Mithra fy1 ASTHMA AND COPD Objectives Differentiate severity of acute asthma exacerbations Pathophysiology of Asthma and COPD Discuss CXR and ABG Type 1 vs Type 2 respiratory failure ID: 235302
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Slide1
Dr sanjena Mithra, fy1
ASTHMA AND COPDSlide2
ObjectivesDifferentiate severity of acute asthma exacerbations
Pathophysiology
of Asthma and COPD
Discuss CXR and ABG
Type 1
vs
Type 2 respiratory failureSlide3
5 mins
–
pretest
10
mins
– case 1
10
mins
– case 2
5
mins
– end of session test
feedbackSlide4
PretestDefine asthma
What constitutes COPD?
Briefly outline the
pathophysiology
of asthma
Describe 4 differences in the airways of acute and chronic asthmatics.
How can you categorise severity of acute asthma attacks?
List 4 classes of drug used to treat Asthma/COPD
What are their mechanisms of action and side effects?
How can you determine severity of COPD?
Compare type 1 and type 2 respiratory failureSlide5
Take a history from this patient who is short of breath…
Cough +/- sputum
Chest pain (
pleuritic
)
Wheeze
SMOKING
Allergies, Pets
Foreign travel
History of DVT, PE*Compliance with meds*Weight lossHaemoptysis
Atopy
Family history
Exercise tolerance
Diurnal
variation
Complications:
Oedema
SOBOE
Recurrent infections
FeverSlide6
CASE 1- Summary
28 year old lady presents to A&E after becoming short of breath whilst visiting friends. She was feeling well during the day and had been to work. Non-smoker
PMH: Asthma since childhood –
Salbutamol
PRN
Inhaler currently not relieving symptoms; SOB worse over last 2 hours. Chest starting to feel tight, she is getting lightheaded.
On examination:
T 36.2 BP 124/71 HR 90 RR26 96%
sats
on airAlert, talking in full sentences but distressed. CVS and Abdo – NADResp – widespread wheeze, no crackles, no friction rubSlide7
What are your differentials for this patient and why?
Acute asthma exacerbation (non-life threatening)
PE
Inhaled foreign body
Allergic reaction
Anxiety
Pathophysiology
Define asthma
4 characteristics of acute and chronic asthmaSlide8
Asthma
ASTHMA –
chronic, inflammatory disease of the airways resulting in variable, often reversible airflow obstruction and airway
hyperresponsiveness
.
Acute asthma airway changes
-
Airway constriction,
microvascular
leakage / oedema, vasodilation, mucus hypersecretionIgE mediated inflammatory response. Cross-linking of IgE
results in
degranulation
of mast cells, histamine release and inflammatory cell infiltration
Chronic asthma
airway changes
– airway remodellingSubepithelial fibrosis, smooth muscle hyperplasia / hypertrophy, goblet cell hyperplasia, new vessel formationSlide9
Investigations
What investigations would you like to do?
Bedside:
Peak flow – 45% of best
Bloods:
ABG
, FBC, U&E, CRP
Imaging: CXR
ABG:
pH 7.46pCO2 4.1pO2 10.3HCO3 26
Respiratory Acidosis
Respiratory Alkalosis
Metabolic Acidosis
Metabolic Alkalosis
pH
↓
pH
↑
pH
↓
pH
↑
Primary problem:
pCO2
↑
Primary problem:
pCO2
↑
Primary problem:
HCO3
↓
Primary problem:
HCO3
↑
Compensation:
HCO3
↑
Compensation
HCO3
↓
Compensation:
pCO2
↓
Compensation:
pCO2
↑Slide10
Reading Chest X-RaysRIP...ABCDE
Adequacy:
Rotation
(symmetry of clavicles)
Inspiration
(ribs)
Penetration
(vertebral bodies)
Mention central lines, NG tubes, pacemakers etc
Airway:
is the trachea central?
Boundaries and Both lungs:
lung borders, consolidation, hazy etc
Cardiac:
Heart size
Diaphragm
Everything else:
soft tissue mass, fracturesSlide11
What investigations would you like to do?
Bedside:
Peak flow – 45% of best
Bloods:
ABG
, FBC, U&E, CRP
Imaging: CXR
Allergic
bronchopulmonary
aspergillosis
: refractory asthma with fever, cough and sputum.
Eosinophilia
and raised
IgESlide12
Acute severe asthmaHow would you like to manage this patient?
Immediate
A to E
Salbutamol
5mg via oxygen driven nebuliser
Repeat
obs
(SpO2, HR, RR) and PEF to assess for progression of severity and risk to life
If clinically stable and PEF >75%, can repeat
Salbutamol nebs and consider oral prednisolone 40-50mgSlide13
Moderate
PEF >50-75%
SpO2 >92%
No features of severe
Acute Severe
PEF 33-50%
RR >25
SpO2 >92%
HR >110
Cannot complete sentences
Life threatening
33-92-CHEST
PEF <33%
SpO
2
<92%
Cyanosis/Confusion, Hypotension, Exhaustion, Silent chest, Tachycardia
Senior help (ITU, anaesthetics)
O SHIT!
O2 to maintain
sats
94-98%
Salbutamol
5mg via O2 driven nebs
Hydrocortisone IV/oral
prednisolone
Ipratropium
via O2 driven nebs
Consider Magnesium Sulphate IV
ABG, CXR
Salbutamol
4 puffs, then 2 puffs every 2
mins
Salbutamol
5mg via O2 driven nebuliser
If life threatening features present
Repeat
salbutamol
nebs, give oral
prednisolone
40-50mgSlide14
Long term managementLong term
Conservative: Follow up by GP, check inhaler technique, refer to chest clinic/asthma liaison nurse
Medical: If PEF <50% on admission, can consider
prednisolone
, adequate inhaler supply
Stepwise treatment of asthmaSlide15
CommunicationPlease explain to Mr X how to correctly use his inhaler
Check understanding
If you haven’t used it for a while, spray in the air to check it works
Shake it
As you breathe in, simultaneously press down on the inhaler
Continue to breathe deeply
Hold your breath for 10 seconds or as long as you comfortably can, before breathing out slowly.
