Arterial Blood Gases Flashcards

1
Q

What are Arterial Blood Gases used for?

A

Used to assess and manage a patient’s respiratory (ventilation) and metabolic (renal) acid-base and electrolyte homeostasis as well as assessing adequacy of oxygenation.

Used to monitor patients on ventilators, monitor critically ill patients, establish preoperative baseline parameters, and regulate electrolyte therapy.

Also used to monitor oxygen flow rates in the hospital and at home

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2
Q

What are the normal findings for the Arterial Blood Gases?

A
Normal findings:
pH: 7.35-7.45 (venous 7.31-7.41) - remember 7.4
PCO2 :  35-45 mm Hg – remember 40
HCO3 : 21-28 mEq/L – remember 24
PO2 : 80-100 mm Hg – remember >= 80
O2 saturation: 95-100% - remember >= 95
Base excess: 0 +/- 2 mEq/L
Alveolar to Arterial O2 difference: < 10 mmHg
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3
Q

What is Acidemia?

A

Low blood pH (<7.38)

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4
Q

What is Alkalemia?

A

high blood pH (>7.42)

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5
Q

What is acidosis? What are its subtypes?

A

Any process that, if left unchecked, will lead to acidemia. This can occur through one of two mechanisms:
Respiratory acidosis and
Metabolic acidosis

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6
Q

What is Respiratory acidosis?

A

PCO2 is high (>44)

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7
Q

What is Metabolic acidosis

A

HCO3 is low (<22)

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8
Q

What is alkalosis? What are its subtypes?

A

Any process that, if left unchecked, will lead to alkalemia. This can occur through one of two mechanisms:
Respiratory alkalosis and
Metabolic alkalosis

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9
Q

What is respiratory alkalosis?

A

PCO2 is low (<36)

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10
Q

What is metabolic alkalosis?

A

HCO3 is high (>26)

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11
Q

How can you make sure it is an arterial sample, not a venous sample?

A

Observe how the blood comes back into the syringe as the sample is being drawn.

Pulsatile flow is seen with an arterial sample but not venous.

Arterial samples fill the syringe much faster than venous.

If the patient was not very hypoxemic when the sample was drawn but the PO2 is very low, most likely it is a venous sample

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12
Q

How do you make sure there are no measurement errors?

A

The bicarbonate value from the blood gas (a calculated value) should closely approximate the bicarbonate from the chemistry panel (a measured value).

This only works if the samples were measured at roughly the same time

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13
Q

What is pH in regards to alkalinity and acidity? Critical values?

A

pH measures alkalinity (pH > 7.45) and acidity ( pH < 7.35)

In respiratory or metabolic alkalosis the pH is elevated while in respiratory or metabolic acidosis it is decreased

Critical values: < 7.25 or >7.55

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14
Q

What is PCO2? Critical values?

A

PCO2 measures the partial pressure of CO2 in the blood.

Measure of ventilation – the faster and more deeply a patient breathes, the more CO2 is blown off, and the level drops.

PCO2 is referred to as the respiratory component in acid base determination as this is mainly controlled by the lungs.

Critical values: < 20 or > 60

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15
Q

When is PCO2 elevated?

A

Elevated in primary respiratory acidosis.

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16
Q

When is PCO2 decreased?

A

Decreased in primary respiratory alkalosis

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17
Q

How do the lungs compensate for primary metabolic acid-base disturbances?

A

Lungs also compensate for primary metabolic acid-base disturbances, so PCO2 levels are affected by metabolic disturbances as well.

In metabolic acidosis the lungs compensate by blowing off CO2 to raise pH.

In metabolic alkalosis the lungs compensate by retaining CO2 to lower pH

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18
Q

What is PO2? Critical value?

A

PO2 is a measure of the tension (pressure) of O2 dissolved in the plasma so is an indirect measure of O2 content of arterial blood.

This pressure determines the force of O2 to diffuse across the pulmonary alveoli membrane.

Used to determine effectiveness of oxygen therapy.

Critical value: <40

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19
Q

When is PO2 decreased?

A

Patients unable to oxygenate the arterial blood because of O2 diffusion difficulties (pneumonia, shock lung, CHF).

Patients in whom venous blood mixes prematurely with arterial blood (congenital heart disease).

