Physiology Flashcards

1
Q

What is internal respiration

A

Intracellular mechanisms which consume oxygen and produce carbon dioxide

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2
Q

What is external respiration

A

Sequence of events leading to exchange of oxygen and carbon dioxide between external environment and cells of the body

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3
Q

Steps of external respiration

A

Ventilation - Gas exchange between atmosphere and alveoli in the lungs
Exchange O2 and CO2 between air in alveoli and blood coming into lungs
Transport O2 and CO2 in blood between lungs and tissues
Exchange O2 and CO2 between blood and tissues

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4
Q

What is ventilation

A

Mechanical process of moving air between atmosphere and alveolar sacs

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5
Q

How is lesser pressure in lungs compared to atmosphere achieved

A

During inspiration, lungs move outwards, increasing volume. This leads to a decrease in pressure exerted by the gas.

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6
Q

What forces hold thoracic wall and lungs close

A

Intrapleural fluid cohesiveness - Water molecules in intrapleural fluid are attracted to each other and resist being pulled apart. Hence, pleural membrane stick
Negative intrapleural pressure - Subatmospheric intrapleural pressure creates a transmural pressure gradient across lung wall and chest wall

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7
Q

What happens to diaphragm during inspiration

A

It flattens out, increasing volume of thorax vertically

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8
Q

Contraction of which muscles help in inspiration

A

External intercoastal muscles, contraction lifts rib cage

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9
Q

Which is an active process, in or exspiration

A

Inspiration

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10
Q

What is Pneumothorax

A

Air in pleural cavity, abolishes pressure gradient

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11
Q

Pneumothorax symptoms

A

Chest pain, shortness of breath (dyspnoea)

Hyperresonant percussion note, decreased or absent breath sounds

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12
Q

Normal pressure gradients in the lung

A

Intraalveolar/Intrapulmonary - 760 mm Hg

Intrapleural/Intrathoracic - 756 mm Hg

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13
Q

What causes lungs to recoil during expiration

A

Elastic connective tissue in lungs and alveolar surface tension

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14
Q

Which alveoli have a higher tendency to collapse

A

Smaller alveoli due to LaPlace law

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15
Q

What is pulmonary surfactant

A

Pulmonary surfactant is a mixture of proteins and lipids secreted by type II alveolar cells

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16
Q

Function of pulmonary surfactant

A

Pulmonary surfactant is interspersed between water molecules lining the alveoli and helps lower surface tension. This prevents collapse of alveoli

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17
Q

What is respiratory distress syndrome of new born

A

New borns may not have enough pulmonary surfactant lining the alveoli. The baby has to make very strenuous inspiratory efforts in an attempt to overcome high surface tension and inflate the lungs

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18
Q

Another factor for keeping the alveoli open

A

Alveolar interdependence

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19
Q

What is alveolar interdependance

A

Mutual supporting structures, termed interdependence, combine with surfactants tension lowering property provide physical stability. If an alveolus starts to collapse, the surrounding alveoli are stretched and then recoil, exerting expanding forces in the collapsing alveolus to open it.

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20
Q

Major inspiratory muscles

A

Diaphragm and external intercoastal muscles

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21
Q

Muscles during forceful inspiration

A

Sternocleiodomastoid, scalenus, pectoral

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22
Q

Muscles of active expiration

A

Abdominal and internal intercoastal muscles

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23
Q

What is tidal volume (TV)

A

Volume of air entering or leaving the lungs during a single breath (0.5L)

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24
Q

What is inspiratory reserve volume (IRV)

A

Extra volume of air that can be inspired over the typical resting tidal volume (3 L)

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25
Q

What is expiratory reserve volume (ERV)

A

Extra volume of air that can be expired beyond the normal volume of air after resting tidal volume (1 L)

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26
Q

What is residual volume (RV)

A

Minimum volume of air in the lungs after maximal expiration (1.2 L)

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27
Q

What are the 4 lung volumes

A

Tidal volume, inspiratory reserve volume, expiratory reserve volume and residual volume

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28
Q

What is inspiratory capacity (IC)

A

Maximum volume of air that can be inspired at the end of a normal quiet expiration (3.5 L)
IC = IRV + TV

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29
Q

What is functional residual capacity (FRC)

A

Volume of air in lungs at end of normal passive expiration (2.2 L)
FRC = ERV + RV

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30
Q

What is vital capacity (VC)

A

Maximum volume of air that can be moved out during a single breath following a maximal inspiration (4.5 L)
VC = TV + IRV + ERV

