Week 2- Acid-Base and Potassium Flashcards
(99 cards)
1
Q
What are sources of hydrogen ion in the body? What is volatile vs. non-volatile acid and which organ deals with which one?
A
Sources of acid
- cellular metabolism (fat, carbs, protein)
- diet
CO2 is a volatile acid produced mainly by fat and carb metabolism and it is blown off in the lung
Phosphates, sulfates are non-volatile and produced mostly from protein metabolism, and these are excreted by the kidney.
2
Q
How is pH regulated (generally)?
A
- with buffers (immediate)
- breathing CO2 out (minutes to hours)
- Excretion of acid or alkaline urine (hours to days)
3
Q
What is the Henderson Equation? What does it signify?
A
- the pH of the blood is decreased with either an increase in PaCO2 or a drop in bicarbonate
4
Q
What are the the buffering systems of the body? Is the cell more or less acidic than the ECF?
A
**Intracellular:
- bicarbonate
- proteins
- phosphate
**Bone (H+ dissolves bone to release buffer)
Extracellular
- bicarbonate
- inorganic acids
**used chronically, not day to day. Extracellular is used in normal circumstances**
5
Q
What are the determinants of PaCO2 and what is the relationship between them?
A
6
Q
How do the lungs respond to low pH?
A
By the Henderson equation, the PaCO2 increases as pH decreases. This is sensed in the brain, then alveolar ventilation and depth is increased, leading to a decrease in PaCO2.
7
Q
Contrast respiratory and metabolic acidosis
A
Respiratory acidosis results from an inability to blow off CO2, and so is defined by an increased PCO2
Metabolic acidosis results from the inability to eliminate acid (or too much production), and so is defined by a decreased HCO3
8
Q
How to calculate the anion gap, what is it normally and what does it tell you?
A
AG = Na+ – (Cl– + HCO3–)
Normal is is 12 +/- 2 because of unmeasured anions in the blood (esp. albumin, phosphate)
It helps you identify the cause of metabolic acidosis. Elevated AG indicates the presence of acids (e.g. lactic, keto…) normal AG with acidosis indicates a loss of HCO3- by some means, bu likely compensated by Cl-
9
Q
What are some causes of anion gap acidosis?
A
KULT
- K= ketones (diabetic, alcoholic, starvation)
- U= uremia (renal failure)
- L= lactate (sepsis)
- T= toxins (toxic alcohols, aspirin)
**more complicated acronym available on wikipedia**
10
Q
What is the osmolar gap? What does a gap mean?
A
The difference between the calculated osmolality of the blood (POsm= 2*[Na] +[urea] + [glucose]) and the measured osmolality in the lab.
If there is a significant difference between the two, there is a large amount of some extra osmole in the blood.
e.g.MADGAS
Mannitol
Alcohols (methanol, ethylene glycol, isopropanol, propylene)
Diatrizoate (contrast agent)
Acetone
Sorbitol
11
Q
What is polycystic kidney disease?
A
An autosomal dominant (ADPKD) or, more rarely, recessive (ARPKD) form of kidney disease where multiple cysts form in the kidney. ADPKD presents in adulthood.
12
Q
What is hydronephrosis?
A
Swelling of the kidney due to urine obstruction (e.g. benign prostate hypertrophy, stones)
13
Q
Is H+ filtered as a free ion? Is HCO3- filtered as a free ion?
A
NO, YES
14
Q
What does the kidney do to maintain acid/base balance?
A
- Secretes H+ (uses titratable acids and NH4+ to get rid of excess acid)
- Reabsorbs HCO3-
- Creates new HCO3-
15
Q
Where is H+ secreted and what can it do ?
A
H+ is secreted in the proximal tubule and it either combines with bicarbonate, and then through CA on the brush border, makes CO2 and H20, which is then reabsorbed.
OR it combines with a titratable acid or ammonium.
