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Respiratory Failure Flashcards

1
Q

Respiratory failure

A

Failure of gas exchange - inability to maintain normal blood gases
Low PaO2 (with or without rise in PaCO2)

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2
Q

Respiratory failure blood gases: PaO2

A

<8 KPa
<60 mmHg

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3
Q

Respiratory failure blood gases: PaCO2

A

> 6.5 KPa
49 mmHg

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4
Q

Sea level PiO2

A

100 KPa x 0.21 = 21 KPa

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5
Q

Normal range PaO2

A

10.5-13.5

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6
Q

Normal range PaCO2

A

4.7-6.5

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7
Q

Acute respiratory acidosis secondary to opiate overdose treatment

A

IV fluids
Supportive care
Opiate antagonists

Possible need for non invasive or invasive ventilation

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8
Q

Type 1 respiratory failure: PaO2

A

Low (hypoxaemia)

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9
Q

Type 1 respiratory failure: PaCO2

A

Low/ normal (hypocapnia/normal)

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10
Q

Type 2 respiratory failure: PaO2

A

Low (hypoxaemia)

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11
Q

Type 2 respiratory failure: PaCO2

A

High (Hypercapnia)

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12
Q

Acute respiratory failure

A

Rapidly
Eg opiate overdose, trauma, pulmonary embolism

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13
Q

Chronic respiratory failure

A

Over a period of time
Eg COPD, fibrosing lung disease

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14
Q

Causes of type 1 respiratory failure

A

Most pulmonary and cardiac produce type 1 failure
Eg
infection = pneumonia, bronchiectasis
Congenital = cyanotic congenital heart disease
Neoplasm = lymphangitis carcinomatosis
Airway = COPD, asthma
Vasculature = pulmonary embolism, fat embolism
Parenchyma = pulmonary fibrosis, pulmonary oedema, pneumoconiosis, sarcoidosis

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15
Q

Causes of hypoxia

A

Mismatching of ventilation and perfusion
Shunting
Diffusion impairment
Alveolar hypoventilation

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16
Q

Similar effects on tissue as type 1 failure as seen with

A

Anaemia
Carbon monoxide poisoning
Methaemoglobinaemia

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17
Q

Hypoxia

A

A reduced level of tissue oxygenation

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18
Q

Hypoxaemia

A

A decrease in the partial pressure of oxygen in the blood

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19
Q

Hypopnoeic

A

Slow respiratory rate

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20
Q

Type 1 respiratory failure treatments

A

Airway patency
Oxygen delivery
Many differing systems
Increasing FiO2

Primary cause (eg antibiotics for pneumonia)

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21
Q

Type 2 respiratory failure mechanisms

A

Lack of respiratory drive
Excess workload
Bellows failure
Increased resistance

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22
Q

Type 2 respiratory failure types

A

Airway = COPD, asthma, laryngeal oedema, sleep apnoea syndrome
Drugs = suxamethonium (paralysis)
Metabolic - poisoning, overdose
Neurological = central, primary hypoventilation, head and cervical spine injury
Muscle = myasthenia
Polyneuropathy = poliomyelitis
Primary muscle disorders

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23
Q

Clinical features of hypoxia

A

Central cyanosis
- may not be obvious in anaemia patients
-Oral cavity
Irritability
Reduced intellectual function
Reduced consciousness
Convulsions
Coma
Death

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24
Q

What is the common cause of type 1 and 2 respiratory failure

A

COPD

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25
Q

Clinical features of Hypercapnia

A

Variable patient to patient

Irritability
Headache
Papilloedema
Warm skin
Bounding pulse
Confusion
Somnolence (tiredness/sleepy)
Coma

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26
Q

Treatments of type 2 respiratory failure

A

Airway patency
Oxygen delivery

Primary cause (eg antibiotics for pneumonia)

Treatment with O2 may be more difficult eg COPD rely on hypoxia to stimulate respiration

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27
Q

Assisted ventilation types

A

Invasive (facial mask) and non invasive (endotracheal tube)

