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medical physiology > Chapter 9- ventilation- Rosen > Flashcards

Chapter 9- ventilation- Rosen Flashcards

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USMLE® Step 1 flashcards
1
Q

Respiratory acidosis

A

Retention of CO2 decreases pH. Ex: COPD CO2 retention

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2
Q

Respiratory alkalosis

A

low CO2= high pH. Ex: hyperventilating before Dr. Walkers test.

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3
Q

A _______ indicates a stronger acid

A

larger K’

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4
Q

Important physiological bufferes

A

Hb in RBC

Phosphate, HCO3-

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5
Q

Buffer capacity of CO2 if pKa is 6.1—is it effective?

A

yes, even though physiological pH is 7.4

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6
Q

When acid added to body…..

A

HCO3- ===>H2CO3 (which then dissociates to H20 and CO2)

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7
Q

CO2 is

A

eliminated by respiration,

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8
Q

COPD

A

Elasticity of the lung is lost. Incomplete exhalation so CO2 is retained.

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9
Q

low pH on O2 dissociation curve?

A

Right shift (decreased affinity)

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10
Q

Hyperventilation

A

CO2 blown off= higher pH= respiratory alkalosis

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11
Q

Primary factor in respiratory control

A

CO2. Low CO2= slower respiration. Respiration may stop ==> hypoxia

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12
Q

Voluntary control system

A

Neurons in cerebral cortex send impulses to respiratory motor neurons via corticospinal tracts. Controls: speech, voluntary breath holding, fear and pain.

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13
Q

Autonomic control system. Where are lower motor neuron cell bodies?

A

neurons in pons and medulla generate rhythmic patterned excitatory output to inspiratory/expiratory muscles. Lower motor neuron cell bodies in phrenic motor nucleus from C3-C5

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14
Q

Transection of brainstem below medulla will:

A

stop breathing completely. Do this if someone is trying to rape you…

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15
Q

Transection of brainstem above medulla will:

A

“not affect breathing greatly”

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16
Q

Medullary neurons that control breathing constitute

A

central pattern generator (CPG)

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17
Q

A CPG is

A

a group of neurons capable of rhythmic patterned output in the absence of outside influence or sensor feedback.

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18
Q

Cutting sensory neurons in the vagus nerve does what to CPG neurons?

A

NOTHING. does not block patterned breathing.

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19
Q

What is the primary stimulus for inspiration?

A

Dorsal respiratory group

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20
Q

DRG (dorsal respiratory group, not dorsal root ganglion) inputs (x5)

A

gets input from 1) central and 2) peripheral chemoreceptors, 3) pulmonary stretch receptors, 4)somatic pain receptors, and 5)mechanoreceptors.

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21
Q

During inspiration, phrenic nerve activity—–

A

increases in terms of rate and number of units discharging (recruitment)

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22
Q

What increases tidal volume? What causes the thing that causes the increase in tidal volume?

A

Increase in number of motor units from increased phrenic nerve activity.

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23
Q

termination of inspiration by?

A

natural CPG rhythm modulated by sensory feedback

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24
Q

Expiration is

A

primarily passive, but there is always tonic expiratory output that can increased for forced expiration

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25
Q

Ventral respiratory group

A

Both inspiratory (accessory) and expiratory neurons.

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26
Q

Accessory inspiratory muscles

A

input from ventral respiratory group

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27
Q

Transection above pons is:

A

without effect on breathing—I guess this means there is not an effect.

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28
Q

Transection at inferior pons

A

causes sustained gasping breathing

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29
Q

What causes sustained gasping breahting

A

Superior pons pneumotaxic center usually regulates inspiratory neurons in the apneustic center. If that regulation stops (if apneustic center goes unregulated) then apneustic center goes nuts and you have long inspirations and gasping.

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30
Q

You cut the vagus nerve, and now are stimulating the proximal stump..?

A

inspiration can be stopped. Basically shows experimentally that the vagus n (which normally carries efferents from lung stretch receptors) is inhibitory

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31
Q

Inhibition of inspiration from vagus?

A

activated stretch receptors in lungs send efferent impulses VIA vagus to inhibit inspiration

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32
Q

Conclusion: Medulla is capable of _______ but___________

this is in bold and italics, guessing it’s important?

