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8 Breathing and Circulation > 8.3 Respiratory physiology > Flashcards

8.3 Respiratory physiology Flashcards

1
Q

Total ventilation (at rest)

A

6 L/min

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2
Q

Respiratory dead space:

A

volume of air that is inhaled that does not take part in the gas exchange.

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3
Q

Concept of partial pressure

A

In a mixture of gases, each constituent gas has a partial pressure which is the notional pressure of that constituent gas if it alone occupied the entire volume of the original mixture at the same temperature.

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4
Q

Resting oxygen consumption:

A

250ml/min (max= 3L/min)

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5
Q

Resting carbon dioxide production

A

200ml/min

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6
Q

Alveolar ventilation (at rest)

A

4L/min

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7
Q

What are normal alveolar partial pressures of oxygen (PAO2) and carbon dioxide(PACO2)?

A

close to normal arterial values.

PaO2=90 mm Hg [12kPa] (range 80-100mmHg [11-13 kPa])

PaCO2=40 mm Hg [5.3kPa] (range 35-45mmHg [4-6 kPa])

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8
Q

Negativity of intra-pleural pressure:

A

At FRC, rib cage has a natural tendency to spring upwards and lungs have intrinsic tendency to collapse. The 2 effects are balanced and generate a negative intrapleural pressure (mean~-6cmH2O).

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9
Q

Compliance=

A

Change in volume/ change in pressure

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10
Q

Surfactant.

A

Important in lowering surface tension.

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11
Q

What is functional residual capacity?

A

volume left after normal tidal volume.

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12
Q

Concept of surface tension

A

Lungs can be inflated much easier with liquid than gas. Inflating with saline means you remove all air-liquid interfaces and you get rid of surface tension, meaning lungs are much easier to inflate.

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13
Q

Pneumothorax

A

Pleural space fills with air and lungs collapse.

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14
Q

What does turbulence of airflow lead to?

A

wheeze

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15
Q

2 types of flow:

A

1) Laminar- Poiseuille’s, orderly, flow∝ pressure
2) Turbulent- fast velocity of blood. Suboptimal because in order to double flow need to more than double pressure. Flow∝ root (pressure)

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16
Q

Peak expiratory flow and its measurement.

A

a person’s maximum speed of expiration, as measured with a peak flow meter, a small, hand-held device.

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17
Q

Forced expiratory volume in one second (FEV1)

A

volume of air exhaled in the first second during forced exhalation after maximal inspiration. Normally, at least 80% of the forced vital capacity (FVC) is exhaled.

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18
Q

Examples of pathologies affecting airways resistance:

A

e.g. asthma, chronic obstructive pulmonary disease (emphysema & chronic bronchitis).

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19
Q

Poiseuille’s Law

A

Ventilation= [(πr^4)/(8nl)]×change in pressure

n=viscosity, l=length of tube

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20
Q

Emphysema

A

Low lung elasticity gives poor airway support and easy collapse. Airways withstand less of a transmural gradient before they collapse.

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21
Q

Concept of diffusion and of the diffusing capacity of the lung.

A

the transfer of gas from air in the lung, to the red blood cells in lung blood vessels. A bigger diffusing capacity means equilibration is more likely.

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22
Q

Fick’s law of diffusion:

A

Flux=d×(A/Δx)×(c1-c2)

d=diffusion constant
x= distance
A=area

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23
Q

Concept of diffusion and of the diffusing capacity of the lung.

A

the transfer of gas from air in the lung, to the red blood cells in lung blood vessels. A bigger diffusing capacity means equilibration is more likely. (depends on solubility of gas in blood and speed of chemical reaction with blood).

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24
Q

Examples of pathologies affecting diffusion:

A

e.g. pulmonary fibrosis, pulmonary oedema, emphysema.

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25
Q

Pulmonary fibrosis:

A

build-up of scar tissue, making lungs stiff.

26
Q

Pulmonary oedema:

A

fluid comes out of the blood to fill the alveoli, hence there’s less volume in the alveoli that air is able to occupy and the lungs become stiff. Creates massive diffusion distances.

27
Q

Normal value for systemic arterial partial pressure of oxygen (PaO2).

A

14kPa

28
Q

Role of haemoglobin in oxygen transport.

A

O2 binds central components (prosthetic group). O2 binds reversibly to iron with no change in valency of iron. Fe2+ held in centre by two ionic and two covalent bonds.

29
Q

Normal value for systemic arterial partial pressure of oxygen (PaO2).

A

PaO2=90 mm Hg [12kPa] (range 80-100mmHg [11-13 kPa])

30
Q

Shape of the oxyhaemoglobin dissociation curve.

A

Sigmoidal curve. P50=3.5kPa

31
Q

Concept of oxyhaemoglobin saturation.

A

the fraction of oxygen-saturated haemoglobin relative to total haemoglobin.

32
Q

Effect of temperature and 2,3-DPG concentration on oxyhaemoglobin dissociation

A

Increases cause a right shift.

NB: 2,3-DPG is necessary for maintaining P50 otherwise Hb would never let go of O2 at tissues.

33
Q

Delivery of oxygen:

A

rate at which O2 is delivered to systemic circulation.

