Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Genitourinary 1 > Basic Principles of Acid/Base Physiology > Flashcards

Basic Principles of Acid/Base Physiology Flashcards

1
Q

How is CO2 produced?

How much CO2 is produced?

A

through aerobic metabolism (complete oxidation) of CHO, fats, and most neutral amino acids

200mL/min = 8.9mmol H+/min

  • if remained as free H+ in tissue, would be fatal in <1min
  • healthy respiratory system readily exhales CO2 as fast as it is produced, so no net load of volatile acid accumulates in the body
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the other acids in the body called (not produced from CO2)?

A

non-volatile acid, non-carbonic acid, non-respiratory acid, metabolic acid, or fixed acid

several metabolic processes produce fixed acids and therefore increase [H+]

  • other metabolic processes produce bases and therefore consume H+
  • GI tract can either be a source or a sink for fixed acids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are three basic processes involved int he body’s response to disturbance in extracellular fluid [H+]?

A
  1. chemical buffers - react very rapidly
  2. respiratory regulation - reacts rapidly
  3. renal regulation - reacts slowly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How does the buffer system help maintain pH in a narrow range?

A

minimize the changes in [H+] that result from the addition or removal of acid from the body fluids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does respiratory regulate changes in pH to keep in a narrow range?

A

chemorecetors in the carotid and aortic bodies in the medulla detect the departure from normal pH

  • triggers the chemoreceptor reflex to change respiratory rate and depth (i.e. to adjust ventilation) to retain or blow off CO2 as needed
  • controls PCO2, which helps return the abnormal pH back to normal

*if respiratory dysfunction is the initiating disturbance, then the chemoreceptor reflex will have limited ability to correct the dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does the kidney regulate pH?

A

vary their excretion of HCO3- and H+ in order to either increase or decrease the amount of ‘new’ [HCO3-] added the body’s extracellular fluid to help bring abnormal pH back to normal

critical role by the kidneys:

  • when acid is added, kidneys continually add enough ‘new HCO3-‘ to the body fluid to match the net daily load of fixed acid (accumulating fro metabolism and from the GI tract)
  • replace any HCO3- lost in the urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is a crtical role of the kidneys?

A

kidneys sustain [HCO3-] in the body fluids

the process of synthesizing new HCO3- and adding it to fluids also synthesizes ‘new’ H+, which they excrete in the urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is pH?

A

pH = -log [H+]

normal pH of arterial blood = 7.4

acidosis = < 7.35

alkalosis = > 7.45

Concentration of H+ is TINY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are some features of H+?

A

H+ is highly reactive

because ion is so small, it is very mobile

has extremely high charge density

extremely high chemical activity

since [H+] in body fluids is so tiny, the addition or removal of tiny amounts of free H+ can change [H+] dramatically

since H+ is so highly reactive, these changes in [H+] significantly alter protein conformation and therefore protein function (especially enzyme function)

  • small change -> BIG effect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are some important features of pH?

A

pH scale = 0-14

pH 7 = neutral (pure water)

each step on the pH scale represents a factor of ten

  • pH 5 vs pH 6 = 10x more acidic
  • change of 2 pH units = 100x more basic/acidic

small variations in ECF (blood) pH are usually fatal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why is H+ so reactive?

A

hydrogen atom has one electron and one proton

hydrogen ion has only a proton

  • responsible for pH
  • only electrons can be changed or lost
  • cation
  • without e-, H+ very reactive

volatile acid = carbonic acid (H2CO2)

non-volatile or ‘fixed’ acid = HCl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is intracellular pH maintained?

A

lower than plasma pH because metabolism of the cells produces acid and because many cellular proteins have a net negative charge that attracts extracellular H+

  • cell membranes are essentially impermeable to ions
  • electrolytes therefore must enter or leave cells via ion channels or carriers
  • transporters control the intracellular concentrations of various electrolytes
  • intracellular fluid has a higher [H+] = lower pH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why is [H+] the same in interstitial fluid and in plasma?

A

electrolytes diffuse freely (and passively) across the capillary endothelium

  • H+ passes freely through intracellular clefts or pores between endothelial cells, or through fenestrations of fenestrated capillaries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why is pH in venous blood lower?

A

metabolism of the cells produces carbon dioxide and hydrogen ions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why does [H+] need to be regulated?