16
Q
How and where is bicarb reabsorbed? How does the process differ between the PCT and the CT?
A
The proximal tubule (80%) and the collecting tubule.
H+ is pumped in the lumen, combines with HCO3-, is converted to CO2 and H20 by luminal CA, CO2 diffuses into the cell and is reconverted to bicarb, which is pumped out the baseloateral side. It’s one big cycle.
In the PCT H+ is exchanged for sodium at the apical side, and in the CT it is a H+ ATPase that pumps it through. Also, bicarb is exchanged for different ions on the basolateral side.
17
Q
How is new bicarb created?
A
When H+ is excreted and combines with a titratable acid, one bicarb is created.
When glutamine is broken down into ammonium and alpha-ketoglutarate, one bicarb is created and pumped into the blood.
18
Q
Where is ammonium formed?
A
In the proximal tubule, from the breakdown of glutamine. It is pumped into the lumen with the Na/H exchanger
19
Q
What are the 3 steps in NH4+ excretion?
A
- Formation (PCT)
- Reabsorption/recycling of NH4+ (TAL-LOH) (via the K position on NKCC)
- Ammonium trapping (collecting duct) (acts as a buffer for secreted H+)
20
Q
What can NH3 in the tubules do ?
A
Diffuse into the blood, go to the liver adn be made into urea. This uses up 2 bicarbs, so it is counter productive
21
Q
What is renal tubular acidosis? Type 1,2,4?
A
Renal tubular acidosis is acidosis resulting from the impairment of the kidney’s usual acid/base functions.
Type 2: PCT can’t absorb bicarb well
Type 1: DT can’t excrete H+ well, so less acid excretion with NH4+
Type 4: aldosterone deficiency/resistance (impaired secretion of H+ and K+)
22
Q
What is the formula for net acid excretion?
A
NAE= NH4+ + titratable acids- bicarb in urine
23
Q
Which part(s) of the kidney’s acid/base function is modifiable?
A
The production of NH4+ is the major modifiable function. Titratable acids are diet dependent.
24
Q
How is potassium content managed? How is potassium concentration managed?
A
Content is managed by the kidneys (ingested potassium= excreted potassium)
Concentration is managed by shift potassium intracellularly (insulin, epinephrine, aldosterone)
25
What is the postassium balance risk:
* B-blockers after ingesting a potassium rich meal
* Primary hyperaldosteronism
* Stress (e.g MI)
* acidosis
* diabetes after a potassium rich meal
* alkalosis
* exercise
* malignant hyperthermia
B-blockers after ingesting a potassium rich meal: hyperkalemia (normally Epi is secreted and promotes uptake)
Primary hyperaldosteronism: hypokalemia (aldosterone promotes K uptake)
Stress (e.g MI): hypokalemia (Epi will be released, K+ shifts into cells)
Acidosis: K/H exchange to maintain electroneutrality --\>hyperkalemia
Diabetes after a potassium rich meal: hyperkalemia (insulin promotes K uptake)
Alkalosis: hypokalemia (K+ enters, H+ exits cells)
Exercise: slight hyperkalemia
Malignant hyperthermia: hyperkalemia (depolarization + rhabdomyolysis)
26
Which kind of acidosis is worse for potassium balance: inorganic (e.g. HCl) or organic (e.g. lactate)?
Organic is better because some of the anion can follow the H+ into the cell, reducing the need for K+ extrusion.
27
What is the normal distribution of potassium between the ECF and ICF? How is K+ usually excreted?
98% ICF
2% ECF
95% renally excreted, 5% excreted in stool/sweat
28
What is the physiologic response after ingesting a high potassium meal?
Potassium promotes the release of:
* insulin from pancreas
* epinephrine from the adrenal medulla
* aldosterone from the adrenal cortex
Insulin and epi act quickly to increase Na/KATPase function, and K is shifted quickly in the the ICF
Aldosterone acts more slowly, but still promotes this shift AND promotes K+ excretion in the CCD
29
Where is K+ reabsorbed and secreted?