Patients who have underventilated and overperfused pulmonary alveoli (pickwickian syndrome – obese patients who cannot breathe well when in supine position or in patients with significant atelectasis)

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20
Q

What is HCO3?

A

Most of the CO2 content in the blood is HCO3.

The bicarbonate ion is a measure of the metabolic (renal) component of the acid-base equilibrium and is regulated by the kidney.

It can be measured directly by the bicarbonate value or indirectly by the CO2 content.

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21
Q

When does HCO3 increase and decrease? Critical values?

A

As HCO3 increases, the pH also increases so they are directly proportional.

HCO3 is increased in metabolic alkalosis and decreased in metabolic acidosis

Critical values: < 15 or > 40

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22
Q

Hoes does the kidney compensate for primary respiratory acid-base abnormalities?

A

Kidneys also compensate for primary respiratory acid-base abnormalities.

In respiratory acidosis, the kidneys compensate by reabsorbing increased amounts of HCO3 while in respiratory alkalosis the kidneys compensate by excreting HCO3 in increased amounts to lower pH

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23
Q

What is O2 Saturation? Critical Value?

A

Indication of the percentage of hemoglobin saturated with O2 .

At 92-100% of hemoglobin carrying oxygen, the tissues are adequately provided with oxygen, assuming normal oxygen dissociation.

Critical value: <75%

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24
Q

How do you measure O2 Saturation?

A

Pulse oximetry is a noninvasive way of determining O2 saturation.

It measures all forms of O2 saturated hemoglobin, including carboxyhemoglobin.

Therefore, in carbon monoxide poisoning, when carboxyhemoglobin is high, oximetry will inaccurately indicate a high O2 saturation.

A clip like sensor is applied to the tip of a finger or the earlobe – the oximeter transmits light from one side and records the amount of light on the other side, determining the O2 saturation.

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25
Q

What is Base excess/deficit? Critical value?

A

Calculated by the blood gas machine using pH, PCO2 , and hematocrit.

Represents the amount of buffering anions in the blood.

Base excess takes all anions into account when determining acid-base treatment based on the metabolic component.

Critical value: +/- 3 mEq/L

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26
Q

What does a negative Base excess/deficit mean?

A

indicates metabolic acidosis (ex. lactic acidosis).

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27
Q

What does a positive Base excess/deficit mean?

A

indicates metabolic alkalosis or compensation to prolonged respiratory acidosis

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28
Q

What is Alveolar (A) to Arterial (a) O2 difference (A-a gradient)? Normal value?

A

Calculated number that indicates the difference between alveolar O2 and arterial O2 .

Normal < 10 mm Hg

If the gradient is abnormally high, there is either a problem in diffusing oxygen across the alveolar membrane (thickened edematous alveoli) OR unoxygenated blood mixing with oxygenated blood

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29
Q

When do thickened alveolar membranes occur?

A

pulmonary edema, pulmonary fibrosis, and acute respiratory distress syndrome (ARDS)

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30
Q

When does mixing of unoxygenated blood occur?

A

congenital cardiac septal defects, arteriovenous shunts, or underventilated alveoli that are still perfused (mucus plug)

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31
Q

What is Respiratory Acidosis? Two types?

A

PCO2 > 40 mmHg and decreased pH due to inadequate elimination of carbon dioxide by the lungs.
Two types:
Acute respiratory acidosis
Chronic respiratory acidosis

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32
Q

What is Acute Respiratory acidosis?

A

acute carbon dioxide retention leading to an increased PCO2 , but a minimal change in HCO3

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33
Q

What is Chronic Respiratory acidosis?

A

pparent after 2-5 days. Renal compensation (increased hydrogen ion secretion and bicarbonate production in the distal nephron) is seen

34
Q

What is Respiratory Alkalosis?

A

Decreased PCO2 and increased pH due to excessive elimination of carbon dioxide by the lungs.

Think HYPERVENTILATION!

Also has acute and chronic types

35
Q

What is Metabolic Acidosis? Two types?

A

Decreased pH and decreased HCO3
Two types:
Anion gap metabolic acidosis (Increased anion gap)

Nonanion gap metabolic acidosis

36
Q

What is Metabolic Alkalosis?

A

Increased pH and increased HCO3

37
Q

What is the Step 1 for interpreting arterial blood gases?

