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Pathophysiology > 5. Fluid, Electrolyte, and Acid-Base Balance > Flashcards

5. Fluid, Electrolyte, and Acid-Base Balance Flashcards

1
Q

60-40-20 rule

A
  • 60% of body weight = total body weight (TBW) - 40% of body weight = intracellular fluid (ICF) - 20% of body weight = extracellular fluid (ECF)
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2
Q

What is ECF composed of?

A
  • interstitial fluid (spaces between cells) - intravascular - lymphatics - transcellular (joint, intraocular, and CSF)
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3
Q

Describe whether each electrolyte is found more in ICF or ECF - Na - Cl - Ca - K - Mg

A
  • Na = ECF - Cl = ECF - Ca = ECF - K = ICF - Mg = ICF
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4
Q

1L of water weighs how much?

A

1kg or 2.2 lbs

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5
Q

Hydrostatic vs osmotic/oncotic pressure

A
  • hydrostatic: fluid pushed out of space due to pressure against walls - osmotic/oncotic: proteins pull/attract water back into space
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6
Q

4 factors in fluid homeostasis

A
  • intake - absorption - distribution - excretion
  1. intake
  2. absorption
    3.
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7
Q

Describe each of the following: - capillary hydrostatic pressure - capillary oncotic pressure - interstitial hydrostatic pressure - interstitial oncotic pressure

A
  • capillary hydrostatic pressure: pushing force of water out of vessels into interstitial space - capillary oncotic pressure: attraction of water from interstitial space into vessels - interstitial hydrostatic pressure: pushing of water from interstitial space into vessels - interstitial oncotic pressure: attraction of water from vessels into interstitial space
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8
Q

What type of pressure is blood pressure?

A

capillary hydrostatic pressure -> pushing against the vessels

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9
Q

What forces favor filtration?

A

capillary hydrostatic pressure and interstitial oncotic pressure -> both move water out of vessels

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10
Q

What forces oppose filtration?

A

capillary oncotic pressure and interstitial hydrostatic pressure -> both move water into vessels

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11
Q

Name 4 factors in the absorption of fluid

A
  • ADH - RAAS - ANP - renal function
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12
Q

What primarily regulates water balance?

A

antidiuretic hormone (ADH); aka vasopressin

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13
Q

Describe the steps of the ADH system

A
  • increase in plasma osmolarity or decrease in fluid volume -> ADH secretion (hypothalamus/ p. pituitary) -> decreased water excretion and increased renal water retention -> increased circulating fluid volume -> decreased osmolarity -> decreased ADH
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14
Q

What is another method the body uses to raise fluid volume or decrease plasma osmolarity other than ADH?

A

thirst -> increase fluid intake

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15
Q

What does RAAS stand for?

A

Renin-Angiotensin-Aldosterone System

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16
Q

Describe the RAAS system

A

decreased renal perfusion (decreased plasma volume) -> renin secreted -> Ang I -> Ang II -> ADH (water absorption) and Aldosterone (salt reabsorption) -> increased blood volume

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17
Q

What secretes renin and when?

A

juxtaglomerular cells when BP is low

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18
Q

What converts angiotensin I to angiotensin II and where?

A

angiotensin-converting enzyme (ACE) in the pulmonary vessels

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19
Q

What releases aldosterone and what stimulates it release?

A

released from the adrenal cortex; stimulated by Ang II or directly by increased plasma K

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20
Q

What produces ANP and BNP?

A

ANP: atria BNP: ventricles

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21
Q

What causes production of ANP and BNP?

A

cardiac distention (ECF volume increased, Na and H2O retention, increased BP)

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22
Q

What will ANP and BNP do?

A
  • decrease RAAS - increase GFR - increase Na and water excretion (natriuresis and diuresis) - vasodilation (decrease BP)
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23
Q

3 lab tests used to measure renal function

A
  • GFR - serum creatinine - serum BUN
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24
Q

What is the minimum normal urine output?

A

30 mL/hr

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25
Q

Normal blood osmolarity

A

275-295 mosm/Kg

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26
Q

high serum osmolarity means what?

