Respiratory control and arterial blood gases

Question 1

Rhythm generator in medulla

Answer 1

Inspiratory/expiratory groups of neurones

Modification by pneumotaxic centre
in the pons

Question 2

Respiratory depression

Answer 2

Opiates/narcotics, alcohol,
anaesthesia, and other sedatives
- Cerebral diseases: ex. cerebral
vascular accident

Question 3

Chemosensing via

Answer 3

Peripheral and central afferent nerve inputs

Question 4

Peripheral chemoreceptors

Answer 4

Carotid and aortic bodies

Carotid body: bundle of cells just outside the bifurcation of carotid arteries

Question 5

Peripheral chemoreceptors action

Answer 5

Respond to hypoxia&raquo_space; CO2 and H (which are largely sensed in medulla)

In normal conditions, increase in ventilation occurs (only) when PaO2 drops significantly

Carotid and aortic bodies provide back up for each other

Question 6

Central chemoreceptors

Answer 6

Clusters of cells scattered throughout the hindbrain

Sense PaO2 and [H+] (indirectly sensing plasma PaCO2)

Question 7

Pneumotaxic centre

Dorsal respiratory group

Ventral respiratory group

Answer 7

Nucleus parabrachialis medialis

Nucleus tractus solitarius

Nucleus ambigualis
Nucleus retroambigualis

Question 8

Efferent nerves - inspiratory

Answer 8

Diaphragm: phrenic nerves, C3-C5
External intercostal muscles: thoracic nerves, T1-T11
Accessory muscles in the neck: sternocleidomastoid (XI cranial nerve) and    
                                                       scalene muscles (C3-C8)

Question 9

Efferent nerves - expiratory

Answer 9

Abdominal wall

Internal intercostal muscles

Question 10

Approach to ABG interpretation

Answer 10

Step 1: Examine the pH, PCO2 and HCO3 – are they abnormal? If so, does the patient have an acidemia or alkalemia?

Step 2: Determine the primary process

Step 3: Calculate the anion gap and base excess

Step 4: Identify the compensatory process (if one is present)

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

Step 6: Generate a differential diagnosis

Question 11

Acidosis

Answer 11

Respiratory acidosis: high PCO2 (> 44)

Metabolic acidosis: low HCO3-(< 22)

Question 12

Alkalosis

Answer 12

Respiratory alkalosis: lowPCO2 (< 36

Metabolic alkalosis: high HCO3- (> 26)

Question 13

CO2 in blood

Answer 13

When CO2 elimination is insufficient, retained CO2 (“CO2 retention”) will drive the equation to the right, thereby increasing [H+] and decreasing the pH.

That’s why CO2 is called a “volatile acid” and why CO2 retention is called a respiratory acidosis.

Question 14

Calculate anion gap

Answer 14

Metabolic acidosis: addition of acid OR loss of bicarbonate

If addition of acid, the process is called an anion gap metabolic acidosis

Question 15

Anion gap - GOLD MARK

Answer 15

Main causes: 
Glycols (ethylene and propylene), 
Oxoproline,
 L-lactate, 
D-lactate, 
Methanol, 
Aspirin, 
Renal failure, 
and Ketoacidosis

Question 16

Non-anion gap (metabolic) acidosis

Answer 16

Renal tubular acidosis (RTA)

All types result in urinary loss of bicarbonate and a hyperchloremic acidosis

Question 17

Base excess

Answer 17

The relationship between a metabolic acidosis/alkalosis and bicarbonate levels is not linear

Base excess/deficit is a measure of a metabolic disturbance

Base excess is the dose of acid to return bloodto normal pH (7.40) under standard conditions (37C and a PCO2 of 40 mm Hg)

Base deficit is the dose of alkali to returnblood to normal pH

Question 18

Compensating acid-base disturbances

Answer 18

Respiratory acidosis ……………………….……. Retain HCO3

Respiratory alkalosis ……………………….……. Reduce HCO3

Metabolic acidosis ………………………….…….. Reduce CO2 (hyperventilation)

Metabolic alkalosis (HCO3 > 14 mmHg) ….. Retain CO2 (hypoventilation)

Question 19

Mixed disorder

Answer 19

two or more primary acid-base disturbances

Question 20

Mixed disorder clues

Answer 20

The anion gap should be similar in value to the reduction in bicarbonate; this calculation is called the “gap of the gap”

An anion gap is present but the pH is alkalemic

Incomplete compensation for any primary process. Note, “complete compensation” does not result in a normal pH, but it gets close.

Question 21

Generate differential diagnosis

Answer 21

Metabolic Acidosis

• Anion gap metabolic acidosis: GOLD MARK
• Non-anion gap metabolic acidosis: RTA, GI loss, Cl- administration, acetazolamide

Metabolic Alkalosis
Increased aldosterone (thiazide diuretic use, ‘contraction alkalosis’); vomiting; other causes

Respiratory Acidosis
- Retention of CO2: increased dead space; weakness

Respiratory Alkalosis
- Hyperventilation due to pain or anxiety, respiratory centre abnormalities; pregnancy; hypoxaemia including from high altitude

Question 22

Gas exchange at alitutude

Answer 22

Barometric pressure decreases with increasing height

Question 23

Normal response to high altitude

Answer 23

Hypoxemia mediated hyperventilation (peripheral chemoreceptors)
Hyperventilation increases alveolar ventilation with a decrease in PaCO2 (respiratory alkalosis)
Reducing PACO2 leaves more space for oxygen in the alveoli
PaCO2 then decreases ventilatory response to hypoxia (central chemoreceptor response to PaCO2)

Hyperventilation decreases and PaO2 falls

Renal compensation (excreting HCO3-) returns acid-base balance to normal

Compensation for alkalosis returns CSF pH to normal and after 1-2 days, overall response to hypoxia recovers