A

Step 1: Evaluate the pH.

If pH < 7.4, acidosis is present
If pH > 7.4, alkalosis is present

38
Q

What is the Step 2 for interpreting arterial blood gases?

A

Step 2: Determine the primary process that led to the change in the pH.

39
Q

What can be the primary process for a patient with a low pH?

A

If the PCO2 is elevated, the primary process is a respiratory acidosis.

If the HCO3 is low, the primary process is a metabolic acidosis.

40
Q

What can be the primary process for a patient with a high pH?

A

If the PCO2 is low, the primary process is a respiratory alkalosis

If the HCO3 is high, the primary process is a metabolic alkalosis

41
Q

What is the Step 3 for interpreting arterial blood gases?

A

Step 3: Calculate the serum anion gap (AG)

Anion gap = Na+ - (Cl- + HCO3 )

Use the bicarbonate from the chemistry panel for this calculation.

42
Q

What does an elevated anion gap mean?

A

If the anion gap is elevated (>12) then there is an elevated anion gap, which implies that the patient has a primary elevated anion gap metabolic acidosis regardless of what other abnormalities are identified or what else is happening with pH and bicarbonate.

There must be an additional disorder because the body does not generate an anion gap to compensate for a primary respiratory disorder.

There may be more than one process occurring

43
Q

What is the Step 4 for interpreting arterial blood gases?

A

Step 4: Identify the compensatory process (if one is present)
Generally, the primary process is followed by a compensatory process, as the body attempts to bring the pH back towards the normal range

44
Q

If the patient has a primary respiratory acidosis (high PCO2 ) leading to acidemia, what is the compensatory process ?

A

The compensatory process is a metabolic alkalosis (rise in the serum bicarbonate)

45
Q

If the patient has a primary respiratory alkalosis (low PCO2 ) leading to alkalemia, what is the compensatory process?

A

Tthe compensatory process is a metabolic acidosis (decrease in the serum bicarbonate)

46
Q

If the patient has a primary metabolic acidosis (low bicarbonate) leading to acidemia, what is the compensatory process?

A

The compensatory process is a respiratory alkalosis (low PCO2 )

47
Q

If the patient has a primary metabolic alkalosis (high bicarbonate) leading to alkalemia, what is the compensatory process ?

A

The compensatory process is a respiratory acidosis (high PCO2 )

48
Q

What are the Compensatory Points to consider?

A

The body never overcompensates for the primary process.

The pace of compensation varies depending on whether it is respiratory or metabolic compensation.

Despite the compensatory mechanisms, the pH may not return all the way to normal.

What may appear to be a compensatory process may not actually represent true compensation.

What appears as a lack of compensation may actually represent an acute process on top of a chronic process

49
Q

Details on The body never overcompensates for the primary process

A

If a patient develops acidemia due to a respiratory acidosis and then develops a compensatory metabolic alkalosis (COPD patient with chronic carbon dioxide retention), the pH will move back towards normal value of 7.4 but will not go to the alkalemic side of normal

If the pH appears to over-compensate then an additional process is occurring

50
Q

What is the speed of Respiratory compensation?

A

Respiratory compensation for primary metabolic disturbance is almost immediate.

Ex:
If a patient was given IV hydrochloric acid to give a metabolic acidosis, the patient would rapidly begin hyperventilating to generate a respiratory alkalosis.

The pH would move back towards normal.

51
Q

What is the speed of metabolic compensation?

A

Metabolic compensation for primary respiratory disturbances is slow and may take several days.

Ex:
If someone travels to high altitude and begins to hyperventilate due to low oxygen levels, initially there will be no metabolic compensation and they will have a high pH.

Over several days, metabolic compensation will occur and the pH will return back towards normal.

52
Q

How does a rise or decrease in PCO2 affect the equation

H2O + CO2 <> H2CO3 <> H + HCO3

A

If there is a large rise in the PCO2 , this equation will shift towards the right and the levels of bicarbonate will transiently increase.

A large fall in the PCO2 will shift the equation to the left and the bicarbonate will transiently decrease

53
Q

When is the base excess simply due to the chemistry of the equation?