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28
Q

Assisted ventilation type 2 respiratory failure

A

Inadequate PaO2 despite increasing FiO2
Increasing PaCO2
Patient tiring

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29
Q

Where to look for cyanosis

A

Under tongue

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30
Q

Oxygen treatments

A

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

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31
Q

Common causes of acute type 1 respiratory failure

A

Pneumonia
Asthma

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32
Q

Common causes of acute type 2 respiratory failure

A

Overdose
Trauma

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33
Q

Common causes of chronic type 1 respiratory failure

A

Fibrosing lung disease

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34
Q

Common causes of chronic type 2 respiratory failure

A

COPD
neuromuscular

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35
Q

Why must you be cautious giving oxygen to type 2 respiratory failure

A

Patients have a new baseline due to habituation (normal level is hypoxaemia)
Giving oxygen will get rid of drive to breathe
Also, will change V/Q ratio due to reduced hypoxia related arterial vasoconstriction

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36
Q

Ageusia

A

Loss of taste

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37
Q

What range of values for SpO2 should aim for

A

94-98%

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38
Q

Rate of oxygen delivery for face mask

A

5-10 L/min

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39
Q

Rate of oxygen delivery for nasal cannulae

A

2-6 L/min

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40
Q

Rate of oxygen delivery for reservoir mask

A

10-15 L/min

If saturation <85% and not at risk of hypercapnic respiratory failure

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41
Q

Aim for SpO2 for Patients with COPD and other risk factors for hypercapnia

A

88-92 % pending blood gases
94-98% if CO2 normal unless previous history of high CO2 or ventilation

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42
Q

Mask

A

Controlled oxygen therapy
Known FiO2

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43
Q

Nasal prongs

A

Uncontrolled oxygen delivery
More stable patients
Unknown FiO2- pockets of high FiO2 develop in nasopharynx

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44
Q

Respiratory alkalosis

A

During hyperventilation, large volume of CO2 lost—> as CO2 is acidic causes blood to become more alkaline (raising pH)
To compensate for loss of CO2, kidneys begin to secrete alkaline HCO3- into the urine in exchange for H+ ions

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45
Q

How does emphysema affect functional residual capacity

A

Increases due to reduced elastic recoil of lung tissue due to reduced elastic tissue

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46
Q

What are patients with chronic CO2 retention reliant on for control of ventilation

A

Hypoxic drive

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47
Q

Workplace causes of asthma- High molecular allergens:

A

Grain
Wood
Laboratory Animals
Fish
Latex
Enzymes

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48
Q

Workplace causes for asthma- low molecular allergens:

A

Glutaraldehyde
Isocyanates
Paints
metal working fluids
Metals
Chemicals
Sterilising agents

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49
Q

Asthma

A

common
chronic inflammatory disease of the airways characterized by

variable and recurring symptoms
reversible airflow obstruction and bronchospasm.
common symptoms include wheezing, coughing, chest tightness, and shortness of breath

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50
Q

Common symptoms of asthma

A

wheezing, coughing, chest tightness, and shortness of breath

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51
Q

Prevalence of asthma

A

5-16% of people worldwide have asthma
Wide variation between countries

Increase in prevalence second half of the 20th century
Now plateaued mostly

US study; Poorer individuals, African-Americans

Many studies identify a wide range of risk factors

Hygiene hypothesis, Berlin

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52
Q

Asthma pollens

A

Emergency attendances
Atlanta
Poaceace (grass) and Quercus (oak) species investigated
Levels associated with emergency room attendances
Oak pollens particularly important in children aged 5-17 years old

Australian thunderstorm data

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53
Q

Proportion of asthma caused by workplace environment

A

15-20%

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54
Q

Asthma infectious agents and microorganisms

A

Farm life protected the subsequent development of asthma

Early and in utero life seem to have an important role

Specific agents not identified, but likely to be a mix of bacterial and other agents, potentially altering gastrointestinal immune response

