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Phase 1 Resp > Physiology > Flashcards

Physiology Flashcards

1
Q

What are the muscles of Resp like?

A

Inspiration: - largely quiet and due to diaphragm C3/4/5 contraction
External intercostal nerve roots at each level

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2
Q

What is expiration as a process?

A

Expiration: - passive during quiet breathing

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3
Q

What is a static lung like?

A

Both chest wall and lungs have elastic properties, and a resting (unstressed) volume

Changing this volume requires force
Release of this force leads to a return to the resting volume
Pleural plays an important role linking chest wall and lungs

This is the lungs ‘midpoint’ - resting position e.g. blow all the way out, without trying to breath in it comes back halfway

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4
Q

What occurs in the Resp pump?

A

Requirement to move 5 litres / minute of inspired gas [cardiac output 5 litres / min]

Generation of negative intra-alveolar pressure
Inspiration active requirement to generate flow

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5
Q

What helps the Resp pump?

A

Bony structures support respiratory muscles and protect lungs
Rib movements; pump handle and water handle

Muscles of Resp, pleura, nerves

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6
Q

What is the innervation of the Resp pump?

A

Sensory;
•Sensory receptors assessing flow, stretch etc..
•C fibres
•Afferent via vagus nerve (10th cranial nerve)
–Autonomic sympathetic, parasympathetic balance

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7
Q

What is ventilation and perfusion?

A

VENTILATION; Bulk flow in the airways allows;
O2 and CO2 movement

PERFUSION; Adequate pulmonary blood supply also needed

Occurs in alveoli and capillaries

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8
Q

What is the SA of gas exchange like?

A

Large surface area required, with minimal distance for gases to move across. Total combined surface area for gas exchange 50-100 m2
300,000,000 alveoli per lung

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9
Q

What is dead space?

A

Alveolar ventilation
Volume of air not contributing to ventilation

Anatomic; Approx 150mls
Alveolar; Approx 25mls

Physiological
(Anatomic+Alveolar) = 175mls

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10
Q

What is the bronchial circulation?

A

Blood supply to the lung; branches of the bronchial arteries

Paired branches arising laterally to supply bronchial and peri-bronchial tissue and visceral pleura

Systemic pressures (i.e. LV/aortic pressures)

Venous drainage; bronchial veins draining ultimately into the superior vena cava

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11
Q

What is the pulmonary circulation?

A

Left and right pulmonary arteries run from right ventricle
Low(er) pressure system (i.e. RV / pulmonary artery pressures)

17 orders of branching
Elastic (>1mm ) and non elastic
Muscular (<1mm )
Arterioles (<0.1mm )
Capillaries

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12
Q

What is the bronchial-vascular bundle?

A

Pulmonary artery and bronchus run in parallel

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13
Q

What does alveolar perfusion involve?

A

Each erythrocyte may come into contact with multiple alveoli
Erythrocyte thickness an important component of the distance across which gas has to be moved
At rest, 25% the way through capillary, haemoglobin is fully saturated

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14
Q

Why is matching V and P important?

A

Hypoxic pulmonary vasoconstriction
Pulmonary vessels have high capacity for cardiac output
–30% of total capacity at rest
Recruiting of alveoli occurs as a consequence of exercise

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15
Q

What is PaCO2, PACO2, PaO2, PAO2?

A

PaCO2 = arterial CO2
PACO2 = alveolar CO2

PaO2 = arterial O2
PAO2 = alveolar O2

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16
Q

What is PiO2, FiO2, VA and VCO2?

A

PiO2 = pressure of inspired O2
FiO2 = Fraction of inspired O2 (0.21)

VA = Alveolar ventilation
VCO2 = CO2 production

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17
Q

What is CO2 elimination?

A
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18
Q

What is Physio causes of high CO2?

A
  • reduced minute vent
  • increased dead space vent by rapid shallow breath
  • increased deade space by VQ mismatch
  • increased CO2 production
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19
Q

What is the alveolar gas equation?