A

If the base excess is between -2 and +2, then the changes in bicarbonate are due to movement based on the equation and there is no metabolic acidosis or alkalosis

54
Q

What does a base excess less than -2 mean?

A

If the base excess is less than -2, then there is a metabolic acidosis which may be the compensatory process (base deficit)

55
Q

What does a base excess greater than 2+ mean?

A

If the base excess is greater than +2, then there is a metabolic alkalosis, which may be the compensatory process

56
Q

What is the Step 5 for interpreting arterial blood gases?

A

Step 5: Determine if a mixed acid-base disorder is present.

57
Q

What is a mixed acid-base disorder?

A

A patient may have a concurrent metabolic acidosis and metabolic alkalosis or a concurrent elevated anion gap acidosis and non-anion gap acidosis.
You can’t have a combined respiratory alkalosis and acidosis as it is impossible for a patient to hyper- and hypo- ventilate at the same time

58
Q

What do you used to determine if a mixed acid-base disorder is present?

A

Calculate the Delta Delta.

This looks at whether the body is holding onto or losing more bicarbonate than you would expect based on looking at the pH, anion gap, and bicarbonate values.

59
Q

How do you calculate the Delta Gap?

Delta Delta?

A

Calculate the Delta Gap:
Measured anion gap – normal anion gap (12)

Calculate the Delta Delta:
Add the Delta Gap to the measured bicarbonate (from the chemistry panel)

Compare the Delta Delta to a normal bicarbonate (22-26)

60
Q

What does a low Delta Delta mean?

A

If the Delta Delta < 22, the patient is losing bicarbonate somewhere and there is a non-gap acidosis.

If a non-gap acidosis (either compensatory or the primary process) in the initial steps above, then the acidosis you identify here represents the same process
If you did not identify an acidosis in the earlier steps or you identified a gap acidosis in the initial steps, then this last step reveals the presence of an additional non-gap acidosis

61
Q

What does a high Delta Delta mean?

A

If the Delta Delta > 26, the patient is holding onto bicarbonate and there is an additional metabolic alkalosis.

If you found an alkalosis (either compensatory or the primary process) in the initial steps, then the alkalosis identified here represents the same process
If you identify an acidosis in the initial steps and then this last step reveals an alkalosis, you have found an additional metabolic process

62
Q

What are arterial blood gas contraindications?

A

No palpable pulse
Cellulitis or open infection at access area
AV fistula proximal to access site
Severe coagulopathy
Allen test is negative – no ulnar artery – if the radial artery is used for access and thrombosis occurs, this could jeopardize the viability of the hand

63
Q

What is the Allen Test?

A

While fist is closed tightly, obliterate both the radial and ulnar arteries simultaneously.
Relax hand and watch for blanching of the palm and fingers
Then release the pressure from the ulnar artery and wait 15 seconds
Observe hand for flushing caused by capillary refilling.
Flushing indicates a positive Allen test, demonstrating that the ulnar artery is capable of supplying the entire hand
If flushing does not occur within 15 seconds, the Allen test is negative and the radial artery cannot be used

64
Q

What are arterial blood gases interfering factors?

A

O2 saturation can be falsely increased due to carbon monoxide
COPD patients are stimulated to breathe not by CO2 levels (as normal) but by O2 levels. If large amounts of oxygen are delivered they will hypoventilate due to lack of drive to breathe. What do you think will happen??????
CO2 levels will rise leading to lethargy and even decreased drive to breathe as well as decreased O2 levels
Sedative hypnotics or narcotics inhibit breathing and cause hypoventilation

Hypothermia can change the position of the oxyhemoglobin dissociation curve – at low temperature the curve is shifted to the left.
As a result, for any given oxygen content, the PO2 is lower than it would be at a normal temperature.
The ABG machine warms the blood to 37o C before doing the analysis – this shifts the curve back to the right to lead to a higher measured PO2 than if the measurement took place without warming the blood.
Therefore, the lab must be notified if the patient is hypothermic.

65
Q

What causes an increased pH (Alkalosis)?

A

Metabolic alkalosis

Respiratory alkalosis

66
Q

What are Clinical causes of Metabolic alkalosis?

A

Chronic and high volume gastric suction, chronic vomiting, hyperaldosteronism, diuretics, Cushing’s syndrome – acid hydrogen ions are lost and HCO3 ions are relatively high

67
Q

What are Clinical causes of Respiratory alkalosis?

