Therapeutics Iv Exam 3- Acid Base Disorders

Front 1

2 main fluid compartments and fluid distribution

Back 1

intracellular fluid (2/3 of volume)
about 30 L


extracellular (1/3)
~13.5 L

Front 2

2 major fluid subdivisions of ECF and fluid distribution

Back 2

▪ Plasma – fluid portion of the blood (25%)
▪ Interstitial fluid (IF) – fluid in spaces between cells (75%)

Front 3

special cases of ECF (where it might be elsewhere than plasma/interstitial) (6)

Back 3

lymph, cerebrospinal fluid, eye humors,
synovial fluid, serous fluid, and gastrointestinal secretions

Front 4

male vs. female water makeup
why the discrepancy?

Back 4

Healthy males are ~ 60% water
Healthy females are ~ 50% water
women have higher body fat and smaller amount of skeletal muscle

Front 5

how to calculate distribution of water into compartments in a person weighing x kg

Back 5

take weight and multiply by % of water (if M or F)

then take 3/4 of ECF and that goes in interstitial, 1/4 into IV

Front 6

intracellular and extracellular- say where the intra/extraVASCULAR fluids are located in each compartment

Back 6

intracellular- extravascular fluid would be in tissues
intravascular would be fluid in erythrocytes

extracellular- intravascular fluids = plasma
extravascular = edema sort of fluids/interstitial fluids

Front 7

3 electrolyte solutes in body

Back 7

▪ Inorganic salts
▪ Acids and bases
▪ Some proteins

Front 8

3 non-electrolytes in body

Back 8

▪ Glucose
▪ Lipids
▪ Creatinine and urea

Front 9

osmotic power of electrolytes vs. nonelectrolytes

Back 9

Electrolytes have greater osmotic power than nonelectrolytes

Front 10

fluid mvmt among compartments is regulated by what 2 types of pressures

Back 10

osmotic and hydrostatic pressures

Front 11

what happens to net leakage of fluid from blood?

Back 11

Net leakage of fluid from blood is picked up by lymphatic vessels and returned to bloodstream

Front 12

Exchanges between interstitial and intracellular fluids are...

Back 12

are complex due to the selective permeability of the cellular membranes

Front 13

two way water flow is...

how does water flow in this case? (in what direction)

Back 13

Two‐way water flow is substantial

Water flows in direction of highest osmolar concentration

Front 14

To remain properly hydrated, what must be true?

Back 14

water intake must = water output

Front 15

Increased plasma osmolality triggers ... (2)

Back 15

thirst
and release of antidiuretic hormone (ADH)

Front 16

7 compounds that go into calculating serum osmolality

Back 16

sodium
gluose
BUN
EtOH
isopropanol
methanol
ethylene glycol

Front 17

normal osmolality range of serum

Back 17

275‐290 mOsm/kg

Front 18

extracellular compartment primary electrolytes (2)
caveat

Back 18

 Sodium = major cation
 Chloride = major anion
 Caveat with high protein content of plasma?? (didn't mention this)

Front 19

intracellular fluids major cation and anion

Back 19

 Potassium = major cation
 Phosphate = major anion

Front 20

osmolality of extra and intracellular should be...

Back 20

equal

Front 21

4 routes of water output (which is biggest)

Back 21

mostly from urine
some are insensible (not sensed?) water losses from skin/lungs (respiration)

poop
sweat

Front 22

3 routes of water input (which is biggest)

Back 22

metabolic water (from oxidation)
food (30%)
most comes from beverages

Front 23

hypothalamic thirst center is stimulated by (4)

Back 23

10-15% decrease in plasma volume
1-2% increase in plasma osmolality (i.e. hypernatremia)
anything that decreases BP or senses BP decrease: baroreceptor input, angiotensin II

Front 24

thirst is quenched when?

