.

ANS: C Bicarbonate is the major buffer in the extracellular fluid. Hemoglobin is in erythrocytes, which are in the vascular compartment, but not in the interstitial portion of extracellular fluid. Albumin is in the vascular compartment, but not in the interstitial portion of extracellular fluid. Phosphate is an important buffer in urine and intracellular fluid.

Cardiogenic shock is characterized by a. hypovolemia. b. reduced systemic vascular resistance. c. reduced cardiac output. d. elevated SvO2.

ANS: C Cardiogenic shock occurs primarily as a result of severe dysfunction of the left or right ventricles, or both, that results in inadequate cardiac pumping. The low cardiac output state is associated with a high left ventricular diastolic filling pressure. Cardiogenic shock is not manifested by hypovolemia. Sympathetic activation leads to increases in heart rate, vasoconstriction, and a narrow pulse pressure. Low cardiac output leads to reduced SvO2.

The patient who requires the most careful monitoring for development of metabolic acidosis is a patient who a. is in the diuretic phase of acute renal failure. b. has had hypokalemia for over a week. c. has had diarrhea for over a week. d. has newly diagnosed Cushing syndrome.

ANS: C Diarrhea causes increased excretion of the base bicarbonate, which can lead to metabolic acidosis. Although the oliguric phase of acute renal failure causes metabolic acidosis, the diuretic phase does not because the kidneys can still excrete metabolic acids. Hypokalemia is associated with metabolic alkalosis. Cushing syndrome is cortisol excess, which can cause metabolic alkalosis from increased renal excretion of hydrogen ions.

Diarrhea causes a. respiratory acidosis. b. respiratory alkalosis. c. metabolic acidosis. d. metabolic alkalosis.

ANS: C Diarrhea causes metabolic acidosis as the intestinal fluids are rich in bicarbonate ions. Diarrhea causes a metabolic acid-base imbalance and is not related to the respiratory system. Diarrhea involves increased excretion of bicarbonate and causes an acidic condition.

Massive release of histamine with consequent vasodilation and hypotension occurs with what type of shock? a. Cardiogenic b. Hypovolemic c. Anaphylactic d. Neurogenic

ANS: C Exposure to a specific antigen causes receptors on mast cells and basophils to cross-link and activate histamine. The release of histamine along with other vasoactive chemicals produces bronchoconstriction. Cardiogenic shock is not associated with histamine release. Hypovolemic shock is not associated with histamine release. Histamine release does not occur with neurogenic shock.

Tumor necrosis factor- and interleukin-1 contribute to shock states because they induce production of a. catecholamines. b. clotting factors. c. nitric oxide. d. vasopressin.

ANS: C In septic shock, tumor necrosis factor-, interleukin-1, and other inflammatory mediators induce vascular cells to produce excessive amounts of the vasodilator nitric oxide. Catecholamines are not produced by TNF- and IL-1. The production of clotting factors is not induced by tumor necrosis factor-a and interleukin-1. Vasopressin production is not induced by TNF- and IL-1.

In contrast to all other types of shock, the hyperdynamic phase of septic shock is associated with a. high afterload. b. low cardiac output. c. high cardiac output. d. reduced contractility.

ANS: C In the hyperdynamic stage of septic shock, blood pressure falls because of the decreased systemic vascular resistance and decreased venous return. The heart rate and stroke volume increase and cardiac output is higher than normal. In the hyperdynamic phase of septic shock, afterload is not high. Cardiac output is high in the hyperdynamic stage of septic shock. The heart rate and stroke volume increase during the hyperdynamic stage of septic shock.

An older patient has been hospitalized several times in 6 months with severe ECV depletion resulting from chronic laxative abuse. Which blood gas results correlate to this condition? a. pH in high part of normal range, PaO2 normal, PaCO2 normal, bicarbonate normal b. pH in high part of normal range, PaO2 normal, PaCO2 high, bicarbonate high c. pH in low part of normal range, PaO2 normal, PaCO2 low, bicarbonate low d. pH in low part of normal range, PaO2 normal, PaCO2 normal, bicarbonate normal

ANS: C Laxative abuse contributes to metabolic acidosis as bicarbonate is lost through the stool and is characterized by a low pH (acidosis), a low HCO3 - (binding excess acids), and a low PaCO2 (due to compensatory hyperventilation). Compensation will help raise the pH to the lower end of normal. The PaO2 should remain normal.

A person who experiences a panic attack and develops hyperventilation symptoms may experience a. neuromuscular depression. b. anxiety acidosis. c. numbness and tingling in the extremities. d. acute compensatory metabolic acidosis.

