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Week 21: Breathless
Important concepts for this PBL:
- Asthma (and its pharmacological treatment)
- Access to treatment in Aboriginal communities
- Acid/ base balance
- paO2 and paCO2
- Gas exchange
TRIGGER 1
- Shona A
- 14 years
- Aboriginal girl
- Nowra Hospital ER
- Distressed
Observations
- Centrally cyanosed
- RR 32/min
- Wheeze (louder in expiration than inspiration)
- Chest over-inflated
- Obvious accessory muscles
- HR 120 bpm (regular)
- Pulse oximetry (oxygen saturation): 88%
- Arterial blood was taken for gases
- High flow oxygen was administered immediately
Video: wheeze on expiration; leaning forward in chair; distressed.
Interpretation of obs
- Central cyanosis
o Lips, tongue
- Wheeze
o Partial bronchial obstruction
o Impacted mucous plugs
o Extrinsic compression (e.g. tumour, lymph node pressing on
bronchi)
- Asthma is an OBSTRUCTIVE condition
- Restrictive conditions are dry; e.g. restrictive lung that is not spongy
- Bronchitis = upper respiratory viral or bacterial infection of the bronchi.
- Bronchiolitis = is swelling and mucous build up in the smallest air
passages of the lungs (bronchioles), usually due to viral infection.
- Over inflation of chest (aka hyper-inflation)
o Must be considered at full insp and distinguished from “air
trapping” on expiration
o A general excess of air in the lungs
o Is she breathing in too much, or too much residual
o After exp if there is a barrel appearance to chest suggests trapping
o Can be diffused (all lobes/ entire lung) or localised (segment of
one or more lobes)
- O2 sats
o Normal is 95%
o Alveolar hypoventilation (not enough air to alveoli)
o Ventilation-perfusion mismatch
o Shunting abnormality - Diffusion abnormality –
o Decrease in fraction of inspired O2
- Pulse oximetry
o Light goes thru finger tip
o Wavelengths of light that are absorbed by Hb
o Dec light going thru indicates good perfusion
o Inc light going thru
o Non invasive, quick way of determining perfusion
- High flow O2
o Treatment because o2 sat is at <95%
o Used where patient requires flow of up to 100% O2 (to inc % sat
O2)
o Involves a mask (the modality of administering O2 is what changes
how much is delivered)
o NB: some patients (“CO2 retainers” e.g. COPD) rely on their low O2
to drive their blow off CO2 – high flow O2 is contraindicated in
these patients.
- Wheeze on expiration suggests peak expiration flow is less than 50%
- Patient is leaning forward; use of accessory muscles of respiration (to
maximise inspiration).
o Accessory muscles: scalenes, sternocleidomastoid, intercostals,
traps, abdominals.
Other possible Dx:
- Asthma
- Anaphalaxis
- Hysterical hyperventilation (probably wouldn’t have low o2 sats)
- Trauma: spontaneous pneumothorax
- Lung injury
- Drugs –
- Inhaled pollutant / inhalation injuries
- Poison
- Bush fire
- Pneumonia
- Rheumatic fever (inflammatory disease that affects heart valves; often
caused by streptococcus viridans, a normal flora of mouth; causes
endocarditis) causes ruptured heart valves pulmonary hypertension
- TB of pericardium/ heart
- Tumour
- Empyema – collection of pus in pleural space; infection; can spread; dry
cough
- CF
- Drowned: cyanosed, lungs full of water;
- Anaemia (unlikely to have wheeze, unless she’s in cardiac failure) heart
trying to beat to get blood to tissues
- Shock
TRIGGER 2
- ABG (breathing room air):
o Pa O2 58 (80-100)mmHg LOW
o Pa CO2 31 (36-44) mmHg LOW
o pH 7.49 (7.35-7.45) HIGH (ALKYLOSIS)
o bicarbonate 24 (21-28 mmol) OK
ABG interpretation:
3 KEY QUESTIONS
1. What is the pH?
a. Below 7.35: acidosis
b. Above 7.45: alkylosis
2. What is the primary problem?
a. pH and CO2 in OPPOSITE directions: respiratory
b. pH and bicarbonate (HCO3) is the SAME direction: metabolic
3. Is there compensation?
a. Respiratory: increased bicarbonate (HCO3)
b. Metabolic: increased paCO2
Shauna’s ABG interpretation: Acute primary respiratory alkylosis (normal
bicarbonate suggests no compensation).