A

Neurophysiology

  • [H+] influences [K+] across the cell membrane
  • pH influences nerves and muscle electrophysiology
  • normal cell membrane permeable to K+ and impermeable to Na+ and anions
  • changes in extracellular [H+] result in changes in extracellular K+ and therefore affect resting membrane potential
  • resting membrane potential = -90mV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is alkalosis?

A

low [H+] (K is Low)

  • reduced H+ in the extracellular fluid
  • H+ to exit the cell (maintaining electro-neutrality)
  • reduced intracellular free H+ causes the negative binding sites on intracellular proteins to release H+. The exposed negative binding sites permits intracellular K+ and Ca2+ to bind
  • results in a reduction in intracellular free K+ and Ca2+. Subsequently, K+ moves into the cell causing hypokalemia
  • an increase in pH of 0.1 units causes a decrease of plasma K+ of 0.5 to 1.0 mEq/L
  • reduced free intracellular Ca2+ reduces cardiac contractility by interfering with excitation-contraction coupling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do you calculate resting membrane potential?

A

Em = -60*log [in]/[out]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What happens in alkalosis?

A

H+ moves out of cellsand K+ moves in

  • hypokalemia -> nerve and muscles hyperpolarized, making RMP more negative, drawing it further from threshold
    • decrease nerve and muscle excitability -> muslce weakness or paralysis

In the heart:

  • H+ come out of cells opening more negative binding sits on proteins -> decrease in free intracellular calcium (more calcium binds to intracellular proteins)
    • reduces cardiac contractility by interfering with excitation-contraction coupling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does a protein’s function depend on?

A

specific conformation

  • proteins have multiple anionic sites that attract and can associate with H+
  • amino acid order determines the protein conformation
  • interactig with H+ alters protien conformation and therefore alters protein function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does the binding (or unbinding) of H+ affects the function of what proteins?

A
  • enzymes involved in intermediary metabolism
  • proteins that act as membrane receptors, channels, or carriers
  • proteins that control the concentration (activity) of oxygen, electrolytes, and hormones in body fluids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Using albumin as an example, how does H+ binding affect function?

A
  1. a decrease in [H+] int he blood plasma
  2. less binding of H+ to albumin
  3. more binding sites available to Ca2+
  4. more binding of Ca2+ to albumin
  5. decreased concentration of Ca2+ in extracellular fluid
  6. decreased allosteric effect of free Ca2+ on other proteins (e.g. voltage-gated Na+ channels)
  7. hyper-excitability of neurons (including motor neurons)
  8. uncontrolled muscle contractions: tetanus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What happens in plasma alkalosis?

A
  1. plasma alkalosis
  2. less binding of hydrogen to albumin
  3. more binding of calcium to albumin
  4. decreased plasma free calcium
  5. change in voltage gated sodium channels
  6. hyperexcitability
  7. tetany
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What happens in acidosis?

A

high [H+] (K is High)

  • acidosis causes H+ to move into cells
  • decreased intracellular pH lessens the binding of K+ and Ca2+ to intracellular anions.
  • K+ is released and moves out of the cell
  • intracellular acidosis also decreases activity of the Na+/K+ ATPase
  • the increased intracellular free calcium promotes arrhythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What happens to skeletal muscle in acidosis?

A

acidosis -> hyperkalemia

skeletal muscle weakness is due to sustained depolarization and inactivation of Na+ channels

arrythmias are a consequence of hyperkalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the major effect of acidosis?

A

depression of the CNS

when pH falls below 7.35, the CNS malfunctions and the individual becomes disoriented and possibly comatose as the condition worsens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the major sources of hydrogen?

A

normal (complete) oxidation of carbohydrates and fat

  • -> CO2 + H2O

incomplete oxidation of carbohydrates

  • -> lactic acid

excessive breakdown of fatty acids in liver

  • -> ketone bodies

oxidation of sulfur-containing amino acids

  • ->H2SO4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What happens in metabolism?

A

depending on the pathways involved, metabolism can produce several acids

  • normal oxidation of carbs and fats -> CO2 + H20
    • CO2 is not itself an acid, but acts as an acid through chemical reactions with water
  • large quantity of CO2 is eliminated by lungs, so typically no impact on acid-base balance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is volatile acid?

A

acid produced from CO2 is called volatile acid, because CO2 is a gas and can be exhaled by the lungs

  • by exhaling more or less CO2, the body can change the [CO2] in body fluid, and thereby regulate the pH of body fluid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What happens in hypoventilation?

