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Medical Studies 1 > Week 5 Respiratory > Flashcards

Week 5 Respiratory Flashcards

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USMLE® Step 1 flashcards
1
Q

what cells compose the alveolar surface

A

Type 1 alveolar cells
Type 2 alveolar cells
fibroblasts
capillaries
pericytes
macrophages
immune cells

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2
Q

function of type 1 alveolar cells

A

95% of alveolar surface, facilitate gas exchange

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3
Q

function of type 2 alveolar cells

A

5% of alveolar surface; secrete surfactant and aid repair

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4
Q

function of fibroblasts

A

ECM production, facilitate repair

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5
Q

what are the capillaries of the lungs

A

consists of endothelial cells and pericytes

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6
Q

function of pericytes

A

enigmatic cells, solicit various functions

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7
Q

function of macrophages

A

phagocytotic ‘engulfing’ of particulate matter

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8
Q

function of immune cells

A

includes T cells, B cells and dendritic cells

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9
Q

what are alveolar macrophages

A

-reside in the mucous layer
-responsible for the clearance of apoptotic cells and cellular debris

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10
Q

Describe the pulmonary circulation

A

RV–>Pulmonary trunk–>Pulmonary arteries–>Smaller arteries–>arterioles –>capillaries–>venules–>smaller veins–>pulmonary veins–>Left atrium–>LV

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11
Q

How do pulmonary arteries respond to hypoxia

A

-constrict in response to alveolar hypoxia
-this diverts blood to better ventilated areas of lung, synchronising perfusion and ventilation

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12
Q

pulmonary arteries vs bronchial arteries

A

-pulmonary arteries and veins are vasa publica, public vessels that are responsible for transport to the lung and gas exchange
-however, bronchial vessels are vasa privata, private vessels that supply lung parenchyma (eg SM, CT,)

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13
Q

features of the bronchial arteries

A

-originate from the thoracic aorta and 3rd right intercostal artery
-in 1/3 of instances, bronchial veins drain into the azygos (right) vein and hemi-azygos or intercostal veins (left)
-in 2/3 of instances, blood from the peripheral bronchial arteries drains into the pulmonary veins

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14
Q

Features of inspiration

A

-diaphragm contracts
-the external intercostals contract
-the rib cage and sternum moves up and out
-the lungs and chest wall expand
-increase in intrathroacic volume
-decrease in intrathoracic pressure
-air moves from environment into lungs (high to low)

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15
Q

Features of expiration

A

-the diaphragm relaxes
-the internal intercostals contract
-the chest wall and lungs contract
-the sternum and rib cage moves down and in
-decrease in intrathroacic pressure
-decrease in intrathoracic volume
-air moves from lungs into environment (high to low)

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16
Q

Describe the lymph drainage of the lungs

A

lung lymph –> lymph (upper)–> ipsilateral lymph nodes –> paratracheal lymph nodes –> bronchomediastinal trunks –> right lymphatic duct

OR

lung lymph –> lymph (lower)–> inferior lymph nodes –> paratracheal lymph nodes –> bronchomediastinal trunks –> right lymphatic duct

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17
Q

outline the normal cough reflex

A

-irritant enters respiratory tract, contacting respiratory epithelium
-innervation of vagal sensory fibres in pharynx, trachea and bronchi
-input via higher order centres–>sensory fibres end in nucleus of solitary tract (NTS in brain stem)
-CPG motor neurons
-VRG motor neurons
-innervation of respiratory muscles (diaphragm, intercostals, intrinsic larangyeal and abdominal muscles)
-forceful expiration against closed glottis (cough)

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18
Q

list the causes of sputum

A

-respiratory infections
-GORD
-bronchitis
-allergies

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19
Q

how do respiratory infections cause sputum production

A

viruses, bacteria, and other pathogens cause inflammation and increased mucus production in the airways as a defence mechanism

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20
Q

how does GORD cause sputum production

A

stomach acid can reach the airways, leading to irritation, inflammation and excess mucous production

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21
Q

how does bronchitis cause sputum production

A

long term irritation from smoking, pollutants, or infection causes chronic inflammation of bronchi, resulting in excess mucous production

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22
Q

how do allergies cause sputum production

A

allergens trigger an immune response that includes inflammation and excess mucous production in the respiratory tract

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23
Q

what is pulmonary ventilation

A

inflow and outflow of air between the atmosphere and alveoli

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24
Q

what is diffusion

A

movement of oxygen and carbon dioxide between the alveoli and pulmonary circulation