ANS: C Numbness and tingling in the extremities occur in alkalosis as a result of increased neuromuscular irritability. Numbness and tingling as a result of hyperventilation result from increased neuromuscular irritability, not neuromuscular depression. Acidosis depresses neuromuscular irritability and thus would not cause numbness and tingling, even in compensation.

The nurse is caring for a patient who has acute hemorrhagic shock. The patient's shock index today is 1.08. What does the nurse understand about this value? a. The patient is in critical condition. b. The patient has fully recovered. c. This value is concerning. d. This value doesn't correlate with the patient's condition.

ANS: C The shock index is calculated by dividing the systolic blood pressure by the pulse rate. A normal index is 0.7 to 0.9. A value above 1 should signal concern. This patient's value indicates ongoing concern, but does not indicate a critical condition nor that the patient has recovered. The value does correlate with the patient's condition of hemorrhagic shock.

The majority of cases of anaphylactic shock occur when a sensitized individual comes in contact with a. perfumes. b. incompatible blood products. c. animal proteins or dander. d. antibiotics.

ANS: D Anaphylactic shock is most frequently associated with antibiotic therapy. Contact with perfumes is not the most frequent cause of anaphylactic shock. Incompatible blood products do not lead to anaphylactic shock. Animal dander may lead to an anaphylactic reaction, but does so less commonly than antibiotics.

Renal compensation for respiratory acidosis is evidenced by a. decreased carbon dioxide. b. elevated carbon dioxide. c. decreased bicarbonate ion concentration. d. elevated bicarbonate ion concentration.

ANS: D Elevated bicarbonate ion concentration is evidence of compensation for a respiratory acidosis. The lungs manage the carbon dioxide concentration. Elevated carbon dioxide is evidence of respiratory acidosis, not of compensation for it. Decreased bicarbonate ion concentration would make acidosis worse.

Emesis causes a. respiratory acidosis. b. respiratory alkalosis. c. metabolic acidosis. d. metabolic alkalosis

ANS: D Emesis causes metabolic alkalosis as the stomach is a major reservoir for acids. Emesis causes a metabolic acid-base imbalance as it is not related to the respiratory system. Emesis involves loss of gastric acid and fluid and causes an alkalotic disruption.

Metabolic alkalosis is often accompanied by a. hypernatremia. b. hyponatremia. c. hyperkalemia. d. hypokalemia

ANS: D Hypokalemia often accompanies metabolic alkalosis because it can cause metabolic alkalosis or be caused by it. Metabolic alkalosis and hypernatremia, hyponatremia, and hyperkalemia are not often associated with each other.

Respiratory acidosis may be caused by a. hyperventilation. b. massive blood transfusion. c. tissue hypoxia. d. hypoventilation

ANS: D Hypoventilation causes carbonic acid retention and respiratory acidosis. Hyperventilation causes excretion of too much carbonic acid and respiratory alkalosis. The liver metabolizes the citrate in transfused blood into bicarbonate. Tissue hypoxia causes lactic acid production during anaerobic metabolism and metabolic acidosis

A patient with cold and clammy extremities, low cardiac output, and profound hypotension is likely to be experiencing a progressive stage of shock. a. cardiogenic b. hypovolemic c. obstructive d. septic

ANS: D In the progressive stage of septic shock, some patients deteriorate to a hypodynamic state. This is characterized by decreased cardiac output and cold, clammy skin as a result of narrowed pulse pressure. Profound hypotension generally occurs which is unresponsive to treatment. Cardiogenic shock is evidenced by decreased cardiac output, elevated left ventricular end-diastolic pressure, S3 heart sounds, and pulmonary edema. Hypotension occurs with hypovolemic shock, but extremities are not likely to be cold and edematous. Cold, clammy extremities along with low cardiac output and profound hypotension are not manifestations of obstructive shock.

Overproduction of nitric oxide is an important aspect of the pathophysiologic process of what type of shock? a. Cardiogenic b. Hypovolemic c. Anaphylactic d. Septic

ANS: D The overproduction of nitric oxide is seen in septic shock as a result of the release of immune cytokines. Nitric oxide is not seen in cardiogenic shock. Hypovolemic shock is not associated with the overproduction of nitric acid. The pathophysiologic process of anaphylactic shock is not associated with the overproduction of nitric oxide.