A

PAO2 = piO2 - PaCO2/R

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20
Q

What is the cause of low PaO2?

A

Hypoxemia

  • alveolar hypoventilation
  • reduced piO2
  • V/Q mismatch
  • diffusion abnormality
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21
Q

Why does the O2/Hb dissociation curve have a sigmoid shape?

A

Sigmoid shape
As each O2 molecule binds, it alters the conformation of haemoglobin, making subsequent binding easier (cooperative binding)

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22
Q

What are the influences of the O2/Hb dissociation curve?

A

Varying influences
2,3 diphosphoglyceric acid
H+
Temperature
CO2

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23
Q

What is acid base control?

A

Body maintains close control of pH to ensure optimal function (e.g. enzymatic cellular reactions)

Dissolved CO2/carbonic acid/respiratory system interface crucial to the maintenance of this control

pH normally 7.40

H+ concentration 40nmol/l [34-44 nmol/l]

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24
Q

What is imp in A-B control?

A

Blood and tissue buffers important
Carbonic acid / bicarbonate buffer in particular
CO2 under predominant respiratory control (rapid)
HCO3- under predominant renal control (less rapid)

The respiratory system is able to compensate for increased carbonic acid production, but;
Elimination of fixed acids requires a functioning renal system

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25
Q

What equations are in A-B control?

A

Carbonic acid equilibrium
CO2+H20 = H2CO3 = H+ + HCO3-

Henderson hasselbach equation
PH = 6.1+log10[HCO3-]/[0.03X?PCO2] CHECK

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26
Q

How does the Henderson hasselbach equation change?

A

In order to keep pH at 7.4, log of the ratio must equal 1.3
As PaCO2 rises (respiratory failure)
HCO3- must also rise (renal compensatory mechanism) to allow this

In order to keep pH at 7.4, log of the ratio must equal 1.3
As PaCO2 rises (respiratory failure)
HCO3- must also rise (renal compensatory mechanism) to allow this

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27
Q

What are the four main acid-base disorders?

A

Resp acidosis
Resp alkalosis
Metabolic acidosis
Metabolic alkalosis

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28
Q

Define Resp acidosis

A

increased PaCO2, decreased pH, mild increased HCO3-

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29
Q

Define Resp alkalosis

A

decreased PaCO2, increased pH, mild decreased HCO3-

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30
Q

Define metabolic acidosis

A

reduced bicarbonate and decreased pH

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31
Q

Define metabolic alkalosis

A

Increased bicarbonate and increased pH

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32
Q

What are measure values of lung physiology?

A

FEV1
Forced expiratory volume in one second
FVC
Forced vital capacity

Breathe in to total lung capacity (TLC)
Exhale as fast as possible to residual volume (RV)
Volume produced is the vital capacity (FVC)

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33
Q

What is Forced expiration like?

A

Take the exact same procedure
Re-plot the data showing flow as a function of volume
PEF; peak flow
FEF25; flow at point when 25% of total volume to be exhaled has been exhaled
FVC; forced vital capacity

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34
Q

What is PEF (peak expiratory flow rate)?

A

Single measure of highest flow during expiration
Peak flow meter, spirometer

Gives reading in litres/minute (L/min)
Very effort dependent
May be measured over time, by giving a patient a PEF meter and chart

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35
Q

What do expiratory procedures measure?

A

Expiratory procedures only measure VC, not RV
Various other ways to measure RV and TLC are needed

These include;
–Gas dilution
–Body box (total body plethysmography; shown in picture)

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36
Q

What are gas dilutions?

A

Measurement of all air in the lungs that communicates with the airways

Does not measure air in non-communicating bullae

Gas dilution techniques use either closed-circuit helium dilution or open-circuit nitrogen washout

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37
Q

What is a total body plethymography?

A

Alterative method of measuring lung volume, (Boyle’s law), including gas trapped in bullae.