Airway bacteria may also play a role in causing asthma, role of rhinovirus

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55
Q

Asthma fungi

A

Important roles in the development of allergic illnesses

Birth cohort study
Development and severity of asthma @ 7 years
Children’s home sampling aged 8 months
24% had asthma aged 7
Associations with fungal exposure (aspergillus and penicillium) and subsequent asthma

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56
Q

Asthma pets

A

Cat ownership and exposure most implicated
Exposure at home is associated with sensitisation as judged by IgE, but;
Timing and intensity to pet exposures appear important

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57
Q

Asthma air pollution

A

Air pollution; aggravating lung diseases;
Responses to pollutants can be analogous to viral responses
Asthma hospitalisations relate to PM2.5 and PM10

Air pollution; inducing allergy less clear
Swedish birth cohort study
NO exposure in the first year of life related to pollen sensitisation at 4 years old
Increasing evidence

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58
Q

Asthma peak flow

A

Variable

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59
Q

Hypersensitivity pneumonitis

A

is an inflammation of the alveoli within the lung caused by hypersensitivity to inhaled agents

Acute, sub acute and chronic forms (fibrotic, non fibrotic)
Immune complex related disease
Antigen reacts with antibody
Normally IgG response

Very significant environmental influences; farmers lung, bird fanciers lung, metal working fluids

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60
Q

Hypersensitivity pneumonitis causes

A

Farmers lung (eg animals, mouldy straw and hay)
Bird fanciers lung
Metal working fluids
Musical instruments
Microbiological and chemical agents from the environment and work place

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61
Q

Hot tub lung

A

Hot tub use in general identified as a cause of EAA (hypersensitivity pneumonitis)
One of the first descriptions; 1997 (Kahana et al 1997)

Two recent cases of HP
Case of a 49 year old male, 2 months of fever, weight loss, shortness of breath and cough
Regular hot tub use

Sputum grew Mycobacterium fortuitum
The hot tub drain and shower drain swabs were smear positive, with cultures demonstrating M fortuitum

Re-presented with further problems 2 months later, and admitted a relapse of his ban on hot tubs

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62
Q

COPD

A

type of obstructive lung disease characterized by chronically poor airflow. It typically worsens over time, with the main symptoms include: shortness of breath, cough, and sputum production

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63
Q

COPD causes

A

Tobacco smoking main cause (contains cadmium)
Other causes include occupational exposures such as;
Silica, Coal, Grain, Cotton, Cadmium
PAH, Isocyanates, Iron/steel processing, Agricultural dust, biomass fuels, Wood dust

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64
Q

Infection

A

Lungs susceptible to infection from inhaled microbiological agents (i) bacteria [e.g. pseudomonas], viral [e.g. COVID-19]

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65
Q

Percentage of COPD caused by occupational exposures

A

10-15%

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66
Q

Which metal exposure is associated with emphysema development

A

Cadmium

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67
Q

What metal causes asthma

A

Chromium

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68
Q

Important COPD occupational exposures

A

Silica
Coal
Grain
cotton
Cadmium

69
Q

Asbestos exposure associated conditions

A

Pleural plaques
Pleural thickening
Benign pleural effusions
Asbestosis
Lung cancer
Malignant mesothelioma

70
Q

Effects of hypersensitivity pneumonitis

A

Regional variation in the lung
Inflammation of bronchioles

71
Q

Silicosis

A

Turkish denim sandblasters

72
Q

Low lung function growth trajectory due to

A

Genetics
Preterm birth
Early life environmental exposures
LRTI
Childhood persistent asthma

73
Q

Asthma and genes

A

Asthma runs in families
Children of asthmatic parents are at increased risk of asthma
Asthma is not caused by a single mutation in one gene
Transmission of the disease through generations does not follow simple Mendelian inheritance typical of classic monogenic diseases
New genotyping technologies has made it possible to sequence the human genome for asthma-associated variants

74
Q

Asthma personalised medicine

A

Individualise pharmacotherapy based on genetic polymorphisms
Certain drugs are administered only to those patients who are most likely to respond
Harmful effects are avoided in patients who are most likely to experience toxicity and adverse reactions
Candidate genes for such studies are those encoding receptor proteins and enzymes involved in drug transportation, processing, degradation and excretion.

