Respiratory Flashcards

1
Q

Causes of breathlessness

A
Lungs -
cardiovascular issues 
Anxiety e.g hyperventilation
poisoning - CO poisoning , cyanide 
Endocrine - Hyperthyroidism 
musculoskeletal - myasthenia gravis, 
Guillain barre syndrome (if you have respiratory breathing difficulties 
Hematology - anaemia 

1;2 ration of inspiration to expiration.

what you may see in a respiratory exam

in obstruction condition - body breathes in fast to give body longer to breathe out to get rid of built up air in the lungs.

pursed lips breathing - tell you someone has got airway obstruction.

accesory muscle - if using other muscle e.g holding on to something - using more effort to breathe - abnormal .

Stridor - (outside chest - inspiration
wheeze - inside chest - expiration)
(but you may hear each of them in either inspiration or expiration)
(all caused by airway narrowing)

cor pulmonale
if they yawn & sigh a lot - if you have strong drive to breathe - feeling like they are not getting enough air in.

if you feel breathless - ASK patient when they get breathless.

onbstructive sleep apnoea
during slee- - gravity is waying on our airways & if the is a weight then the airways narrow.
as they stop ventilation - oxygen sat drops, when ventilation starts again - oxygen sats pick up.

peak flow - reduction with reduction in airway diameter
asthma etc - cause airway narrowing

spirometry - how much you have breathed out related to time ( 70 % in the 1 sec - normal )

on the spirometry page - if there is a restrictive picture - the graph will have the same shape , only the litres of air involved will be less.
(fev1/FVC - small

gas transfer measurement - residual volume. 
##
ventilation /perfusion ratio - dye defects back were blood is . if area of black is less - lack of perfusion (PE)

pulse oximerty around the block -

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2
Q

What is COPD ?

A

Chronic Obstructive pulmonary disease.

Group of lung conditions tat cause breathing difficulties including :

0 emphysema (damage to air sacs —–> loss of elasticity —–> means unable to maintain shape & become larger (unable to rebound) , smaller SA : V ratio (less efficient gas exchange)

0 Chronic bronchitis long term inflammation of bronchi ——> causes mucus build up——–> swelling + mucus make it hard for CO2 to get out (C02 retention)

(These are types of COPD)

CAUSES :
Exposure to irritants e.g. smoking

SIGNS/ SYMPTOMS - * (means most important )

    • Cough (usually initial symptom) - usually productive (sputum)
  • starts as a morning cough usually then becomes constant
  • *SOB ( on exercise at first progresses to SOB on rest)
    • Chronic Sputum production
  • Barrel chest - (anterior - posterior diameter of the chest is increased - (appears like it is always inflated - Suggest hyperinflation and air trapping due to incomplete expiration)
    • Recurrent lower tract infections
  • Hyper resonance (louder ?) - indicates hyperinflation .
  • Distant breath sounds

*WHEEZE - common in excaerbations
- expiratory wheeze
or
polyphonic wheeze (multiple pitches / notes starting & ending at the same time.

(sign of inflammation & resistance

COARSE CRACKLES - indicates airway inflammation & muscus over -secretion.

  • pursed lip breathing ( action done by patient to prolong expiration to decrease air trapping)
  • use of accessory muscles

RISK FACTORS

  • Cigarette smoking
  • advancing age
  • genetic factors - Alpha - 1 - antitrypsin (smoking in this group can activate lung manifestations of this disease)

WEAKER

  • exposure to air pollution , burning solid / biomass fuel , ocupational exposure to dust , chemicals , fumes & gases.

COMPLICATIONS OF CO2
(breathing difficulties ———————> drop in serum 02 levels ————-> body increase BP ———————————-> pulmonary hypertension ——————————> Right sided heart failure ————————————–> Cor pulmonale ( impairment of right side of heart bcc of respiratory disease)

SIGNS

0  Distended neck veins
0 cyanosis
0 Loud P2 
0 hepatosplenomegaly
0 hepatojugular reflux ( manual pressure applied to liver - if neck veins , distend - positive)
- ankle swelling (peripheral oedema)
- systolic parasternal heave.
-
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3
Q

DIagnosis of COPD ?

A

Spirometry - needed for confirmation of diagnosis
(FEV1/FVC ration below 0.7 )

  • consider COPD in young PL with symptoms indicative of COPD even if FEV1 /FVC lower than 0.7 ( in under 40 yrs consider Alpha - 1 - antitryspin deficiency if FHX)
  • for older people , if no typical symptoms of COPD & FEV1/FVC below 0.7 - consider alternative cause.

COPD can exist with other conditions.

0 FBC
0 CXR

CONSIDER

0 ECG & serum natriuretic peptides - if cardiac disease r pulmonary hypertension suspected.

0 echocardiogarm - if pulomary hypertension suspected .

0 CT thorax - if sysmptoms seem disproportionate to spirometry results - may indicate another condition e.g fibrosis , bronchiectasis.

0 Serum alpha - 1 - antitryspin.

if acute presentation & breathing difficulties :

  • check 02 sat (Pulse oxim)
  • ABG

0 SERIAL PEAK FLOW MEASUREMENT - to exclude asthma if in doubt.

0 Sputum culture -if frequent excaberations , sever airflow limitation , exacberations requirng mechanical ventilation (SPUTUM SHOULD BE SENT FOR CULTURE - IN THESE CASES. )

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4
Q

What are the criteria for stages of COPD ?