Back 24

as soon as we start to drink

Front 25

feedback signals that inhibit thirst center (2)

Back 25

 Moistening of the mucosa of the mouth and throat
 Activation of stomach and intestinal stretch receptors

Front 26

thirst mechanism flow chart

Back 26

---skipped over

Front 27

Obligatory water losses (2)

Back 27

 Insensible water losses from lungs and skin
 Water that accompanies undigested food residues
in feces

Front 28

Obligatory water loss reflects the fact that (didn't go over this in class...) (2)

Back 28

 Kidneys excrete 900‐1200 mOsm of solutes to
maintain blood homeostasis
 Urine solutes must be flushed out of the body in
water

Front 29

what receptors regulate ADH release

Back 29

hypothalamic osmoreceptors trigger or inhibit ADH release

Front 30

triggers for ADH release (7)

Back 30

▪ Prolonged fever
▪ Excessive sweating, vomiting, or diarrhea
▪ Severe blood loss
▪ Traumatic burns
hypoglycemia
pregnancy (total body volume doubles so thirst to achieve this)
meds like SSRI, carbamazepine, NSAIDs via SIADH??

Front 31

Water reabsorption in collecting ducts is proportional to...

low vs. high lvls of said hormone and effect on urine

Back 31

to ADH release...so:

Low ADH levels = dilute urine and reduced volume of body
fluids

High ADH levels = concentrated urine and increased volume of
body fluids

Front 32

mechanisms and consequences of ADH release slide

Back 32

didn't go over

Front 33

dehydration definition in terms of water in body

Back 33

Water loss > water intake and the body is in negative fluid balance

Front 34

hypovolemia vs. dehydration

Back 34

hypovolemia = depletion of SODIUM and water

dehydration = depletion of water

treated a little differently

Front 35

causes of dehydration (6)

Back 35

 Hemorrhage
 Severe burns
 Prolonged vomiting or
diarrhea
 Profuse sweating
 Water deprivation
 Diuretic abuse

Front 36

4 sx, 1 lab indicating dehydration

Back 36

 Dry mouth and thirst
 BUN: SCr ratio > 20:1
 Dry, flushed skin
 Oliguria
 Hypotension, tachycardia

Front 37

prolonged dehydration may lead to...(5)

Back 37

 Weight loss
 Fever
 Mental confusion
 Loss of electrolytes
 Eventually hypovolemic
shock

Front 38

2 of body's reactions to dehydration (activate what 2 systems)

Back 38

SNS- vasoconstriction, increased HR
RAAS- kidneys reabsorb more Na and water

Front 39

mechanism of dehydration (3)

Back 39

1) excessive loss of water from ECF
2) ECF osmotic pressure will now rise and suck water out of cells
3) cells shrink

Front 40

etiology (2) of "hypotonic hydration" (overhydration/water intoxication)

sodium levels?

Back 40

Renal insufficiency or an extraordinary amount of water ingested quickly can lead to cellular overhydration (AKA “water intoxication”)

Sodium content is normal BUT diluted because excess water is present

Front 41

pathophysiology of hypotonic hydration (2)

Back 41

Resulting hyponatremia (due to dilution) promotes net osmosis into tissue cells, causing swelling

These events must be quickly reversed to prevent severe metabolic disturbances, particularly in neurons

Front 42

edema definition

pathophysiology (2 ways)

Back 42

Atypical accumulation of fluid in interstitial space*** (not extra fluid in vasculature) → tissue swelling

Increased flow of fluids out of bloodstream and/or hindered fluid return from bloodstream

Front 43

diuretic for pedal edema- thing to keep in mind

Back 43

slowly pull fluid out of vasculature so fluid moves out of interstitial space into vessels...so it takes a while to fix

Front 44

Interstitial fluid accumulation causes what? (2)

Back 44

low blood pressure and severely
impaired circulation

Front 45

factors that accelerate fluid loss causing edema (6)

Back 45

Hypertension, capillary permeability
Incompetent venous valves, localized blood vessel blockage (backed up fluids)
Congestive heart failure, high blood volume

