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Respiratory > 4. Pulmonary Ventilation I > Flashcards

4. Pulmonary Ventilation I Flashcards

1
Q

BREATHING aka

A

PULMONARY VENTILATION

accomplished by changing Thoracic cavity/Lung VOLUME

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2
Q

CHARACTERISTICS needed for THORAX

A

RIGID enough for PROTECTION

FLEXIBLE enough to act as BELLOWS for breathing

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3
Q

what is the ACTIVR part of the BREATHING PROCESS

A

INSPIRATION

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4
Q

what is INSPIRATION INITIATED by

A

the RESPIRATORY CONTROL CENTRE
- in the MEDULLA OBLONGATA (part of brain stem)

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5
Q

what does ACTIVATION of the MEDULLA CAUSE

A

CONTRACTION of the DIAPHRAGM and the EXTERNAL INTERCOSTAL MUSCLES

  • leading to EXPANSION of THORACIC CAVITY and
    DECREASE in PLEURAL SPACE PRESSURE
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6
Q

what is the PASSIVE part of BREATHING

A

EXPIRATION

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7
Q

what is EXPIRATION due to

A

ELASTIC RECOIL of LUNGS (and diaphragm)

  • INTERNAL INTERCOSTAL and ANTERIOR ABDOMINAL MUSCLES can ACCELERATE EXPIRATION by RAISING PLEURAL PRESSURE
    (when more air has to be removed quickly)
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8
Q

PRESSURE DIFFERENCES between the 2 ends of the CONDUCTING ZONE occur due to..

A

CHANGING LUNG VOLUMES

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9
Q

Important PHYSICAL PROPERTIES of the LUNGS

A

COMPLIANCE
ELASTICITY
SURFACE TENSION

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10
Q

what is
- ATMOSPHERIC PRESSURE
- INTRAPULMONARY / INTRA-ALVEOLAR PRESSURE
- INTRAPLEURAL PRESSURE

A
  • pressure of AIR OUTSIDE BODY
  • pressure in the LUNGS
  • PRESSURE within the INTRAPLEURAL SPACE
    (between Parietal and Visceral Pleura)
    (contains thin layer of FLUID - LUBRICANT)
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11
Q

how are the PRESSURES during INSPIRATION (inhalation) that allows AIR to flow INTO LUNGS

A

INTRAPULMONARY PRESSURE is LOWER than ATMOSPHERIC

(high to low)

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12
Q

how are the PRESSURES during EXPIRATION (exhalation) that allows AIR to flow OUT OF LUNGS

A

INTRAPULMONARY PRESSURE is GREATER than ATMOSPHERIC PRESSURE

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13
Q

what is TRANSPULMONARY PRESSURE

A

DIFFERENCE between INTRAPULMONARY and INTRAPLEURAL PRESSURE

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14
Q

PURPOSE of TRANSPULMONARY PRESSURE

A

keeps the LUNGS AGAINST THORACIC WALL (stuck together)

  • allows LUNGS to EXPAND as the THORACIC WALL EXPANDS
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15
Q

FORCES in the LUNG, PLEURAL SAC and CHEST WALL

A

Lung: ELASTIC RECOIL of lung (away from pleural sac)

Pleural Sac: Force pulling away from Lung, Force pulling away from Chest Wall

Chest wall: ELASTIC RECOIL of chest wall (away from pleural sac)

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16
Q

how is INTRAPULMONARY PRESSURE

A

INSPIRATION:
DECREASES as LUNG VOLUME INCREASES

  • NEGATIVE PRESSURE

EXPIRATION: INCREASES (POSITIVE)

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17
Q

how is INTRAPLEURAL PRESSURE

A

starts off NEGATIVE (-4)

INSPIRATION: MORE NEGATIVE as the Chest Wall EXPANDS

RECOIL: returns to initial value -4 mm Hg

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18
Q

VOLUME OF BREATH drawn in/out of lungs during each breath

A

0.5 LITRE

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19
Q

what does BOYLE’S LAW state

A

the PRESSURE of a GAS is INVERSELY PROPORTIONAL to its VOLUME

During INSPIRTION: INCREASE in LUNG VOLUME DECREASES INTRAPULMONARY PRESSURE to SUBATMOSPHERIC LEVELS (air in)