The __________system compensates for metabolic acidosis and alkalosis. a. gastrointestinal b. renal c. cardiovascular d. respiratory

ANS: D When metabolic acids are out of balance, the respiratory system compensates for the altered pH by adjusting the amount of carbon dioxide in the blood. The gastrointestinal system is not a major compensatory mechanism in acid-base imbalances. The kidneys are overwhelmed or dysfunctional in a metabolic acid-base imbalance. The cardiovascular system is not a major compensatory mechanism in acid-base imbalances.

A patient has a positive Chvostek sign. The nurse interprets this as a sign of a. hypercalcemia. b. hypermagnesemia. c. decreased neuromuscular excitability. d. increased neuromuscular excitability.

ANS: D Positive Chvostek sign indicates increased neuromuscular excitability, which can be caused by hypocalcemia, hypomagnesemia, or other factors. Hypercalcemia and hypermagnesemia cause decreased neuromuscular excitability and do not cause positive Chvostek sign. Hypokalemia and hyperkalemia cause skeletal muscle weakness and do not cause positive Chvostek sign.

Which event is likely to lead to hyponatremia? a. Insufficient ADH secretion b. Excess aldosterone secretion c. Administration of intravenous normal saline d. Frequent nasogastric tube irrigation with water

ANS: D Sodium is lost from gastric secretions when nasogastric tubes are irrigated with water. The sodium diffuses into the irrigating water and is then lost when the aspirate is withdrawn. Excessive ADH would lead to hyponatremia by retention of water in the body, thus diluting the sodium. Excess aldosterone would increase serum sodium. Normal saline is an isotonic solution and will not alter the serum sodium

Signs and symptoms of clinical dehydration include a. decreased urine output. b. increased skin turgor. c. increased blood pressure. d. decreased heart rate.

ANS: A One clinical manifestation of dehydration is decreased urine output. Skin turgor and blood pressure decrease in clinical dehydration. Heart rate increases in clinical dehydration.

Fully compensated respiratory acidosis is demonstrated by a. pH 7.36, PaCO2 55, HCO3 - 36. b. pH 7.45, PaCO2 40, HCO3 - 28. c. pH 7.26, PaCO2 60, HCO3 - 26. d. pH 7.40, PaCO2 40, HCO3 - 24.

ANS: A Compensation for respiratory acidosis involves conservation of HCO3 - in the body; an HCO3 - of 36 is a key finding; the normal pH (7.36) indicates compensation. Low HCO3 - is not indicative of compensated respiratory acidosis. Low pH indicates no compensation or only partial compensation. Values of pH 7.40, PaCO2 40, and HCO3 - 24 are all normal.

An increase in the resting membrane potential (hyperpolarized) is associated with a. hypokalemia. b. hyperkalemia. c. hypocalcemia. d. hypercalcemia

ANS: A Hypokalemia increases the resting membrane potential. Hypocalcemia and hypercalcemia do not affect the resting membrane potential.

The body compensates for metabolic alkalosis by a. hypoventilation. b. decreasing arterial carbon dioxide. c. increasing bicarbonate ion excretion. d. hyperventilation

ANS: A In metabolic alkalosis, the lungs compensate by hypoventilation to conserve CO2 in the body. Decreasing arterial carbon dioxide would worsen metabolic alkalosis. The respiratory system compensates for metabolic acid and base disturbances; the lungs do not increase bicarbonate ion excretion. Hyperventilation would blow off CO2 and cause respiratory alkalosis.

What age group has a larger volume of extracellular fluid than intracellular fluid? a. Infants b. Adolescents c. Young adults d. Older adults

ANS: A Infants have a larger volume of extracellular fluid than intracellular fluid. Adolescents, young adults, and older adults have a larger volume of intracellular fluid than extracellular fluid.

For general good health, the nurse advises the older patient to do which of the following? a. Drink fluids on a schedule rather than waiting to feel thirsty. b. If laxatives are needed, use ones that are magnesium based. c. If antacids are needed, use ones that are magnesium based. d. Due to nocturia seen in older adults, restrict fluid intake after 6 pm

ANS: A Older adults are a high-risk group for clinical dehydration, in part because they have a reduced thirst response to increased body fluid osmolality. Magnesium-containing laxatives and antacids place older adults at risk of hypermagnesemia due to changes in renal function. A decreased ability to concentrate urine leads to nocturia; the older adult may or may not need to restrict fluids but if they do, 6 pm may be too early and the adult should be instructed to increase fluids during the rest of the day to maintain the typical intake.

Respiratory acidosis is associated with a. increased carbonic acid. b. hypokalemia. c. increased neuromuscular excitability. d. increased pH.