Front 46

Hindered fluid return in edema usually reflects

Back 46

an imbalance in
colloid osmotic pressures

Front 47

2 causes of hindered fluid return in edema and explain how they cause edema

Back 47

hypoproteinemia- forces fluids out of capillary beds at arterial ends, then fluids fail to return (oncotic pressure issue) at venous ends

blocked or surgically removed lymphatics- leaked proteins accumulate in interstitial fluid, and exert increasing colloid osmotic pressure, which draws fluid from blood and we don't have the lymphatics to return it to the blood stream

Front 48

3 causes of hypoproteinemia

Back 48

▪ Protein malnutrition
▪ Liver disease
▪ Glomerulonephritis

Front 49

adult avg fluid requirement (per kg, per day)

generally in a male that is how much per hour?

exception to this rule

Back 49

Average fluid requirement = 30‐35 mL/kg/day

Generally in a guy, this is ~ 125 mL/h

really heavy- 200kg+...adipose tissue doesn't have as much vasculature so equations don't apply

Front 50

children total body water vs. adults

what do you use to calc fluid reqs in kids

Back 50

higher % of total body water than adult

so kids need weight based maintenance IVFs via 4/2/1 rule

Front 51

4/2/1 rule for fluids
used for whom?

Back 51

4-2-1 rule: 4mL/kg/h for 1st 10 kg of weight
then 2mL/kg/h for 2nd 10kg
for each kg above 20, it is 1 mL/kg/h

can also be used for adults

Front 52

daily water transfer to/from tract lumen- explain the input and output of water and how it balances out

sources of water to lumen (5)

Back 52

8000-8400 mL of water is reabsorbed out of intestine +400 from colon


ingest 2-3 L per day
bile
pancreatic juice
saliva swallowed
intestinal secretion

total excreted to tract lumen ~ 9 L which balances out the 9 L absorbed

Front 53

electrolyte composition of bodily fluid graph- take home msg: blood/interstitial fluids primarily made up of..(2)

intracellular is primarily (3)

Back 53

blood and interstitial fluid are primarily NaCl and bicarb

intracellular is K+, phosphate, protein

Front 54

ions in stomach (2)
duodenum (2)
ileum (3)
colon (3)
pancreas (4)
bile (3)


importance of this?

Back 54

fluids in stomach- Na+ and Cl
duodenum- Na+, Cl
ileum- Na, Cl, bicarb
colon- Na, K, Cl
Pancreas- Na, K, Cl, TONS of bicarb
bile- Na, Cl, some bicarb

important when deciding what ions to replace

Front 55

lactated ringers composition (5)

Back 55

sodium (130 mEq/L)
Cl (100)
Lactate (28)
potassium (4)
calcium (3)

Front 56

0.9% NaCl how much Na and Cl per liter?

drawback to NaCl

Back 56

sodium/Cl = 154 mEq/L

can cause hyperchloremic metabolic acidosis- use LR instead (less Cl)

Front 57

LR- when to be careful with use (2)

Back 57

in CKD/AKI pt- due to having potassium
lactate is cleared by liver- so avoid large amounts in liver issues-->lactic acidosis- or watch carefully and switch when K+/lactic acid starts creeping up

Front 58

gastric losses (e.g. NG suction)
losing what lytes? (2)
fluid replacement choice?

Back 58

- will be losing acids (H+/Cl-) - replace with NS, 0.5 NS with or without K+

Front 59

pancreatic losses- lose what lytes? (2)

replace with what?

Back 59

Na, bicarb - LR with bicarb (idk why LR...)

Front 60

Biliary, small bowel- lose which lytes? (3)
replace with what?

Back 60

lose Na, Cl, bicarb but not as much bicarb so can get away with just LR

Front 61

diarrhea- lose which lytes (4)

use what to replace?

Back 61

lose a lot of everything- Na, K, Cl, bicarb- so use LR with or without bicarb

Front 62

fluids used for rescucitation (in emergencies) (4)

Back 62

 Crystalloids
 Colloids
 Hypertonic solutions- risk for hypernatremia, not a good option
 Oxygen‐carrying fluids

Front 63

change in Mean arterial pressure by fluid- list order of fluids from best to worst (5)

Back 63

best option in changing MAP is blood, followed by dextran, albumin, lactate then glucose (dextrose)

Front 64

when picking fluids for rescucitation, what compartment do we want the fluids to be in?