From the FRC, patient “pants” with an open glottis against a closed shutter to produce changes in the box pressure proportionate to the volume of air in the chest

The volume measured (TGV) represents the lung volume at which the shutter was closed

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38
Q

How to calculate TLC?

A

FRC, inspiratory capacity, expiratory reserve volume, vital capacity all measured

From these volumes and capacities, the residual volume and total lung capacity can be calculated

TLC = VC+RV

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39
Q

What estimates TLCO?

A

Carbon monoxide used to estimate TLCO, as has high affinity for haemoglobin
•TLCO is an overall measure of the interaction of;
–alveolar surface area
–alveolar capillary perfusion
–physical properties of the alveolar capillary interface
–capillary volume
–haemoglobin concentration, and the reaction rate of carbon monoxide and hemoglobin.

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40
Q

What is the breath-holding technique?

A

Single 10 second breath-holding technique
–10% helium, 0.3% carbon monoxide, 21% oxygen, remainder nitrogen.

•Alveolar sample obtained;
–DLCO is calculated from the total volume of the lung, breath-hold time, and the initial and final alveolar concentrations of carbon monoxide.

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41
Q

What are the normal ranges?

A

Each measured value has its own normal range
•Derived normally from regression equations based on normal populations
•Wide range of values hence normal
•Lowest 5% arbitrarily defined as abnormal (and upper 5%)

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42
Q

What are the normal measured values in men?

A

Men - predicted, equation RSD

  1. FEV1 (L)
  2. FVC (L)
  3. PEF
  4. 4.30H - 0.029A - 2.49
  5. 5.76H - 0.026A - 4.34
  6. 6.14H - 0.043A + 0.15
  7. 0.51 (0.75)
  8. 0.61 (0.89)
  9. 1.21 ( 1.98)
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43
Q

What are the normal measured value ranges in women?

A

Women predicted, equation and RSD

  1. FEV1 (L)
  2. FVC (L)
  3. PEF
  4. 3.95H - 0.025A - 2.60
  5. 4.43H - 0.026A - 2.89
  6. 5.50H - 0.030A - 1.11
  7. 0.38 (0.64)
  8. 0.43 (0.67)
  9. 0.90 (1.45)
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44
Q

What is FEV 1 and FVC?

A

FEV1
Forced expiratory volume in one second
FVC
Forced vital capacity

Normal values?

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45
Q

What are abnormal values of FEV 1?

A

Forced expiratory volume in one second in litres
Good overall assessment of lung health

Compare with predicted value
80% or greater “normal”
Above the lower limit of normal for that patient (LLN)
Above mean minus 1.645 SD

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46
Q

What are the normal values of FVC?

A

Compare with predicted value
80% or greater “normal”
Above the lower limit of normal for that patient (LLN)
Above mean minus 1.645 SD

Low value indicates likely Airways Restriction

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47
Q

What is airway restriction?

A

FVC <80% predicted
Low FVC value indicates likely airways restriction

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48
Q

What ima airway obstuction?

A

FEV1/FVC

There is a predicted ratio for each individual, but..

Abnormal ratio < 0.70 = airways obstruction

[Can also use the LLN* for each individual patient]
*Lower limit of normal

FEV1 / FVC ratio < 0.70 = airways obstruction

FEV1/FVC ratio <0.70

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49
Q

What are transfer estimates?

A

Carbon monoxide used to estimate TLCO, as has high affinity for haemoglobin
•TLCO is an overall measure of the interaction of;
–alveolar surface area
–alveolar capillary perfusion
–physical properties of the alveolar capillary interface
–capillary volume
–haemoglobin concentration, and the reaction rate of carbon monoxide and hemoglobin.

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50
Q

Watch lung physio 3 lecture - cases!

A
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51
Q

What is the requirement of respiration?