ANS: A Respiratory acidosis causes an excess of carbonic acid that may be because of impaired gas exchange, inadequate neuromuscular function, and impairment of respiratory control of the brainstem. Hypokalemia is associated with alkalosis. Acidosis is associated with decreased neuromuscular excitability. Increased pH is associated with alkalosis; in acidosis the pH is low.

A patient diagnosed with chronic compensated heart failure reports that, ―My feet swell if I eat salt but I don't understand why.‖ The nurse's best response is: a. ―Salt holds water in your blood and makes more pressure against your blood vessels, so fluid leaks out into your tissues and makes them swell.‖ b. ―Gravity makes more pressure down by your feet than up at the top of your body, so more fluid leaks into your tissues at your feet and they swell.‖ c. ―Salt makes your blood vessels relax and the blood does not flow as fast, so some of it leaks into your tissues and makes swelling.‖ d. ―Salt binds to the proteins in your blood and changes the osmotic pressure so more fluid can leak out and stay in the tissues, causing swelling.‖

ANS: A Salt holds water in the ECV, thus increasing capillary hydrostatic pressure. Gravity leads to feet swelling, but it does not explain what the patient is asking. Salt does not cause vasodilation, nor does it bind to blood proteins and change osmotic pressure.

Manifestations from sodium imbalances occur primarily as a result of a. cellular fluid shifts. b. vascular collapse. c. hyperosmolarity. d. hypervolemia.

ANS: A Sodium imbalances alter osmolality of fluid compartment leading to osmosis of water from the hypo-osmolar compartment to the hyperosmolar compartment. In brain cells, this leads to swelling or shrinkage of cells, and associated manifestations.

Hypotension associated with neurogenic and anaphylactic shock is because of a. hypovolemia. b. peripheral pooling of blood. c. poor cardiac contractility. d. high afterload.

ANS: B Profound peripheral vasodilation of both arterioles and veins leads to peripheral pooling of blood and hypotension. Decreased venous return to the heart results in decreased cardiac output and hypotension. Hypovolemia is not the source of the hypotension involved in neurogenic and anaphylactic shock. Cardiac contractility is generally adequate in neurogenic and anaphylactic shock. Hypotension in neurogenic and anaphylactic shock is not related to high afterload.

The nurse is caring for a patient being treated with an Impella device. What statement by the nurse shows good understanding of this treatment? a. ―It is like an external heart-lung bypass machine.‖ b. ―It is a tiny device that assists the left ventricle.‖ c. ―It is a flow-directed catheter to measure pressures.‖ d. ―It is a new type of Intra-Aortic Balloon Pump.‖

ANS: B The Impella device is a catheter-based miniaturized ventricular assist device placed through the femoral artery, through the aortic valve, into the left ventricle. Extracorporeal membrane oxygenation is an external heart-lung bypass machine. A pulmonary artery catheter can be used to measure systemic hemodynamic pressures. An Intra-Aortic Balloon Pump is a counter-pulsation device to augment heart function.

A patient who was involved in a fall from a tree becomes short of breath. The lung sounds are absent on one side. This patient is experiencing ___ shock. a. cardiogenic b. obstructive c. hypovolemic d. distributive

ANS: B This type of obstructive shock is the result of a tension pneumothorax and is caused by shifting and compression of mediastinal structures including the heart, which compromise left ventricular filling. Accumulation of air in the pleural space may occur because of trauma. Prompt relief of the obstructive event is necessary to restore cardiac output and prevent cardiovascular collapse. Cardiogenic shock is not related to a traumatic event. Hypovolemic shock results when circulating blood volume is inadequate to perfuse tissues. Distributive shock is characterized by an abnormally expanded vascular space caused by excessive vasodilation.

When providing teaching to new parents about fluid and electrolytes in their newborn, what information does the nurse include? a. Infants are prone to dehydration because their body water content is so small. b. A newborn loses 5% to 10% of its body weight through fluid losses in the first few days c. Crying children become dehydrated quickly due to respiratory fluid loss. d. Adding extra powdered formula when mixing a bottle will help baby conserve fluid.

ANS: B A newborn loses 5% to 10% of its body weight through fluid losses in the first few days of life as a normal adjustment to extrauterine life. An infant's body is 75% water by weight. Crying will not lead to dehydration although some fluid is lost through the respiratory tract. Adding extra powder to formula increases the baby's risk for hypernatremia.

