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CVPR > CVPR Week 5: Acid and Base prework > Flashcards

CVPR Week 5: Acid and Base prework Flashcards

1
Q

How much of the human body is water?

A

~60% of human body weight is composed of water

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2
Q

Where is the water in the human body distributed?

A

2/3 ICF (28L) and 1/3 ECF (14L)

TBW equation =

0.6 x Wt (Kg) = V (L)

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3
Q

What are the main anions and cations in ICF and ECF?

A
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4
Q

How does H+ effect the cellular environment?

A

H+ concentration modifies protein structure and enzyme function therefore it is paramount to regulate H+ concentration within tight limits (35-45 nmol/L)

What is the typical H+ concentration in the body?

35-45 nmol/L

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5
Q

H+ concentrations in the ECF compared to other elements

A

In the ECF, the concentration of H+ is much less compared to other elements. Such as Na is 35 million times higher than that of H+

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6
Q

Why are buffer systems necessary?

A

Large amounts of H+ are produced during metabolic processes daily

The concentration of H+ must be maintained at low and tight levels

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7
Q

What is a buffer system?

A

A buffer is a solution that resists changes in pH when an acid or an alkali is added to it

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8
Q

What are buffer’s composed of?

A

Typically involve a weak acid or an alkali together with one of their salts

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9
Q

How does a buffer system work?

A

Addition of a strong acid results in the formation of a weak acid and similarly, the addition of a strong base results in the formation of a weak base. Thus a buffer system prevents large changes in pH

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10
Q

Are buffer systems reusable?

A

If the constituents of a buffer system are consumed and the buffer system loses efficacy if they are not replaced.

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11
Q

Buffer system of the ECF?

A

Bicarbonate buffer system (H2CO3/HCO3)

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12
Q

Buffer system of the ICF?

A

Hemoglobin (H/Hb)

Proteins (H/Proteins)

Phosphate (HPO4/H2PO4)

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13
Q

Isohydrolic principle

A

since the H+ concentration in the body is finite, all of the buffers in a common solution are in equilibrium with the same H+ concentration. So by knowing the status of one system then we know the functioning status of all the buffer systems in the body and thus can assess the acid/base status

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14
Q

How is acid/base status assessed?

A

Arterial blood gasses (ABGs), serum osmolarity and chemistries (Na, K, Cl, CO2, albumin), urine chemistries (Na, K, Cl) are a few tools used to assess the functioning of the bicarbonate buffer system

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15
Q

ABGs AKA

A

Arterial blood gases

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16
Q

What are ABGs?

A

A series of tests that are performed on arterial blood and provide valuable information to assess the oxygenation and acid/base status

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17
Q

PaO2 =

A

A value that represents the partial pressure of oxygen dissolved in the arterial blood The PaO2 is the primary indicator of whether a patient is hypoxic and is used to diagnose Acute Respiratory Failure

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18
Q

ARF AKA

A

Acute respiratory failure

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19
Q

What is partial pressure?

A

In a mixture of gases, the partial pressure exerted by a gas is equal to the amount of gas present in that mixture provided the temperature remains constant

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20
Q

Changes in PaO2 with altitude

A

At sea level the atmospheric pressure is 760 mmHg. The concentration in air is 21%, therefore the PO2 at sea level will be (760 x 0.21) 159 mmHg. Albuquerque is at an altitude of 6000 ft and the atmospheric pressure here is approximately 603 mmHg. PO2 in Albuquerque is 126 mmHg. Note that the concentration of O2 remains constant but is only represented by a total pressure of 603 mmHg. 603 mmHg x 21% O2 = 0.21 126 mmHg PO2

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21
Q

What serum level of O2 represents hypoxia?

A

<65 mmHg

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22
Q

SaO2 =

A

Represents the % of hemoglobin which is saturated with O2

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23
Q

Normal SaO2 levels

A

Normal SaO2 = > 92%

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24
Q

What describes the relationship between PaO2 and SaO2?

A

The O2-Hb dissociation curve

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25
Q

FiO2 =

A

The fraction O2 in the inspired air. An ABG result should list the FiO2 at which the ABG was collected. Room air has a FiO2 of 21%

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26
Q

Shunt equation relevance

A

This value is calculated by taking the PaO2 from the ABG results and dividing this by the FiO2 being delivered to the patient.

For example: PaO2 of 75 mmHg divided by room air which has a FiO2 of 0.21 (21% oxygen) would give us a ratio of 357

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27
Q

Shunt equation normal values

A

A PaO2/FiO2 ratio of > 300 is considered normal

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28
Q

pH definition

A

A term used to indicate the hydrogen ion concentration in the blood. It is the H ion concentration in the negative log (base 10) scale.

