Resp Flashcards
Whats Dyspnoea?
Shortness of breath
What could the presenting complaint be in a respiratory examination?
Dyspnoea
Wheeze
Haemoptysis
Chest pain
Sputum
Cough
Whats used to grade breathlessness?
The MRC Dyspnoea Score
Grades of the MRC dyspnoea score:
- No breathlessness unless on strenuous exertion
- SoB when hurrying or walking up a slight hill
- Walks slower than others due to SoB on flat level, or has to stop for breath when walking at own pace
- Stops for breath after walking 100m or after a few minutes on level ground
- Too breathless to leave the house, or breathless when dressing or undressing
Whats Forced vital capacity (FVC)?
The volume of air that can be forcibly expelled from the lungs from a position of maximal inspiration.
Whats vital capacity?
Volume of air that can be expired from the lungs from a maximal inspiration using a relaxed/slow manoeuvre
Forced expired volume (FEV1)?
Following a maximal inspiration - The Volume of air forcibly expelled from the lungs in the first second.
FEV1/FVC
Volume of air forcibly expired in the first second as a percentage of the total volume exhaled.
What does a Restrictive volume time plot look like?
What does a Obstructive volume time plot look like?
What would the flow volume loop look like for:
- Normal
- Early small airways obstruction
- Chronic obstructive disease
- Fixed large airway obstruction
- Variable extrathoracic large airway obstruction
- Restrictive disease
Whats an obstructive lung disease briefly?
Difficulty with expiring air. FEV1 is reduced. (typically FVC is the same)
Examples of obstructive lung diseases?
COPD, asthma
Whats a restrictive lung disease briefly?
Cause problems by restricting a person’s ability to inhale (enough) air. FVC is decreased. (FEV1 can be reduced though proportionately).
Examples of restrictive lung disease:
Interstital lung disease, Myasthenia gravis
Pathophysiology of restrictive lung diseases
Occurs if lungs become too stiff or if inspiratory effort is compromised by muscle weakness/ injury/ deformity (or both)
Pathophysiology of obstructive lung conditions
Its all to do with resistance.
During expiration the small airways are compressed. This increases flow resistance, hence helping to reach a point where no more air can be driven out of the alveoli.
In COPD there is greater airway narrowing than normal, thus greater outflow resistance, thus expiratory outflow is compromised much earlier. Hence expiratory outflow is not satisfactory.
In asthma, the already narrowed airways (due to mucosal inflammation and smooth muscle hypertrophy) are further constricted due to increased smooth muscle tone. This causes resistance to airflow to become very high. This means the patient must work harder to overcome the increased resistance. This can lead to turbulent flow, causing the characteristic wheeze of an asthma attack.
COPD involves a balance between which two diseases?
Emphysema and chronic bronchitis.
Pathophysiology of emphysema
-Elastin breakdown and hence loss of alveolar integrity. Leading to destructive enlargement of airspaces distal to the terminal bronchioles.
-Also, the small bronchioles are narrowed due to the loss of elastic fibres in the surrounding alveoli. These fibres exert an outward pull on the small bronchioles and keep them open (radial traction). These airways can also therefore collapse when pressure increases e.g. during expiration (as they have no cartilage and reduced radial traction)
-Loss of elastic recoil, gain in compliance. Lungs are hyperinflated.
Pathology of Chronic Bronchitis
Excessive mucous secretions and impaired removal of the secretions (ciliary dysfunction)
How does Chronic Bronchitis lead to increased airway resistance
luminal obstruction of airways by secretions.
2 ways that airway resistance is increased by COPD
1) luminal obstruction of airways by secretions.
2) small bronchioles are narrowed due to the loss of elastic fibres exerting an outward pull (radial traction) on the small bronchioles.
In an Obstructive defect what happens to the FVC, FEV1, FEV1/FVC ratio?
- FEV1 is reduced
- FVC nearly normal (worsens as disease progresses, thus increasing residual volume at the cost of FVC)
- FEV1/FVC is <0.7
In a restrictive defect what happens to FVC, FEV1, FEV1/FVC ratio?
FVC is reduced
FEV1 is reduced proportionately
FEV1/FVC ratio is normal = greater than or equal to 0.7
Whats Hypoxia?
Deficiency of oxygen in the tissues
(correlates with low PaO2 I guess)
low PaO2 = hypoxemia
4 causes of low PaO2:
1) Hypoventilation
2) Diffusion impairment
3) Shunt
4) V/Q mismatch
pH ∝ ?
pH ∝ [HCO3-]/[(pCO2*0.23)]
CO2 + H2O ⇌ H+ + HCO3-
CO2 + H2O ⇌ H+ + HCO3-
Normal ratio of HCO3- to CO2? (this is to maintain normal blood pH!)
[HCO3-] : [CO2]
20:1
Normal ratio of HCO3- to CO2? (this is to maintain normal blood pH!)
