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ANPH 1105 > Week 1- Fluids, Electrolytes, Acid Base Status > Flashcards

Week 1- Fluids, Electrolytes, Acid Base Status Flashcards

1
Q

How much fluid is in:
1) a full-term baby?
2) Lean Adult Male?
3) Aged client?

A

1- 80%, 2- 60%, 3- 40%

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2
Q

What % of the body is solid vs Fluid?

A

40-45%, 55-60%

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3
Q

what portion of fluid is ECF vs ICF?

A

2/3 ICF
1/3 ECF

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4
Q

What % of ECF is interstitial fluid vs plasma?

A

IF- 80%, Plasma- 20%

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5
Q

what happens if there is more space between cells?

A

harder for glucose/ O2 etc. to go through, more space to travel

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6
Q

Compartments of ECF

A
  • Cerebrospinal fluid (surrounds brain and spine)
  • lymph
  • synovial fluid (joints, adds lubrication)
  • pleural fluid (protect lungs & heart)
  • peritoneal fluid (abdominal)
  • pericardial fluid (heart)
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7
Q

Functions of water in body?

A

1) solvent- dissolves salts + electrolytes
2) chemical reactant
3) lubricant
4) moderate temp changes
5) coolant: perspiration cools body

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8
Q

where does the most water GAIN come from?

A
  1. Ingested liquids
  2. Ingested foods
  3. metabolic water
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9
Q

where is the most water LOSS?

A
  1. Kidneys (pee)
  2. Skin (sweat)
  3. lungs (heat when you breathe out)
  4. GI tract
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10
Q

Sensible fluid losses

A

Measurable losses
- urination
- defecation
- wound drainage

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11
Q

Insensible fluid losses

A

Unmeasurable losses, require estimation for replacement
- Evaporation from skin
- Evaporation from breathing

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12
Q

paths of body fluid movement between body compartments? (2 beginnings)

A
  1. Arterial capillaries→ Interstitium→ cells
  2. Cells → interstitium → route A and B
    A→ lymphatics (~15%)
    B→ Venous capillaries (~85%)
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13
Q

2 Key factors of bulk flow

A
  1. Hydrostatic Pressure
  2. Osmotic Pressure
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14
Q

Hydrostatic Pressure

A
  • BP in capillaries from cardiac contraction
    → exerts outward force on walls of the vessels
    → movement of water out of capillaries
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15
Q

Osmosis

A
  • requires concentration gradient
  • diffusion of water across membrane from area of high to low concentration of water molecules
  • Applied pressure to raised side = osmotic pressure
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16
Q

Oncotic Pressure / Colloid osmotic pressure

A
  • osmotic pressure of a colloid in solution
  • caused by presence of large, charged, insoluble particles such as proteins
    • can not cross the semi-permeable membrane
  • particles draw water towards them
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17
Q

MAJOR factor of movement in interstitium and cells

A

differing ion concentrations btw these two compartments
- Na+/K+ pumps → Increase [Na+] outside cell
- Na+ tends to flow in → Na+ can be used to bring in other substances

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18
Q

Second factor of movement in interstitium and cells

A

cytosol contains large # of negatively charged ions (proteins and phosphates)
- positively charged substances then are attracted

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19
Q

4 regulatory Mechanisms

A
  1. Baroreceptors
  2. Volume receptors
  3. Renin-Angiotensin-aldosterone mechanism
  4. Antidiuretic hormone
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20
Q

Baroreceptor Reflex

A
  • Pressure sensors
  • Respond to fall in arterial BP
  • In atrial walls, vena cava, aortic arch and carotid sinus
  • constricts afferent arterioles of kidneys resulting in retention of fluid → sends less blood to kidneys, & holds onto more water
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21
Q

Volume Receptors

A
  • Respond to fluid excess in atria and great vessels
  • Stimulation of these receptors creates a strong renal response that increases urine output
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22
Q

Renin in RAAS

A
  • Enzyme secreted by kidneys when arterial pressure or volume drops
  • Interacts with angiotensinogen to angiotensin I (vasoconstrictor)
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23
Q

Angiotensin in RAAS

A
  • Angiotensin I converted in lungs to Angiotensin II using ACE
  • produces vasoconstriction to elevate BP
  • stimulates adrenal cortex to secrete aldosterone
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24
Q

Aldosterone in RAAS

A
  • mineralocorticoid that controls Na+ and K+ blood levels
  • Increases [Cl-] and [HCO3-] and fluid volume
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25
Q

Dehydration

A
  • Only water loss (hypotonic fluid loss)
  • Loss of body fluids→ increase conc. of solutes in blood and rise in serum Na+ levels
  • fluid shifts out of cells into blood to restore balance
  • cells shrink from fluids loss, no longer function properly
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26
Q

Hypovolemia

A
  • Isotonic fluid loss from the EC space
  • can progress to hypovolemic shock
  • caused by:
    • Ecessive fluid loss (hemorrhage)
    • decreased fluid intake/ not eating over time
    • third space fluid shifting
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27
Q

1st space? 2nd space? 3rd space?

