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Respi > V:Q mismatch, ventilatory depression and gas toxicities (physio) > Flashcards

V:Q mismatch, ventilatory depression and gas toxicities (physio) Flashcards

1
Q

What is the O2 cascade?

A

O2 transfer from air to tissues

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2
Q

Consequence of O2 cascade

A

When one starts of w/ low pO2 than at sea lvl -> cascadic effect -> subsequent O2 levels at alveolus and systemic arteries are much lower -> compromise O2 supply at tissue

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3
Q

Changes in atmospheric pO2 at high altitude

A

pO2 decreases

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4
Q

How does ventilation change at high altitude?

A

Ventilation increases -> decreased pCO2 and H+ and increased pH

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5
Q

Symptoms of acute mountain sickness

A

Fatigue, headache, dizziness, nausea, palpitations

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6
Q

What is acute mountain sickness due to?

A

Hypoxia

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7
Q

Consequence of acute mountain sickness

A

Alkalosis -> decreased H+ -> increased pH

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8
Q

How does body acclimate to sustained low pO2 levels to relieve hypoxia?

A

Increase 2,3 DPG in RBC -> reduced Hb affinity for O2 -> more O2 released to tissues

Increased erythropoietin -> increased RBC -> more O2 carried in blood

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9
Q

How does body acclimate to high altitudes to relieve alkalosis?

A

Restoration of pH by kidneys -> H+ excretion decrease and HCO3- reabsorption decrease

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10
Q

Solns to acute ascent problems

A

Physio -> strong hypoxic drive to increase ventilation

Human intervention -> artificially increase atmospheric O2 in the internal environment

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11
Q

Describe oxygenation of blood at normal alveolar capillary unit

A

Alveolar ventilation and capillary diffusion matched such that there is oxygenation of blood flow thru unit and CO2 is removed -> pO2 rise from 40-60mmHg
- efficient gas exchange takes place -> at steady state -> ventilation and perfusion well matched

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12
Q

Define dead space

A

Vol of air inspired which doesn’t undergo gas exchange

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13
Q

How does alveolar dead space affect gas exchange?

A

Alveolar is ventilated but there is no perfusion -> gas exchange decreases

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14
Q

What is a shunt?

A

Deoxygenated blood returns to systemic circulation w/o passing thru ventilated alveoli

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15
Q

What happens to gas exchange during shunt condition?

A

No alveolar ventilation but there continues to be capillary perfusion thru the alveolar capillary unit -> gas exchange decreases

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16
Q

How to describe alveolar dead space and shunt in terms of ventilation/perfusion?

A

Alveolar dead space = wasted ventilation

Shunt = wasted perfusion

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17
Q

How does alveolar dead space and shunt affect arterial blood gas?

A

Decreased O2 uptake -> decreased pO2

Increased CO2 retained -> increased pCO2

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18
Q

Normal V/Q ratio and what it indicates

A

Normal = 1
- there is ventilation and perfusion

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19
Q

What does V/Q value of infinity indicate?

A

Alveolar dead space -> have ventilation but no perfusion

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20
Q

What does V/Q value of 0 indicate?

A

Shunt -> have ventilation but no perfusion

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21
Q

Describe gas composition when V/Q ratio is infinity

A

Resembles that of atmospheric gas composition as air continues to be replenished by atmosphere

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22
Q

Describe gas composition when V/Q ratio is normal

A

Resembles that of capillary blood that leaves alveolar capillary unit due to replenishment of alveolar gas w/ atmospheric air as alveolar is being ventilated and gas exchange w/ capillary blood that flows through

23
Q

Describe gas composition when V/Q ratio is 0

A

No ventilation -> no replenishment of air from atmosphere but gas exchange takes place btw air in alveolus and blood that comes to it -> alveolar gas resembles blood that comes to alveolar capillary unit b4 it’s oxygenated/CO2 removal takes place/similar to gas composition of venous blood that enters right heart

24
Q

Eg of conditions causing alveolar dead space

A

Pulmonary circulation blocked by blood clots -> pulmonary embolism

25
Q

Eg of conditions causing shunt

A

Pneumonia

Collapsed alveoli/alveoli w/ fluid

26
Q

What effect does hypoxic vasoconstriction do to shunt?

