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Medicine > Respiratory case > Flashcards

Respiratory case Flashcards

1
Q

functions of the respiratory system? (4)

A
  • Gas exchange
  • Filtering particle matter
  • Defense against inhaled particles and pathogens
  • Processing of endogenous compounds by the pulmonary vasculature
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2
Q 
Emergency assessment:
A
B
C
D
E
F
A 
AIRWAY 
BREATHING
CIRCULATION 
DISABILITY 
EXPOSURE 
don't ever FORGET to measure blood glucose
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3
Q

Emergency assessment: BREATHING

  • What to do:
  • Normal:
  • Tachypnoea:
  • Apnoea:
A
  • Count the number of breaths per minute
  • Normal: 10-15 breaths per min
  • Tachypnoea: rapid breathing rate
  • Apnoea: breathing arrest
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4
Q

Emergency assessment: Look for

A
  • Abnormal blue-purple discolouration of the mucus membranes particularly the tongue
  • Abnormal patterns of breathing
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5
Q

Abnormal breathing patterns:

  • Keyne-stokes:
  • Kussmaul:
A
  • Cheyne-Stokes: often occurs towards the end of life.
  • Fast shallow breathing followed by slow deep breathing
  • Kussmaul breathing: indicates increased acidity of arterial blood (e.g. diabetic ketoacidosis)
  • Deep, rapid and laboured breathing
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6
Q

Auscultating: listening to the breath sounds using a stethoscope

  • Normal sounds
  • Abnormal sounds
A
  • Normal sounds are known as vesicular

- Abnormal sounds include; wheeze, stridor and bronchial breathing

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7
Q

Abnormal auscultation sounds: stridor

A
  • High-pitched, musical breathing sound

- Caused by a blockage in throat or larynx

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8
Q

Abnormal auscultation sounds: bronchial breathing

A
  • Loud, harsh breathing sounds. Midrange pitch
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9
Q

Hypoxia definition:

A
  • Inadequate oxygen supply to maintain homeostasis in tissues
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10
Q

Hypercapnia:

A
  • Increased arterial pressure of CO2 (PaCO2)
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11
Q

Normal blood oxygen saturation (SaO2):

A
  • 95-100% saturation
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12
Q

Nasopharynx function: (2)

  • Function
  • Protective reflex
A
  • Warms, humidifies and filters air

- Sneezing is a protective reflex

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13
Q

Laryngeal function: (3)

A
  • Phonation
  • Closing the airway during swallowing
  • Cough reflex
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14
Q

dead space:

A
  • Volume of gas in respiratory tract that is not involved in gas exchange
  • Physiological
  • Anatomical
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15
Q

Physiological dead space:

A
  • Anatomical deadspace plus the volume of gas in alveoli that have inadequate perfusion
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16
Q

Anatomical deadspace:

A
  • Volume of gas in upper airways and the conducting zone of the airways
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17
Q

Closing capacity:

  • Definition
  • Age
  • Equation
A
  • Maximal lung volume where airway closure can be detected in the lungs during expiration
  • Increases with age
  • CC = CV + RV
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18
Q

Factors affecting airways resistance: (2)

A
  • Contraction of bronchial smooth muscle

- Closing capacity

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19
Q

Control of bronchial smooth muscle: neural pathways

  • Parasympathetic:
  • Sympathetic:
A
  • Postganglionic parasympathetic fibres release acetylcholine, agonising M3 muscarinic receptors
  • Causes bronchoconstriction
  • NANC: bronchodilator
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20
Q

Control of bronchial smooth muscle: humoral control

A
  • Elevated adrenaline levels in blood agonise beta2-adrenoceptor
  • Causes bronchodilation
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21
Q

Control of bronchial smooth muscle:

  • Physical effects
  • Chemical effects
A
  • stimulation of the respiratory epithelium can cause bronchoconstriction (cold air, dust, smoke)
  • Gastric acid aspiration and gas inhalation cause bronchoconstriction
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22
Q

Control of bronchial smooth muscle: local cellular mechanisms

A
  • Inflammatory cells in the lungs (mast cells) may be activated by pathogens or allergens
  • Causes bronchoconstriction
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23
Q