A

Ensure haemoglobin is as close to full saturation with oxygen as possible
–Efficient use of energy resource
–Regulate PaCO2 carefully
•variations in CO2 and small variations in pH can alter physiological function quite widely

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52
Q

How is breathing automatic?

A

Breathing is automatic

–No conscious effort for the basic rhythm
–Rate and depth under additional influences
–Depends on cyclical excitation and control of many muscles
•Upper airway, lower airway, diaphragm, chest wall
•Near linear activity
•Increase thoracic volume

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53
Q

What are the input signals of breathing?

A
  • Central chemoreceptors
  • Voluntary Control (cerebrum)
  • Lung Receptors
    1.Stretch, 2.J receptors, 3.Irritant
    ->
  • Respiratory control centres (Medulla and Pons)->
  • Spinal Motor Neurons ->
    Muscles of Respiration
    Intercostal muscles
    Accessory muscles
    Diaphragm

Muscle proprioceptors and peripheral chemoreceptors - carotid and aortic ->resp control centres (medulla and pons)

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54
Q

What are the basic breathing rhythms?

A

Pons
–Pneumotaxic and Apneustic Centres

•Medulla Oblongata
–Phasic discharge of action potentials
–Two main groups
•Dorsal respiratory group (DRG)
•Ventral respiratory group (VRG)

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55
Q

What are the basic breathing rhythms?

A

Pons
–Pneumotaxic and Apneustic Centres

•Medulla Oblongata
–Phasic discharge of action potentials
–Two main groups
•Dorsal respiratory group (DRG)
•Ventral respiratory group (VRG)

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56
Q

What is active during breathing?

A

DRG; predominantly active during inspiration
•VRG; active in both inspiration and expiration

•Each are bilateral, and project into the bulbo-spinal motor neuron pools and interconnect

57
Q

What influences basic breathing rhythms?

A
  • IX Glossopharyngeal nerve
  • X Vagus nerve
  • E neurons
  • Medulla
  • I neurons
  • Inspiratory motorneuron
  • Expiratory motorneuron
  • VRG
  • Spinal cord
  • DRG
58
Q

What are central pattern generators?

A

Neural network (interneurons)
•Located within DRG/VRG
–Precise functional locations not known
–Start, stop and resetting of an integrator of background ventilatory drive

59
Q

What are central pattern generators?

A

Neural network (interneurons)
•Located within DRG/VRG
–Precise functional locations not known
–Start, stop and resetting of an integrator of background ventilatory drive

60
Q

What is inspiration?

A

Inspiration
–Progressive increase in inspiratory muscle activation
•Lungs fill at a constant rate until tidal volume achieved
•End of inspiration, rapid decrease in excitation of the respiratory muscles

61
Q

What is expiration?

A

Expiration
–Largely passive due to elastic recoil of thoracic wall
•First part of expiration; active slowing with some inspiratory muscle activity
•With increased demands, further muscle activity recruited
•Expiration can be become active also; with additional abdominal wall muscle activity

62
Q

What are chemoreceptors?

A

Central (60% influence from PaCO2) and peripheral (40% influence from PaCO2)

–Stimulated by [H+] concentration and gas partial pressures in arterial blood
–Brainstem [primary influence is PaCO2]

•Carotids and aorta [PaCO2, PaO2 and pH]
–Significant interaction

63
Q

What are central chemoreceptors?

A

Located in brainstem
•Pontomedullary junction
•Not within the DRG/VRG complex

–Sensitive to PaCO2 of blood perfusing brain
–Blood brain barrier relatively impermeable to H+ and HCO3-
–PaCO2 preferentially diffuses into CSF

64
Q

What are peripheral chemoreceptors?

A

These are located in;
–Carotid bodies
•Bifurcation of the common carotid
•(IX) cranial nerve afferents
–Aortic bodies
•Ascending aorta
•Vagal (X) nerve afferents

65
Q

What are peripheral chemoreceptors responsible for?

