Arterial Blood Gases Flashcards
What is SaO2?
Hemoglobin-bound O2 -> Saturation of arterial O2
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
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
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
What is the typical PiO2?
(760 mmHg atmospheric at sea level - 47 mmHg H2O) * 21% O2
= 150 mmHg
What is PAO2 normally? PaCO2?
Around 100 mmHg, with PaCO2 normally at 40 mmHg
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
What does increased A-a O2 gradient imply?
Primary parenchymal lung disease
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.
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)
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.
What is the P50 on the oxyhemoglobin dissociation curve?
27 mmHg -> 50% saturation of SaO2
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
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
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
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?
- 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 - 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)