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29
Q

pH =

A

pH = - log(H+) where H+ is expressed in mol/L

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30
Q

Normal pH range of arterial blood

A

Normal Arterial blood pH = 7.35 - 7.45

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31
Q

pH relation to [H+]

A

pH is inversely related to H+ ion concentration

A low pH is associated with a high [H+]

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32
Q

Is a given pH considered acidic or basic?

A

Any values under 7.40 is considered acidic

Any values over 7.40 is considered alkaline

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33
Q

How to calculate H+ ions from pH

A

[H+] = 10^-pH

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34
Q

PaCO2 =

A

A value that represents the partial pressure of CO2 in the arterial blood

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35
Q

CO2 in the blood is considered?

A

CO2 in the blood is considered a volatile acid

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36
Q

How is CO2 regulated in the body?

A

CO2 is regulated in the lungs, a change in pH due to a change in PaCO2 is labeled as a respiratory abnormality

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37
Q

Normal PaCO2 levels

A

PaCO2 > 42 mmHg indicates respiratory acidosis

PaCO2 <38 mmHg indicates respiratory alkalosis

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38
Q

HCO3 =

A

A value that represents the bicarbonate content of the blood

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39
Q

How is HCO3 regulated?

A

Kidneys regulate HCO3 concentration by reabsorbing and making new HCO3-. A change in pH due to a change in HCO3- is labeled as a “metabolic” abnormality

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40
Q

Normal HCO3 levels

A

HCO3 < 22 indicates metabolic acidosis

HCO3 > 26 indicates metabolic alkalosis

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41
Q

Acid =

A

An acid is a substance that can donate a proton

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42
Q

Base =

A

A substance that can accept a proton

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43
Q

Acidemia =

A

Acidic blood has a pH < 7.35 (or a H ion concentration > 42 nmol/L)

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44
Q

Acidosis =

A

A clinical condition or disease process producing a state where the blood pH is < 7.35

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45
Q

Alkalemia =

A

Basic blood has a pH > 7.45 (or a H ion concentration < 38 nmol/L)

a pH of > 7.45 is labeled as alkalemia

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46
Q

Alkalosis =

A

A clinical condition or disease process producing a state where the blood pH is > 7.45

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47
Q

How does the bicarbonate system work?

A

Cells produce H+ ions which enter the circulation Bicarbonate buffer system which comprises a weak acid (H2CO3) and its salt (NaHCO3), prevents sudden changes in the concentration of H+. H+ binds with the salt (Na)HCO3 and forms Carbonic acid (H2CO3) which is catalyzed by carbonic acid

H2CO3 is unstable and immediately breaks down into H2O and CO2

Thereby preventing an increase in H+ ion concentration by converting a strong acid into a weak acid, however, there was depletion of HCO3 and addition of CO2 in the system

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48
Q

What happens to carbonic acid after it is catalyzed by carbonic anhydrase?

A

H2CO3 is unstable and immediately breaks down into H2O and CO2

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49
Q

For the bicarbonate buffer system to continue preventing pH changes what needs to happen?

A

CO2 needs to be released and HCO3 needs to be repleted

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50
Q

How is HCO3 replenished?

A

Kidneys generate new HCO3

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51
Q

How is CO2 removed?

A

Lungs remove CO2

52
Q

What is the significance of the Henderson-Hasselbalch Equation?

A

It is a mathematical representation of the bicarbonate buffer system and tells us the ratio of HCO3 and PCO2 that govern the pH

53
Q

Bicarbonate buffer system Henderson-Hasselbalch Equation =

A
54
Q

How is pH governed in the blood?

A

pH is governed by the ratio of HCO3 / PCO2

The Henderson-Hasselbalch Equation tells us that pH can only change if PCO2 and/or [HCO3] change

55
Q

Changes in PCO2 are labeled as?

A

Respiratory

56
Q

Changes in [HCO3] are labeled as?

A

Metabolic

57
Q

If PCO2 increases then pH will? And lead to?

A

pH will decrease and lead to respiratory acidosis

58
Q

If PCO2 decreases then pH will? And lead to?

A

pH will increase and lead to respiratory alkalosis

59
Q

If HCO3 increases then pH will? And lead to?

A

pH will increase and lead to metabolic alkalosis

60
Q

If HCO3 decreases then pH will? And lead to?

A

pH will decrease and lead to metabolic acidosis

61
Q

pH is inversely related to which part of the HHE?

A

pH is inversely related to PCO2

62
Q

PH is directly related to which part of the HHE?

A

pH is directly related to HCO3

63
Q

The body tries to limit changes to pH by?

A

Keeping the HCO3/PCO2 ratio constant which is called Compensation

64
Q

What is compensation?