Reabsorbed:
* 75% in PCT
* 25% in TAL (NKCC)
Secreted
* CCD (under regulation of aldosterone)
30
How does aldosterone act to increase K secretion?
It promotes the expression of ENaC, and the activity of the basolateral Na/KATPase. This makes the lumen more negative and promotes K secretion.
31
What are the two broad reasons for hyperkalemia? What can cause each
impaired renal excretion
* low GFR (renal failure, volume depletion)
* impaired secretion (e.g. decreased aldosterone due to adrenal insufficiency..)
shift of K+ from ICF into ECF
* insulin deficiency
* B-blockers
* metabolic acidosis
* digoxin toxicity (impairs N/K pump)
* cell breakdown (e.g. rhabdomyolysis, tumour cell lysis)
32
What is the normal range for serum potassium? What is hyperkalemic?
Normal 3.5-5, hyperkalemic above that. Emergency is above 6.5 OR EKG changes.
33
What is the treatment for hyperkalemia?
1. IV calcium to antagonize cardiac effects of hyperkalemia
2. Shift K into cells: insulin + glucose, can also use B-blocker (e.g. salbutamol)
3. Remove K from the body
* GI excretion: resin enemas
* Renal excretion: loop diuretics
* Hemodialysis
34
What does secretion of K+ depend on?
1. Aldosterone (promotes K secretion)
2. Tubular luminal flow (high flow promotes K secretion)
3. Delivery of luminal Na (high delivery promotes K secretion)
4. Acid-Base (acidosis decreases K secretion, H+ is secreted instead)
35
What factors influence movement of potassium from ICF into ECF?
**Hormones**
* insulin, epinephrine, aldosterone
**Acidosis/alkalosis**
**Osmolality of ECF** (water drawn into ECF concentrates K+ in cell, so K+ is released into ECF to maintain the concentration gradietn across the membrane)
36
How does acid-base balance after potassium regulation in the cell and in the kidney?
In the cell:
* H+ and K+ are exchanged to maintain electroneutrality (acidemia--\> K+ release, alkalemia --\> K+ retention)
In the kidney
* in acidemia H+ is secreted instead of K+ to some extent --\> hyperkalemia
37
What are the general etiologies of hypokalemia, and some examples of each?
1) increased shift from ECF --\> ICF
* B- agonists
* insulin
* refeeding (e.g. after starvation)
* alkalosis
2) increased losses (e.g. cholera, diuretics, hyperaldosteronism)
38
Treatment for hypokalemia
1. cardiac monitor
2. replace K+ (KCl infusion) rapidly to a safe concentration, then increase the total content slowly
39
What is metabolic alkalosis?
Increased [HCO3-]
Can concomittanly have:
* alkalemia (increased pH)
* compensatory increase in PaCO2
40
What are the two events required to generate a metabolic alkalosis?
1. elevation of plasma HCO3-
* volume contraction most important.
* H+ shift (e.g. hypokalemia)
* exogenous HCO3-
* H+ loss (e.g. vomiting)
2. Increase in renal HCO3- reabsorption +/- generation
* e.g. decreased GFR --\> RAAS --\> Na retention, HCO3- retention
* hypokalemia (intracellular acidosis in kidney --\> increased H+ extrusion)
41
What is polyuria? What are the determinants of urine output?
Polyuria is an excessive output of urine. Affected by:
* fluid and salt intake (e.g. psychogenic diabetes insipidus)
* the ability of the kidney to reabsorb water and solute
* adding an osmole (e.g. glucose) to the filtrate alters this
* transporters
Urine production is relatively steady, but hormones control the reabsorption of solutes and the reabsorption of water. But the ability of the kidney to reabsorb/concentrate the urine depends on its ability to generate the medullary concentration gradient, the correct amount of solute reabsorption upstream, and the osmolality of the filtrate.
