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PA10315 2nd semester > Respiratory system: chemical and neuronal control mechanisms > Flashcards

Respiratory system: chemical and neuronal control mechanisms Flashcards

1
Q

neural control of respiration

A

central rhythm generator in medulla (automatic)
Receptors in respiratory tract causing sneezing, coughing and hyperpnoea (incr rate and depth of breathing)
Nociceptors- detect noxious substances

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2
Q

Chemical control of respiration

A

central and peripheral chemoreceptors

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3
Q

Medulla control

A

ventral and dorsal respiratory group:

  • discharge rhythmically
  • efferent (output) neurones to respiratory motor nerves
  • receives afferent input from periphery and pons
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4
Q

Pons control

A

Apneustic centre:
prolongs medullary centre firing
so depth of breathing incr

Pneumotaxic centre:
Inhibits apneustic centre
Controls rate of breathing

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5
Q

Pre-Botzinger complex

A

Region of ventral respiratory group
Spontaneous rhythmic discharge
stimulates rhythmic discharge of motor nerves, resulting in contraction of diaphragm
Key in regulation of breathing- without it there is a loss of regular rhythm and CO2 responsiveness

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6
Q

Are cortical/higher centres essential for breathing

A

No, but no longer voluntary control without them

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7
Q

Transection above pons

A

loss of voluntary control

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8
Q

Transection above medulla

A

loss of feedback regulation from pons (above medulla)

breathing continues

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9
Q

Transection of spinal cord

A

breathing abolished

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10
Q

Voluntary control of breathing

A

via cerebral cortex

sends signals direct to respiratory motor neurones

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11
Q

lung transplant

A

Motor innervation is to skeletal muscle, so ventilation carries on
Preservation of cough
from tracheal stimulation
But loss of cough stimulation in lower airway
Loss of Hering-Breuer reflex (prevents over inflation of the lung)

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12
Q

chemoreceptors

central and peripheral

A

Central (medullary)- H+, CO2

Peripheral- cartoid and aortic bodies. Primary peripheral signal is O2, but also input from H+

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13
Q

PO2

A

partial pressure of oxygen

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14
Q

PCO2

A

partial pressure of CO2

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15
Q

PaO2

A

partial pressure of arterial oxygen

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16
Q

PaCO2

A

Partial pressure of arterial CO2

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17
Q

PAO2

A

partial pressure alveolar oxygen

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18
Q

Central control of respiration

A

HCO3- and H+ don’t easily cross BB
CO2- uncharged- does cross BBB and dissociates in CSF
Hence CO2 larger influence on ventilation than pH

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19
Q

carbon dioxide effect

A

has little effect in stimulating neurones in the chemosensitive area, but does have a potent indirect effect by reacting with H2O in tissues to from H2CO3, dissociates into HCO3- and H+ ions, and H+ have direct effect on respiration
Hence whenever blood PCO2 incr, so does PCO2 of ISF in medulla and CSF, and H+ ions incr when CO2 reacts with water , so respiratory center activity incr by changes in blood CO2

20
Q

How does H+ act on respiratory center

A

Stimulate central chemo receptors (CO2 can’t)
Incr ventilation
Reduction in blood PCO2

21
Q

Regulation of CO2 during sustainable exercise

A

Ventilation incr prior ro rise in blood CO2- due to anticipatory stimulation in the higher CNS
Arterial PCO2 levels fall
As exercise goes on, more CO2 generated and arterial CO2 returns to normal
CO2 passes from muscles into venous blood and efficiently removed in the lung

22
Q

Peripheral control respiration- O2

A

Fall in o2 stimulates glomus cells in cartoid and aortic bodies
Contains O2 sensitive K+ channels and dopamine

23
Q

O2 falling sequence

A 
O2 falls
K+ channels close
Depolarisation
DA release which stimulates afferent fibres, signals to medulla
Nerve firing increases at low PaO2
24
Q

Doxapram

A

Closes K+ channels on glomus cell (cartoid body)
Glomus cell depolarises and sends afferent signals to medullary respiratory centre
used in respiratory failure

25
Q

Caffeine

A

Non-specific CNS stimulation, including respiratory centre

bronchodilator

26
Q

Acetazolamide

A

respiratory stimulant
carbonic anhydrase inhibitor
Stimulates respiration by creating mild metabolic acidosis via decr renal absorption of bicarbonate and hence reduced acid buffering
Cartoid bodies respond to decr in pH

27
Q

Respiratory depressants?

