ACT Respiratory Flashcards by Euan Mckeating

Describe panic hyperventilation

Stress and anxiety causes a heightened awareness of breathing and hyperventilation. Hypocapnia causes a rise in blood pH, increasing the binding of Calcium to albumin. The reduction in ionised calcium causes the symptoms: numbness, tingling, tinnitus, muscle excitability.
If severe, LOC can be caused by hypocapnia induced vasoconstriction of cerebral vasculature

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Assessment and investigation of hyperventilation

ABG if concerned - respiratory alkalosis
CXR - normal
Bloods - FBC ?anaemia, TFT ?hyperthyroid

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Management of hyperventilation

Educate that symptoms of tingling/numbness are harmless
Breathing into a bag is no longer recommended
Placing palms (usually cold) to the cheeks can suppress breathing impulse (divers reflex)
If required – sedation with diazepam

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What signs define a moderate asthma attack:

Peak flow >50% normal
Increasing symptoms but
No features of severe asthma

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What signs define a severe asthma attack:

Peak Expiratory flow rate of 33-50% of predicted or best
RR 25 or more
HR 110 or more
Inability to complete sentences in one breath

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What signs define a life threatening asthma attack

Peak Expiratory flow of < 33% of predicted or best
02 sats < 92%
Silent chest, Cyanosis
Hypotension, Arhythmia 
Exhaustion, Confusion, Coma 
ABG - p02 = < 8kPa
- normal C02

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What defines a near fatal asthma attack

PaCO2 > 6.0 kPa (Normal Range 4.5 – 6kPa)

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Management of acute asthma attack

Oxygen - aim sats 94-98%
Salbutamol 5mg nebulised oxygen driven
Prednisolone 40mg for 5 days
Ipratropium bromide 500micrograms 4-6hrly
Senior help - consider ITU admission
Magnesium 1.2-2g IV infusion over 20mins

Check inhaler technique
Follow-up within 48 hours of presentation, if not admitted to hospital.
Follow-up all people admitted to hospital within 2 working days of discharge.
Follow up by Respiratory for at least 1 year if severe
Or for the rest of their life if near fatal attack

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What are the indications for intensive care referral in acute asthma attack

Refer any patient:
1. Requiring ventilatory support
2. Acute severe or life-threatening asthma, who
is failing to respond to therapy, as evidenced by:
- deteriorating PEF
- persisting or worsening hypoxia
- hypercapnia
- ABG analysis showing acidosis
- exhaustion, feeble respiration
- drowsiness, confusion, altered conscious state
- respiratory arrest.

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When should patients with acute asthma attacks be admitted

Admit all patients with any feature of a life-threatening or near-fatal asthma attack.

Admit patients with any feature of a severe asthma attack persisting after initial treatment.

Patients whose peak flow is greater than 75% best or predicted one hour after initial treatment may be discharged from ED, unless there are other reasons why admission may be appropriate.

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What are the colours of venturi mask in order and what percentage oxygen to they deliver

Blue = 24%  2-4L
White = 28% 4-6L
Yellow = 35%  8-10L
Red = 40%  10-12L
Green = 60% 12-15L

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Medical management of stable asthma

SABA for all - step up if used 3+ times a week

1st: low dose ICS
2nd: LABA + low dose ICS
3rd: stop or continue LABA depending on response and
- consider medium dose of ICS
- or trial of other therapy: TRA, S-R theophylline, LAMA
4th: Refer to specialist and consider
- High dose ICS
- or adding fourth drug

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Non pharmacological management of asthma

Patient education 
Written personalised self management plan
Avoidance of triggers
Smoking cessation 
Weight loss if overweight
Breathing exercise programs

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Description of asthma

More than one of: ‘wheeze, breathlessness, chest tightness, cough’ with variable airflow obstruction.

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Aetiology of asthma

Extrinsic - Dust mites, pollen, chemicals
Atopy - circulating IgE in the blood
Hygiene hypothesis

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Description of Chronic Obstructive Pulmonary Disorder

Airflow obstruction that is not fully reversible and is both progressive and associated with inflammation in response to noxious particles or gasses.
Combines emphysema, where there is widening of distal airspaces and destruction of alveolar walls, and chronic bronchitis, where there is increased number of mucus secreting goblet cells and infiltration of bronchial walls with inflammatory cells.
This leads to scarring and thickening of the walls and poorer gas exchange.

Aetiology of COPD

Long term exposure to toxic particles
SMOKING - 20 per day = 30 x risk
Urban population
Age > 35

Management of stable COPD

Patient education
Personalised written self management plan
Smoking cessation - nicotine, varenicline or bupropion
Pneumococcal + annual influenza vaccine
Manage comorbidities
Pulmonary rehabilitation + Chest physiotherapy

Inhaled therapies - ensure good technique
All get SABA or SAMA when needed
Asthmatic features: 1st LABA + ICS. 2nd + LABA
No asthmatic: 1st LABA + LAMA
Consider spacer or nebulisers
Mucolytics for chronic productive cough
Oral theophylline - only after failed inhaled or can’t inhale
- requires monitoring, many interactions, caution elderly
Rescue pack for exacerbations

Management of acute exacerbation of COPD

Target sats depend on if CO2 retainer or not
Titrate Oxygen therapy - Blue or White Venturi to start
Salbutamol 5mg nebulised back to back if needed
Ipratropium bromide 500mcg nebulised 4-6hrly
Prednisolone 30mg for 7-14 day
ABx if purulent sputum or clinical signs of pneumonia
1st: Amoxicillin 500mg TDS for 5 days
or Clarithromycin 500mg BD for 5 days
or Doxycycline 200mg first day, 100mg OD till 5 days
2nd: Alternative first drug, if no improvement after 3 days
Consider NIV

Most common causative organisms of acute exacerbation of COPD?

