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Baz: Y1 Semester 2 > Respiritory: Physiology > Flashcards

Respiritory: Physiology Flashcards

1
Q

Which parts of the brain are responsible for voluntary/ involuntary breathing?

A

Voluntary: Cortex
Involuntary: Pons, Medulla and Spinal Chord aka brain stem

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2
Q

What are the names of the three respiritory groups

A
  • Pontine Respiritory Group
  • Ventral Respiritory Group
  • Dorsal Respiritory Group
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3
Q

Describe the positioning of the three main respiritory groups from a dorsal view

A
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4
Q

What are more passive, the inspiritory neurons or the expiritory neurons?

A

Expiritory neurons, in normal breathing the only thing they do is inhibit the inspirtory neurons

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5
Q

Describe the process of neuron activation during normal breathing?

A

By activating the inspiratory neurons this causes contraction of the inspiritory muscles. It also causes activation of the expiritory neurons which in turn inhibit the inspiritory muscles thus relaxing the muscles of inspiration allowing expiration to take place.

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6
Q

Normal muscles of inspiration

A

Diaphragm and Intercostals

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7
Q

Describe the prrocess of neuron activation during large respiration

A

In order to have a large expiration you must first take a large inpiration. This large activation of inspiration neurons has a large activation on the expiritory nuerons. When this happens the activate muscles of expiration as well as inhibiting muscles of inspiration

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8
Q

5 receptors which effect respiration

A
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9
Q

Which nerve carries the lung receptors

A

Vagus Nerve

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10
Q

How do the vagal nerves effect your breathing pattern?

A

Cutting the vagus nerve produces a reflec of slow deep breaths

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11
Q

Why does a normal breathing pattern look like this?

A

Inspiration is steep because it is active while expiration is slower because it is passive

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12
Q

Which of this receptors is rapidly/slowly adapting?

A

Slowly adapting receptors keep firing in response to a stimuus whereas rapidly adpating receptors slettle down quickly.

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13
Q

What are the slowly adapting receptors responsible for?

A

These are stretch receptors and are responsible for sensing when the airways are streched therefore activating expiration. The take a bit of time to settle down after stimulating because you want expiration to continue fully even when the airways aren’t fully stretched anymore

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14
Q

What are the rapidly adapting receptors responsible for?

A

These are irritant receptors and are responsible for sensing obnoxious substances in the airways and triggering things like the cough mechanism. Because these reactions are extreme you want them to settle quickly after the stimulus is dealth with.

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15
Q

What are c-fibre ending responsible for?

A

Stimulated by interstitial fluid and inflammatory mediators

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16
Q

Peripheral vs Central chemoreceptors

A

Peripherals sense changes in PCO2, PO2 and H+ and have a fast response. These signals are carried by the vagus nerve.

Central detects shifts in PCO2 once it has diffused over the blood brain barrier hence has a slower response.

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17
Q

Vagus nerve vs Phrenic nerve

A

Both and for breathing. Vagus is afferent, Phrenic is efferent

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18
Q

What are the terms for the different ammounts of oxygen and CO2 in the blood?

A
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19
Q

Why is it dangerous to give COPD patients high O2 therepy.

A

After chronic hypoxia and hypercapnia the central chemoreceptors become desenitised.

The drive to breath then comes from hypoxia rather than hypercapnia.

If they are given high O2 then they loose the drive to breath completely leading to further hypercapnia, CO2 narcosis and acidosis and evnetually death

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20
Q

Drugs that inhibit respiration

A
  • Anaesthetics
  • Opioids
  • Sedatives e.g. benzos
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21
Q

Drugs that stimulate respiration

A
  • Primary: these actually drive the respiritory drive e.g. doxapram. However these aren’t used due to nasty side effects
  • Secondaries: these are things like bronchodialators that make breathing easier such as B2 agonists
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22
Q

What happen’s if control of your respiritory function is too common for example surpressing a tickly cough? And what is the name of the dissorder?

A

If you overide your autonomic respiritory system too often it gives up and then you rely on the cortex for breathing. This is called breathing pattern dissorder.

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23
Q

What is Obstructive Sleep Apnoea?

A

This occurs because of a loss of the tonic neural drive to maintain the upper the airways during sleep.

If you have a condition which already means your upper airways are impaired such as obesity, alcohol or anatomical abnormalities when you sleep then can get completely obstructed resulting in you waking up in order to breath therefore disrupting sleep. However you might not always fully wake up so might not know why you are so tired.

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24
Q

What is the tonic drive?

A

This is the continuous background drive that maintains our upper airways and keeps then clear.

