Respiratory System - Lec 6 Flashcards

1
Q

Explain the transport of oxygen to the peripheral tissues via tissue systemic capillaries

A

The oxygenated blood from the pulmonary capillaries will travel through the systemic circuit and to the tissue capillaries to deliver oxygen

The tissue capillaries allow the O2 to diffuse across the membrane into the IF following a pressure gradient (partial pressure of O2 on IF is variable amongst regions of tissue - AV. 40 mmHg).

The O2 will then diffuse from IF and into cells. We will find that the intracellular P O2 is always lower than IF because oxygen is always used by cells

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2
Q

What’s the partial pressure of oxygen in cells

A

Can be very variable (but lower than IF)

Ranging from 5 - 60 mmHg (av. 25 mmHg)

But literally a P O2 1-3 mmHg is suffiecnt to support the cellular processes, like metabolism

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3
Q

How is oxygen situated in blood for travel?

A

Oxygen can be found in 2 forms in blood

  • physically dissolved
  • bound to Hb molecules within erythrocytes
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4
Q

How much oxygen is actually in blood and how much is transported during a normal cardiac output?

A

There’s only 3mL of oxygen physically dissolved for every litre of blood, but there’s a P O2 of 100 mmHg in the arterial blood!
Normal Q = 5 L of blood/min, therefore 15 ml of oxygen is dissolved and is delivered to tissues

BUT normal oxygen consumption at rest should be around 250 ml/min
And this can be adhered to by oxygen being bound to Hb molecules (98.5% of oxygen is in this form, where 1 g of Hb is combined with 1.36mL of oxygen)
- 100 mL of blood has 15 g Hb (decreases if anemic )
- therefore, 100 mL of blood has 20.4 ml of oxygen bound to Hb
- therefore, 1 L of blood has 204 ml of oxygen
-therefore, normal Q = 5 L of blood/min which will now have has 1020 ml of oxygen delivered to tissues every min (60-70 times greater than dissolved form alone)

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5
Q

What’s the reaction that occurs where Oxygen is bounded to Hb

A

Reduced Hb + O2 <>HbO2 (Oxyhaemoglobin)

Each Hb bind with 4 molecules of oxygen

It’s a reversible reaction because we need to allow oxygen gas to diffuse across the systemic (tissue) capillary and into the IF, so oxyhaemoglobin would need to unbind from the oxygen in order to allow diffusion

DIFFUSION OF OXYGEN CAN ONLY OCCUR WHEN OXYGEN IS IN ITS DISSOLVED FORM IN THE BLOOD (hence for reversible nature)

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6
Q

Explain the axis on the oxygen-Hb dissociation curve

A

Y axis:

  • % Hb saturation = proportion of Hb bound to oxygen. Have all the Hb become saturated with oxygen binding?
  • Volume % of O2 in blood (oxygen saturation test)= how many ml of oxygen in 100 ml of blood is carried. Normally 20.4 ml of oxygen, and 15 g Hb in 100 ml blood, unless the person is anaemic (don’t have enough Hb). YOU CANT WORK OUT THE AMOUNT OF OXYGEN IN BLOOD UNTIL WE FIND OUT THE AMOJNT OF Hb IN BLOOD.
    IE. a oxygen saturation test with 100% suggests that all oxygen molecules and bound to Hb, but we don’t know how much oxygen that is tho, unless we find out the amount of Hb (BECAUSE THE PERSON CAN BE ANAEMIC AND STILL HAVE 100% oxygen saturation)

x axis:
Partial pressure of oxygen in blood (systemic capillary region and pulmonary capillary region)

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7
Q

Explains on the concepts of features of the oxygen-Hb dissociation curve

A

You can see that the curve is much more flatter with very little deviation in Hb saturation between the P O2 of 70-100 mmHg, therefore, travelling to altitudes up to 3000m or experiencing a respiratory disease that reduces arterial P O2 to 70 mmHg will have no drastic effect on arterial blood content

The curve is steep in 10-50 mmHg range of P O2 because this is the the blood that has delivered oxygen to tissues that metabolise (and has become “deoxygenated”). SO IF THERES LESS OXYGEN, means Hb saturation (binding) will also decrease (that’s why it’s steep)

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8
Q

What’s the utilisation coefficient, how is it relevant to the curve?

A

So during rest, we have a P O2 of 40 mmHg (venous blood in systemic vessels), this indicates that we still have 75% of Hb still saturated (bound to oxygen),

Therefore, we’ve really only delivered 25% of our oxygen content to our tissue. 25% = 5 mL of blood from the 100 ml (you have 20 mL O2). And this is what we call the utilisation coefficient, since we delivered this to tissues

BUT the utilisation coefficient can increase greatly during exercise because more oxygen will be required by the muscles

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9
Q

What happens to the curve when you increase the P O2 to greater than 100 mmHg

A

Very little effect will be noticed as the individual has already reached 97.5% Hb saturation at 100 mmHg, thus, increasing oxygen supply won’t do anything since there aren’t any active sites on the Hb.

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10
Q

What factors can effect the affinity of oxygen for Hb?

A

Increase in P CO2 and decreased pH, increase in temp. at tissue level

  • this will cause more oxygen to be unloaded (as there’s high metabolic activity occurring) than during controlled condition of the given P O2 on the curve, thus, the curve is moved more to the right and brought down
  • occurs due to increase to metabolism (ie exercise)
  • THUS O2-Hb affinity is decreased
  • vice versa can occur
  • so in the lungs, we see more of a controlled curve but in the tissues we see more of a rightward shifted curve as there’s high metabolic activity

2, 3-Bisphosphoglycerate (BPG)

  • produced in red blood cells
  • when oxygen levels decrease (chronic hypoxia), BPG levels increase and causes more oxygen to be unloaded into tissues
  • moves curve to the right as well
  • occurs in tissue with high metabolic activity
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11
Q

Why is carbon monoxide such a dangerous gas?

A

CO is produced through anaerobic reaction of combustion of organic matter (ie. wood, coal, natural gas, petrol)

It can bind to Hb active sites just like oxygen with a much greater affinity (200 timer greater affinity) to form carboxyhaemoglobin. Therefore, even small amounts of CO can deplete Hb of oxygen binding., OXYGEN CARRYING CAPACITY DECREASED

Literally a P CO of 0.8 mmHg, 0.1% of atmosphere conc (1/200th of P O2 in atmosphere) can bind to half of the Hb active sites.
Meaning if CO conc in atmosphere exceeds 0.15%, will be lethal.
Under these circumstances, P O2 still stays the same but it’s just it’s in very low content in blood due to affinity being less significant than CO

Therefore, CO causes hypoxia of tissues

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12
Q

Why does CO induced hypoxia not cause sensation of breathlessness?

A

process doesn’t occur as the molecule isn’t oxygen

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13
Q

Explain how CO2 is carried in the blood

A

CO2 is carried in 3 forms

  • physically dissolved
  • bound to Hb
  • as bicarbonate ions

The amount of CO2 that’s physically dissolved is proportional to its P CO2. CO2 is more soluble that O2 but only 10% is able to dissolve

30% combines with Hb to form carbamino Hb (HbCO2)
- Reduced Hb has a greater affinity to CO2 than oxygen, thus, when HbO2 breaks apart in order for oxygen to diffuse out, this will allow CO2 from the tissue cells to diffuse across and readily bind to Hb more easily

60% of CO2 is carried in form of bicarbonate ions (most are) where the reactions go:

  1. CO2 + H2O <>H2CO3
  2. H2CO3 <> H+. + HCO3-

Carbonic anhydrase = enzyme that accelerates the rate of reaction In red blood cells

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14
Q

What muscles are involved in breathing?

A

Respiratory muscles (skeletal muscles) like the diaphragmatic and intercostal muscles contract during inspiration and so require somatic and motor neurone activation of muscular contraction

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15
Q

How is breathing done and how is it regulated?

A

Breathing is rhythmic, involuntary and occurs without conscious thought, therefore, because it’s involuntary it’s controlled by the brain stem rather than motor cortex

It’s regulated by

  • increase with exercise, fear, arousal
  • holding breath or hyperventilating
  • cough (forced expiration)
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16
Q

Explain what’s the respiratory centre

A

It’s made of neuronal groups are located in medulla oblangata and pons (brain stem region)

Initiation of inspiration = increase in firing rate of these neuronal groups

These groups of neurons in respiratory centre make connection with motor neurons in cervical and upper thoracic spinal cord THUS INNERVATING THE INSPIRATORY MUSCLES (DIAPHRAGMTIC AND INTERCOSTAL) to allow inspiration

17
Q

What factors regulate the RATE AND DEPTH of respiration?

