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
Minute volume (VE) equation:
VE = tidal volume x respiratory rate
26
Alveolar ventilation rate (VA):
VA = (tidal volume - physiological dead space) x respiratory rate
27
Surface tension: - Alveolus lining - Bubble - Cohesive forces - transmural pressure
- 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
28
Laplace equation: | Transmural pressure=
- Transmural pressure = (2 surface tension) / radius
29
transmural pressure at Functional Residual Capacity: - Equation - P(alv) - P(ip)
- P(alv) - P(ip) = 0cmH2O - (-5cmH2O) - At FRC alveolar pressure must be equal to atmospheric pressure (0) - Intrapleural is below atmospheric (negative)
30
Intrapleural pressure is below atmospheric, so what?
- A penetrating chest injury will allow air to be sucked in to the intrapleural space - Lung will collapse causing severe respiratory distress
31
First breaths: (3)
- 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
32
Surfactant in embryo's:
- Surface tension reduced by surfactant produced by type 2 alveolar cells - Premature babies may lack surfactant and develop respiratory distress
33
Mechanics of breathing: compliance
- The distensibility of the lungs and chest wall | - compliance = change in volume / change in pressure
34
Changes in compliance: - Fibrotic lung disease - Emphysema
- 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)
35
Boyle's law: pressure is inversely proportional to .....
Pressure is inversely proportional to volume | P = 1/v
36
Breathing cycle: Inspiration
- Inspiration leads to an increase in thoracic volume and a decrease in alveolar pressure to below atmospheric. - This sucks in the tidal volume
37
Breathing cycle: expiration
- Passive process - Decrease in thoracic volume leads to an increase in alveolar pressure to above atmospheric pressure - Tidal volume blown out
38
The work of breathing:
- 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
39
Pulmonary circulation: - Pressure generated by: - Systolic and diastolic pressures: - Resistance: - Blood flow: - Response of small arteries/arterioles to hypoxia
``` 1- Right ventricle 2- 25/8 3- Lower (pulmonary vascular region) 4- Slightly less than 5 L/min 5- Vasoconstriction ```
40
Systemic circulation: - Pressure generated by: - Systolic and diastolic pressures: - Resistance: - Blood flow: - Response of small arteries/arterioles to hypoxia
``` 1- Left ventricle 2- 120/80 3- higher (total peripheral resistance) 4- 5L/min 5- vasodilation ```
41
Physiological shunt: - Pulmonary vein - Thebesian vein - Effect on PA02 and Pa02 - Effect on venous return
- 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
42
V(A):Q=1
- The amount of ventilation with fresh gas equals perfusion with blood - End capillary blood is fully oxygenated/arterialized
43
V(A):Q = 0
- Normal perfusion but complete absence of alveolar ventilation - End capillary blood remains deoxygenated - Shunt/venous admixture
44
V(A):Q = infinite
- Normal ventilation but complete absence of perfusion | - No gas is transferred, this is wasted ventilation, increasing physiological dead space
45
Effects of gravity on V(A):Q
- More ventilation than perfusion at the top of the lung | - V(A):Q will be higher here, as will PAO2
46
Advantages of hypoxic vasoconstriction: (2)
- 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
47
Disadvantages of hypoxic vasoconstriction: - Barometric pressure - COPD
- 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
48
Cor pumonale:
- Right-sided heart failure due to hypoxic lung disease | - Symptoms: blue bloated appearance
49
- Alveolar ventilation (VA)
- The amount of fresh gas delivered to the alveoli | - VA = (tidal volume - physiological) x respiratory rate
50
Alveolar ventilation equations: | PACO2=
PACO2 = PaCO2 = Rate of CO2 by metabolism/ rate of CO2 removal PACO2 directly proportional to rate of CO2 production by metabolism PACO2 indirectly proportional
51
Simplified Alveolar ventilation equation:
PACO2 : Rate of CO2 by metabolism / Rate of CO2 removal by alveolar ventilation
52
Daltons law:
P(TOTAL)= P1 + P2 + P3 ......