A

1- blood
2- inside cell
3- interstition

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28
Q

Hypervolemia

A
  • excess fluid in EC compartment as result of fluid or Na retention, excessive intake, or renal failure
  • occurs when compensatory mechanisms fail to restore fluid balance
  • leads to congestive heart failure (CHF) and pulmonary edema
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29
Q

Edema

A
  • abnormal accumulation of IF
  • 4x causes
  • giving them fluid but can’t force it to stay where we want it
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30
Q

4 causes of Edema

A
  1. increase in blood hydrostatic pressure
    - venous congestion, circulatory failure, thrombi
  2. decrease in blood colliod osmotic pressure
    - hypoalbuminemia, kidney or liver disease,
    severe burns
  3. increase in IF osmotic pressure
    - inflammation → exudate formation
    - * increase IFOP due to increase capillary
    permeability
  4. Obstruction of lyphatics
    - surgery
    - tumor growth
    - parasitic infections
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31
Q

Elephantiasis

A

as angiotensin II hits kidneys, aldosterone tells kidneys to absorb water
- swollen limbs

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32
Q

Electrolytes

A
  • compound that dissociates into ions when in solution
  • ions are charged particles and
  • resulting solution can carry an electric current
33
Q

4 general functions of electrolytes

A
  1. control osmosis of water between compartments
  2. help maintain the acid-base balances need for cellular activity
  3. carry electrical current
  4. serve as cofactors
34
Q

Sodium

A
  • Major EC cation
  • Attracts fluid and helps preserve fluid volume
  • Combines with Cl and HCO3 to help regulate acid-base balance
  • Normal range of serum Na 135-145 mEq/L
35
Q

Normal Levels of Sodium?

A

135-145 mEq/L

36
Q

What happens if sodium intake increases?

A
  • [ECF] increases
  • increased thirst and release of ADH (antidiuretic)
  • tiggers kidneys to retain more water
  • aldosterone also increases Na+, H2O and Fluid
37
Q

Functions of Sodium-Potassium Pump

A
  • Na+ outside tries to get inside
  • K+ inside tries to get outside
  • pump maintains normal conc. using ATP, magnesium, and an enzyme
  • pump prevents cell swelling, creates electrical charge allowing neuromuscular impulse transmission
38
Q

Potassium

A
  • Major INTRAcellular cation
  • untreated changes in K+ levels lead to serious neuromuscular and cardiac problems
  • Normal levels: 3.5-5mEq/L
39
Q

Normal Potassium levels

A

3.5-5 mEq/L

40
Q

Factors influencing K+ balance

A
  • Na+/K+ pump
  • Renal regulation
  • pH levels
41
Q

How does Renal Regulation influence K+ balance?

A
  • increased K+ levels→ increased K+ loss in urine
  • Aldosterone secretion causes Na+ reabsorption and K+ excretion
42
Q

How does pH influence K+ balance?

A
  • Potassium ions and hydrogen ions exchange freely across cell membrane
  • Acidosis → hyperkalemia (K+ moves out of cell)
  • Alkalosis → hypokalemia (K+ moves into cell)
43
Q

Hyperkalemia

A
  • K+ > 5mEq/L
  • less common
  • caused by altered kidney function, increased intake (salt substitutions), blood transfusions, meds (K+ sparing diuretics), cell death (trauma)
44
Q

Magnesium

A
  • helps produce ATP
  • Role in protein synthesis & carbohydrate metabolism
  • helps cardiovascular system function (vasodilation)
  • regulates muscle contractions
  • Normal levels Mg2+: 1.5-2.5 mEq/L
45
Q

Normal levels of Magnesium

A

1.5-2.5 mEq/L

46
Q

Hypermagnesemia

A
  • Mg++ > 2.5mEq/L
  • not common
  • renal dysfunction most common cause
    ~ renal failure
    ~ Addison’s disease
    ~ Adrenocortical insufficiency
    ~ untreated Diabetic Ketoacidosis (DKA)
47
Q

Hypomagnesemia

A
  • Mg++ < 1.5mEq/L
  • caused by poor dietary intake, poof GI absorption, excessive GI/urinary losses
  • High risk clients
    ~ chronic alcoholism
    ~ Malabsorption
    ~ GI/ urinary system disorders
    ~ Sepsis
    ~ burns
    ~ wounds needing debridement
48
Q

Calcium

A
  • 99% in bones, 1% serum and soft tissue (measure by serum)
  • works with phosphorus to form bones and teeth
  • role in cell membrane permeability
  • affects cardiac muscle contraction
  • participates in blood clotting
49
Q

Normal Calcium levels (serum and ionized)

A

Serum: 8.9-10.1 mg/dl
ionized: 4.5-5.1 mg/dl

50
Q

Hypocalcemia

A

serum: <8.9 mg/dl
ionized: <4.5 mg/dl
- caused by inadequate intake, malabsorption, pancreatitis, thyroid or parathyroid surgery, loop diuretics, low magnesium levels

51
Q

Hypercalcemia

A

serum: >10.1 mg/dl
ionized: > 5.1 mg/dl
Two major causes:
- cancer
- hyperparathyroidism

