Arterial Blood Gases Flashcards by Matthew Miller

What is SaO2?

Hemoglobin-bound O2 -> Saturation of arterial O2

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How is the oxygen content of blood calculated?

CaO2 = (1.39 * Hgb * SaO2) + 0.003 * PaO2

Where PaO2 is the arterial oxygen tension, used to calculate dissolved arterial O2 (makes a much smaller contribution than hemoglobin)

Hgb is hemoglobin concentration

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How can the partial pressure of O2 gas in an alveolus be predicted?

Alveolar gas equation

PAO2 = PiO2 - PaCO2 / R

PiO2 = inspired O2 partial pressure
PaCO2 = arterial partial pressure of CO2
R = respiratory quotient

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What is the respiratory quotient and its normal value?

rate of production of CO2 / consumption of oxygen

Normal value = 0.8, under normal dietary conditions

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What is the typical PiO2?

(760 mmHg atmospheric at sea level - 47 mmHg H2O) * 21% O2

= 150 mmHg

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What is PAO2 normally? PaCO2?

Around 100 mmHg, with PaCO2 normally at 40 mmHg

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What is the normal A-a gradient and how does it change as you age?

About 10mmHg

Gradient increases about 2.5 mmHg per decade.

Equation:
PaO2 = 100 mmHg - (age in years/3)

I.e. if PAO2 = 100 mmHg, then 2 decades after age 20 (age 40), PaO2 = 85 mmHg expected.

60 years:
PaO2 = 100 - (60/3) = 80 mmHg

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What does increased A-a O2 gradient imply?

Primary parenchymal lung disease

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What relationship does the oxyhemoglobin dissociation curve describe? Why is this important?

PaO2 and the SaO2

Important because poor ventilation can drop your PaO2, and make large differences in SaO2 depending on where you are on the dissociation curve.

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What is the PaO2 which qualifies patients for home oxygen?

55mmHg -> corresponds to 88% on SaO2. Below this level, there is a rapid decrease in SaO2 with decreasing PaO2 (highly sloped portion of the curve)

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What PaO2 marks the beginning of the plateau phase of the curve?

60 mmHg -> 90% SaO2. Increases in PaO2 will only result in small increases in SaO2.

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What is the P50 on the oxyhemoglobin dissociation curve?

27 mmHg -> 50% saturation of SaO2

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What does a rightward shift on the oxyhemoglobin dissociation curve indicate, and what changes in temperature, 2,3-BPG, PaCO2, and pH cause this?

Affinity of hemoglobin for O2 is decreased

Temperature -> increased
2,3-BPG -> increased
PaCO2 -> increased
pH -> decreased

All conditions which happen at high elevation / in muscles

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What do alternative hemoglobins generally do to the oxyhemoglobin curve, and what is the exception?

Shift it to the left (i.e. fetal hemoglobin, carboxyhemoglobin, methemoglobin)

Exception: sickle cell disease

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What does a leftward shift on the oxyhemoglobin dissociation curve indicate, and what changes in temperature, 2,3-BPG, PaCO2, and pH cause this?

Affinity of hemoglobin for O2 is increased

Temperature -> decreased
2,3-BPG -> decreased
PaCO2 -> decreased
pH -> increased

All conditions which happen at low elevation / in lungs

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What is normal body pH and the Henderson-Hasselbalch equation which describes it?

7.4

pH = pKa + log ([HCO3-] / (0.03*PaCO2))

What are the three ways which CO2 is transported in blood?

Dissolved CO2 (PaCO2)
Bicarbonate anion
Carbamino compounds (most important in venous blood, when O2 is exchanged for CO2)

What is the chloride shift / what causes it?

CO2 enters RBC. HCO3- starts to accumulate due to carbonic anhydrase. Membrane is impermeable to H+, and so it is buffered by hemoglobin to HHb. As HCO3- begins to build in the cell, HCO3- is antiported with Cl-, dropping Cl- in venous blood (chloride shift)

What is the Haldane effect?

Low oxygen conditions allow RBCs / hemoglobin to carry more H+ / CO2

What are respiratory acidosis and alkalosis, and their compensation?

