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POEM > Breathing Part 2 - Critical Illnesses > Flashcards

Breathing Part 2 - Critical Illnesses Flashcards

1
Q

How does acute asthma present?

A

Features:

  • worsening dyspnoea, wheeze and cough that is not responding to salbutamol
  • maybe triggered by a respiratory tract infection
  • BTS guidelines split into moderate, severe, and life-threatening
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2
Q

Outline the features of moderate acute asthma.

A
  • PEFR 50-75% best or predicted
  • Speech normal
  • RR < 25 / min
  • Pulse < 110 bpm
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3
Q

Outline the features of severe acute asthma.

A
  • PEFR 33 - 50% best or predicted
  • Cannot complete sentences
  • RR > 25/min
  • Pulse > 110 bpm
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4
Q

Outline the features of life-threatening asthma.

A
  • PEFR < 33% best or predicted
  • Oxygen sats < 92%
  • Silent chest, cyanosis or feeble respiratory effort
  • Bradycardia, dysrhythmia or hypotension
  • Exhaustion, confusion or coma
NB/ remember with 33-92 CHEST
C = cyanosis 
H = hypotension
E = exhaustion (normal pCO2)
S = silent chest
T = tachycardia
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5
Q

What is the importance of a normal PaCO2 in acute asthma?

A

A normal pCO2 in an acute asthma attack indicates exhaustion and should, therefore, be classified as life-threatening.

NB/FREQUENT MCQ!

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6
Q

Outline ‘near-fatal asthma’.

A

Characterised by a raised pC02 and/or requiring mechanical ventilation with raised inflation pressures.
Essentially requires an anaesthetist (they should be here before this ever happens!)

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7
Q

What investigations are appropriate in acute asthma?

A
  • PEFR
  • Pulse oximetry
  • ABG (sats <92%)
  • CXR (only if pneumothorax suspected; life-threatening asthma; or failure to respond to treatment)
  • Bloods - U+E including regular K+ monitoring
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8
Q

Explain the treatment of acute asthma (O SHIT ME!).

A
  • Provide high flow O2
  • Sit patient up - instruct to hold onto rails
  • Check trachea and chest for signs of pneumothorax
  • Administer high-dose (O2 driven) nebulised salbutamol 5mg/terbutaline 10mg, or 10 puffs of salbutamol into a spacer device with face mask.
  • Give a corticosteroid to all patients with acute asthma - either prednisolone 40-50 mg PO or hydrocortisone 100mg IV
  • Add nebulised ipratropium bromide 500mcg 4-6 hourly to B2-agonist treatment for patients with acute severe or life-threatening asthma
  • Use IV aminophylline only after consultation with senior medical staff
  • Remember patients unable to talk cannot drink or eat (IV fluids required)
  • Repeat ABG after an hour if: initial PaO2 <8Kpa; or pCO2 normal or increased; or if patient deteriorates
  • Correct electrolyte abnormalities exacerbated by B2 agonist or steroid therapy.
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9
Q

What are the criteria for discharge in acute asthma?

A

Criteria for discharge:

  • been stable on their discharge medication (i.e. no nebulisers or oxygen) for 12–24 hours
  • inhaler technique checked and recorded
  • PEF >75% of best or predicted
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10
Q

Outline acute asthma pathogenesis (if you want)

A

Exposure to the antigen will result in CD4 T cells
differentiating into T helper cells, and they will begin
to secrete IL-4 (causes B cells to become plasma
cells and being secreting IgE) and IL-5 (bind to
eosinophils and mast cells, making them reactive
to the antigen)
Mast cells release histamine & prosta-glandin (as
well as leukotrienes; LTC4).

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11
Q

What are some features of acute exacerbation of COPD?

A

Features:

  • increase in dyspnoea, cough, wheeze
  • there may be an increase in sputum suggestive of an infective cause
  • patients may be hypoxic and in some cases have acute confusion
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12
Q

List the 3 most common infective cause of acute exacerbation of COPD.