A

leads to an increase in CO2, which leads to an increase H+, which causes a decrease pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What happens in hyperventilation?

A

leads to a decrease CO2, which leads to decrease H+, which causes an increase pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What happens if excess CO2 is retained in the body?

A

due to inadequate ventilation called hypoventilation

creates an acid load and an increased [H+] -> decreased pH

hypoventilation -> increased CO2 -> increased [H+] -> decreased pH

OR

hyperventilation -> decreased CO2 -> decreased [H+] -> increased pH

32
Q

What is the solubility of CO2?

A

volume of gas in the liquid depends on its solubility

Henry’s law: greater solubility of CO2 than O2 and N2

33
Q

What are the concentrations vs. partial pressures of gases dissolved in liquids?

A

concentration of gas dissolved in liquid is directly related to its soliubility in the liquid

  • concentration of a highly soluble gas will be greater than that of a less soluble gas at the same partial pressure
34
Q

How do you calculate dissolved CO2?

A

solubility of CO2 = 0.03mmol/L/mmHg

At equilibrium, the concentration of dissolved CO2 is proportional to the pressure of CO2 (PCO2)

[CO2]d = PCO2 * (0.03mM CO2/mmHg)

ex: if PCO2 = 40 mmHG, then [CO2]d = 1.2mM

35
Q

What is the Henderson-Hasselbach equation as it relates to CO2?

A

pH = pKa + log ([HCO3-]/0.03*pCO2)

[HCO3-] is regulated by kidneys

pCO2 is regulated by respiration

36
Q

How is CO2 transported in blood?

A

tissue-produced CO2 is transported in systemic venous blood to the lung where it is excreted by exhalation

  • CO2 diffuses as a physically dissolved gas into capillary blood by simple diffusion
  • CO2 must continually be excreted to avoid acid-base problems
  • systemic arterial blood entering the tissue capillary already contains a considerable amount of CO2
  • a certain amount is retained and maintained in the blood for the purpose of acid-base balance

amount of CO2 exhaled by the lungs needs to equal the amount of CO2 produced by the tissues of the body

37
Q

What forms of CO2 are present in the blood?

A

bicarbonate ions

dissolved CO2 gas

carbonic acid

carbamino groups of proteins

38
Q

How is CO2 in systemic arterial blood?

A

most CO2 present in systemic arterial blood is not in the form of a physically dissolved gas

CO2 hydration reaction:

  • CO2 reacts with water (hydration) to produce carbonic acid (H2CO3)
  • H2CO3 is unstable and readily dissociates into bicarbonate (HCO3-) and hydrogen (H+) ions
    • the H+ formed from the dissociation of carbonic acid is buffered so the concentration of free H+ ions is negligible compared to HCO3-
39
Q

Why does loading of CO2 in the tissue capillary occur in red blood cells?

A

RBCs contain carbonic anhydrase, the enzyme that facilitates the hydration reaction of H2CO3 -> HCO3- + H+

  • a diffusion gradient of HCO3- causing it to exit the RBC to the plasma, leaving behind a net positive charge on the inside of the RBC membrane
  • to preserve electrical neutrality of the RBC membrane, Cl- move into the RBC from plasma (chloride shift/Hamburger effect)
  • H+ is buffered by Hb
    • as H+ attach to Hb, they displace K+ -> net gain in the number of osmotically active particles inside the RBC and prompts a net inward diffusion of H2O from the plasma to maintain osmotic balance
    • inward flex of water causes the volume and size of the RBC to increase slightly as it traverses the tissue capillary
40
Q

What is a non-volatile acid?

A

any acid not produced from CO2 is called:

  • non-volatile acid
  • non-carbonic acid
  • non-respiratory acid
  • metabolic acid
  • fixed acid
41
Q

What are features of a non-volatile acid?

A

cannot be eliminated from the body via the lungs

  • must instead be eliminated via the GI tract (in the feces or vomit) or via the kidneys (in the urine)
  • kidneys play the prime role by excreting more acid or less acid in the urine
42
Q

What are the sources of non-volatile acid?

A

metabolism of carbohydrates, fats, and amino acids

43
Q

How is lactic acid a source of non-volatile acid?

A

incomplete oxidation of carbohydrates (in hypoxic conditions) -> lactic acid

lactic acid ⇋ H+ and lactate-

44
Q

How are ketone bodies a source of non-volatile acid?