A
4 stages
(GOLD - Global initiative for Chronic Obstructive Lung disease)

0 Gold 1- mild (FEV1 > 80 % )
0 Gold 2 - moderate - 50 % - 80 %
0 Gold 3 - Severe - below 50 %
0 Gold 4 - Very severe - below 30 % FEV1

FEV1 - forced expiratory volume (the amount of air you can force out in one second - COPD prevents breathing out (causing co2 uild up)

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5
Q

What is mMRC dyspnoea scale ?

A

Modified medical research council dyspnea scale

Determines the severity of dyspnoea in respiratory disease i.e. COPD.

0 - 4 Points

0 - dyspnoea on excretion
1- Dyspnoea when hurrying or walking up slight hill
2- walks slower than pl of same age bcc of dyspnoea or has to stop for breath when walking at own pace
3- Stop for breath after walking 91 m (100 YARDS ) or after a few mins.
4 - Too dyspneic to leave house or breathless when dressing.

This can be incorpated into the GOLD critera for COPD when trying to assess more breathless patients .

0 Group A: low risk (0-1 exacerbation per year, not requiring hospitalisation) and fewer symptoms (mMRC 0-1 or CAT <10)

0 Group B: low risk (0-1 exacerbation per year, not requiring hospitalisation) and more symptoms (mMRC≥ 2 or CAT≥ 10)

0 Group C: high risk (≥2 exacerbations per year, or one or more requiring hospitalisation) and fewer symptoms (mMRC 0-1 or CAT <10)

0 Group D: high risk (≥2 exacerbations per year, or one or more requiring hospitalisation) and more symptoms (mMRC≥ 2 or CAT≥ 10).

  • CAT - means COPD Assessment test - questionaire used for people with COPD - assess impact of COPD on a person’ life , how this changes over time ( used to aid management. )
    ( assesses cough , phlegm , chest tightness , breathlessness , activities , confidence , sleep . energy)
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6
Q

Treatment of COPD ?

A

(if patient is breathless and has exercise limitation)

1ST LINE - short acting or long acting bronchodilator (short acting BETA -2 - AGONIST (SABA) , short acting muscarinic antagonist (SAMA)

0 short acting Beta - 2 - agonist (salbutamol )

or

0 short acting muscarinic antagonist (SAMA) - ipratropium

( these used to reduce breathlessness & increase excercise tolerance.

  • PLUS - Supportive care e.g smoking cessation, inhaler training , vaccinatio against influenza & streptococcus pneumoniae. )

if not working & supportice care (non -pharmological ) is optimal use & NO ASTHMATIC FEATURES use:

2ND LINE

LABA + LAMA
( long acting beta -2 agonist ( salmeterol , formoterol , vilanterol ) + long acting muscarinic anatgonist - aclidinium , glycopyrronium , umeclidium )

3RD LINE
(trail of LABA + LAMA + inhaled cortiocosteriod (ICS ) - for 3 months
(if improved keep combination - review anually )

4TH LINE - if no improvement - go back to LABA + LAMA

  • If a person has asthmatic features or respond (improve ) when steriod use (steriod responsiveness - consider LABA + ICS.
  • however if they still have day to day symptoms affecting life or 1 severe exacerbations (need hopitalalisation or 2 moderate ones with 1 year - offer LAMA + LABA + ICS

add on treatments
- Oral mucolytic therapy ( if person with stable COPD develops chronic productive cough)
(erdosteine , acetylcysteine , carbocisteine
(mucolytics - dissolve thick mucus)
(STEINES)

  • oral theophylline - only considered if both short & long acting bronchiodilatoes used or ICS can’t be used.
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7
Q

Mechanism of action of different types of bronchiodilators ?

A

examples of bronchiodilators

0 Beta - 2 - agonist
( B2 receptors when activated cause smooth muscle dilation of airways )
( (salbutamol , Terbutaine-SABA - short acting ) , salmeterol , formoterol , vilanterol - LABA (rest of these are Long acting - TEROLS)

0 Anticholinergics / muscarinic anatgonists
(block actelycholine which is responsible for involuntary muscle movements )
(ipratropium - SABA, tiotropium , aclidinium , glycopyrronium, umeclidium - LABA - PIUM)

0 ADD ON TREATMENT Theophylline (Xanthines - relax muscles around airways so they open up more easily , also decrease lungs response to irritants
(
Oral theophylline - should only be considered after trail of short & long bronchiodilators have beem used & inhaled corticosteriods cannot be used) - hIGH RISK , NARROW THERAPEUTIC RATIO , FREQUENT DRUG-DRUG INTERACTIONS

  • ADD ON TREATMENTS - oral Corticosteriods should not be started in primary acre - refferal needed.
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8
Q

Which groups should use Beta - 2 agonists with caution ?

A

Effects Potassium levels (so will affect cardiac system - be careful in cardiovascular disease)

Hyperthyroidism — beta-2 agonists may stimulate thyroid activity.

0 Diabetes mellitus — there is a rare risk of ketoacidosis (especially after intravenous beta-2 agonist administration). Additional blood glucose measurements are recommended when treatment with a beta-2 agonist is commenced.

0 Cardiovascular disease (including hypertension) — beta-2 agonists may cause an increased risk of arrhythmias and significant changes to blood pressure and heart rate.
Susceptibility to QT-interval prolongation.

  • RISK OF ADVERSE EFFECTS IF PRE - DISPOSED TO ARRYTHMIAS OR PRE - EXOSTING CARDIOVASCULAR DISEASE OR HYPERTENSION)

0 Hypokalaemia — plasma potassium concentration may be reduced by beta-2 agonists (particularly high doses).

0 Convulsive disorders.

Side effects - 
heart
 - QT prolongatiion
- palapitations 
- cardiac arrythmias - rare
(Neurological)
Seizures 
Fine tremour 
headache
anxiety

(Lungs )
- bronchospasm - rare

  • Acute angle closure glaucoma - risk in patients using nebulised SABAs - advise to wear mouthpiece rather than mask to reduce exposure to eyes.
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9
Q

Differenitals of COPD ?