Back 64

intravascular space (of ECF)

Front 65

what are crystalloids?
2 examples

Back 65

Solutions containing sodium as their major
osmotically active particle

NS, lactated ringers

Front 66

indications for crystalloids (4)

Back 66

Plasma volume expansion
Correct extracellular electrolyte and volume deficits
Fluid challenge for oliguric patient (to see if they are dehydrated or not, or if it's kidney shit)
Hemorrhagic shock

Front 67

2‐liter rule for oliguric pt

Back 67

if you give them 2 L of crystalloid and look for increase in UoP to determine reason for oliguria

Front 68

3:1 rule for hemorrhagic shock- give reasoning

Back 68

3 mL of crystalloid should be given for every 1 mL of blood loss (due to third...space...loss)

Front 69

NS distribution in body and why we have the 3:1 rule

Back 69

3L of NS- all stays in ECF but distributes between interstitial space and IV space

so 75% goes into interstitial and 25% in IV...that's why 3:1 rule

Front 70

distribution of D5W in body- how much in IV space?

Back 70

distribution of D5W- equally between ICF and ECF due to being metabolized to free water

so 3 L--> 2/3 of it goes into ICF, then of the 1/3 remaining fluids, 25% of THAT will be IV

Front 71

3 ML of NS + D5W-->so 1.5 of each- how to work out distribution into IV space

Back 71

just...calculate each separately...add together

Front 72

for trauma...which fluid do you not want to give..

Back 72

D5W...it sucks for IV space

Front 73

D5W, 1/2 NS, NS and hypertonic NaCl (3%)- list their tonicities and how much free water they provide (free water goes into cells)

Back 73

D5W- hypotonic, 1L of free water

1/2 NS- hypotonic- 73% ECF, 27% ICF- 500mL free water

NS- isotonic, 0 free water

3% NaCl- hypertonic, -2k free water (draws...water out?)

Front 74

3 potential AE of crystalloids

Back 74

 Peripheral and pulmonary edema
 Electrolyte disturbances
 Hyperchloremic acidosis (too much NS- switch to LR

Front 75

colloid definition

Back 75

Large molecular weight substances that do not pass readily across capillary walls

Front 76

3 colloids

Back 76

 Hetastarch (Hespan) 6%
 Albumin
 Dextrans

Front 77

stop-gap measure for blood- what does this mean

Back 77

no O2 carrying capacity- so you can give this if they're bleeding but must be temporary

Front 78

hetastarch comes in what form

Back 78

6% solution in normal saline – 500 mL bag

Front 79

hetastarch- amt of plasma volume expansion

when to use

administer with what?

Back 79

Plasma volume expansion ≥ infusion volume
Plasma volume expanding agent for use after cystalloids
Does not carry O2 → administer with packed RBCs

Front 80

hetastarch elimination (2)

renal dysfunction effect?

issue with the elimination rate

Back 80

Broken down slowly by body
 50% eliminated by 2 days
 64% eliminated by 8 days

even slower in renal dysfunction

issue is coagulopathy if it builds up

Front 81

hetastarch ADRs (4)

Back 81

 Coagulopathy – usually in volumes greater than 1500 mL/day (20 mL/kg/day)
 Volume overload (pulmonary edema)
 Anaphylaxis in 0.1%
 Hyperamylasemia

Front 82

albumin- 2 formulations

Back 82

Available in 5% and 25% (both 12.5 g)

Front 83

5% vs. 25% albumin- what's the difference?

Back 83

500 mL of 5% increases IV space by 500 mL (due to staying in IV space)

use 25% if fluid expansion not desired

Front 84

4 indications for albumin and which one (5 or 25%) to use

what NOT to use albumin for

Back 84

hemorrhagic shock after crystalloids and CI to hetastarch- use 5% to expand volume (have moved away from using albumin though)

paracentesis- 8g/L withdrawn -helps with cardiorenal perfusion (use 25%)

hypotension due to fluid shifts during dialysis use (25%); but same effect as NS so...

