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Paige - MOD > Lecture 13: Acid/Base > Flashcards

Lecture 13: Acid/Base Flashcards

1
Q

Define an acid and base.

A

Acids are molecules that release H+.

Bases are molecules that accept H+.

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2
Q

Define pH.

A

Power of hydrogen, aka the amount of hydrogen ions present on a logarithmic scale.

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3
Q

What is the normal range for body pH?

A

7.35-7.45

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4
Q

What is the basic formula for carbonic acid to bicarb and hydrogen ions?

A

CO2 + H2O <=> H2CO3 <=> HCO3- + H+

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5
Q

What is the Henderson-Hasselbalch equation used for?

A

Determining pH, given the concentration of bicarb and pCO2.

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6
Q

What 3 systems are responsible for maintaining the body’s acid/base balance?

A

Chemical buffer systems, which include:
Bicarbonate buffer systems
Proteins
H+/K+ transcellular system
(Bone buffer system)

Respiratory acid/base control
Renal acid/base control

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7
Q

What is the acid and base in the bicarbonate buffer system?

A

HCO3- is the base, as it can accept H+.
H2CO3 is the acid, as it contributes H+.

(Our body can readily eliminate the components that are not needed)

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8
Q

What is the largest buffering system in the body?

A

Proteins.

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9
Q

Why are proteins able to buffer the pH of the body?

A

They are amphoteric, aka they have binding sites for both bases and acids.

They are found in essentially all cells, but they have delayed onsets due to the transmembrane movement of an acid/base.

They can also help buffer the ECF/plasma.

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10
Q

How does the H/K transcellular system work?

A

Both ions can freely move across a membrane.

Cells can exchange them for each other to maintain equilibrium.

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11
Q

How does the bone buffering system work?

A

Excess H+ can be exchanged for Na and K on bone surface.

Bone breakdown releases Sodium and Calcium bicarb.

Note:
It is technically not a buffering system, as it is only active during acute acid loads and chronic acidemia.
Chronic acidemia can also cause weak bones as a result.

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12
Q

How does the respiratory acid/base control work?

A

Controlling pCO2, which is in ECF.
Causes RAPID changes in pH, maximizing in 12-24 hours.
NOT AS EFFECTIVE as renal management.

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13
Q

What receptors monitor our pCO2 and where are they found?

A

Chemoreceptors, which are found in the brainstem, carotids, and aorta.

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14
Q

How do the lungs respond to acidemia and what is the chemical adjustment that occurs?

A

They will increase ventilation.

This decreases pCO2, which decreases the formation of carbonic acid.

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15
Q

How do the lungs respond to alkalemia and what is the chemical adjustment that occurs?

A

They will decrease ventilation.

This increases pCO2, which increases the formation of carbonic acid.

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16
Q

How does the renal acid/base control work?

A

Controls H+/HCO3- excretion via kidneys.

Takes several hours to days to reach full effect.
Can be sustained long-term.

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17
Q

What functions do the kidneys play in renal acid/base control?

A

They excrete H+ ions freely and through making compounds like sodium phosphate or ammonia/ammonium.

They can also reabsorb HCO3- if needed.

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18
Q

How do the kidneys respond to acidemia?

A

They will excrete H+ while reabsorbing HCO3-.

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19
Q

How do the kidneys respond to alkalemia?

A

They will reabsorb H+ while excreting HCO3-.

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20
Q

What two ions in the kidney are generally exchanged for one another?

A

H+ and K+.

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21
Q

What happens to our ions in hyperkalemia?

A

We have increased K+ secretion, which means we have impaired H+ secretion. (aka we can get acidotic while in hyperkalemia)

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22
Q

What happens to our ions in hypokalemia?

A

We have increased K+ reabsorption, which means we have impaired H+ reabsorption. (aka we can get alkalotic while in hypokalemia)

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23
Q

What is hypochloremic alkalosis?

A

An inappropriate excess of HCO3- and loss of Cl-.

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24
Q

What is hyperchloremic acidosis?

A

An inappropriate excess of Cl- and loss of HCO3-.

(Think carbonic anhydrase inhibitor)

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25
Q

What are some acute conditions that can affect our acid-base balance?

A

URI/LRI (respiratory infections), V/D, AKI (acute kidney injury), malnutrition, electrolyte disorder, abnormal volume status, and substance OD.