[HCO3-] : [CO2]
20:1
Flow =
Flow = ΔP/R
Pathophysiology of COPD
(is an airflow limitation problem that is not fully reversible)
Lots… Main two:
1) Changes leading to increased airway resistance (especially on expiration, as pressure increases try to narrow the smaller airways). - luminal obstruction of airways by secretions. -Small bronchioles narrowing due to loss of radial traction.
Overall, meaning that expiratory flow is compromised much earlier in expiration. Hence expiratory outflow is not satisfactory
2) Decreased elastic recoil
This leads to:
-reduced expiratory force (flattens diaphragm)
-hyperinflation of the lungs
Overall both lead to expiratory flow limitation, therefore promoting air trapping in the lungs. This leads to “old” and “new” air mixing in the lungs.
https://pubmed.ncbi.nlm.nih.gov/15325838/
The poor airflow seen in COPD is due to emphysema or the small airways disease?
Both
https://en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_disease#cite_note-Robbins1-87
My notes:
Obstructive is basically an airflow problem (airway obstruction)
Restrictive is basically a reduced volumes problem
My notes:
Obstructive is basically an airflow problem (airway obstruction)
Restrictive is basically a reduced volumes problem
What measure is useful when analysing the cause of a metabolic acidosis?
Anion Gap
Anion gap equation:
Anion gap = Na+ - (Cl- + HCO3-)
Normal anion gap is…
8-12
High anion gap metabolic acidosis is due to increased acid or decreased acid?
Increased acid (reacts with HCO3- and the anion of the acid replaces HCO3-)
Normal anion gap metabolic acidosis is due to decreased HCO3- or increased acid?
HCO3- will be decreased (losses often). Cl- will rise to maintain the anion gap
A-a gradient why is it useful?
Is a measure of the difference between the alveolar concentration (A) of oxygen and the arterial (a) concentration of oxygen. It is an useful parameter for narrowing the differential diagnosis of hypoxemia. If increased ∴ problem with the lungs!
A-a gradient equation?
PAO2 - PaO2
A=alveolar a=arterial
How to work out PAO2?
PAO2=PIO2 - PaCO2/0.8
Type 1 vs type 2 respiratory failure
Type 1 respiratory failure involves hypoxaemia (PaO2 <8 kPa / 60mmHg) with normocapnia (PaCO2 <6.0 kPa / 45mmHg).
Type 2 respiratory failure involves hypoxaemia (PaO2 <8 kPa / 60mmHg) with hypercapnia (PaCO2 >6.0 kPa / 45mmHg).
20:1
As calculated by the Henderson–Hasselbalch equation, in order to maintain a normal pH of 7.4 in the blood (whereby the pKa of carbonic acid is 6.1 at physiological temperature), a 20:1 ratio of bicarbonate to carbonic acid (assumed to be CO2) must constantly be maintained; this homeostasis is mainly mediated by pH sensors in the medulla oblongata of the brain and probably in the kidneys, linked via negative feedback loops to effectors in the respiratory and renal systems.
https://en.wikipedia.org/wiki/Bicarbonate_buffer_system
Normal A-a gradient values?
Less than 2kPa in young people
Less than 4 kPa in old people.
Greater then 4 kPa implies lung pathology
When is airflow most impeded in asthma and COPD? Inspiration or Expiration?
**Expiration! **
during expiration theres a rise in intrathoracic pressure, this causes increased pressure on the narrowed airways further narrowing them
Dead space
Ventilation, no perfusion
Which causes of Hypoxemia cause a deranged (increased) A-a gradient?
1)diffusional impairment
2)Shunt e.g. pneumonia
3) V/Q mismatch e.g. PE
interestingly asthma mechanism is initially by V/Q mismatch, but I’m unsure if A-a gradient should be used in the case of asthma (I don’t understand how asthma causes A-a gradient increase) *see in obsessions notes
Which cause of hypoxemia causes a normal A-a gradient?
1) Hypoventilation
2) High altitudes (low Po2 in air)
Whats a respiratory shunt?
Continuing to perfuse an unventilated alveolus
How severe is the asthma exacerbation/ attack criteria?