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25
Q

What is tidal volume?

A

Tidal volume is your standard breath volume without forced respiration

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26
Q

What is dynamic hyperinflation in COPD?

A

Due to damage of lung structure the lung loses it’s elastic property and the patient loses the ability to passively deflate their lungs. Therfore without force expiration breaths stack

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27
Q

Quick refresher on oxygen haemoglobin dissociation curve: What is on the axis and what 4 things cause a right shift?

A
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28
Q

What does V and Q mean in a V/Q missmatch?

A

V = Ventilation (oxygen)
Q = Perfusion (blood flow)

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29
Q

Why isn’t gas diffusion in the lungs perfect?

If it were perfect equilibrium would be reached between alveolar and arterial blood and these two lines would be the same

A

Shunting and Dead Space

A shunt refers to blood passing through the lungs without participating in gas exchange.

Dead space is the volume of air not participating in gas exchange due to ventilation without perfusion

30
Q

Normal forms of anatomical shunting?

A
  • A small ammount of arterial blood doesn’t come form the the lung (Thebesian veins - these are tiny veins that drain blood directly from the myocardium into the heart’s chambers)
  • A small amount of blood passes through the lungs without seeing gas exchange (bronchial circulation)
31
Q

What are physiological shunts?

A

Physiological shunts are areas where there isn’t sufficient ventilation hence the blood isn’t getting oxygen as it should.

32
Q

What is alveolar dead space?

A

This is areas of the lung with insufficient blood supply to allow for perfususion. Occurs with age and disease.

33
Q

What is the natural V/Q distribution in the lungs?

A

In the top of the lung both Q and V are reduced however V>Q therefore V/Q is raised. PO2 is greater but there is simply less of it.

In the middle it is the average which is about 0.8 (4L Oxygen pass through the lungs for every 5L of blood)

In the bottom both Q and V are raised however Q>V therefore V/Q is reduced. PO2 is less but there is simply more blood.

It all averages out in healthy lungs.

34
Q

What happens to the gas content in blood during hypoventilation and hyperventilation.

Think about the shape of the oxygen dissociation curve

A

In hypoventilation blood oxygen goes down due to decreased PO2 and blood CO2 goes up

In hyperventilation blood CO2 goes down but blood oxygen doesn’t really go up as the curve is already maxed out at normal ventilation

35
Q

What is the main difference in presentation of type 1 and type 2 respiritory failure?

A

In type 1 (V/Q missmatch) only part of the lung is affected. In the part where this is occuring PaO2 is low and PaCO2 is high, high PaCO2 triggers an increased respitatory response however this fresh air will disproportionately go to the areas that have normal V/Q. Here oxygen saturation is healthy therefore no more oxygen goes in yet more CO2 goes out. This results in a low PaO2 with a normal PaCO2.

In type 2, respiration is completely affected therefore PaO2 is low and PaCO2 is high.

36
Q

Causes of type 1 vs type 2 respiratory failure

A
37
Q

What is anatomical dead space?

A

This is normal areas where air might go but where gas exchange doesn’t happen either because blood doens’t go there or it doesn’t conduct.

E.g. bronchus and trachia

38
Q

What is physiological dead space?

A

This is anatomical dead space and alveolar dead space combined

39
Q

Physiologically what do we need hydrogen ions (acid) for

A
  • Energy in mitochondria
  • Protein conformation/function
  • Metabolism
40
Q

How is hydrogen ion balance (homeostasis) acheived?

A
  • Regulating production/excretion
  • Buffering
41
Q

What are the different forms of hydrogen ion production in the body?

A
42
Q

What is a buffer solution?

A

A buffer solution resists changes in pH when and acid or base is added to it

43
Q

Types of buffer systems in the body?

A
  • Bicarbonate system
  • Haemoglobin
  • Others (don’t need ot know the details of these) : phosphate, proteins, exchange of intracellular K+ for H+
44
Q

Basic equation of the bicarbonate buffering system

A
45
Q

Priciple of the haemoglobin buffering system?

A

CO2 can enter an RBC causing an increase in H+. H+ can actually bind to haemoglobin encouraging it to release oxygen. At the same time the left over HCO3- is exchanged for a Cl- ion outwitht he cell. This is another way CO2 and HCO3- can effect one another.

46
Q

In what way is the bicarbonate buffering system regulated?

A

It is open on both ends.

CO2 is excreted through the lungs and regenerated in respiration. On the other side H+ is excreted through the kidneys and HCO3- is regenerated through the kidneys.

47
Q

When end of the bicarb buffering system is the fastest?

A

The lung side

48
Q

What is the Hb buffering system an example of?