EXPIRATION: DECREASE LUNG VOLUME INCREASES INTRAPULMONARY PRESSURE ABOVE ATMOSPHERIC levels

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20
Q

BOYLE’S LAW
what happens when LUNG VOLUME INCREASES (Inspiration)

A

INTRAPULMONARY PRESSURE DECREASES

to SUBATMOSPHERIC levels

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21
Q

BOYLE’S LAW

what happens when LUNG VOLUME DECREASES (Expiration)

A

INTRAPULMONARY PRESSURE INCREASES

ABOVE ATMOSPHERIC levels

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22
Q

DIAPHRAGM during INSPIRATION and EXPIRATION

A

Inspiration: CONTRACTS, FLATTENS, INCREASES VOLUME of THORACIC CAVITY

Expiration: RELAXES, RAISES, DECREASES VOLUME of Thoracic Cavity

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23
Q

EXTERNAL INTERCOSTAL MUSCLES

A

RAISE RIB CAGE during Normal/Quiet INSPIRATION

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24
Q

INTERNAL INTERCOSTAL MUSCLES

A

LOWER RIB CAGE during FORCED EXPIRATION

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25
Q

which MUSCLES used for FORCED INSPIRATION

A

SCALENES, PECTORALIS MINOR and STERNOCLEIDOMASTOID

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26
Q

which MUSCLES used for FORCED EXPIRATION

A

INTERNAL INTERCOSTAL
&
ABDOMINAL Muscles (give highest expiratory flow) (rectus abdominus, transversus abdominus, internal and external obliques)

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27
Q

when does the VOLUME of THORACIC CAVITY INCREASE VERTICALLY

A

Inspiration-

when DIAPHRAGM CONTACTS

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28
Q

when does the VOLUME of THORACIC CAVITY INCREASE LATERALLY

A

Inspiration

when PARASTERNAL and EXTERNAL INTERCOSTALS RAISE the RIBS

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29
Q

when does the VOLUME of the THORACIC CAVITY DECREASE VERTICALLY

A

Expiration

when DIAPHRAGM RELAXES (Dome)

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30
Q

when does the VOLUME of the THORACIC CAVITY DECREASE LATERALLY

A

Expiration

  • when External and Parasternal intercostals RELAX for QUIET EXPIRATION
    or
  • when INTERNAL INTERCOSTALS CONTRACT in FORCED EXPIRATION to LOWER RIBS
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31
Q

what are PRECISELY REGULATED in order to maintain normal levels of PARTIAL OXYGEN and CARBON DIOXIDE PRESSURE

A

DEPTH and RATE OF BREATHING

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32
Q

BASIC ELEMENTS of the RESPIRATORY CONTROL CENTRE:

A
  1. CENTRAL CONTROLLER
  2. STRATEGICALLY places SENSORS (Mechanoreceptors and Chemoreceptors)
  3. Respiratory MUSCLES
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33
Q

BREATHING is MAINLY CONTROLLED at the level of the…

A

BRAINSTEM

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34
Q

the NORMAL AUTOMATIC and PERIODIC nature of BREATHING is TRIGGERED and CONTROLLED by the..

A

RESPIRATORY CENTRES located in the PONS and MEDULLA

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35
Q

RESPIRATORY CENTRES in the PONS and MEDULLA are…

A

POORLY DEFINED COLLECTION of NEURONES

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36
Q

3 Important Areas of the CENTRAL CONTROL

A
  • MEDULLARY Respiratory Centre comprising of DORSAL Medullary NEURONES and VENTRAL medullary NEURONES
  • APNEUSTIC CENTRE
  • PNEUMOTAXIC CENTRE
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37
Q

the DRG (DORSAL RESPIRATORY GROUP) is associated with… and responsible for..