Flow/volume loop measured using a spirometer:

A
  • Starts at residual volume (RV)
  • Inhales to fill lungs to Total Lung Capacity (TLC)
  • Maximum effort to exhale to achieve Peak Expiratory Flow (PEF)
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24
Q

Terminology:

  • Ventilation (V)
  • Perfusion (Q)
  • Minute volume (VE)
  • Alveolar ventilation (VA)
A
  • V: refers to the flow of respiratory gases
  • Q: the flow of blood
  • VE: tidal volume volume of gas exhaled in one minute
  • VA: the amount of fresh gas delivered to the alveoli per minute
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25
Q

Minute volume (VE) equation:

A

VE = tidal volume x respiratory rate

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26
Q

Alveolar ventilation rate (VA):

A

VA = (tidal volume - physiological dead space) x respiratory rate

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27
Q

Surface tension:

  • Alveolus lining
  • Bubble
  • Cohesive forces
  • transmural pressure
A
  • Alveolus is lined with a thin film of fluid
  • Behaves like a bubble
  • Cohesive forces between water molecules attempt to reduce the surface area and may favour collapse of the alveoli
  • To prevent collapse a transmural pressure is required that is predicted via Laplace equation
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28
Q

Laplace equation:

Transmural pressure=

A
  • Transmural pressure = (2 surface tension) / radius
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29
Q

transmural pressure at Functional Residual Capacity:

  • Equation
  • P(alv)
  • P(ip)
A
  • P(alv) - P(ip)
    = 0cmH2O - (-5cmH2O)
  • At FRC alveolar pressure must be equal to atmospheric pressure (0)
  • Intrapleural is below atmospheric (negative)
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30
Q

Intrapleural pressure is below atmospheric, so what?

A
  • A penetrating chest injury will allow air to be sucked in to the intrapleural space
  • Lung will collapse causing severe respiratory distress
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31
Q

First breaths: (3)

A
  • High transmural pressure to open alveoli for the first time
  • must overcome effects of surface tension and elastin
  • Surface tension is reduced by surfactant, produced by pneumocyte
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32
Q

Surfactant in embryo’s:

A
  • Surface tension reduced by surfactant produced by type 2 alveolar cells
  • Premature babies may lack surfactant and develop respiratory distress
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33
Q

Mechanics of breathing: compliance

A
  • The distensibility of the lungs and chest wall

- compliance = change in volume / change in pressure

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34
Q

Changes in compliance:

  • Fibrotic lung disease
  • Emphysema
A
  • Fibrotic lung diseases (restrictive): lead to scarring of the lungs, reducing compliance and FRC
  • Emphysema (obstructive disease): results in loss of elastin fibres and increase in compliance and FRC (barrel-shaped chest)
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35
Q

Boyle’s law: pressure is inversely proportional to …..

A

Pressure is inversely proportional to volume

P = 1/v

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36
Q

Breathing cycle: Inspiration

A
  • Inspiration leads to an increase in thoracic volume and a decrease in alveolar pressure to below atmospheric.
  • This sucks in the tidal volume
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37
Q

Breathing cycle: expiration

A
  • Passive process
  • Decrease in thoracic volume leads to an increase in alveolar pressure to above atmospheric pressure
  • Tidal volume blown out
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38
Q

The work of breathing:

A
  • Respiratory muscles require energy to do work
  • Work must overcome resistance of airways and elasticity of tissues/effects of surface tension
  • Elastic energy stored during inspiration allows expiration to be passive
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39
Q

Pulmonary circulation:

  • Pressure generated by:
  • Systolic and diastolic pressures:
  • Resistance:
  • Blood flow:
  • Response of small arteries/arterioles to hypoxia
A 
1- Right ventricle 
2- 25/8
3- Lower (pulmonary vascular region)
4- Slightly less than 5 L/min 
5- Vasoconstriction
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40
Q

Systemic circulation:

  • Pressure generated by:
  • Systolic and diastolic pressures:
  • Resistance:
  • Blood flow:
  • Response of small arteries/arterioles to hypoxia
A 
1- Left ventricle 
2- 120/80
3- higher (total peripheral resistance)
4- 5L/min
5- vasodilation
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41
Q

Physiological shunt:

  • Pulmonary vein
  • Thebesian vein
  • Effect on PA02 and Pa02
  • Effect on venous return
A
  • Some deoxygenated blood drains in to the pulmonary veins from bronchial circulation
  • Some deoxygenated blood drains in the coronary circulation (5%) into thebesian veins in to the left ventricle
  • PA02 > Pa02
  • venous return to left ventricle greater than right
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42
Q

V(A):Q=1

A
  • The amount of ventilation with fresh gas equals perfusion with blood
  • End capillary blood is fully oxygenated/arterialized
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43
Q

V(A):Q = 0

A
  • Normal perfusion but complete absence of alveolar ventilation
  • End capillary blood remains deoxygenated
  • Shunt/venous admixture
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44
Q

V(A):Q = infinite

A
  • Normal ventilation but complete absence of perfusion

- No gas is transferred, this is wasted ventilation, increasing physiological dead space

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45
Q

Effects of gravity on V(A):Q

A
  • More ventilation than perfusion at the top of the lung

- V(A):Q will be higher here, as will PAO2

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46
Q

Advantages of hypoxic vasoconstriction: (2)

A
  • Diverts blood away from poor ventilated alveoli e.g. alveoli full of pus in pneumonia
  • In utero: low PAO2 results in a high pulmonary vascular resistance, reversed by first breath via lungs
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47
Q

Disadvantages of hypoxic vasoconstriction:

  • Barometric pressure
  • COPD
A
  • Barometric pressure decreases with altitude, leading to a fall in PAO2 in the lungs, increasing pulmonary vascular resistance, hypertrophy of the right ventricle generates higher pressure
  • COPD can also lower PAO2 and cause right ventricular hypertrophy, right ventricular fails in some patients causing cor pumonale
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48
Q

Cor pumonale:

A
  • Right-sided heart failure due to hypoxic lung disease

- Symptoms: blue bloated appearance

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49
Q
  • Alveolar ventilation (VA)
A
  • The amount of fresh gas delivered to the alveoli

- VA = (tidal volume - physiological) x respiratory rate

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50
Q

Alveolar ventilation equations:

PACO2=

A

PACO2 = PaCO2
= Rate of CO2 by metabolism/ rate of CO2 removal

PACO2 directly proportional to rate of CO2 production by metabolism
PACO2 indirectly proportional

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51
Q

Simplified Alveolar ventilation equation:

A

PACO2 : Rate of CO2 by metabolism / Rate of CO2 removal by alveolar ventilation

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52
Q

Daltons law:

A

P(TOTAL)= P1 + P2 + P3 ……

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53
Q

Alveolar gas equation use:

A
  • Used to predict a patients PAO2 depending upon the amount of oxygen they’re breathing
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54
Q

Gas exchange: (3)

  • Definition
  • Diffusion
  • Direction
A
  • Refers to diffusion of O2 and CO2 in the lungs and peripheral tissue
  • Diffusion occurs due to random thermal motion of molecules
  • Gases diffuse down their partial pressure gradient
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55
Q

Diffusing capacity:

  • Definition
  • Measured by
  • Decreased by
  • Increased by
A
  • Rate of transfer of gas from alveoli to capillary
  • Measured using a single breath with a gas mixture containing a low conc. of carbon monoxide
  • Decreased: emphysema, pulmonary oedema, pulmonary fibrosis
  • Increased: during exercise(increased capillary perfusion)
56
Q

Perfusion-limited gas exchange:

A
  • At rest capillary partial pressure of O2 rapidly becomes equal to the partial pressure of oxygen in the alveolus
57
Q

Diffusion limited gas exchange:

A
  • Caused by lung fibrosis and strenuous exercise
  • There is a partial pressure gradient or O2 along the entire capillary, decreasing PaO2
  • Greater partial pressure gradient required to increase gas transfer
58
Q

Calculating the total oxygen content of blood:

A

C = amount bound to haemoglobin + amount dissolved in plasma
= (O2 binding capacity x SaO2) + (PaO2 x solubility)

59
Q

Rate of O2 delivery:

A

O2 delivery = cardiac output (Q) x O2 content (C)

60
Q

Haemoglobin variants: foetal haemoglobin (HbF)

  • Structure
  • Affinity
  • Lifespan
A
  • Two alpha and two gamma subunits
  • Higher affinity for O2 than HbA
  • Replaced by HbA within a year of birth
61
Q

Haemoglobin A (HbA)

  • Structure
  • Haem moiety
  • Bound
A
  • Two alpha subunits and two beta subunits
  • Subunits contain a haem moiety, an iron-binding porphyrin with iron in the ferrous state
  • Each subunit can bind to one molecule of oxygen
62
Q

Haemoglobin variants: Methaemoglobin

A

Iron moiety oxidised to ferric (Fe3+) state

  • Does not bind O2
  • Congenital form due to deficiency of methaemoglobin reductase
63
Q

Haemoglobin variants: Methaemoglobin

A

Iron moiety oxidised to ferric (Fe3+) state

  • Does not bind O2
  • Congenital form due to deficiency of methaemoglobin reductase
64
Q

Haemoglobin variants: Haemoglobin S

A
  • Abnormal B subunits

- Sickle cell disease, distorts RBCs causing anaemia

65
Q

Oxygen Haemoglobin dissociation curve:

A
  • Sigmoidal
  • Due to increasing affinity for oxygen with each O2 molecule that binds
  • P50 is the PO2 where 50% saturation is achieved
66
Q

Loading and unloading of oxygen:

A
  • Areas with higher PO2 will have higher saturation, signalling loading
  • Areas with low PO2 have lower saturation, signalling unloading
67
Q

Bohr effect:

A
  • CO2 produced by peripheral tissues results in the generation of H+ ions
  • H+ ions bind to HbA, decreasing O2 affinity, facilitating unloading
  • In lungs, O2 binding releases H+ ions that react with HCO3- to produce CO2 that is exhaled
68
Q

Carbon monoxide (CO) poisoning:

A
  • CO binds to HbA with affinity 250 times higher than oxygen
  • Decreases O2 binding sites
  • Shifts curve to the left, reducing ability to unload O2
69
Q

CO2 transport in the blood:

A
  • Dissolved in plasma
  • Bound to HbA forming carbaminohaemoglobin
  • Converted to bicarbonate (HCO3-)
70
Q

Chloride shift in HbA:

A
  • HCO3- transported out of cell in exchange for Cl- ions
71
Q

CO2 dissociation curve:

A
  • Linear in shape, CO2 exertion increases with increased ventilation in all areas
72
Q

Ventilation perfusion mismatch (VQ):

A
  • Defect in the V(A):Q ratio

- Causes arterial hypoxaemia but an increase in alveolar ventilation prevents hypercapnia

73
Q

Fick’s law: rate of diffusion =

A

Rate of diffusion (a)

(surface area x concentration) / thickness of membrane

74
Q

Henry’s law: amount of gas in liquid

A

At constant temperature, the amount of gas dissolved in a given type and volume of liquid is DIRECTLY PROPORTIONAL to the partial pressure of the gas in equilibrium with that liquid

75
Q

Control of respiration (PaO2,PaCO2, arterial pH):

- CPG

A
  • A central pattern generator in the brainstem with inputs from the cerebral cortex and multiple types of receptors/sensors
76
Q

Cerebral (voluntary) respiratory control:

  • Voluntary hyperventilation
  • Voluntary hypoventilation
A

If the rate of CO2 production remains constant:

  • Voluntary hyperventilation must lead to hypocapnea
  • Voluntary hypoventilation must lead to hypercapnia
77
Q

Respiratory acidosis:

A
  • Hypercapnia drives equilibrium to the right, increasing H+conc. lowering pH
78
Q

Respiratory Alkalosis:

A
  • Hypocapnia drives equilibrium to the left, decreasing H+conc. raising the pH
79
Q

