4. Pulmonary Ventilation I Flashcards
(91 cards)
1
Q
BREATHING aka
A
PULMONARY VENTILATION
accomplished by changing Thoracic cavity/Lung VOLUME
2
Q
CHARACTERISTICS needed for THORAX
A
RIGID enough for PROTECTION
FLEXIBLE enough to act as BELLOWS for breathing
3
Q
what is the ACTIVR part of the BREATHING PROCESS
A
INSPIRATION
4
Q
what is INSPIRATION INITIATED by
A
the RESPIRATORY CONTROL CENTRE
- in the MEDULLA OBLONGATA (part of brain stem)
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
6
Q
what is the PASSIVE part of BREATHING
A
EXPIRATION
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)
8
Q
PRESSURE DIFFERENCES between the 2 ends of the CONDUCTING ZONE occur due to..
A
CHANGING LUNG VOLUMES
9
Q
Important PHYSICAL PROPERTIES of the LUNGS
A
COMPLIANCE
ELASTICITY
SURFACE TENSION
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)
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)
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
13
Q
what is TRANSPULMONARY PRESSURE
A
DIFFERENCE between INTRAPULMONARY and INTRAPLEURAL PRESSURE
14
Q
PURPOSE of TRANSPULMONARY PRESSURE
A
keeps the LUNGS AGAINST THORACIC WALL (stuck together)
- allows LUNGS to EXPAND as the THORACIC WALL EXPANDS
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)
16
Q
how is INTRAPULMONARY PRESSURE
A
INSPIRATION:
DECREASES as LUNG VOLUME INCREASES
- NEGATIVE PRESSURE
EXPIRATION: INCREASES (POSITIVE)
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
18
Q
VOLUME OF BREATH drawn in/out of lungs during each breath
A
0.5 LITRE
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
20
Q
BOYLE’S LAW
what happens when LUNG VOLUME INCREASES (Inspiration)
A
INTRAPULMONARY PRESSURE DECREASES
to SUBATMOSPHERIC levels
21
Q
BOYLE’S LAW
what happens when LUNG VOLUME DECREASES (Expiration)
A
INTRAPULMONARY PRESSURE INCREASES
ABOVE ATMOSPHERIC levels
22
Q
DIAPHRAGM during INSPIRATION and EXPIRATION
A
Inspiration: CONTRACTS, FLATTENS, INCREASES VOLUME of THORACIC CAVITY
Expiration: RELAXES, RAISES, DECREASES VOLUME of Thoracic Cavity
23
Q
EXTERNAL INTERCOSTAL MUSCLES
A
RAISE RIB CAGE during Normal/Quiet INSPIRATION
24
Q
INTERNAL INTERCOSTAL MUSCLES
A
LOWER RIB CAGE during FORCED EXPIRATION
25
which MUSCLES used for FORCED INSPIRATION
SCALENES, PECTORALIS MINOR and STERNOCLEIDOMASTOID
26
which MUSCLES used for FORCED EXPIRATION
INTERNAL INTERCOSTAL
&
ABDOMINAL Muscles (give highest expiratory flow) (rectus abdominus, transversus abdominus, internal and external obliques)
27
when does the VOLUME of THORACIC CAVITY INCREASE VERTICALLY
Inspiration-
when DIAPHRAGM CONTACTS
28
when does the VOLUME of THORACIC CAVITY INCREASE LATERALLY
Inspiration
when PARASTERNAL and EXTERNAL INTERCOSTALS RAISE the RIBS
29
when does the VOLUME of the THORACIC CAVITY DECREASE VERTICALLY
Expiration
when DIAPHRAGM RELAXES (Dome)
30
when does the VOLUME of the THORACIC CAVITY DECREASE LATERALLY
Expiration
- when External and Parasternal intercostals RELAX for QUIET EXPIRATION
or
- when INTERNAL INTERCOSTALS CONTRACT in FORCED EXPIRATION to LOWER RIBS
31
what are PRECISELY REGULATED in order to maintain normal levels of PARTIAL OXYGEN and CARBON DIOXIDE PRESSURE
DEPTH and RATE OF BREATHING
32
BASIC ELEMENTS of the RESPIRATORY CONTROL CENTRE:
1. CENTRAL CONTROLLER
2. STRATEGICALLY places SENSORS (Mechanoreceptors and Chemoreceptors)
3. Respiratory MUSCLES
33
BREATHING is MAINLY CONTROLLED at the level of the...
BRAINSTEM
34
the NORMAL AUTOMATIC and PERIODIC nature of BREATHING is TRIGGERED and CONTROLLED by the..
RESPIRATORY CENTRES located in the PONS and MEDULLA
35
RESPIRATORY CENTRES in the PONS and MEDULLA are...