75
Q

Cystic fibrosis

A

Chronic genetic disease
Multi-organ involvement
In UK >10,000 people affected
Median age of death improving
Most common lethal autosomal recessive genetic disorder in Caucasians
Static incidence with an increasing prevalence

76
Q

Cystic fibrosis genes

A

Defect in long arm of chromosome 7 coding for the cystic fibrosis transmembrane regulator (CFTR) protein (anion channel)

> 1600 mutations of CFTR gene identified

90% within a panel of 70 mutations

F508del most common mutation causing CF

77
Q

Proportion of carriers of cystic fibrosis

A

1:25

78
Q

CTFR protein

A

Transport protein on membrane of epithelial cells

Abnormal CFTR protein leads to dysregulated epithelial fluid transport

80% Lung and gastrointestinal involvement
15% Lung alone

79
Q

Pathophysiology - cystic fibrosis

A

Bronchitis —> bronchiectasis —>fibrosis

80
Q

Cystic fibrosis diagnosis

A

Genetic profile and neonatal screening (day 5 IRT)

Clinical symptoms – frequent infections, malabsorption, failure to thrive

Abnormal salt / chloride exchange – raised skin salt

Late diagnoses via infertility services – azoospermia or via gastroenterology team with recurrent pancreatitis / malabsorption

50% diagnosed @ 6 months
90% diagnosed @ 8 years of age

81
Q

What percentage of patients with cystic fibrosis diagnosed at 6 months

A

50%

82
Q

What percentage of patients with cystic fibrosis diagnosed at 8 years

A

90%

83
Q

CF respiratory symptoms

A

Persistent cough with productive thick mucus
Wheezing and shortness of brewth]frequent chest infections
Sinusitis
Nasal polyps

84
Q

CF digestive symptoms

A

Bowel disturbances
Weight loss
Obstructive
Constipation

85
Q

CF MSK symptoms

A

Osteoporosis
Arthritis

86
Q

Prevalence of CF

A

1 in 2500

87
Q

CF reproductive symptoms

A

95% men and 20% women are infertile

88
Q

Normal lung function growth trajectory

A

FEV1 increases to 100% as you age up until mid-20s as lungs are still growing
Lung function then plateaus and begins to decrease

89
Q

CF pathophysiology : in the pancreas

A

blockage of exocrine ducts, early activation of pancreatic enzymes, and eventual auto-destruction of the exocrine pancreas
Most patients require supplemental pancreatic enzymes

90
Q

Asthma inheritance

A

Does NOT follow Mendelian inheritance
But runs in families

91
Q

CF pathophysiology : in the intestine

A

Bulky stools can lead to intestinal blockage

92
Q

CF pathophysiology : in the respiratory system

A

mucus retention, chronic infection, and inflammation that eventually destroy lung tissue
There are multiple hypotheses regarding the pathogenesis of lung disease, each of which is supported by data in vitro and in vivo
Lung disease is the most common cause of morbidity and mortality

93
Q

Which chromosome codes for CFTR protein

A

Long arm of chromosome 7
7q

94
Q

Most common mutation causing CF

A

F508del
2 abnormal genes

95
Q

Number of CFTR gene mutations identified

A

> 1600

96
Q

Mutant CFTR channels

A

Does not move Cl-, causing sticky mucus to build up on the outside of the cell
Leads to dysregulated epithelial fluid transport

97
Q

The vicious cycle

A

Respiratory tract infection (microbial insults OR defect in host defence) —> bronchial inflammation—> respiratory tract damage —> more liable onto infection…
Progressive lung disease