A

The most common bacterial organisms that cause infective exacerbations of COPD are:

- Haemophilus influenzae (most common cause)
- Streptococcus pneumoniae
- Moraxella catarrhalis
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13
Q

Outline the NICE guidelines on acute exacerbation of COPD.

A

NICE guidelines from 2010 recommend the following:

  • increase frequency of bronchodilator use and consider giving via a nebuliser
  • give prednisolone 30 mg daily for 5 days
  • it is common practice for all patients with an exacerbation of COPD to receive antibiotics. NICE do not support this approach. They recommend giving oral antibiotics ‘if sputum is purulent or there are clinical signs of pneumonia’
  • the BNF recommends one of the following oral antibiotics first-line: amoxicillin or clarithromycin or doxycycline.
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14
Q

Outline the oxygen management of acute exacerbation of COPD.

A

Give O2:

aim to maintain SpO2 of 88-92% without precipitating respiratory acidosis or worsening hypercapnia.

  • If known COPD and drowsy, or history of type 2 RF then give an FiO2 of 24-28% via Venturi mask and obtain an ABG.
  • Titrate the FiO2 up with serial ABG sampling until the minimum FiO2 that achieves SpO2 of 88-92% is achieved.
  • Reduce inhaled O2 if SpO2 is >92%
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15
Q

Outline the bronchodilator/steroid management of acute exacerbation of COPD.

A

Give bronchodilators and steroids:

  • Nebulised salbutamol 5mg or terbutaline 5-10 mg
  • Consider adding nebulised ipratropium 0.5 mg
  • Use O2 driven nebulisers unless patient is hypercapnic, acidotic
  • Prednisolone 30 mg PO stat, then continued once daily for 7 days
  • Hydrocortisone 100mg IV if cannot take prednisolone PO
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16
Q

Outline the antibiotic management of acute exacerbation of COPD.

A

Give antibiotics:

  • Amoxicillin/doxycycline/clarithromycin if the patient reports increase of purulent sputum or if clinical evidence of pneumonia/consolidation on CXR
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17
Q

Outline other drug management of acute exacerbation of COPD.

A
  • Only consider IV aminophylline if there is an inadequate response to neb bronchodilators.
  • Consider naloxone if the patient is taking an opioid analgesic that may cause respiratory depression
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18
Q

Outline the role of non-invasive ventilation in acute exacerbation of COPD.

A
  • Standard early therapy for type 2 RF in COPD
  • Improves blood gas measurements in ED
  • Reduces intubation rates
  • CPAP or BiPAP
  • Check CXR before starting - will convert a pneumothorax to a tension pneumothorax (cause of cardiac arrest)
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19
Q

Describe the pathogenesis of COPD (if you want).

A

COPD is characterised by chronic airflow limitation due to impedance to expiratory airflow, mucosal oedema, infection, bronchospasm, and bronchoconstriction due to decreased lung elasticity.

Smoking is the main risk factor. Other causes are alpha-1-antitrypsin deficiency, and chronic infection (e.g. bronchiectasis)

It is a mix of chronic bronchitis and emphysema.

Emphysema is defined pathologically as the
dilatation and destruction of tissue distal to the
terminal bronchioles; this leads to loss of elastic
recoil that causes a closing of airways in
expiration. Pink puffers (mainly emphysema) and
blue bloaters (mainly chronic bronchitis) are
described but most patients have a mix

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20
Q

What is pneumonia?

A

Symptoms and signs of lower respiratory infection (SOB; productive cough; fever) usually associated with CXR abnormalities. Always consider pneumonia in patients with septicaemia and acute confusional states.

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21
Q

What are the causes of community acquired pneumonia?

A

Bacteria (most common):

  • Streptococcus pneumoniae most commonly
  • Mycoplasma pneumoniae
  • Haemophilus influenzae
  • Legionella
  • Chlamydia psittaci
  • Staphylococcus aureus

Viruses:

  • COVID-19
  • Influenza A and B
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22
Q

Outline the signs and symptoms of CAP.

A
  • Cough
  • Fever
  • Sputum
  • SOB
  • Pleuritic chest pain
  • Myalgia
  • Rigors
  • Haemoptysis (rarely)

NB/pneumonia can present without obvious chest signs.

