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Final Year > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is the most significant cause of lung cancer?

A

Smoking

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2
Q

What is the most common type of lung cancer?

A

Non-small-cell lung cancer (80%):
Adenocarcinoma (40%)
Squamous cell carcinoma (20%)
Large-cell carcinoma (10%)
Other types (10%)

Small-cell lung cancer (SCLC) (20%)

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3
Q

What is mesothelioma?

A

Lung malignancy affecting mesothelial cells of pleura
Strongly linked to asbestos
Can take up to 45y to develop

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4
Q

What is the prognosis of mesothelioma?

A

Very poor
Chemo can improve survival, but is essentially palliative

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5
Q

Outline small-cell lung cancer

A

Contains neurosecretory granules that release neuroendocrine hormones
May be responsible for various paraneoplastic syndromes

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6
Q

Outline presentation of lung cancer

A

SOB
Cough
Haemoptysis
Finger clubbing
Recurrent pneumonia
Weight loss
Lymphadenopathy (often supraclavicular nodes 1st to be found)

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7
Q

List extrapulmonary manifestations of lung cancer

A

Recurrent laryngeal nerve palsy
Phrenic nerve palsy
SVC obstruction
Horner’s syndrome
Syndrome of inappropriate ADH (SIADH)
Cushing’s syndrome
Hypercalcaemia
Limbic encephalitis
Lambert-Eaton myasthenic syndrome

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8
Q

What is the association between lung cancer and recurrent laryngeal nerve palsy?

A

Presents with hoarse voice
Caused by tumour pressing on or affecting recurrent laryngeal nerve as passes through mediastinum

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9
Q

What is the association between lung cancer and phrenic nerve palsy?

A

Due to nerve compression
Causes diaphragm weakness and presents with SOB

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10
Q

What is the association between lung cancer and SVC obstruction?

A

Caused by direct tumour compression on SVC
Presents with facial swelling, difficulty breathing, distended neck and upper chest veins
Pemberton’s sign
MEDICAL EMERGENCY

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11
Q

What is Pemberton’s sign?

A

Raising hands over head causes facial congestion and cyanosis

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12
Q

What is the association between lung cancer and Horner’s syndrome?

A

Triad of partial ptosis, anhidrosis and miosis
Caused by Pancoast tumour (in pulmonary apex) pressing on sympathetic ganglion

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13
Q

What is the association between lung cancer and SIADH?

A

Caused by ectopic ADH secreted by SCLC
Presents with hyponatremia

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14
Q

What is the association between lung cancer and Cushing’s syndrome?

A

Caused by ectopic ACTH secretion by SCLC

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15
Q

What is the association between lung cancer and Hypercalcaemia?

A

Caused by ectopic PTH secreted by squamous cell carcinoma

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16
Q

What is the association between lung cancer and Limbic encephalitis?

A

Paraneoplastic syndrome
SCLC causes immune system to make antibodies to tissues in brain (limbic system), causing inflammation
Associated with anti-Hu antibodies

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17
Q

List the symptoms of limbic encephalitis

A

Short-term memory impairment
Hallucinations
Confusion
Seizures

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18
Q

What is the association between lung cancer and Lambert-Eaton Myasthenic Syndrome?

A

Caused by antibodies against SCLC
Antibodies target and damage voltage-gated calcium channels on presynaptic terminals in motor neurones

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19
Q

List the symptoms of Lambert-Eaton Myasthenic Syndrome

A

Weakness in proximal muscles
Affect intraocular muscles causing diplopia (double vision)
Levator muscles in eyelid, causing ptosis
Pharyngeal muscles, causing slurred speech and dysphagia (difficulty swallowing)
Dry mouth, blurred vision, impotence, dizziness due to autonomic dysfunction

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20
Q

Outline the referral criteria for lung cancer

A

Suspected cancer- Recommend chest xray within 2wks to patients over 40y with signs of:
Clubbing
Lymphadenopathy (supraclavicular/persistent abnormal cervical nodes)
Recurrent/persistent chest infections
Raised platelet count (thrombocytosis)
Chest signs of lung cancer

Offer chest xray to patients over 40y with:
2+ unexplained symptoms in patients that have never smoked
1+ unexplained symptoms in patients that have smoked/had asbestos exposure

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21
Q

What are unexplained lung cancer guidelines as NICE guidelines suggest

A

Cough
SOB
Chest pain
Fatigue
Weight loss
Loss of appetite

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22
Q

What are the 2 key examination findings that automatically indicate an urgent chest xray for lung cancer?

A

Finger clubbing
Supraclavicular lymphadenopathy

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23
Q

Outline investigations for lung cancer

A

Chest xray 1st line
Staging CT scan- Chest, abdomen, and pelvis- Should be contrast-enhanced
PET-CT- Inject radioactive tracer- Identify metastases by highlighting areas of increased metabolic activity
Bronchoscopy with endobronchial US (EBUS)- Detailed assessment of tumour and US-guided biopsy
Histological diagnosis (biopsy)

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24
Q

List some potential findings of lung cancer on xray

A

Hilar enlargement
Peripheral opacity (visible lesion in lung field)
Pleural effusion (usually unilateral in cancer)
Collapse

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25
Q

Outline management options in non-SCLC

A

Surgery 1st line if disease isolated to single area
Radiotherapy
Chemotherapy (adjuvant (to improve outcomes) or palliative)

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26
Q

Outline management of SCLC

A

Chemo and radiotherapy
Prognosis generally worse for SCLC than non-SCLC

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27
Q

When is endobronchial treatment used in lung cancer?