34
Q

Normal value for systemic arterial partial pressure of carbon dioxide(PaCO2)

A

PaCO240 mm Hg [5.3kPa] (range 35-45mmHg [4-6 kPa])

35
Q

Factors affecting delivery of O2 to tissues:

A

O2 delivery=([Hb]×c× arterial O2 saturation×cardiac output)+ (O2 solubility×PaO2× cardiac output)

1st bracket= reacted O2
2nd bracket= dissolved O2

36
Q

The Henderson-Hasselbalch equation.

A

pH=pK+ log10 ([HCO3-]/αPCO2)

α= CO2 solubility
K= equilibrium constant
37
Q

Concept of buffering and its importance in carbon dioxide transport.

A

In carbonic anhydrase reaction, [H+] quickly becomes proportionally massive compared to where it started so reaction would be a useless way of transporting CO2 without a mechanism to buffer the protons formed. Hb is the most important buffer of H+ (due to many histidine residues).

38
Q

Carbonic anhydrase

A

present in RBCs and on pulmonary endothelium. Catalyses the normally slow reaction:

CO2+H2O⇌H2CO3⇌H+ + HCO3-

39
Q

The chloride shift

A

CO2+H2O⇌H+ + HCO3- runs to far greater extent inside than outside RBC because there’s a ready source of protons from Hb. Because of depletion of HCO3- from inside the cell, more HCO3- moves in from plasma. Therefore to keep electrical neutrality, Cl- moves out… CHLORIDE SHIFT!!!!

40
Q

Partial pressure units of measurement:

A

kPa & mmHg. Conversion: multiply kPa by 7.5 or divide mmHg by 7.5

41
Q

Pulmonary circulation pressure?

A

a low-pressure circulation.

42
Q

Normal values for pulmonary arterial blood pressures (systolic and diastolic).

A

20/10 mmHg

43
Q

Concept of pulmonary shunt.

A

blood is shunted from a particular region of the lung. In health, the shunt faction (Qs/Qt where Qs= pulmonary shunt ml/min and Qt= cardiac output ml/min) is typically 0.05, but this increases in different respiratory diseases. In extreme cases of V/Q mismatch, pure shunting can occur where V/Q=0. Pulmonary emboli may result in this sort of shunting.

44
Q

What increases both regional perfusion and regional ventilation from top to bottom of the lung?

A

Gravity

45
Q

Effect of regional mismatch of perfusion to ventilation on pulmonary gas exchange (including consequences of the shape of the oxyhaemoglobin dissociation curve).

A

Stagnant hypoxia: low perfusion e.g. cardiac failure.

SEE PICTURE

46
Q

Hypoxic pulmonary vasoconstriction

A

acts to counter hypoxia by reducing blood flow to the lung. Low O2 causes blood vessels to contract down.

47
Q

Acute pulmonary hypertension

A

global hypoxic vasoconstriction will increase pulmonary artery pressure and may cause right-sided heart failure (cor pulmonalae).

48
Q

Acute airway obstruction types:

A

By Foreign Bodies: Consequences of acute airway obstruction (upper and lower) by foreign bodies.- perfusion increases.

Unconsciousness and in sleep: Consequences and relief during basic resuscitation of upper airways obstruction.

49
Q

Where is breathing rhythm generated?

A

Brainstem

50
Q

Location of central chemoreceptors

A

Major ones lie within 0.2mm of anterior surface of medulla (bottom of brainstem).

51
Q

What constitute peripheral chemoreceptors?

A

Carotid bodies (generate respiratory effects) and aortic bodies (generate vascular effects).

52
Q

What mediates the response of ventilation to arterial blood gases (PaO2and PaCO2)?

A

respiratory control system

53
Q

Pulmonary stretch receptors.

A

1) Slowly-adapting stretch receptors: between smooth muscle cells in large airways, large myelinated fibres within Vagus. Reflexes: inhibition of inspiration (the Hering-Breuer reflex), bronchodilation (relaxing smooth muscle).
2) Rapidly-adapting stretch (irritant) receptors: between epithelial cells in large airways, small myelinated fibres within Vagus. Refelxes: cough, bronchoconstriction, tachypnoea (rapid breathing).
3) J-receptors: by alveoli and capillaries, unmyelinated C fibres within Vagus (visceral pain receptor). Stimulated by oedema in lung interstitium. Refelxes: rapid shallow breathing.

54
Q

Normal stimulants of carotid bodies:

A

decrease in PO2 and a rise in H+/ PCO2

55
Q

Normal stimulants of carotid bodies:

SEE IMAGE

A

decrease in PO2 and a rise in H+/ PCO2 (increases in PCO2 affect carotid body through increases in H+). Cause intracellular Ca inside type I cell to trigger transmitter release.

56
Q

Location of aortic bodies:

A

aortic arch

57
Q

Innervation of aortic bodies:

A

Vagus nerve (X)

58
Q

Normal stimulants of aortic bodies:

A

particularly sensitive to changes in pH. More sensitive detectors of arterial blood oxygen content than carotid bodies.

59
Q

Effect of ventilation on alveolar pressures of O2 and CO2 (PAO2and PACO2)

A

(SEE IMAGE)

60
Q

What is ventilated?

A

ventilation of the alveoli

61
Q

(the concept of the metabolic hyberbolae).

A

Hyperbolae can be derived by considering CO2 production and O2 consumption as constants set by metabolism in the steady state. Varying inspired gases will vary asymptotes. Varying metabolic rates will vary area constant.

8 Breathing and Circulation (5 decks)

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