A

Medulla is capable of SUSTAINED PATTERNED BREATHING but the patter can be FINE TUNED BY NEURONS IN THE PONS AND FEEDBACK VIA VAGUS.

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33
Q

Chemical control of ventilation- Central

A

CO2 and H+ concentrations of CSF on central chemoreceptors

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34
Q

Chemical control of ventilation- Principal control

A

Principal control is via arterial CO2 acting at central chemoreceptors (idk how it’s arterial…i thought it was CSF?)

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35
Q

CO2 production is directly related to _____ and ____.

A

rate of oxidative metabolism and pH via bicarb system

36
Q

chemical control of ventilation- peripheral

A

via pH, CO2 and O2 on carotid body and aortic body receptors. MOSTLY O2!!!

37
Q

Location of carotid and aortic bodies. Size?

A

2-3mm diameter (idk why anyone would ask this…but its W LA campus..)

Carotid bodies at bifurcation of common carotid
Aortic bodies near aortic arch

38
Q

Aortic body/carotid bodies contain:

A

islands of 2 cell types (I and II) surrounded by sinusoidal capillaries

39
Q

Type I cells in carotid/aortic bodies

A

Type I= glomus cells. Make synapses with nerve endings.

40
Q

Aortic/carotid body afferents via?

A

Aortic bodies to medulla via Vagus nerve

Carotid bodies to medulla via glossopharyngeal

41
Q

Fibers carrying afferents from aortic bodies/carotid bodies

Diameter and conduction speed

A

CN IX, X
2-5 micrometers in diameter
Speed: 7-12m/s

42
Q

when pH decreases, what happens to peripheral receptors?

A

Neurons from carotid and aortic bodies INCREASE discharge when pH decreases===> increased ventilation rate AND increased tidal volume

43
Q

_____ receive among the highest blood flow in the body, per gram weight. 40x’s great than brain.

A

carotid bodies

44
Q

Carotid bodies account for ____ of ventilatory drive

A

20%

45
Q

carotid bodies account for _____ of ventilatory response to high CO2

A

30%

46
Q

How do we know that the influence of aortic bodies in response to high CO2 is minimal?

A

Ablation of just carotid bodies = -30% response to high CO2

Ablation of carotid bodies AND aortic bodies= pretty much same result.

47
Q

What can enhance the response to lowered O2?

A

high CO2= hypercapnea

Acidosis

48
Q

Maximal receptor activity at carotid/aortic bodies is to:

A

very low O2 values. So the high CO2 and acidosis “enhance” the response, but are not the major contributors to the response.

49
Q

Central chemoreceptors -location

A

ventral surface of medulla near cranial nerves VI-X

50
Q

Central chemoreceptors contact?

A

DO NOT CONTACT BLOOD. Bathed in CSF. CSF is close to the choroid plexus (which has a high blood flow) so CO2 equilibrates rapidly.

51
Q

CSF CO2 is close to?

A

arterial CO2

52
Q

BBB is poorly permeable to

A

H+

53
Q

BBB is permeable to

A

CO2. It crosses and is hydrated to H2CO3 and then dissociates to HCO3- and H+.

54
Q

______ in the medullary CSF enhances _____.

A

Acidosis enhances tidal volume

55
Q

What if we increase CO2 without changing pH (CSF in medulla)?

A

No effect. they did an experiment or something.

56
Q

THE CENTRAL CHEMORECEPTORS RESPOND DIRECTLY TO _____ BUT INDIRECTLY TO ____.

A

directly to H+, indirectly to CO2 (experiment thing, remember?)

57
Q

What happens if high PCO2 persists for hours? Why?

A

ADAPTATION: ventilatory response wanes. Compensatory HCO3- transport via anion exchange for Cl-.

58
Q

What is the clinical importance of the adaptation to chronic high CO2? What is the major drive/influence for ventilation.

A

Patients with COPD will return to normal breathing even though they have high CO2 (it’s high because they can’t exhale and retain CO2).

PO2 drive from periphery becomes major influence on ventilation.

59
Q

Metabolic acidosis-definition

A

Accumulation of ketone acids during diabetes mellites

60
Q

Metabolic acidosis causes ______ to happen?

A

respiratory stimulation. Hyperventilation to blow off CO2 and increase pH.

61
Q

Hyperventilation is ___ and causes ____.

A

respiratory alkalosis==> fall in blood H by blowing off too much CO2

62
Q

What can cause metabolic alkalosis?