53
Alveolar gas equation use:
- Used to predict a patients PAO2 depending upon the amount of oxygen they're breathing
54
Gas exchange: (3) - Definition - Diffusion - Direction
- 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
55
Diffusing capacity: - Definition - Measured by - Decreased by - Increased by
- 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
Perfusion-limited gas exchange:
- At rest capillary partial pressure of O2 rapidly becomes equal to the partial pressure of oxygen in the alveolus
57
Diffusion limited gas exchange:
- 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
Calculating the total oxygen content of blood:
C = amount bound to haemoglobin + amount dissolved in plasma = (O2 binding capacity x SaO2) + (PaO2 x solubility)
59
Rate of O2 delivery:
O2 delivery = cardiac output (Q) x O2 content (C)
60
Haemoglobin variants: foetal haemoglobin (HbF) - Structure - Affinity - Lifespan
- Two alpha and two gamma subunits - Higher affinity for O2 than HbA - Replaced by HbA within a year of birth
61
Haemoglobin A (HbA) - Structure - Haem moiety - Bound
- 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
Haemoglobin variants: Methaemoglobin
Iron moiety oxidised to ferric (Fe3+) state - Does not bind O2 - Congenital form due to deficiency of methaemoglobin reductase
63
Haemoglobin variants: Methaemoglobin
Iron moiety oxidised to ferric (Fe3+) state - Does not bind O2 - Congenital form due to deficiency of methaemoglobin reductase
64
Haemoglobin variants: Haemoglobin S
- Abnormal B subunits | - Sickle cell disease, distorts RBCs causing anaemia
65
Oxygen Haemoglobin dissociation curve:
- Sigmoidal - Due to increasing affinity for oxygen with each O2 molecule that binds - P50 is the PO2 where 50% saturation is achieved
66
Loading and unloading of oxygen:
- Areas with higher PO2 will have higher saturation, signalling loading - Areas with low PO2 have lower saturation, signalling unloading
67
Bohr effect:
- 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
Carbon monoxide (CO) poisoning:
- 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
CO2 transport in the blood:
- Dissolved in plasma - Bound to HbA forming carbaminohaemoglobin - Converted to bicarbonate (HCO3-)
70
Chloride shift in HbA:
- HCO3- transported out of cell in exchange for Cl- ions
71
CO2 dissociation curve:
- Linear in shape, CO2 exertion increases with increased ventilation in all areas
72
Ventilation perfusion mismatch (VQ):
- Defect in the V(A):Q ratio | - Causes arterial hypoxaemia but an increase in alveolar ventilation prevents hypercapnia
73
Fick's law: rate of diffusion =
Rate of diffusion (a) | (surface area x concentration) / thickness of membrane
74
Henry's law: amount of gas in liquid
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
Control of respiration (PaO2,PaCO2, arterial pH): | - CPG
- A central pattern generator in the brainstem with inputs from the cerebral cortex and multiple types of receptors/sensors
76
Cerebral (voluntary) respiratory control: - Voluntary hyperventilation - Voluntary hypoventilation
If the rate of CO2 production remains constant: - Voluntary hyperventilation must lead to hypocapnea - Voluntary hypoventilation must lead to hypercapnia
77
Respiratory acidosis:
- Hypercapnia drives equilibrium to the right, increasing H+conc. lowering pH
78
Respiratory Alkalosis:
- Hypocapnia drives equilibrium to the left, decreasing H+conc. raising the pH
79
Dangers of acute respiratory acidosis: (3)
- Decreased cardiac contractility - Cardiac arrhythmias and potential cardiac arrest - Alterations in pH dependent biochem pathways
80
Hypocapnia symptoms:
- Reduced cerebral blood flow due to vasoconstriction
81
Central chemoreceptors: - Location - Role of CO2
- 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
Peripheral chemoreceptors:
- Found in carotid sinus | - Stimulated by acidemia, hypoxia, hypercapnia and decreased perfusion (hypotension)
83
Influence of CO2 on respiratory control: (3) - Rise effects - Max - Min
- 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
Influence of oxygen on respiratory control
- Linear relationship between PaO2 and minute volume until SaO2 drops too far, stimulating a powerful stimulus
85
Influence of pH on respiratory control:
Arterial pH depends upon ratio of bicarbonate to PaCO2 | pH = [HCO3-] / PaCO2
86
Metabolic acidosis:
- A pathological decrease in [HCO3-] causes a fall in blood pH - Often seen in uncontrolled type 1 diabetes mellitus
87
Metabolic acidaemia correction:
- Peripheral chemoreceptors stimulated, increasing alveolar ventilation, decreasing PaCO2 - Reduces pH disturbance
88
Influence of opioids in respiratory control: | MOP receptors
- Opioids bind the MOP receptors and depress alveolar ventilation - Pathological rise in PaCO2 causes respiratory acidosis, pH falls - Reversed using the antagonist naloxone
89
Cellular respiration:
- 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
Oxidation of glucose (cellular respiration):
- Cell oxidises glucose in a series of enzyme-catalysed steps, gradually releasing energy which is captured by activated carrier molecules
91
Glycolysis:
- 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
Glycolysis steps (3): 1. Investment 2. 6-carbon sugar 3. Energy generation
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