SBP- risk of renal failure due to intravascular volume depletion- give on days 1/3 (idk which %)

NOT for hypoalbuminemia in chronic diseases (malnutrition, cirrhosis, etc)- because of short half life- temporary solution to long standing problem wastes albumin

Front 85

in shock...what would you use

Back 85

you'd think albumin because it all goes into IV space but NS is just as good

Front 86

3 ADR for albumin

what 2 things do you not have to worry about

Back 86

Pulmonary edema, especially during sepsis/ARDS
Intestinal obstruction (moa unknown)
Anaphylaxis in 0.5‐1.5%

purified so don't have risk of hep and HIV

Front 87

what is dextran?

2 forms

Back 87

 Large glucose polymer
 Dextran‐40
 Dextran‐70

Front 88

2 uses of dextran

Back 88

 Plasma volume expander
 VTE prevention- wat- prevent clots? doesn't make much sense if you're trying to fix blood loss and yet prevent coagulation so not used much

Front 89

dextran ADRs (4)

Back 89

 Anaphylaxis in 1‐5%
 Osmotic diuresis
 Bleeding diathesis
 Reticuloendothelial blockade

Front 90

Blood usage (2)

Back 90

Volume expansion + oxygen‐carrying
capacity

Front 91

blood disadvantages (4)

Back 91

 Cost
 Compatibility error
 Infection
 Citrate- causes hypocalcemia because it binds calcium in LR? wtf didn't talk about it

Front 92

acid/bases on charts- how to read
x/x/x/x

Back 92

pH/ PCo2/PO2/HCO3-

Front 93

normal pH of bodily fluids (arterial blood, venous blood/interstitial fluid, intracellular fluid)

Back 93

Arterial blood: 7.4
Venous blood and interstitial fluid: 7.35 (more CO2)
Intracellular fluid: 7.0

Front 94

Alkalosis/alkalemia – pH

Back 94

arterial pH > 7.45

Front 95

Acidosis/acidemia – pH

Back 95

arterial pH < 7.35

Front 96

respiratory acidosis/alkalosis results from...

Back 96

result from failure of the respiratory system
to balance pH

Front 97

single most important indicator of
respiratory inadequacy

Back 97

PCO2

Front 98

normal PCO2 fluctuates between what?

values that signal respiratory acidosis and alkalosis

Back 98

Normal PCO2 fluctuates between 35‐45 mmHg
Values > 45 mmHg signal respiratory acidosis
Values < 35 mmHg signal respiratory alkalosis

Front 99

[H+] (acidity) equation for blood

Back 99

[H+] = 24x(pCO2/[HCO3-])
basically CO2 treated like acid

Front 100

Most common acid‐base imbalance

Back 100

respiratory acidosis- hypercapnea (too much CO2)

Front 101

2 causes of respiratory acidosis

Back 101

shallow breathing- e.g. narcotics
hampered gas exchange

Front 102

4 causes of hampered gas exchange that causes resp acidosis

Back 102

▪ COPD
▪ Pneumonia
▪ Cystic fibrosis
▪ PE

Front 103

respiratory alkalosis causes

Back 103

Hyperventilation (“blowing off the CO2”)

Front 104

sx of respiratory acidosis (3) and mechanism

Back 104

headache
papilledema-optic disc swelling that is caused by increased intracranial pressure
CO2 is vasodilator --> increases cerbral blood flow -->CNS changes (obtundation?)

Front 105

metabolic acidosis/alkalosis definition

Back 105

All pH imbalances except those caused by abnormal PCO2 levels

Front 106

HCO3- levels- normal range

values that signal alkalosis and acidosis

Back 106

Normal HCO3‐ fluctuates between 22‐26 mEq/L
Values > 26 mmHg signal metabolic alkalosis
Values < 22 mmHg signal metabolic acidosis

Front 107

Second most common cause of acid‐base
imbalance

Back 107

metabolic acidosis

Front 108

sx of respiratory alkalosis (4)

Back 108

cardiac arrhythmias
decreased cerebral BF because decreased CO2 (vasoconstriction?)-->HA, syncope, seizures

Front 109

when you see metabolic acidosis- 2 types you need to distinguish

how to calculate?