42
What is osmotic diuresis?
When an osmole is added to the filtrate, it hinders the ability of the kidney to properly concentrate the urine and diuresis results. E.g. hyperglycemia, glucose keeps water into the lumen, so in the PCT the Na cannot be absorbed isotonically and an unfavorable gradient quickly develops. Sodium follows glucose!!
43
What is the ADH status in hyperglycemia?
ADH is released because water is drawn out of the osmoreceptor cells
44
What is the relationship between plasma sodium concentration and plasm osmolality?
Physiologically: POsm= 2\* pNa + [glucose] +[urea]
Practically, the serum sodium cannot definitively tell us anything about the POsm. Low pNa suggesst low POsm (hyposmolar hyponatremia) but if another osmole is present (e.g. glucose) you can have hyperosmolar hyponatremia
45
How is ECF volume evaluated? What about effective circulating volume?
All clinical evaluation
* urine output (high=high)
* JVP (high=high)
* blood pressure (high=high)
* peripheral or pulmonary edema (present=high)
* serum sodium (low=high)
* thirst (present=low)
But these are all just pieces of the puzzle. The ECF doesn't reflect the ECV and we don't have a good test to determine that.
46
How is ICF evaluated?
A high POsm means that the ICF is contracted (and vice versa).
47
How is a depleted ECF managed?
* Give fluids:
* isotonic saline will increase volume of ISF/IVF
* hypertonic saline will increase volume of ISF/IVF, but at the expense of pulling fluid out of the ICF
* D5W is like giving free water because the dextrose is metabolized right away. It will distribute to all three compartments (2/3 ICF 1/3 ECF)
48
How can ECF volume changes contribute to acid-base distrubances?
* A decrease in ECF can concentrate HCO3- --\> alkalosis
* A decrease in ECF could decrease GFR (RAAS activation--\> HCO3- retention)
49
What is the relationship between total body Na and ECF volume?
Increase in sodium content increases ECF volume.
50
What is the effect fo hyperglycemia on ECF and ICF osmolality, volume and pNa?
ECF Osm: increases with the addition of glucose
ECF volume: increases as water is drawn out of cells by the higher pOsm
ICF Osm: increases as water is drawn out of cells
ICF: decreases as water is drawn out of cells
pNa: decreases as the volume of ECF increases.
51
How is pH regulated (generally)?
- with buffers (immediate)
- breathing CO2 out (minutes to hours)
- Excretion of acid or alkaline urine (hours to days)
52
What is the Henderson Equation? What does it signify?
* the pH of the blood is decreased with either an increase in PaCO2 or a drop in bicarbonate
53
What are the the buffering systems of the body? Is the cell more or less acidic than the ECF?
\*\*Intracellular:
* bicarbonate
* proteins
* phosphate
\*\*Bone (H+ dissolves bone to release buffer)
Extracellular
* bicarbonate
* inorganic acids
\*\*used chronically, not day to day. Extracellular is used in normal circumstances\*\*
54
What are the determinants of PaCO2 and what is the relationship between them?
55
How do the lungs respond to low pH?
By the Henderson equation, the PaCO2 increases as pH decreases. This is sensed in the brain, then alveolar ventilation and depth is increased, leading to a decrease in PaCO2.
56
Contrast respiratory and metabolic acidosis
Respiratory acidosis results from an inability to blow off CO2, and so is defined by an increased PCO2
Metabolic acidosis results from the inability to eliminate acid (or too much production), and so is defined by a decreased HCO3
57
How to calculate the anion gap, what is it normally and what does it tell you?
AG = Na+ – (Cl– + HCO3–)
Normal is is 12 +/- 2 because of unmeasured anions in the blood (esp. albumin, phosphate)
It helps you identify the cause of metabolic acidosis. Elevated AG indicates the presence of acids (e.g. lactic, keto...) normal AG with acidosis indicates a loss of HCO3- by some means, bu likely compensated by Cl-
58
What are some causes of anion gap acidosis?