A

A protein buffering system

49
Q

Definition of acidosis/alkalosis

A
50
Q

Normal blood acidity (H+ concentration and pH)

A
51
Q

What is the [H+] relationship to [CO2] and [HCO3-]

A
52
Q

Fill in this table

Think about how each one occurs

A
53
Q

How does respiratory acidosis occur?

A

Respiration is decreased

pCO2 increases

H+ increases

54
Q

How does compensated respiratory acidosis occur?

A

In response to the acidosis more HCO3- is made resulting in a normal pH but with elevated CO2 levels

55
Q

How does respiratory alkalosis occur?

A

Respiration increases

pCO2 decreases

H+ decreases

56
Q

How does matabolic acidosis occur?

A

If there is a problem with your metabolism and your body is making too much H+.

You sense this acidosis and your body body responds by increasing respiration however this can only work so far.

Eventually you end up with high H+ and low pCO2

57
Q

How does metabolic alkalosis occur?

A

The body isn’t making enough acid either kidneys excrete too much or you have consumed to much alkaline medication.

Start breathing less to compensate. Can only do this so far until you need oxygen.

If it goes this far you end up with low H+ and high pCO2

58
Q

Biomarkers of acute, chronic & acute on chronic respiratory acidosis?

A
59
Q

Biomarkers of acute and chronic alkalosis

A

You get a small drop in bicarb as well because renal compensation of decreased H+ excretion also includes a decrease is bicarbonate generatio

60
Q

Examples of causes of matabolic acidosis

A
61
Q

Effects of metabolic acidosis

A
62
Q

Example causes of metabolic alkalosis

A
63
Q

Effects of metabolic alkalosis

A
64
Q

What’s going on here?

A

This is metabolic acidosis.

H+ raised but pCO2 lowered to compensate.

Think renal failure, DKA (diabetic ketone acidosis), salicylate OD (found in plants, aspirin, acidosis caused by inhibtion os citric acid cycle and ultimately lactic acidosis), lactic acidosis.

Would do a urine analysis to look for glucose, salicylate and lactate

65
Q

What’s going on here?

A

pCO2 raised, H+ only slightly raised, pO2 low, pHCO3- raised

Chronic compensated respritory acidosis.

Most likely COPD

66
Q

Acid base disturbance cheat sheet just to look at

A
67
Q

What’s going on here?

A
  • H+ lowered - alkalosis
  • pCO2 lowered - correlates therefore cause
  • HCO3- normal - no metabolic compensation

Acute respiratory alkalosis

68
Q

What’s going on here?

Any changes you might expect over the next few days?

A
  • H+ raised - acidosis
  • pCO2 raised - correlated therefore cause
  • HCO3- normal - no metabolic response

Acute respiratory acidosis

After a couple days you would expect the HCO3- to increase as metabolic compensation. However in accidents it is common to also have renal impairement leading to further acidosis.

69
Q

What is going on here?

A
  • H+ lowered - alkalosis
  • pCO2 raised - opposite so respiratory compensation
  • HCO3- raised - metabolic cause

Chronic metabolic alkalosis with respiratory compensation

The vomitting leads to a loss of acid in the system thus lowering overall H+. In order to replenish this stomach acid you end up with HCO3- getting pumped into the blood further increasing the alkalosis.

70
Q

What’s going on here?

A
  • H+ raised - acidosis
  • pCO2 lowered - respiratory response
  • HCO3- lowered - metabolic cause
  • AG (anion gap) raised - anions taken up by H+

Metabolic acidosis with respiratory compensation

DKA - diabetic ketone acidosis.

Without insulin the liver begins to break down fats for fuel resulting in a build up of acidic ketones

71
Q

What’s going on here?

A
  • H+ raised - acidosis
  • pCO2 lowered - respiratory response
  • HCO3- lowered - metabolic cause
  • AG (anion gap) raised - anions taken up by H+

Metabolic acidosis with full respiratory compensation

Aspirin is broken down into salicylic acid

72
Q

What’s going on here?

A
  • H+ raised - acidosis
  • pCO2 lowered - respiratory response
  • HCO3- lowered - metabolic cause
  • AG (anion gap) raised - anions taken up by H+

Metabolic acidosis with respiratory compensation

Carbon monoxide poisoning. CO bind to haemoglobin blocking oxygen and causing a left shift of the oxygen dissociation curve reducing haemoglobin’s ability to give up the oxygen it does have. This reduces delivery to tissues causing them to produce lactic acid from anaerobic respiration resulting in acidosis

Baz: Y1 Semester 2 (42 decks)

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