The fraction of total body water (TBW) volume contained in the intracellular space in adult males is a. three-fourths. b. two-thirds. c. one-half. d. one-third.

ANS: B Approximately two-thirds of TBW are contained inside the cells of an adult male. Two-thirds, not three fourths, of TBW are contained inside the cells of an adult man. Two-thirds, not one-half, of TBW are contained inside the cells of an adult man. One-third of the TBW is extracellular in adults of an adult ma

Hypernatremia may be caused by a. decreased aldosterone secretion. b. decreased antidiuretic hormone secretion. c. compulsive water drinking. d. excessive dietary potassium.

ANS: B Decreased antidiuretic hormone secretion (diabetes insipidus) prevents water reabsorption in the kidneys, which creates large volumes of dilute urine and causes hypernatremia. Aldosterone causes sodium and water retention. Compulsive water drinking that overwhelms the kidneys would dilute the blood, causing hyponatremia. Excessive dietary potassium would not affect the serum sodium concentration.

Diarrhea and other lower intestinal fluid losses will contribute to a. metabolic alkalosis. b. metabolic acidosis. c. respiratory acidosis. d. mixed acid-base disorders

ANS: B Diarrhea results in loss of bicarbonate and leads to metabolic acidosis. Loss of bicarbonate (a base) would not lead to metabolic alkalosis. Respiratory conditions lead to respiratory acid and base disturbances; diarrhea is not a respiratory condition. Bicarbonate loss through diarrhea would not lead to any respiratory acid/base disturbance.

The process responsible for distribution of fluid between the interstitial and intracellular compartments is a. filtration. b. osmosis. c. active transport. d. diffusion.

ANS: B Distribution of fluid between the interstitial and intracellular compartments occurs by the process of osmosis. Filtration is responsible for the distribution of fluid between the vascular and interstitial compartments. Active transport moves ions across membranes, but does not move water. Diffusion involves movement of particles, not movement of water.

Excessive antidiuretic hormone (ADH) secretion can cause ___ concentration. a. increased serum sodium b. decreased serum sodium c. increased serum potassium d. decreased serum potassium

ANS: B Excessive ADH stimulates excessive water reabsorption by the kidneys, which dilutes the blood, thus decreasing the serum sodium concentration. Excessive ADH secretion does not cause increased serum sodium or potassium concentrations, or decreased serum potassium concentration.

A patient, who is 8 months pregnant has developed eclampsia and is receiving intravenous magnesium sulfate to prevent seizures. To determine if her infusion rate is too high, you should regularly assess which of the following? a. Deep tendon reflexes. b. The Chvostek sign. c. Capillary refill. d. Skin turgor.

ANS: B Hypermagnesemia would manifest with severely decreased deep tendon reflexes. A positive Chvostek sign is indicative of hypomagnesemia and hypocalcemia. Capillary refill and skin turgor are assessments for fluid volume status. Hypermagnesemia causes decreased neuromuscular excitability and testing the patellar reflex can detect that. Hypermagnesemia causes decreased, not increased, neuromuscular excitability. If the patellar reflex stays the same, the infusion rate is therapeutic. Watching for seizure activity is a dangerous course of action. Hypermagnesemia can cause respiratory depression and cardiac arrest, so you need to assess for its development.

The imbalance that occurs with oliguric renal failure is a. metabolic alkalosis. b. hyperkalemia. c. hypokalemia. d. hypophosphatemia.

ANS: B Oliguric renal failure decreases potassium excretion, which causes hyperkalemia. Oliguric renal failure decreases acid excretion and causes metabolic acidosis (not alkalosis). Oliguric renal failure does not cause hypokalemia or hypophosphatemia.

How is a patient hospitalized with a malignant tumor that secretes parathyroid hormone monitored for the resulting electrolyte imbalance? a. Serum calcium, Chvostek and Trousseau signs b. Serum calcium, bowel function, level of consciousness c. Serum potassium, Chvostek and Trousseau signs d. Serum potassium, bowel function, level of consciousness

ANS: B Parathyroid hormone increases the plasma calcium concentration, and constipation and lethargy are manifestations of hypercalcemia. Chvostek and Trousseau signs are assessments for hypocalcemia. Potassium levels are not related.

Which acid are the kidneys unable to excrete? a. Metabolic b. Carbonic c. Bicarbonate d. Ammonia

ANS: B The kidneys can excrete any acid except carbonic acid. The kidneys are able to excrete metabolic acids and ammonia. The kidneys are able to excrete bicarbonate, but bicarbonate is a base, not an acid.

