[Exam 2] Chapter 13: Fluid and Electrolytes: Balance and Disturbances (Page 283-288) Flashcards Preview

NRSG 110: Med Surg 2 > [Exam 2] Chapter 13: Fluid and Electrolytes: Balance and Disturbances (Page 283-288) > Flashcards

Flashcards in [Exam 2] Chapter 13: Fluid and Electrolytes: Balance and Disturbances (Page 283-288) Deck (134)
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1
Q

Acid-Base Disturbances: What is plasma pH?

A

An indicator of hydrogen ion (H+) concentration and measures the acidity of alkalinity of the blood

2
Q

Acid-Base Disturbances: Normal plasma pH?

A

7.35 - 7.45

3
Q

Acid-Base Disturbances: The greater the concentration of H+, the more…

A

acidic the solution and the lower the Ph.

4
Q

Acid-Base Disturbances: The lower the H+ concentration, the more

A

alkaline the solution and the higher the pH.

5
Q

Acid-Base Disturbances: The hydrogen ions are buffered by

A

both intracellular and extracellular buffers.

6
Q

Acid-Base Disturbances: Major extracellular buffer system is , and is assessed when?

A

Bicarbonate-carbonic acid buffer system,

And assessed when arterial blood gasses are measures

7
Q

Acid-Base Disturbances: Normally, what is the pare of bicarbonate to carbonic acid?

A

20 Pair to 1 Pair.

If altered, pH will change.

8
Q

Acid-Base Disturbances: CO2 is a potential acid, when dissolved in water it becomes

A

carbonic acid.

9
Q

Acid-Base Disturbances: When CO2 is increased, what also happens?

A

Carbonic acid content is also increased. and vice versa.

10
Q

Acid-Base Disturbances: What happens if either bicarbonate or carbonic acid is increased or decreased?

A

20:1 ratio is no longer maintained , and acid-base imbalance results

11
Q

Acid-Base Disturbances: Less important buffer systems in the ECF include

A

inorganic phosphates and plasma proteins

12
Q

Acid-Base Disturbances: Intracellular buffers include

A

proteins, organic, and inorganic phosphates and in RBCs, hemoglobin

13
Q

Acid-Base Disturbances: What do the kidneys regulate?

A

Bicarbonate level in the ECF. , and can regenerate bicarbonate ions as well as reabsorb them from the renal tubular cells

14
Q

In respiratory acidosis, what do the kidneys do?

A

Kidneys excrete hydrogen ions and conserve bicarbonate ions to help restore balance.

15
Q

Acid-Base Disturbances: What do the kidneys do in respiratory alkalosis?

A

Kidneys retain hydrogen ions and excrete bicarbonate ions to help restore balance.

16
Q

Acid-Base Disturbances: What do the lungs do for disturbances?

A

Lungs, under the control of medulla, control the CO2 and this the carbonic acid content of the ECF.

Do so by adjusting ventilation in response to amount of CO2 in the blood

17
Q

Acid-Base Disturbances: Rise in the partial pressure of CO2 in arterial blood is a powerful stimulant of

A

respiration.

18
Q

Acid-Base Disturbances: What happens to the respiratory system in metabolic acidosis?

A

Respiratory rate increases, causing greater elimination of CO2

19
Q

Acid-Base Disturbances: What happens to the respiratory system in metabolic alkalosis?

A

Respiratory rate decreases, causing CO2 to be retained (to increase acid load)

20
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit): Metabolic acidosis is a common clinical disturbance characterized by a low

A

pH (Increased H+ concentration) and low plasma bicarbonate concentration

21
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit): This is produced by

A

a gain of hydrogen ions or a loss of bicarbonate

22
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit): Can be divided into what two forms?

A

High anion gap acidosis and normal anion gap acidosis

23
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit): Anion gap refers to

A

the difference between the sums of all measured positively charged electrolytes (cations) and the sum of all negatively charged electroytes (anions) in blood.

Because cations usually are more, there is usually a gap

24
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit): Anion gap equations

A

Anion Gap = Na + K - (Cl + HCO3)

or

Na - (Cl + HCO3)

Potassium often omitted, so 2nd equation is used more often than the first

25
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit): Normal value for anion group without Potassium is

A

8-12 mEq/L

26
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit): Anion gap range is potassium is included?

A

12-16 mEq/L

27
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit): How much do the unmeasures anions in the serum account for?

A

16 mEq/L or less

28
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit): Person is diagnosed with metabolic acidosis is determined to have normal anion gap normal anion gap metabolic acidosis if the anion gap is in what range?

