13.1 Introduction to ABGs (arterial blood gas analysis)

Question 1

What does effective gas exchange require?

Answer 1

1. Adequate flow of gas to the alveoli
2. Adequate flow of blood to the pulmonary capillaries

Question 2

Give examples of perfusion mismatch and explain them

Answer 2

1. PHYSIOLOGICAL SHUNTING
   
   • Low V/Q ratio (ventilation rate/perfusion)
   • Poorly oxygenated blood mixes with blood from normally ventilated side
     
     • Leads to REDUCTION in arterial pO2
     • e.g. obstructive/severe asthma attack
2. PHYSIOLOGICAL DEAD SPACE
   
   • High V/Q ratio (ventilation rate/perfusion)
   • Reduction in effective alveolar ventilation could lead to reduction in arterial PO2
   • e.g. pulmonary emboli

Question 3

What is the compensation mechanism for the types of perfusion mistmatch?

Answer 3

1. Physiological shunting
   
   • ​HYPOXIC VASOCONSTRICTION
     
     • ​Helps divert blood to well ventilated alveoli
2. Physiological dead space
   
   • BRONCHOCONSTRICTION & REDUCED SURFACTANT
     
     • ​Helps divert air to well-perfused alveoli

Question 4

What are the different types of respiratory failure & explain them

Answer 4

1. TYPE 1 (HYPOXAEMIC) respiratory failure
   
   • ​​Localised mismatching of ventilation/perfusion ratios
   • pO2 = LOW
   • pCO2 = NORMAL/LOW
2. TYPE 2 (HYPERCAPNIC) respiratory failure
   
   • ​​Global reduction in flow of either air to alveoli or blood to pulmonary capillaries
   • pO2 = LOW
   • pCO2 = HIGH

Question 5

What would an increase in arterial pCO2/pHCO3- do to the pH?

Answer 5

1. Increasing the arterial PCO2, will also cause a drop in arterial pH (more acidic)

↑CO2 + H2O ↔ H2CO3 ↔ HCO3- + ↑H+

2. Increasing the arterial PHCO3-, will also cause an increase in arterial pH (more alkali)

CO2 + ↑H2O ↔ H2CO3 ↔ ↑HCO3- + H+

• This is because of this equation:

Question 6

What happens in response to chronic respiratory acidosis (not repiratory)?

Answer 6

1. The kidney’s can increase plasma [HCO3-]
2. The liver reduces urea production and starts producing more glutamine
3. The kidney’s produces more glutamate dehydrogenase and PEPCK which catalyses the breakdown of glutamine into NH4+ and HCO3- in the PCT
4. NH4+ lost in urine, HCO3- increased in blood
5. INCREASING plasma pH

Question 7

Explain and draw the production of HCO3- in the PCT of the kidneys

Answer 7

Question 8

What happens in response to chronic respiratory alkalosis?

Answer 8

1. The kiddneys can decrease plasma [HCO3-]
2. In the collecting ducts there is an increased number and activity of TYPE-B INTERCALATED CELLS in the collecting ducts
   
   • ​​These help secrete HCO3- INTO the tubule lumen
     
     • Helps INCREASE their concentration in the final urine
3. ↑HCO3- lost in urine
4. ↓plasma [HCO3-]
5. ↓plasma pH

Question 9

What metabolic factors can disrupt acid/base balance?

Answer 9

• Alkaline tide (the production of hydrochloric acid by parietal cells in the stomach, the parietal cells secrete bicarbonate ions across their basolateral membranes and into the blood, causing a temporary increase in pH)
  
  • ↑HCO3-
• Kidney failure
  
  • ​↑HCO3-
• Ketone bodies
  
  • ​↑H+
• Lactic acid
  
  • ​↑H+
• Vomiting
  
  • ​↑H+

CO2 + H2O ↔ HCO3- + H+

Question 10

What metabolic factors can affect breathing pattern?

Answer 10

KUSSMAUL breathing

Question 11

Give examples of physiological buffering

Answer 11

1. Proteins - + H+ –> Proteins
2. HPO4(2-) + H+ –> H2PO4-
3. HCO3- + H+ –> CO2 + H20

• This way lungs excrete excess non-volatile acids in the form of CO2

Question 12

What is the physiological process behind INCREASING ventilation rate?

Answer 12

NTS = nucleus tractus solitarii

Question 13

What is the repiratory compensation for chronic metabolic acidosis?

Answer 13

1. ↓HCO3-
2. ↓pH

• NTS = nucleus tractus solitarii

Question 14

What is the 1st step in interpreting ABGs?

Answer 14

1. STEP O (OXYGENATION)
   
   • ​pO2 = 10-13.3kPa (NORMAL)
     
     • pO2 < 10kPa
       
       • Likely RESPIRATORY PROBLEM
       • ​pCO2 normal/low = TYPE 1 respiratory failure
       • pCO2 high = TYPE 2 respiratory failure
     • pO2 > 10kPa
       
       • Likely METABOLIC PROBLEM
   • However if subject is breathing artificially high oxygen concentrations then it should be around 10 KPa less than the inspired PO2

Question 15

What is the 2nd step in interpreting ABGs?

Answer 15

2) STEP A = ACIDOSIS or ALKALOSIS

• Normal pH = 7.35-7.45
  
  • pH < 7.35 = ACIDOSIS
  • pH > ALKALOSIS

REMEMBER: Type I respiratory failures or mixed acid/base disorders should be considered in patients with normal pH

Question 16

What is the 3rd step in interpreting ABGs?

Answer 16

3) STEP B = BUFFERS (CO2/HCO3-)

Question 17

What is the 4th step in interpreting ABGs?

Answer 17

3) STEP C = CHRONIC/COMPENSATED

Question 18

What is the 5th step in interpreting ABGs?

Answer 18

5) BASE EXCESS
* A negative value indicates a base deficit – i.e. the amount of strong base needed to be added to return to normal pH
* Useful in conjunction with [HCO3-] to confirm any metabolic component of an acid-base disorder
* -2 to +2 mM = Normal Range

> +2 mM = Metabolic Alkalosis

< -2 mM = Metabolic Acidosis