Lecture 5: Resp control Flashcards Preview

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Flashcards in Lecture 5: Resp control Deck (55)
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1
Q

What efferent nerves are required for inspiratory muscles?

A

Diaphragm(s): phrenic nerves, C3-C5

External intercostal muscles: thoracic nerves T1-T11

Accessory muscles: sternocleidomastoid (XI cranial nerve) and scalene muscles (C3-C8)

2
Q

What efferent nerves are required for expiratory muscles?

A

Abdominal wall: T5-T12

External intercostal muscles: T1-T12

3
Q

What is the role of the pons?

A

Not essential for respiration but exerts fine control over medullary neurons

4
Q

What are the dorsal respiratory group of neurons required for?

A

Trigger inspiratory impulses

5
Q

What are the ventral respiratory group of neurons required for?

A

Trigger inspiratory and expiratory impulses (during exercise or other times of active exhalation)

6
Q

What is the role of the rhythm generator in the medulla?

A

Controls the basic, automatic pattern of breathing - the pacemaker for breathing is not a single cell but a group of neurons concentrate in the Pre-Botzinger complex

7
Q

Where are the group of neutrons that act as the pacemaker for breathing?

A

In the Pre-Botzinger complex

8
Q

What afferent inputs may impact breathing rate?

A
  • Emotional inputs from the cerebral cortex
  • Lung mechanoreceptors
  • Chemoreceptors (central and peripheral)
9
Q

What is the role of lung stretch receptors(vagal nerve afferent fibres)?

A

Sense lung stretch during breathing to terminate breath to prevent over-stretching

Sense abnormal changes in airway mechanical properties

10
Q

What is the role of irritant and particulate receptors (vagal nerve afferent fibres)?

A

C-fibre neurons: activated by oedema and molecules such as bradykinin

Irritant receptors (sometimes called ‘cough receptors’): respond to punctate mechanical stimuli

11
Q

What is detected by the central chemosensors?

A

[H+] in the CSF

[H+] in the CSF reflects blood [H+], PaCO2 and CSF CO2 but these are NOT directly sensed by central chemoreceptors

12
Q

What area of the brain responds to input from central chemoreceptors?

A

Hindbrain

13
Q

Where are the peripheral chemosensors?

A

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

Aortic body: bundle of cells within aortic arch

Carotid and aortic bodies are back up for each other, but normally the carotid bodies do bulk of peripheral sensing

Both respond to PO2 (hypoxaemia) and CO2. Carotid bodies also detect pH.

14
Q

What is detected by carotid body?

A

PO2, CO2 and pH

15
Q

What is detected by the aortic body?

A

PO2 and CO2

16
Q

What is the relationship between sensitivity to PO2 and PCO2?

A

Sensitivity to PO2 is altered by PCO2: more sensitive to hypoxaemia in setting of hypercarbia

17
Q

Give an example of a volatile acid?

A

CO2

18
Q

What is respiratory acidosis?

A

The build up (retention) of CO2

19
Q

What are fixed acids?

A

Non-volatile acids have to be physically eliminated from the body, typically via the kidneys

They are products from the oxidation of dietary substrates. Baseline production is well managed by the kidneys and liver, where lactate is converted to glucose in the liver

Increased production of acids, especially lactic acid, can outstrip normal clearance

20
Q

How do the kidneys eliminate fixed acids?

A

Filtration and elimination of the conjugate base of acids: urate, lactate, and ketones are main types

21
Q

What are the 6 steps to ABG interpretation?

A

Step 1: Examine the pH, PCO2 and HCO3 –

Step 2: Determine the primary process. Does the patient have an acidaemia or alkalaemia based on the pH? If so, what type is it?

Step 3: If a metabolic acidosis is present, calculate the anion gap

Step 4: Identify the compensatory process

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

Step 6: Determine the cause

22
Q

What pH is suggestive of acidaemia?

A

A low blood pH (< 7.38)

23
Q

What pH is suggestive of alkalaemia?

A

A high blood pH (> 7.42)

24
Q

How do you determine respiratory acidosis?

A

High PCO2 (> 44 mmHg / 5.9 kPa)

25
Q

How do you determine metabolic acidosis?

A

Low HCO3- (< 22 mmHg / 2.9 kPa)

26
Q

How do you determine respiratory alkalosis?

