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Primary FRCA > Physiology 10 > Flashcards

Physiology 10 Flashcards

1
Q

What is the alveolar gas equation?

A

PAO2 = PIO2 - PICO2 / RQ

RQ = respiratory quotient

RQ depends on mix of dietary intake but is commonly quoted as 0.8

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2
Q

What is the A-a gradient?

What is its normal value?

A

A-a gradient = PAO2 - PaO2

Under normal conditions this is <2 kPa

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3
Q

What factors affect O2 carrying capacity in the blood?

A

Hb
SaO2
PaO2

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4
Q

How is HbO2 carrying capacity calculated?

A

HbO2 carrying capacity = [Hb] x 1.39 x SaO2/100

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5
Q

How is dissolved oxygen in the blood calculated?

A

Dissolved O2 = 0.023 x PaO2 ml/100ml

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6
Q

What is the equation for calculating total blood O2 content?

A

O2 content = [Hb] x 1.39 x SaO2/100 + (0.023 x PaO2)

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7
Q

Regarding the HbO2 dissociation curve what is the P50 at pH 7.4?

A

3.5kPa

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8
Q

How is oxygen delivery to tissues (DO2) defined?

A

DO2 = blood O2 content x CO

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9
Q

Regarding the HbO2 dissociation curve what is the P75 at pH 7.4?
Why is this number important?

A

5.3 kPa

This is a typical value for mixed venous blood

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10
Q

How is VO2 derived?

A

VO2 = CO x (Ca02 - CvO2)

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11
Q

For a ‘normal’ person, what is the O2 content of 100% saturated blood?

A

Approx 20ml/100ml

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12
Q

Using normal values to calculate, what is a normal VO2?

A

VO2 = 5000 x (20 - 15)/100

= 250 ml/min

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13
Q

Outline the concept of tissue hypoxia

A

When intracellular PO2 is insufficient to sustain normal aerobic metabolism for cellular functions

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14
Q

How is tissue hypoxia classified?

A
  • Hypoxic hypoxia (low PO2)
  • Anaemic hypoxia (reduced or dysfunctional Hb)
  • Ischaemic hypoxia (low CO or vascular abnormality)
  • Histotoxic hypoxia (inability of cells to utilise available oxygen)
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15
Q

What are the phases of cellular metabolism?

A

Phase 1: Production of 2-carbon compounds
Phase 2: Citric acid cycle
Phase 3: Electron transport chain

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16
Q

Outline processes relevant to phase 1 metabolism

A

Glycolysis (Glucose 6c -> 2x Pyruvate 3c) - Produces 2 NADH2+ and [net] 2 ATP (4 -2)
Glycolysis occurs in the cytoplasm

Oxidative decarboxylation (Pyruvate 3c + CoA -> Acetyl CoA 2c + CO2) - Produces 2 NADH2+
Oxidative decarboxylation occurs in the mitochondria

Beta-oxidation of free fatty acids in mitochondria produces Acetyl CoA

Oxidation of amino acids produces Pyruvate, Acetyl CoA and other intermediates

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17
Q

Outline the key points of Phase 2 metabolism

A

Citric Acid Cycle

  • Acetyl CoA combines with Oxaloacetate to form citrate
  • Citrate goes through a series of reactions producing intermediary compounds, energy-containing compounds and CO2
  • The cycle ends with oxaloacetate, allowing the cycle to start again.
  • Per glucose molecule, 2 cycles will produce 2 ATP, 6 NADH2+, 2 FADH2 and 4 CO2
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18
Q

Outline the key points of phase 3 metabolism

A

Electron Transport Chain

  • Reduced energy-containing compounds are re-oxidised producing electrons and energy, used to phosphorylate ADP -> ATP
  • Each NADH2+ produces 3 ATP in the ETC
  • Each FADH2+ produces 2 ATP in the ETC
  • Oxygen is the final electron acceptor in the chain
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19
Q

What is the breakdown of net ATP production from one glucose molecule during aerobic respiration?

A

Glycolysis: 8 ATP (2 ATP + 2 NAHD2+)

Oxidative decarboxylation: 6 ATP (2 NADH2+)

Citric acid cycle: 24 ATP (2 ATP + 6 NADH2+ + 2 FADH2)

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20
Q

What is the breakdown of net ATP production from one glucose molecule during anaerobic respiration?

A

Glycolysis: 2 ATP

The NADH2+ is used in the metabolism of pyruvate to lactate.