Acidosis - primary rise in PaCO2, compensated by reabsorption HCO3- (really by increasing H+ excretion in kidney)

Alkalosis - primary drop in PaCO2, compensated by excretion of HCO3- (really by refusing to lose H+ in kidney)

This compensation is delayed since it takes a while for kidneys to do this

What are metabolic acidosis and alkalosis, and their compensation?

Acidosis - primary drop in HCO3- due to loss of HCO3-
or addition of acid, compensated by increased respiration to lose CO2 (extra made from acid combining with HCO3-)

Alkalosis - primary increase in HCO3- due to addition of base or loss of acid, compensated by decreased respiration to increase CO2 (CO2 is lost making carbonic acid to neutralize the base)

This compensation is immediate since the respiratory system can rapidly respond

What are normal ranges for PaCO2 and HCO3-?

PaCO2: 35-45 mmHg

HCO3-: 23-28 mEq/L

What does this mean for ABG:

7.40/40/90/24/100%?

7.40 = pH
40 = PaCO2
90 = PaO2
24 = [HCO3-]
100% = SaO2

How do you calculate anion gap and what is the normal range?

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

Normal = 10-12 mEq/L

What is anion gap useful for?

Differential diagnosis of metabolic acidosis - > increased = unmeasured anions in the blood - > normal = loss of base caused acidosis

What is the primary cause of decreased anion gap metabolic acidosis and how?

Hypoalbuminemia Albumin is a base and an anion -> loss = acidosis Loss of albumin also causes retention of negatively charged anions such as Cl- and HCO3- which will decrease the anion gap.

What are some endogenous acids which can increase the anion gap?

Phosphate, sulfate Ketoacids, lactic acid

What are exogenous acids which can increase the anion gap?

Drug or toxin: methanol, polyethylene glycol, salicylate

Give acute causes of respiratory acidosis?

``` Asthma Drug overdose (opioid) Stroke COPD Neuromuscular diseases like Guillain-Barre ```

Give chronic causes of respiratory acidosis?

Obesity-hypoventilation syndrome (restrictive) COPD Kyphoscoliosis Neuromuscular: ALS, myasthenia gravis

What are the causes of respiratory alkalosis and what is the only chronic one?

Hypoxemia of any cause (will cause hyperventilation) Anxiety, pain, fevever Airway disorders: asthma and COPD can go both ways, pulmonary edema and pneumonia as well Salicylates (increases breathing frequency to cause respiratory alkalosis along with metabolic acidosis) Pregnancy: mild, chronic hyperventilation

What are the causes of metabolic acidosis WITH anion gap?

Acid increases: ``` Ketoacidosis (diabetic or alcoholic) Lactic acidosis Intoxicants Renal failure (increased phosphates and sulfates) ```

What are the causes of metabolic acidosis WITHOUT anion gap?

Base loss: HCO3- loss from diarrhea Diuretics: acetazolamide -> causes loss of HCO3- Pure acid: HCl Renal tubular acidoses and early renal failure

What metabolic disturbance can furosemide cause and why?

Metabolic alkalosis - > Increased Na+ in distal tubule increases K+ excretion by principle cell - > K+ is exchanged for H+ excretion by alpha-intercalated cell - > HCO3- accumulation causes alkalosis

What are the two types of metabolic alkalosis and which is most common?

1. Chloride responsive (in blood levels, low urine chloride) - > most common, due to volume depletion (RAA system activation), H+ loss in vomiting, diuretics like furosemide, and ingestion of base 2. Chloride unresponsive (in blood levels, high urine chloride) - > less common, due to adrenal tumors

If pH is <7.35 and CO2 < 35 mmHg, what do we have?

``` Metabolic acidosis (CO2 is being blown off to compensate for HCO3- combining with acid. HCO3- must be less than 23 to confirm) ```

If pH is <7.35 and CO2 > 45 mmHg, what do we have? What if HCO3- is >27? Within normal range?

Respiratory acidosis Within normal range: acute >27: chronic (compensated)

If pH is >7.45 and CO2 > 45 mmHg, what do we have?

Metabolic alkalosis (confirm with HCO3- > 27) CO2 is accumulating to compensate for an increase in base (pH is high despite high CO2)

If pH is >7.45 and CO2 < 35 mmHg, what do we have? What if HCO3- is within normal range? What will it be if compensated?

Respiratory alkalosis ``` Normal = acute Compensated = chronic, when HCO3- (<23) ```