A
Asthma 
- usually happens early in life ,
- personal history of allergic rhinitis :
0 eczema 
0 allergic rhinitis
(atopy triad - together with asthma)
  • Overt wheeze which rapidly responds to bronchiodilators.
  • Cough variant of COPD mimics COPD.

Investiagtions - Spirometry & PFTs show reversibility with bronchiodilators.
* if sputum or blood shows eosinophillia (high levels of eosinphils )- sign of type of severe asthma - marked by high WBC - high levels of eosinophils cause swelling & inflammation of airway - rare)

0 Bronchiectasis ( long term condition where airways become widened & mucus builds up)
* some patients can develop bronchiectasis as a result of COPD)
(Bronchiectasis - is caused by lung infection , immunodieficency, aspiration (airway is senstive to gastric contents so can trigger inflammation, Cystic fibrosis - complication - as mucus is a good evironment for infection) , cillia abnormalities , connective tissue disorders (RA , Sjogren’s syndrome , crohn’s disease , UC)
* 1 IN 3 CASES ARE ASSOCIATED WITH SEVERE LUNG INFECTION IN CHILDHOOD ( TB , whooping cough , measles , severe pneumonia)
- history of recurrent lung infection in childhood (especially Hx of TB or whooping cough (pertussis)
- Large volume of prulent content present.

0 CHF -
usually :

history of Cardiovascular disease present , othropnoea & inspiratory crackles
(raised B -nauiretic protein X ray shows pulmonary vascular congestion & echo confirms this)

0 TB -
signs - Hx of fever , night sweats , weight loss , chronic productive cough
microbiological confirmation
- granuloma , fibrosis , inflitates seen on X RAY
- positive skin test for TB

0 ACE inhibitor induced cough - ACE inhibitors cause chronic cough - NOT USUALLY PRODUCTIVE. (cough improves when ACE stopped )

0 Chronic sinusitis / rhinitis - common cause of chronic cough
(Hx of sinus pressure , runny nose (rhinorrhoea , non -productive cough , headache)
rrhoea - flow / discharge

0 GORD - chronic cough can occur especially when supine - worsens at night
(accompained with GORD symptoms (dyspepsia , frequent bletching )

0 LUNG CANCER - COPD INCREASED RISK OF LUNG CANCER
(weight loss , neight sewats , haempytsis , chest , back pain.

0 Upper airway dysfunction

0 Bronchiolitis - inflammation of the bronchioles (post infectious , Hx of connective tissue disorders , fume exposure)
CXR - hyperinflation

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10
Q

What is a COPD excaebation ?

A

exacerbation of COPD - acute worsening of respiratory symptoms that results in additional therapy .

SIGNS /SYMPTOMS

  • increased level of dyspnoea
    (change from baseline can test with questionaires , scales - breathlessness can be described by patients as reduced excercise capacity e.g. can only walk 10 min instead of 15. )
  • worsening of chronic cough (in frequency or severity )
  • increase in volume , thickness , colour or purulence (pus) of sputum produced (change in purulence may indicate presence of bacteria .
    0 The most frequently identified bacterial pathogens include : *Haemophilus influenzae, *Streptococcus pneumoniae, *Moraxella catarrhalis.- VIRAL INFECTIONS CAN HAPPEN ALONGSIDE BACTERIAL.

0 Wheeze
(beware of decreased breath sound - indicates impending respiratory failure.)

0 tachypnoea - could be respiratory failure

0 Cor pulmonale 
(could occur due to exacerbation - induced hypoxaemia )
- peripheral oedema 
 elevated JVP
- hepatojugular reflux
 systoluc parasternal heave 
- relative hypotension
- loud pulmonary second heart sounds
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11
Q

Just for knowledge - practical tip to differentiate upper airway sound from wheeze?

A

Transmitted upper airway noise ‘wheeze’ is common both as a symptom and as a sign. Be aware that patients or relatives may describe ‘wheeze’, especially on exertion, that is actually upper airway transmitted noise and not wheeze. Consider this on auscultation. Likewise wheeze heard at the end of the bed is often from the upper airway rather than small airways and may not improve with usual COPD treatment.

  • GORD - can trigger excaberations.

INVESTIGATIONS

  • Arterial blood gas (in hospital )
    (if moderate - severe excaberations)
    ( may see chronic hypercapnia , acute respiratpry acidosis) - COMPARE WITH PRIOR ABG to determine difference from baseline levels.
  • Pa02 < 8KPA
  • <7.35 or PaCO2 > 6.5 KPA - Respiratory acidosis.
  • ACIDAEMIA IMPLIES SEVERE EXCABERATION & 30 - DAY MORTALITY
    (DO ABG wiithin 2 hours of starting acute NIV)

0 Pulse oximetry (community & hoospital )
0 ECG, Vitamin D ( can be done commmunity if possible & hospital )

REST CAN ONLY BE DONE IN HOSPITAL - FOR MODERATE TO SEVERE EXACERBATIONS) do :

  • CXR - (or if pneumonia is suspected)
  • FBC
  • CRP (elevation - possible infection)
  • Urea & electrolytes , creatinine
  • Sputum microscopy , culture & gram stain.
  • serum theophylline levels ( for anyone on theophylline)
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12
Q

Signs of respiratory failure ?

A

0 Change in mental status

  • drowsiness
  • confusion
  • personality change
  • irritability

0 Morning headaches
(sign of worsening hypercapnic ventilatory failure. )

0 accessory muscle use
& pursed lips breathing.