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25
Q

what is gas transport

A

transport of oxygen and carbon dioxide in the blood stream

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26
Q

what is gas exchange

A

exchange of gases within body tissue

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27
Q

Whats Boyles law

A

-pressure of gas is inversely proportional to its volume

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28
Q

Outline features of air flow

A

-air flows from high pressure to low pressure
-increasing lung volume results in negative alveolar pressure, air inflow, expansion of chest wall pulls outwards on the lungs, creating more negative pleural pressure
-relaxation of diaphragm and elastic recoil of lungs results in positive alveolar pressure, air outflow and pleural pressure decreases back to baseline

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29
Q

what is lung compliance

A

-‘stretchiness of lungs’
= change in volume/change in pressure

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30
Q

factors that impact compliance

A

-elastic forces of the lungs and elastic forces caused by surface tension
-lung is more compliant during inspiration compared to expiration, due to difficulty inflating alveoli

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31
Q

what is surface tension

A

-tension of the surface film of a liquid, caused by attraction of particles in the surface layer
-in the lungs surface tension causes alveoli to collapse

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32
Q

features of the pleura

A

-double layered membrane
-outer parietal pleura, attaches to the chest wall, diaphragm and mediastinum
-inner visceral pleura adheres closely to surface of lungs
-pleural pressure is negative to create a vacuum between lung surface and thoracic cavity

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33
Q

role of diaphragm

A

primary respiratory muscle, contracts to increase thoracic volume during inhalation and relaxes to decrease thoracic volume during exhalation

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34
Q

role of external intercostals

A

elevate ribs during inhalation, aiding in expanding chest cavity

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35
Q

role of internal intercostals

A

depress the ribs during forced exhalation, assisting in decreasing thoracic volume

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36
Q

role of sternocleidomastoid

A

accessory muscle involved in elevating the sternum and aiding in deep inhalation

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37
Q

define quiet breathing

A

normal, rhythmic inhalation and exhalation during rest or light activities primarily driven by the diaphragm and external intercostal muscles

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38
Q

define forced breathing

A

active, intense inhalation and exhalation involving additional respiratory muscles to meet increased oxygen demands during strenuous activities or when additional ventilation is needed

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39
Q

whats Tidal volume (TV)

A

the amount of air inhaled or exhaled during normal breathing

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40
Q

what is Inspiratory reserve volume

A

the additional air that can be forcibly inhaled beyond tidal volume

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41
Q

what is expiratory reserve volume

A

the additional air that can be forcibly exhaled beyond tidal volume

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42
Q

what is total lung capacity

A

maximum volume of air the lungs can hold, sum of all lung volume (including residual volume)

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43
Q

what is residual volume

A

the air remaining in the lungs after forceful exhalation

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44
Q

what is inspiratory capacity

A

total volume of air that can be inhaled after a normal exhalation (TV + IRV)

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45
Q

what is functional residual capacity

A

volume of air remaining in the lungs after normal exhalation (RV + ERV)

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46
Q

what is forced vital capacity

A

the maximum amount of air that can be exhaled after a maximal inhalation (IRV + TV + ERV)

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47
Q

Describe how pressure, volume, flow and resistance are related

A

V= QR
Volume = flow x resistance

“airflow is inversely proportional to resistance”

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48
Q

state pleural pressure during inspiration and expiration

A

-negative pleural pressure during inspiration
-negative pleural pressure during expiration

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49
Q

state alveolar pressure during inspiration and expiration

A

-negative alveolar pressure during inspiration
-positive alveolar pressure during expiration

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50
Q

define work of breathing

A

refers to the energy expenditure required to overcome the resistance and compliance of respiratory system during ventilation

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51
Q

define transmural pressure

A

the pressure difference across a structures wall, determining its distension or collapse

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52
Q

define trans pulmonary pressure

A

the pressure difference between alveolar and pleural pressure, maintain lung expansion (needs to be +)

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53
Q

define lung compliance

A

measure of the lungs ability to stretch and expand in response to applied pressure, typically during inhalation
-change in lung volume per unit change in transpulmonary pressure

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54
Q

how does compliance link to pressure

A

high lung compliance indicated the lungs can easily expand with little pressure, whereas low compliance suggests stiffness or resistance