A

The body attempting to limit pH changes by keeping the HCO3/PCO2 ratio constant

65
Q

The compensatory response accuracy?

A

The compensatory response may overshoot or undershoot

66
Q

Compensatory response to metabolic acidosis

A

A decrease in HCO3 will lead to a decreased pH.

Lungs will counteract this by decreasing PCO2 and thus pH will increase

67
Q

Compensatory response to metabolic acidosis AKA

A

Respiratory compensation of metabolic acidosis

68
Q

Respiratory compensation of metabolic alkalosis

A

An increase in HCO3 will lead to an increased pH

Lungs will counteract this by increasing PCO2 and thereby increasing pH

69
Q

Metabolic compensation of respiratory acidosis

A

An increase in PCO2 will lead to a decreased pH

The kidneys will counteract this by increasing HCO3 and thereby increasing pH

70
Q

Metabolic compensation of respiratory alkalosis

A

A decrease in PCO2 will lead to an increased pH

The kidneys will counteract this by decreasing HCO3 and thereby decreasing pH

71
Q

Normal pH values

A

7.35 - 7.45

72
Q

Normal PaCO2 levels

A

38 - 42 mmHg

73
Q

Normal HCO3 levels

A

22-26mEq/L

74
Q

Normal PaO2

A

80-100 mmHg

75
Q

Normal SaO2

A

>92%

76
Q

Normal Hypoxemic score/shunt equation

A

>300

77
Q

How to identify ventilation/perfusion problems?

A

Evaluate PaO2/FiO2 whenever hypoxia is present

78
Q

How to determine the acid/base balance

A

pH is the indicator

pH <7.35 = Acidosis

pH >7.45 = Alkalosis

79
Q

Is the cause of acidosis respiratory or metabolic?

A

If PaCO2 is > 42 mmHg then the cause is respiratory

If the HCO3 is < 22 mEq/L then the cause is metabolic

80
Q

Is the cause of alkalosis respiratory or metabolic?

A

If PaCO2 is < 38 mmHg then the cause is respiratory

If the HCO3 is > 26 mEq/L then the cause is metabolic

81
Q

Has compensation occurred?

A

Find out the magnitude of the compensatory response and assess whether the compensatory response was appropriate or inappropriate

82
Q

Respiratory Acidosis is caused by?

A

Decreased elimination of CO2 usually due to a perfusion/ventilation mismatch

83
Q

Causes of a perfusion/ventilation mismatch?

A

Depression of the respiratory center in CNS

Interference with gas exchange across alveolar membrane

Reduction in the amount of blood pumped to the lungs

84
Q

Lab findings of respiratory acidosis

A

pH < 7.35

PaCO2 > 42 mmHg

85
Q

Respiratory acidosis compensation

A

Kidneys increase HCO3 and thereby attempt to increase pH towards normal but not all the way

86
Q

Respiratory acidosis compensation timeline

A

It takes time for the kidneys to produce new channels and enzymes to produce new HCO3, therefore metabolic compensation of respiratory acidosis has 2 phases; an acute phase where the compensation is less robust and a chronic phase where the compensation is more robust

87
Q

Acute phase respiratory Acidosis compensation magnitude

A

For each 10 mmHg increase in PCO2, the HCO3 increases by 1 mmHg

88
Q

Chronic phase Respiratory Acidosis compensation magnitude

A

For each 10 mmHg increase in PCO2, the HCO3 increases by 4 mmHg

89
Q

Respiratory alkalosis primary defect

A

CO2 deficit

90
Q

Causes of the CO2 deficit in respiratory alkalosis

A

Overstimulation of the respiratory center in the CNS

Hyperventilation - due to exercise

91
Q

Lab findings in respiratory alkalosis

A

pH > 7.45

PaCO2 < 38 mmHg

92
Q

Metabolic compensation of respiratory alkalosis

A

Kidneys reabsorbs less HCO3-

Compensation corrects pH towards nromal but not all the way

93
Q

Metabolic compensation of respiratory alkalosis timeline

A

Metabolic compensation of respiratory alkalosis takes time so there are 2 phases; an acute phase where the compensation is less robust and a chronic phase where the compensation is more robust

94
Q

Metabolic compensation of respiratory alkalosis Result

A

A decrease in pH towards normal

95
Q

Acute phase respiratory Alkalosis compensation magnitude

A

For each 10 mmHg decrease in PCO2, the HCO3 decreases by 2 mmHg

96
Q

Chronic phase Respiratory Alkalosis compensation magnitude

A

For each 10 mmHg decrease in PCO2, the HCO3 decreases by 5 mmHg

97
Q

Question

A
98
Q

Dissociation constant (Ka)