A

Stents or debulking as part of palliative treatment to relieve bronchial obstruction

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28
Q

Outline surgical options for removing lung tumour

A

Segmentectomy or wedge resection
Lobectomy (remove lung lobe)- Most commonly used
Pneumonectomy (remove entire lung)

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29
Q

What are the types of surgery that can be used to remove a lung tumour?

A

Thoracotomy
Video-assisted thoracoscopic surgery (VATS)- Minimally invasive ‘keyhole’ surgery
Robotic surgery

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30
Q

What is pneumonia?

A

Infection of lung tissue, causing inflammation in alveolar space
Seen as consolidation on chest xray
LRTI

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31
Q

What is acute bronchitis?

A

Infection and inflammation in bronchi and bronchioles
LRTI

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32
Q

Outline classification of pneumonia

A

Community-acquired pneumonia (CAP)
Hospital-acquired pneumonia (HAP)- Develops after >48h in hospital
Ventilator-acquired pneumonia (VAP)- Develops in intubated patients in ICU
Aspiration pneumonia

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33
Q

Outline aspiration pneumonia

A

Infection due to aspiration of food or fluids
Usually in patients with impaired swallowing (eg: Following a stroke or advanced dementia)
Associated with anaerobic bacteria

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34
Q

Outline presentation of pneumonia

A

Cough
Sputum production
SOB
Fever
Feeling generally unwell
Haemoptysis (coughing up blood)
Pleuritic chest pain (sharp chest pain, worse on inspiration)
Delirium (acute confusion)

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35
Q

What are the characteristic chest signs of pneumonia?

A

Bronchial breath sounds- Harsh inspiratory and expiratory breath sounds- Due to consolidation around the airway
Focal coarse crackles- Caused by air passing through sputum in airways
Dullness to percussion- Due to lung tissue filled with sputum/colapse

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36
Q

Outline indications of sepsis associated with pneumonia

A

Tachypnoea
Tachycardia
Hypoxia
Hypotension
Fever
Confusion

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37
Q

Outline the severity assessment scale of pneumonia

A

C- Confusion
U- Urea >7mmol/L
R- RR >30
B- BP <90 systolic or <60 diastolic
65- Age >65y

0-1= Consider treatment at home
>2= Consider hospital admission
>3= Consider intensive care

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38
Q

What is the most common cause of typical bacterial pneumonia?

A

Streptococcus pneumoniae (most common)
Haemophilus influenzae

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39
Q

When is Moraxella catarrhalis more likely to be a cause of pneumonia?

A

Immunocompromised patients
Chronic pulmonary disease

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40
Q

When is Pseudomonas aeruginosa more likely to be a cause of pneumonia?

A

Patients with cystic fibrosis or bronchiectasis

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41
Q

When is Staphylococcus aureus more likely to be a cause of pneumonia?

A

Cystic fibrosis

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42
Q

When is Methicillin-resistant Staphylococcus aureus (MRSA) more likely to be a cause of pneumonia?

A

Hospital-acquired infections

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43
Q

What is atypical pneumonia?

A

Caused by organisms that can’t be cultured in the normal way or detected using a gram stain

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44
Q

How is atypical pneumonia treated?

A

Penicillin is ineffective
Treat with macrolides (eg: Clarithromycin), fluoroquinolones (eg: Levofloxacin) and tetracyclines (eg: Doxycycline)

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45
Q

When is Legionella pneumophilia more likely to be a cause of pneumonia?

A

Atypical pneumonia
Caused by inhaling infected water from infected water systems, such as air conditioning
Causes a syndrome of SIADH, resulting in hyponatremia
Typical patient- Cheap hotel holiday, presents with pneumonia and hyponatremia
Diagnosis- Urine antigen test

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46
Q

When is Mycoplasma pneumoniae more likely to be a cause of pneumonia?

A

Atypical pneumonia
Milder pneumonia
Rash- Erythema multiforme- Target lesions
Neurological symptoms in young patients

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47
Q

When is Chlamydophilia pneumoniae more likely to be a cause of pneumonia?

A

Atypical pneumonia
Mild to moderate chronic pneumonia and wheezing in school-age children

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48
Q

When is Coxiella burnetii more likely to be a cause of pneumonia?

A

Atypical pneumonia
Q fever
Linked to exposure to bodily fluids of animals
Patient- Farmer with flu-like illness

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49
Q

When is Chlamydia psittaci more likely to be a cause of pneumonia?

A

Contracted from contact with infected birds
Patient example- Parrot owner

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50
Q

Outline pneumocystis jirovecii pneumonia (PCP)

A

Fungal pneumonia
Occurs in immunocompromised patients
Poorly controlled HIV and low CD4 count at particular risk

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51
Q

How does PCP present?

A

Subtle
Dry cough
SOB on exertion
Night sweats

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52
Q

Outline management of PCP

A

Co-trimoxazole (trimethoprim/sulfamethoxazole)
Low CD4 count prescribed prophylactic co-trimoxazole to protect against PCP

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53
Q

List complications of pneumonia

A

Sepsis
ARDS
Pleural effusion
Empyema
Lung abscess
Death

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54
Q

How is mild community-acquired pneumonia typically managed?