A

Responsible for [all] ventilatory response to hypoxia (reduced PaO2)

Generally not sensitive across normal PaO2 ranges

When exposed to hypoxia, type I cells release stored neurotransmitters that stimulate the cuplike endings of the carotid sinus nerve

66
Q

What are peripheral chemoreceptors response to PaCO2?

A

Linear response to PaCO2

Interactions between responses

[Poison (e.g. cyanide) and blood pressure responsive]

67
Q

What are the Lung receptors?

A

Stretch, J and irritant
•Afferents; vagus (X)
•Combination of slow and fast adapting receptors
•Assist with lung volumes and responses to noxious inhaled agents

68
Q

How do lung receptors act?

A

Stretch
–Smooth muscle of conducting airways
–Sense lung volume, slowly adapting
•Irritant
–Larger conducting airways
–Rapidly adapting [cough, gasp]
•J; juxtapulmonary capillary
–Pulmonary and bronchial C fibres

69
Q

What are the airway receptors?

A

Nose, nasopharynx and larynx
–Chemo and mechano receptors
–Some appear to sense and monitor flow
•Stimulation of these receptors appears to inhibit the central controller
•Pharynx
–Receptors that appear to be activated by swallowing
•respiratory activity stops during swallowing protecting against the risk of aspiration of food or liquid

70
Q

What are muscle propria receptors?

A

Joint, tendon and muscle spindle receptors
•Intercostal muscles > > diaphragm
•Important roles in perception of breathing effort

71
Q

What is the bodies response to ascent?

A

Ascending; PiO2 falls (FiO2 remains constant)
Decreased PAO2
Decreased PaO2
Peripheral chemoreceptors fire (e.g carotid)
Activates increased ventilation (VA)
Increased PAO2
Increased PaO2

72
Q

What are the importance of chemoreceptors?

A

•PaCO2 most important factor
–Central chemoreceptors; PaCO2
–Peripheral; PaO2, PaCO2 and p

73
Q

What’s respiration control like?

A

Positive and negative feedback systems
•Basic rhythm from brainstem
•Modified by various reflexes
•Vagal afferents of lung stretch

74
Q

What is pulmonary and bronchial circulation like?

A

Unique dual blood supply of the lungs

•Pulmonary Circulation
–From Right Ventricle
–100% of blood flow

•Bronchial Circulation
–2% of Left Ventricular Output

75
Q

What are the measurements of pulmonary circulation?

A

Receives 100% of cardiac output (4.5-8L/min.)

•Red cell transit time ≈5 seconds.

•280 billion capillaries & 300 million alveoli.

•Surface area for gas exchange 50 – 100 m2

76
Q

What is the difference between pulmonary vs systemic arteries?

A

Pulmonary vs systemic
Vessel wall: thin vs thick
Muscularisation: minor vs significant
Need for redistribution: not in normal state vs yes

77
Q

Difference between structure/histology of systemic and pulmonary artery

A

Adventitia
Intima
Media

78
Q

What are the pressures (mmHg) of pulmonary circulation?

A

Pulmonary Circulation

•RA 5

•RV 25/0

•PA 25/8

79
Q

What are the pressures of systemic circulation?

A

Systemic Circulation

•LA 5

•LV 120/0

•Aorta 120/80

80
Q

Difference between ventricles

A

Left Ventricle “sees” higher pressure than the right ventricle

81
Q

What is pulmonary arterial wedge pressure?

A
82
Q

What is Ohm’s law?

A

Voltage across circuit = Current x Resistance
V = I R

Pressure across circuit = Cardiac Output x Resistance

mPAP – PAWP = CO x PVR

83
Q

What is Pouiseuille’s law?

A

Resistance = (8 x L x viscosity)/(π r4)
- r = 4 r = 2
- r4 = 256 r4 = 16

84
Q

What happens in exercise?

A

mPAP – PAWP = CO x PVR

•On exercise CO increases significantly but mPAP remains stable/increases slightly

85
Q

What is the response to increased pulmonary artery pressure?

A

Recruitment and Distention in Response to Increased Pulmonary Artery Pressure

86
Q

What is respiratory failures?

A

Type I Respiratory Failure
–pO2 < 8 kPA
–pCO2 <6 kPA

•Type II Respiratory Failure
–pO2 < 8 kPA
–pCO2 >6 kPA

87
Q

What are the causes of hypoxaemia?

A

Hypoventilation
•Diffusion Impairment
•Shunting
•V/Q mismatch

88
Q

What is hypoventilation?

A

Type II Respiratory Failure
–pO2 < 8 kPA
–pCO2 >6 kPA
•Failure to ventilate the alveoli

•Muscular weakness
•Obesity
•Loss of respiratory drive

89
Q

What is hypoventilation?

A

Type II Respiratory Failure
–pO2 < 8 kPA
–pCO2 >6 kPA
•Failure to ventilate the alveoli

•Muscular weakness
•Obesity
•Loss of respiratory drive

90
Q

What is diffusion impairement?

A

•Gaseous Diffusion
–Pulmonary Oedema

•Blood Diffusion
–Anaemia

•Membrane Diffusion
–Interstitial Fibrosis

91
Q

What is perfusion?

A
92
Q

What is perfusion?

A
93
Q

What is ventilation?

A

Average V/Q = 0.8

94
Q

What is Shunt v V/Q Mismatch?

A

Decreased V/Q
Pneumonia
COPD
Lobar collapse
?????

95
Q

What is shunt?

A

•Pulmonary
–Complete Lobar Collapse
–ArterioVenous Malformation (AVM)
•Intracardiac
–eg VSD - R-L Shunt (Eisenmenger’s Syndrome)
•Physiological
–Bronchial Arteries

96
Q

What is shunt?

A

•Pulmonary
–Complete Lobar Collapse
–ArterioVenous Malformation (AVM)
•Intracardiac
–eg VSD - R-L Shunt (Eisenmenger’s Syndrome)
•Physiological
–Bronchial Arteries

97
Q

What is shunt?

A

•Pulmonary
–Complete Lobar Collapse
–ArterioVenous Malformation (AVM)
•Intracardiac
–eg VSD - R-L Shunt (Eisenmenger’s Syndrome)
•Physiological
–Bronchial Arteries

98
Q

What is Eisenmenger’s Syndrome?

A

Cyanosis
•Clubbing
•Erythrocytosis

High pulmonary artery pressure
Shunt reverses because of high RV pressure

99
Q

What is Hypoxic Pulmonary Vasconstriction?

A

Local action of hypoxia on pulmonary artery wall
•Weak response as little muscle
•Aims to maintain V/Q matching
–Local hypoxia (eg peanut)
–Generalised hypoxia (eg altitude)

100
Q

What is Hypoxic Pulmonary Vasconstriction?

A

Local action of hypoxia on pulmonary artery wall
•Weak response as little muscle
•Aims to maintain V/Q matching
–Local hypoxia (eg peanut)
–Generalised hypoxia (eg altitude)

101
Q

What is Dead Space Ventilation v V/Q Mismatch?

A

Peripheral Pulmonary Embolism
Alveolar dead space
V/Q = infinity
Central Pulmonary embolism

102
Q

What are diseases of pulmonary circulation?

A

Pulmonary Embolism
•Pulmonary Hypertension
•Pulmonary AVMs

103
Q

What are diseases of pulmonary circulation?

A

Pulmonary Embolism
•Pulmonary Hypertension
•Pulmonary AVMs

104
Q

What is a pulmonary embolism?

A

CENTRAL = ISCHAEMIA
PERIPHERAL = INFARCTION

Lung infarction: minor PE

Pleuritic pain
Peripheral arteries

Central “Major” PE

•Shock
•Central Chest Pain

•Hypoxia
•Risk of Immediate Mortality

105
Q

What is a Ventilation/Perfusion Scan: V/Q Mismatch?