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23
Q

Outline important components of examining patients with suspected pneumonia.

A
  • Auscultate (bronchial breathing - harsh breath sounds/patch of inspiratory crackles - sign of consolidation)
  • Assess for signs of sepsis
  • RR, pulse, BP
  • Check SpO2
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24
Q

What investigations are appropriate in CAP?

A
  • ABG if SpO2 <90% or known to have COPD
  • U+E, FBC, and CRP.
  • Blood cultures before giving antibiotics.
  • Obtain CXR.
  • Obtain sputum cultures and consider urinary pneumococcal and Legionella antigen testing.
  • COVID-19 nasopharyngeal swab for testing.
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25
Q

Outline the CURB-65 score.

A 
Confusion = 1
Urea >7 mmol/L = 1 
RR >30/min = 1
Low BP (sBP <90/dBP <=60) = 1
Age >= 65 years = 1

Patients with ‘mild’ ilness and good social circumstances may be safely discharged with amoxicillin 0.5-1g PO TDS for 5 days, simple analgesia.

Patients who score 2 are at increased risk of death and should be admitted as inpatients.

Patients >=3 are at high risk of death (severe pneumonia)

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26
Q

Describe the treatment of pneumonia.

A

Suitable for discharge:

  • Analgesia, oral abx 5 days, GP follow-up (GP will decide if CXR after 6 weeks)

Admitted, but not severely unwell:

  • Amoxicillin 0.5-1g PO tds + erythromycin 500mg PO qds (or clarithromycin mg bd)
  • Monitor SpO2 and provide O2 accordingly
  • Provide simple analgesia

Sepsis (BUFALO):

  • Blood cultures
  • Urinary catheter (aim for output of > 0.5 mg/kg/hr)
  • IV crystalloid fluids
  • IV antibiotics (e.g. co-amoxiclav 1.2 IV tds + clarithromycin 500mg IV bd)
  • ABG for lactate
  • Administer O2 if required
  • Aim for MAP of >65 mmHg
  • Contact ICU
27
Q

Outline how patients present with pulmonary embolism.

A
  • Most dyspnoea (commonly without other symptoms)
  • Syncope (+/- cyanosis, cardiac arrest, angina - signs of massive PE)
  • Pleuritic chest pain (minority)
  • In any patient with unexplained SOB or hypoxia always consider PE
28
Q

List some important things to ask about in a history in suspected PE.

A
  • Concurrent illness
  • Surgical procedures
  • Recent hospital admission
  • Past history - DVT/PE
  • Travel
  • Family history
29
Q

What may be seen on examining a patient with suspected PE?

A
  • Normal
  • Tachycardia/tachypnoea common
  • Pyrexia following lung infarction common
  • Hypoxia (30% normal SpO2)
  • BP - hypotension = massive PE
  • Full respiratory and cardiovascular examination required
  • Always examine legs for signs of DVT
30
Q

What is the Wells score?

A

A clinical probability assessment score for PE.

31
Q

Outline the Wells score (clinical features and scoring)

A 
Signs of DVT (leg swelling/tenderness = 3
IV drug use = 3
PE most likely diagnosis = 3
HR >100 = 1.5 
Prior PE/DVT = 1.5 
Bedridden >3 days or surgery in last 4 weeks = 1.5 
Cancer = 1
Haemoptysis = 1

Total score >= 4.5 OR have an elevated D-dimer requires pulmonary imaging. ONLY a normal D-dimer AND a PE unlikely Wells score will exclude PE.

32
Q

Which investigations must be performed in suspected PE?

A
  • Insert an IV cannula
  • Blood taken for FBC and U&E
  • Take D-dimer test on any patient Wells <= 4.0 (a normal D-dimer in patient scoring <4.0 excludes PE)
  • ECG (MI/pericarditis)
  • CXR (pneumothorax/pneumonia)
33
Q

What is the appropriate diagnostic imaging in PE?