A

5 days oral ABs:
Amoxicillin or doxycycline or clarithromycin

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55
Q

How is moderate/severe pneumonia managed?

A

IV ABs
Respiratory support (eg: Oxygen/intubation/ventilation)

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56
Q

Outline investigations of pneumonia

A

Point-of-care test for CRP level
Chest xray
FBC- Raised WCC
Renal profile- Urea level for CURB-65 and AKI
CRP- Raised in inflammation and infection
Sputum cultures
Blood cultures
Pneumococcal and Legionella urinary antigen tests

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57
Q

What is PaO2 a marker of on an ABG

A

Partial pressure of oxygen
Amount of oxygen dissolved in blood
Low PaO2- Indicates hypoxia and respiratory failure

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58
Q

What is FiO2 a marker of?

A

Fraction of inhaled oxygen
Room air= FiO2 of 21%
Venturi masks control FiO2

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59
Q

How can you distinguish the type of respiratory failure?

A

Normal PaCO2 with low PaO2- Type 1 respiratory failure (only one affected)
Raised PaCO2 with low PaO2- Indicates Type 2 respiratory failure (2 affected)

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60
Q

Outline respiratory acidosis

A

CO2 makes blood acidotic by breaking down into carbonic acid (H2CO3)
Low pH (acidosis) with raised PaCO2- Respiratory acidosis
Suggests patient is retaining CO2

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61
Q

What is the role of bicarbonate in the body?

A

Kidneys produce bicarbonate
Bicarbonate acts as buffer to neutralise acid in blood and maintain normal pH
In acute resp acidosis- Bicarbonate not produced fast enough to compensate rising CO2

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62
Q

What does a raised bicarbonate suggest?

A

Patient chronically retains CO2
Kidneys respond to CO2 by producing additional bicarbonate
Seen in COPD

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63
Q

Outline respiratory alkalosis

A

Occurs when patient has raised respiratory rate and ‘blows off’ too much CO2
Hyperventilation syndrome
High pH and low PaCO2

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64
Q

Outline metabolic acidosis

A

Low pH, low bicarbonate

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65
Q

List causes of metabolic acidosis

A

Raised lactate- Lactate released during anaerobic respiration (indicating tissue hypoxia)
Raised ketones- DKA
Increased hydrogen ions- Due to renal failure, type 1 renal tubular acidosis or rhabdomyolysis
Reduced bicarbonate- Due to diarrhoea, renal failure or type 2 renal tubular acidosis

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66
Q

Outline metabolic alkalosis

A

Raised pH, raised bicarbonate

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67
Q

What are the causes of metabolic alkalosis?

A

Results from loss of H+ ions: GI tract- Vomiting
Kidneys- Due to increased activity of aldosterone- Increased H+ ion excretion

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68
Q

List causes of increased aldosterone activity

A

Conn’s syndrome (primary hyperaldosteronism)
Liver cirrhosis
HF
Loop diuretics
Thiazide diuretics

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69
Q

List respiratory support options from least to most invasive

A

Oxygen therapy
High flow nasal cannula
Intubation and mechanical ventilation
ECMO

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70
Q

What is Acute Respiratory Distress Syndrome (ARDS)?

A

Occurs due to severe inflammatory reaction in lungs
Often secondary to sepsis or trauma

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71
Q

Outline features of ARDS

A

Collapse of alveoli and lung tissue (atelectasis)
Pulmonary oedema (not related to HF or fluid overload)
Decreased lung compliance (reduced lung inflation when ventilated)
Fibrosis of lung tissue (typically after 10+ days

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72
Q

List the clinical signs of ARDS

A

Acute respiratory distress
Hypoxia with inadequate response to oxygen therapy
Bilateral infiltrates on chest xray

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73
Q

Outline management of ARDS

A

Respiratory support
Prone position
Careful fluid management to avoid excess fluid collecting on lungs
PEEP

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74
Q

Why is PEEP used in ARDS?

A

In ARDS- Only small portion of total lung volume is aerated
During mechanical ventilation, low volumes and pressures used to avoid over-inflating small functional portion of lung
PEEP prevents lungs from collapsing further

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75
Q

List the benefits of prone positioning

A

Reduces compression of lungs by other organs
Improving blood flow to lungs, especially well-ventilated areas
Improves clearance of secretions
Improves overall oxygenation
Reduces required assistance from mechanical ventilation

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76
Q

Outline basic methods of oxygen therapy

A

FiO2 depends on oxygen flow rate
Nasal cannula: 24-44% oxygen
Simple face mask: 40-60% oxygen
Venturi mask: 24-60% oxygen
Face mask with reservoir (non-rebreather): 60-95% oxygen

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77
Q

What is the maximum oxygen flow rate of a nasal cannula?

A

4L/min

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78
Q

What is the function of a venturi mask?

A

Used to deliver exact conc. oxygen in COPD CO2 retainers
Blue- 2L, 24% FiO2
White- 4L, 28% FiO2
Orange- 6L, 31%
Yellow- 8L, 35%
Red- 10L, 40%
Green- 15L, 60%

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79
Q

What is end-expiratory pressure?

A

Pressure that remains in airways at end of exhalation

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80
Q

How can PEEP be delivered?

A

High-flow nasal cannula
Non-invasive ventilation (NIV)
Mechanical ventilation

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81
Q

What is PEEP?