NAD+ and FAD are not re-formed so the citric acid cycle cannot continue

Lack of oxygen means the ETC cannot operate

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21
Q

How long can the body’s supply of ATP last?

A

Approx 90 seconds

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22
Q

What is the lowest possible mitochondrial PO2 compatible with oxidative phosphorylation?

A

0.4 kPa

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23
Q

What are the main mechanisms by which cellular hypoxia causes loss of function?

A
  • Fall in ATP levels

- Fall in pH

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24
Q

How does the body compensate for hypoxia?

A
  • Early / Late
  • Local / Ventilatory / Cardiovascular

Early local: Changes to HbO2 affinity, vasodilatation

Early ventilatory: Hypoxic (<7 kPa) / hypercarbic response

Early CV: Vasoconstriction, tachycardia (to ^CO/MAP)

Late: Polycythaemia (detectable in 3-5 days)

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25
Q

How does the cerebral circulation respond to hypoxia?

A

PO2 <7 kPa leads to exponential increases in cerebral blood flow due to vasodilatation

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26
Q

How does cardiac circulation respond to hypoxia?

A

Local arteriolar dilatation through vasoactive metabolites, direct O2 effect and myogenic reduction in tone

27
Q

What are normal values for CO2 tension?

A

PICO2: 0 kPa
PaCO2: 4.7-5.3 kPa
PvCO2: 6.1 kPa

PACO2 is = to PaCO2 due to the rapid equilibration across the alveolar wall.

28
Q

What are the main factors affecting CO2 exchange in the alveoli?

How is alveolar CO2 calculated?

A
  • AMV
  • CO2 production

%PACO2 = CO2 output / AMV

eg. 200ml/min / 4000ml/min = 5%

29
Q

What are the main causes of hypercapnia?

A
  • Increased FiCO2
  • Primary respiratory
  • Increased CO2 production
  • Compensatory
30
Q

What are the complications of hypercapnia?

A
  1. Neurological:
    - Increased CBF
    - Increased ICP
    - Narcosis >12kPa (likely pH mediated)
    - Autonomic effects
  2. Respiratory
    - Tachypnoea
    - Pulmonary vasoconstriction (>7kPa)
    - Bohr effect -> reduction in HbO2 affinity
    - Alveolar dilution of O2
  3. Cardiovascular
    - HR and contractility reduced (though overcome by catecholamines)
    - Vasodilatation
    - Arrhythmia due to myocardial intracellular acidosis and catecholamines
  4. Biochemical
    - Acidosis -> K+ leakage from cells -> hyperkalaemia
    - Acidosis -> increase in relative UNionised Calcium
31
Q

What changes in respiratory gas properties occur at altitude?

A
  • Pressures decrease
  • Fractional values stay the same
  • Alveolar SVP of water stays the same
32
Q

How would you calculate PIO2 at sea level?

A

PIO2 = FiO2 x (ambient pressure - SVP H20 37°C)

PIO2 = 0.21 x (101 - 6.3) = 19.9 kPa

33
Q

What are the changes to inspired oxygen relevant to air travel?

A

At 35,000ft, cabins are pressurised to ~5-6,000ft, equivalent to breathing 17% O2 at sea level

34
Q

At what altitude does PO2 = O kPa?

A

63,000 ft

35
Q

What temperature does water boil at on the top of Everest?

A

69°C

36
Q

What would happen if a sea level dweller ascended to Everest summit quickly?

A

Initial hypoxic respiratory drive but this only lasts ~1hr. Following this hypoxia will develop

37
Q

How does the body acclimatize to low PO2 at altitude?

A
  • Hyperventilation and hypocapnia
  • Respiratory alkalosis -> renal HCO3- excretion -> metabolic acidosis -> increased AMV
  • Increased haematopoeisis
  • Increase in 2,3 DPG, though counteracted by alkalosis

Takes days to weeks

38
Q

How is mountain sickness classified?

A

Acute (Mild/Severe) ; Chronic

39
Q

Above what altitude may acute mountain sickness occur?

A

6000ft

40
Q

What are the clinical features of mild acute mountain sickness?

A
  • Dyspnoea
  • Headache
  • Nausea
  • Fatigue
  • Sleep disturbance
  • Cheyne-Stokes respiration
41
Q

What are the clinical features of severe acute mountain sickness?