52
Q

Chloride

A
  • Major Extracellular anion
  • Na+ and Cl- maintain water balance
  • secreted in stomach as HCl
  • Aids CO2 transport in blood
53
Q

Normal Chloride levels

A

96-106 mEq/L

54
Q

Hypochloremia

A

<96 mEq/L
- caused by decreased intake or decreased absorption, metabolic alkalosis, and loop, osmotic, or thiazide diuretics

55
Q

Hyperchloremia

A

> 106 mEq/L
- not common, rarely occurs alone
- causes: dehydration, renal failure, resipiratory alkalosis, salicylate toxicity, hyperpara-thyroidism, hyperaldosteronism, hypernatremia

56
Q

Normal pH in blood

A

7.35-7.45
- narrow, crucial for enzyme activity and to prevent tissue damage

57
Q

Acidosis vs Alkalosis

A
  1. pH < 7.35
  2. pH > 7.45
58
Q

Sources of H+ in body (3 major)

A
  1. Cell Respiration
    - complete combustion of glucose yeilds CO2 + H2O)
  2. Incomplete combustion of glucose yeild organic acids
    - lactic acid, ketones
  3. ingestion of acid products
    - drug overdose (asprin, TCA, increase breathing)
59
Q

3 Acid-Base Regulatory systems

A
  1. Buffers
    - major buffer = HCO3- (carbonic acid system)
  2. Respiratory therapy system
    - regulates CO2 loss
  3. Kidneys
    - secrete H+
    - Reabsorb HCO3-
60
Q

What is a buffer system

A
  • SA/SB converted to WA/WB
  • modifies release of H+ and prevents drastic pH change
  • done w/in fraction of a second
61
Q

types of buffer systems

A
  1. carbonic acid- bicarbonate
  2. phosphate
  3. protein
62
Q

Carbonic Acid-Bicarbonate System

A
  • plasma and ECF buffer (in blood)
  • kidney nomally maintains 20:1 supply of HCO3-:H2CO3
  • respiratory system regulates amount of CO2
63
Q

Phosphate Buffers

A
  • Intracellular buffer (also used to buffer in urine)
  • phoasphates can bind and release H+
  • can buffer and acid or base
64
Q

Protein buffers

A
  • intracellular and plasma buffer
    ~ ex. hemoglobin in RBCs buffers H2CO3
  • each protein has a carboxyl terminal and an amino terminal
  • can buffer both acid or base
65
Q

What happens during Hyperventilation?

A
66
Q

What happens during hypoventilation?

A
67
Q

How is pH monitored and what happens?

A
  • chemoreceptors (medulla, aortic, carotid bodies)
  • monitor [CO2]/[H+] of blood
  • send a message to inspiratory control center (brainstem) to alter rate of respiration
68
Q

How do kidneys regulate pH?

A

Excreting H+:
- secrete H+ into urine in exchange for Na+; H+ competes with K+ regulating bicarbonate concentration
~ reabsorbs and synthesizes new HCO3-
*renal failure can quickly cause death
kidneys → slow system → hours to days

69
Q

How to maintain acceptable Urine pH

A
  • two buffers in urinary filtrate to combine with H+ and prevent Urine becoming too acidic
  • HPO4– → H2PO4-
  • NH3 → NH4+
70
Q

Normal PaCO2

A

35-45 mmHg

71
Q

Normal HCO3 conc.

A

22-26 mmol/L

72
Q

Respiratory Acidosis

A

→ decrease exhalation of CO2
(hypoventilation) (think: resp=lungs)
→ increase PaCO2, pH < 7.35
causes:
- ephysema (smoking too much, cant breathe out)
- pulmonary edema (too much fluid in lungs)
- brainstem injury ( signal isn’t happening)
- airway obstruction

73
Q

How do you compensate Respiratory Acidosis

A
  • kidneys compensate by increasing H+ secretion and HCO3- reabsorption
  • slow: hrs, days
74
Q

Respiratory Alkalosis

A

→ increase exhalation of CO2
(hyperventilation) (think: resp=lungs)
→ decreas PaCO2, pH > 7.45
causes:
- CVA (cerbrovascular accident/ stroke)
- anxiety
- O2 deficiency (eg. high altitude)

75
Q

How do you compensate Respiratory Alkalosis

A
  • kidneys compensate by decreasing H+ secretion and HCO3- reabsorption
76
Q

Metabolic Acidosis

A

Loss of HCO3-
- Severe diarrhea
- renal dysfunction
- or buffer overwhelmed:
drug overdose, ketosis, lactic acidosis

77
Q

Metabolic Acidosis Compensation

A

hyperventilation to increase CO2 exhalation
- decrease CO2 in system +H2O → H2CO3 → decrease HCO3- + H+

78
Q

Metabolic Alkalosis

A
  • loss of acid
    causes:
  • vomiting (loss of stomach HCl)
  • alkaline drugs
  • too much HCO3- in IV
79
Q

Metabolic Alkalosis Compensation

A

Hypoventilation (decrease CO2 release)

ANPH 1105 (3 decks)

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