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31
Q

What is total lung capacity (TLC)

A

Total volume of air lungs can hold (5.7 L)

TLC = VC + RV

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32
Q

When does residual volume increase

A

When elastic recoil of lungs is lost, e.g. emphysema

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33
Q

What do volume time curves help determine

A

FVC - Forced vital capacity which is the maximum volume that can be forcibly expelled from lungs following a maximum inspiration
FEV1 - Forced expiratory volume in 1 s which is volume of air that can be expired in the first second of expiration

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34
Q

Normal FEV1/FVC ratio

A

FEV1/FVC > 70% is normal

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35
Q

What are dynamic lung volumes

A

Lung volumes that depend on rate of air flow

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36
Q

FEV1/FVC ratio in obstructive vs restrictive lung disease

A

Obstructive lung disease, FEV1/FVC < 70%

Restrictive lung disease, FEV1/FVC > 70%, FVC is reduced

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37
Q

What is reduced in restrictive lung disease, FEV1 or FVC

A

FVC and FEV1 hence ratio of FEV1/FVC is unchanged

However they are both reduced

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38
Q

What part of ANS causes bronchodilation

A

Sympathetic stimulation

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39
Q

Which is harder, expiration or inspiration when diseased

A

Expiration

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40
Q

What happens to intrapleural pressure during in and expiration

A

Intrapleural pressure follows intralveolar pressure

Intrapleural pressure falls during inspiration and rises during expiration

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41
Q

What is dynamic airway compression

A

Rising pleural pressure during expiration compresses the alveoli and airway. This causes the wheezing sound heard in patients with obstructive disease

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42
Q

When is peak flow useful

A

To assess obstructive lung disease: Asthma and COPD

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43
Q

What pattern does decreased pulmonary compliance cause in spirometry

A

Restrictive pattern of lung volume

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44
Q

What can cause increased pulmonary compliance

A

Is elastic recoil is lost: emphysema. Patients have to work harder to get air out of lungs

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45
Q

Relation between compliance and age

A

Compliance increases with age

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46
Q

When does work of breathing increase?

A

Pulmonary compliance is decreased, airway resistance increased, elastic recoil decreased or need to increase ventilation

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47
Q

Formula for pulmonary ventilation

A

Pulmonary ventilation = Tidal volume * Respiratory rate (

0.5 L * 12 breaths/min = 6 L

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48
Q

What is alveolar ventilation

A

(Tidal volume - dead space) * Respiratory rate

(0.5 - 0.15) * 12 = 4.2 L

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49
Q

Why is it better to increase depth of breathing than RR

A

Due to presence of anatomical dead space

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50
Q

What does transfer of gases between body and atmosphere depend on

A

Ventilation - Rate at which air passes the lungs

Perfusion - Rate at which blood passes the lungs

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51
Q

Which part of lung has maximum blood flow and ventilation

A

Bottom lung has maximum blood flow whereas top lung has maximum ventilation

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52
Q

What is alveolar dead space

A

Ventilated alveoli not adequately perfused with blood

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53
Q

What is physiological dead space

A

Anatomical dead space - Alveolar dead space

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54
Q

Ventilation perfusion match in the lungs

A

Increase in CO2 due to increased perfusion decreases airway resistance leading to increase airflow
Increase in 02 due to increased ventilation causes pulmonary vasodilation which increases blood flow

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55
Q

Effect of O2 on arterioles

A

O2 vasodilates pulmonary arterioles whereas it vasoconstricts systemic arterioles

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56
Q

What affects rate of gas exchange across alveolar membrane

A

Partial pressure gradient of O2 and CO2
Diffusion coefficient for O2 and CO2
Surface area of alveolar membrane
Thickness of alveolar membrane

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57
Q

What is the respiratory exchange ratio (RER)

A

Ratio between amount of CO2 produced in metabolism and O2 used. RER = 0.8

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58
Q

Equation for partial pressure of oxygen in alveolar air

A

Alveolar gas equation -

PAO2 = PiO2 - (PaCO2/0.8)

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59
Q

Which gas is more soluble in membranes

A

CO2 is more soluble than O2. Solubility of gas in membranes is diffusion coefficient. The diffusion coefficient of CO2 is 20 times that of O2.