0 Paradoxial movement of the abdomen ( SEE SAW BREATHING)

Respiratory failure ( Pa02 below 8.0 KPA)

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13
Q

Types of breathing support / assistance ? - oxygen delivery devices ?

A

NIV - NON - INVASIVE VENTILATORY SUPPORT - delivery of O2 via a face mask - no need for endotracheal airway.

  • Mask
    0 Non -rebreathe (reservior )
    0 Bag valve mask
    0 Venturi mask
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14
Q

Treatment of excaberbation of COPD ?

A

1ST LINE

Oral corticosteriods - Prednisolone 5 days 30mg- FOR ALL THOSE ADMITTED TO HOSPITAL OR SIGNIFICANT INCREASE IN BREATHLESSNESS.

IF BACTERIAL INFECTION PRESENT

ORAL ANTIBIOTICS
- (amoxicillin, doxycycline , clathromyocin )

2ND LINE - if this does not work (pick another of those 3 )

if higher risk of treatment failure
(Co - amoxiclav , , Co - trimoxazole , IF THESE NOT POSSIBLE / WORKING levofloxacin)

3RD LINE

IV ANTIBIOTICS

  • Amoxicillin
  • Co - amoxiclav
  • Clarithromycin
  • Piperacillin with tacobactam
  • if Oxygen needed use - NIV
  • IF in hospital - can use :
  • invasive ventilation
  • intravenous theophylline (on if inadquate response to nebulised bronchodilators) - monitor levels of theo within 24 hrs of starting
  • Pulmonary rehabilitation (supervised program including excercise training , health education , breathing techniques etc. )
  • monitor pulse oximetry during recovery for non - hypercapnic / acidotic respiratory failure
  • monitor with ABG for acidiotic respiratory failure
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15
Q

What is asthma ?

same guy that did tonsilitis .

A

Chronic respiratory condition associated with airway inflammation & hyper-responsiveness
(airway hyperresponsiveness - pre - disposition of airways to narrow excessively in response to stimuli) that would not really affect heathy pl. ————————-> leads to recurrent wheezing , breathlessness , chest tightness , coughing - resulting in variable airway obstruction that is reversible either spontaneously or with treatment.

SIGNS & SYMPTOMS

(MAINLY LOOK FOR
0 Cough , breathlessness , expiratory wheeze & daily or seasonal changes in symptoms
0 FHx or Hx of atopic disorders
0 Any triggers that make it worse. )

  • Recent upper respiratory tarct infection
  • dyspnoea , breathelessness
  • Cough , expiratory wheeze (precipitated by allergen exposure , cold air , tobacco smoke , worse with emotions e.g laughing hard.
  • Nasal polyposis
    (single or mutiple polyps in nasal cavity. )

RISK FACTORS

  • Family history
  • allergens
  • atopic history
    (atopic dermatitis , eczema , allergic rhinitis )
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16
Q

Investigations / Diagnosis of asthma ? - 17 & above (note children aged 5 - 16 are similar but slight differences )

A

Diagnose asthma :

  • FeNO > 40 ppm + postive BDR or positive peak flow varibility / bronchial hyperreactivity

or

  • FeN0 btw 25 & 39 + positive bronchial challenge

or Postive BDR + Positive peak flow varibility

Suspect asthma with :
- Negative BDR , FeN0 > 40 ppm or btw 25 & 39 with peak flow varibility

or

Positive BDR + FeN0 level btw 25 - 29 ppb with negative peak flow varibility .
(review diagnoses 6 -10 weeks after)

  • NOTE IN CHILDREN - POSITIVE FeN0 = > 35ppb

Order of diagnosis

HIstory ————> Exam (respiratory - may be normal in people with asthma )———————> Objective testing - offer all 3 - (Spirometry , feNO , peak flow) ———————-> Bronchodilator reversibility test (BDR)( for aged over 17 with obstructive spirometry (FEV1 /FVC < 70 %) ——————–> Diagnostic uncertainity do : monitoring of peak flow variability for 2 to 4 weeks - 20 % variability - POSITIVE / ——> Bronchial challenge test (see requirements below) —————————->

Explanation of test

spirometry - aged over 5
FeNO - aged over 17

0 Spiromtery (FEV1/FVC 40 ppm + no variability in peak flow

or

0 FeN0 < 40 ppm + variability in peak flow)
(may be used if spirometry has been done but doctors not sure if you still have asthma.
(other names - airway provocation test - look to see if patient has sensitive airways - increasing doses of medicine that constrict / irritate the airways (e.g histamine , methacholine ) are breathed in. Pl with sensitive airways / asthma are affected by much lower doses. )

0 FeNO - fractional exhaled nitric oxide test ( test how much NO is in you breath - higher levels indicate asthma - MORE THAN 40 PPB (parts per billion)
* beware that smoking can lower levels.

0 Bronchodilator reversibility test (IMPROVEMENT OF FEV1 OF MORE THAN 12 % + increase in volume of 200 or more - POSITIVE )

OTHER TEST - NOT DIAGNOSTIC

  • peripheral eosiophil count
  • excercise challenge (17 & over)

FOLLOWING TEST ARE NOT DIAGNOSTIC - USED TO IDENTIFY ALLERGEN AFTER FORMAL DIAGNOSIS MADE (on if allergy is present ) :

  • Skin prick allergy test
  • immunoassay for allergen specific IgE
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17
Q

Treatment of asthma for ages 17 & over ?

A

Infrequent asmtha symptoms , short lived wheeze + normal function

1 ST LINE

reliever therapy
SABA - e.g salbutamol

2ND LINE

Low dose ICS

If maintence therapy needed e.g frequent asthma symptoms (3 or more times a weeks ) or waking at night.

