Respiratory Alfred Flashcards

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
Q

What is the most common cause of hypercapnia

A

Hypoventilation

Then severe V/Q mismatch

26
Q

Motor neuron disease lung volumes

A

Everything decreases

27
Q

Does HbF and metHb have a higher or lower affinity for oxygen? (compared with normal adult Hb)

A

HbF and metHb have a higher affinity

28
Q

PaO2, SaO2 and CaO2 in altitude

A

all reduced

29
Q

Why is the haematocrit more in venous blood compared with arterial blood

A

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
Q

Which way does carbon monoxide cause the Hb-O2 curve shift?

A

Left

31
Q

How does P50 (in the Hb-O2 curve) change with left and right shift of the curve?

A

lower P50 is left shift (corresponds with PaO2 with 50% of haemoglobn saturation)

32
Q

Stepwise approach to ABGs

A
  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
Q

Amount of compensation of HCO3 in respiratory acidosis

A

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
Q

What abnormality causes no response to 100% FiO2

A

Shunt

35
Q

ABG in carbon monoxide poisoning

A

normal PaO2

normal SaO2 (unless you specifically ask for CO)

lactic acidosis causing metabolic acidosis

36
Q

hepatopulmonary syndrome cause of hypoxia

A

shunt

37
Q

What happens to the Respiratory quotient during exercise

A

Resp quotient is VCO2/VO2

The CO2 output increases during exercise so the R quotient increases from around 0.8 -> 2

38
Q

What causes the hypocapnia in extreme exercise?

A

Normal exercise has normocapnia.

In extreme exercise, the lactic acidosis causes hypocapnia

39
Q

What is the cause of hyperventilation in acclimatisation to high altitude?

A

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
Q

What happens to the O2 Hb curve at high altitude

A

moderate altitude = right shift

high altitude = left shift

41
Q

Treatment for acute mountain sickness complications - high altitude cerebral oedema, high altitude pulmonary oedema

A
  1. Oxygen
  2. Pressurisation
  3. Acetazolamide (but mainy used prophylacticly)
  4. Dex (for cerebral oedema)

Don’t use diuretics

42
Q

What is MetHb?

A

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
Q

Treatment of Met Hb

A

<20% no therapy - stop offending agent

>20% use methylene blue (cannot use for G6PD deficiency)

44
Q

cyanosis and normal PaO2 with normal or low sats

A

MetHb

Absorbs waves of both the oxy and deoxyHb wavelengths

45
Q

Lung volume changes in pregnancy

A

TLC only slight reduction

More significant reductions (20%) in FRC, ERV, RV after 2nd trimester

46
Q

What is the sniff test and what does it show

A

The diaphragm goes up instead of down. Indicates diaphragmatic paralysis