A

excessive breakdown of fatty acids in liver (in fasting state or uncontrolled diabetes) -> ketone bodies (ketoacids)

acetoacetic acid ⇋ H+ + acetoacetate- -> acetone + CO2 (pKa = 3.8)

ß-hydroxybutyric acid ⇋ H+ + ß-hydroxybutyrate-

45
Q

How do ketone bodies affect the entry of acetyl CoA into the TCA cycle?

A

entry of acetyl CoA into the TCA cycle depends on the avaialbility of oxaloacetate, which is lowered if carbohydrates are unavailable (starvation) or improperly utilized (diabetes)

  • oxaloacetate is normally formed from pyruvate by pyruvate carboxylase
  • fats burn in the flame of carbohydrates
  • in fasting or diabetes the gluconeogenesis is activated and oxaloacetate is consumed in this pathway
  • fatty acids are oxidized producing excess acetyl CoA, which is converted to ketone bodies
    • ketone bodies synthesized in the liver MT and exported to different organs
  • ketone bodies are fuel molecules (can fuel brain and other cells during starvation)
46
Q

How is sulfuric acid a source of non-volatile acid?

A

oxidation of sulfur-containing amino acids (e.g. methionine, cysteine) -> H2SO4

cysteine and methionine - contain sulfur and are catabolized to produce sulfuric acid

47
Q

How is phosphoric acid a source of non-volatile acid?

A

metabolism of phosphorous-containing proteins and phosphoesters in nucleic acids -> H3PO4

nucleic acids and phosphoproteins catabolized to produce phosphoric acid

48
Q

What are the sources of bicarbonate?

A

apical membrane of parietal cell, which faces the lumen of the stomach, contains an H+-K+ ATPase (proton pump)

basolateral membrane, which faces the blood, contains a Na+-K+ ATPase and a Cl-HCO3- exchanger

inside the parietal cell, CO2 and H2O combine to form H2CO3, which dissociates into H+ and HCO3-

H+ secreted into lumen of stomach

HCO3- is exchanged for CL- across basolateral membrane and is absorbed into gastric venous blood (‘alkaline tide’); eventually it is secreted into the lumen of the small intestine where it neutralizes the acidic chyme delivered from the stomach and some is filtered into the urine

loss of H+ from GI tract occurs during vomiting and nasal gastric suctioning -> alkalosis

49
Q

How do the intestines handle bicarbonate?

A

HCO3- secreted into the proximal duodenum moves to the jejunum, where both Cl- and HCO3- are absorbed in large amounts

  • most HCO3- is absorbed in the distal jejunum
  • Cl- is absorbed and HCO3- is secreted in the ileum
  • Cl- is absorbed and HCO3- is secreted in the colon

Thus, loss of HCO3- occurs with diarrhea

50
Q

How do the typical loads of volatile and fixed acids compare?

A

excess of fixed acid must be excreted in order to maintain acid/base balance - kidneys & lungs play crucial roles in acid excretion

51
Q

How is acid regulated?

A

the lungs by themselves are of no use in excreting a fixed acid load, which requires the kidneys

  • normal kidneys can readily excrete an amount of acid equal to the daily fixed load in the urine
  • fixed acids usually referred to by their anion (e.g. lactate, phosphate, sulphate, acetoacetate, or beta-hydroxybutyrate) - dissociation of acid must have produced H+ for every anion
52
Q

How do the kidneys work in collaboration with the lungs to excrete fixed acid?

A

Step 1: the kidneys hydrate CO2 to synthesize H+ and HCO3-

  • reaction takes place within the renal tubular epithelial cells

Step 2: the kidneys excrete this ‘new H+’ in the urine, but the ‘new HCO3-‘ gets added to the body fluid

Step 3: in body fluid, this ‘‘new HCO3-“ combines with H+ that was formed from fixed acids

Step 4: the resulting CO2 is exhaled by the lungs; the H2O remains in the body fluid or is excreted (as needed to maintain water balance)

Step 5: the load of H+ from fixed acids is removed from the body without any net loss of body fluid HCO3-

  • the ‘new H+’ appears int he urine in the form of acids (titratable acids or NH4+)
  • amount of free H+ in urine is negligible
53
Q

How is the acid-base balance mantained?