A

vomiting, nasogastric suctioning, diuretics, corticoid treatment, alkali treatment, sever K+ depletion, Cl- restriction

63
Q

Metabolic alkalosis causes (ventilation response to it)

A

depressed ventilation==>rise in arterial CO2 and H+ and eventually restoring pH.

64
Q

Things that cause metabolic acidosis

A

hyperchloremic (diarrhea, interstitial renal disease, renal tubular acidosis)
Increased undetermined anion (generalized renal failure, diabetic/alcoholic ketoacidosis, lactic acidosis).

65
Q

Things that cause respiratory acidosis

A

Respiratory failure (obstructive lung disease, chest wall disease, hypoventilation), CNS depression, pulmonary edema, pneumothorax, abdominal distension

66
Q

Things that cause Respiratory alkalosis

A

hyperventilation, gram (-) sepsis, pulmonary emboli, pneumonia, hepatic failure, high altitude sever anemia

67
Q

The relationship between alveolar pCO2 and ventilation rate is _____

A

“nearly linear”

68
Q

When metabolism increases, PCO2 ______ and ventilation _____ in order to ______.

A

When metabolism increases, PCO2 increases and ventilation increases in order to lower PCO2

69
Q

What happens if you inhale elevated CO2 (rebreathing)?

A

Ventilation increases and alveolar pCO2 will come to equilibrium at a higher value.

70
Q

What happens if pCO2 of inspired air reaches alveolar pCO2? (what is normal alveolar pCO2?)

A

Normal alveolar pCO2= 40 mmHg

Elimination is difficult.

71
Q

When inhaled CO2 levels are > ____, arterial CO2 _______ resulting in ______. Finally, ___ and ___.

A

When inhaled CO2 levels are >7%, arterial CO2 rises rapidly, resulting in CNS depression (including respiratory center). Finally CO2 narcosis and coma.

72
Q

PO2 must ______ before ventilation is affected. What happens to ventilation?

A

must drop below 60mm Hg. When this happens, discharge from peripheral chemoreceptors increases.

73
Q

CO poisoning binds ___ and makes __.

A

binds Hb to make carboxyhemoglobin. CO: Hb affinity is 230x’s stronger than O2: Hb affinity. So, if CO binds, the rest of the O2 bound to Hb wont be able to leave for tissues. Shifts curve to the left

74
Q

Hypoxia caused by high altitude

A

compensation with erythrocytosis

75
Q

Increased oxygen demand is

A

a pathological condition in his notes. Cause by exercise.

76
Q

Proprioreceptors and stretch receptors-role in respiration?

A

in muscle, tendons and joints. they can stimulate ventilation in response to physical disturbance (slap and tickle??) and possibly anticipatory exercise

77
Q

Receptors to irritants (what are irritants?)

A

Irritants can be chemical or mechanical. Histamine and bradykinin during an allergic reaction

Receptors in the trachea and extrapulmonary bronchi cause coughing

In lungs: cause rapid shallow breathing and bronchoconstrition

78
Q

A receptor in your lung was activated and caused shallow breathing and bronchoconstriction–what is it?

A

irritant receptor

79
Q

stretch receptors in smooth muscle of airway

A

Exercise or tidal volume >1L excite sensory neurons running in vagus===> inhibition of respiration

80
Q

Hering Breurer Reflex

A

Inhibition of respiration via stretch receptors in smooth muscle. Acts on respiratory center in medulla and pneumotaxic center in pons to inhibit inspiration (inhibition of apneustic center indirectly.)

81
Q

Deflation receptors

A

stimulate rapid shallow breathing

82
Q

Ventilatory response during pulmonary congestions/edema?

A

Deflation receptors contribute to response.

83
Q

Off switch neurons inhibited by? stimulated by?

A

inhibited by expiratory neurons

stimulated by pneumotaxic center and vagus nerve carry afferents from airway stretch receptors.

84
Q

Inspiration is terminated when?

A

When off-switch neuron inhibition stops (it decreases with time.

85
Q

CC- girl jumped into the pool

A

severed spinal cord too high= quadriplegic and unable to breathe on her own

86
Q

CC-Yelling too much causes?

A

respiratory alkalosis. Sx: light headed, syncope, tonic seizure. paresthesia in fingers and mouth, thirsty and dry mouth.

medical physiology (9 decks)

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