A
  1. CTPA: higher dose of radiation (worse for younger patients) but gives definite diagnosis (and can see other conditions like aortic dissection)
  2. V/Q mismatch scan: lower dose of radiation and may not give definitive answer.
34
Q

Describe the management of DVT/PE.

A
  • If ambulant and normal observations - treat in outpatients after senior review
  • Admit if hypoxic, hypotensive, tachycardic, tachypnoeic or unable to cope at home
  • If Wells score 5 or more and D-dimer positive - give treatment dose LMWH 1.5 mg/kg OD prior to CTPA
  • Once confirmed stop LMWH and commence therapeutic anticoagulant for SIX months
  • Give a dose of anticoagulant e.g. apixaban 10mg PO bd for 7 days, then 5 mg PO bd SIX months
  • Thrombolysis only indicated if MASSIVE PE
35
Q

Describe the management of suspected massive PE.

A
  • CV compromise - urgent ICU help.
  • Bedside ECHO for dilated RV.
  • Bedside USS to demonstrate DVT.
  • Do NOT take unstable patients for CT or V/Q scanning.
  • If suspicion of PE high and patient haemodynamically stable - administer thrombolytic therapy. No delay. IV alteplase.
  • If contraindicated or not tolerated - discuss with experts - consider alternatives such as surgical embolectomy; catheter directed thrombolysis)
  • After thrombolysis, start unfractionated heparin IVI; dose based on patient’s weight
36
Q

What is a pneumothorax?

A

An abnormal collection of air in the pleural space between the lung and the chest wall. May be primary spontaneous (no underlying cause) or secondary spontaneous (underlying cause).

37
Q

What are the risk factors for secondary spontaneous pneumothorax?

A

Risk factors:

  • pre-existing lung disease: COPD, asthma, cystic fibrosis, lung cancer, Pneumocystis pneumonia
  • connective tissue disease: Marfan’s syndrome, rheumatoid arthritis
  • ventilation, including non-invasive ventilation
38
Q

Outline the presentation of a spontaneous pneumothorax.

A
  • Unilateral pleuritic chest pain (most)
  • Dyspnoea (most)
  • Tachypnoea
  • Tachycardia
  • Normal/hyperresonant percussion note with reduced air entry on affected side

Severe symptoms:

  • Inability to speak
  • Gasping
  • Hypoxia

Look for tracheal deviation, tachypnoea, tachycardia, and hypotension when these symptoms occur.

39
Q

Outline the initial assessment and management of spontaneous pneumothorax.

A
  • Monitor pulse, SpO2, and BP.
  • Gain IV access.
  • Administer high flow O2.
  • When no signs of tension, an ABG to help assess patient’s chronic lung disease and guide O2 therapy.
  • Erect CXR - principal way to make diagnosis.
40
Q

Describe the management of a primary pneumothorax?

A

BTS guidelines:

Recommendations include:

  • if the rim of air is < 2cm and the patient is not short of breath then discharge should be considered
  • otherwise, aspiration should be attempted
  • if this fails (defined as > 2 cm or still short of breath) then a chest drain should be inserted
41
Q

Describe the management of a secondary pneumothorax?

A

BTS guidelines:

Recommendations include:

  • if the patient is > 50 years old and the rim of air is > 2cm and/or the patient is short of breath then a chest drain should be inserted.
  • otherwise aspiration should be attempted if the rim of air is between 1-2cm. If aspiration fails (i.e. pneumothorax is still greater then 1cm) a chest drain should be inserted. All patients should be admitted for at least 24 hours
  • if the pneumothorax is less the 1cm then the BTS guidelines suggest giving oxygen and admitting for 24 hours
42
Q

Describe the aspiration technique in pneumothorax.

A
  • Confirm side of pneumothorax
  • Sit patient upright
  • Infiltrate 1% lidocaine, then insert 16G IV cannula just about the third rib in the second intercostal space MCL
  • Alternatively, lay the patient on their side with the pneumothorax upwards
  • Insert cannula in the 5th ICS in the anterior axillary line (triangle of safety)
  • Remove the needle; attach a three-way tap, then aspirate with a 50 mL syringe
  • Continue aspiration until the patient coughs excessively or until 2.5 L of air is removed
43
Q

What is a tension pneumothorax?