A

Positive end-expiratory pressure
Additional pressure in airways at end of exhalation that keeps them inflated
Keeps airways from collapsing and improves ventilation
Reduces atelectasis
Decreases effort of breathing

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82
Q

Outline high-flow nasal cannulas

A

Allows controlled flow rates up to 60L/min of humidified and warmed oxygen
High flow rate reduces amount of room air patient inhales alongside O2, increasing conc. inspired O2
Adds PEEP
Provides dead space washout- Adds O2 to dead space

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83
Q

What is CPAP?

A

Continuous positive airway pressure
Constant pressure added to lungs to keep airways expanded
Used in OSA
Not technically NIV as ventilation is still dependant on respiratory muscles

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84
Q

Outline non-invasive ventilation (NIV)

A

Full face mask, hood or tight fitting nasal mask to blow air forcefully into lungs
BiPAP (Bilevel)
Involves a cycle of high and low pressure to correspond with inspiration and expiration

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85
Q

Outline NIV IPAP and EPAP

A

High and low pressure to correspond to inspiration and expiration
IPAP (inspiratory PAP)- Pressure during inspiration- Air forced into lungs
EPAP (expiratory PAP)- Pressure during expiration- Stops airways collapsing

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86
Q

Outline mechanical ventilation

A

Used when other forms of respiratory support (NIV and oxygen) inadequate or CI
Ventilator machine used to move air in and out of lungs
Patients generally require sedation whilst on ventilator
ETT or tracheostomy
Delivers controlled pressures and volumes into lungs

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87
Q

Outline Extracorporeal Membrane Oxygenation (ECMO)

A

Blood removed from body and oxygenated, CO2 removed, then pumped back into body
Only used short term in potentially reversible cause of respiratory failure

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88
Q

What is spirometry?

A

Establishes objective measures of lung function
Involves different breathing exercises into machine and measures volume of air and flow rates

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89
Q

What is reversibility testing?

A

Give bronchodilator (eg: Salbutamol) before repeating spirometry

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90
Q

What is FEV1?

A

Air a person can forcefully exhale in 1s
Measures how easily air moves out of lungs
Reduced with airflow obstruction

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91
Q

What is FVC?

A

Total air a person can forcefully exhale in 1s
Measures total volume of air a person can take into their lungs
Reduced with restricted lung capacity

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92
Q

How is obstructive lung disease diagnosed?

A

FEV1:FVC ratio <70%
Suggests obstruction is slowing air passage out of lungs

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93
Q

What is the difference between asthma and COPD?

A

Asthma- Obstruction is a narrowed airway due to bronchoconstriction
COPD- Chronic airway and lung damage causing obstruction
Test reversibility- Give bronchodilator- Typically reversible in asthma, less so in COPD

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94
Q

Outline restrictive lung disease

A

FEV1 and FVC equally reduced
FEV1:FVC ratio >70%
Limits ability of lungs to expand and sill with air
Leads to inadequate ventilation of alveoli and insufficient blood oxygenation
FEV1:FVC ratio normal/raised in restrictive without obstructive pathology affecting airflow- FVC reduced due to restriction of lung expansion and capacity

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95
Q

List conditions of restrictive lung disease

A

Interstitial lung disease- Idiopathic pulmonary fibrosis
Sarcoidosis
Obesity
Motor neurone disease
Scoliosis

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96
Q

What does a low FVC and normal FEV1:FVC ratio indicate?

A

Restrictive lung disease

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97
Q

What does a low FVC and low FEV1:FVC ratio indicate?

A

Combination of obstructive lung disease and restrictive lung disease

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98
Q

What does a low FEV1:FVC ratio indicate?

A

Obstructive lung disease

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99
Q

Outline peak flow

A

Measures fastest point of expiratory flow of air
Demonstrates how much obstruction to airflow is present in lungs

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100
Q

What is predicted peak flow based on?

A

Sex
Height
Age

Result can be recorded as percentage of the predicted

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101
Q

What is asthma?

A

Chronic inflammatory airway disease leading to variable airway obstruction
Smooth muscle in airways is hypersensitive and responds to stimuli by constricting and causing airflow obstruction
Bronchoconstriction reversible with bronchodilators

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102
Q

List the atopic conditions

A

Asthma
Eczema
Hay fever
Food allergies

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103
Q

Outline presentation of asthma

A

SOB
Chest tightness
Dry cough
Wheeze
Diurnal variability- Symptoms fluctuate at different times of day- Typically worse at night
Widespread ‘polyphonic’ wheeze

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104
Q

What are the top differentials of a localised monophonic wheeze?

A

Inhaled foreign body
Tumour
Thick sticky mucus plug obstructing an airway

Chest xray is next step

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105
Q

What are the typical triggers of asthma?

A

Infection
Night time/early morning
Exercise
Animals
Cold, damp, dusty air
Strong emotions

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106
Q

What are the meds that can worsen asthma?

A

Non-selective BBs- Propanolol
NSAIDs- Ibuprofen or naproxen

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107
Q

Outline investigations of asthma

A

Spirometry
Reversibility testing- >12% increase in FEV1 supports diagnosis of asthma
FeNO- Measures conc. NO exhaled- Marker of airway inflammation- >40ppb +ve test result- Smoking can lower FeNO making results unreliable
Peak flow variability- >20% supports diagnosis
Direct bronchial challenge

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108
Q

How is direct bronchial challenge testing done?