1ST LINE

low dose ICS

2ND LINE

Lose dose ICS + LTRA (leukotriene receptor antagonist e.g . Montelukast , zafirlukast)

3RD LINE

Low dose ICS + LABA +/- LTRA

( discuss whether to continue LTRA)

4TH LINE

MART - maintence and reliever therapy combines ICS with LABA in single inhaler) - low dose ICS used +/= LTRA

5TH LINE

MART - medium dose of ICS

or fixed dose of ICS , LABA with a SABA

( + /- LTRA)

6TH LINE

  • increase to High dose ICS

or trail of addition drug e.g. LMRA (muscarinic antagonist) or theophylline.

SELF MANAGEMENT - ADVICE ON AVOIDANCE OF EXPOSURE TO POLLUTANTS , ALLERGENS
- they have self management plan on how to deal with asthma if deteroriates e.g . Doctor prescribes a specific increased dose to take for 7 days etc.

CONSIDER REDUCING MAINTENCE THERAPY IF SYSMPTOMS CONTROLLED FOR 3 MONTHS .
(only consider stopping low ICS treatment if symptoms free)

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18
Q

Treatment of asthma aged below 5 ?

A

1ST LINE

SABA - reliever therapy

IF maintence therapy needed bcc frequent asthma symptoms or SABA not enough

1ST LINE - use SABA alongside as reliever therapy

8 week trial of moderate of ICS
(stop after 8 weeks to monitor child symptoms)

  • no response - consider alternative dose
  • resolved withing 4 weeks after stopping ICS therapy - RESTART a LOW DOSE ICS
  • Resolved but reoccured within 4 weeks of stopping - restart 8 week trial of moderate dose of ICS.
2ND LINE
- if uncontrolled on low dose ICS 
ADD LTRA (Montelukast etc)

3RD LINE - stop LTRA - refer to specialist

19
Q

Treatment of asthma of those aged 5 -16 ?

A

Infrequent asmtha symptoms , short lived wheeze + normal function

1 ST LINE

reliever therapy
SABA - e.g salbutamol

f maintence therapy needed e.g frequent asthma symptoms (3 or more times a weeks ) or waking at night.

1ST LINE

pediatric low dose ICS

2ND LINE

Lose dose ICS + LTRA (leukotriene receptor antagonist e.g . Montelukast , zafirlukast) ( review treatment response in 4 tp 8 weeks .

3RD LINE
consider Lose dose ICS + LABA (stop LTRA)

4TH LINE

consider MART ( containing pedriatric low dose ICS & A LABA)

5TH LINE

consider seeking opinion of specialist
and consider :

  • increaseing to pedriatric high dose ICS (only part of fixed dose regimen with SABA as reliever)
  • starting trial of additional drug e.g.
    Theophylline

SELF MANAGEMENT - ADVICE ON AVOIDANCE OF EXPOSURE TO POLLUTANTS , ALLERGENS
- they have self management plan on how to deal with asthma if deteroriates e.g . Doctor prescribes a specific increased dose to take for 7 days etc.

-

20
Q

How to treat severe asthma ?

A

Not controlled by standard therapy

Omalizumab (AGED OVER 6)- if severe persistent confirmed allergic IgE mediated asthma.

for severe eosphillic asthma

Mepolizumab
Benralizumab
reslizumab

(there are some conditions for their usage but could not be bothered to write )

21
Q

Diagnostic criteria for asthma (5 - 16 years )

A

0 FeN0 >/= 35ppm + peak flow varibility

0 or obstructive spirometry and positive BDR.

  • beware in some case children aged 5 are not able to perform objective test - treat based on clinical judgement or ask for advice from specialist , try doing test every 6 -12 months until satisficatory results recieved.

Under 5s dont do objective test , clinical jugdement is used + symptoms.

22
Q

What is acute exacerbation of asthma ?

A

Subacute worsening of symptoms of asthma including :

  • SOB
  • Wheezing
  • cough
  • chest tightness
    (can be progressive)

( will reduction in baseline levels on objective tests e.g peak flow , spirometry , FeNO etc.)

may also be :

  • exercise limitation
  • collapse

life threatening

  • altered conciousness
  • exhausted
  • have arrythmias

OE :

  • tachypnoea (above 25 RR - indicates severe asthma )
  • silent chest (indicates impending repsiratory failure )
  • accessory muscle use (sign of respiratory distress)(muscles ribs , shoulders neck )
  • cyanosis (severe hypoxaemia ) - rare but serious
  • Hypotension - serious

RISK FACTORS

  • Viral infection
    (very common) - Influenza , rhinovirus , respiratory syncytial virus / common respiratory virus.
  • uncontrolled asthma symptoms
  • inadquate usage of ICS
  • Incorrect inhaler technique
  • poor adherence to treatment
  • use of oral (vs ICS ) steriods - indicates asthma is more severe
  • low FEV1
  • high bronchodilator reversibility
  • blood eosinphils
    elevated fractional nitric oxide.
  • Current smoker or exposure to 2nd hand smoke.
  • air pollution
  • poor indoor air quality
  • exposure to allergens
  • atopic ezcema
  • chronic rhinosinistius
  • Hx of exacerbations
    (especially if 1 or more severe in last 12 months )
  • confirmed food allergy
  • pregnancy
23
Q

Diagnosis of asthma excaerbation ?

A

non verbal behaviour e.g agigitation (especially children), altered conciousness —————–> appearence (is there signs of hpoxia - cyanosis , use of accessory muscles ) ——————-> examine - RR , BP , pulse —————————–> record Peak flow expiratory rate———————-> measure oxygen sat .