Dangers of acute respiratory acidosis: (3)

A
  • Decreased cardiac contractility
  • Cardiac arrhythmias and potential cardiac arrest
  • Alterations in pH dependent biochem pathways
80
Q

Hypocapnia symptoms:

A
  • Reduced cerebral blood flow due to vasoconstriction
81
Q

Central chemoreceptors:

  • Location
  • Role of CO2
A
  • Ventral surface of medulla oblongata responds to increases in H+
  • H+ ions cannot cross the blood brain barrier (BBB), CO2 diffuses across the BBB and is converted to H+
82
Q

Peripheral chemoreceptors:

A
  • Found in carotid sinus

- Stimulated by acidemia, hypoxia, hypercapnia and decreased perfusion (hypotension)

83
Q

Influence of CO2 on respiratory control: (3)

  • Rise effects
  • Max
  • Min
A
  • A rise in PaCO2 above 5.3KPa causes an incremental rise in minute volume
  • Max PaCO2 is 13.3-26.7KPa, after which CO2 narcosis occurs with respiratory fatigue
  • Hyperventilation resulting in PaCO2 less than 5KPa can lead to apnoea until levels are restored
84
Q

Influence of oxygen on respiratory control

A
  • Linear relationship between PaO2 and minute volume until SaO2 drops too far, stimulating a powerful stimulus
85
Q

Influence of pH on respiratory control:

A

Arterial pH depends upon ratio of bicarbonate to PaCO2

pH = [HCO3-] / PaCO2

86
Q

Metabolic acidosis:

A
  • A pathological decrease in [HCO3-] causes a fall in blood pH
  • Often seen in uncontrolled type 1 diabetes mellitus
87
Q

Metabolic acidaemia correction:

A
  • Peripheral chemoreceptors stimulated, increasing alveolar ventilation, decreasing PaCO2
  • Reduces pH disturbance
88
Q

Influence of opioids in respiratory control:

MOP receptors

A
  • Opioids bind the MOP receptors and depress alveolar ventilation
  • Pathological rise in PaCO2 causes respiratory acidosis, pH falls
  • Reversed using the antagonist naloxone
89
Q

Cellular respiration:

A
  • Food molecules digested to produce fatty acids, glycerol, amino acids and sugar
  • These products are oxidised to form ATP, NADH and other activated carrier molecules
90
Q

Oxidation of glucose (cellular respiration):

A
  • Cell oxidises glucose in a series of enzyme-catalysed steps, gradually releasing energy which is captured by activated carrier molecules
91
Q

Glycolysis:

A
  • Major metabolic pathway for sugar oxidation
  • Occurs in the cytosol of cells
  • 6-carbon glucose is converted into 2X 3-carbon molecules of pyruvate
92
Q

Glycolysis steps (3):

  1. Investment
  2. 6-carbon sugar
  3. Energy generation
A
  1. Energy investment to be recouped of 2 ATP’s to drive unfavourable reactions
  2. 6-carbon sugar is cleaved into 2X 3-carbon sugars
  3. Energy generation: two NADHs, two pyruvate and 4 ATPs are formed
93
Q

ATP functions:

A
  • A building block of DNA, RNA
  • Combine with other groups to form coenzymes
  • as cyclic AMP, a signalling molecule
94
Q

ATP functions:

A
  • A building block of DNA, RNA
  • Combine with other groups to form coenzymes
  • as cyclic AMP, a signalling molecule
95
Q

Anaerobic energy generation:

A
  • When oxygen is limited pyruvate is converted into lactate (muscle) or ethanol and CO2 (yeast)
  • NADH is oxidised to NAD+ to allow glycolysis to continue
96
Q

Metastasize:

Warburg effect:

A
  • Malignant tumours reproduce very quickly

- They consume large amounts of glucose and produce lots of lactate

97
Q

Glycogen:

A
  • Stores sugars in small granules in the cytoplasm of many cells
  • Used during short periods of fasting
98
Q

Triglycerides:

A
  • Stores fatty acids in adipocyte cells
  • Used for longer periods of fasting
  • Adipose tissue can be white or brown, brown containing more mitochondria
99
Q