A

daily net load of fixed acid must be excreted

this is done by combining H+ from fixed acid with HCO3- in the body fluid to form CO2 and H2O and exhaling the CO2

The HCO3- needed for this purpose must be created by the kidneys as ‘new HCO3-‘

the kidneys must add a net amount of HCO3- to the body fluid each day equal to the net load of fixed acid

54
Q

What are buffers in body fluid physiology?

A

a partially dissociated acid (i.e. weak acid) in solution

  • minimizes the decrease in pH that results from the addition of a strong acid to the solution
  • minimizes the increase in pH that results fromt he addition of a strong base

to be effective, a buffer must be able to accept or donate protons, depending on whether acid or base is added

55
Q

What do buffer systems do? Examples?

A

prevent rapid changes in pH of a body fluid

principle buffer system:

  • phosphate buffer system
  • protein buffer system
  • carbonic acid-bicarbonate buffer system
56
Q

What is the respiratory control system designed to do?

A

designed to more closely regulate physically dissolved CO2 (i.e. pCO2)

  • since CO2 readily reacts with water to yield H+ and HCO3- to control CO2 by ventilation helps to maintain a proper acid-base environment that is essential for the proper enzyme function
  • geared towards the regulation of extracellular fluid CO2 and pH with secondary emphasis on maintaining adequate blood oxygenation

when ventilation is sufficient to maintain a proper CO2 and pH of blood, the oxygenation of blood will in omst instances also be adequate

57
Q

How is CO2 sensed and regulated?

A

chemoreceptor reflexes

  • specialized cells capable of detecting changes in the concentration of physically dissolved O2, CO2, or H+ in the extracellular fluid immediately surrounding them
  • divided functionally, anatomically, and geographically into peripheral and central chemoreceptors
  • function to regulate ventilation so CO2 is maintained nearly constant and at a level consistent with CO2 production and O2 consumption by the tissues of the body
58
Q

How are peripheral chemoreceptors stimulated?

A

carotid and aortic bodies are able to monitor the physically dissolved O2 and CO2 and H+ concentration of arterial blood

  • stimulated by a decline in the PO2, especially when falls below 60 Torr
  • stimulated by an increase in the arterial blood H+ concentration (decreased pH) or an increase in physically dissolved CO2 (or PCO2)
  • only sensors capable of detecting a fall in pO2
  • account for inreases in ventilation resulting from hypoxemia
  • only detect levels of physically dissolved O2 and not the O2 that is chemically attached to hemoglobin
59
Q

How are central chemoreceptors stimulated?

A

chemosensitive areas (CSA) are located along the ventrolateral surface of the medulla near the CSF of the 4th ventricle

  • stimulated by an increase in the PCO2 or H+ concentration
  • NOT stimulated by O2
  • appear to be more sensitive to changes in H+ or PCO2 of CSF than of cerebral blood
  • blood brain barrier limits access of certain blood constituents, such as HCO3- and H+ to the CSF
  • not sensitive to changes in the PO2 of cerebral blood or CSF
    *
60
Q

What is respiratory acidosis?

A

process that acidifies the blood by increasing pCO2

Hypoventilation -> increase in CO2 -> increase in H+ = decrease pH

61
Q

What is metabolic acidosis?

A

any other process that acidifies the blood (i.e. process that adds fixed acid to the blood, or removes HCO3- from the blood)

  • losing bicarbonate is equivalent to gaining acid
    • any HCO3- lost via urine or GI tract becomes unavailable to combine with H+ in body fluid and participate in acid excretion via lungs, so losing a HCO3- has effect of ‘stranding’ a fixed H+ in body fluid
62
Q

How is HCO3- removed from the blood?

A

diarrhea causes a loss of bicarbonate as the bowel is generally rich in bicarbonate

-> acidosis

63
Q

How are fixed acids added to the blood?

A

ketone bodies

  • excessive breakdown of fatty acids in liver (in fasting state or uncontrolled diabetes) -> ketone bodies (ketoacids)

lactic acid

  • incomplete oxidation of carbs (in hypoxic conditions) -> lactic acid

consuming aspirin

64
Q

What is respiratory alkalosis?

A

process that makes the blood less acidic by decreasing arterial pCO2

hyperventilation -> decrease CO2 -> decrease H+ and increase pH

65
Q

What is metabolic alkalosis?

A

any other process that decreases the acidity of the blood (i.e. process that removes fixed acid from the blood or adds HCO3- to the blood)

  • gaining of bicarbonate is equivalent to losing an acid
    • any HCO3- is added and becomes available to combine with H+ and participate in acid excretion via the lungs
66
Q

How is fixed acid removed from the blood?