0 arterial blood gas
0 peak flow
0 pulse oximetry
0 CXR

consider :
0 FBC - eosinophilla (eosinophil asthma )
0 U & E 
0 CRP 
0 Theophylline 
(if on this )
0 ECG
24
Q

Grading of severity of acute exacerbation?
Adults
Children

A

0 MODERATE -

  • PEFR > 50 - 75 %
  • PEFR (more thna 50 % - children)

+ normal speech with no features of acute severe or threatening asthma.

ACUTE SEVERE - PEFR 33 - 50 %
- PEFR (less than 50 % children )
or 
RR - 25 or more / Pulse rate of 110 or above 
( above 12 yrs) 

RR- 30 or more (5 -12 yrs )
PR - 125 or more

RR - above 40
PR - above 140 (below 2- 5 )

OR either one of these;
inability to complete sentences in one breath 
- acessory muscle use
- inability ro feed (infants )
WITH OXYGEN SAT OF 92 % or above 

LIFE- THREATENING
- PEFR 33 % below
or
- oxygen sat - below 92 %

either of these :

  • altered conciousness
  • exhaustion
  • cardiac arrythmias
  • hypotension
  • cyanosis
  • poor respiratory effort
  • silent chest
  • confusion.
25
Q

Management / treatment of patients with acute exacerbation asthma ?

hospital admittance

A

ADMIT ALL WITH LIFE THREATENING ASTHMA TO HOSPITAL .

IF HYPOXIC -
Give supplementary oxygen using face mask .
(maintain oxygen sat at 94-98%)

IF ADMITTED TO HOSPITAL

life threatening

1ST LINE

0 Nebulized salbutamol (SABA) 
5mg - over 5 years 
2.5mg - 2-5 years
( * oxygen driven nebuliser - 1st
(air driven nebuliser - 2nd - risk of oxygen desaturation - be careful ))

Pressurised metered dose inhaler with large volume spacer SALBUTAMOL.
( used if nebulised salbutamol not possible or moderate severity)

2ND LINE

SALBUTAMOL + NEBULIZED IPRATROPIUM BROMIDE (SAMA)

  • Consider quadrupling dose of ICS :
    prednislone
    (consider IM methypred or IV hydrocortisone if not able to swallow)
26
Q

Management / treatment of acute exacerbation of asthma ?

Not admitted to hospital .

A

SABA (salbutamol) via large volume spacer.

  • Consider quadrupling dose of ICS
  • before doing this consider adherence (pl who are highly adherent may experience the ceiling effect & gain no additional benefit from increasing ICS.

ceiling effect - drug reaches it’s maximum effect.

after symptoms subsided return to original dose. & monitor symptoms & PEFR.

Follow up patient with 48 hrs.

  • Review symptoms, Lifestyle advise (pollutants avoidance etc. ), make sure patient has received self - management education and a personalised asthma action plan.
27
Q

What are the target oxygen saturations ?

A

Normal : 94 -98%

COPD / Risk of hypercapnia respiratory failure/ risk of c02 retention (morbid obesity , cystic fibrosis , chest wall deformities or spinal disease ( kyphosis-sclerosis), neuromuscular disorders , bronchchietasis): 88 - 92%

reason - both C02 / 02 Can bind haemoglobin (so competing with each other - if there is a lot of 02 less C02 will bind to haemoglobin
Haldene effect - 02 affecting decreases the affinity of Hb for C02/ H+———-> less C02 binds ——–>reduces body capacity to remove C02 from tissues. etc.

  • Note - Bohr effect - C02 / h + (causes low PH) affecting the affintiny of Hb for 02. = reduces hb affinity for 02
  • also in COPD as well as targets sat - keep Pa02 levels < 10Kpa
28
Q

Prescribing 02 in critically ill patients ?

TARGET SAT 88 -92 %

A

critically ill

Commence 15l/min oxygen via reservoir mask(non -rebreathe or bag valve mask )

oxygen sat target is 88% - 92 % on alert card change to :
24 % or 28 % oxygen or 1-2l/min nasal oxygen (nasal cannula)
+ obtain aterial blood gas results

  • if target sat on alert card is 88 -92% but Pc02 = 6.0 kpa (this is the normal ) - change target to 94 -98%
  1. if in respiratory acidosis
    - seek senior review & consider NIV or IV ———————————————————> TREAT WITH 24 - 28 % Venturi mask to maintain target o2 sat.
  2. if hypercapnia ( i.e. no low PH) ——————————–> Treat with 24 -28 % Venturi or 1 -2 l/min nasal o2. ——————————-> repeat blood gas at 30 -60 mins ———————–> (if gone into respiratory acidosis - senior review , consider NIV or IV . ) / Consider reducing P02 if . 8.0Kpa
29
Q

TYPES OF MASK ?

A

Venturi mask

0 Delivers 24-60% oxygen
0 Different colours deliver different rates
Flow rate: Varies with colour. The correct flow rate to use with each colour it is shown on mask, along with the percentage of oxygen delivered.
Types:
- BLUE = 2-4L/min = 24% O2
- WHITE = 4-6L/min = 28% O2
- YELLOW = 8-10L/min = 35% O2
- RED = 10-12L/min = 40% O2
- GREEN = 12-15L/min = 60% O2
Venturi masks are often used in COPD, where it is important not to over-oxygenate the patient.

30
Q

Prescribing 02 in critically ill patients ?