POORLY DEFINED COLLECTION of NEURONES
36
3 Important Areas of the CENTRAL CONTROL
- MEDULLARY Respiratory Centre comprising of DORSAL Medullary NEURONES and VENTRAL medullary NEURONES
- APNEUSTIC CENTRE
- PNEUMOTAXIC CENTRE
37
the DRG (DORSAL RESPIRATORY GROUP) is associated with... and responsible for..
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
when the DRG NEURONES are ACTIVE, what do their ACTION POTENTIALS travel through to finally STIMULATE RESPIRATORY MUSCLES
through RETICULOSPINAL TRACT (in the SPINAL CORD)
and PHRENIC and INTERCOSTAL NERVES
39
VRG (VENTRAL RESPIRATORY GROUP) is associated with
EXPIRATION
40
how are the VRG NEURONES
SILENT during QUIET BREATHING (expiration is PASSIVE)
- ACTIVATED during FORCED EXPIRATION when the Rate and Depth of respiration INCREASES
41
what happens to DRG and VRG during HEAVY BREATHING (eg exercise)
INCREASED ACTIVTY of DRG ACTIVATES VRG (expiratory system)
-> INCREASED ACTIVITY of VRG (Expiratory system) INHIBITS DRG (inspiratory centre)
and STIMULATES MUSCLES of EXPIRATION
42
how are the DORSAL and VENRRAL GROUPS in MEDULLARY RESPIRATORY CENTRE and how are their communications
BILATERALLY PAIRED
CROSS COMMUNICATION between them
- therefore behave in SYNCHRONY and Respiratory Movements are SYMMETRIC
43
where is the APNEUSTIC CENTRE located
LOWER PONS
44
LESIONS covering the area of the APNEUSTIC CENTRE of the PONS cause a..
PATHOLOGIC RESPIRATORY RHYTHM
with INCREASED APNOEA FREQUENCY (pauses in breathing)
45
NERVE IMPULSES from the APNEUSTIC CENTRE STIMULATE...
what happens to respiration without...
INSPIRATORY CENTRE
- WITHOUT constant influence of Apneustic Centre, respiration becomes SHALLOW and IRREGULAR
46
where is the PNEUMOTAXIC CENTRE Located
UPPER PONS
47
the PNEUMOTAXIC CENTRE is a group of NEURONES with what EFFECT
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
PNEUMOTAXIC CENTRE has an INHIBITORY EFFECT on WHICH CENTRES
INSPIRATORY / DRG and APNEUSTIC
49
what does the PNEUMOTAXIC CENTRE PRIMARILY regulate
VOLUME of respiration
50
what does the PNEUMOTAXIC CENTRE SECONDARILY regulate
RATE of respiration
51
it is generally believed that the UPPER PONS is responsible for the..
FINE-TUNING of the Respiratory RYTHM
52
HYPOACTIVATION of the PNEUMOTAXIC CENTRE causes...
allows INSPIRATION CENTRE to remain ACTIVE for LONGER than normal (no inhibition)
- PROLONGED, DEEP INSPIRATIONS
- BRIEF, LIMITED EXPIRATIONS
53
HYPERACTIVATION of the PNEUMOTAXIC CENTRE results in..
SHALLOW INSPIRATIONS
(more inhibition of inspiratory DRG and APNEUSTIC)
54
STEPS in the RESPIRATORY CYCLE
(Apneustic and Pneumotaxic centres in co-ordination providing rhythmic respiratory cycle)
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
where are the MECHANORECEPTORS (Stretch receptors)
WALLS of BRONCHI and BRONCHIOLES
56
main FUNCTION of MECHANORECEPTORS
PREVENT OVER-INFLATION
57
how do MECHANORECEPTORS PREVENT OVER-INFLATION
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
ACTIVATION of MECHANORECEPTORS INHIBITS neurones in INSPIRATORY CENTRE via which NERVE
VAGUS NERVE
59
what is the HERING-BREUER REFLEX
reflex triggered by MECHANORECEPTORS to INHIBIT OVER-INFLATION of the LUNGS
- by INHIBITING INSPIRATORY CENTRE neurones (VAGUS nerve)
60
HERING-BREUER REFLEX is particularly important for..