ASTHMA: inflammatory disease, with the following pathological characteristics:
- Infiltration of the mucosa with inflammatory cells (especially eosinophils)
- Oedema of the mucosa, thickening of the basement membrane
- Damaged mucosal epithelium
- Hypertrophy if mucous glands with inc mucous secretion
- Smooth muscle constriction
Explaining why this patient has LOW paO2 and LOW paCO2:
- She is “blowing off” CO2, but her O2 is still low.
- Her respiratory rate is high (to breathe off CO2) but she has an impaired
ability to breath in O2.
- There is something impairing/ obstructing O2 into the lungs.
- What is the difference between the two gases (O2 and CO2)?
o CO2 occupies a different binding site on the Hb than O2;
o CO2 is more readily removed (“Haldane effect” i.e. deoxygenation
of the blood increases its ability to carry CO2; allows CO2 to move
in opposite direction to O2).
o Respiratory drive is caused by CO2 – the higher it is, the more you
want to inhale air.
o CO2 binds with greater affinity than O2
- Shunting: low O2 causes vasoconstriction of pulmonary vessels; however,
some bronchioles are narrowed/ blocked with mucous because of
asthma, therefore not getting O2.
- Asthma (trachea is blocked)not enough air BVs start to shunt away
from the blocked alveoli limited ability to oxygenated the blood.
The movement of oxygen and carbon dioxide across the respiratory membrane is
influenced by:
(1) The partial pressure gradients and gas solubilities.
(2) Matching of alveolar ventilation and pulmonary blood perfusion
(ventilation-perfusion ratio)
(3) Structural characteristics of the respiratory membrane.
For next PBL, need to understand:
- V/Q mismatch (ventilation/ perfusion)
- Oxygen dissociation curve
Is the patient hyperventilation or underventilating (hypoventilating)?
- What is causing the blood gas picture?
- Hypoxia (low O2) and hypocapnia (low CO2).
Pathophysiology of asthma and gas exchange:
- In asthma, there are some airways that are restricted and others that are
OK i.e. asthma has a “patchy” arrangement.
- The “drivers of respiration” are CO2 and hypoxia (low O2).
- Arterioles (vasoconstriction or vasodilation) respond to pO2.
- Bronchioles (constriction or dilation) respond to pCO2.
- CO2 has a smaller partial pressure gradient than O2 across the
alveoli/pulmonary capillaries:
o pCO2 gradient is 5mmHg (45mmHg in blood:40mmHg in alveoli)
o pO2 gradient is 60mmHg (104mmHg in alveoli: 40mmHg in
venous blood)
- CO2 is much more soluble in liquid (blood) than O2.
- Hypoxia has made her increase her respiration rate (leading to decrease
in CO2).
Dr Fotheringham’s note:
- Let’s assume, hypothetically, that the LEFT lung is NOT working (due to
inflammation associated with asthma the bronchioles constrict and
airflow is reduced) and the RIGHT lung is working OK.
- Blue, deoxygenated blood returns to the heart via veins with a pO2
40mmHg (¼ of its Hb is deoxygenated). Blood then goes thru the right
side heart, to pulmonary arteries, and the lungs.
- Suppose an endotrachial tube is pushed down R main bronchus (i.e. only
the R lung gets air flow –-> disaster)
- We compensate for the LEFT lung by overventilating (overcompensating)
on the right side with the hope of increasing our O2. BUT, we cannot
increase the O2 content indefinitely because Hb becomes saturated
with O2 (equilibrium point) – see oxygen dissociated curve where Hb
saturates/plateaus at 104mmHg. i.e. there is a point where more O2 is of
NO benefit because it cannot diffuse into the blood. Thus when blood
from L and R sides of heart mix, we end up with reduced O2 content and
reduced pO2 overall.
Hypocalemia (low CO2):
Because O2 is low, hypoxia is telling her to breathe more – using accessory
muscles etc – she over-ventilates. Therefore by increasing her respiration rate,
pCO2 is decreased as it is removed from the pulmonary capillaries, into the
alveoli, and “blown off”.