98
Q

Clinical symptoms cystic fibrosis diagnosis

A

Frequent infections
Malabsorption
Failure to thrive

99
Q

Abnormal salt/chloride exchange

A

A mild electrical current pushes medicine into skin to cause sweating
Sweat is collected and salt content measured

100
Q

CF general treatment strategy

A

Maintenance and prevention management
Rescue
Personalised approaches

101
Q

CF prevention management

A

Segregation
Surveillance- frequent reviews minimum every 3 months
Airway clearance- physio and exercise
Nutrition- pancreatic enzymes, diet high calorie and fat, supplements including vitamins, percutaneous feeding
Psychosocial support

102
Q

CF geneotype classification

A

Class I: no functional CFTR protein is made (e.g. G542X)
Class II: CFTR protein is made but it is mis-folded (e.g. F508del)
Class III: CFTR protein is formed into a channel but it does not open properly (e.g. G551D)
Class IV: CFTR protein is formed into a channel but chloride ions do not cross the channel properly (e.g. R347P)
Class V: CFTR protein is not made in sufficient quantities (e.g. A455E)
Class VI: CFTR protein with decreased cell surface stability (e.g. 120del123)

More than 2000 CF - causing CFTR mutations have been found
Most common of which is F508del [a class II mutation found in up to 80% to 90% of patients]

103
Q

Classes of CF

A

Different classes of genotype abnormality for development of CTFR protein
Class I- Class VI

104
Q

CF medications

A

Suppression of chronic infections – antibiotic nebulisation
Bronchodilation – salbutamol nebulisation
Anti inflammatory – azithromycin, corticosteroids
Diabetes – insulin treatment
Vaccinations – influenza, pneumococcal, SARS CoV 2

105
Q

CF rescue antibiotics

A

2 week course IV antibiotics

Home vs hospital

Issues with frequent antibiotics
Allergies
Renal impairment
Resistance
Access problems

106
Q

Issues with frequent antibiotics

A

Allergies
Renal impairment
Resistance
Access problems

107
Q

CF personalised approaches

A

Individual tailored or targeted medicine
Move away from a ‘one size fits all’ approach
Stratified based on predicted response or risk of disease
Genetic information major factor
Monogenic disorder (i.e. is the result of mutation(s) in a specific gene)
Well-characterised pathophysiology with clear therapeutic targets
Genotype directed therapies
Targeted treatments based on infectious organisms and resistance patterns

108
Q

Ivacaftor (kalydeco)

A

CFTR potentiator- potentiates chloride secretion via increased CFTR channels opening time
Class III mutations

109
Q

Lumacaftor (orkambi)

A

CFTR corrector - corrects cellular misprocessing of CFTR (e.g. folding) to facilitate transport from the endoplasmic reticulum

Class II mutation - F508del/F508del

110
Q

CF phage therapies

A

Bacteriophage therapy is the use of lytic phases to kill infectious diseases

111
Q

Challenges treating CF

A

adherence to treatment
High treatment burden
High cost of certain treatments
Allergies/intolerances to treatment
Different infectious organisms and resistance to drugs

112
Q

Alpha-1 antitrypsin deficiency (AATD)

A

Autosomal recessive genetic disorder

80 different mutations of SERPINEA1 gene on chromosome 14

Serum antiprotease

M phenotype normal and healthy

S and Z phenotypes major disease associations

113
Q

Which gene is mutated AATD

A

SERPINEA1 gene on chromosome 14

114
Q

AATD M phenotype

A

Normal and healthy
PiMM

115
Q

AATD S and Z phenotypes

A

Major disease associations

116
Q

Consequences of AATD

A

Early onset emphysema (proteases in lung breakdown lung proteins) and bronchiectasis
Liver cirrhosis
Unopposed action of neutrophil elastase in the lung