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55
Q

x and y axis for pressure volume loop

A

x = pressure
y =volume

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56
Q

key features of pressure volume loop

A

-lung compliance is directly related to slope
-in compliant lung, the graph demonstrates a steep slope, indicating small increase in pressure leads to significant increase in lung volume
-less complaint lung has a flatter slope
-hysterisis present (inflation curve differs to deflation curve)

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57
Q

list the factors that provide resistance to air flow

A

airway resistance
pulmonary resistance
chest wall resistance

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58
Q

how does airway resistance impact air flow

A

the resistance encountered by air moving through the airways, influenced by airway diameter and the smooth muscle tone in bronchi and bronchioles

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59
Q

how does pulmonary resistance impact air flow

A

the overall resistance to airflow within the lungs, incorporating airway resistance, lung tissue elasticity, and the viscoelastic properties of the lung parenchyma

60
Q

how does chest wall resistance impact air flow

A

the resistance from the chest wall and diaphragm during breathing, influenced by muscle tone, rib cage stiffness, and the compliance of the thoracic cavity

61
Q

define surface tension

A

the force exerted by the cohesive properties of water molecules at the interface between the air and fluid lining the alveoli, which creates a tendency for alveoli to collapse

62
Q

what is the role of pulmonary surfactant

A

a mixture of lipids and proteins secreted by type II alveolar cells into the alveolar surface, its primary role is to reduce surface tension, thereby decreasing work of breathing and preventing alveolar collapse (atelectasis)

63
Q

what regulates surfactant release and synthesis

A

mechanical stretching of alveoli and hormonal signals eg cortisol

64
Q

describe the role of surface tension in the elastic recoil of the lung

A

-contributes to the forces that drive lung deflation, surface tension drives deflation and surfactant drives inflation

65
Q

define elastic recoil

A

the tendency of the lungs to return to their original shape and size after being stretched, driven by elastic forces and surface tension

66
Q

compare and contrast the pulmonary and systemic circulation

A

-In SC veins carry deO2blood towards the heart vs in PC veins carry o2blood toward the heart
-In SC arteries carry O2 blood vs in PC arteries carry deO2 blood
-In SC arteries and veins travel adjacently vs in PC arteries travel with airways, veins travel with septa
-In SC arteries have thicker walls vs in PC arteries have thinner walls
-In SC arteries are highly elastic vs in PC arteries are less elastic
-in SC pressure change (12 to 5 at capillaries) vs in PC pressure change (100 to 12 at arterioles)

67
Q

List the regional differences in blood flow of lungs

A

-when upright, blood flow in lower parts of lungs>apex
-Zone 1: lack of blood flow as alveolar pressure is higher than venous and arterial pressure
-Zone 2: blood flow occurs in systole but not diastole, as arterial pressure is higher than alveolar pressure (but alveolar pressure is still greater than venous)
-Zone 3:constant supply of blood flow as arterial AND venous pressure is higher than alveolar pressure

68
Q

factors impacting PVR

A

-endothelin 1 increases PVR
-Histamine increases PVR
-Catecholamines increase PVR
-NO decreases PVR
-adenosine decreases PVR

69
Q

what is PVR

A

refers to the resistance that blood faces when flowing through the blood vessels in the lungs
-impacted by vessel width

70
Q

Features of internal respiration

A

Location: Body tissues
Process: Gas exchange between blood in systemic capillaries and tissues.
Oxygen: Moves from blood to tissues.
CO2: Moves from tissues to blood, carried back to lungs.
Purpose: Deliver oxygen to cells, remove CO2.

71
Q

Features of external respiration

A

Location: Lungs
Process: Gas exchange between alveoli and blood in pulmonary capillaries.
Oxygen: Moves from alveoli to blood.
CO2: Moves from blood to alveoli, then exhaled.
Purpose: Oxygenate blood, remove CO2.

72
Q

Describe the principle of gas diffusion

A

-net movement of gas molecules from a. region of high to low partial pressure
-partial pressure = product of total pressure and fractional concentration of gas

73
Q

what factors influence O2 dissociation

A

-increase H+ (lower pH)
-increased temperature
-increased CO2

74
Q

what is Bohr effect

A

increased H+ and CO2, promotes offloading of O2 in the peripheral tissues (where PCO2 is high) and promotes O2 loading in the lungs (where PCO2 is low)

75
Q

what is a left shift in the O2-Hb dissociation curve

A

-increased affinity for O2
-decreased PCO2
-decreased [H+]
-decreased temp
-decreased 2-3 DPG