Haemophilus influenzae (most common cause)
Streptococcus pneumoniae
Moraxella catarrhalis

Criteria for NIV and ITU in acute COPD exacerbation

Respiratory acidosis (pH <7.35 or pCO2 > 6 kPa) on controlled oxygen therapy and after usual medical treatment is an indication for Non Invasive Ventilation

ICU referral when pH < 7.25 or PaO2 < 7.3 for consideration of intubation

Management of acute bronchitis

Usually viral - influenza most common
Patient education on self care strategies:
- Keep hydrated, paracetamol, ibuprofen
- Expectation of 14 days
Smoking cessation
Abx not usually indicated, but are if:
- Systemically very unwell
- CRP > 100mg/L
- at risk of serious complications due to comorbidities
- 65+yo with two, or 80+yo with one of the following:
- Hospital admission in the previous year.
- Type 1 or type 2 diabetes mellitus.
- Known heart failure.
- Concurrent use of oral corticosteroids.

The three main causes of a metabolic acidosis

Ketoacidosis - Diabetics with high ketones
Renal acidosis - High Urea and Creatinine
Lactic acidosis - Tissue hypoxia eg. Shock

Treatment of tension pneumothorax

Sit up + Oxygen 15L
Needle thoracocentesis:
- 14/16G cannula attached to syringe with saline
- 2nd ICS, mid-clavicular line, just above rib
- aspirate quickly, then remove plunger
- Air should bubble through fluid
- LEAVE IN SITU
- No hiss/bubbling? Needle may be too short/blocked.
- Insert another cannula 5th ICS mid-auxiliary line
Insert a chest drain same side asap

Description of tension pneumothorax

A one way valve is created letting air in to the pleural space but not out again. Pressure builds and and compresses the great vessels, preventing venous return to the heart causing harm-dynamic instability

Symptoms and signs during tension pneumothorax

Symptoms: Severe SOB, Chest pain
Vitals: Tachycardia, Tachypnea, Hypotension
Signs: Deviated trachea, Raised JVP,
Unilateral hyper- resonance, Reduced air entry

Management of pulmonary embolism

If suspicious do 2 level PE WELLS score
If score 4 or less - PE unlikely - do D-dimer
If score 5 or more - PE likely - do CTPA
Give treatment dose LMWH whilst waiting for CTPA
If haemodynamically unstable - thrombolysis

What is in the two level PE WELLS score

Clinical DVT = 3
Alternative diagnosis less likely than PE = 3
HR > 100/min = 1.5
Immobilisation for >3/7 or surgery in previous 3/52 = 1.5
Previous DVT/PE = 1.5
Haemoptysis = 1
Malignancy = 1

What are the typical community acquired pneumonia causative organisms and their associations

Streptococcus pneumoniae - 80% of all, lobar
Haemophilius influenza - COPD
Staphlococcus aureus - following influenza
Klebsiella pneumoniae - Alcoholics
Pseudomonas (gram -ves) - CF and bronchiectasis
Moraxella catarrhalis

What are the atypical community acquired pneumonia causative organisms and their associations

Not detectable on gram stain, won’t grow in normal media

Mycoplasma pneumoniae - common ‘walking pneumonia’
Legionella pneumophilia - Hyponatraemia + lymphopenia
Chlamydophillia pneumoniae
Chlamydiophila psittaci - psittacosis from birds
Coxiella burnetii - Q fever in farmers
Tuberculosis
Fungi - Pneumocystis jiroveci - Immunocompromised

Describe Hospital acquired pneumonia and what are its likely causative organisms

Pneumonia that occurs 48hrs after admission and hasn’t been intubated

Gram negative bacilli eg. E.coli and Klebsiella
Pseudomonas
Anaerobes

What scoring system is used in pneumonia and what are the criteria

CURB65 score out of 5

Confusion - 8 or less out of 10 on AMTS
Urea >7 mol/L
RR > 30
BP <90 systolic or <60 Diastolic 
65 years or older

What does CURB65 recommend for patients with each score out of 5

0-1: Consider suitability for discharge home
- Oral Amoxycillin 500mg tds + General advice

2: Needs hospital admission - PO (?IV)
- Amoxycillin 500mg tds + Clarithromycin 500mg bd

3+: Consider need for higher dependency environment
IV Co-amoxiclav 1.2g tds + Clarithromycin 500mg bd
or IV Levofloxacin 500mg bd if penicillin allergy

What is the aetiology of tuberculosis

Mycobacterium tuberculosis
Primary: Ghon focus - macrophages unable to degrade
Macrophages migrate to regional lymph nodes.
Ghon focus + lymph nodes = Ghon complex.
Granuloma - collection of epithelioid histiocytes with caseous necrosis in the centre.
Type 4 hypersensitivity reaction.

Secondary: Immunosupression = Reactivation
Dissemination = Millary TB

Presentation and risk factors for tuberculosis

Cough, Haemopytsis
Fever, Malaise, Night sweats 
Anorexia, Weight loss
Clubbing, Erythema nodosum 
Presence of risk factors:
- Exposure to infection eg. Travel, Family 
- Born in high risk country
- Immunocompromise eg. HIV
- Immunosupression eg. Steroids 
- Silicosis

Investigation of suspected tuberculosis infection

3 sputum samples obtained
- Not able = Bronchoscopic levage or gastric aspiration
Microscopy: Ziehl-Nielsen stain for acid-fast bacilli,
Nucleic acid amplification testing (NAAT) on at least one
Cultures and sensitivity
Bloods: FBC, U&Es, HIV test
Imaging: CXR

Screening for latent tuberculosis infection

Tuberculin skin test
- intradermal injection, read 2-3 days later

Interferron-Gamma release assays (IGRA)
- Blood test

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