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26
Q

What are some chronic conditions that can affect our acid-base balance?

A

Liver, lung, CKD (chronic kidney disease), DM, intestines.

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27
Q

What do I examine on a PE that could affect acid-base balance?

A

Respiratory Rate, lung auscultation
Edema, ascites
BP, HR, skin turgor, mucous membranes
Mental status, reflexes

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28
Q

What lab tests can I order that are essential to determining acid-base balance?

A

A BMP (or CMP)

ABG (arterial blood gas):
Provides PaCO2, PaO2, HCO3-, and pH

Note:
You can also order a VBG, which gives PvCO2, SvO2 (venous O2 sat)

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29
Q

Why is an ABG preferred over a VBG? When do I use a VBG?

A

VBGs require adjustments for their values, as venous pH is usually 0.02-0.05 lower and PvCO2 is higher by 3-8 mm Hg than PaCO2.
HCO3- is also 1-2 mEq/L higher.

We get VBGs usually if an ABG is unobtainable.

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30
Q

What lab value is used as our approximate bicarb in a BMP?

A

Carbon dioxide.

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31
Q

What is an anion gap?

A

Difference between measured cations and anions in ECF.

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32
Q

How do I calculate anion gap?

A

[Na+] - ( [Cl-] + [HCO3-] )

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33
Q

What is the normal anion gap range?

A

8-16

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34
Q

Why do we care about anion gap, and when do we measure it?

A

It helps us determine the etiology of metabolic acidosis.

If the anion of the acid added is Cl-, we would see a normal anion gap.

If the anion of the acid added is something else, we would see an increased anion gap.

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35
Q

What kind of things can cause increased anion gap?

A

Some common examples are diabetic ketoacidosis and salicyclic acid OD (aka aspirin).

36
Q

What values do I care about in an ABG for determining acid-base balance?

A

pH
pCO2
HCO3- (more accurate than a BMP)

37
Q

Why is an ABG useful in determining acid-base balance?

A

Used to work-up a patient
Determine the severity of an illness
Help guide treatment
Determine a patient’s response to treatment

38
Q

When do we order an ABG?

A

Suspected hypercapnia (increased PaCO2)
Suspected severe hypoxemia
Suspected ventilatory difficulty

39
Q

What kind of patients do we monitor with ABGs?

A

Ventilated patients
Dyspneic patients
O2 therapy

40
Q

Define acidosis and alkalosis.

A

Acidosis is a PROCESS that increases H+ by increasing PCO2 or by reducing HCO3-.

Alkalosis is a PROCESS that reduces H+ by reducing PCO2 or by increasing HCO3-.

41
Q

What does increased CO2 in the blood do to the acid/base equation?

A

Increased H+ ions.

42
Q

What are the main causes of respiratory acidosis?

A

Depression of CNS respiratory center
Lung disease
Airway obstruction and/or MSK disease
Breathing air with high CO2 content

43
Q

What are the symptoms of respiratory acidosis?

A

Neuro:
HA, CONFUSION, WEAKNESS, DROWSINESS/STUPOR, muscle twitching, tremors, paralysis, COMA

CV:
Vasodilation (warm, flushed skin)

Signs of underlying disease

44
Q

What happens to a person’s respiratory drive if they have chronic hypercapnia?

A

Their CO2 chemoreceptors started getting desensitized, so the body relies of PaO2 chemoreceptors instead. This means that the body will switch to hypoxic drive instead.

PaO2 will then become the principal ventilatory stimulus.

45
Q

Why is hypoxic drive concerning?

A

People on hypoxic drive will suffer greatly if placed on too much supplemental oxygen. They will become acidotic because they will breathe less.

Supplemental oxygen => increased PaO2 => less drive to breathe => less CO2 breathed out => respiratory acidosis.

Note:
Overzealous correction of hypoxemia with supplemental O2 requires ABG monitoring!

46
Q

What happens to our H+ ions if we have less CO2 in our blood?

A

We have less H+, so we enter alkalosis.

47
Q

What are some causes of respiratory alkalosis?

A

Excessive ventilation (pain, anxiety, mechanical ventilation, psychogenic)

Increased stimulus of CNS Respiratory center (Encephalitis, fever, salicylate toxicity, elevated blood ammonia, hypoxemia)

48
Q

What are some symptoms of respiratory alkalosis?