A

Tests for diagnosis of asthma
Opposite of reversibility testing
Inhaled histamine or metacholine stimulates bronchoconstriction, reducing FEV1 in patients with asthma

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109
Q

Outline beta-2 adrenergic receptor agonists

A

Bronchodilators (open airways)
Adrenalin acts on smooth muscle of airways to cause relaxation
Stimulating adrenalin receptors dilates bronchioles and reverses bronchoconstriction
SABA (salbutamol)- Work quickly, effects last a few hrs- Rescue/reliever medication
LABA (salmeterol)- Slower to act, last longer

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110
Q

Outline inhaled corticosteroids

A

Beclometasone
Reduce inflammation and reactivity of airways
Used as maintenance or preventer medications

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111
Q

Outline Long-acting muscarinic antagonists (LAMA)

A

Tiotropium
Block acetylcholine receptors
Acetylcholine receptors are stimulated by parasympathetic nervous system and cause contraction of bronchial smooth muscles
Blocking acetylcholine receptors dilate bronchioles, reverse bronchoconstriction

112
Q

Outline leukotriene receptor antagonists

A

Montelukast
Block effects of leukotrienes
Leukotrienes cause inflammation, bronchoconstriction and mucus secretion in airways

113
Q

How does theophylline work?

A

Relaxes bronchial smooth muscle and reduces inflammation
Has very narrow therapeutic window- Can be toxic in excess- Requires monitoring

114
Q

Outline maintenance and reliever therapy (MART)

A

Combination inhaler containing ICS and fast and long-acting beta-agonist (eg: Formoterol)
Replaces all other inhalers- Used as a preventer and a reliever

115
Q

Outline long-term asthma management (NICE guidelines)

A
  1. SABA (salbutamol)
  2. ICS (low dose)
  3. LRT (montelukast)
  4. LABA (salmeterol)
  5. Consider changing to MART
  6. Increase ICS to moderate dose
  7. High dose ICS or add LAMA or theophylline
  8. Specialist management (eg: Oral corticosteroids)
116
Q

Outline the additional management of asthma

A

Asthma self management plan
Yrly flu jab
Yrly asthma review
Regular exercise
Avoid smoking
Avoid triggers where possible

117
Q

List features of an acute exacerbation of asthma

A

Progressive SOB
Use of accessory muscles
Tachypnoea
Symmetrical expiratory wheeze on auscultation
Tight chest

118
Q

What is seen on an ABG in a patient with an acute exacerbation of asthma?

A

Respiratory alkalosis
Raised RR causes drop in CO2
Normal pCO2 or low O2 is concerning- Getting tired
Respiratory acidosis due to high pCO2 is a very bad sign

119
Q

List features of moderate exacerbation of asthma

A

Peak flow 50-75% best or predicted

120
Q

List features of severe exacerbation of asthma

A

Peak flow 33-50% best or predicted
RR >25
HR >110
Unable to complete sentences

121
Q

List features of life-threatening exacerbation of asthma

A

Peak flow <33%
O2 sats <92%
PaO2 <8kPa
Becoming tired
Confusion or agitation
No wheeze or silent chest
Haemodynamic instability (shock)

122
Q

Outline management of mild exacerbations of asthma

A

Inhaled salbutamol via spacer
Quadrupled dose ICS (for up to 2wks)
Oral steroids (prednisolone) if higher ICS is inadequate
ABs if convincing evidence of bacterial infection
Follow up within 48h

123
Q

Outline management of moderate exacerbations of asthma

A

Consider hospital admission
Nebulised beta-2 agonists
Steroids (eg: Oral prednisolone or IV hydrocortisone)

124
Q

Outline management of severe exacerbations of asthma

A

Hospital admission
Oxygen to maintain sats 94-98%
Nebulised ipratropium bromide
IV magnesium sulphate
IV salbutamol
IV aminophylline

125
Q

Outline management of life-threatening exacerbations

A

Admission to HDU or ICU
Intubation and ventilation

126
Q

What needs monitoring with salbutamol treatment?

A

Serum potassium
Salbutamol causes potassium to be absorbed from blood into cells- Hypokalaemia
Also causes tachycardia and lactic acidosis

127
Q

Outline management of asthma after an acute attack

A

Consider rescue pack of oral steroids to start early in exacerbation
Prednisolone (1 to 2mg/kg for 5d)

128
Q

Outline obstructive sleep apnoea

A

Caused by collapse of pharyngeal airway
Patient stops breathing for up to a few minutes

129
Q

List risk factors for OSA

A

Middle age
Male
Obesity
Alcohol
Smoking

130
Q

Outline presentation of OSA

A

Episodes of apnoea during sleep
Snoring
Morning headache
Waking up unrefreshed from sleep
Daytime sleepiness
Conc. problems
Reduced oxygen saturation during sleep
Severe cases- HTN, HF- Increase risk of MI and stroke

131
Q

Outline Epworth Sleepiness Scale

A

Used to assess symptoms of sleepiness associated with OSA

132
Q

Outline investigations of OSA

A

Epworth sleepiness scale
Sleep studies
Respiratory polygraphy

133
Q

Outline management of OSA

A

Reversible risk factors- Reduce alcohol, smoking cessation, weight loss
CPAP
Surgery- Involves significant surgical reconstruction of soft palate and jaw- Uvulopalatopharyngoplasty (UPPP)

134
Q

What is sarcoidosis?