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60
Q

What does a big gradient between arterial (PaO2) and alveolar oxygen indicate (PAO2)

A

Problem with gas exchange or left-right shunt in heart

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61
Q

Ficks’s law of diffusion

A

Amount of gas that moves across a sheet of tissue in unit time is proportional to the area of the sheet but inversely proportional to to it’s thickness

62
Q

What do walls of alveoli contain

A

Flattened type 1 alveolar cells. Space inside contains alveolar macrophage whereas type 2 alveolar cells secrete pulmonary surfactant

63
Q

Major influence on the rate of gas transfer

A

Partial pressure gradient of O2 and CO2

64
Q

What is Henry’s law

A

Amount of gas dissolved in a liquid is proportional to the partial pressure of the gas in equilibrium with the liquid

65
Q

How is most oxygen transported in the body

A

Bound to heamoglobin and dissolved oxygen in blood

66
Q

Oxygen binding to haemoglobin

A

Each haemoglobin has 4 haem groups. One haem group can bind to one O2 molecule.

67
Q

What determines oxygen delivery to tissues

A

Oxygen content of arterial blood and cardiac output

68
Q

What is oxygen delivery index

A
DO2I = CaO2 * Cl
DO2I = Oxygen content of arterial blood * Cardiac index
69
Q

What determines oxygen content of blood

A
CaO2 = 1.34 * Hb * SaO2
CaO2 = 1.34 * Haemoglobin concentration * %Hb saturation with O2
70
Q

Convert kPa to mmHg

A

Multiply by 7.5

71
Q

Binding of one O2 to Hb increase affinity for more?

A

True, sigmoid shape curve

72
Q

Significance of steep lower part of sigmoid curve in % Hb saturation vs blood PO2

A

Peripheral tissues get a lot of oxygen for a small drop in capillary PO2 as easier for O2 to dissociate

73
Q

What is the Bohr effect

A

Bohr effect states that Hb O2 binding affinitiy is inversely related to acidity and concentration of CO2. Since more CO2 is released from metabolically active tissue, there is a fall in pH leading to release O2 from Hb

74
Q

By what effect do metabolically active tissues get more O2

A

Bohr effect, oxygen dissociation curve shifts right

75
Q

How is foetal haemoglobin (Hb) different from adult heamoglobin

A

Foetal hemoglobin has 2 alpha and 2 gamma subunits. This interacts less with 2,3 - bisphosphoglycerate in red blood cells. Hence, HBf has higher affinity for O2 than Hb and O2-Hb dissociation curve shifts to the left

76
Q

Significance of foetal haemoglobin

A

Foetal haemoglobin allows O2 transfer from mother to foetus even if PO2 is low

77
Q

Where is myoglobin present

A

In skeletal and cardiac muscle

78
Q

Myoglobin-PO2 dissociation curve

A

Hyperbolic curve, releases O2 at very low PO2

79
Q

Presence of myoglobin in blood indicates?

A

Muscle damage and can damage kidneys eventually

80
Q

Function of Myoglobin

A

Provides short term storage of O2 for anaerobic conditions

81
Q

How is CO2 transported in blood

A

Dissolved (10), bicarbonate (60) and carbamino (30)

82
Q

How is bicarbonate formed in blood

A

CO2 + H2O = H2CO3 = H+ + HCO3-

This is mediated by Carbonic Anhydrase in RBC

83
Q

What is choride shift

A

HCO3- forms from CO2 in RBCs. Thus, rise in intracellular bicarbonate leads to bicarbonate export and chloride intake using anion exchanger protein. This ensures the reaction proceeds from CO2 to HCO3- and not the other way round

84
Q

Haemoglobin has a higher affinity for?

A

CO2 to form carbamino-haemoglobin

85
Q

What is the Haldane effect

A

Removing O2 from Hb increases the ability of Hb to pick up CO2 and CO2 generated H+

86
Q

What effects work in synchrony to facilitate O2 liberation and CO2 and CO2 generated H+ at tissues

A

Bohr effect and Haldane effect

87
Q

Haldane effect shifts CO2 dissociation curve to?

A

The right

88
Q

Haldane effect at lungs

A

Blood picks up O2 at the lungs, decreasing affinity for CO2 and CO2 generated H+

89
Q

How do red blood cells exchange CO2 for O2 in alveoli

A

Closer to the lungs, CO2 concentration falls. This leads to dissociation of H+ from Hb shifting the concentration towards CO2 formation. The decrease in bicarbonate (HCO3_) levels reverses chloride shift with HCO3- moving into RBC. This leads to more formation of CO2 via carbonic anhydrase which is exchanged for O2 due to concentration gradient.