A

Reduces effect of shunt
- local response to low alveolar pO2n -> smooth muscle walls of arterioles contract -> redirects blood to better ventilated regions

27
Q

Blood flow in pulmonary shunt

A

De-O2 blood returns to systemic circulation w/o passing thru ventilated alveoli -> no gas exchange

28
Q

Blood flow in vascular shunt

A

Blood flow bypasses alveoli into systemic circulation -> aft supplying tissues w/ O2, bypasses alveolar capillaries -> left heart

29
Q

Eg of normal shunt in vascular sys

A

Bronchial capillaries drain directly into pulmonary veins -> left heart

30
Q

Eg of abnormal shunt in vascular sys

A

Direct connection btw R and L heart

31
Q

Do airways need oxygenated blood for metabolism?

A

Yes

32
Q

How are airways supplied w/ O2?

A

Aorta -> systemic arteries -> bronchial arteries and capillaries -> supply oxygenated blood to bronchi and pleura -> deoxygenated blood flow to bronchial veins -> systemic veins -> RA and RV -> pulmonary artery -> alveoli -> pulmonary veins -> LA and LV -> systemic arteries

33
Q

Blood flow in normal shunt

A

Aorta -> systemic arteries -> bronchial arteries and capillaries -> supply oxygenated blood to bronchi and pleura -> deoxygenated blood flow to bronchial veins while some blood bypasses alveoli
- blood that flows to bronchial veins -> systemic veins -> RA and RV -> pulmonary artery -> alveoli -> pulmonary veins -> LA and LV -> systemic arteries
- blood that bypass alveoli -> pulmonary veins -> LA and LV -> systemic arteries

34
Q

What can blunt ventilatory response?

A

Altered response to arterial pCO2

Depression of respi control centres in brain

35
Q

How can normal response to increase in arterial pCO2 be altered?

A

Chronic increase pCO2 -> adaptation of central chemoreceptors -> less ventilation response (compared to acute setting)

36
Q

What can depress respi control centre in brain?

A

Sedative and narcotic drugs

Anaesthetics and alcohol

37
Q

Changes in arterial blood when respi control centre is depressed?

A

Decreased ventilation and normal ventilatory response -> CO2 accumulates -> increase in arterial pCO2
- increase in pCO2 usually stimulates ventilation but severely increased pCO2 depresses CNS -> depress respi control centre in brain -> CO2 narcosis -> ventilation decreases further

38
Q

Eg of toxic gases

A

CO2

CO

N2

O2

39
Q

What is CO2 narcosis?

A

Severely increased pCO2 -> depress CNS and ventilation

40
Q

Source of CO

A

Incomplete combustion

41
Q

Pathophysio of CO poisoning

A

CO binds Hb w/ greater affinity than O2 -> COHb (carboxyhaemoglobin) -> prevents Hb from carrying O2 -> no O2 delivery to tissues

42
Q

Colour of COHb

A

Cherry-pink

43
Q

What is cyanosis?

A

Blue discolouration of tissues due to lack of O2 -> excess deoxygenated Hb in blood

44
Q

If cyanosis isn’t detected in a pt, does it mean that the pt’s O2 saturation is normal?

A

No
- absence of cyanosis doesn’t mean normal SaO2 -> doesn’t rule out that pt may have decreased SaO2

45
Q

Treatment for pt w/ CO poisoning

A

100% O2 at high atm pressure

46
Q

What happens to inert gases at high atmospheric pressure?

A

They become toxic

47
Q

How do you get N2 narcosis?

A

Breathing compressed air during diving -> rapid ascent from deep diving
- N2 dissolves into tissues during diving and comes out of tissues during rapid ascent -> obstruct blood flow and and cause pain in joints

48
Q

Pathophysio of N2 narcosis

A

Increase in pN2 affects CNS -> anaesthetic-like effect

49
Q

Symptoms of N2 narcosis

A

Euphoria, loss of coordination, coma, disorientation

50
Q

Treatment for people w/ decompression sickness

A

Recompression in a hyperbaric/high pressure chamber then slow release of atm. pressure till surface pressure released -> prevent N2 from coming out as bubbles

51
Q

When does O2 become toxic?

A

At high pressure and percentage

52
Q

Eg of O2 toxicity

A

80-100% O2 administered for many hrs -> irritation of respi passages

100% O2 administered at vry high atm pressure -> CNS toxicity -> muscle twitching, convulsions

53
Q

What is hyperbaric O2 therapy? What are some precautions to take?

A

100% O2 administered at moderately high atm pressure for treatment but only for limited period

54
Q

Eg of conditions that are treated w/ hyperbaric chamber

A

High O2 pressure to treat
- decompression sickness
- CO poisoning -> high pO2 to displace CO from Hb

High pO2 improves tissue oxygenation for acute ischaemic injury and bad wounds

Respi (16 decks)

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