A

Chronic granulomatous disorder
Granulomas- Inflammatory nodules full of macrophages
Usually associated with respiratory symptoms but has many extra-pulmonary manifestations

135
Q

Outline epidemiology of sarcoidosis

A

20-39y or around 60y
Women
Black ethnic origin

136
Q

20-40y black female with dry cough and SOB
May have nodules on shins

A

Sarcoidosis (with erythema nodosum)

137
Q

What are the skin features of sarcoidosis?

A

Erythema nodosum- Nodules of inflamed SC fat on shins- Raised, red, tender, painful, SC nodules on both shins
Inflammation of fat = Panniculitis

Lupus pernio- Specific to sarcoidosis- Raised purple skin lesions on cheeks and nose

138
Q

How can sarcoidosis affect the lungs?

A

Mediastinal lymphadenopathy
Pulmonary fibrosis
Pulmonary nodules

139
Q

List the systemic symptoms of sarcoidosis

A

Fever
Fatigue
Weight loss

140
Q

How can sarcoidosis affect the liver?

A

Liver nodules
Cirrhosis
Cholestasis

141
Q

How can sarcoidosis affect the eyes?

A

Uveitis
Conjunctivitis
Optic neuritis

142
Q

How can sarcoidosis affect the heart?

A

Bundle branch block
Heart block
Myocardial muscle involvement

143
Q

How can sarcoidosis affect the kidneys?

A

Kidney stones (hypercalcaemia)
Nephrocalcinosis
Interstitial nephritis

144
Q

How can sarcoidosis affect the CNS?

A

Nodules
Pituitary involvement (diabetes insipidus)
Encephalopathy

145
Q

How can sarcoidosis affect the PNS?

A

Facial nerve palsy
Mononeuritis multiplex

146
Q

How can sarcoidosis affect bones?

A

Arthralgia
Arthritis
Myopathy

147
Q

What is Lofgren’s syndrome?

A

Specific presentation of sarcoidosis
Classic triad- Erythema nodosum, bilateral hilar lymphadenopathy, polyarthralgia

148
Q

List differential diagnosis of sarcoidosis

A

TB
Lymphoma
Hypersensitivity pneumonitis
HIV
Toxoplasmosis
Histoplasmosis

149
Q

Which blood tests are used to investigate sarcoidosis?

A

Raised angiotensin-converting enzyme (ACE)- Used as a screening test
Raised calcium (hypercalcaemia)

150
Q

Outline imaging used in sarcoidosis

A

Chest xray- May show hilar lymphadenopathy
High resolution CT- Hilar lymphadenopathy and pulmonary nodules
MRI- CNS involvement
PET scan- Active inflammation

151
Q

Outline histology of sarcoidosis

A

Often bronchoscopy with US-guided biopsy of mediastinal lymph nodes
Shows non-caseating granulomas with epithelioid cells

152
Q

List other tests used to investigate sarcoidosis

A

U&Es- Kidney involvement
Urine ACR- Look for proteinuria
LFTs
Ophthalmology
ECG and ECHO
US liver and kidney

153
Q

Outline management of sarcoidosis

A

Conservative- If no/mild symptoms
Oral steroids (for 6-24mths)- 1st line
Bisphosphonates protect against osteoporosis if on long-term steroids
Methotrexate- 2nd line
Lung transplant- In severe pulmonary disease

154
Q

What is the prognosis of sarcoidosis?

A

Spontaneously resolves in around half of patients, usually within 2yrs
Sometimes progresses to pulmonary fibrosis and pulmonary HTN
Overall mortality <10%

155
Q

What is pulmonary HTN?

A

Increased resistance and pressure in pulmonary arteries
Causes strain on R side of heart as tries to pump blood through lungs
Back pressure through R side of heart and into systemic venous system
Defined as mean pulmonary arterial pressure >20mmHg

156
Q

List the causes of pulmonary HTN

A

Group 1- Idiopathic or connective tissue disease (eg: SLE)
Group 2- Left HF, usually due to MI or systemic HTN
Group 3- Chronic lung disease (eg: COPD or pulmonary fibrosis)
Group 4- Pulmonary vascular disease (eg: Pulmonary embolism)
Group 5- Miscellaneous- Sarcoidosis, glycogen storage disease, haematological disorders

157
Q

What are the signs and symptoms of pulmonary HTN?

A

SOB
Syncope (LOC)
Tachycardia
Raised JVP
Hepatomegaly
Peripheral oedema

158
Q

Outline ECG changes in pulmonary HTN

A

Indicate R sided heart strain
P pulmonale (peaked P waves)
Right ventricular hypertrophy (tall R waves in V1 and V2 and deep S waves in V5 and V6)
Right axis deviation
RBBB

159
Q

Outline chest xray changes in pulmonary HTN

A

Dilated pulmonary arteries
RV hypertrophy

160
Q

Outline other investigations in pulmonary HTN

A

Raised NT-proBNP- Indicates RV failure
ECHO- Can be used to estimate pulmonary artery pressure

161
Q

Outline management of idiopathic pulmonary HTN

A

CCBs
IV prostaglandins (eg: Epoprostenol)
Endothelin receptor antagonists (eg: Macitentan)
Phosphodiesterase-5 inhibitors (eg: Sildenafil)

162
Q

How is secondary pulmonary HTN managed?

A

Treat underlying cause- Such as PE, COPD, SLE

163
Q

What are the supportive treatments of pulmonary HTN?