90
Q

FVC is reserved in Asthma or COPD

A

Asthma

91
Q

What is peak expiratory flow rate (PEFR)

A

Person’s maximum speed of expiration as measured by peak flow meter

92
Q

PEFR in obstructive vs restrictive

A

Less in obstructive, unchanged in restrictive

93
Q

FEV1 in obstructive vs restrictive

A

Less in obstructive and restrictive

94
Q

FVC in obstructive vs restrictive

A

Normal in asthma, reduced in COPD and restrictive

95
Q

FEV1/FVC in obstructive vs restrictive

A

< 75% in obstructive, >75% in restrictive

96
Q

FEV1 response to B2-agonist in obstructive vs restrictive

A

> 15% in Asthma, <15% in COPD, no response in restrictive

97
Q

What is bronchial challenge testing

A

Patient is adminstered methacholine/histamine/mannitol. These are markers of airway hyper-responsiveness and cause bronchoconstriction. A fall of 20% in FEV1 is calculated and compared to healthy individuals

98
Q

What is bronchial challenge testing used for

A

To assess allergic or occupational asthma

99
Q

How can exercise induced asthma be tested for

A

Exercise testing. Decrease in FEV1 or PEF post exercise is indicative.

100
Q

Use of full cardiopulmonary exercise test (CPET)

A

Differentiate cardiac vs respiratory dyspnoea

It monitors heart rate vs oxygen uptake vs ventilatory rate

101
Q

TCL in emphysema

A

Increase

102
Q

TLC in restrictive lung disease

A

Decreases

103
Q

What is transfer factor for carbon monoxide (TLCO)

A

Also called diffusing capacity of lungs for carbon monoxide (DLCO). It measures ability of the lungs to transfer gas from inhaled air to RBC in pulmonary capillaries.

104
Q

DLCO manoeuvre advantage

A

Easier for elderly patients to perform the ten second breath holding in DLCO that forced exhalation in spirometry

105
Q

How can airway resistance be measured

A

Plethysmography or impulse oscillometry

106
Q

More sensitive method than spirometry in differentiating small and large airway obstruction

A

Impulse oscillometry; sound waves are superimposed on normal tidal breathing and disturbances to flow and pressure by external waves are used to calculate resistance to airflow

107
Q

Exhaled breath nitric oxide (FeNO)

A

Non-invasive marker of eosinophilic airway inflammation in asthma. Not useful in smokers with COPD as nitric oxide is suppressed by smoking

108
Q

What do high levels of nitric oxide in asthmatics show

A

(> 35ppb) Uncontrolled asthmatic inflammation. Used as as adjunct to bronchial challenge

109
Q

Major respiratory rhythm generator

A

Medulla oblongata by network of neurons called Pre-Botzinger complex. They display pacemaker activity near the upper end of medulla respiratory control centre

110
Q

Neural activity leading to inspiration

A

Rhythm is generated by Pre-Botzinger complex. This excites dorsal respiratory group neurones (inspiratory) which fire in bursts. This firing causes contraction of inspiratory muscles - inspiration. Cessation of firing causes passive expiration

111
Q

How does active expiration occur

A

Increase firing of dorsal neruones excites ventral neurones. These activate internal intercoastal muscles, abdominals etc to cause forceful expiration.

112
Q

Parts of pons respiratory centre

A

Pneumotaxic center and apneustic center

113
Q

How is inspiration terminated

A

Firing of dorsal neurones causes stimulation of the pneumotaxic center. This terminates inspiration.

114
Q

What is apneusis

A

Breathing with prolonged inspiratory gasps and brief expiration due to absence of pneumotaxic center in pons.

115
Q

Function of apneustic center in pons

A

Apneustic neurones stimulates inspiratory area of medulla prolonging inspiration.

116
Q

Respiratory rhythm control in the brain

A

Rhythm is generated in medulla: Pre-Botzinger complex (generates rhythm), dorsal neurones (contraction and inspiration) and ventral neurones (forceful expiration). Rhythm is controlled in the pons: pneumotaxic center (terminates inspiration) and apneustic center (prolongs inspiration)

117
Q

Respiratory centers are influenced by?