A

associated with INSPIRATION

proposed that the spontaneous intrinsic periodic FIRING of these neurones is responsible for the basic RHYTHM OF BREATHING

have cycle of activity that arises spontaneously every few seconds

38
Q

when the DRG NEURONES are ACTIVE, what do their ACTION POTENTIALS travel through to finally STIMULATE RESPIRATORY MUSCLES

A

through RETICULOSPINAL TRACT (in the SPINAL CORD)

and PHRENIC and INTERCOSTAL NERVES

39
Q

VRG (VENTRAL RESPIRATORY GROUP) is associated with

A

EXPIRATION

40
Q

how are the VRG NEURONES

A

SILENT during QUIET BREATHING (expiration is PASSIVE)

  • ACTIVATED during FORCED EXPIRATION when the Rate and Depth of respiration INCREASES
41
Q

what happens to DRG and VRG during HEAVY BREATHING (eg exercise)

A

INCREASED ACTIVTY of DRG ACTIVATES VRG (expiratory system)

-> INCREASED ACTIVITY of VRG (Expiratory system) INHIBITS DRG (inspiratory centre)
and STIMULATES MUSCLES of EXPIRATION

42
Q

how are the DORSAL and VENRRAL GROUPS in MEDULLARY RESPIRATORY CENTRE and how are their communications

A

BILATERALLY PAIRED

CROSS COMMUNICATION between them

  • therefore behave in SYNCHRONY and Respiratory Movements are SYMMETRIC
43
Q

where is the APNEUSTIC CENTRE located

A

LOWER PONS

44
Q

LESIONS covering the area of the APNEUSTIC CENTRE of the PONS cause a..

A

PATHOLOGIC RESPIRATORY RHYTHM
with INCREASED APNOEA FREQUENCY (pauses in breathing)

45
Q

NERVE IMPULSES from the APNEUSTIC CENTRE STIMULATE…

what happens to respiration without…

A

INSPIRATORY CENTRE

  • WITHOUT constant influence of Apneustic Centre, respiration becomes SHALLOW and IRREGULAR
46
Q

where is the PNEUMOTAXIC CENTRE Located

A

UPPER PONS

47
Q

the PNEUMOTAXIC CENTRE is a group of NEURONES with what EFFECT

A

INHIBITORY EFFECT on the DRG (Inspiratory Centre) and APNEUSTIC CENTRE

PROBABLY responsible for the TERMINATION of INSPIRATION by INHIBITING the activity of the DORSAL medullary NEURONES

48
Q

PNEUMOTAXIC CENTRE has an INHIBITORY EFFECT on WHICH CENTRES

A

INSPIRATORY / DRG and APNEUSTIC

49
Q

what does the PNEUMOTAXIC CENTRE PRIMARILY regulate

A

VOLUME of respiration

50
Q

what does the PNEUMOTAXIC CENTRE SECONDARILY regulate

A

RATE of respiration

51
Q

it is generally believed that the UPPER PONS is responsible for the..

A

FINE-TUNING of the Respiratory RYTHM

52
Q

HYPOACTIVATION of the PNEUMOTAXIC CENTRE causes…

A

allows INSPIRATION CENTRE to remain ACTIVE for LONGER than normal (no inhibition)

  • PROLONGED, DEEP INSPIRATIONS
  • BRIEF, LIMITED EXPIRATIONS
53
Q

HYPERACTIVATION of the PNEUMOTAXIC CENTRE results in..

A

SHALLOW INSPIRATIONS

(more inhibition of inspiratory DRG and APNEUSTIC)

54
Q

STEPS in the RESPIRATORY CYCLE
(Apneustic and Pneumotaxic centres in co-ordination providing rhythmic respiratory cycle)

A
  1. ACTIVATION of the INSPIRATORY centre stimulates MUSCLES of Inspiration and the PNEUMOTAXIC centre
  2. PNEUMOTAXIC centre INHIBITS the APNEUSTIC and the INSPIRATORY Centre
  3. Initiation of EXPIRATION
  4. SPONTANEOUS activity of the NEURONES (DRG) in the INSPIRATORY Centre starts another similar cycle again
55
Q

where are the MECHANORECEPTORS (Stretch receptors)

A

WALLS of BRONCHI and BRONCHIOLES

56
Q

main FUNCTION of MECHANORECEPTORS

A

PREVENT OVER-INFLATION

57
Q

how do MECHANORECEPTORS PREVENT OVER-INFLATION

A

INFLATION of Lungs ACTIVATES mechanoreceptors

-> INHIBITS neurones in INSPIRATORY CENTRE via the VAGUS NERVE

activation of mechanoreceptors gradually ceases when Expiration starts, so neurones in Inspiratory Centre become Active again

58
Q

ACTIVATION of MECHANORECEPTORS INHIBITS neurones in INSPIRATORY CENTRE via which NERVE

A

VAGUS NERVE

59
Q

what is the HERING-BREUER REFLEX

A

reflex triggered by MECHANORECEPTORS to INHIBIT OVER-INFLATION of the LUNGS

  • by INHIBITING INSPIRATORY CENTRE neurones (VAGUS nerve)
60
Q

HERING-BREUER REFLEX is particularly important for..