ATP functions:
- A building block of DNA, RNA - Combine with other groups to form coenzymes - as cyclic AMP, a signalling molecule
94
ATP functions:
- A building block of DNA, RNA - Combine with other groups to form coenzymes - as cyclic AMP, a signalling molecule
95
Anaerobic energy generation:
- 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
Metastasize: | Warburg effect:
- Malignant tumours reproduce very quickly | - They consume large amounts of glucose and produce lots of lactate
97
Glycogen:
- Stores sugars in small granules in the cytoplasm of many cells - Used during short periods of fasting
98
Triglycerides:
- Stores fatty acids in adipocyte cells - Used for longer periods of fasting - Adipose tissue can be white or brown, brown containing more mitochondria
99
Liver specialities:
- 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
Mitochondria: | - Membranes (4)
- 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
Mitochondria function:
- Pyruvate pumped into the mitochondrial matrix and converted into acetyl CoA and CO2 by Pyruvate Dehydrogenase Complex
102
Citric acid cycle overview:
- 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
Citric acid cycle products:
- 3 NADH - 1 GTP - 1 FADH2 - 2 CO2
104
Oxidative Phosphorylation:
- 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
Oxidative phosphorylation overview:
- 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
How is Vo2 (O2 consumption rate) measured:
- Measured using a spirometer filled with 100% oxygen
107
Phases of respiration during exercise: (3)
- 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
Oxygen debt:
- 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
Vo2MAX:
- An individuals maximum oxygen consumption rate | - Used as a measure of respiratory fitness
110
Exercising above Vo2 MAX:
- 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
Effects of lactic acid:
- 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
Oxygen delivery (O2) =
O2 delivery = Cardiac output (Q) x O2 content (C)
113
Effects of increased mean pulmonary artery pressure:
- Increases pulmonary blood flow - Increases perfusion of the lung apices - Reduces physiological dead space, improves VA:Q
114
Fick equation and limiting factors of Vo2MAX:
- Vo2MAX= MAX CO X difference in arterial and venous O2 content
115
Effects of training upon the heart:
``` Increases: - Myocardial capillaries - Size of ventricular chamber - Vagal tone, resulting in resting bradycardia Results in increased Cardiac output (Q) ```
116
Effects of training upon skeletal muscle: - Increases - Effects
``` Increases: - Capillaries - Mitochondria - Myoglobin Allows an increase in oxygen extraction, increasing anaerobic threshold and livers ability to clear lactate ```
117
Ergoreflex:
- Mechanoreceptors and metaboloreceptors in skeletal muscle cause an increase in ventilation and HR during exercise
118
The oxygen cascade:
- 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
Normal arterial PaO2:
- PaO2 = 13.6 (0.044 x age)
120
Hypoxaemia:
- Abnormally low arterial partial pressure of oxygen (PaO2) | - Associated with central cyanosis (blue tongue)
121
Hypoxia:
- Low tissue partial pressure of oxygen | - Hypoxaemia is one cause of tissue hypoxia
122
Causes of hypoxaemia: (5) | -Compared how?
``` 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
Hypoxaemia causes: High altitude - Notes - PaO2 effect - Aa difference - Does O2 help?
- Fall in barometric pressure leads to a decrease in PIO2 and PAO2 - Decrease - Aa normal - Yes
124
Hypoxaemia causes: Hypoventilation - Notes - PaO2 effect - Aa difference - Does O2 help?
- Decreases PAO2 - Decreases PaO2 - Aa normal - Yes
125
Hypoxaemia causes: Diffusion defect - Notes - PaO2 effect - Aa difference - Does O2 help?
- Decreases PaO2 - Increased Aa difference - Yes
126
Hypoxaemia causes: VA:Q mismatch - Notes - PaO2 effect - Aa difference - Does O2 help?
- Decreases PaO2 - Increased Aa difference - Yes
127
Hypoxaemia causes: R-to-L cardiac shunt - Notes - PaO2 effect - Aa difference - Does O2 help?
- 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
Causes of tissue hypoxia: Stagnant hypoxia
- Decrease in cardiac output causes a decrease in rate of O2 delivery
129
Causes off tissue hypoxia: Hypoxaemia
- A decrease in SaO2 and PaO2 reduces total O2 content, reducing rate of O2 delivery
130
Causes of tissue hypoxia: anaemic hypoxia:
- Concentration of haemoglobin falls, lowering oxygen binding capacity, which lowers O2 content
131
Causes of tissue hypoxia: histotoxic hypoxia:
- An inability of the cells to utilise oxygen
132
``` Hypoxia symptoms: _ A - E - C/L of C - T - U/C/S ```
- Anxiety - Euphoria - Confusion/lack of coordination - Tachypnoea, use of accessory muscles - unconsciousness/coma/seizures
133
Pressure of inspired air (PIO2) - FIO2 - PB - PH2O
PIO2 = FIO2 x [PB - PH2O] ``` FIO2= fractional O2 composition PB = Barometric pressure PH2O = Water vapour pressure ```
134
The challenge of high altitude: | PIO2 = FIO2 x [PB - H2O]
- At high altitudes PB falls, lowering PIO2
135
Acclimatisation: - Definition - Respiratory changes
- 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
Acute altitude sickness: - Symptoms - Treatment
- Headaches, anorexia, insomnia | - Evacuate patient to lower altitude