Liver specialities:

A
  • Use of glucokinase (KM=10mM) as opposed to hexokinase (KM=0.1mM)
  • Following a meal, only liver cells can increase their rate of glucose phosphorylation
  • G6P in liver cells can be used to synthesise glycogen
100
Q

Mitochondria:

- Membranes (4)

A
  • Outer membrane permeable to many molecules
  • Inner impermeable to all, unless specific transport proteins are present
  • Inner membrane is the site for oxidative phosphorylation (ATP synthesis)
101
Q

Mitochondria function:

A
  • Pyruvate pumped into the mitochondrial matrix and converted into acetyl CoA and CO2 by Pyruvate Dehydrogenase Complex
102
Q

Citric acid cycle overview:

A
  • Two carbons from acetyl CoA combine with 4-carbon oxaloacetate, forming six carbon citrate
  • Citrate is progressively oxidised, producing NADHm FADH2, GTP.
  • CO2 is a waste product
103
Q

Citric acid cycle products:

A
  • 3 NADH
  • 1 GTP
  • 1 FADH2
  • 2 CO2
104
Q

Oxidative Phosphorylation:

A
  • Uses high-energy electrons in NADH, GTP and FADH2 to produce a concentration gradient of H+ out of the mitochondrial matrix.
  • H+ renters the matrix via ATP Synthase channels
105
Q

Oxidative phosphorylation overview:

A
  • Electrons move across three complexes in the inner mitochondrial membrane
  • Pumping protons out of the cell, creating an electrochemical gradient
  • ATP synthase uses protons flowing down the gradient to form ATP
106
Q

How is Vo2 (O2 consumption rate) measured:

A
  • Measured using a spirometer filled with 100% oxygen
107
Q

Phases of respiration during exercise: (3)

A
  • Phase I: instant increase in ventilation at, or slightly before exercise begins
  • Phase II: Further increase to reach phase III
  • Phase III: equilibrium level
108
Q

Oxygen debt:

A
  • During phase II some of the energy required is produced by anaerobic metabolism
  • This generates lactate
  • During recovery minute volume remains elevated to allow lactate to be metabolised (repaying O2 debt)
109
Q

Vo2MAX:

A
  • An individuals maximum oxygen consumption rate

- Used as a measure of respiratory fitness

110
Q

Exercising above Vo2 MAX:

A
  • A subject can exercise at a higher intensity than Vo2MAX via anaerobic respiration
  • This produces lactic acid, ionised to H+ and lactate ions
  • This causes a rise in arterial pH, stimulating chemoreceptors, causing increases in minute volume and alveolar ventilation
111
Q

Effects of lactic acid:

A
  • causes a rise in arterial pH, stimulating chemoreceptors, causing increases in minute volume and alveolar ventilation
  • Causes distress above levels of 11 mmol/L, a limiting factor for sustained heavy work
112
Q

Oxygen delivery (O2) =

A

O2 delivery = Cardiac output (Q) x O2 content (C)

113
Q

Effects of increased mean pulmonary artery pressure:

A
  • Increases pulmonary blood flow
  • Increases perfusion of the lung apices
  • Reduces physiological dead space, improves VA:Q
114
Q

Fick equation and limiting factors of Vo2MAX:

A
  • Vo2MAX= MAX CO X difference in arterial and venous O2 content
115
Q

Effects of training upon the heart:

A 
Increases:
- Myocardial capillaries 
- Size of ventricular chamber 
- Vagal tone, resulting in resting bradycardia
Results in increased Cardiac output (Q)
116
Q

Effects of training upon skeletal muscle:

  • Increases
  • Effects
A 
Increases:
- Capillaries 
- Mitochondria 
- Myoglobin 
Allows an increase in oxygen extraction, increasing anaerobic threshold and livers ability to clear lactate
117
Q

Ergoreflex:

A
  • Mechanoreceptors and metaboloreceptors in skeletal muscle cause an increase in ventilation and HR during exercise
118
Q

The oxygen cascade:

A
  • Process by which Oxygen partial pressure reduces from 21.2KPa (dry air, sea-level) to 0.5-3 KPa (in mitochondria)
  • A pathological disturbance can lead to tissue hypoxia and dysfunction
119
Q

Normal arterial PaO2:

A
  • PaO2 = 13.6 (0.044 x age)
120
Q

Hypoxaemia:

A
  • Abnormally low arterial partial pressure of oxygen (PaO2)

- Associated with central cyanosis (blue tongue)

121
Q

Hypoxia:

A
  • Low tissue partial pressure of oxygen

- Hypoxaemia is one cause of tissue hypoxia

122
Q

Causes of hypoxaemia: (5)

-Compared how?

A 
Five possible pathological causes: 
- High altitude 
- Hypoventilation
- Diffusion defect 
- VA:Q mismatch 
- R to L cardiac shunt 
Compared by their effects on Alveolar-arterial difference 
Aa Dif. = PA02 - PaO2
123
Q

Hypoxaemia causes: High altitude

  • Notes
  • PaO2 effect
  • Aa difference
  • Does O2 help?
A
  • Fall in barometric pressure leads to a decrease in PIO2 and PAO2
  • Decrease
  • Aa normal
  • Yes
124
Q

Hypoxaemia causes: Hypoventilation

  • Notes
  • PaO2 effect
  • Aa difference
  • Does O2 help?
A
  • Decreases PAO2
  • Decreases PaO2
  • Aa normal
  • Yes
125
Q

Hypoxaemia causes: Diffusion defect

  • Notes
  • PaO2 effect
  • Aa difference
  • Does O2 help?
A
  • Decreases PaO2
  • Increased Aa difference
  • Yes
126
Q

Hypoxaemia causes: VA:Q mismatch

  • Notes
  • PaO2 effect
  • Aa difference
  • Does O2 help?
A
  • Decreases PaO2
  • Increased Aa difference
  • Yes
127
Q

Hypoxaemia causes: R-to-L cardiac shunt

  • Notes
  • PaO2 effect
  • Aa difference
  • Does O2 help?
A
  • Shunted blood bypasses the alveoli and cannot be ventilated, resulting in very low PaO2
  • Decreased
  • increased Aa difference
  • Limited effect only on non-shunted blood
128
Q

Causes of tissue hypoxia: Stagnant hypoxia

A
  • Decrease in cardiac output causes a decrease in rate of O2 delivery
129
Q

Causes off tissue hypoxia: Hypoxaemia

A
  • A decrease in SaO2 and PaO2 reduces total O2 content, reducing rate of O2 delivery
130
Q

Causes of tissue hypoxia: anaemic hypoxia:

A
  • Concentration of haemoglobin falls, lowering oxygen binding capacity, which lowers O2 content
131
Q

Causes of tissue hypoxia: histotoxic hypoxia:

A
  • An inability of the cells to utilise oxygen
132
Q 
Hypoxia symptoms:
_ A 
- E
- C/L of C
- T
- U/C/S
A
  • Anxiety
  • Euphoria
  • Confusion/lack of coordination
  • Tachypnoea, use of accessory muscles
  • unconsciousness/coma/seizures
133
Q

Pressure of inspired air (PIO2)

  • FIO2
  • PB
  • PH2O
A

PIO2 = FIO2 x [PB - PH2O]

FIO2= fractional O2 composition 
PB = Barometric pressure 
PH2O = Water vapour pressure
134
Q

The challenge of high altitude:

PIO2 = FIO2 x [PB - H2O]

A
  • At high altitudes PB falls, lowering PIO2
135
Q

Acclimatisation:

  • Definition
  • Respiratory changes
A
  • increase in tolerance to high altitude when subject gradually ascends to high altitude
    Ventilatory changes:
  • Polycythaemia (Increase in Hb)
  • Hypoxic vasoconstriction, increases PVR
  • Raised pulmonary artery pressure and R.ventricular hypertrophy
136
Q

Acute altitude sickness:

  • Symptoms
  • Treatment
A
  • Headaches, anorexia, insomnia

- Evacuate patient to lower altitude

Medicine (18 decks)

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