A

too many particles compared to plasma -> dehydration

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27
Q

low serum osmolarity means what?

A

not enough particles compared to plasma -> overload of fluid

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28
Q

high urine osmolarity means what?

A

concentrated urine -> dehydration

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29
Q

What is responsible for the ECF water balance

A

Na

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30
Q

What will isotonic IV solution do?

A

remain in vessels -> add to blood volume

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31
Q

Ex of isotonic IV solution

A

normal saline or 0.9% NaCl

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32
Q

What will hypertonic IV solution do?

A

contains high Na -> will pull fluid from cells into vessels (useful in cerebral edema)

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33
Q

Ex of hypertonic IV solution

A

3-5% normal saline

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34
Q

What will hypotonic IV solution do?

A

contains low Na -> fluid will be pulled into the tissues from the vessels

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35
Q

Ex of hypotonic IV solution

A

0.45% normal saline

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36
Q

What will happen to a cell in the following solutions: isotonic, hypotonic, hypertonic?

A
  • isotonic: equal movement of water in and out of cell - hypotonic: less concentration in fluid -> fluid moves into cell -> cell ruptures - hypertonic: more concentration in fluid -> fluid moves out of cell -> cell shrinks
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37
Q

What does filtration depend on (4)?

A
  • normal serum albumin/protein - normal fluid level - normal heart function - normal BP = controlled peripheral vascular resistance (PVR)
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38
Q

Explain how fluid moves in the arterial and venous sides of circulation

A
  • arterial side of capillary: hydrostatic pressure greater than oncotic pressure -> fluid moves to interstitial space - venous side of capillary: oncotic pressure in capillary greater than hydrostatic pressure -> fluid moves into circulation
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39
Q

Pathophysiology of edema (3)

A
  • increased capillary permeability (proteins moves to interstitial space) - low levels of serum proteins - hydrostatic pressures increased due to venous obstruction, Na or water retention
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40
Q

list some causes of edema

A
  • CHF - liver and renal failure - venous or lymphatic obstruction - inflammation - malnutrition - trauma/tissue injury
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41
Q

edema limited to site of trauma

A

local edema

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42
Q

edema over a larger area of the body due to liver or renal failure

A

generalized edema

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43
Q

Describe third spacing and 3 places it can occur. What is the most common cause?

A
  • too much fluid shifts to a nonfunctional area - can occur in an interstitial space, pleural space, or pericardial space - most commonly due to burns
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44
Q

Non-pitting vs pitting edema

A
  • Non-pitting: swollen cells due to increased ICF volume - Pitting: increased interstitial fluid volume
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45
Q

T/F: A loss or gain of saline affects the volume of both ICF and ECF

A

False; saline is confined to the extracellular compartment -> does not affect volume of the intracellular compartment

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46
Q

Causes of isotonic fluid loss

A
  • hemorrhage - wound drainage - severe diaphoresis - hyposecretion of aldosterone
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47
Q

How does serum Na change in isotonic fluid loss and excess

A

will see Normal serum Na

48
Q

Clinical presentation of isotonic fluid loss

A
  • orthostatic hypotension - tachycardia - weight loss - decreased skin turgor and slow capillary refill - low urine output - hypovolemic shock
49
Q

Clinical presentation of isotonic fluid excess

A
  • hypertension - weight gain - edema - signs of CHF - may have increased urine output
50
Q

Causes of isotonic fluid excess

A
  • fluid excess of IV solution - hypersecretion of aldosterone
51
Q

Tx of isotonic fluid excess

A
  • diuretics - reduce rate of isotonic fluid administration - investigate: what is kidney function?
52
Q

Cause of hyponatremia

A
  • excessive hypotonic IV - excess water intake (includes psychogenic polydipsia, tap water enemas, and NG irrigation) - vomiting/diarrhea - fresh water drowning - SIADH
53
Q

occurs when there is a loss of Na without a significant loss of water (pure Na deficit)

A

isovolemic hyponatremia

54
Q

occurs when total body Na level increases -> leads to increase in TBW and dilution of Na in extracellular space

A

hypervolemic hyponatremia

55
Q

occurs w/ a loss of TBW but there is a greater loss of Na; extracellular volume is decreased

A

hypovolemic hyponatremia

56
Q

occurs when there is intake of large amounts of free water or replacement of fluid loss w/ IV 5% dextrose in water (dilutes Na)

A

dilution hyponatremia (water intoxication)

57
Q

What will happen to serum Na and cells with hyponatremia?