A
99
Q

Dissociation constant equation

A
100
Q

Henderson-Hasselbalch equations

A
101
Q

Causes of acute respiratory acidosis

A
102
Q

Causes of chronic respiratory acidosis

A
103
Q

Causes of respiratory alkalosis

A
104
Q

Acidosis symptoms

6 listed

A
  • Hyperventilaton (Kussmaul breathing)
  • Depression of myocardial contractility
  • Cerebral vasodilation
    • increased blood flow can cause ICP
  • Can also get CNS depression
  • Hyperkalemia
    • H+ shifts into cells in exchange for K+
  • Shift in O2Hb dissociation curve to the right reducing Hb’s affinity to O2 and causing more O2 release into tissues
105
Q

Alkalosis symptoms

5 listed

A
  • Inhibition of respiratory drive
  • depression of myocardial contractility
  • cerebral vasoconstriction
    • decrease in cerebral blood flow
  • hypokalemia
    • shifts K+ into cells in the absence of H+
  • Shift in HbO2 dissociation to the left dcreasing O2 offloading to the tissues
106
Q

Alkalosis potassium levels

A

hypokalemia

because in the absence of H+, K+ is more readily shifted into cells

107
Q

Acidosis potassium levels

A

Hyperkalemia because the excess of H+ is shifted into cells in the place of K+

108
Q

Anion gap

A

for metabolic acidosis only

109
Q

Renal compensation for acidosis

3 listed

A
  • Excess H+ filtered/secreted into the nephron
  • H2CO3- is reabsorbed
  • Urinary buffers are excreted (these serve as buffers and bind H+ preventing severe drops in pH)
    • HPO42- excreted as H2PO4- (phosphate)
    • NH3 is ecreted as NH4+ (ammonium)
110
Q

Urinary buffers

2 listed

A

HPO42- excreted as H2PO4- (phosphate)

NH3 is excreted as NH4+ (ammonium)

111
Q

Renal compensation for alkalosis

3 listed

A
  • Excess H+ reabsorbed from the nephron
  • H2CO3- is secreted and excreted
  • Urinary buffers are excreted (these serve as buffers and bind H+ preventing severe drops in pH)
    • HPO42- reabsorbed H2PO4- (phosphate)
    • NH3 is reabsorbed NH4+ (ammonium)
112
Q

How to recognize mixed acid-base disorders

A
  • Need to determine the expected compensatory response
  • and if the actual response isn’t the expected response then a 2nd disorder is present
  • If the body cannot compensate for the pH all the way back to the normal range
113
Q

Common cause of a mixed acid-base disorder

A

Nausea and Vomiting

  • Nausea causes acidosis
  • Vomiting causes alkalosis
114
Q

Mixed acid-base disorder possible combinations

A

can only have 1 respiratory ventilation imbalance (either acidosis or alkalosis)

Can have 1 or 2 metabolic disorders (can have an alkalotic and acidotic or 2 of the same)

115
Q

Compensation formulas

A
  • Winter’s Formula
  • Metabolic Alkalosis Formula
  • Acute/Chronic Respiratory Equations
  • Delta-Delta
116
Q

Metabolic acidosis compensation and the possibility of a mixed disorder

A

Always hyperventilation to decrease CO2

Winter’s formula tells you the expected PCO2

If the actual ≠ expected then there is a mixed disorder

117
Q

Metabolic alkalosis compensation and the possibility of a mixed disorder

A

hypoventilation to increase PCO2

Rule of thumb is ↑ PCO2 0.7 mmHg per 1.0meq/L ↑[HCO3-]

ΔPCO2 = 0.7 x (Δ[HCO3-])

if the actual PCO2 ≠ expected then a mixed disorder is present

118
Q

Respiratory acidosis compensation and the possibility of a mixed disorder

A

Acute compensation

  • minutes
  • Intracellular budders raise [HCO3-]
  • Hemoglobin and other proteins
  • results in small ↑pH

Chronic compensation

  • Days
  • Renal generation of ↑[HCO3-]
  • results in a ↑↑pH (but not back to normal!)
119
Q

Compensating back to a normal pH

A

The body cannot do this so if this is the case there is a mixed disorder

120
Q

Respiratory alkalosis compensation and the possibility of a mixed disorder

A
121
Q

Compensation timeframe for respiratory compensation

A
  • Rapid (minutes)
  • change in respiratory rate
122
Q

Compensation timeframe for metabolic compensation

A
  • Acute occurs in minutes by mild compensation from cells
  • Chronic takes days to get a significant compensation from the kidneys
123
Q

Alkalosis and acidosis compensation summary

A
124
Q

Most commonly tested mixed disorder formula

A

Winters formula

125
Q

Shunt equation and normal values

A

PaO2/FiO2

>300 is normal

CVPR (93 decks)

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