76
Q

what is a right shift in the O2-Hb dissociation curve

A

-decreased affinity for O2
-increased PCO2
-increased [H+]
-increased temp
-increased 2-3 DPG

77
Q

describe the diffusion of oxygen at the lungs

A

-alveoli have a standard PO2 of 104 mmHg
-pulmonary capillary carrying deoxygenated blood has a PO2 of 40 mmHg
-Thus, as blood enters pulmonary circulation, its PO2 increases significantly, hence oxygenating blood via diffusion between the capillary and alveolus

78
Q

describe the diffusion of oxygen at tissues

A

-oxygen supply to tissues follows a similar principle, arterial ends of capillaries have PO2 of 95, the interstitial tissue has a PO2 of 40 and the intracellular solution a PO2 of 23
-hence, oxygen diffuses from the arterial end to intracellular space via interstitial space, oxygenating the tissue

79
Q

PCO2 and PO2 at arterial capillary

A

PCO2=40 mmHg
PO2=95 mmHg

80
Q

PCO2 and PO2 at interstitial cells

A

PCO2=45 mmHg
PO2=45 mmHg

81
Q

PCO2 and PO2 at intracellular space

A

PO2= 23mmHg
PCO2=46 mmHg

82
Q

PCO2 and PO2 at Venous capillary cells

A

PO2=45 mmHg
PCO2=45 mmHg

83
Q

how is oxygen transported in the body

A

-via Hg (97-98%)

84
Q

how is carbon dioxide transported in the body

A

-dissolved state (5-10%)
-As bicarbonaten ion ,HCO3 (70%)
-As carbaminohaemoglobin (CO2Hb) (20-25%)

85
Q

Describe the Haldane effect

A

greater binding of oxygen with haemoglobin increases the release (offloading) of CO2, thus, CO2 release is promoted when venous blood is arterialised

86
Q

what is Fick’s law of diffusion

A

rate of gas transfer is proportional to the product of diffusing capacity across a membrane (size of membrane) and the pressure gradient

87
Q

Define diffusing capacity

A

the net rate of gas transfer for a partial pressure gradient of 1 mmHg

88
Q

What factors affect diffusing capacity

A

membrane SA
membrane diffusion barrier
Gas uptake

89
Q

How does membrane SA impact diffusing capacity

A

-body size (height)
-lung volume
-ventilation/perfusion
ALL impact diffusion capacity

90
Q

How does membrane diffusion barrier impact diffusing capacity

A

-Pulmonary congestion ‘
-interstitial oedema
-membrane thickening

91
Q

How does gas uptake impact diffusing capacity

A

-Hb capacity
-capillary transit time

92
Q

Describe the process of gas exchange at lungs and tissues

A

Pressure gradients drive gas exchange:
Partial pressure of oxygen (PO2) is higher in the alveoli (about 100 mmHg) than in the blood (about 40 mmHg), so oxygen moves into the bloodstream.
Partial pressure of carbon dioxide (PCO2) is higher in the blood (about 45 mmHg) than in the alveoli (about 40 mmHg), so carbon dioxide moves into the alveoli to be exhaled.

*same partial pressure values at tissues and same movement ; however, occurs between blood and tissues instead

93
Q

describe regional mismatches to v/q in lungs

A

In an upright individual, the base of the lungs receives more blood flow due to gravity. This matches well with the greater ventilation in the lower regions, optimizing gas exchange. In contrast, the apex receives less blood flow, and despite being well-ventilated, the V/Q ratio is higher, meaning less efficient gas exchange.

94
Q

what is the v/q ratio

A

measure of the efficiency of gas exchange in the lungs

95
Q

what factors influence regional ventilation

A

-gravity
-anatomical expansion (base of lungs larger)
-lung compliance (base more compliant)
-breathing pattern

96
Q

what factors influence regional perfusion

A

-gravity
-hypoxic pulmonary vasoconstriction (redirection)
-pulmonary vascular structure
-lung volume

97
Q

identify the primary features of the respiratory centre

A

dorsal respiratory group
ventral respiratory group
pontine respiratory group

98
Q

function of dorsal respiratory group

A

inspiratory neurons responsible for timing respiratory cycle (inspiration)

99
Q

function of ventral respiratory group

A

neurones that influence both inspiration and expiration

100
Q

function of pontine respiratory group

A

includes the pneumotaxic centre (shortens inspiration) and apneustic centre (prolongs inspiration)