If you need to take another puff, wait for 30 seconds, shake your inhaler again then repeat
Advise on using a spacerSlide16
Chronic Management of AsthmaSlide17
Case 2 – Summary
A 64 year old gentleman presents to A&E with increasing SOB over the last 3 days. This is associated with a cough productive of thick, green sputum.
Gets SOB normally after about 5-10
mins
walking on the flat
PMH: “asthma”
SH: 50 cigarettes a day for the past 40 years.
On examination he is alert but visibly SOB
T 37.7 RR 25 HR 110 O2
sats 89% on air, you notice he is using his accessory muscles to breathe. Resp: hyperinflated chest, diffuse coarse crepitations
, widespread wheeze, reduced air entry bilaterally
CVS: JVP raised, ankle oedema (non-pitting)
Abdo
SNTSlide18
Case 2Slide19
What are your differentials for this patient and why?
Acute infective exacerbation of COPD
Pneumonia
Cor
pulmonale
Bronchiectasis
Pathophysiology
Define COPD clinically
Histopathology?Pathophysiology?Slide20
Definitions
COPD
: Umbrella term encompassing chronic bronchitis (chronic cough and sputum production on most days for at least 3 months per year for 2 years) and emphysema (pathological diagnosis of permanent destructive enlargement of distal air spaces)
Chronic bronchitis
: airway narrowing due to bronchiole inflammation, mucosal oedema and mucus
hypersecretion
Emphysema
: Destruction and enlargement of alveoli that reduces elastic recoil and results in
bullae
.Slide21
Investigations
What investigations would you like to do?
Bedside: ECG, sputum culture
Bloods:
ABG
, FBC, U&E, CRP, blood cultures
Imaging: CXR
Special tests: ECHO,
α
1-antitrypsin levelsABG: assess the oxygenationChecking for respiratory failure- failure to fully oxygenate the blood passing through the lungs giving rise to hypoxia +/- hypercapnea.Slide22
ABG
pH 7.29
pCO2 6.8
pO2 7.9
HCO3 25Slide23
Respiratory failureType 1- hypoxia with low or normal pCO2 – anything that
impairs gas exchange
Atelectasis
, pulmonary oedema, pneumonia,
pneumothorax
Type 2 – hypoxia with hypercapnea –
alveolar hypoventilation
Same causes for a respiratory acidosis
COPD, neuromuscular disorders (GBS, MND), CNS depression (drugs, brainstem injuries) Slide24
Initial management – infective exacerbation of COPD
How would you like to manage this patient?
Immediate
A to E
Maintain
sats
88-92% (titrate to ABG)
Corticosteroids (oral/IV)
Empirical antibiotics
Salbutamol 5mg and Ipratropium via O2 driven nebulisersConsider need for NIV – if desaturating/decompensating
Admit, chest physiotherapySlide25
Flow volume loops - SpirometrySlide26
FEV1/FVCDetermines the severity of COPD
Describes the proportion of a person’s vital capacity (maximum air expelled after maximum inhalation) that can be expired in the first second.
Normal ~ 70%
Mild 50-70%
Moderate 30-50%
Severe <30%Slide27
Management Long term
Conservative – smoking cessation, pulmonary rehabilitation, flu vaccination,
Spirometry
Medical – LTOT (
only if not smoking
), bronchodilators, steroids (can consider if more than 2 infective exacerbations/year), prophylactic antibiotics
Surgical – Transplant,
lobectomy
,
bullectomyLTOT criteriaPaO2 <7.3 kPa on air during period of clinical stabilityPaO2 7.3-8.0
kPa
and signs of secondary
polycythaemia
, nocturnal
hypoxaemia
, peripheral oedema or pulmonary hypertensionSlide28
Drugs 1Bronchodilators:
Beta-2 agonists – Short acting/Long acting (Salbutamol/
Salmeterol
)
MOA: increases
cAMP
production in the lung which decreases calcium concentration
Effect: Smooth muscle relaxation, bronchial dilatation
S/e: tachycardia, sweating, tremor
Anticholinergics:Ipratropium (Atrovent), Tiotropium (Spiriva
)
MOA: Anti-
muscarinic
.
Ipratropium
is non-selective,
Tiotropium is selective (M3)s/e: dry mouth, sedation, skin flushing, tachycardiaSlide29
Drugs 2
Methyxanthines
Theophylline
,
Aminophylline
MOA:
Phosphodiesterase
antagonists – raise intracellular
cAMP
levels. Works well with beta-2 agonistss/e: narrow therapeutic windowLeukotriene receptor antagonists Montelukast,
Zafirlukast
s/e: GI upset, drowsiness
Corticosteroids
Prednisolone,
Beclamethosone
MOA:
upregulates intracellular proteins after binding with receptor and causes expression of anti-inflammatory agentss/e: weight gain, immunosuppression, skin thinning, bruising, osteoporosis, cataractsSlide30
PretestDefine asthma
What constitutes COPD?
Briefly outline the
pathophysiology
of asthma
Describe 4 differences in the airways of acute and chronic asthmatics.
How can you categorise severity of acute asthma attacks?
List 4 classes of drug used to treat Asthma/COPD
What are their mechanisms of action?
How can you determine severity of COPD?Compare type 1 and type 2 respiratory failureSlide31
Take home message33-92 CHEST
Focussed history taking: Symptoms, red flags, complications
Structure your answers
Questions?