Important points:
- Why patient has hypoxia despite overventilation?
- Crux is understanding dissociation curve of 2 gases
- Pathophysiology of asthma
- V/Q mismatch
TRIGGER 3
- Shona’s colour improves promptly with oxygen via mask
- Sulbutamol inhaler (12 puffs)
- Ipratropium (4 puffs) is administered via spacer device
- Shona’s color continues to improve
- Inhalers repeated twice more and after 40mins she is no longer
distressed.
- 1mg/kg oral prednisolone
- Spirometry is also performed
- Resident attempts to obtain hx, but Shona is dismissive – “they want me
to give up smoking and take the useless orange puffer. That steroid stuff
doesn’t help my asthma attacks”
- Leaves hospital against advice without seeing the Aboriginal Health
worker.
Treatments:
- Oxygen treatment via mask
o Ensures that all viable alveoli (i.e. those areas of the lung that are
not inflamed) are fully saturated with O2 (i.e. are receiving as
much O2 as poss.)
o Also helps with the over/hyper-ventilation and the work of
breathing (by reducing it).
o High flow O2 is appropriate when respiratory drive is high (by
reducing hyperventilation).
- Salbutamol inhaler
o A bronchodilator; Beta-2 adrenoreceptor agonist; short acting;
binds to adrenoreceptors
o Example is Ventolin
o Max effect within 30mins. Lasts 3-5hrs.
- Ipratropium
o Anticholinergic agent
o A muscurinic acetylcholine receptor antagonist
o Muscarinc receptors are in the parasympathetic nervous system -
at the junction of the post-ganglionic fibre and the effector.
o Used for COPD
o Prevent bronchoconstriction.
o Used with a spacer to increase the dose that arrives at the lung/
enables you to absorb it over a number of breaths (4-6 breaths);
rinse afterwards.
- Prednisolone
o Corticosteroid
o Oral form used in more severe cases (vs. inhaled form)
o Preventative role re: asthma attacks
o Plays a role in reducing the inflammation associated with asthma
o Inhibit T cell activation and therefore the inflammatory response
o Long term complications with use:
Suppress response to injury and infection;
Adrenal suppression,
Hyperglycaemia,
Hypocalameia,
Growth retardation -this is a common concern of parents:
worried about feedback loop and suppression of GnRH
(growth hormone);
Cataracts and mood swings
o Safe levels of corticosteroids: – aim to keep below 500mg/day in
kids; <1000mg/day for adults; dose can be once or twice daily –
start low and build up; given in combination with inhalers/
bronchodilators etc.
o Up to 1mg/kg/day.
- Spirometry
o Indicates pulmonary abnormalities by determining respiratory
volumes and flow rates
o Obstructive conditions e.g asthma – low FEV1
o Restrictive conditions – total lung capacity is reduced e.g. TB,
asbestos exposure; low FVC
o FVC –Forced Vital Capacity - amount of a gas forcibly expelled after
deep breath.
o FEV1 – Forced Expiratory Volume - volume expelled over 1 sec (or
another period of time)
o Ratio (FEV1/FVC)
Treatments for asthma: mechanisms of action for the diff classes of asthma
medications.
- Relievers – “inhalers” (salbutamol, iprattroium)
- Preventers – inhaled corticosteroids
- Combination drug (long acting bronchodilator + anti-inflammatory
corticosteroids) e.g. seratide inhaler (blue) – tend to inc. compliance.
- Also used often is the corticosteroid, Pulmicort (twist).
- Long acting bronchodilators e.g. Salmeterol, Terbutaline, Eformoterol.
Murtagh’s p1274 : Pharmacological treatment of bronchial asthma
Vehicle of administration
Generic types Examples Nebulising Oral Aerosol Dry powder Injection
solution (MDI) (inhalation)
Bronchodilators
-andrenoreceptor Salbutamol Ventolin X X X X X
agonists
Salmeterol Serevent X X
Terbutaline Bricanyl X X X X
Eformoterol Foradile X
Anticholinergics Ipratropium Atrovent X X
bromide
Methylxanthines Theophylline Brondecon X
Nuelin X
Aminophylline X
Mast cell Sodium Intal X X X
stabilisers cromoglycate
Intal forte X
Nedrocromil Tilade X
sodium
Corticosteroids Beclomethasone QVAR (50, 100) X X
Becloforte X
Becotide X
Budesonide Pulmoicort X X X
Ciclesonide Alvesco X
Prednisolone X
Hydrocortisone Solu-cortef X
Leukotriene agents Montelukast Singulair X
Zafirlukast Accolate X
- Compliance in teenagers
o Stormy time for chronic diseases
o Promotion of compliance by sports figures in South Africa.