Mild: - No features of severe asthma - PEFR >75%
Moderate: - No features of severe asthma - PEFR =50-75%
Severe: Any one of: - PEFR =33%-50%, - cannot complete sentences in one breath, - RR > 25, - HR >110
Life threatening: Any one of: - PEFR <33%, - Sats <92% or ABG pO2<8kPa, - cyanosis, poor respiratory effort, near or fully silent chest
Near Fatal: Raised pCO2
Management of Asthma in secondary care:
1)ABCDE
2)Aim for SpO2 of 94-98% can use oxygen too. If SpO2 is <92% therefore order ABG
3) 5mg nebulised Salbutamol (can repeat every 15mins)
4) PO 40mg Prednisolone STAT (give IV Hydrocortisone if PO not possible)
Management of severe asthma:
Management of Asthma in secondary care card
+
1) Nebulised Ipratropium Bromide 500 micrograms
2) Consider Salbutamol back to back
Management of life threatening asthma:
Management of Asthma in secondary care card
+
1) Urgent ITU or anaesthetist assessment
2) Urgent portable CXR
3) IV Aminophylline
4) Consider IV Salbutamol if nebulised route is ineffective
Mechanism of Anaphylaxis, Angioedema:
Type 1 hypersensitivty reaction
Sensitized individual exposed to specific antigen
IgE bound to mast cells and basophils
When antigen binds to IgE causes release of histamine from mast cells
Causes symptoms
Symptoms of anaphylaxis
Airways → Stridor, broncial obstruction, wheeze, chest tightness. (from bronchospasm)
Pruritus, urticaria, angioedema, hoarseness
Management of Anaphylaxis
Are COPD exacerbations always infective?
No could be due to seasonal variation, re exposure to smoking, ect
What makes you think that the COPD exacerbation is infective in nature?
Fever
Increase in sputum volume
Sputum colour change
Increased WCC +/- CRP
COPD exacerbation in secondary care management?
Diagnosis of Pneumonia in secondary care?
Consolidation on CXR with fever +/- purulent sputum +/- raised WCC and/or CRP
check this
Whats Sepsis?
Life threatening organ dysfunction caused by an overwhelming, systemic host response to an infection
Features of Sepsis:
Poor EWS and/or SEPSIS RED Flags
Sepsis six managment?
Management of Pneumonia in secondary care?
1) ABCDE
2) If features of sepsis, treat using sepsis pathway
3) Otherwise treat with antibiotics as per hospital guidelines and CURB 65.
4) Be aware of drug allergies when prescribing
5) Use CURB 65 to determine where patient should be
5) Also give anti pyretics (paracetamol), analgesia, good fluid intake
CURB 65 criteria?
C – new-onset confusion
U – Urea >7mmol/L
R – Respiratory rate >30 breaths per minute
B – Blood pressure <90mmHg systolic or <60mmHg diastolic
65 – Age ≥65
What do the scores of the CURB 65 mean?
A score of 0 or 1 with signs and symptoms typical of pneumonia warrants antibiotics in the community according to clinical judgement. Any patient with a score of 2 or more should be admitted to hospital, and a patient with a score of 4 or 5 may require treatment in intensive care.
Patient has Massive Haemoptysis, how would you manage this?
Bohr effect?
Describes how the O2 dissociation curve is influenced by PCO2
Increase pCO2, rightward shift, increase O2 unloading
Bohr effect?
Increase in CO2 in the blood causes O2 to be displaced from the hemoglobin (the Bohr effect)
Haldane effect?
Binding of O2 with hemoglobin tends to displace CO2
from the blood.
Haldane effect?
Describes how the CO2 dissociation curve is influenced by pO2
Increase in pO2 causes decrease in CO2 content in blood for a relative pCO2
(High pO2 reduces haemoglobin affinity for CO2)
What are the three forms of CO2 in blood?
1) Dissolved
2) CO2 reacts with water to form HCO3- (+H+)
3) CO2 reacts with haemoglobin to from Carbamino-haemoglobin compound
ECG changes in PE?
S1Q3T3
Lead I s wave
Lead III Q wave
Lead III inverted T wave
or
None
or Sinus tachycardia
Youngs syndrome triad?
Sinusitis
Bronchiectasis
Reduced male fertility
Muscles of inspiration, expiration and accessory muscles
Does myoglobin have a higher or lower affinity for oxygen than haemoglobin?
Higher.
Myoglobin function?
Store of oxygen for cardiac and skeletal muscle. At low partial pressures of oxygen it will provide additional oxygen to the respiring/working muscle.
Signs of a tension pneumothorax:
Hypotension
Tachycardia
Deviation of trachea away from the side of the pneumothorax
Mediastinal shift away from pneumothorax
In tension pneumothorax cXr or chest drain first?
Chest drain!
Management of tension pneumothorax?
Large bore intravenous cannula into 2nd ICS MCL
Chest drain into the affected side
PE is difficult to diagnose. But what can be the symptoms?
What are the 6 major risk factors for acquiring a PE?
Development of PE, relates to what triad?
Virchow’s Triad
Sometimes a PE may be unprovoked (i.e. no risk factors), in which case, what conditions would you consider?
Underlying malignancy
Thrombophilia
SLE
Polycythaemia
Management of PE?
Whats a CTPA?
CT pulmonary angiogram often used to diagnose a PE
Whats a Well’s score used for?
Clinical probability score for a DVT
Thromobolysis in used in certain situations (for example in a Massive PE), however what are the contraindications to thrombolysis?
Absolute thrombolysis contraindications?
Relative thrombolysis contraindications?
Management of Massive PE?
Numbers correlate to order
page 819 oxford medical handbook