A

low serum Na and cellular swelling

58
Q

Clinical presentation of hyponatremia and why?

A
  • confusion, lethargy, coma - headache, weight gain - nausea - seizure, weakness, muscle twitching - decrease in Na concentration changes the cell’s ability to depolarize and repolarize normally -> alters APs of neurons and muscles - will also see cerebral edema (causes many neurological changes)
59
Q

Most important way to determine if someone is retaining fluid or losing fluid

A

Daily weights

60
Q

Normal Na level

A

135-145 mEq/L

61
Q

Causes of hypernatremia

A
  • chronic diarrhea, vomiting and fever (water loss) - no access to water (decreased thirst) - diabetes insipidus - drowning in salt water - tube feedings - diaphoresis and diuresis - primary hyperladosteronism - Cushing syndrome
62
Q

What will happen to serum Na with hypernatremia?

A

elevated serum Na

63
Q

clinical manifestations of hypernatremia and why?

A
  • confusion, lethargy, coma - seizure - fever - dry mucous membranes - hyperreflexia - pulmonary edema - CNS signs due to brain cells shrinking and Na can’t cross BBB; also due to alterations in membrane potential
64
Q

occurs w/ loss of free water and near normal body Na concentration

A

isovolemic hypernatremia

65
Q

occurs where there is loss of Na accompanied by a greater loss of body water

A

hypovolemic hypernatremia

66
Q

rare and occurs when there is increased TBW and greater increase in total body Na level

A

hypervolemic hypernatremia

67
Q

normal K levels

A

3.5-5.0 mEq/L

68
Q

4 factors that enhance cellular uptake of K

A
  • insulin - epinephrine - aldosterone - alkalosis (K is lo)
69
Q

4 factors that enhance K release

A
  • acidosis (H+ takes over cells) - cell lysis - strenuous excersice - increased ECF osmolarity
70
Q

causes of hyperkalemia

A
  • excess K intake - diuretics - large blood transfusions - decreased renal excretion - Addison’s disease (decreased aldosterone) - crush injuries and burns (cell lysis)
71
Q

Clinical signs of hyperkalemia

A
  • muscle weakness/paralysis - cardiac dysrhythmias/arrest - hypopolarization (lowering) of RMP (easier to excite) - anxiety, numbness/tingling, N/V/D
72
Q

EKG signs of hyperkalemia

A
  • flattened P wave - prolonged PR interval - tall, peaked, T wave - bradycardia
73
Q

Causes of hypokalemia

A
  • anorexia or NPO - diuretics - V/D - NG suction - intestinal drainage
74
Q

Clinical signs of hypokalemia

A
  • hyperpolarization (increasing) of RMP - muscle weakness/paralysis - paralytic ileus - dysrhythmias
75
Q

EKG signs of hypokalemia

A
  • sinus bradycardia - ventricular tachycardia - AV block - low T wave
76
Q

Normal total Ca level

A

9-11 mg/dL

77
Q

Normal ionized Ca level

A

4.5-6 mEq/L

78
Q

Causes of hypercalcemia

A
  • hyperparathyroidism (increased PTH secretion) - immobilization (stimulation breakdown of bones) - leukemia - diuretics
79
Q

Clinical signs of hypercalcemia

A
  • weakness and CNS depression - decreased NM excitability
80
Q

Causes of hypocalcemia

A
  • dietary deficiency (vitamin D) - laxative abuse - diarrhea - pancreatitis - malabsorption
81
Q

Clinical signs of hypocalcemia

A
  • cramps and seizures - increased NM excitability
82
Q

What is trousseau sign

A
  • identifies hypocalcemia - inflate BP cuff on arm and will see flexion at wrist (carpal spasm)
83
Q