101
Q

what are the three predominant receptors in lungs

A

-slow adapting stretch receptors (SASR)
-rapidly adapting stretch receptors (RASR)
-vagal C fibre nociceptors

102
Q

function of SASR

A

predominantly in the airways, acts as a lung volume sensor

103
Q

function of RASR: rapidly acting stretch receptors

A

located in superficial mucosa, stimulated by changes in tidal volume ,breathing frequency and lung compliance

104
Q

function of vagal C fibre nociceptors

A

free never endings found in bronchi and pulmonary capillaries, stimulated by oxidative stress, inflammation or inhaled irritants

105
Q

Outline the chemical control of respiration

A

-CO2 passes BBB, increasing PCO2 within CSF, pH decreases, H+ can’t penetrate BBB
-CO2–> carbonic acid, dissociates into H+ and bicarbonate ion
-respiratory activity is varied based on CO2 levels

106
Q

where are peripheral chemoreceptors located

A

aortic arch
carotid body

107
Q

what are peripheral chemoreceptors sensitive to

A

PO2, PCO2, H+

108
Q

how is information sent from the aortic arch to medullary respiratory neurons

A

vagus nerve

109
Q

how is information sent from the carotid body to medullary respiratory neurons

A

glossopharyngeal nerve

110
Q

function of J receptors

A

located near pulmonary capillaries, respond to capillary changes, stimulation leads to tachypnoea

111
Q

describe chest wall reflex

A

activated by receptors in the chest muscles, joints and skin; prevent over inflation or sudden deflation of lung (includes hering breur and deflation reflex)

112
Q

describe lung reflexes

A

activated by irritant and stretch receptors in lung tissues; detect harmful particles and chemicals; activate coughing and bronchoconstriction; assist in maintaining overall tidal volume

113
Q

outline hering breur reflex

A

-inflated lung
-activation of stretch receptors
-impulses generated
-inhibition of inspiratory centre
-expiration reduces lung inflation

114
Q

outline deflation reflex

A

-extreme lung deflation (pneumothorax)
-activation of compression receptors
-impulse generated
-stimulation of respiratory centre
-rapid respiration attempt to restore lung volume

115
Q

explain the homeostatic control of respiration and how the body responds to correct hypoventilation and hyperventilation

A

Hypoventilation triggers increased ventilation to correct hypercapnia and hypoxia, while hyperventilation leads to a reduction in ventilation to correct hypocapnia.

116
Q

Explain how the respiratory system is involved in the regulation of acid-base balance.

A

An increase in PCO₂, as seen in hypoventilation, leads to respiratory acidosis, while a decrease in PCO₂, as seen in hyperventilation, results in respiratory alkalosis.

117
Q

How does the body respond to exercise hyperpnea

A

-aerobic exercise
-metabolic acidosis and stress on muscles
-acidosis detected by chemoreceptors, muscle stress detected by proprioceptors
-initiation of respiratory centres
-hyperventilation
-expulsion of CO2

118
Q

list the types of PFT

A

-spiromtery
-single breath diffusing capacity of carbon monoxide (DLCO)
-subdivisons of lungs volume

119
Q

describe spirometery

A

Spirometry is a common pulmonary function test used to measure lung function, specifically the amount (volume) and speed (flow) of air a person can inhale and exhale.

120
Q

describe DLCO

A

Measures the lung’s ability to transfer gas from inhaled air to the bloodstream.

121
Q

How is spirometery conducted

A

Preparation: The patient is seated or standing, with their nose clipped and lips sealed around a mouthpiece.
Initial Test: They fully inhale, then forcefully exhale until empty, followed by a rapid inhalation.
Repetition: This process is repeated 3 to 8 times.
Bronchodilator Test: After administering a bronchodilator, the test is repeated 20 minutes later to assess lung function changes.

