Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Respiratory > 16. Hypoxia > Flashcards

16. Hypoxia Flashcards

1
Q

Hypoxia

A

Describes a low oxygen (PO2) environment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Hypoxaemia

A

Describes low blood oxygen levels (PaO2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Ischaemia

A

Describes tissues receiving inadequate O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

List 3 situations that can put the body under hypoxic stress

A

Altitude
Exercise (only in a way: before physiological response)
Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does PAO2 and PaO2 change with age?

A

DECREASES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the amount of O2 that will bind to haemoglobin dependent on?

A

Partial pressure (PO2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Oxygen cascade

A

describes the decreasing oxygen tension from inspired air to respiring cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does Fick’s law of diffusion state

A

flow rate is proportional to the pressure gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does the partial pressure of oxygen in the alveoli (after mixing) change?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A
  1. 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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why are changes in O2 and CO2 not equal?

A

ODC is sigmoid shaped

CO2 dissociation curve is linear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

State 4 factors affecting the oxygen cascade.

A

V/Q mismatch
Alveolar Ventilation
Diffusion Capacity
Cardiac Output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

State the 5 challenges of altitude.

A

Hypoxia: much less O2 than ambient air
Solar Radiation: less atmospheric screening, reflection off snow
Thermal stress: freezing cold, high wind-chill factor
Hydration: water lost humidifying inspired air, hypoxia induced diuresis
Dangerous: windy, unstable terrain, hypoxia-induced confusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What would immediate exposure to high altitude (hypoxic environment) result in?

A

1 min: Incapacitation

2 mins: Death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is a consequence of the reduction in ambient pressure at high altitude result in?

A

Completely lowers the gradient of PO2 between air and tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe how the body tries to acclimatise to low atmospheric oxygen by increasing oxygen loading

A
  1. Reduction in alveolar O2 (PAO2)
  2. Reduction in arterial O2 (PaO2): recognised by peripheral chemoreceptors
    3.a) Increased sympathetic activation: increased ventilation: increase in PAO2, increase amount of O2 in blood
    3.b) Sympathetic outflow increases CO (through SV and HR): increases delivery of O2
    3.c) Increases erythropoietin secretion; increased production of RBCs; increases capacity for O2 loading
    3.d) Increase oxidative enzymes, Increases rate of aerobic mechanisms, Increased O2 utilisation
    3.e) Increase mitochondrial density, More ATP produced, Increased O2 utilisation
    3d and 3e cause a slight increase in 2,3 DPG in RBCs, shifts ODC right, increases O2 unloading
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe the consequences of the body trying to acclimatise to low atmospheric oxygen

A

Decrease PaCO2: Interferes with baseline control of breathing, decreases ventilation (counterproductive as decreases O2 loading)
Decrease PaCO2: Rise in pH, shifts ODC to the left, decrease in O2 unloading

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does the body cope with the consequences of trying to acclimatise to low atmospheric oxygen?

A 
Alkalosis is detected by carotid bodies 
Changes way kidneys react: 
Increase HCO3- excretion 
Increase H+ in blood
Normalises ODC, increases O2 unloading
Initially responses are quick but when kidneys get involved, takes increased time to fix
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Prophylaxis

A

Treating something before it has happened

20
Q

Acclimation

A

Like acclimatisation but stimulated by an artificial environment e.g. hyperbaric chamber

21
Q

2 prophylactic measures for dealing with low atmospheric oxygen

A

Acclimation

Acetazolamide (drug)

22
Q

Describe the effects of Acetazolamide

A

Carbonic anhydrase inhibitor:
Accelerates the slow renal compensation to hypoxia-induced hyperventilation
If inhibited can reduce initial alkalotic response to low O2

23
Q

Describe 4 innate/ developmental adaptations to low atmospheric oxygen

A

‘Barrel chest’: larger TLC, more alveoli and greater capillarisation: More O2 into the body
Increased haematocritL greater O2 carrying-capacity of the blood: More O2 carried in blood
Larger heart to pump through vasoconstricted pulmonary circulation: Greater pulmonary perfusion
Increased mitochondrial density: greater O2 utilisation at cellular level: More O2 utilised

