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LSS 2- Respiration > Hpoxia****** > Flashcards

Hpoxia****** Flashcards

1
Q

What parameter defines hypoxaemia?

A

PO2 < 8 kPa.

-Describes the blood environment.

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2
Q

what factors can put your body under hypoxic stress?

A
  • Disease, if you impeded the ability of outside air to get to the cells
  • Altitude, if the air you’re breathing in has a low oxygen content, then that reduces the starting point of the oxygen cascade.
  • Exercise
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3
Q

Describe how the partial pressure of oxygen changes from inspired air to the tissues.

A

21.3 —> 20 (conducting airways) —> 13.5 (alveoli) —> 13.5 (PaO2 immediately past exchange surface) —> 13.3 (diluted by return of bronchial circulation) —> 5.3 (mixed venous blood)

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4
Q

where does the lungs receive its blood supply from?

A

the lungs have their own blood supply to keep them alive- they don’t get this via the pulmonary circulation.

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5
Q

How does PAO2 and PaO2 change with age?

A

DECREASES

Mean PO2 in the alveolar space and in the arterial blood decreases with age

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6
Q

How can the partial pressure of oxygen in the alveoli (after mixing) be changed?

A

It’ll continue to move down its concentration into the blood until it reaches equilibrium.

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7
Q

what does p50 show?

A

gives the overall impression of the position of the curve at any point- this can be used to determine whether it is a loading or an unloading environment.

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8
Q

Why does the oxygen dissociation curve vary?

A

It varies depending on how much metabolism is happening

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9
Q

if the curve moves up and down does the p50 change ?

A

NO

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10
Q

what is polycythaemia ?

A

An abnormally increased concentration of haemoglobin in the blood

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11
Q

what is the oxygen cascade?

A

Describes the decreasing oxygen tension from inspired air to respiring cells.

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12
Q

Explain the oxygen cascade?

A
  1. Initially 21.3 kPa of oxygen at atmospheric pressure - can be shifted up (oxygen therapy) or down (humid air)
  2. Humidification - lose a little bit of oxygen when air in airways humidified
  3. As you go further down the airways you mix with the air that is already in the airways
    This bar can be moved up (hyperventilation) or down (hypoventilation)
  4. There should be no change between the alveolar air and the post-alveolar capillaries (provided you can get the air to your alveoli you should be able to get it to your arteries)
  5. There is a slight decrease between post-alveolar capillaries and arteries because of the bronchial drainage
  6. About 1% of the cardiac output on your arterial side ends up perfusing the bronchial tree and this 1% gets dumped back into the circulation and causes a slight decrease in saturation
  7. The difference between arteries, veins, and tissues depends on the demand at the time (in tissues, the PO2 decreases with increased exercise)
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13
Q

what change occurs between the alveolar air and the post-alveolar capillaries and then from post-alveolar capillaries and arteries

A
  • There should be NO change

- there is a slight decrease between post-alveolar capillaries and arteries because of the bronchial drainage.

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14
Q

What percentage of cardiac output goes to perfuse the bronchial tree?

A

1%

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15
Q

State the normal arterial and venous PO2.

A

Arterial = 13.3
Venous = 5.3
NOTE: only 25% of haemoglobin desaturates when going from arteries to veins

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16
Q

How is oxygen transported?

A
  • Dissolved: 2%

- Bound to haemoglobin: 98%

17
Q

How does dissolved oxygen affect the oxygen that is bound to haemoglobin?

A

The PO2 (dissolved oxygen) only counts for a small part of oxygen transport in the blood (the rest is bound to haemoglobin) but it is like the conductor of an orchestra. Uptake of dissolved oxygen into tissues is NOT keeping you alive directly, but it is accompanied by a LARGE unloading of oxygen from haemoglobin, which provides a sufficient supply of oxygen to the tissues.

18
Q

State four factors affecting the oxygen cascade and explain them

A
  • Alveolar ventilation:
  • Ventilation/Perfusion matching: won’t achieve efficient gas exchange. if you perfuse unventilated alveoli then you’re going to leave with the same saturation that you came with
  • Diffusion capacity: some diseases can affect the parenchyma ( the functional sub-units-the alveolar capillary membranes) can become thickened and less conductive to exchange.
  • Cardiac output: if you increase cardiac output then you increase the amount of blood flowing through and getting the opportunity to oxygenate hence increasing oxygen delivery.
19
Q

what is VO2 max?

A

Total capacity to deliver oxygen to tissues

20
Q

Describe how ventilation changes with submaximal exercise.

A

If we initiate submaximal exercise we increase the oxygen demand. Ventilation takes a little bit of time to meet these demands.
So, once exercise is finished, ventilation will remain higher for a little while longer to repay the oxygen debt from the start.

21
Q

Describe and explain the ventilatory response to exercise.

A

When exercise begins, respiratory rate rapidly increases from around 12-20 then it remains stable for a long time.
Tidal volume then increases considerably (more efficient at increasing ventilation than increasing respiratory rate).
Eventually you get to a point where increasing tidal volume any further is energy inefficient.
Then respiratory rate increases further.