A
  1. Inputs to the neurons in respiratory centre signalling changes in P O2, P CO2 and pH of arterial blood (SIGNALS VIA CHEMORECPTORS)
    - pH if blood changes according to the amount of CO2 and all that right, so high CO2 means more acidic blood and therefore, this stimulus picked up by chemoreceptors and sends it to the respiratory centre to adjust this by increasing ventilation
  2. Afferent (sensory) inputs from receptors in lugs ie. stops lungs from overinflating (lung stretch receptors)
  3. Inputs arising from higher centres of the brain, like motor cortex
    - exercising = sends signal to legs for movement, also sends signal to respiratory centre that your metabolic activty increSed and so rate of breathing should increase
18
Q

What’s the meaning of increase in rate and depth of respiration?

A

Hyperventilation

Caused by increase in alveolar ventilation

So short shallow breaths will not lead to hyperventilation

19
Q

Name and describe the functions of the different components of the respiratory centre (in brain stem)

A

The centre is made up of the medulla oblaganta and the pons so we have two regions

Dorsolateral pons

  • pneumotaxic centre = inhibit inspiratory neurons, that limit inspiration
  • apneustic centre = excite inspiratory neurons, that promote inpiration

Medullary respiratory center

  • Dorsal respiratory group = inspiratory neurons (Fire during inspiration)
  • ventral respiratory group = inspiratory and expiratory neurons (Fire during expiration)
  • pre-botzinger complex = auto-active neurons
20
Q

What do these inspiratory neurons in the respiratory center do?

A

They have axons which descend to the spinal cord and control motor neurons that supply the inspiratory muscles

They drive inspiration to begin

21
Q

How is expiratory conducted in a neurological sense

A

It’s usually a passive process when it’s normal breathing

But during active respiration, some expiratory neurons have axons that descend into the spinal cord and drive expiration

22
Q

What conducts the respiratory rhythm?

A

It’s thought to be the medulla since damage to the pons does not stop respiration, but the exact neurons that generate the respiratory rhythm is not known

But some studies show the auto active neurons in pre botzinger compkex May be the origin, but this is refuted because researchers think that the Rhythm comes from a neural network that initiates a “pattern generator” (ie. like walking rhythm)

Even then, we have no idea what neurons make up the pattern but they would definitely involve the DRG and VRG

23
Q

How is an increase in CO2 in the arterial blood reformed by the respiratory center?

A

Increase in CO2 in the arterial blood is a very strong stimulus, as an increase in CO2 produces an increase in H+ ions in the IF of the brainstem, this can be detected by central chemoreceptors located in brainstem and send in a transmission that will increase the rate and depth of respiration.

The specific location of the CENTRAL chemoreceptors is ear the Ventral surface of medulla oblongata

24
Q

How can low oxygen levels be detected? Low P O2

A

By peripheral chemoreceptors = in carotid body (small vascular organ on carotid artery)

Stimulus - receptor - signal enters the brain via 9th cranial nerve - inputs the info to DRG AND VRG

This causes

  • increase in rate and depth of ventilation
  • SNS activity increased causing vasoconstriction of blood vessels to peripheral tissues, but maintains blood flow and oxygen to vital organs (Brain and heart)
25
Q

Explain what’s the hering-Breuer reflex

A

It’s a mechanism to prevent the over inflation of the lungs

Pulmonary stretch receptors = located in walls of bronchi and bronchioles

These receptors get excited when lungs inflate and send impulses via the nerve fibres in vagus to respiratory centre and cause inhibition of inspiration (done by pneumotaxic center in pons)

Therefore, limiting inspiration thus, decrease depth of breathing, but increase rate

It’s said that this reflex also minimises the work of breathing

26
Q

What other factors can influence respiratory rate and depth, by minimising respiratory wOr

A

Receptors in the chest wall