A
106
Q

What is Virchow’s Triad?

A
107
Q

What is Pulmonary Arterial Hypertension: Increased Pulmonary Vascular Resistance?

A
108
Q

What does Pulmonary Arteriovenous Malformation: Shunt look like?

A
109
Q

What are the two circulations like?

A

•2 Circulations
–Pulmonary circulation: low pressure system
–Systemic circulation: high pressure system

110
Q

What are 4 causes of hypoxaemia?

A

4 main causes of hypoxaemia
–Hypoventilation
–Diffusion abnormality
–V/Q mismatch
–Shunt

111
Q

What are 4 causes of hypoxaemia?

A

4 main causes of hypoxaemia
–Hypoventilation
–Diffusion abnormality
–V/Q mismatch
–Shunt

112
Q

What are 3 diseases of pulmonary circulation?

A

–V/Q Mismatch: Pulmonary Embolism (↑V/Q)
–Increased PVR: Pulmonary Arterial Hypertension
–Shunt: Pulmonary Arteriovenous Malformation

113
Q

How is CO2 carried?

A
  • Bound to Hb (protein chain)
  • plasma dissolved
  • as carbonic acid

Normally PaCO2 = 4-6KPa

PaCO2 = kVco2/VA

114
Q

What are physiological causes of high CO2?

A
  • reduced minute ventilation
  • increased dead space ventilation by rapid shallow breathing
  • Increased dead space by V/Q mismatch
  • increased CO2 production
115
Q

What is the alveolar gas equation?

A

Alveolar Gas Equation

PAO2 = PiO2 – PaCO2/R

Causes of low PaO2 (hypoxaemia)

Alveolar hypoventilation
Reduced PiO2
Ventilation/perfusion mismatching (V/Q)
Diffusion abnormality

R=Respiratory Quotient [ratio of Vol CO2 released/Vol O2 absorbed, assume = 0.8]

116
Q

What determines PaCO2?

A

PaCO2 - proportional 1/alveolar ventilation
PaCO2 = kVco2/ VA

117
Q

What is oxygenation?

A

PAO2 = PiO2 – PaCO2/R

PAO2 = 20KPa – 6KPa/0.8
= 20 – 7.5
= 12.5 KPa

R=Respiratory Quotient [ratio of Vol CO2 released/Vol O2 absorbed, assume = 0.8]

118
Q

What is the definition of respiratory failure?

A

Failure of gas exchange
Inability to maintain normal blood gases

Low PaO2
With or without a rise in PaCO2

Respiratory failure can occur with normal or abnormal lungs

119
Q

What are the blood gases of respiratory fsailure?

A

At sea level PiO2 = 100KPa x 0.21 = 21 KPa

PaO2 <8KPa <60mmHg [10.5 - 13.5]

PaCO2 >6.5KPa >49mmHg
[4.7 – 6.5]

PAO2 = alveolar PaO2 = arterial

120
Q

What are the types of respiratory failure?

A

Resp Failure: I, PaO2-Low hypoxia), PaCO2 - Low / Normal hypocapnia/normal)

Resp Failure 2: PaO2-low (hypoxia), PaCO2 - High (hypercapnia)

121
Q

What time course can resp failure take?

A

Acute, rapidly
For example; opiate overdose, trauma, pulmonary embolism

Chronic, over a period of time
For example; COPD, fibrosing lung disease

122
Q

What is type 1 mechanisms of resp failure?

A

Most pulmonary and cardiac causes produce type I failure

Hypoxia
Mismatching of ventilation and perfusion
Shunting
Diffusion impairment
Alveolar hypoventilation

Similar effects on tissues seen with;
Anaemia, carbon monoxide poisoning, methaemoglobinaemia

123
Q

What are the causes for respiratory failure type 1?