TARGET SAT 94-98%

A

Initially
give nasal cannula 2-6 l / min ( best ) or simple face mask (5 - 10l / min ) - target sat 94 -98 %

once

(If this not reach change to reservoir - 15l/min)

if oxygen sat below 85 % and no risk of C02 retention :

Reservior mask (15l/min)
(if oximetry not available give this oxygen and wait for arterial blood gas)
 can change back to nasal can or simple face mask once stabilised.
31
Q

Prescribing 02 in hypoxemia but not critically ill ?

Oxygen sat - target

A

Nasal cannula or simple face mask (if nasal not tolerate / not possible )

32
Q

Random notes from respiratory therapeutics tutorial ?

A

All age groups normally desaturate to 90.4 % during the night.

33
Q

What is a pneumothorax ?

A

Air gets inside & accumulates in the pleural space ( btw visceral & parietal pleura )

TENSION PNEUMOTHORAX - MEDICAL EMERGENCY ——> Pneumothorax leads to shift of medistinal structures.

CLASSIFICATIONS /TYPES

SPONTANEOUS - no trauma or preceeding event
(this divided into primary & secondary)

  • Primary - no known respiratoty illness brought it on.
  • Secondary - occurs in patients with pre-existing pulmonary illnesses e.g . COPD , asthma , catamenial pnuemothorax etc.
  • In practice a patient with only mild respiratory illness e.g. intermittent asthma with no exacerbation of symptoms.
    at presentation may be treated as a primary sponatenous pneumothorax.

NON SPONTANEOUS - caused by trauma or accentidenal (iatrogenic) :

0 Traumatic pneumo - caused penetrating or blunt injury to chest

0 Iatrogenic pneumo - medical prodcedures e.g. aspiration , thoracentesis , Central venous catheter placement , barotrauma
]
* Barotrauma - means damage to body because of changes in barometric pressure

  • Barotauma ( to do with lungs ) - due to mechanical ventilation
    ( causes build up of transaveloar pressure causing rupture of air sacks——-> air leaks into surroudning extra alveolar space. )

OTHER TYPES

Pneumothorax ex vaco , Catameinal pneuo

SIGNS/ SYMPTOMS

  • Chest pain (typically pleuritic )
  • Primary spontaneous pneumothorax (PSP) may experience shoulder tip pain instead. )
  • Dyspnoea
    (more prominent in SSP) e.g. secondary SP
  • Ipsilateral reduced breath sounds (may indicate tension Pneumothorx but can happen with non - tension)
  • Ipisilateral hyperinflation of hemitorax (one side of lungs ) with hyper-resonance on percussion !!!!
    (NOT PRESENT IN PNEUMOTHORAX EX VACUO - TRAPPED LUNG)
  • hypoxia - generally late sign
    (more common in tension & SSP)

If there is cardiopulonary deterioration indicates tension pneumo :

0 Hypotension (suggest imminent cardiac arrest)
0 Tachycardia 
0 Respiratory distress
0 Low oxygen sats 
0 Shock 
0 Loss of conciousness 

other signs of tension pnuemo
(tracheal deviation - shifted to contralateral side. ) , Sweating

RISK FACTORS

0 Smoking - most common (important) - risk 22x for men , 9 x - women

0 Fx of Pneumothorax
0 Tall slender body build
0 Structural abdnomalities 
- marfans syndrome 
- Ehlers - Danlos syndrome 
)

0 Male
0 Young age (though SSP more common > 55 yrs)

0 Presence of underlying lung disease 
- COPD
- Severe asthma 
- TB
- Pneumocystis
- Cystic Fibrosis 
- bronchiectasis 
- fibrotic lung disease
(especially acute presentation e.g bullous COPD , asthma )
0 lung disease  
0 recent invasive procedures 
0 trauma 
0 Ventilated patients , NIV( barotrauma)
0 Hyperbaric oxygen treatment

0 * Mensturation ( risk of catamenial pneumothorax)
suspect if history of recurrent pneumothorax , endometrosis )

34
Q

What are the special /other rarer forms of pneumothorax ?

A

Pneumothorax ex vaco (Complication of lung collaspe)- precipated by lobar collaspe / aceletasis ——————–> elevated negative pressure in intrapleural spce the pleural cavity (btw visceral & parietal )

*( COLLASPE CAN BE CAUSED BRONCHIAL OBSTRUCTION FROM MUCOUS PLUGS , ASPIRATED FOREIGN BODIES OR MALPOSITIONED ENDOTRACHEAL TUBES) - important for treatment as pneumothorax can be relieved by relieveing obstruction rather than chest drain etc.

Negative pressure (in this case ) - means air pressure in pleural cavity is lower than that around it . 
( * air flows from high pressure to low pressure (into pleural cavity , so accumulation of air -----> puemothorax  )

CATAMENIAL PNEUMOTHORAX -VERY RARE

Affects women
Have recurrent episodes of pneumothorax 72 hours before & after menstration .
- CAUSE UNKNOWN
however possible causes :
0 Endometrosis - endometrial tissue migrates from areas over than the uterus to diaprgam & pleural space (lungs )for example—————————> enometrosis can cause small holes in diapragm allowing air into & fluid to pass into pleural space.
( Thoracic endometrosis - endometrial tissue in the lungs )

Hormonal cause - Ovulation has elevated levels of prostogaldin F2 ——————–> causes constriction of bronchicles ———————> rapture of alveoli ———————————-> air leaks into pleural space.

Anatomical cause - absence of normal mucous plug in menstration allows air to move from Genital tract through fenestrations in the diapragm.

  • MAJORITY OF CASES RIGHT LUNG AFFECTED.