A

loss of H+ ions from the stomach through vomiting, forcing the stomach to produce more acid, thus raising serum bicarbonate levels (alkalosis)

67
Q

How are acid-base disorders analyzed?

A
  1. acquire a history and PE that raises suspicion of an acid-base disorder. obtain arterial blood gases (ABG)
  2. analyze the pH. labeled as acidic, alkalotic, or normal
  3. analyze the CO2. label pCO2 as acidic (increase), alkalotic (decrease), or normal; analyze HCO3. label HCO3- as acidic (decrease), alkalotic (increase), or normal.
  4. match the CO2 or the HCO3 with the pH. if acidotic and CO2 is acidotic, then primary acid base disturbance is respiratory acidosis; if pH is alkalotic and HCO3 is alkalotic, then primary acid base disturbance is metabolic alkalosis
  5. look for combination disorders.
  • in respiratory acidosis, if HCO3- is lower than expected, condition is combined metabolic acidosis & respiratory acidosis
  • in respiratory alkalosis, if HCO3- is higher than expected, condition is combined metabolic alkalosis & respiratory alkalosis
  • in metabolic acidosis, if low PaCO2, then respiratory compensation for a metabolic acidosis
  • in metabolic alkalosis, if high PaCO2, then respiratory compensation for a metabolic alkalosis
  1. compensation: does CO2 or HCO3 go in the opposite direction of pH?
  2. if patient has metabolic acidosis, calculate serum anion gap (AG)
  • AG is difference between measured serum cations and the measured serum anions
  • anion gap = [Na+] - [Cl-] - [HCO3-]
    • lactate increases the anion gap
    • acetoacetate increases the anion gap
  1. in patient with wide anion gap metabolic acidosis, calculate the delta gap
  • delta gap = AG - 12
  • measures how much bigger AG is than ‘normal’
68
Q

What are the compensation mechanisms in metabolic acidosis?

A

respiratory compensation:

  • expect hyperventilation, which decreases PaCO2 below normal

‘full compensation’:

  • expect PaCO2 to decrease to a value (in mmHg) = [(1.5*[HCO3-])+8] +/- 2

timing:

  • hyperventilation begins immediately
  • steady-state compensation reached in 12-24hrs
69
Q

What are the compensation mechanisms in metabolic alkalosis?

A

Respiratory compensation:

  • expect hypoventilation, which increases PaCO2 above normal

‘full compensation’:

  • expect PaCO2 to increase 0.5mmHg for every 1 mEq/L increase in [HCO3-]

important note:

  • both the amount and timing of respiratory compensation are less predictable than for metabolic acidosis
70
Q

What are the compensation mechanisms in acute respiratory acidosis?

A

by mass action:

  • expect 1mEq/L increase in HCO3- for every 10 mmHg increase in PaCO2

equivalently:

  • expect pH to be down by 0.08 for every 10mmHg increase in PaCO2
71
Q

What are the compensation mechanisms in chronic respiratory acidosis?

A

renal compensation:

  • with ‘full compensation’, expect 3-5 mEq/L increase in HCO3- for every 10mmHg increase in PaCO2

equivalently:

  • expect pH to be down by only 0.03 for every 10mmHg increase in PaCO2
72
Q

What are the compensation mechanisms in acute respiratory alkalosis?

A

by mass action:

  • expect 1-2 mEq/L decrease in HCO3- for every 10mmHg decrease in PaCO2

roughly equivalent:

  • expect pH to be up by 0.08 for every 10mmHg decrease in PaCO2
73
Q

What are the compensation mechanisms in chronic respiratory alkalosis?

A

renal compensation:

  • with ‘full compensation’, expect 5 mEq/L decrease in HCO3- for every 10mmHg decrease in PaCO2

roughly equivalent:

  • expect pH to be up by only 0.03 for every 10mmHg decrease in PaCO2
74
Q

What is normal-AG acidosis?

A

metabolic acidosis with normal AG

e. g. severe diarrhea -> loss of NaHCO3 -> decreased [HCO3-]
* if lost NaHCO3 is replaced with NaCl, AG remains normal

75
Q

What is wide-AG acidosis?

A

metabolic acidosis with elevated AG

e.g. increased [organic anions] from increased production of lactic acid or ketoacids

Genitourinary 1 (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions