56: Control of Respiration Flashcards

1
Q

Central Controller

A

Pons, medulla, other parts of brain

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2
Q

Effectors

A

Respiratory muscles, diaphragm, intercoastals

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3
Q

Sensors

A

Chemo and mechanoreceptors, muscle proprioceptors

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4
Q

What are the three respiratory centers in the Medulla Oblongata?

A

DRG – dorsal resp. group

VRG – ventral resp. group

PRG - Pontine resp. group

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5
Q

Dorsal Resp. Group

A

control muscles during inspiration

Output via the
phrenic nerves and intercostal nerves

Receives sensory info from
peripheral chemo and mechanoreceptors
through cranial nerves IX and X

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6
Q

Ventral Resp. Group

A

active expiration or for greater than normal
inspiration

pre-Botzinger complex

spontaneously firing
neurons, may act as the pacemaker

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7
Q

Pontine Resp. Group

A

tonic input to medulla to control smooth resp. rhythm

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8
Q

Latent period

A

after expiration – then a ramp pattern develops

increase action potentials, increase in diaphragm muscle tone, action potential reach max diaphragm muscle tone, action potential cease and diaphragm relaxes

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9
Q

Sensors 1: central

chemoreceptors

A

ventral surface of the medulla

Responds to a change in PCO2 and pH of (CSF)

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10
Q

CSF

A

separated from the blood by the BBB – which is largely impermeable to
H+ and HCO3-

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11
Q

Does metabolic acidosis or alkalosis affect CSF pH?

A

little effect of CSF pH

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12
Q

What is the BBB very permeable to?

A

O2 and CO2

PCO2 has a strong
effect on CSF pH

raising PCO2, large decrease in CSF pH

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13
Q

Sensors 2: peripheral

chemoreceptors

A

located in carotid and aortic bodies

Detect changes in PCO2, PO2 and pH

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14
Q

Carotid body

A

small sensory organ at carotid artery, signals to CNS via the glossopharyngeal
nerves

detect ↓PO2 (below 100 mmHg) and pH
changes

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15
Q

Aortic bodies

A

multiple bodies along aorta

afferents feed CNS via vagus nerve

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16
Q

Glomus cells

A

site of chemoreception

↓PO2 – depolarizes glomus cell and
stimulates afferents to the CNS

↑PCO2 in the cells causes acidification – also causes depolarization

H+- causes acid loading into cell - depolarization

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17
Q

Integrated response

A

Central chemoreceptors primarily involved

but peripheral chemoreceptors also help and respond faster

18
Q

What is the most important stimulus to ventilatory drive?

A

PCO2 of arterial blood

19
Q

When PO2 low

A

PCO2 is high

20
Q

Cerebrum

A

voluntary control

21
Q

Medulla oblongata

A

site of dorsal respiratory
center and ventral respiratory center

generate
the basic rhythmic pattern of breathing

22
Q

Pons

A

apneustic and pneumotaxic centers can
modulate the basic pattern of the medulla but
are not essential

23
Q

limbic system and

hypothalamus

A

Emotional responses

anxiety, rage, fear

24
Q

Pulmonary Stretch Receptors

A

in smooth muscle layer of airways

fire in response to transmural pressure

Cause excitation of inspiratory offswitch
& prolongs expiration

25
Q

Irritant Receptors

A

in airway epithelium

Respond to touch, noxious substances (smoke or particles) or lung edema

stimulated by histamines, serotonins
and prostaglandins (inflammation)

results in coughing/gasping

26
Q

Juxtapulmonary capillary Receptors

A

AKA C-fiber endings

Alveolar and bronchial groups

27
Q

Alveolar C-fibers

A

fire in response to lung injury,
overinflation, pulmonary edema, pulmonary embolism

not sensitive to inflammatory mediators

28
Q

Bronchial C-fibers

A

are sensitive to inflammatory

mediators

29
Q

Stimulation bronchial C fibers

A

rapid shallow breathing,
bronchoconstriction, airway secretion and cardiovascular
depression (i.e. hypotension and bradycardia)

30
Q

Proprioceptors

A

Present in joints, tendons and muscle

inform brain of position of body through reception of tension

31
Q

Patient without proprioception…

A

brain has no

information on the location of your extremities must watch their limbs

32
Q

What is sobriety test testing?

A

proprioception

33
Q

What happens during repeat inflammation in the lungs?

A

destruction of alveolar septa and lungs with large air sacs rather than small alveoli

leads to hypoxemia and dyspnea

34
Q

Davenport Diagram

A

When respiratory acidosis occurs:

Renal Compensation through ‘Metabolic alkalosis’

Secrete H+into urine
blood pH↑
HCO3- ↑

35
Q

CSF pH with chronic hypercapnia

A

Choroid plexus will restore CSF pH by secreting HCO3 into the CSF to compensate for chronic acidosis

36
Q

Minute ventilation during oxygen

induced hypercapnia

A

high O2 administered, initial decrease in minute ventilation but then increases

hypercapnia continues to increase

37
Q

Carbon dioxide retention

A

consequence of
ventilation-perfusion mismatching rather than respiratory
center depression

38
Q

How can you reduce risk of oxygen-induced

hypercapnia in COPD patients?

A

titrate oxygen delivery to maintain the PaO2 at 60-65 mm Hg

achieve
saturations of 88% to 92%

39
Q

Consequences of Hypoxaemia

A

Regional pulmonary vasoconstriction

Peripherally vasodilation increase Cardiac output

Erythropoietin secretion increases

Loss of cognitive and motor functions

Impaired judgement

headache,
breathlessness, palpitations, tremor ,
restlessness

loss of consciousness

Detrimental long term effects: pulmonary
HT, Right Ventricular failure, polycythaemia

40
Q

Why treat Hyoxaemia?

A

Immediate benefits – Alleviate of hypoxaemia,
reduce dyspnea, sleep consolidation

Long term benefits – improves survival
-slight reduction in
pulmonary artery pressure