Treatment
( thoracic surgery statergies + hormonal manipulation
ex - plaicng patches over fenestrations in diaphragm
- electrocoagulation of endrometrosis depsoits & pleurodosis
- Gonadotropin relasing hormone analagoues
( risk of amennhroea but less risk of reocurrance )

35
Q

Diagnosis of Pneumothorax ?

A

0 CXR - main one
( Tension p - not really imaged bcc emergency and treatment urgently)
Order a Posterior - anterior CXR
(an (AP) - anterior posterior not really used to assess things like cardiomegaly etc - bcc natural enlargement of mediastinal structures from the front)

findings :
- absent lung markings btw lung margin & chest wall

  • visible rim btw lungs & chest wall
  • surgical / subcatenous emphysema
    ( air in subcanteous soft tissue (tissue just under skin ) - felt as swelling in affected area & crepitus)

Blood test -
0FBC
0 Clotting screen
need to check INR > /=1.5 or platelets = 50 x 10^9 before you can insert a chest drain.

CONSIDER

Chest ultrasound - becoming increasingly used - especially immbolised patients following trauma when erect PA cannot be obtained.

0 CT scan - if CXR uncertain & patient still symptomatic.

0 ABG - if o2 sats <92 %

36
Q

How to measure the size a pneumothorax ?

A

> 2cm between lung margin & chest wall (LARGE )

<2cm - small

37
Q

Treatment of tension pneumothorax >

A

Immediate decompression (with large bore cannula ) - unless Tension pneumothorax secondary to trauma.

PLUS - high flw O2 + chest drain + hospital admission.

(PUT OUT IMMEDIATE CARDIAC ARREST CALL.
( & dont wait for imaging to confirm)

38
Q

Treatment of secondary Spontaneous Pneumothorax ?

A

If Bilateral or patient haemodymacally unstable ———————> 1ST LINE - Chest drain

First thing - need decide whether primary or secondary spontaneous P
(secondary often tolerated less well )

If secondary :
& :

> 2cm or breathless ————————–> small bore (8 -14 F) chest drain

1-2 cm ——————————–> aspirate 2.5 L with 16g -18 g cannula ————->
1. if successful (below 1cm ) —————–> Admit , HFO , Observe 24
if not successful ( Chest drain)

<1cm ———————–> admit , high flow oxygen ( unless 02 sensitive ) & observe 24hrs
(admit , HFO , observe 24 )

39
Q

Treatment of primary Spontaneous Pneumothorax ?

A

If Bilateral or patient haemodymacally unstable ———————> 1ST LINE - Chest drain

First thing - need decide whether primary or secondary spontaneous P
(secondary often tolerated less well )

If Primary & :

  • > 2cm or breathless aspiate 2.5 L with 16 -18 G cannula —————–> if sucessful ( less than 2cm with improved breathing )—————————–> Consider discharge , review in OPD (OUTPATIENTS ) in 2-4 weeks
    (IF NOT >2CM or breathless ——–> discharge, review in OPD in 2-4 w)
40
Q

Treatment of non - spontaenous pneumothorax ?

A

iatrogenic - must resolve spontaneously (so onservation) ———————————–> if not - simple aspiration (needle?)

Traumatic - high flow oxygen + observation + refer to thoracic surgeon

41
Q

How to when to use needle aspiration or chest drain ?

A

depends on size of Pneumothorax.

NA should not be repeated if there are technical diffuclties ———————————–> if failed use Small bore (<14F ) chest drain.

42
Q

What is pulmonary fibrosis ?

A

Progressive - Build up of scar tissue in the lungs making it difficult to breathe as oxygen transport in blood is impaired.

(Common type of interstitial lung disease - affects lungs & intersitium (support network of tissue the alveoli )

Sub types

Idiopathic PF - no known cause (most common )

SIGNS / SYMPTOMS

0 Dyspnoea on excretion (most common)
0 Crackles - end expiratory crackles basilar crackles (typcially dry & velcro quality )
0 Cough - typically (non -productive )

  • weight loss
  • fatigue
  • malasie
  • clubbing
  • also may be pulmonary hypertension ( as pulmonary arterioles constrict to shuttle blood away from damaged areas —–> if there is widespread damage then widespread vasoconstriction —————-> pulmonary hypertension————–> right ventricular hypertrophy ( Cor pulmonale)aru.

RISK FACTORS

  • advanced age ( most above 60 yrs)
  • Male sex
  • Fx of interstitual lung disease or FPF (familial pulmonary fibrosis)
  • cigarette smoking - 60 x more likely .

Less common

  • organic & inorganic dust exposure
    GORD ( pre - dispose patients due acid aspiration)
  • infection
  • Diabetes
43
Q

Investigation of pulmonary fibrosis ?

A

CXR
- Opacities

0 High resolution CT ( HRCT) - ordered in all suspected patients.

0 Anti -nuclear antibodies 
0 Rheumatoid factor
0 anti - CCP 
0 myositis panel 
(if elevated these 2 may indicate collagen vascular disease - link to Connective tissue disease (auto immune - attacking collagen - can cause Interstitial lung disease))

CONSIDER
0 PFTs - restrictive - reduced VC , TLC ,
0 surgical lung biopsy - used in pl who history , HCT , clincial evaluation do not support clear diagnosis of PF.
- should see fibrosis of varying ages etc.
0 bronchoalveolar lavage (BAL)
0 CRP
0 ESR

44
Q

Treatment of PF ?

A

1ST LINE

Antifibrotic therapy e.g. pirfenidone or ninetanib

+ smoking cessation + pulmonaey rehab + 02

ADJUNCT - PPI if GORD

2ND LINE
- Lung transplantation

ACUTE EXACERBATION

1ST LINE
- admission to hospital + high dose corticosteriod.

(sometimes a cytoxic agent is added. )