What is Chovstek sign

A
  • identifies hypocalcemia - tap the facial nerve anterior to the ear to elicit ipsilateral facial contraction
84
Q

Normal Mg level

A

1.5-2.5 mEq/L

85
Q

causes of hypermagnesemia

A

laxatives and antacids

86
Q

Clinical signs of hypermagnesemia

A
  • decreased reflexes - muscle weakness - drowsiness - respiratory depression - cardiac arrhythmias
87
Q

causes of hypomagnesemia

A

alcoholism, poor nutrition, and malabsorption

88
Q

Clinical signs of hypomagnesemia

A
  • muscle cramps/spasm - tetany - seizures - hyperactive reflexes - cardiac arrhythmias
89
Q

Normal Pi levels

A

2.5-4.5 mg/dL

90
Q

causes of hypophosphatemia

A
  • alcoholism - malabsorption - diarrhea - DKA - diuretics - antacids - dialysis
91
Q

Clinical signs of hypophosphatemia

A
  • anorexia - malaise - paresthesias - muscle weakness - decreased reflexes - confusion - impaired cardiac function
92
Q

causes of hyperphosphatemia

A
  • phosphate containing enemas - crushing injury - adrenal insufficiency - hypoparathyroid disease
93
Q

Clinical signs of hyperphosphatemia

A
  • increased NM excitability - Ca deposits in body tissues - hypocalcemia
94
Q

Which electrolyte imbalances will cause weakness/poor muscle tone?

A
  • hyperkalemia - hypokalemia - hypercalcemia - hypermagnesemia
95
Q

Which electrolyte imbalances will cause twitchy/crampy muscles?

A
  • hypocalcemia - hypomagnesemia
96
Q

Major plasma buffer system

A

carbonic acid (weak acid) H20 + CO2 -> H2CO3 -> HCO3 + H+

97
Q

How are CO2 and H2O produced and removed?

A

produced by aerobic metabolism; blown off by lungs

98
Q

How are HCO3 and H+ produced and removed?

A

produced by anaerobic metabolism; regulated by kidneys

99
Q

How does Hb act as an intracellular blood buffer?

A

binds with H+ and CO2

100
Q

What acts as buffers in ICF?

A

phosphate and proteins

101
Q

Normal blood pH

102
Q

Normal blood PaCO2

A

35-45 mmHg

103
Q

Normal blood HCO3 (bicarb)

A

22-26 mEq/L

104
Q

causes of metabolic acidosis

A
  • loss of base or addition of acid - DKA - lactic acidosis - EtOH poisoning
105
Q

What is the compensation of metabolic acidosis?

A

hyperventilation (respiratory compensation) -> excrete more CO2

106
Q

Clinical presentation of metabolic acidosis

A
  • N/V/D - confusion/coma - Kussmaul breathing (deep and rapid)
107
Q

causes of metabolic alkalosis

A
  • addition of base or loss of acid - vomiting (loss of acid) - antacid tablets (gain HCO3) - diuretics (volume contraction)
108
Q

What is the compensation of metabolic alkalosis?

A

hypoventilation (respiratory compensation) -> retain more CO2

109
Q

Clinical presentation of metabolic alkalosis

A
  • increased NM irritability - tetany - seizures - confusion - lethargy - coma
110
Q

Respiratory acidosis compensation

A

decreased ventilation -> CO2 goes up -> kidneys increase HCO2 regeneration and acid excretion

111
Q

causes of respiratory acidosis

A

CNS depression, airway obstruction, pneumonia, PE, COPD

112
Q

Clinical presentation of respiratory acidosis

A
  • headache - lethargy - confusion - tremors/seizures - cardiac arrhythmias
113
Q

Respiratory alkalosis cause and compensation

A

increased ventilation (hyperventilation) -> CO2 decreases -> kidneys decrease acid excretion

114
Q

Clinical presentation of respiratory alkalosis

A
  • diaphoresis - NM irritability - carpopedal spasms - tingling around fingers/mouth - seizures/coma
115
Q

What is the relationship between calcium and phosphate?

A

extracellular concentrations are inversely related -> both regulated by the same hormones

Pathophysiology (20 decks)

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