INFANTS
- only functional in ADULTS during EXERCISE when tidal volume larger than normal
61
what is the Normal state of INSPIRATORY NEURONES
ACTIVE
(spontaneous)
62
what are CHEMORECEPTORS
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
where are PERIPHERAL CHEMORECEPTORS
at the Bifurcation of the CAROTID ARTERY in the neck
and the AORTIC ARCH (where aorta bends over the heart)
64
PERIPHERAL CHEMORECEPTORS are .. SENSITIVE
O2 - SENSITIVE
small, vascular sensory organs encapsulated with the connective tissue
65
PERIPHERAL CHEMORECEPTORS are connected to the RESPIRATORY CENTRE in the MEDULLA by which NERVES
- GLOSSOPHARYNGEAL NERVE (Carotid body)
- VAGUS NERVE (Aortic body)
66
Where are CENTRAL CHEMORECEPTORS Located
and what are they exposed to
BILATERALLY in the Chemo-sensitive area of the MEDULLA OBLONGATA
EXPOSED to CEREBROSPINAL FLUID (CSF), local BLOOD flow and local METABOLISM
67
what do the CENTRAL CHEMORECEPTORS respond to
CHANGES in H+ CONCENTRATION
- when PCO2 is INCREASED,
CO2 DIFFUSES into CSF from cerebral vessels
Liberates H+
(CO2 + H2O -> CARBONIC ACID -> H+ + HCO3-)
68
INCREASE in H+ STIMULATES CHEMORECEPTORS resulting in..
HYPERVENTILATION
- REDUCES PCO2 in BLOOD and CSF
69
what accompanies INCREASED PCO2 and what does it do
CEREBRAL VASODILATION (dilation blood vessels in Brain)
- ENHANCES DIFFUSION of CO2 into CSF
70
CENTRAL CHEMORECEPTORS
why does CO2 DIFFUSE into CSF to INCREASE H+ rather than Blood
CSF has a much LOWER BUFFERING CAPACITY THAN BLOOD
- has LESS PROTEINS
therefore, for a given change in PCO2, BIGGER pH CHANGES
71
what STIMULATES CENTRAL CHEMORECEPTORS
INCREASED H+ (In CSF/BLOOD)
- resulting in Hyperventilation which REDUCES PCO2
72
what is the MAJOR REGULATOR of Respiration
CO2
73
is CO2 or O2 more important to MAINTAIN NORMAL RESPIRATION and why
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
what is HYPOCAPNIA
LOWER than normal PCO2 level in the Blood
- causes in periods where RESPIRATORY MOVEMENTS DO NOT OCCUR
75
what is HYPOXIA
DECREASE in PO2
76
when only can PO2 DECREASE cause SIGNIFICANT CHANGES in Respiration
and why?
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
BREATHING in some extent is also controlled CONSIOUSLY from.
HIGHER BRAIN CENTRES
(eg Cerebral Cortex)
78
what is the name of the NEURAL CENTRE for VOLUNTARY Respiratory Control
PRIMARY MOTOR CORTEX
works by sending signals to the SPINAL CORD which sends signals to the MUSCLES eg diaphragm
79
VOLUNTARY RESPIRATION from the PRIMARY MOTOR CORTEX is known as what pathway and when is it required
ASCENDING RESPIRATORY PATHWAY
when we TALK, COUGH, VOMIT
(also possible to voluntarily change the RATE of breathing)
80
EFFECT of HYPERVENTILATION
DECREASE PCO2 (loss of CO2)
resulting in PERIPHERAL VASODILATION and DECREASE in BLOOD PRESSURE
81
when happens when you STOP BREATHING VOLUNTARILY
- 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
STIMULATION of what can also STIMULATE RESPIRATORY SYSTEM
PAIN, TOUCH and THERMAL RECEPTORS
83
what is the VENTILATION/PERFUSION (V/Q) RATIO
dynamic RELATIONSHIP between the amount of VENTILATION (air flow) in the ALVEOLI and the amount of PERFUSION (BLOOD flow) through the ALVEOLAR CAPILLARIES
84
what does the V/Q RATIO determine
QUALITY of GAS EXCHANGE
- amount of OXYGEN entering Blood
- amount of CO2 Off-loading from blood
85
how would the V/Q RATIO be in an IDEAL LUNG
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
what is a SHUNT
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
what is PHYSIOLOGICAL DEADSPACE
when there is VENTILATION but POORLY PERFUSED Alveoli (poor/no blood flow)
ie. Cardiovascular shock, COPD, Pulmonary Embolus
88
what is it called when the ALVEOLI is PERFUSED but NOT VENTILATED
SHUNT
89
what is HYPOXIC PULMONARY VENTILATION (HPV)
Physiological Mechanism to COMBAT SHUNT
Low PO2
-> CONSTRICTION of ARTERIOLES
-> DIVERTS BLOOD FLOW to better Ventilated alveoli
90
what can it lead to when there are A LOT of UNDER-VENTILATED ALVEOLI (SHUNT)
PULMONARY HYPERTENSION
-> can contribute to ALTITUDE SICKNESS
91
How does HYPOXIC PULMONARY VASOCONSTRICTION occur - MOLECULAR MECHANISM, what causes the activation
- 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)