A

INFANTS

  • only functional in ADULTS during EXERCISE when tidal volume larger than normal
61
Q

what is the Normal state of INSPIRATORY NEURONES

A

ACTIVE

(spontaneous)

62
Q

what are CHEMORECEPTORS

A

SPECIALISED NEURONES

ACTIVATED by CHANGES is O2 or CO2 LEVELS in the BLOOD and BRAIN TISSUE

involved in the Regulation of Respiration according to the CHANGES in PO2 and pH

63
Q

where are PERIPHERAL CHEMORECEPTORS

A

at the Bifurcation of the CAROTID ARTERY in the neck
and the AORTIC ARCH (where aorta bends over the heart)

64
Q

PERIPHERAL CHEMORECEPTORS are .. SENSITIVE

A

O2 - SENSITIVE

small, vascular sensory organs encapsulated with the connective tissue

65
Q

PERIPHERAL CHEMORECEPTORS are connected to the RESPIRATORY CENTRE in the MEDULLA by which NERVES

A
  • GLOSSOPHARYNGEAL NERVE (Carotid body)
  • VAGUS NERVE (Aortic body)
66
Q

Where are CENTRAL CHEMORECEPTORS Located

and what are they exposed to

A

BILATERALLY in the Chemo-sensitive area of the MEDULLA OBLONGATA

EXPOSED to CEREBROSPINAL FLUID (CSF), local BLOOD flow and local METABOLISM

67
Q

what do the CENTRAL CHEMORECEPTORS respond to

A

CHANGES in H+ CONCENTRATION

  • when PCO2 is INCREASED,
    CO2 DIFFUSES into CSF from cerebral vessels
    Liberates H+

(CO2 + H2O -> CARBONIC ACID -> H+ + HCO3-)

68
Q

INCREASE in H+ STIMULATES CHEMORECEPTORS resulting in..

A

HYPERVENTILATION
- REDUCES PCO2 in BLOOD and CSF

69
Q

what accompanies INCREASED PCO2 and what does it do

A

CEREBRAL VASODILATION (dilation blood vessels in Brain)
- ENHANCES DIFFUSION of CO2 into CSF

70
Q

CENTRAL CHEMORECEPTORS
why does CO2 DIFFUSE into CSF to INCREASE H+ rather than Blood

A

CSF has a much LOWER BUFFERING CAPACITY THAN BLOOD
- has LESS PROTEINS

therefore, for a given change in PCO2, BIGGER pH CHANGES

71
Q

what STIMULATES CENTRAL CHEMORECEPTORS

A

INCREASED H+ (In CSF/BLOOD)

  • resulting in Hyperventilation which REDUCES PCO2
72
Q

what is the MAJOR REGULATOR of Respiration

A

CO2

73
Q

is CO2 or O2 more important to MAINTAIN NORMAL RESPIRATION and why

A

CO2 MORE IMPORTANT than o2

  • even small CHANGES in PCO2 in the blood cause LARGE INCREASES in RATE and DEPTH of RESPIRATION (100% increase ventilation)

(Hypercapnia is 5 mm Hg increase PCO2)

EFFECTS of PO2 on respiration is very MINOR

74
Q

what is HYPOCAPNIA

A

LOWER than normal PCO2 level in the Blood

  • causes in periods where RESPIRATORY MOVEMENTS DO NOT OCCUR
75
Q

what is HYPOXIA

A

DECREASE in PO2

76
Q

when only can PO2 DECREASE cause SIGNIFICANT CHANGES in Respiration
and why?

A

ONLY AFTER 50% DECREASE

  • due to the nature of O2-HAEMOGLOBIN SATURATION
  • at any level above 80 mm Hg, Hb saturated with O2

so only BIG changes in PO2 produce Symptoms otherwise COMPENSATED by O2 BOUND with Hb

77
Q

BREATHING in some extent is also controlled CONSIOUSLY from.