A
  • Life-threatening emergency.
  • One-way valve forms - gas progressively enters pleural space and is unable to leave.
  • Increased pressure causes complete lung collapse on affected side and shifts mediastinum to the contra-lateral side.
  • Leads to kinking of great vessels
  • Reduces venous return and therefore cardiac output.
  • May occur rapidly, resulting in cardiac arrest in minutes.
44
Q

What are the causes of tension pneumothorax?

A
  • Trauma trauma trauma
  • Iatrogenic - insertion of central venous line
  • Small simple pneumothorax –> IPPV commenced = tension pneumothorax
45
Q

Outline some signs/symptoms of tension pneumothorax.

A
  • Dyspnoea, tachypnoea, and ARDS
  • Absent breath sounds on affected side
  • Hyper-resonance over affected lung
  • Distended neck veins (unless hypovolaemic), tachycardia, and hypotension - then loss of consciousness
  • Trachea deviated WAY from the affected side (rarely apparent clinically)
  • Increased airway pressure in patient receiving IPPV
46
Q

What must you NOT waste time doing if you have clinical suspicion of a tension pneumothorax?

A

Do NOT waste time on a chest X-ray.

47
Q

How is tension pneumothorax managed?

A
  • Performing a finger thoracostomy decompression followed by a chest drain
  • Or, 16G IV cannula in 2nd ICS MCL - will get a hiss after needle withdrawn then insert axillary chest drain.
  • Check position of drain with chest X-ray.
48
Q

What is an open pneumothorax?

A

Pneumothorax associated with a chest wall defect
that, when a negative pressure is generated, air is
entrained into the chest cavity through the defect
instead of trachea as it provides less resistance. If
the hole is more than 0.75 times the size of the
trachea, air preferentially enters through defect.
This results in inadequate oxygenation and
ventilation, and a progressive build-up of air in the
pleural space. The pneumothorax may become
tension if a flap has been created that allows air in,
but not out

49
Q

What are some features of an open pneumothorax?

A

A wound in the chest wall is identified that appears to be ‘sucking in’ air into the chest and may be visibly bubbling. If large, reduced breath sounds at affected area and hyper-resonant percussion note.

50
Q

How is an open pneumothorax managed?

A
  • Three-sided dressing: allows air to escape during expiration but not enter during inspiration
  • ASAP insert a chest drain and close the wound
51
Q

What are some symptoms and signs of a massive haemothorax?

A
  • SOB
  • Trauma to chest wall
  • Palpable crepitus at chest (#ribs)
  • Decreased chest expansion
  • Dullness to percussion
  • Reduced breath sounds
  • Mediastinal/tracheal deviation (only if massive)
52
Q

Define a haemothorax.

A
  • Collection of blood in the pleural space.
  • Penetrating or blunt injuries.
  • Most a result of rib fractures, lung parenchymal, and minor venous injuries.
  • Therefore self-limiting.
53
Q

How is massive haemothorax managed?

A
  • Large bore chest drain (prevent intramural clotting)

- Thoracotomy

54
Q

Define flail segment.

A
  • Fracture of >= ribs in two places allowing part of the chest wall to move independently.
  • Usually indicates underlying pulmonary contusion.
  • Lateral flail segment: ribs fracture anteriorly and posteriorly
  • Anterior flail segment: all ribs fracture anteriorly; free portion is sternum, costal cartilages, and medial ends of ribs
55
Q

How does flail segment present?

A
  • Chest pain
  • Moves paradoxically with breathing compared to rest of chest wall
  • Clinical diagnosis: look for areas that move inward on inspiration and outward on expiration
56
Q

What two conditions much you be suspicious of in flail segment?

A
  • Pneumothorax

- Haemothorax

57
Q

How do you investigate a flail chest segment?