A

Neuro (increased excitability):
Dizziness, panic, light-headedness, TETANY, NUMBNESS/TINGLING, seizures, CHVOSTEKS/TROSSEAU signs.

CV:
Arrhythmias

Signs of underlying disease

49
Q

What are Chvostek and Trosseau signs? Cause?

A

Chvostek = twitching of facial in response to tapping of facial nerve

Trosseau = carpopedal spasm when BP cuff is inflated for 2-3 minutes

Note:
Caused by calcium binding to albumin. Usually, albumin binds to H+, but in respiratory alkalosis, there is less H+ to bind to.

50
Q

What lab test can confirm chvostek and trosseau?

A

Ionized calcium test.

Once calcium binds to albumin, it will become deionized, so ionized calcium counts would be low while BMP calcium would be normal.

51
Q

What are the 4 primary causes of metabolic acidosis?

A

Increased production or ingestion of acids.
Inability to renally excrete acid (H+)
Increased plasma Cl-
Excessive loss of HCO3- (renally or GI tract)

52
Q

Why does diarrhea cause HCO3- loss?

A

There is not enough time for the GI tract to extract the bicarb out.

53
Q

How is normal anion gap preserved during hyperchloremic metabolic acidosis?

A

Even with a loss of HCO3- via kidneys or GI, the kidneys will preserve Cl- to maintain a neutral electrical charge.

54
Q

What can caused an elevated anion gap?

A

Ingestion of an exogenous acid OR elevation of an unmeasured endogenous acid.

Exogenous would be like salicylate poisoning.
Endogenous would be like lactic acid elevation.

55
Q

What can cause a decreased anion gap?

A

Decreased anions, such as in hypoalbuminemia (albumin is negatively charged)

OR

Increased IgG/cations: multiple myeloma; elevations in Ca, K, or Mg

56
Q

What is the purpose of a delta gap?

A

It allows us to determine if a secondary, “hidden” acid-base disturbance is also present.

57
Q

How do I calculate delta gap and how do I interpret it?

A

Delta gap = anion gap - normal AG (12)
Then you add the delta gap to your HCO3-.

It should be 24.
<24 means that something else is contributing to the metabolic acidosis.

> 24 means that something else is contributing as a metabolic ALKALOSIS.

58
Q

How do I calculate modified gap and how do I interpret it?

A

It is a delta gap done without adding the bicarb.

Na + Cl -36

-6 or less = mixed high and normal AG metabolic acidosis.

-6 to 6 = only high AH metabolic acidosis.

6 or more = mixed high AG metabolic acidosis and metabolic ALKALOSIS.

59
Q

What are some common causes of increased anion gaps in metabolic acidosis?

A

Excess production of metabolic acids:
Lactic acidosis
Ketoacidosis
Poisoning

Renal failure:
Accumulation of renal wastes

60
Q

What are some common causes of a normal anion gap in metabolic acidosis?

A

HCO3- loss (renal tubular acidosis, diarrhea, carbonic anhydrase inhibitors, urinary diversion/fistula)

Inability to excrete H+ (Adrenal insufficiency or renal failure)

Excess administration of Cl (IV infusions, ammonium chloride)

Note:
Hyperchloremic metabolic acidosis causes a NORMAL anion gap! Your body is able to compensate using chloride.

61
Q

What is the acronym for high AG metabolic acidosis?

A

MUDPILES!

Methanol
Uremia
DKA
Paraldehyde and phenformin
Isoniazid
Lactic acidosis
Ethylene glycol
Salicylates

62
Q

What is the acronym for normal AG metabolic acidosis?

A

HARD UP!

Hyperalimentation (artificial supply of nutrients, aka TPN)

Acetazolamide (carbonic anhydrase inhibitor!)
Renal tubular acidosis (RTA) (loss of bicarb)
Diarrhea (loss of bicarb)
Ureteral diversion (loss of bicarb)
Pancreatic fistula

63
Q

What general things does acidosis do?

A

CNS depression!

64
Q

What are the neuro symptoms of metabolic acidosis?

A

Confusion
Weakness
Drowsiness/stupor
Coma

65
Q

What are the other non-neuro symptoms of metabolic acidosis?

A

CV:
Vasodilation (warm, flushed skin)
Cardiac arrhythmias

GI:
Abd pain
N/V and anorexia

Respiratory:
Increased depth and rate or respiration (aka Kussmaul)

Bone:
Decreased density/osteoporosis

Signs of underlying disease

66
Q

What kind of medication is metabolic acidosis resistant to?

