Respiratory Physiology Flashcards

1
Q

McFadden et al (1968)

A

Measured minute and alveolar ventilation in relation to FEV1 and found that asthma is associated with alveolar -hyper-ventilation

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2
Q

V/Q matching in asthma

A

Studies have shown V/Q mismatch in asthma

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3
Q

What is type I respiratory failure also called?

What is the Co2 level?

A

Gas exchange failure

Co2 level is low or normal

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4
Q

West et al (1964)

A

Characterised the distribution of blood flow in the vertical plane of the lung.
In a dog, inhaled radioactive xenon isotope, scanned the lungs(A). Then rebreathed into a bag for 2 mins and rescanned (A). Dividing A by B gives pulmonary blood flow per unit lung volume,
They showed very little blood flow at the top of the lung.

They described 3 zones, zone I at the top of the lungs where alveolar pressure is greater than arterial pressure and so there is arterial collapse. Zone II where alveolar pressure is lower than arterial but greater than venous (waterfall zone). Here, blood flows in pulses as pressure builds up in the artery due to too high a resistance at the venous end of the capillary until it is enough to overcome the alveolar pressure and then it flows.
Zone III where arterial and venous pressure are both greater than alveolar pressure. This is the biggest zone of the lung in health.

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5
Q

When does zone I and II of the lung become bigger?

A

During positive airway pressure ventilation.

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6
Q

Prisk et al (1994)

A

Showed that even in space where there is the absence of gravity, pulmonary blood flow remains inhomogenous.

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7
Q

Grunig et al (1997)

A

Showed that during exercise, pulmonary vascular resistance falls, allowing pulmonary arterial pressure to remain relatively constant.
Pressure measured using doppler cardiography.

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8
Q

Pulmonary arterial hypertension

A

Vessel walls become thickened and less compliant, flow cannot increase without an accompanying increase in pressure. Leads to pulmonary oedema. Can cause peripheral odema as the right heart cannot keep up, produces a venous backlog.

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9
Q

What is Cor pulmonale?

A

It is heart problems arising from a pulmonary cause.

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10
Q

Smith et al (2009)

A

Showed acute pulmonary hypertension in healthy volunteers ascending to 4300m

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11
Q

Hodson et al 2016

A

Hypoxia induced proliferation in the carotid body and ventilatory acclimation to altitude is HIF-2 but not HIF-1 dependant.

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12
Q

Calbet et al (2002)

A

Isovolaemic haemodilution at altitude doesn’t reduce execercise capacity at altitude. No benefit to the increased haematocrit?

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13
Q

Krogh and Lindhard, 1913

A

Proposed the concept of cortical irradiation in control of breathing during exercise.
They used tasks where the power output was the same but the degree of conscious effort was greater (through partial muscle paralysis) - breathing increased in that group

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14
Q

Effect of hypnosis on ventilatory response to exercise

A

Using hypnosis to reduce conscious effort reduces exercise induced hypernea.

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15
Q

Eldridge et al

A

Stimulated the hypothalamic motor area in cats, produced an increase in heart rate and ventilatory rate. However, unlike exercise as blood pressure rose as well.

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16
Q

Dejours

A

First person to suggest that only a neurohumoral response could account for the step change response in control of breathing during exercise.

17
Q

What are the 3 phases of the ventilatory response to excercise?

A

Phase I: initial rapid increase in ventilation, neurally mediated as so rapid

Phase II: gradual increase in breathing over several minutes, humorally mediated

Phase III: If below the AT, breathing plateaus, if above the AT, continual steady increase.

18
Q

What happens to arterial PCO2 during exercise?

A

Importantly, it remains constant. This means that there is no feedback signal from CO2 to manipulate breathing.

CO2 does rise in very high intensity exercise, by definition this is not sustainable.

19
Q

What happens PO2 and pH during exercise?

A

They remain constant

20
Q

Eldridge et al

A

Showed that fictive activity increases phrenic nerve activity. This shows the importance of the central drive to breathe during exercise.

21
Q

Neural and Humoral dog experiment (Kao 1963)

A

Vascular system of a dog re-plumbed so that the humeral demands are met by a separate dog. Stimulation of the muscles of the “neural dog” increased the ventilatory rate, showing the role for a neural feedback from muscles in control of breathing during exercise.

22
Q

Adams et al (1984)

A

Stimulation of muscles in paraplegic humans does not cause an increase in ventilation.
This is evidence against the neural muscle feedback theory, but can be explained by compensation by other mechanisms

23
Q

Mcclosky and Mitchell (1972)

A

Showed that stimulation of muscle in decorticate cats increased blood pressure and that this response was abolished by lesion at the dorsal root.

24
Q

Role for cardio dynamic hyperpnoea in control of breathing during exercise?

A

Wasserman (1974): increased cardiac output by infusion of isoproterenol, measured ventilation and found that it increased. Simultaneous infusion with propranolol (to inhibit the increase in cardiac output) inhibited the rise in breathing.

Banner et al (1988) showed a normal ventilatory response to exercise when the early rise in CO was inhibited, evidence against the theory but can be explained by redundancy in the system.

25
Q

Somjen 1992

A

Proposed that the brain has learned the adequate ventilatory response to excercise through trial and error over many years during development. Learned through comparison of ventilatory response, perceived effort and blood gas composition.

26
Q

Holdsworth et al (2020)

A

British soldiers on expedition in the Himalayas, Iron infusion to see if it affected pulmonary arterial pressure, no change seen in pulmonary pressure (but maybe because low sample size and many soldiers had to drop out of the study). Improved metrics of RV function, SpO2, index of SV

27
Q

Metabolic changes at altitude

A
  • Increased angiogenesis (Wahl et al)
  • Downregulation of mitochondrial oxygen consumption (Papandreou et al)
  • With towards anaerobic metabolism
  • Reduction in mitochondrial density, in acclimatised climbers and Tibetan Sherpas (Howald, 1990) (Kayser, 1991)
28
Q

Aragones et al (2008)

A

Phd KO mouse

29
Q

Formenti et al (2010)

A

Metabolic changes in Chuvash polycythemia.

30
Q

Ballester et al 1989

A

Demonstrated that V/Q mismatch is worsened by high flow oxygen

31
Q

Eckert 2013 (2 points)

A

Heterogeneity of OSA

PCRIT values -5 to 2

32
Q

Sutherland 2019

A

Obesity as a risk factor in OSA, most pronounced in asian population

33
Q

Sands 2014

A

Genioglossus muscle activity is protective OSA

34
Q

OSA studies

A
Sands 2014
Sutherland 2019
Eckert 2013
Eckert 2013
Loop gain
MND
PCRIT
Arousal threshold