A

Higher brain centres - cerebral cortex, hypothalamus
Stretch receptors - Hering-Breuer reflex guards against hyperinflation of lungs
Juxtapulmonary (J) receptors - Stimulated by pulmonary capillary congestion and pulmonary oedema; also pulmonary emboli causes rapid, shallow breathing
Joint receptors - Joint movement
Baroreceptors - Decrease blood pressure, increase respiratory rate

118
Q

Pulmonary stretch receptors are also known as

A

Hering-Breuer reflex

119
Q

What contributes to increased ventilation during exercise

A

Joint receptors that increase breathing due to movement at joints

120
Q

Factors increasing ventilation during exercise

A

Reflexes originating from body movement
Adrenaline release, impulse from cerebral cortex, increase in body temperature, accumulation of CO2 and H+ by active muscles

121
Q

Where is the cough reflex centre

A

Medulla

122
Q

Steps in cough reflex

A

Short intake of breath, closure of larynx, contraction of abdominal muscles (increase intra-alveolar pressure) and opening of larynx and expulsion of air

123
Q

Chemical control of respiration is by

A

Blood gas tension especially CO2

124
Q

Peripheral chemoreceptors that sense tension of O2, CO2 and H+ in the body are situated at

A
Carotid body (Hering's nerve part of glossopharyngeal)
Aortic body (Vagus nerve)
125
Q

Central chemoreceptors that response to H+ of CSF are

A

Surface of medulla of brainstem

126
Q

Only CO2, not H+ or HCO3-, can diffuse across blood-brain barrier. What can this cause?

A

CO2 and diffuse across the barrier and react with H20 leading to the formation of HCO3- and H+. This increases acidity of blood. This activates central chemoreceptors leading to an increase in depth and rate of inspiration.

127
Q

What causes hypoxia at high altitudes

A

Decrease partial pressure of inspired oxygen (PiO2)

128
Q

Acute response to hypoxia

A

Hyperventilation and increased cardiac output

129
Q

Symptoms of acute mountain sickness

A

Nausea, headache, fatigue, tachycardia, dizziness, sleep disturbance, exhaustion, SOB, unconsciousness

130
Q

Chronic adaptation to high altitudes hypoxia

A

Increased RBC production, 2,3-BPG produced within RBC (O2 offloaded more easily into tissues), number of capillaries, number of mitochondria, kidneys conserve acid to decrease arterial pH

131
Q

Hypoxic drive is via what receptors

A

Peripheral chemoreceptors

132
Q

H+ drive of respiration

A

Via peripheral chemoreceptors. Increase in non-carbonic acid H+ (eg: lactic acid during exercise, diabetic ketoacidosis) leads to hyperventilation in an attempt to remove CO2 from the body. This is imporant in acid-base balance in body

133
Q

When does arterial oxygen level become important

A

If PO2 < 8 kPa

134
Q

Type 1 vs type 2 respiratory failure

A

Type 1 - Hypoxia

Type 2 - Hypoxia + Hypercarbia

135
Q

What percentage do we try and keep the percent saturation at

A

90% sO2 which corresponds to oxygen partial pressure pO2 of 60mmHg

136
Q

What is percent saturation of oxygen

A

The amount of haemoglobin bound by oxygen

137
Q

What can very high oxygen levels cause

A

High CO2 levels leading to acidosis

138
Q

Do all COPD patients retain oxygen

A

No, only 1 in

139
Q

What chemoreceptors does the body generally use

A

CO2 chemoreceptors. Normal respiration is driven by amount of CO2 in arteries. Increase in CO2 leads to an increase in respiration

140
Q

What is the hypoxic drive

A

A form of respiration in which the body uses oxygen chemoreceptors instead of CO2 chemoreceptors to regulate respiratory cycle

141
Q

Where do you get low inspired oxygen

A

High altitudes with low barometric pressure

142
Q

What is Ondine’s curse

A

Central hypoventillary synrome (CHS) is a respiratory disorder that results in respiratory arrest during sleep

143
Q

Shunting and dead space

A

Perfusion without ventilation is shunting

Ventilation without perfusion is dead space

144
Q

Is oxygen the therapy for breathlessness

A

No but it can help maximise potential, target the cause of breathlessness while eliminating hypoxaemia

145
Q

Oxygen target for type 2 respiratory failure

A

88 - 92 %

146
Q

Oxygen target for type 1 respiratory failure

A

94 - 98 %

147
Q

Risk factors for type 2 hypercapnic respiratory failure

A

Moderate or severe COPD, kyphoscoliosis, severe obesity, neuromuscular disease, cystic fibrosis, brochiectasis.

148
Q

What flow can nasal cannulae be used till

A

1 to 4 l/min

149
Q

Variable performance mask flow limit

A

5 - 15 l/min

150
Q

Venturi mask flow limit

A

Upto 250 l/min