KULT
* K= ketones (diabetic, alcoholic, starvation)
* U= uremia (renal failure)
* L= lactate (sepsis)
* T= toxins (toxic alcohols, aspirin)
\*\*more complicated acronym available on wikipedia\*\*
59
What is the osmolar gap? What does a gap mean?
The difference between the calculated osmolality of the blood (POsm= 2\*[Na] +[urea] + [glucose]) and the measured osmolality in the lab.
If there is a significant difference between the two, there is a large amount of some extra osmole in the blood.
e.g.MADGAS
Mannitol
Alcohols (methanol, ethylene glycol, isopropanol, propylene)
Diatrizoate (contrast agent)
Acetone
Sorbitol
60
What is polycystic kidney disease?
An autosomal dominant (ADPKD) or, more rarely, recessive (ARPKD) form of kidney disease where multiple cysts form in the kidney. ADPKD presents in adulthood.
61
What is hydronephrosis?
Swelling of the kidney due to urine obstruction (e.g. benign prostate hypertrophy, stones)
62
Is H+ filtered as a free ion? Is HCO3- filtered as a free ion?
NO, YES
63
What does the kidney do to maintain acid/base balance?
1. Secretes H+ (uses titratable acids and NH4+ to get rid of excess acid)
2. Reabsorbs HCO3-
3. Creates new HCO3-
64
Where is H+ secreted and what can it do ?
H+ is secreted in the proximal tubule and it either combines with bicarbonate, and then through CA on the brush border, makes CO2 and H20, which is then reabsorbed.
OR it combines with a titratable acid or ammonium.
65
How and where is bicarb reabsorbed? How does the process differ between the PCT and the CT?
The proximal tubule (80%) and the collecting tubule.
H+ is pumped in the lumen, combines with HCO3-, is converted to CO2 and H20 by luminal CA, CO2 diffuses into the cell and is reconverted to bicarb, which is pumped out the baseloateral side. It's one big cycle.
In the PCT H+ is exchanged for sodium at the apical side, and in the CT it is a H+ ATPase that pumps it through. Also, bicarb is exchanged for different ions on the basolateral side.
66
How is new bicarb created?
When H+ is excreted and combines with a titratable acid, one bicarb is created.
When glutamine is broken down into ammonium and alpha-ketoglutarate, one bicarb is created and pumped into the blood.
67
Where is ammonium formed?
In the proximal tubule, from the breakdown of glutamine. It is pumped into the lumen with the Na/H exchanger
68
What are the 3 steps in NH4+ excretion?
1. Formation (PCT)
2. Reabsorption/recycling of NH4+ (TAL-LOH) (via the K position on NKCC)
3. Ammonium trapping (collecting duct) (acts as a buffer for secreted H+)
69
What can NH3 in the tubules do ?
Diffuse into the blood, go to the liver adn be made into urea. This uses up 2 bicarbs, so it is counter productive
70
What is renal tubular acidosis? Type 1,2,4?
Renal tubular acidosis is acidosis resulting from the impairment of the kidney's usual acid/base functions.
Type 2: PCT can't absorb bicarb well
Type 1: DT can't excrete H+ well, so less acid excretion with NH4+
Type 4: aldosterone deficiency/resistance (impaired secretion of H+ and K+)
71
What is the formula for net acid excretion?
NAE= NH4+ + titratable acids- bicarb in urine
72
Which part(s) of the kidney's acid/base function is modifiable?
The production of NH4+ is the major modifiable function. Titratable acids are diet dependent.
73
How is potassium content managed? How is potassium concentration managed?