A

Vasopressors!

67
Q

What ion in the bloodstream causes metabolic alkalosis primarily?

A

Excess bicarb.

Note:
Loss of H+ is not as significant BECAUSE our kidneys can correct it by getting rid of more bicarb. However, H+ retention comes at the cost of increasing serum potassium, which is high detrimental.

68
Q

What kind of medications in general cause impaired HCO3- excretion?

A

Drugs that cause you to vomit or pee a lot. This depletes the other electrolytes, such as Cl, K, and Na.

Note:
Cl is used to trade for bicarb, since they have the same electrical charge. Losing too much Cl means the body needs to keep bicarb to compensate for the loss of electrical charge.

69
Q

What are the common causes of metabolic alkalosis?

A

Excess amounts of bicarb/alkali substances (Sodium bicarb IV, or alkaline IV solutions)

Excessive loss of H+ (Vomiting, NG tubes, Hypokalemia, Milk-alkali syndrome)

Increased bicarb retention (loss of Cl)

Volume depletion (Diuretics)

70
Q

Why does hypokalemia cause metabolic alkalosis?

A

Because the body is low on potassium, it gets rid of H+ instead, since they are exchanged for each other. This increases the pH as we have barely any H+ ions.

71
Q

If I lose a lot of chloride, how does my kidney compensate?

A

It will retain HCO3-, which will cause us to get metabolic alkalosis.

72
Q

If I lose a lot of Na or K, how does my kidney compensate?

A

It will retain Na/K in exchange for H+, causing excess H+ LOSS, leading to metabolic alkalosis.

73
Q

What does alkalosis cause in general to neuro?

A

Increased neuronal excitability

74
Q

What are the neuro symptoms of metabolic alkalosis?

A

Dizziness
Panic
Light-headedness
Tetany
Numbness/tingling
Seizures
Chvostek/trosseau

75
Q

What are the CV symptoms of metabolic alkalosis?

A

Arrhythmias

76
Q

What does ROME stand for?

A

Respiratory
Opposites

(HIGH pH = respiratory alkalosis = LOW PaCO2)
(LOW pH = respiratory acidosis = HIGH PaCO2)

Metabolic
Equivalent

(HIGH pH = metabolic alkalosis = HIGH HCO3-)
(LOW pH = metabolic acidosis = LOW HCO3-)

77
Q

What are the two ways a mixed acid-base disorder can turn out?

A

If both go in the same direction…
You can have profound/severe/refractory alkalemia or acidemia.

If both go in OPPOSITE directions….
You can have a compensated acid-base disorder with a minimal pH change.

78
Q

Define compensation.

A

Process by which either kidneys/lungs make automatic adjustments when the other system is overwhelmed.

79
Q

If I have a primary metabolic acid-base disorder, how will my lungs compensate?

A

They will increase/decrease ventilation.

80
Q

If I have a primary respiratory acid-base disorder, how will my kidneys compensate?

A

Proximal tubule will adjust its HCO3-
Distal tubule will adjust its H+

81
Q

What is the goal of compensation?

A

Maintaining PCO2/HCO3- ratio.

Note:
Compensation NEVER overcorrects.

82
Q

What kind of disorder has acute and chronic compensation?

A

A primary respiratory disorder can have acute or chronic metabolic compensation.

Note:
Respiratory compensation is always the same.

83
Q

What is the direction of the compensatory system in response to a disorder?

A

It is always the SAME direction.

High PCO2 will be compensated by having HIGH HCO3-

84
Q

Why is metabolic compensation acute and chronic?

A

The acute response is due to cell buffering.
The chronic response is from renal adaptation.

85
Q

Given an ABG, what is the process for determining the acid-base disorder?

A

First, I would check what the pH is.

After that, I would check which HCO3- and PCO2 match up with primary metabolic or respiratory.

After I determine the primary disorder, I would check the compensation to see if it is partial or full.

86
Q

What are the special considerations I need to note when considering what acid-base disorder I am dealing with?

A

For a primary respiratory disorder, I need to also check if the metabolic compensation is acute or chronic.

For metabolic acidosis, I need to check the anion gaps and delta gaps to see if a secondary acid or base is contributing.

Paige - MOD (16 decks)

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