A

W/O Potassium, 8-12

W Potassium , 12-16

29
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit): An anion gap greater than 16 meQ suggests

A

excessive accumulation of unmeasured anions and would indicate high anion gap metabolic acidosis as the type

30
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit): Why does an anion gap occur?

A

Because not all electrolytes are measured. More anions left unmeasured than cations

31
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit): Low or negative anion gap may be attributed to

A

hypoproteinemia

32
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit): Normal anion gap acidosis results from the direct loss of

A

bicarbonate, as in diarrhea, lower intestinal fistulas, ureterostomies, and use of diretics

REnal insufficiency

Excessive administration of chloride

33
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit): Normal anion gap acidosis is referred to as

A

hypercholermic acidosis

34
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit): High anion gap acidosis results from

A

excessive accumulation of fixed acid

35
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit): IF increased to 30 mEq or more, than high anion gap metabolic acidosis is preseent regardless of

A

values of pH and HCO3.

36
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit): High anion gap occurs in

A

ketoacidosis, lactic acidosis, and late phase of salicylate positioning.

37
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit): In high anion gap, the hydrogen is buffered by HCO3 causing

A

the bicarbonate concentration to fall.

38
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit): Metabolic acidosis is characterized by

A

a low pH and low plasma bicarbonate concentration

39
Q

Reduced or Negative Anion Gap without potassium range?

A

<8

40
Q

Reduced or negative anion gap with potassium?

A

> 12

41
Q

Reduced or negaive anion gap clinical significance ?

A

Hypoproteinemia

42
Q

Normal Anion Gap without Potassium range?

A

8-12

43
Q

Normal Anion Gap with Potassium range?

A

12-16

44
Q

Normal Anion Gap Clinical Significance

A

Normal anion gap metabolic acidosis

45
Q

High Anion Gap Without Potassium?

A

> 12

46
Q

High Anion Gap with Potassium?

A

> 16

47
Q

High Anion Gap CLinical Significance?

A

High anion gap metabolic ACidosis

48
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit), Clinical Manifestations: Signs include

A

headache, confusion, drowsiness, increased respiratory rate and depth, N/V.

49
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit), Clinical Manifestations: When does peripheral vasodilation and decreased cardiac output occur?

A

When pH drops to less than 7

50
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit), Clinical Manifestations: Physical assessment findings include

A

decreased blood pressure, cold and clammy skin, dysrhythmias, and shock

51
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit), Clinical Manifestations: Chronic acidosis is usually seen in those with

A

kidney disease

52
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit), Assessment and Diagnostic Findings: What is valueable in diagnosing metabolic acidosis?

A

Arterial blood gas measurements

53
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit), Assessment and Diagnostic Findings: Expected blood gas changes?

A

Low Bicarb Level (<22 mEq)

Low pH (Less than 7.35)

54
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit), Assessment and Diagnostic Findings: Cardinal feature of metabolic acidosis is

A

decrease in serum bicarbonate level, with hyperkalemia potentially following as well due to potassium leaving the cells

55
Q

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit), Assessment and Diagnostic Findings: Why are low seurm calcium levels treated before chronic metabolic acidosis?

A

Treated to avoid tetany resulting from an increase in pH and decrease in ionized calcium

56
Q

Acute and Chronic Metabolic Alkalosis (Base Bicarbonate Excess): What is this?

A

Clinical disturbance characterized by a high pH (decreased h+ concentration adna high plasma bicarbonate concentration

57
Q

Acute and Chronic Metabolic Alkalosis (Base Bicarbonate Excess), Patho: A common cause is

A

vomiting or gastric suction with loss of hydrogen and chloride ions The gastric fluid loss would increase the alkalinity of body fluids

58
Q

Acute and Chronic Metabolic Alkalosis (Base Bicarbonate Excess), Patho: Hypokalemia produces alkalosis in what two ways?

A

Kidneys conserve potassium, and therefore H+ excretion increases

  1. CEllular potassium moves out of the cell into the ECFin attempt to maintain near normal serum levels
59
Q

Acute and Chronic Metabolic Alkalosis (Base Bicarbonate Excess), Patho: Chronic metabolic alkalosis can occur with

A

long-term diuretic therapy, villous adenoma, external drainage of gastric fluids, or significant potassium depletion

60
Q

Acute and Chronic Metabolic Alkalosis (Base Bicarbonate Excess), Clinical: Primarily manifested by symptoms related to decreased calcium ionization, such as

A

tingling of the fingers and toes, dizzinenss, and hypertonic muscles.