The person at highest risk for developing hypernatremia is a person who a. self-administers a daily tap water enema to manage a partial bowel obstruction. b. receives tube feedings because he or she is comatose after a stroke. c. has ectopic production of ADH from small cell carcinoma of the lung. d. is receiving IV 0.9% NaCl at a fast rate.

ANS: B Tube feedings are associated with hypernatremia as a result of intake of highly concentrated solution that causes the kidneys to excrete extra water to remove the solute load. Absorption of excessive water from daily tap water enemas would cause hyponatremia. Uncontrolled secretion of ADH causes renal retention of water that leads to hyponatremia. An IV solution of 0.9% NaCl (normal saline) is isotonic.

A patient is diagnosed with starvation ketoacidosis. What signs and symptoms should you anticipate in your assessment? a. Slow, shallow breathing, belligerence, hyperexcitability b. Slow, shallow breathing, numbness and tingling around his mouth c. Rapid, deep breathing, lethargy, abdominal pain d. Rapid, deep breathing, tremors, elevated blood pressure

ANS: C Rapid, deep breathing, lethargy, and abdominal pain are clinical manifestations of metabolic acidosis and its respiratory compensation. The other answer options are not clinical manifestations of metabolic acidosis and its respiratory compensation.

If an individual has a fully compensated metabolic acidosis, the blood pH is a. high. b. low. c. in the normal range. d. either high or low, depending on the type of compensation.

ANS: C The blood pH is in the normal range if an individual has fully compensated for an acid-base imbalance. High blood pH indicates alkalosis. Low blood pH indicates uncompensated or partially compensated acidosis.

Causes of metabolic acidosis include a. hyperventilation. b. massive blood transfusion. c. tissue anoxia. d. hypoventilation.

ANS: C Tissue anoxia can cause metabolic acidosis resulting from lactic acid production during anaerobic metabolism. Hyperventilation causes excretion of too much carbonic acid and respiratory alkalosis. The liver metabolizes the citrate in transfused blood into bicarbonate. Hypoventilation causes CO2 retention and respiratory acidosis

Improvement in a patient with septic shock is indicated by an increase in a. cardiac output. b. SvO2. c. systemic vascular resistance. d. serum lactate level.

ANS: C Vasodilation in all forms of distributive shock results in intravascular pooling in the venous system. Some portions of tissue are overperfused, and some are underperfused. Improvement in systemic vascular resistance is an indication of improvement in septic shock. In septic shock, the heart rate and stroke volume increase, and cardiac output is higher than normal. In septic shock, SvO2 levels may already be higher than normal. An increase in serum lactate levels may increase levels of acidosis and tissue hypoxia

Administration of a vasodilator to a patient in shock would be expected to a. increase vascular resistance. b. increase contractility. c. decrease left ventricular afterload. d. increase tissue perfusion.

ANS: C Vasodilators are used to decrease the workload of the heart by decreasing left ventricular afterload. Nitroprusside and nitroglycerin are examples of vasodilators. Dobutamine is used to decrease vascular resistance. Positive inotropic drugs are used to increase contractility. Positive inotropes include -adrenergic agonists, which have the ability to increase tissue perfusion.

A person who overuses magnesium-aluminum antacids for a long period of time is likely to develop a. hypokalemia. b. hyperkalemia. c. hypophosphatemia. d. hyperphosphatemia

ANS: C Antacid overuse for a long time can cause hypophosphatemia by binding phosphate in the gastrointestinal tract and preventing its absorption. Magnesium-aluminum antacids do not cause hypokalemia, hyperkalemia, or hyperphosphatemia.

Signs and symptoms of extracellular fluid volume excess include a. tachycardia. b. increased serum sodium concentration. c. bounding pulse. d. increased hematocrit.

ANS: C Bounding pulse is one of the signs of extracellular fluid volume excess. Tachycardia is one of the signs of extracellular fluid volume deficit. Increased serum sodium concentration is found in hypernatremia. Hematocrit can be decreased with extracellular fluid volume excess.

The inward-pulling force of particles in the vascular fluid is called ___pressure. a. capillary hydrostatic b. interstitial osmotic c. capillary osmotic d. interstitial hydrostatic

ANS: C Capillary osmotic pressure is the inward-pulling force of particles in the vascular fluid. Capillary hydrostatic pressure is an outward-pulling force. The question pertains to vascular fluid rather than interstitial fluid. Interstitial hydrostatic pressure is an outward-pulling force.