A

HIGHER BRAIN CENTRES
(eg Cerebral Cortex)

78
Q

what is the name of the NEURAL CENTRE for VOLUNTARY Respiratory Control

A

PRIMARY MOTOR CORTEX

works by sending signals to the SPINAL CORD which sends signals to the MUSCLES eg diaphragm

79
Q

VOLUNTARY RESPIRATION from the PRIMARY MOTOR CORTEX is known as what pathway and when is it required

A

ASCENDING RESPIRATORY PATHWAY

when we TALK, COUGH, VOMIT

(also possible to voluntarily change the RATE of breathing)

80
Q

EFFECT of HYPERVENTILATION

A

DECREASE PCO2 (loss of CO2)

resulting in PERIPHERAL VASODILATION and DECREASE in BLOOD PRESSURE

81
Q

when happens when you STOP BREATHING VOLUNTARILY

A
  • DECREASE PO2 (ARTERIAL PARTIAL OXYGEN PRESSURE)
  • produces an URGE to BREATHE
  • ARTERIAL PCO2 INCREASES
  • when PCO2 HIGH enough, OVERRIDES CONSCIOUS influence from the Primary Motor Cortex and
    STIMULATES INSPIRATORY SYSTEM

if held breath long enough to decrease PO2 very low, may LOOSE CONSCIOUSNESS
UNCONSCIOUS person: AUTOMATIC CONTROL TAKES OVER and NORMAL BREATHING RESUMES

82
Q

STIMULATION of what can also STIMULATE RESPIRATORY SYSTEM

A

PAIN, TOUCH and THERMAL RECEPTORS

83
Q

what is the VENTILATION/PERFUSION (V/Q) RATIO

A

dynamic RELATIONSHIP between the amount of VENTILATION (air flow) in the ALVEOLI and the amount of PERFUSION (BLOOD flow) through the ALVEOLAR CAPILLARIES

84
Q

what does the V/Q RATIO determine

A

QUALITY of GAS EXCHANGE
- amount of OXYGEN entering Blood
- amount of CO2 Off-loading from blood

85
Q

how would the V/Q RATIO be in an IDEAL LUNG

A

V/Q RATIO = 1

VENTILATION = PERFUSION

matching amount of blood flow to ventilation

*DONT GET due to effects of GRAVITY on Blood Flow, STRUCTURE of Lungs, SHUNTING of Blood

86
Q

what is a SHUNT

A

when there is PERFUSION but POORLY VENTILATED Alveoli

ie. Pneumonia (fluid etc in alveoli) or Acute Asthma (bronchioles constricted, no ventilation)

therefore DECREASED OXYGENATION

87
Q

what is PHYSIOLOGICAL DEADSPACE

A

when there is VENTILATION but POORLY PERFUSED Alveoli (poor/no blood flow)

ie. Cardiovascular shock, COPD, Pulmonary Embolus

88
Q

what is it called when the ALVEOLI is PERFUSED but NOT VENTILATED

A

SHUNT

89
Q

what is HYPOXIC PULMONARY VENTILATION (HPV)

A

Physiological Mechanism to COMBAT SHUNT

Low PO2

-> CONSTRICTION of ARTERIOLES

-> DIVERTS BLOOD FLOW to better Ventilated alveoli

90
Q

what can it lead to when there are A LOT of UNDER-VENTILATED ALVEOLI (SHUNT)

A

PULMONARY HYPERTENSION

-> can contribute to ALTITUDE SICKNESS

91
Q

How does HYPOXIC PULMONARY VASOCONSTRICTION occur - MOLECULAR MECHANISM, what causes the activation

A
  • INHIBITION of HYPOXIA (low O2) SENSITIVE Voltage Gated POTASSIUM CHANNELS in PULMONARY ARTERY SMOOTH MUSCLE
    -> DEPOLARISATION
  • Activates Voltage Dependent CALCIUM CHANNELS,
    INCREASES INTRACELLULAR CALCIUM and Activates SMOOTH MUSCLE
    -> VASOCONSTRICTION

(later studies show ion channels and mechanisms play a role)
(recently proposed hypoxia sensed at alveolar/capillary level not pulmonary artery smooth muscle cell)

Respiratory (16 decks)

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