A

Oxygen and diuretics
Used for complications- Respiratory failure, oedema, arrhythmias

164
Q

What is the prognosis of pulmonary HTN?

A

Poor
Mean survival of 2-3yrs after diagnosis if untreated

165
Q

What is a pulmonary embolism?

A

Thrombus in pulmonary arteries
Embolus- Thrombus that has travelled in blood from a DVT
Blocks lung tissue and strains R side of heart

166
Q

List risk factors for pulmonary embolism

A

Immobility
Recent surgery
Long-haul travel
Pregnancy
Hormone therapy with oestrogen
Malignancy
Polcythaemia (raised Hb)
SLE
Thrombophilia

167
Q

Outline VTE prophylaxis

A

LMWH- Enoxaparin
Anti-embolic compression stockings

168
Q

What are the CIs of LMWH?

A

Active bleeding
Existing anticoagulation (warfarin or DOAC)

169
Q

What are the CIs of anti-embolic compression stockings?

A

Peripheral arterial disease

170
Q

Outline presentation of PE

A

Can be asymptomatic
SOB
Cough
Haemoptysis
Pleuritic chest pain (sharp pain on inspiration)
Hypoxia
Tachycardia
Raised RR
Low-grade fever
Haemodynamic instability causing hypotension
Signs of DVT

171
Q

What is the PERC rule?

A

Pulmonary embolism rule-out criteria
Clinician estimates <15% probability of PE to decide whether further investigations for PE are needed

172
Q

What is the Wells score?

A

Predicts probability of patient having PE

173
Q

Outline how PE is diagnosed

A

Chest xray- Usually normal in PE, but required to rule out other pathology
Wells score- Outcome decides next step:
- Likely- Perform CTPA
- Unlikely- Perform d-dimer- If positive perform CTPA

174
Q

Outline d-dimer for use in diagnosing PE

A

Sensitive but not specific for VTE

175
Q

Which conditions can cause a raised d-dimer?

A

Pneumonia
Malignancy
HF
Surgery
Pregnancy

176
Q

List the 3 imaging options for diagnosing PE

A

CT pulmonary angiogram- With IV contrast
Ventilation perfusion single photon emission computed tomography (V/Q SPECT) scan
Planar ventilation-perfusion (VQ) scan

177
Q

What is a VQ scan?

A

Uses radioactive isotopes and gamma camera to compare ventilation with perfusion of lungs
Used in patients with renal impairment/contrast allergy/risk from radiation, where CTPA unsuitable
Isotopes inhaled to fill lungs, picture taken to demonstrate ventilation- Then contrast containing isotopes injected and demonstrates perfusion
2 images compared

178
Q

What is the result of a PE on a VQ scan?

A

Deficit in perfusion
Lung tissue ventilated but not perfused

179
Q

What is the difference between Planar V/Q and V/Q SPECT scans?

A

Planar- 2D
SPECT- 3D- More accurate

180
Q

What can an ABG show in PE?

A

Respiratory alkalosis
Hypoxia causes raised RR
Breathing fast- Blow off extra CO2
Low CO2- Blood becomes alkalotic

181
Q

How can you tell the difference between PE and hyperventilation on ABG?

A

PE- Low pO2
Hyperventilation- High pO2

182
Q

Outline supportive management of PE

A

Admission as required, oxygen as required, analgesia as required, monitor for deterioration

183
Q

Outline anticoagulation management in PE

A

1st line- Treatment-dose apixaban or rivaroxaban
LMWH- An alternative

184
Q

How is a massive PE with haemodynamic compromise treated?

A

Continuous infusion of unfractionated heparin
Consider thrombolysis

185
Q

What are the 2 ways of delivering thrombolysis?

A

IV using peripheral cannula
Catheter-directed thrombolysis (directed into pulmonary arteries using central catheter)

186
Q

What is thrombolysis?

A

Inject fibrinolytic that rapidly dissolves clots
Streptokinase, alteplase, tenecteplase

187
Q

What is the risk of thrombolysis?

A

Bleeding

188
Q

Outline long-term anticoagulation used in VTE

A

DOAC, warfarin or LMWH

189
Q

What are the CIs to DOACs?

A

Severe renal impairment (creatinine clearance <15ml/min)
Antiphospholipid syndrome
Pregnancy

190
Q

What is the target INR for warfarin when treating DVTs and PEs?

A

Between 2 and 3

191
Q

When is warfarin 1st line in patients with a DVT or PE?

A

In patients with antiphospholipid syndrome (who also require initial concurrent treatment with LMWH)

192
Q

When is LMWH the 1st line anticoagulant in DVT or PE?

A

Pregnancy

193
Q

How long is anticoagulation continued following PE or DVT?

A

3mths with reversible cause
Beyond 3mths with unprovoked PE, recurrent VTE, or irreversible underlying cause (eg: Thrombophilia)
3-6mths in active cancer

194
Q

What is a pneumothorax?

A

Air enters pleural space, separating lung from chest wall
Can occur spontaneously or secondary to trauma/medical interventions/lung pathology

195
Q

What are the risk factors for a spontaneous pneumothorax?