A

Majority of drugs with depressant action on CNS

28
Q

Why do we breathe?

A

O2 needed for respiration- krebs can’t proceed without regeneration of NAD+, ETC dependent on O2
ATP generated from respiration required for: active transport (maintaining ionic gradients, nutrient uptake), anabolic reactions, muscle contraction, phosphorylation of targets, precursor for cAMP
O2 also needed to pay O2 debt after bursts of anabolic metabolism

29
Q

Pgas

A

barometric pressure x fraction of particular gas

30
Q

PAO2

A

Alveolar pressure

O2 inspired - O2 consumed

31
Q

How much O2 is consumed?

A

Estimate O2 consumption from CO2 in arterial blood

CO2 produced divided by O2 consumed is the respiratory quotient

32
Q

PAO2 also equals

A

O2 inspired - (CO2 produced/RQ)

33
Q

Uptake of oxygen in the pulmonary capillary

A

Alveolar O2 equilibrates with the blood in the capillaries

As blood in capillary gets oxygenated

34
Q

How is oxygen transported

A

Most bound to haemoglobin
Binding is co-operative- 4 molecules of oxygen per haemoglobin molecule
Some O2 dissolved in blood

35
Q

Myoglobin

A

O2 storage and transport in metabolically active cells
Skeletal and cardiac muscle
Doesn’t bind co-operatively- one O2 binding site
High affinity, affinity not affected by pH or CO2, so able to capture O2 released by Hb (when pH falls)
Myoglobin saturated by O2 at a much lower concentration

36
Q

CO2 transport

A

Mainly as HCO3-
some as dissolved CO2
Some as carbamino haemoglobin (HbCO2)

37
Q

what happens when CO2 diffuses tissues to plasma

A

Most enters RBC and converted to bicarbonate by carbonic anhydrase

38
Q

When CO2 production increased (exercise/disease)

A

Fraction of CO2 increases relative to HCO3-

Passes into CSF and detection by central chemoreceptors

39
Q

High PO2 in lungs causes the blood to release CO2

A

O2 binding to Hb makes it more acidic
Less formation of HbCO2
Excess H+ bind HCO3- to form H2CO3, Co2 released

40
Q

Ventilation-Perfusion matching

A

For optimum GE ventilation must match blood perfusion

Mismatched in disease- reduced blood PO2

41
Q

Hypoxaemia

A 
Low O2
Shunting: unventilated alveoli
ventilation-perfusion mismatch
Diffusion abnormalities: thickened alveolar wall
Hypoventilation (ventilation inadequate)
42
Q

shunting

A

In shunting, venous blood enters the bloodstream without passing through functioning lung tissue. Often from blood flowing through unventilated portions of the lung

43
Q

Hypercapnia

A

Incr CO2
Incr dead space: pulmonary embolus
Hypoventilation

44
Q

Physiological response to low inspired O2

A

Incr ventilation: immediate, driven by peripheral chemosensors, not sustained
Pulmonary vasoconstriction: rapid, sustained, shunts blood away from poorly ventilated areas
Increased hematocrit: rbc cell fraction of blood incr, HIF activation (hypoxia inducible factors) which regulate oxygen-sensitive gene transcription and EPO production by kidneys (stimulate RBC production)

45
Q

Acute mountain sickness

A

Flu-like, ahngover
Breathlessness
Hypoxic pulmonary vasoconstriction
Pulmonary and cerebral oedema (incr fluid in the lungs)

46
Q

Chronic mountain sickness

A 
Low PO2 cannot be matched by ventilation
Incr EPO production in kidney
Too high hematocrit, viscous blood
Increased load on right heart
Acetazolamide drug (carbonic anhydrase inhibitor) inhibits EPO production and incr ventilation
47
Q

Genetic adaptions for high altitude populations

A

higher hematocrit

higher myoglobin levels

PA10315 2nd semester (27 decks)

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