Back 109

Determine if anion gap or non‐anion gap

Anion gap = Na – (Cl‐ + HCO3
‐)

Front 110

anion gap vs. non-anion gap metabolic acidosis- AG ranges for both and etiology

Back 110

if AG < 12, it is non-anion gap and due to excessive loss of HCO3-

if AG >=12, it is an anion gap metabolic acidosis and due to accumulation of organic acids

Front 111

4 sx of metabolic acidosis

Back 111

hyperventilate to blow off CO2 to compensate
CNS depression, though more common with resp acidosis
GI symptoms
peripheral vasodilation

Front 112

non-gap metabolic acidosis etiologies (2 are drugs) (8)

Back 112

bicarb loss-->so diarrhea
pancreatic bicarb loss
renal tubular acidosis
post respiratory alkalosis
potassium sparing diuretics (causing hypoaldosteronism)
carbonic anhydrase inhibitors
ureteral diversions into bowel (peeing out of your butt so diarrhea)
acids (HCl, NH4Cl)

Front 113

anion gap metabolic acidosis etiologies (10) all these things are adding acids

remember the mnemonic

Back 113

MUDPILES

Methanol
Uremia
Diabetic ketoacidosis
Paraldehyde
Isoniazid, ingestions (of toluene)
Lactic acidosis from variety of causes (metformin, seizures, sepsis, shock,
rhabdomyolysis)
Ethanol, ethylene glycol
Salicylates (ASA od)

Front 114

metabolic alkalosis definition

Back 114

Rising blood pH and HCO3‐ levels

Front 115

typical causes of metabolic alkalosis (6)
losing acids

Back 115

Vomiting (excessive stomach acids lost)
Intake of excess base (i.e., antacids)
Constipation (excessive HCO3‐ reabsorbed)
Volume contraction (i.e., “contraction alkalosis”- from diuresing)
Hypochloremia
Excessive black licorice intake

Front 116

respiratory and renal complications

Back 116

Acid‐base imbalance due to inadequacy of a
physiological buffer system is compensated for by the
other system

Front 117

treating metabolic acidosis (2)

Back 117

if PH < 7 can give bicarb, otherwise address underlying cause

Front 118

respiratory and renal compensations for acid/base disorders- explain what occurs generally, then specifically in each system what the limits are for compensation

Back 118

Acid‐base imbalance due to inadequacy of a physiological buffer system is compensated for by the other system

Respiratory system will attempt to correct metabolic acid‐base imbalances instantly but cannot fully compensate and can't over compensate

Kidneys will work to correct imbalances caused by respiratory
disease by altering bicarb absorption/secretion - can fully compensate but not over compensate but takes like 4 days to fix things

Front 119

6 steps for interpreting ABG

Back 119

Determine if acidotic or alkalotic (pH)
Assess possible metabolic imbalance (look to see what is more screwy, bicarb or PCO2- off more is probably the issue)
If other item isn't screwy, probably acute (no time for compensation)
Assess possible respiratory imbalance
Mixed metabolic‐respiratory imbalance
Assess for compensatory process

Front 120

IDK if have to know exact ranges...
venous blood values compared to arterial blood- pH, PO2, O2 sat, PaCO2, HCO3

Back 120

pH lower because more CO2 (7.38)
PO2 lower because O2 has been delivered (35-40)
SaO2 same as above (70-75)
PaCO2 higher (41-51)
HCO3 higher (24-28)

Front 121

how to use goldberg graph

Back 121

- take ABG- plot PCO2 on bottom axis, HO3 on top, then look at pH and it'll tell you what it is...

Front 122

look at samples for ABG

Back 122

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