A
  • ABCDE
  • Assess for respiratory compromise
  • SpO2 (pulse oximetry)
  • ABG - combination of hypoxia and respiratory acidosis (inc. pCO2, [H+]) indicates severe respiratory compromise
  • CT more useful than CXR for demonstrating fractures and other injuries (pulmonary contusions/pneumothorax/haemothorax)
58
Q

How is flail segment managed?

A
  • ABCDE
  • High-flow O2
  • Treat any life-threatening problems as they arise
  • Contact ICU/anaesthesia
  • Regular analgesia/PCA/epidural/regional anaesthesia
59
Q

What is pulmonary contusion?

A

Pulmonary contusion is an injury to lung
parenchyma, leading to oedema and blood
collecting in alveolar spaces and loss of normal
lung structure & function. This blunt lung injury
develops over the course of 24 hours, leading
to poor gas exchange, increased pulmonary
vascular resistance and decreased lung
compliance. There is also a significant inflammatory
reaction to blood components in the lung, and 50-
60% of patients with significant pulmonary
contusions will develop bilateral Acute
Respiratory Distress Syndrome (ARDS). Other
complications are: respiratory failure, atelectasis
and pneumonia.

60
Q

How is pulmonary contusion investigated?

A
  • ABCDE
  • Assess for respiratory compromise
  • SpO2 (pulse oximetry)
  • ABG - combination of hypoxia and respiratory acidosis (inc. pCO2, [H+]) indicates severe respiratory compromise
  • CT more useful than CXR for demonstrating pulmonary contusions
61
Q

Outline the pathophysiology of acute heart failure.

A
  • HF causes a drop in MAP that initially stimulates
    baroreceptors that feed into medullary
    cardiovascular center [MCVC].
  • MCVC tries to increase MAP by reducing vagal tone and increase sympathetic tone leading to increase
    heart contractility and rate.
  • Sympathetic activtiy also contracts arteries [inc. TPR] and veins [inc. venous return] and the release of adrenaline from adrenal medulla, which stimulate all of the above actions.
  • Renin-angiotensin-system [RAS] is also
    stimulated in heart failure due to reduced kidney
    perfusion. The end product, Angiotensin II,
    causes vasoconstriction, aldosterone release and
    ADH release causing Na+ and H2O retention by the
    kidneys.
  • These mechanisms are beneficial initially
    as they increase blood volume, therefore venous
    return and SV, TPR and HR, therefore maintaining a
    high CO, however, these compensatory
    mechanisms worsen HF: increase cardiac
    workload > increase O2 demands > stretching of
    ventricles > reduced contractility > peripheral
    and pulmonary edema
  • Acute HF can evolve into cardiogenic shock,
    which is an acute circulatory failure
62
Q

Outline the management of acute heart failure.

A
  1. Sit the patient upright
  2. 100% high flow O2 (if no underlying respiratory disease)
  3. Gain IV access and perform ECG (treat arrhythmias e.g. AF as they arise)
  4. Diamorphine 1.25-5mg IV slowly
  5. Furosemide 40-80 mg IV slowly (monitor weight and urine output)
  6. Do not routinely offer the following unless concomitant MI, severe HTN, or valve disese:
    - Sublingual GTN 2 sprays
    - if sBP > 90 then give IV infusion isosorbide dinitrate 2-10 mg/h
    - if sBP <90 treat as cardiogenic shock
63
Q

Outline the investigation of suspected acute heart failure.

A
  • ECG
  • FBC/U&E
  • Cardiac enzymes (Troponin/BNP (<100 ng/L rules out acute HF)
  • ECHO
  • ABG
  • CXR: ABCDE mnemonic
A = Alveolar shadowing ("bat's wings' sign")
B = B-lines (interstitial oedema)
C = Cardiomegaly
D = Diversion of blood to upper lobe/dilated vessels
E = Effusion (blunting of costophrenic angles)
64
Q

Outline CXR findings in acute heart failure.

A 
A = Alveolar shadowing ("bat's wings' sign")
B = B-lines (interstitial oedema)
C = Cardiomegaly
D = Diversion of blood to upper lobe/dilated vessels
E = Effusion (blunting of costophrenic angles)

POEM (11 decks)

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