A
  • High-altitude pulmonary oedema (HAPO): Associated with exercise, caused by excessive pulmonary vasoconstriction. High untreated mortality.
  • High-altitude cerebral oedema (HACO): Hallucinations/coma
42
Q

How is acute mountain sickness treated?

A

NIfedipine / acetazolamide

Immediate descent

43
Q

What are the features of chronic mountain sickness?

A
  • Poor hypoxic ventilatory response
  • Polycythaemia
  • Cyanosis
  • Clubbing
  • CO2 retention
44
Q

How can patients be tested before flying if concerned about altitude?

A

Those with SpO2 <92% on air can undergo a 15% hypoxic challenge

45
Q

By how much does pressure increase with depth underwater?

A

1atm per 10m

46
Q

What are the possible complications of rapid decompression?

A
  • Barotrauma
  • Arterial air embolus
  • Neurological damage
  • Bubbles in vessel-poor tissues (eg. cartilage) with subsequent AVN
47
Q

Define hyperbaric O2 therapy

A

Delivery of 100% O2 at an ambient pressure of 2-3 atm. Usually for 1-2h per day over a course of days.

48
Q

What physiological benefit does hyperbaric O2 therapy confer?

A

Arterial O2 content shows a modest increase (from 19 - 25 ml/dL) at pressure but venous oxygen content increases significantly. This forms the basis for treating tissue hypoxia.

49
Q

What are current indications for hyperbaric O2 therapy?

A

CO poisoning
Anaerobic infections

Possibly MS and burns

50
Q

What are the challenges associated with managing air transfer of an anaesthetised patient?

A
  • Precipitation of hypoxia at altitude
  • Expansion of air-filled spaces on takeoff
  • Breathing system valves may stick
  • Boiling point of volatiles reduced, though low temperatures reduce this effect
51
Q

Where are the Hbα genes encoded?

How many a-as make up the Hbα molecule?

A

Chromosome 16

141 a-as

52
Q

Where are the Hbβ genes encoded?

How many a-as make up the Hbβ molecule?

A

Chromosome 11

146 a-as

53
Q

Describe the structure of haem

A

Composed of an organic part and an iron atom in its ferric (Fe2+) state

The organic part is a protoporphyrin ring.

The Fe2+ forms six bonds

  • 4x bonds to N in the protoporphyrin ring
  • 1x bond to ‘proximal histidine’ of associated globin molecule
  • 1x bond to O2 molecule

Close to the O2 binding site, a ‘distal histidine’ residue prevents oxidisation of other haem groups and prevents CO from binding to the Fe2+

54
Q

Outline the production of haem

A

Glycine + Succinyl CoA -> Protoporphyrin

Protoporphyrin + Fe2+ -> Haem

55
Q

Outline the breakdown of haem

A

Protoporphyrin -> biliverdin

Biliverdin -> bilirubin

Bilirubin is bound to albumin and glucuronidated in the liver and excreted in bile

In the bowel, bilirubin -> stercobilin. Some is reabsorbed and excreted via the kidney as urobilinogen

56
Q

What is Hufner’s constant?

A

Describes the O2 carrying capacity of Hb

In vivo value is 1.34 ml/g

Differs from the theoretical value of 1.39 ml/g is likely due to small percentages of HbA2, HbF and COHb

57
Q

What is the P50 of HbA?

A

3.5 kPa

58
Q

What is the P50 of HbF?

A

2.5 kPa

59
Q

What is the ‘double Bohr effect’ seen in pregnancy?

A

Maternal uptake of CO2 from the foetal circulation shifts the maternal HbO2 curve to the right and the foetal HbO2 curve to the left.

60
Q

How is 2,3-DPG formed?

A

As a product of glycolysis

61
Q

Where does 2,3 DPG exert its effect on Hb?

A

β-globin chains

62
Q

What situations may lead to abnormal oxidation of haem?

A

CO toxicity
Physiological NO scavenging by Hb
Treatment with NO
Prilocaine or nitrate therapy

63
Q

What artificial means of increasing O2 delivery have been explored?

A

Stroma free Hb-based carriers

Synthetics eg. Perfluorocarbons

64
Q

What are some of the problems associated with development of stroma-free Hb-based O2 carrying solutions?

A
  • Free Hb dissociates into nephrotoxic α/β dimers
  • Concerns re prion contamination of bovine Hb
  • Free Hb has a short IV half-life -> bilirubin
  • Excessive scavenging of NO may lead to hypertension

Primary FRCA (34 decks)

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