The nurse provides teaching regarding dietary intake of potassium to avoid an electrolyte imbalance when a patient a. takes very large doses of vitamin D to supplement during chemotherapy for breast cancer. b. has fatty stools from taking an OTC weight loss product that decreases absorption of fat. c. has chronic heart failure that is treated with diuretics. d. experiences anorexia and chronic oliguric renal failure.

ANS: C Chronic heart failure causes increased secretion of aldosterone, which often causes hypokalemia by increasing renal excretion of potassium; most diuretics used to treat heart failure also increase renal excretion of potassium. Vitamin D and malabsorption of fat decreases absorption of calcium, not potassium. Chronic oliguric renal failure causes decreased excretion of potassium. An anorexic patient with chronic oliguric renal failure should not increase dietary potassium.

Clinical manifestations of hyponatremia include a. weak pulse, low blood pressure, and increased heart rate. b. thirst, dry mucous membranes, and diarrhea. c. confusion, lethargy, coma, and perhaps seizures. d. cardiac dysrhythmias, paresthesias, and muscle weakness.

ANS: C Clinical manifestations of hyponatremia include confusion, lethargy, coma, and perhaps seizures, as they are manifestations of CNS dysfunction. Weak pulse, low blood pressure, and increased heart rate are characteristics of clinical dehydration. Hyponatremia does not cause thirst, dry mucous membranes, and diarrhea. Cardiac dysrhythmias, paresthesias, and muscle weakness are manifestations of imbalances in potassium, calcium, and phosphorus.

Clinical manifestations of severe symptomatic hypophosphatemia are caused by a. excess proteins. b. renal damage. c. deficiency of ATP. d. hypocalcemia.

ANS: C Clinical manifestations of severe symptomatic hypophosphatemia are caused by a deficiency of ATP. Phosphate is an important component of ATP, which is the major source of energy for many cellular substances. Severe symptomatic hypophosphatemia does not cause excess protein accumulation, damage the kidneys, or cause hypocalcemia.

What is the most likely explanation for a diagnosis of hypernatremia in an elderly patient receiving tube feeding? a. Too much sodium in the feedings b. Excess of feedings c. Inadequate water intake d. Kidney failure

ANS: C Failure to provide adequate water when a patient is receiving tube feedings could result in hypernatremia. The feedings may have too much sodium, or the patient may be receiving too much feeding solution, but most likely the patient is not receiving enough water. Kidney failure is most likely not the cause of hypernatremia in this patient.

Which electrolyte imbalances cause increased neuromuscular excitability? a. Hypokalemia and hyperphosphatemia b. Hyperkalemia and hypophosphatemia c. Hypocalcemia and hypomagnesemia d. Hypercalcemia and hypermagnesemia

ANS: C Hypocalcemia and hypomagnesemia both cause increased neuromuscular excitability. Hypokalemia, hyperkalemia, hypophosphatemia, hypercalcemia, and hypermagnesemia do not cause increased neuromuscular excitability

A known cause of hypokalemia is a. oliguric renal failure. b. pancreatitis. c. insulin overdose. d. hyperparathyroidism

ANS: C Insulin overdose causes hypokalemia by shifting potassium into cells. Oliguric renal failure decreases electrolyte excretion. Pancreatitis causes fat malabsorption, which binds calcium and magnesium, but not potassium, in the gastrointestinal tract. Hyperparathyroidism regulates calcium, not potassium.

Which alteration can lead to edema? a. Decreased capillary hydrostatic pressure b. Increased capillary colloid osmotic pressure c. Decreased lymphatic flow d. Decreased capillary membrane permeability

ANS: C Lymphatic obstruction prevents the drainage of accumulated interstitial fluid and proteins, which can lead to severe edema. Decreased capillary hydrostatic pressure would push less fluid into the interstitial space. Increased capillary colloid osmotic pressure would remove fluid from the interstitial space. Decreased capillary membrane permeability would allow less fluid movement into the interstitial space.

Total body water in older adults is a. increased because of decreased adipose tissue and decreased bone mass. b. increased because of decreased renal function and hormonal fluctuations. c. decreased because of increased adipose tissue and decreased muscle mass. d. decreased because of renal changes that cause diuresis with sodium excretion

ANS: C Older adults have decreased total body water because of increased adipose tissue and decreased muscle mass. Older adults have increased adipose tissue. Hormonal fluctuations and diuresis with sodium excretion are not characteristic of older adults.