117
Q

Flat diaphragm

A

Sign of emphysema

118
Q

Dyspnoea

A

Sense of awareness of increased respiratory effort
Inappropriate

119
Q

Orthopnoea

A

Breathless on lying down

120
Q

Tachypnoea

A

Increased respiratory rate

121
Q

Bradypnoea

A

Reduced respiratory rate

122
Q

Hyperventilation

A

Inappropriate over breathing

123
Q

Paroxysmal nocturnal dyspnoe

A

Episodes of shortness of breath

124
Q

Genetic inheritance of asthma

A

Is not caused by a single mutation (at least chromosome 2,6,9,15,17 and 22 are involved)

125
Q

Type I respiratory failure

A

• involves low oxygen, and normal or low carbon dioxide levels. (hypoxaemia (PaO2 <8 kPa / 60mmHg) with normocapnia (PaCO2 <6.0 kPa / 45mmHg))
• It usually occurs due to ventilation/perfusion (V/Q) mismatch –the volume of air flowing in and out of the lungs is not matched with the flow of blood to the lung tissue
• As a result of the ventilation/perfusion mismatch, PaO2 falls, and PaCO2 rises. The rise in PaCO2 rapidly triggers an increase in a patient’s overall alveolar ventilation, which corrects the PaCO2 but not the PaO2 due to the different shapes of the CO2 and O2 dissociation curves.

126
Q

Entire lung failure…

A

Type II respiratory failure

127
Q

COPD and type II respiratory failure

A

COPD causes habituation of high PaCO2
Begin to rely on low PaO2 for drive to breathe

128
Q

What causes the drive to breathe

A

PaCO2
Small changes causes difference as very sensitive

129
Q

Type II respiratory failure flow diagram

A

Hypoventilation —> increase PCO2 (acidic) —> increase H2CO3 —> decrease pH
Respiratory acidosis

130
Q

Acute phase of type II respiratory failure

A

CO2 moving into RBCs combines with H2O- carbonic anhydride converts to H2CO3 which dissociates into HCO3 -

131
Q

Chronic phase of type II respiratory failure

A

Renal:
Increased HCO3 - reabsorption
Increased H+ excretion in ammonia (NH3+ -> NH4)

132
Q

Causes of decreased pH (metabolic acidosis)

A

Renal failure
GI HCO3 - loss eg cholera
Diabetic ketoacidosis
Dilution of blood with H2O
Failed H+ excretion (hypoalosteronism)

133
Q

Metabolic acidosis pathway

A

Decreased pH—> chemoreceptors increase respiratory rate —> decreases PCO2 —> decreases H2CO3

134
Q

Causes of increased pH (metabolic alkalosis)

A

Vomiting (HCL loss)
Alkali ingestion
Renal acid loss: hyperaldosteronism, hyperkalaemia

135
Q

Metabolic alkalosis pathway

A

Increased pH —> chemoreceptor inhibition —> decrease’s respiratory rate- hypoventilation—> increases PCO2 —> decreases pH

136
Q

Type I respiratory failure flow diagram

A

Hyperventilation—> decreases PCO2 (acidic) —> decreases H2CO3 —> increases pH
Respiratory alkalosis

137
Q

Chronic type I respiratory failure

A

Renal:
Decreased HCO3 - reabsorption
Decreased H+ excretion

138
Q

Gaseous diffusion impairment

A

Pulmonary oedema

139
Q

Blood diffusion impairment

A

Anaemia

140
Q

Membrane diffusion impairment

A

Interstitial fibrosis

141
Q

Complete airway blockage

A

Shunt
V/Q= 0

142
Q

Partial airway blockage

A

Decreased V/Q
Local hypoxia

143
Q

Complete blood blockage

A

V/Q = infinty

144
Q

Partial blood blockage

A

Increased V/Q

145
Q

What is V/Q mismatch counteracted by

A

Local Bronchoconstriction
Hypoxic pulmonary vasoconstriction (weak-little muscle) diverts blood to better-oxygenated lung segments

146
Q

FeNO (fractional expired nitric oxide)

A

Marker of eosinophilic airway inflammation
>50 ppb

147
Q

Chronic bronchitis

A

Inflammation
Increased mucus

148
Q

Emphysema

A

Decreased lung surface area
Destruction of alveoli and capillaries
Decreased elastic recoil
Distended thorax (barrel chest)

149
Q

Class 2 CF

A

Misfolded CFTR
Eg F508del (most common)

150
Q

Class 3 CF

A

CFTR channel doesn’t open properly

151
Q

Treatment of AATD

A

Antiproteases inhibit neutrophil elastase from damaging elastin

152
Q

which is the most clinical significant form of alpha 1 anti trypsin deficiency

A

PiZZ

153
Q

A 67 year old patient is being investigated for shortness of breath.