122
Q

what is forced expiratory volume1

A

maximum amount of air that can be expelled in one second

123
Q

what is forced vital capacity

A

maximum amount of air that can be expired in one breath

124
Q

what is peak expiratory flow

A

fastest speed at which air is expired

125
Q

what is mid forced expiratory flow

A

averaged flow rate between 25% and 75% of FVC

126
Q

what is forced expiratory time

A

time taken for FVC to become completely expired

127
Q

Obstructive ventilatory defects findings on spirometery

A

-decreased FEV
-decreased or normal FVC
-decreased FEV1/FVC

128
Q

Restrictive ventilatory defects findings on spirometery

A

-decreased or normal
FEV
-decreased FVC
-increased or normal
FEV1/FVC

129
Q

examples of obstructive respiratory conditions

A

-asthma
-emphysema
-chronic bronchitis
-foreign bodies

130
Q

examples of restrictive respiratory conditions

A

congestion
kyphoscolisosis
pleural effusion
fibrosis
ILD
Pulmonary fibrosis
sarcoidosis

131
Q

Describe the significance of bronchodilator response in the obstructive pattern

A

The bronchodilator response is used to determine if airway obstruction is reversible. After administering 200 µg of salbutamol post-spirometry, a 10% or greater improvement in FEV1 or FVC indicates reversibility, which is key in diagnosing conditions like asthma.

132
Q

Describe steps in lung dilution

A
  1. The patient inhales a helium-oxygen mixture with a known helium concentration.
  2. The helium mixes with lung gases until equilibrium is reached, ensuring even distribution in the lungs.
  3. The patient exhales the mixture, and the spirometer measures the helium concentration in the exhaled breath.
  4. Comparing the initial and exhaled helium concentrations allows calculation of lung volume and other pulmonary parameters.
133
Q

reduced DLCO indicates

A

-less Hb available for CO binding
-anaemia, PE, emphysema

134
Q

elevated DLCO indicates

A

-more Hb available for CO binding
-polycythaemia, erythrocytosis

135
Q

how does CAD lead to dyspnoea

A

-CAD
-stenosis/occlusion
-MI
-reduced oxygen to myocardium
-damage to heart
-reduced CO
-inadequate circulation of oxygenated blood
-increased workload of breathing
-dyspnoea

136
Q

how does cardiomyopathy lead to dyspnoea

A

-cardiomyopathy
-heart enlargement/stiffening
-reduced CO
-inadequate circulation of oxygenated blood
-increased workload of breathing
-dyspnoea

137
Q

how does anaemia lead to dyspnoea

A

-anaemia
-decreased RBC count
-reduced Hg
-reduced oxygen capacity
-insufficient oxygen delivery tissue and cells
-reduced oxygen availability at the lungs
-dyspnoea

138
Q

how does COPD lead to dyspnoea

A

-COPD
-inflammation leads to narrowed airways
-obstructed flow of air in/out lungs
-reduced oxygen uptake
-reduced oxygen availability at lungs
-dyspnoea

139
Q

how does asthma lead to dyspnoea

A

-asthma
-bronchoconstriction
-reduced airway diameter, reduces oxygen intake
-increased work of breathing
-dyspnoea

140
Q

how does pneumonia lead to dyspnoea

A

-pneumonia
-inflammation and fluid buildup in the lungs
-reduced gas exchange capacity
-inadequate circulation of oxygenated blood
-increased workload of breathing
-dyspnoea

141
Q

how does valvular disease lead to dyspnoea

A

-valvular disease
-stenosis/regurgitation
-increased pulmonary pressure puts strain on the right heart
-RV becomes weakened
-less blood to the lungs
-inadequate circulation of oxygenated blood
-increased work of breathing
-dyspnoea

(RV dysfunction can eventually lead to decreased venous return and decreased preload hence causing left sided failure which leads to pulmonary congestion)

142
Q

how does inflammation of the pericardium lead to dyspnoea

A

-inflammation of the pericardium
-fluid build up (pericardial effusion)
-reduced contractility of the heart
-reduced CO
-inadequate circulation. of oxygenated blood
-increased workload of breathing
-dyspnoea

143
Q

control of ventilation using peripheral chemoreceptors

A

-peripheral chemoreceptors in aortic arch–> vagus nerve–> medullary respiratory neurons–> changes to pulmonary ventilation (dependent on CO2) and decreased metabolism if chronic

-peripheral chemoreceptors in aortic arch–> glossopharngyeal nerve–> medullary respiratory neurons–> changes to pulmonary ventilation (dependent on CO2) and decreased metabolism if chronic

144
Q

control of ventilation using central chemoreceptors

A

-central chemoreceptors of the brain and spinal chord
-medullary respiratory neurons
-changes to pulmonary ventilation and decreased metabolism if chronic (decreases CO2 produced)

145
Q

systematic approach to interpret spirometry results

A

-if FEV/FVC is low then it has to be obstructive
-if FEV/FVC is high then it could be restrictive, but only if the FVC is less that LLN

Medical Studies 1 (15 decks)

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