Abnormalities in intracellular regulation of enzyme activity and cellular production of ATP are associated with a. hyponatremia. b. hypocalcemia. c. hypophosphatemia. d. hypokalemia

ANS: C Phosphate is an important component of ATP. Hypophosphatemia results in decreased ATP to cells. Hyponatremia, hypocalcemia, and hypokalemia do not affect ATP production

Sepsis has been recently redefined as a. a systemic infection with viable organisms in the bloodstream. b. a systemic inflammatory response to ischemia. c. a systemic inflammatory response to infection. d. severe hypotension in an infected patient.

ANS: C The current definition of sepsis is SIRS (systemic inflammatory response syndrome) secondary to infection. The current definition does not include having viable organisms in the bloodstream, a response to ischemia, or hypotension.

A person who has hyperparathyroidism is likely to develop a. hypokalemia. b. hyperkalemia. c. hypocalcemia. d. hypercalcemia.

ANS: D A person who has hyperparathyroidism is likely to develop hypercalcemia because parathyroid hormone causes calcium to come out of the bones and go to the ECF. Hypokalemia, hyperkalemia, and hypocalcemia are not the result of hyperparathyroidism.

Which change in a patient's assessment has the greatest urgency? a. Serum potassium concentration is decreasing; abdominal distention, but denies any difficulty breathing. b. Serum calcium concentration is decreasing; reports constipation; is alert and denies any discomfort. c. Serum calcium concentration is increasing; reports constipation; is alert and denies any discomfort. d. Serum potassium concentration is increasing; has developed cardiac dysrhythmias, but denies any difficulty breathing.

ANS: D Cardiac dysrhythmias from hyperkalemia need rapid attention to prevent potentially life-threatening consequences and are therefore the highest priority for reporting. None of the other manifestations are as critical to report as the priority.

When a parent asks how they will know if their 2-month-old baby, who is throwing up and has frequent diarrhea, is dehydrated, the nurse's best response is: a. ―Clinical dehydration is the combination of extracellular fluid volume deficit and hypernatremia, so those are the diagnostic criteria.‖ b. ―If he doesn't wet his diaper all afternoon and his neck veins look flat when he is lying down, then he is probably dehydrated.‖ c. ―If he sleeps more than usual and acts tired when he is awake, then he is probably dehydrated.‖ d. ―If the soft spot on the top of his head feels sunken in and his mouth is dry between his cheek and his gums, then he is probably dehydrated.‖

ANS: D Checking whether the head feels sunken and the mouth is dry between cheek and gums are useful assessments of ECV deficit in an infant, which is an important part of clinical dehydration. It is true that clinical dehydration is the combination of extracellular fluid volume deficit and hypernatremia, but it does not address the question the parent is asking. Although the diaper information provides a useful assessment, neck veins are not a reliable assessment in an infant. Drowsiness and fatigue are not reliable assessments for dehydration.

How do clinical conditions that increase vascular permeability cause edema? a. Through altering the negative charge on the capillary basement membrane, which enables excessive fluid to accumulate in the interstitial compartment b. By causing movement of fluid from the vascular compartment into the intracellular compartment, which leads to cell swelling c. Through leakage of vascular fluid into the interstitial fluid, which increases interstitial fluid hydrostatic pressure d. By allowing plasma proteins to leak into the interstitial fluid, which draws in excess fluid by increasing the interstitial fluid osmotic pressure

ANS: D Clinical conditions that increase vascular permeability cause edema by allowing plasma proteins to leak into the interstitial fluid, which draws in excess fluid by increasing the interstitial fluid osmotic pressure. The capillary basement membrane does not change its charge with increased vascular permeability. Increased vascular permeability does not move water into the cells. Increasing the interstitial fluid osmotic pressure would not cause edema.

Osmoreceptors located in the hypothalamus control the release of a. angiotensin. b. atrial natriuretic peptide. c. aldosterone. d. vasopressin (antidiuretic hormone, ADH).

ANS: D Factors that increase secretion of ADH into the blood include increased osmolality of the blood, which is sensed by osmoreceptors in the hypothalamus. Release of angiotensin, atrial natriuretic peptide, and aldosterone is not controlled by osmoreceptors in the hypothalamus.

Two primary acid-base disorders that are present independently are referred to as a. metabolic acidosis. b. metabolic alkalosis. c. respiratory alkalosis. d. mixed acid-base imbalance.

ANS: D Mixed acid-base disorders occur when two primary acid-base disorders are present independently. They may arise from simultaneous dysfunction of the respiratory system and kidneys. Metabolic acidosis is an acid disorder. Metabolic alkalosis and respiratory alkalosis are base disorders.