A
Low PCO2 (< 36 mmHg / 4.8 kPa)
Metabolic alkalosis: high HCO3- (> 26 mmHg / 3.5 kPa)
27
Q

How do you determine metabolic alkalosis?

A

High HCO3- (> 26 mmHg / 3.5 kPa)

28
Q

What is metabolic acidosis?

A

Loss of bicarbonate or the addition of acid

29
Q

What are the main causes of metabolic acidosis (loss of bicarb)?

A

Renal tubular acidosis (RTA)
- all types result in urinary loss of bicarbonate and a hyperchloremic acidosis

GI losses

Acetazolamide (carbonic anhydrase inhibitor)

Excessive chloride administration (intravenous fluids with NaCl)

30
Q

What is the anion gap?

A

There are more uncounted anions than uncounted cations. The uncounted anions minus the uncounted cations is called the ANION GAP.

31
Q

What are the causes of anion gap metabolic acidosis?

A

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

GOLD MARK.

32
Q

What is anion gap metabolic acidosis?

A

If it is acidosis as a result of addition of acid (rather than loss of bicarb)

33
Q

What does an anion gap of >12 mean?

A

There is a hidden/extra anion present

The conjugate base of fixed acids are the source of this extra anion.

34
Q

What is the compensatory response to resp acidosis?

A

Retain HCO3

35
Q

What is the compensatory response to resp alkalosis?

A

Reduce HCO3

36
Q

What is the compensatory response to metabolic acidosis?

A

Reduce CO2

37
Q

What is the compensatory response to metabolic alkalosis?

A

Retain CO2

38
Q

What type of compensation is faster?

A

Respiratory compensation occurs quickly - the lungs are FAST (seconds)

Metabolic compensation can take days - the kidneys are SLOW (days)

39
Q

What is a mixed disorder?

A

Two or more primary acid-base disturbances

40
Q

What are the clues that a mixed disorder exists?

A

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 alkalaemic

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

41
Q

What is a base excess?

A

The dose of acid that would be needed to return bloodto normal pH (7.40) under standard conditions (37C and a PCO2 of 40 mm Hg)

42
Q

What is base deficit?

A

The dose of alkali to returnblood to normal pH

In reality, the term “base excess” is used: a metabolic acidosis is described as a “negative” base excess rather than a base deficit

43
Q

What are the causes of metabolic alkalosis?

A

Increased aldosterone (some medications, ‘contraction alkalosis’)

Vomiting

44
Q

What are the causes of respiratory acidosis?

A

Increased dead space (emphysema)

Weakness

Depression of respiratory centre

45
Q

What are the causes of respiratory alkalosis?

A

Hyperventilation due to pain or anxiety

Pregnancy

Hypoxaemia

46
Q

What are the causes of metabolic acidosis (anion gap and non-anion gap)?

A

Anion gap: GOLD MARK

Non-anion gap: RTA, GI loss

47
Q

What are the results from the respiratory centre becoming less sensitive to chronic PaCO2 elevations

A

Respiratory responses become blunted

  1. Chronic respiratory acidosis with metabolic compensation
  2. Hypoxaemia due to hypoventilation.
48
Q

What causes respiratory depression?

A

Opiates/narcotics (heroin, legal prescription narcotics)

Alcohol

Anaesthesia and other sedatives

Cerebral diseases: ex. cerebral vascular accident

49
Q

What is caused by respiratory depression?

A

Hypercarbia

Hypoxaemic hypoxia

Acute respiratory acidosis

50
Q

Where can you get a DVT?

A

Legs > pelvis > arms

51
Q

What is an embolism?

A

Any intravascular material that migrates from its original location to occlude a distal vessel

52
Q

What is a PE?

A

Pulmonary embolism, and the result of migration of all or part of a peripheral DVT to the lungs

53
Q

What are the signs and symptoms of a PE?

A
Hypoxaemia 
Dyspnea
Cough 
Pleuritic chest pain
Pleural rub
Haemoptysis
Syncope
Tachycardia
54
Q

What are the symptoms of a DVT?

A

Calf pain

Leg swelling

55
Q

What tests can be used to diagnose DVT or PE?

A

Blood D-dimer level: to screen for a possible clot (not specific for PE)

Duplex ultrasound: to diagnose DVT

Ventilation perfusion scan (V/Q scan): specific for PE

CT pulmonary angiography (not CXR): specific for PE