Which of the following conditions would normally lead to Type 2 Respiratory Failure?

A

Increased airways resistance - chronic obstructive pulmonary disease

Reduced breathing effort (drug effects, brain stem lesion, extreme obesity)

A decrease in the area of the lung available for gas exchange (such as in chronic bronchitis)

Neuromuscular problems

154
Q

70 year old has an X-ray to investigate their shortness of breath. It reveals a suspicious lesion associated with the pleura.

What is the term used to describe a malignant tumour of the pleural membranes?

A

Mesothelioma

155
Q

An 83 year old patient is admitted with shortness of breath and is diagnosed with Type 1 respiratory failure.

Which of the following arterial blood gas results characterizes Type 1 Respiratory Failure?

A

low pO2, normal/low pCO2

156
Q

A 67 year old patient is being investigated for shortness of breath.

Which of the following arterial blood gas results is typical of chronic Type 2 Respiratory Failure?

A

low pO2, high pCO2, normal-high HCO3-

157
Q

type 1 respiratory failure is caused by conditions that affect oxygenation such as:

A

Low ambient oxygen (e.g. at high altitude)

Ventilation-perfusion mismatch (parts of the lung receive oxygen but not enough blood to absorb it, e.g. pulmonary embolism)

Alveolar hypoventilation due to reduced respiratory muscle activity, e.g. in acute neuromuscular disease (this form can also cause type 2 respiratory failure if severe)

Diffusion problem (oxygen cannot enter the capillaries due to parenchymal disease, e.g. in pneumonia)

Shunt (oxygenated blood mixes with non-oxygenated blood from the venous system, e.g. right to left shunt)

158
Q

A 5 year old is scheduled for theatre to remove an inhaled peanut.

Where is the inhaled peanut most likely to become lodged in their airway?

A

Right main bronchus

159
Q

In chronic hypercapnia, which pathway controls respiratory drive

A

Chemoreceptors in the carotid bodies detect low blood oxygen and send signals via cranial nerves to the dorsal respiratory group.
Motor output is sent via the phrenic nerve to stimulate contraction of the diaphragm and increase respiratory rate

160
Q

Chronic hypercapnia and respiratory drive

A

Central chemoreceptors in dorsal medulla less able to respond to carbon dioxide levels
Body becomes reliant on peripheral chemoreceptors and hypoxic drive

161
Q

Respiratory acidosis blood gases

A

PaO2 <8 KPa
PaCO2 > 6KPa

162
Q

What is the effect of a marked increase in pulmonary capillary pressure in lung compliance

A

Decrease in compliance as pulmonary oedema occurs

163
Q

How does emphysema affect lung compliance

A

Increases due to loss of elastic tissue

164
Q

How does pulmonary fibrosis affect lung compliance

A

Decrease

165
Q

Flapping tremor/ asterixis

A

Sign of CO2 retention - type 2 respiratory failure

166
Q

Shallow breathing leads to

A

Respiratory acidosis

167
Q

Hyperventilating leads to

A

Respiratory alkalosis

168
Q

Joe is a 50 year old man who has just returned to Blackburn after living in Thailand for a year. Over the next few days he notices that he’s finding it more difficult to breathe, and that when he does he feels a sharp pain. He goes to his GP who diagnoses him with a pulmonary embolism. What is the main kind of hypoxia that a pulmonary embolism would cause

A

V/Q mismatch

CVR (22 decks)

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