Calcium decreased because it combines with serum proteins

61
Q

Acute and Chronic Metabolic Alkalosis (Base Bicarbonate Excess), Clinical: Predominant symptom of alkalosis?

A

Signs and symptoms of hypocalcemia. This includes decreased respiration and atrial tachycardia.

62
Q

Acute and Chronic Metabolic Alkalosis (Base Bicarbonate Excess), Clinical: Signs of chornic metabolic alkalosis include

A

Same as acute mtabolic alkalosis, potassium decreases, and U waves being seen

63
Q

Acute and Chronic Metabolic Alkalosis (Base Bicarbonate Excess), Assessment and Diagnostic Findings: Arterial blood gasses reveal what?

A

pH greater than 7. 45 and a serum bicarbonate concentration greater than 26 mEq.

64
Q

Acute and Chronic Metabolic Alkalosis (Base Bicarbonate Excess), Assessment and Diagnostic Findings: PaCO2 increases as the lungs attempt to compensate for

A

the excess bicarbonate by retaining CO2. This results in hypoventilation which may lead to hypoxemia.

65
Q

Acute and Chronic Metabolic Alkalosis (Base Bicarbonate Excess), Assessment and Diagnostic Findings: Urine Chloride Levels are useful why?

A

MAy be more accurate estimate of fluid volume than urine sodium concentration.

Help to differentiate between vomiting, diuretic therapy, and excessive adrenocorticosteroiod secretions

66
Q

Acute and Chronic Metabolic Alkalosis (Base Bicarbonate Excess), Assessment and Diagnostic Findings: Those with vomiting or cystic fibrosis, nutritional replacement, or those recieving diuretic therapy shw a urine chloride of what

A

Lower than 25 mEq

67
Q

Acute and Chronic Metabolic Alkalosis (Base Bicarbonate Excess), Assessment and Diagnostic Findings: Urine Chloride values when patient as mineralcorticoid excess or alkali loading?

A

Hypovolemia not present, and concentration for Urine Chloride greater than 40.

Normal value should be less than 15

68
Q

Acute and Chronic Metabolic Alkalosis (Base Bicarbonate Excess), Medical Management: Why must I/O be monitored?

A

Because of volume depletion from GI loss,

69
Q

Acute and Chronic Metabolic Alkalosis (Base Bicarbonate Excess), Medical Management: Sufficient chloride must be available for the kidney why?

A

To absorb sodium with chlorice (allowing excretion of excess bicarbonate)

70
Q

Acute and Chronic Metabolic Alkalosis (Base Bicarbonate Excess), Medical Management: Treatment includes

A

restoring normal fluid volume by administering sodium chloride fluids

71
Q

Normal pH range?

A

7.35 - (7.4) - 7.45

72
Q

Normal PaCO2 range?

A

35 - (40) - 45 mm Hg

73
Q

Normal HCO3 range?

A

22 - (24) - 26 mEq/L

74
Q

Normal PaO2 range?

A

80 - 100 mm Hg

75
Q

Normal Oxygen Saturation level?

A

> 94%

76
Q

Acute and Chronic Respiratory Acidosis (Carbonic Acid Excess) : What is this?

A

Clinical disorder when pH is less than 7.35 and PaCO2 is greater than 42 mm Hg and a compensatory increase in the plasma HCO3 occurs. Either acute or chronic

77
Q

Acute and Chronic Respiratory Acidosis (Carbonic Acid Excess) , Patho: What is this always due to?

A

Inadequate excretion of CO2, with inadequate ventilation resulting in elevated plasma CO2 concentrations and increased levels of carbonic acid

78
Q

Acute and Chronic Respiratory Acidosis (Carbonic Acid Excess) , Patho: This occurs in emergency situations, such as

A

acute pulmonary edema, aspiration, pneumothorax, and overdose of sedatives

79
Q

Acute and Chronic Respiratory Acidosis (Carbonic Acid Excess) , Clinical Manifestations: Sudden increases in PaCO2 can cause

A

increased pulse and RR, increased BP, mental cloudiness, or confusion, and a feeling of fullness in the head.

80
Q

Acute and Chronic Respiratory Acidosis (Carbonic Acid Excess) , Clinical Manifestations: First sign in anesthetized patients?

A

Ventricular fibrillation

81
Q

Acute and Chronic Respiratory Acidosis (Carbonic Acid Excess) , Clinical Manifestations: Signs of this is severe?