TRIGGER 4
- 3am the following morning Shona comes back to ED
- Asthma attack has not responded to salbutamol puffer (bronchodilator)
- Cyanosed
- Fatigue
- Slight wheeze
- Breath sounds are quiet
- Started on high flow O2
- Given nebulised salbutamol 10mg
- Ipratropium 500mcg
- Blood gas report (20 mins later) showed:
o PaO2 55 (80-100) dec
o PaCO2 47 (36-44) inc*
o pH 7.31 (7.35-745 dec* – acidotic
o Bicarbonate 26 (21-28) normal
o PAO2-PaO2 37 (<10mmHg) *don’t worry too much about this one.
- Respiratory acidosis (pH and paCo2 in opposite directions)
- Compensation –bicarb is normal therefore no compensation.
- RESPIRATORY ACIDOSIS WITH NO COMPENSATION
However, the emergency staff had not waited for investigation. They had reacted
to the clinical situation with urgency.
Signs of acute asthma attack (i.e. with more swelling of mucosal membrane)
indicative of impending respiratory failure:
- Silent chest
- Sweating
- Feeble respiratory effort (no use of resp accessory muscles)
- Vomiting
- Panicking
- Pulse ox <90%
- Hx of childhood onset
- Previous ICU admission
- Inability to speak in sentences
- Altered mental status, confusion
- Poor air entry
- Low FEV
Additional comments on acute asthma:
- Blood gases normally not necessary, however markers of very severe life
threatening attack:
o Low pH (or high H+)
o Normal or high pCO2
o Severe hypoxia (<60mmHg)
- May need to be incubated
- Immediate treatment:
o Nebulised salbutamol (pressurized)
o Concurrently prepare adrenalin and incubation equipment
o Secure IV lines
o May add Ipratropium.
- Wheeze and quiet breath sounds indicate underventilation something
is happening that the brain is not firing off resp centres (she is fatiguing
and unable to compensate any longer) therefore cant blow off O2
acidic in the blood acidosis
- If she is not taking the steroids, she is not treating the inflammation
airways are narrowing
- Potassium (K) can drop quite low during asthma attack
- Salbutamol (inhaler and nebuliser) can induce tachycardia because there
are beta receptors in the heart.
- Cycle:
- * another feature of severe asthma attack is overinflated lungs
-
TRIGGER 5– MANAGEMENT
After emergency treatment, including continuous inhaled bronchodilators and IV
hydrocortisone Shona admitted to ICU
- Intravenous salbutamol was commenced
- The following day she recommenced on oral prednisolone
- Trained in the use of a peak flow meter, correct use of metered dose
inhalers with fluticasone and salbutamol
- A mgmt plan was worked out with Shona
- Discharge 5 days later feeling better than she had for months
- Met with Aboriginal liason social worker who arranged transport to
enable Shona to return to outpatients for review in 10 days.
Peak flow meter
- Quick reading of FEV
- Cheap, convenient good for home monitoring
- Need to be educated well for then
IV hydrocortisone
- Another form of corticosteroid
- Used for further treatment
- Injected if patient has swallowing difficulties/ administration difficulties
- Because of reduced consciousness
- 5mg prednisolone (oral) is equivalent to 20mg hydrocortisone (IV) (ie a
much higher dose)
Salbutamol
- IV recommended when failure to respond to beta2 agonists
- Check Cochrane reviews **
Fluticasone
- Alternative type of corticosteroid
- Can be administered by: (i) nebulising solution, (ii) given in aerosol form
(autohaler)/ MDI (metered dose inhalation), or (iii) dry powder
(tubuhaler).
Management plan
- Electronic resources of BB
- Asthma action plan
Follow up
- Using preventor?
- Any other attacks?
- Encourage to continue using preventers.