Content is managed by the kidneys (ingested potassium= excreted potassium)
Concentration is managed by shift potassium intracellularly (insulin, epinephrine, aldosterone)
74
What is the postassium balance risk:
* B-blockers after ingesting a potassium rich meal
* Primary hyperaldosteronism
* Stress (e.g MI)
* acidosis
* diabetes after a potassium rich meal
* alkalosis
* exercise
* malignant hyperthermia
B-blockers after ingesting a potassium rich meal: hyperkalemia (normally Epi is secreted and promotes uptake)
Primary hyperaldosteronism: hypokalemia (aldosterone promotes K uptake)
Stress (e.g MI): hypokalemia (Epi will be released, K+ shifts into cells)
Acidosis: K/H exchange to maintain electroneutrality --\>hyperkalemia
Diabetes after a potassium rich meal: hyperkalemia (insulin promotes K uptake)
Alkalosis: hypokalemia (K+ enters, H+ exits cells)
Exercise: slight hyperkalemia
Malignant hyperthermia: hyperkalemia (depolarization + rhabdomyolysis)
75
Which kind of acidosis is worse for potassium balance: inorganic (e.g. HCl) or organic (e.g. lactate)?
Organic is better because some of the anion can follow the H+ into the cell, reducing the need for K+ extrusion.
76
What is the normal distribution of potassium between the ECF and ICF? How is K+ usually excreted?
98% ICF
2% ECF
95% renally excreted, 5% excreted in stool/sweat
77
What is the physiologic response after ingesting a high potassium meal?
Potassium promotes the release of:
* insulin from pancreas
* epinephrine from the adrenal medulla
* aldosterone from the adrenal cortex
Insulin and epi act quickly to increase Na/KATPase function, and K is shifted quickly in the the ICF
Aldosterone acts more slowly, but still promotes this shift AND promotes K+ excretion in the CCD
78
Where is K+ reabsorbed and secreted?
Reabsorbed:
* 75% in PCT
* 25% in TAL (NKCC)
Secreted
* CCD (under regulation of aldosterone)
79
How does aldosterone act to increase K secretion?
It promotes the expression of ENaC, and the activity of the basolateral Na/KATPase. This makes the lumen more negative and promotes K secretion.
80
What are the two broad reasons for hyperkalemia? What can cause each
impaired renal excretion
* low GFR (renal failure, volume depletion)
* impaired secretion (e.g. decreased aldosterone due to adrenal insufficiency..)
shift of K+ from ICF into ECF
* insulin deficiency
* B-blockers
* metabolic acidosis
* digoxin toxicity (impairs N/K pump)
* cell breakdown (e.g. rhabdomyolysis, tumour cell lysis)
81
What is the normal range for serum potassium? What is hyperkalemic?
Normal 3.5-5, hyperkalemic above that. Emergency is above 6.5 OR EKG changes.
82
What is the treatment for hyperkalemia?
1. IV calcium to antagonize cardiac effects of hyperkalemia
2. Shift K into cells: insulin + glucose, can also use B-blocker (e.g. salbutamol)
3. Remove K from the body
* GI excretion: resin enemas
* Renal excretion: loop diuretics
* Hemodialysis
83
What does secretion of K+ depend on?
1. Aldosterone (promotes K secretion)
2. Tubular luminal flow (high flow promotes K secretion)
3. Delivery of luminal Na (high delivery promotes K secretion)
4. Acid-Base (acidosis decreases K secretion, H+ is secreted instead)
84
What factors influence movement of potassium from ICF into ECF?
**Hormones**
* insulin, epinephrine, aldosterone
**Acidosis/alkalosis**
**Osmolality of ECF** (water drawn into ECF concentrates K+ in cell, so K+ is released into ECF to maintain the concentration gradietn across the membrane)
85
How does acid-base balance affect potassium regulation in the cell and in the kidney?
In the cell:
* H+ and K+ are exchanged to maintain electroneutrality (acidemia--\> K+ release, alkalemia --\> K+ retention)
In the kidney
* in acidemia H+ is secreted instead of K+ to some extent --\> hyperkalemia
86
What are the general etiologies of hypokalemia, and some examples of each?