22
Q

what is EPOC?

A

Excess post exercise oxygen consumption: this is because you are trying to reverse the metabolic consequences of an oxygen deficit.

23
Q

State the five challenges of altitude.

A

Hypoxia: much less oxygen in the amblent air
Solar Radiation: less atmospheric screening. Reflection of snow
Thermal: Freezing cold weather. High wind-chill factor
Hydration: water lost humidifying inspired air. Hypoxia induced diuresis
Dangerous: windy, unstable terrain, hypoxia-induced confusion and malcoordination

24
Q

What’s the difference between accommodation and acclimatisation.

A 
Accommodation = ACUTE response to this kind of change - rapid physiological change in response to a change in oxygen in the oxygen environment 
Acclimatisation = physiology becomes more efficient so that you can get as much out of the air as possible
25
Q

During acclimatisation, what happens to PaO2 and PaCO2 levels

A

PaO2 increases and PaCO2 falls

26
Q

What have the benefits of increased ventilation and PaO2 been attributed to?

A

Renal compensation for the respiratory alkalaemia

Increased ventilatory sensitivity to hypoxia

27
Q

Where is erythropoietin produced?

A

Renal cortex

28
Q

What does low PaO2 stimulate and what is the name given to this response?

A

Hypobaric Hyperventilation

Decreased PaO2 –> Increase Ventilation –> Increase PAO2 –> Increase PaO2

29
Q

what are the four innate adaptations of native highlanders?

A 
Barrel Chest: Larger chest and a bigger set of lungs thus increasing SA. Larger TLC, more alveoli and greater capillarisation. This allows more O2 into the body.
Increased Haematocrit: More RBCs due to the chronic secretion of erythropoietin. This increases the oxygen carrying capacity of the blood. This allows more O2 into the blood and to tissues
Large Heart(right ventricular hypertrophy): Pulmonary vasculature constricts in response to hypoxia, so you need a stronger right side of the heart to push blood through the increased resistance. This allows more O2 into the blood and to tissues. 
Increased Mitochondrial Density: There is greater oxygen utilisation at cellular level. This means more O2 is utilised.
30
Q

What causes chronic mountain sickness and what are the consequences of CMS?

A

Acclimatised individuals can spontaneously acquire chronic mountain sickness ( Monge’s disease)
CMS is thought to be due to secondary polycythaemia in response to hypoxia - RBCs are overproduced to the point where they are no longer beneficial
Consequences - heart failure, eventual death

31
Q

What causes acute mountain sickness and what are the consequences?

A

Maladaptation to the high altitude environment
Consequences: High altitude cerebral oedema and high altitude pulmonary oedema are associated with LOW oxygen environments.
Ataxia: impaired ability to coordinate movement

32
Q

What causes High Altitude Cerebral Oedema (HACE)?

A

Vasodilation of vessels in response to hypoxaemia

More blood going to the capillary beds and so more leakage —> cerebral oedema —> rise in ICP —> herniation

33
Q

What causes High Altitude Pulmonary Oedema (HAPE)?

A

Pulmonary arteries VASOCONSTRICT in response to hypoxaemia - leading to pulmonary hypertension.
This means that hydrostatic pressure in the capillaries is increased so more fluid moves out of the capillaries and into the tissue.

34
Q

What are the two main types of respiratory failure? State the parameters that define them.

A

Type 1 = Hypoxaemic (PO2 < 8 kPa)
Type 2 = Hypercapnic (PCO2 > 6.7 kPa)
There is also a third type: Mixed = PO2 < 8kPa AND PCO2 > 6.7 kPa

35
Q

What causes type 1 and type 2 respiratory failure?

A

Type 1 (hypoxic)

  • V/Q mismatch
  • typically a ventilation/perfusion mismatch in the lungs; perfused alveoli are hypoventilated or ventilated alveoli are hypoperfused

Type 2 (hypercapnic)

  • Hypoventilation
  • typically hypoventilated lungs; inadequate gas exchange as alveolar air stagnates and concentration gradients are poor
36
Q

How do the kidneys control blood pH?

A
  • By secretion and retention of weak acids
  • They can eliminate or replenish H+ by altering the plasma bicarbonate concentration
  • The excretion of HCO3- in the urine increases the plasma H+ concentration just as if a hydrogen ion had been added to the plasma
  • Similarly, addition of HCO3- to the plasma decreases the plasma hydrogen ion concentration just as if hydrogen ions had been removed from the plasma
  • When the plasma H+ concentration decreases (alkalosis), the kidneys’ homeostatic response is to excrete large quantities of HCO3- (this increases plasma H+ concentration towards normal)
  • When acidotic, the kidneys do NOT excrete HCO3- in the urine
  • Instead, the kidney tubular cells produce new HCO3- and add it to the plasma
37
Q

what is respiratory failure?

A

failure to maintain adequate gas exchange in the lungs

LSS 2- Respiration (17 decks)

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