24
Q

Onset of chronic mountain sickness

A

Acclimatised individuals can spontaneously acquire chronic mountain sickness

25
Q

Pathophysiology of chronic mountain sickness

A

Secondary polycythaemia increases blood viscosity, which sludges through systemic capillary beds impeding O2 delivery (despite adequate oxygenation)

26
Q

Symptoms and consequences of chronic mountain sickness

A

Symptoms: cyanosis, fatigue (due to inadequate O2 supply)
Consequences: ischaemic tissue damage, heart failure, eventual death

27
Q

Treatment of chronic mountain sickness

A

Descent to lower altitude

28
Q

Cause of acute mountain sickness

A

Maladaptation to the high-altitude environment.
Usually associated with recent ascent (within 24 hours)
Can last > week

29
Q

Pathophysiology of acute mountain sickness

A

Associated with a mild cerebral oedema: fluid accumulating inside cranium causing compression in head

30
Q

Symptoms and consequences of acute mountain sickness

A

Symptoms: nausea, vomiting, irritability, dizziness, insomnia, fatigue, and dyspnoea
Consequences: development into HAPE or HACE

31
Q

Treatment of acute mountain sickness

A

Stop ascent
Medication (acetazolamide)
Hyperbaric O2 therapy

32
Q

Causes of High altitude pulmonary oedema (HAPE) and High altitude cerebral oedema (HACE)

A

Rapid ascent

Inability to acclimitise

33
Q

Pathophysiology of High altitude pulmonary oedema (HAPE)

A

Vasoconstriction of pulmonary vessels in response to hypoxia
Increases pulmonary pressure
Permeability and fluid leakage from capillaries
Fluid accumulates once production exceeds the max. rate of lymph drainage

34
Q

Symptoms and consequences of High altitude pulmonary oedema (HAPE)

A

Symptoms: dyspnoea, dry cough, bloody sputum, crackling chest sounds
Consequences: impaired gas exchange, impaired ventilatory mechanics

35
Q

Treatment of High altitude pulmonary oedema (HAPE)

A 
Descent
Hyperbaric O2 therapy
Nifedipine (CCB)
Salmeterol (relaxes airway smooth muscle)
Sildenafil (vasodilation)
36
Q

Pathophysiology of High altitude cerebral oedema (HACE)

A

Vasodilation of vessels in response to hypoxaemia (to increase blood flow)
More blood going into the capillaries
Increased fluid leakage
Cranium is a ‘sealed box’ – no room to expand so intracranial pressure increases

37
Q

Symptoms and consequences of High altitude cerebral oedema (HACE)

A

Symptoms: confusion, ataxia, behavioural change, hallucinations, disorientation
Consequences: irrational behaviour, irreversible neurological damage, coma, death

38
Q

Treatment of High altitude cerebral oedema (HACE)

A

Immediate descent
Hyperbaric O2 therapy
Dexamethasone

39
Q

What’s the difference between accommodation and acclimatisation?

A

Accommodation: ACUTE response, rapid physiological change in response to a change in the oxygen environment
Acclimatisation = physiology becomes more efficient so that you can get more out of the environment

40
Q

Respiratory failure

A

Failure to maintain adequate pulmonary gas exchange

41
Q

Hypoxic respiratory failure (Type I)

A

PaO2: < 8kPa
PaCO2: low/ normal
Diffusion issue
O2 moving into body is impaired

42
Q

3 Causes of Type I respiratory failure

A

Pulmonary oedema
Pneumonia
Atelectasis

43
Q

Hypercapnic respiratory failure (Type II)

A 
PaO2: < 8kPa
PaCO2: > 6.7 kPa
"Getting the gas there" problem 
Decreased CNS drive
Increased work of breathing
44
Q

Broad causes of Type II respiratory failure

A

May be increased production of CO2 and unable to clear it
May be an elimination issue
Maybe a combination of both

45
Q

4 Causes of Type II respiratory failure

A

Pulmonary fibrosis
Neuromuscular disease
Increased physiological dead space
Obesity

46
Q

How to remember the differences in type I and type II respiratory failure

A

Type I: 1 thing wrong (low O2)

Type II: 2 things wrong (low O2, high CO2)

Respiratory (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions