Respiratory Alfred Flashcards

(46 cards)

1
Q

What does central chemoreceptors respond to?

What are peripheral chemoreceptors respond to?

A

Central - CO2, pH

Peripheral - O2, CO2, pH (smaller effect)

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2
Q

Where do inspiratory neurons get stimulated?

A

Dorsal respiratory group in the medulla - diaphragm

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3
Q

What is activated at the end of inspiration to termination inspiration and start expiration?

A

Vagus nerve which negatively feeds back to the central respiratory controls

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4
Q

Where are central chemoreceptors located?

A

Ventral surface of medulla

Responds to changes in H+ (mediated by CO2) in the CSF (which is not regulated by HCO3 buffers in the blood)

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5
Q

Where is the lowest level of transection of the brainstem that would terminate respiration

A

Below medulla

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6
Q

How does arterial baroreceptors modulate breathing?

A

Responds to blood pressure

Hypertension causes hypoventilation

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7
Q

What is the volume of dead space? And how many generations of airways?

A

150mL

16 generations (terminal bronchioles)

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8
Q

Which way does the diaphgarm move during inspiration?

A

Moves down normally, but paradoxically moves up if the diaphgram is paralysed

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9
Q

What happen with lung compliance with:

  • age
  • atelectasis
  • pulmonary oedema
A
  • age - increases
  • atelectasis - decreases
  • pulmonary oedema - decreases
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10
Q

What produces pulmonary surfactant?

A

Type II alveolar epithelial cells

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11
Q

Which part of the lung has more ventilation in normal respiration??

A

Base because it is closer to the linear section of the intrapleural pressure and volume

However, at residual volume, there is more ventilation at the top of the lungs because the section on the curve changes

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12
Q

Where is equal pressure point normally?

A

Respiratory bronchioles

In COPD and asthma, there is earlier obstruction.

The asthma patient has increased resistance in the airways so the fall in pressure is very quick. In COPD patients, the airways is floppy so the airways will collapse at a lower pressure difference

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13
Q

Where is the party of the airways with the most airway resistance?

A

Medium-sized bromchi (up to generation 7)

Particularly affected in asthma

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14
Q

What is the shape of the pulmonary vascular resistance - lung volume curve and when is the pulmonary vascular resistance the lowest?

A

U shaped

Lowest at the functional residual capacity

This is because at the high lung volumes, the capillaries are stretches. In small lung volumes, the capillaries are squished and constricted

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15
Q

What is the change of VQ ratio throughout the lung

A

Top of the lung = high V/Q

Bottom of the lung = low V/Q

THis is because the change of perfusion throughout the lung is a lot more than the change in perfusion (even though both ventilation and perfusion is greater at the bottom)

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16
Q

Type A vs Type B VQ mismatch

A

Type A - emphysema - lots of dead space - normal CO2 but hypoxia

Type B - chronic bronchitis - shunting - mild hypoxia but increased CO2

Most COPD is on the spectrum

High paCO2 is due to MORE SHUNTING

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17
Q

Why does bronchodilation create an initial V/Q mismatch (especially IV administration) in asthma?

A

Initially bronchodilation in the vessels occur before the lungs, creathing more V/Q mismatch

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18
Q

What is the most common cause of hypoxia?

A

V/Q mismatch

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19
Q

What happens to lung volumes in elderly normal

A

Slightly increased FRC due to increased RV

20
Q

Obstruction of lung function tests

A

<0.7 in FEV1/FVC (the ratio, not the percentage compared to normal)

21
Q

What is differences in lung volumes between restrictive diseases due to intrinsic lung disease vs extrinsic chest wall?

A

Intrinsic lung disease - equal reduction in RV/TLC

Extrinsic - more reduction in TLC than RV

22
Q

Best indication of gas trapping in COPD in lung volumes

A

Functional residual capacity or residual volume

23
Q

How does smoking affect DLCO?

A

Decreases DLCO because it creates back pressure of carbon monoxide.

Hence, patients are supposed to not smoke for 12 hours prior pulmonary function tests

24
Q

How to calculate amount of shunting

A

Ideal PO2 on 100% oxygen is 670 mmHg

every 20 mmHg below is a 1% shunt

25
What is the most common cause of hypercapnia
Hypoventilation Then severe V/Q mismatch
26
Motor neuron disease lung volumes
Everything decreases
27
Does HbF and metHb have a higher or lower affinity for oxygen? (compared with normal adult Hb)
HbF and metHb have a higher affinity
28
PaO2, SaO2 and CaO2 in altitude
all reduced
29
Why is the haematocrit more in venous blood compared with arterial blood
The exit of HCO3- causes entrance of Cl-, which is always coupled with Na+, which draws water into the RBC, causing them to be slightly bigger
30
Which way does carbon monoxide cause the Hb-O2 curve shift?
Left
31
How does P50 (in the Hb-O2 curve) change with left and right shift of the curve?
lower P50 is left shift (corresponds with PaO2 with 50% of haemoglobn saturation)
32
Stepwise approach to ABGs
1. pH - determines acidosis vs alkalosis 2. Look at pCO2 and HCO3 3. pCO2 \<35mmHg is resp alkalosis, \>45 resp acidosis 4. HCO3 \<22 is met acidosis, \>30 met alkalosis
33
Amount of compensation of HCO3 in respiratory acidosis
Acute compensation: * HCO3 increases by 1-1.5 for each 10mmHg increase in pCO2 Chronic compensation: * HCO2 increases by 3-4 mEq/L for each 10 mmHg increase in pCO2
34
What abnormality causes no response to 100% FiO2
Shunt
35
ABG in carbon monoxide poisoning
normal PaO2 normal SaO2 (unless you specifically ask for CO) lactic acidosis causing metabolic acidosis
36
hepatopulmonary syndrome cause of hypoxia
shunt
37
What happens to the Respiratory quotient during exercise
Resp quotient is VCO2/VO2 The CO2 output increases during exercise so the R quotient increases from around 0.8 -\> 2
38
What causes the hypocapnia in extreme exercise?
Normal exercise has normocapnia. In extreme exercise, the lactic acidosis causes hypocapnia
39
What is the cause of hyperventilation in acclimatisation to high altitude?
Hypoxic stimulation of the **peripheral chemoreceptors** acclimatisation is limited by the time it takes for the kidneys to respond to the alkalosis from hyperventilation
40
What happens to the O2 Hb curve at high altitude
moderate altitude = right shift high altitude = left shift
41
Treatment for acute mountain sickness complications - high altitude cerebral oedema, high altitude pulmonary oedema
1. Oxygen 2. Pressurisation 3. Acetazolamide (but mainy used prophylacticly) 4. Dex (for cerebral oedema) Don't use diuretics
42
What is MetHb?
The normal HbFe2+ loses an electron to the O2 making HbFe3+ and O2- met Hb reductase is able to reverse the reaction Fe3+ haemes are unable to bind O2 O2 dissociation curve is left-shifted MetHb is absorbing both waves lengths in the pulse oximetry (used normally to measure oxy and de-oxyhaemoglobin
43
Treatment of Met Hb
\<20% no therapy - stop offending agent \>20% use methylene blue (cannot use for G6PD deficiency)
44
cyanosis and normal PaO2 with normal or low sats
MetHb Absorbs waves of both the oxy and deoxyHb wavelengths
45
Lung volume changes in pregnancy
TLC only slight reduction More significant reductions (20%) in FRC, ERV, RV after 2nd trimester
46
What is the sniff test and what does it show
The diaphragm goes up instead of down. Indicates diaphragmatic paralysis