A

Intracranial pressure may increase, resulting in papilledema, dilated conjunctival blood vessels.

82
Q

Acute and Chronic Respiratory Acidosis (Carbonic Acid Excess) , Clinical Manifestations: Chronic occurs in what diseases?

A

Pulmonary diseases such as chronic emphysema and chronchitis . sleep apnea, and obesity

83
Q

Acute and Chronic Respiratory Acidosis (Carbonic Acid Excess) , Clinical Manifestations: If PaCO2 increases rapidly, what happens??

A

Cerebral vasodilation will increase the intracranial pressure and cyanosis and tachypnea will develop

84
Q

Acute and Chronic Respiratory Acidosis (Carbonic Acid Excess) , Assessment and Diagnostic Findings: Arteriral blood gas analysis reveals pH and PaCO2 to be?

A

7.35 and PaCO2 greater than 42 mmHg

85
Q

Acute and Chronic Respiratory Acidosis (Carbonic Acid Excess) , Assessment and Diagnostic Findings: OTher diagnostic measures include

A

monitoring of serum electrolyte levels, chest x-ray for deterining respiratory disease, adn screening to see if overdose suspected

86
Q

Acute and Chronic Respiratory Acidosis (Carbonic Acid Excess) , Treatment: Treatment directed at and may include

A

Improving ventilation, and pharmacologic agents are used as indicated such as bronchodilators

87
Q

Acute and Chronic Respiratory Acidosis (Carbonic Acid Excess) , Treatment: Whys is 2/3 L of water recommended?

A

To keep the mucous membranes moist and thereby facilitate the removal of secretions

88
Q

Acute and Chronic Respiratory Acidosis (Carbonic Acid Excess) , Treatment: Inapprorpaite mechanical ventilation is a problem because

A

it may cause rapid excretion of CO2 and that the kidneys are unable to eliminate excess bicarbonate quickly enough to prevent alkalosis and seizures

89
Q

Acute and Chronic Respiratory Alkalosis (Carbonic Acid Deficit):What is this?

A

pH is greater than 7.45 and PaCO2 is less than 38 mmHg

90
Q

Acute and Chronic Respiratory Alkalosis (Carbonic Acid Deficit), Patho: Always caused by

A

hyperventilation, which causes excessive “blowing off” of CO2 and hence a decrease in the plasma carbonic acid concentration

91
Q

Acute and Chronic Respiratory Alkalosis (Carbonic Acid Deficit), Patho: Causes include

A

extreme anxiety, hypoxemia, early phase of salicylate intoxication, and gram negativef bacteremia.

92
Q

Acute and Chronic Respiratory Alkalosis (Carbonic Acid Deficit), Patho: Chronic respiratory alkalosis results form

A

chronic hypocapnia, and decreased serum bicarbonate levels are teh consequence

93
Q

Acute and Chronic Respiratory Alkalosis (Carbonic Acid Deficit), Clinical Manifesatations: Signs consist of

A

lightheadedness due to vasoconstriction and decresed cerebral blood flow, inability to concentrate, numbness and tingless from decreased calcium, tinnitus, and someitmes loss of consciousness.

94
Q

Acute and Chronic Respiratory Alkalosis (Carbonic Acid Deficit), Assessment and Diagnostic Findings: How is this diagnosed?

A

Analysis of arterial blood gases.

95
Q

Acute and Chronic Respiratory Alkalosis (Carbonic Acid Deficit), Assessment and Diagnostic Findings: In the acute state, the pH is elevated above normal because of

A

low PaCO2 and a normal bicarbonate level.

96
Q

Acute and Chronic Respiratory Alkalosis (Carbonic Acid Deficit), Assessment and Diagnostic Findings: In the compensated state, kidneys had sufficient time to lower

A

bicarbonate level to a near-normal level

97
Q

Acute and Chronic Respiratory Alkalosis (Carbonic Acid Deficit), Medical Managemen: If cause is due to anxiety, what must be done?

A

Patient is instructed to breathe more slowly to allow CO2 to accumulate or to breathe into a closed system. Antianxiety agent may be required to relieve hyperventilation

98
Q

Mixed Acid-base Disorders: Example of a mixed disorder is

A

the simultaneous occurence of metabolic acidosis and respiratory acidosis durign respiratory and cardiac arrest

99
Q

Mixed Acid-base Disorders: What mixed disorder cannot occur?