A

Hypoxemic states, including CHF, cystic fibrosis, carbon monoxide poisoning, pulmonary emboli, shock, acute severe pulmonary diseases – hypoxemia causes breathing rate to increase and CO2 is blown off
Anxiety, pain, pregnancy – all have hyperventilation
Salicylate intoxication

68
Q

What causes a decreased pH (Acidosis)?

A

Metabolic acidosis

Respiratory Acidosis

69
Q

What are Clinical causes of Metabolic acidosis?

A

Ketoacidosis, lactic acidosis – acid anions build up
Severe diarrhea, renal failure – base ions are lost
Seizures, shock

70
Q

What are Clinical causes of Respiratory acidosis?

A

COPD, hypoventilation - PCO2 builds up causing acidosis

71
Q

What causes increased PCO2?

A

Respiratory Acidosis.

COPD (bronchitis, emphysema), oversedation, head trauma, over-oxygenation in COPD or pickwickian syndrome – reduced ventilation causes increased levels of PCO2

72
Q

What causes decreased PCO2?

A

Respiratory Alkalosis

Hypoxemia, pulmonary emboli – hypoxemia drives respiratory center to increase ventilation
Anxiety, pain, pregnancy – rapid ventilation

73
Q

What causes increased HCO3?

A

Metabolic alkalosis

Chronic vomiting or chronic high volume gastric suction, aldosteronism, diuretics – acid hydrogen ions are lost so HCO3 ions are relatively high causing metabolic alkalosis
COPD – HCO3 ions are increased to compensate for chronic hypoventilation (high PCO2 ). Compensation occurs for respiratory acidosis

74
Q

What causes decreased HCO3?

A

Metabolic acidosis

Chronic and severe diarrhea, chronic use of loop diuretics – persistent loss of base ions, including HCO3
Starvation, DKA, acute renal failure – ketoacids are built up; HCO3 neutralizes these acids and decreases

75
Q

What causes increased PO2 and O2 content?

A

Polycythemia – Hgb is increased

Increased inspired oxygen, hyperventilation – increased alveolar oxygen leads to increased PO2 and O2 content

76
Q

What causes decreased PO2 and O2 content?

A

Anemias – Hgb is decreased.
Mucus plug, bronchospasm, atelectasis, pneumothorax, pulmonary edema, ARDS, restrictive lung disease, atrial or ventricular septal defects, emboli.
Inadequate oxygen in inspired (suffocation), severe hypoventilation states (oversedation or neurologic somnolence) – without air exchange the PO2 decreases

77
Q

What causes an increased A-a O2 Gradient?

A

Mucus plug, bronchospasm, atelectasis, pneumothorax, pulmonary edema, ARDS – nonventilated lung tissue is still perfused but the perfused blood does not get oxygenated because there is no ventilation in that area of the lung to bring oxygen to the blood. The perfused unoxygenated blood mixes with the oxygenated blood in the pulmonary veins, and by dilution, the O2 content of mixed blood returning to the heart is lowered.

Atrial or ventricular cardiac septal defects, emboli – unoxygenated blood gains access to oxygenated blood by direct shunting, and by dilution, the O2 content of the mixed blood returning to the heart is lowered

78
Q

What is carboxyhemoglobin (COHb) used for?

Normal?

A

Used to detect CO poisoning. Can be measured from arterial or venous sample

Normal findings:
Nonsmoker: < 3% saturation of total Hgb
Light smoker: 2-5%
Heavy smoker: 5-10%
Critical value: > 20%
79
Q

What does carboxyhemoglobin (COHb) measure?

A

Measures the amount of COHb, which is formed by the combination of CO and Hgb.

80
Q

How does CO combine with Hgb? How does this affect Hgb and O2?

A

CO combines with Hgb 200 X more readily than O2 can combine with Hgb resulting in fewer Hgb bonds available to combine with oxygen.

Also, when CO occupies the oxygen binding sites, the Hgb molecule is changed so it binds the remaining oxygen more tightly.

These changes do not allow the oxygen to readily pass from the RBCs to the tissue leading to hypoxemia

81
Q

How do you treat CO toxicity?

A

high concentrations of oxygen to displace the COHb