A

Most pulmonary and cardiac causes produce type I failure

Specific causes;
Infection
Pneumonia
Bronchiectasis
Congenital
Cyanotic congenital heart disease
Neoplasm
Lymphangitis carcinomatosis

Most pulmonary and cardiac causes produce type I failure

Specific causes;
Airway
COPD
Asthma
Vasculature
Pulmonary embolism
Fat embolism
Parenchyma
Pulmonary fibrosis
Pulmonary oedema
Pneumoconiosis
Sarcoidosis

124
Q

What are the treatments of respiratory failure type 1?

A

Airway patency
Oxygen delivery
Many differing systems
Increasing FiO2

Primary cause (e.g. antibiotics for pneumonia)

125
Q

What are the treatments of respiratory failure type 1?

A

Airway patency
Oxygen delivery
Many differing systems
Increasing FiO2

Primary cause (e.g. antibiotics for pneumonia)

126
Q

What are the mechanisms of respiratory failure type 2?

A

Lack of respiratory drive
Excess workload
Bellows failure

127
Q

What are the mechanisms of respiratory failure type 2?

A

Lack of respiratory drive
Excess workload
Bellows failure

128
Q

What are the causes of respiratory failure 2?

A

Airway
COPD
Asthma
Laryngeal oedema
Sleep apnoea syndrome
Drugs
Suxamethonium
Metabolic
Poisoning
Overdose

Neurological
Central
Primary hypoventilation
Head and Cervical spine injury
Muscle
Myasthenia
Polyneuropathy
Poliomyelitis
Primary muscle disorders

129
Q

What are the clinical features of hypoxia?

A

Central Cyanosis
Oral cavity
May not be obvious in anaemic patients
Irritability
Reduced intellectual function
Reduced consciousness

Convulsions
Coma
Death

130
Q

What are the clinical features of hypoxia?

A

Central Cyanosis
Oral cavity
May not be obvious in anaemic patients
Irritability
Reduced intellectual function
Reduced consciousness

Convulsions
Coma
Death

131
Q

What are the clinical features of hypercapnia?

A

Variable patient to patient

Irritability
Headache
Papilloedema
Warm skin
Bounding pulse
Confusion
Somnolence
Coma

132
Q

What are the treatments for respiratory failure type 2?

A

Airway patency
Oxygen delivery

Primary cause (e.g. antibiotics for pneumonia)

Treatment with O2 may be more difficult
For example; COPD patients rely on hypoxia to
stimulate respiration

133
Q

What is assissted ventilation for respiratory failure type 2?

A

Assisted ventilation
Invasive
Non invasive

Inadequate PaO2 despite increasing FiO2
Increasing PaCO2
Patient tiring

134
Q

What are some oxygen treatments?

A

Oxygen Treatments
Serious illnesses needing high levels of FiO2
5-10 litres/min face mask or 2-6 litres/min nasal cannulae
Aim for SpO2 of 94-98%

If saturation <85% and not at risk of hypercapnic respiratory failure
10-15 litres / minute reservoir mask

Patients with COPD and other risk factors for hypercapnia;
Aim for SpO2 of 88-92% pending blood gases
Adjust to SpO2 of 94-98% if CO2 normal unless previous history of high CO2 or ventilation

135
Q

What is failure of gas exchange?

A

Failure of gas exchange
Inability to maintain normal blood gases

136
Q

When does resp failure occur?

A

Low PaO2
With or without a rise in PaCO2

Respiratory failure can occur with normal or abnormal lungs

137
Q

What is type 1 respiratory failure values?

A

PaO2 <8KPa
PACO2 low or normal
Common causes: Acute: pneumonia, asthma
Chronic: fibrosing lung disease
O2 - yes

138
Q

What is type 2 respiratory failure like?

A

PaO2 <8KPa
PaCO2 - >6.7KPa
Common causes: Acute: overdose, trauma
Chronic: COPD, neuromuscular
O2 yes, certain conditions

Phase 1 Resp (4 decks)

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