A

Mixed respiratory acidosis and alkalosis, because you cannot have hypoventilation and hyperventilation at the same time

100
Q

Mixed Acid-base Disorders, Compensation: What compensates for each other to return pH to normal ?

A

Pulmonary and Renal Systems

101
Q

Mixed Acid-base Disorders, Compensation: What does the body do in a single base disorder to compensate?

A

Tries to compensate by returning the ratio of bicarbonate to carbonic acid to the normal 20:1

102
Q

Mixed Acid-base Disorders, Compensation: How do lungs compensate for metabolic disturbances?

A

Changing CO2 excretion

103
Q

Mixed Acid-base Disorders, Compensation: How do the kidneys compensate for dysfunctions?

A

by altering bicarbonate retention and H+ secretions

104
Q

Mixed Acid-base Disorders, Compensation: How to compensate in respiratory acidosis?

A

Excess hydrogen is excreted in exchange for bicarbonte ions

105
Q

Mixed Acid-base Disorders, Compensation: How does the body compensate for respiratory alkalosis?

A

The renal excretion of bicarbonate increases and hydrogen ions retained

106
Q

Mixed Acid-base Disorders, Compensation: How does the body compensate for metabolic acidosis?

A

Compensatory mechanisms increase the ventilation rate and the renal retention of bicarbonate.

107
Q

Mixed Acid-base Disorders, Compensation: How does the body compensate for metabolic alkalosis?

A

Respiratory systme compensates by decreasing ventilation to conserve CO2 and increase the PaCO2

108
Q

Mixed Acid-base Disorders, Compensation: Does compensation for metabolic imbalances or respiratory imablances work faster?

A

Metabolic imbalances

109
Q

Blood Gas Analysis: Why is this used?

A

Often used to identify the specific-acid base disturabance and the degree of compensation that has occured

110
Q

Blood Gas Analysis: BLood sample usually based on

A

an arterial blood sample

111
Q

Blood Gas Analysis: Results of arterial blood gas analysis provide information about

A

alveolar ventilation, oxygenation, and acid-base balance

112
Q

Blood Gas Analysis: What must you evaluate in the sample?

A

Electrolytes (Na, K, Cl) and CO2

113
Q

Metabolic Acidosis, Primary Disturbance

A

Decrease in pH

HCO3 < 22 mEq.

114
Q

Metabolic Acidosis, Respiratory Compensation and Predicted Response

A

Increase Ventilation anddecrease of PCO2

115
Q

Metabolic Alkalosis, Primary Disturbances

A

Increase pH and HCO3 > 26 mEq

116
Q

Metabolic Alkalosis, Respiratory Compensation and Predicted Response

A

Decrease ventilation and increased PCO2

117
Q

Metabolic Alkalosis, Renal Compensation and Predicted Response

A

Decreased H+ excretion and Decreased HCO3 reabsorption if no renal disease

118
Q

Respiratory Acidosis, Primary Disturbance

A

DEcrease pH and Increased PCO2 > 45 mmHg

119
Q

Respiratory Acidosis, Respiratory Compensation and Predicated Response

A

None

120
Q

Respiratory Acidosis, Renal Compensation and Predicted Response

A

Increased H+ excretion and Increased HCO3 reabsorption

121
Q

Respiratory Alkalosis, Primary Disturbance

A

Increased pH and decreased PCO2 < 35 mm Hg

122
Q

Respiratory Alkalosis, Respiratory Compensation and Predicted Response

A

None

123
Q

Respiratory Alkalosis, Renal Compensation and PRedicted REsponse

A

DEcreased H+ excretion and Decreased HCO3 reabsorption

124
Q

Normal Value of Arterial Blood, pH

A

7.35 - 7.45

125
Q

Normal Value of Arterial Blood, PCO2

A

35-45 mmHg

126
Q

Normal Value of Arterial Blood, PO2

A

> 80 mmHg

127
Q

Normal Value of Arterial Blood, HCO3

A

22-26

128
Q

Normal Value of Arterial Blood, Base Excess/Deficit

A

+2 mEq

129
Q

Normal Value of Mixed Venous BLood, pH

A

7.32-7.42

130
Q

Normal Value of Mixed Venous BLood, PCO2

A

38-52

131
Q

Normal Value of Mixed Venous BLood, PO2

A

24-48

132
Q

Normal Value of Mixed Venous BLood, HCO3

A

19-25

133
Q

Normal Value of Mixed Venous BLood, Base Excess/Deficit

A

+5 mEq

134
Q

Normal Value of Mixed Venous BLood, Oxygen Saturation

A

65-75 %

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