1) increased shift from ECF --\> ICF
* B- agonists
* insulin
* refeeding (e.g. after starvation)
* alkalosis
2) increased losses (e.g. cholera, diuretics, hyperaldosteronism)
87
Treatment for hypokalemia
1. cardiac monitor
2. replace K+ (KCl infusion) rapidly to a safe concentration, then increase the total content slowly
88
What is metabolic alkalosis?
Increased [HCO3-]
Can concomittanly have:
* alkalemia (increased pH)
* compensatory increase in PaCO2
89
What are the two events required to generate a metabolic alkalosis?
1. elevation of plasma HCO3-
* volume contraction most important.
* H+ shift (e.g. hypokalemia)
* exogenous HCO3-
* H+ loss (e.g. vomiting)
2. Increase in renal HCO3- reabsorption +/- generation
* e.g. decreased GFR --\> RAAS --\> Na retention, HCO3- retention
* hypokalemia (intracellular acidosis in kidney --\> increased H+ extrusion)
90
What is polyuria? What are the determinants of urine output?
Polyuria is an excessive output of urine. Affected by:
* fluid and salt intake (e.g. psychogenic diabetes insipidus)
* the ability of the kidney to reabsorb water and solute
* adding an osmole (e.g. glucose) to the filtrate alters this
* transporters
Urine production is relatively steady, but hormones control the reabsorption of solutes and the reabsorption of water. But the ability of the kidney to reabsorb/concentrate the urine depends on its ability to generate the medullary concentration gradient, the correct amount of solute reabsorption upstream, and the osmolality of the filtrate.
91
What is osmotic diuresis?
When an osmole is added to the filtrate, it hinders the ability of the kidney to properly concentrate the urine and diuresis results. E.g. hyperglycemia, glucose keeps water into the lumen, so in the PCT the Na cannot be absorbed isotonically and an unfavorable gradient quickly develops. Sodium follows glucose!!
92
What is the ADH status in hyperglycemia?
ADH is released because water is drawn out of the osmoreceptor cells
93
What is the relationship between plasma sodium concentration and plasm osmolality?
Physiologically: POsm= 2\* pNa + [glucose] +[urea]
Practically, the serum sodium cannot definitively tell us anything about the POsm. Low pNa suggesst low POsm (hyposmolar hyponatremia) but if another osmole is present (e.g. glucose) you can have hyperosmolar hyponatremia
94
How is ECF volume evaluated? What about effective circulating volume?
All clinical evaluation
* urine output (high=high)
* JVP (high=high)
* blood pressure (high=high)
* peripheral or pulmonary edema (present=high)
* serum sodium (low=high)
* thirst (present=low)
But these are all just pieces of the puzzle. The ECF doesn't reflect the ECV and we don't have a good test to determine that.
95
How is ICF evaluated?
A high POsm means that the ICF is contracted (and vice versa).
96
How is a depleted ECF managed?
* Give fluids:
* isotonic saline will increase volume of ISF/IVF
* hypertonic saline will increase volume of ISF/IVF, but at the expense of pulling fluid out of the ICF
* D5W is like giving free water because the dextrose is metabolized right away. It will distribute to all three compartments (2/3 ICF 1/3 ECF)
97
How can ECF volume changes contribute to acid-base distrubances?
* A decrease in ECF can concentrate HCO3- --\> alkalosis
* A decrease in ECF could decrease GFR (RAAS activation--\> HCO3- retention)
98
What is the relationship between total body Na and ECF volume?
Increase in sodium content increases ECF volume.
99
What is the effect fo hyperglycemia on ECF and ICF osmolality, volume and pNa?
ECF Osm: increases with the addition of glucose
ECF volume: increases as water is drawn out of cells by the higher pOsm
ICF Osm: increases as water is drawn out of cells
ICF: decreases as water is drawn out of cells
pNa: decreases as the volume of ECF increases.