A

Tall, thin, young man presenting with sudden breathlessness and pleuritic chest pain, possibly whilst playing sports

196
Q

List causes of pneumothorax

A

Spontaneous
Trauma
Iatrogenic- Due to lung biopsy/mechanical ventilation/central line insertion
Lung pathologies- Infection, asthma, COPD

197
Q

Outline investigations of pneumothorax

A

Erect chest xray- Simple pneumothorax- Shows area between lung tissue and chest wall with no lung markings- Will be a line demarcating edge of lung
CT thorax- Detects pneumothorax too small to be seen on chest xray

198
Q

Outline management of pneumothorax

A

No SOB and <2cm rim of air on CXR- No treatment required as spontaneously resolves, follow up in 2-4wks

SOB or >2cm rim of air on CXR- Aspiration and reassessment- If aspiration fails twice insert chest drain

199
Q

When are chest drains required in pneumothorax?

A

If aspiration fails twice
Unstable patients
Bilateral or secondary pneumothoraces

200
Q

Outline chest drains

A

Triangle of safety- 5th ICS, midaxillary line (lateral edge of latissimus dorsi), anterior axillary line (lateral edge of pec major)

Needle inserted just above rib to avoid NV bundle
Once inserted, CXR to assess positioning

201
Q

What are the key complications of chest drains?

A

Air leaks around the drain site (indicated by persistent bubbling of fluid, particularly on coughing)
Surgical emphysema- Air collects in SC tissue

202
Q

When may a pneumothorax require surgical management?

A

Chest drain fails to correct pneumothorax
Persistent air leak in drain
Pneumothorax reoccurs

203
Q

Outline surgical management of pneumothorax

A

Video-assisted thoracoscopic surgery (VATS)

Abrasive pleurodesis
Chemical pleurodesis
Pleurectomy

204
Q

List signs of tension pneumothorax

A

Tracheal deviation away from side of pneumothorax
Reduced air entry on affected side
Increased resonance to percussion on affected side
Tachycardia
Hypotension

205
Q

What is a tension pneumothorax?

A

Caused by trauma to chest wall that creates 1 way valve that lets air in, but not out of pleural space
Air is trapped in pleural space
Creates pressure inside thorax to push mediastinum across, kink big vessels in mediastinum and cause cardiorespiratory arrest

206
Q

Outline management of tension pneumothorax

A

Insert a large bore cannula into 2nd intercostal space in midclavicular line
Chest drain required for definitive management once pressure relieved

207
Q

What are the 2 categorisations of pleural effusion?

A

Exudative- High protein content (>30g/L)
Transudative- Lower protein content (<30g/L)

208
Q

What is Light’s criteria?

A

Establishes exudative effusion
Uses protein or lactate dehydrogenase (LDH)

Pleural fluid protein/serum protein >0.5
Pleural fluid LDH/serum LDH >0.6
Pleural fluid LDH >2/3 of normal upper limit serum LDH

209
Q

What are the exudative causes of pleural effusion?

A

Related to inflammation

Cancer (lung or mesothelioma)
Infection (pneumonia or TB)
RA

210
Q

What are the transudative causes of pleural effusion?

A

Related to fluid moving across or shifting into pleural space

Congestive HF
Hypoalbuminaemia
Hypothyroidism
Meigs syndrome

211
Q

What is Meigs syndrome?

A

Triad of:
Benign ovarian tumour
Pleural effusion
Ascites

212
Q

Outline presentation of pleural effusion

A

SOB
Dullness to percussion over effusion
Reduced breath sounds
Tracheal deviation away from effusion in large effusions

213
Q

Outline CXR findings in pleural effusion

A

Blunting of costophrenic angle
Fluid in lung fissures
Larger effusions have meniscus (curving upwards where it meets chest wall and mediastinum)
Tracheal and mediastinal deviation away from effusion in very large effusions

214
Q

List investigations of pleural effusions

A

CXR
US and CT- Detect smaller effusions
Pleural fluid analysis- Requires sample taken by aspiration or chest drain

215
Q

Outline treatment of pleural effusions

A

Conservative- If small
Pleural aspiration- Needle in chest wall and aspirate fluid, may recur
Chest drain- Prevents reoccurring

216
Q

What is empyema?

A

Infected pleural effusion
Pleural aspiration- Pus, low pH, low glucose, high LDH
Treat- Chest drain and ABs

217
Q

What is interstitial lung disease?

A

Includes conditions that cause inflammation and fibrosis (scarring) of lung parenchyma

218
Q

List types of ILD

A

Idiopathic pulmonary fibrosis
Secondary pulmonary fibrosis
Hypersensitivity pneumonitis
Cryptogenic organising pneumonia
Asbestosis

219
Q

Outline presentation of ILD

A

SOB on exertion
Dry cough
Fatigue

220
Q

What are the typical findings of idiopathic pulmonary fibrosis on examination?

A

Bibasal fine end-inspiratory crackles
Finger clubbing

221
Q

Outline diagnosis of ILD

A

Clinical features
High-resolution CT scan of thorax- Ground glass
Spirometry- FEV1 and FVC equally reduced , FEV1:FVC ration >70%- Restrictive pattern
Lung biopsy
Bronchoalveolar lavage

222
Q

Outline general management of ILD

A

Remove/treat underlying cause
Home oxygen if hypoxia
Stop smoking
Physiotherapy and pulmonary rehab
Pneumococcal and flu vaccine
Advanced care planning and palliative care if appropriate
Lung transplant

223
Q

What is idiopathic pulmonary fibrosis?

A

Progressive pulmonary fibrosis with no apparent cause

224
Q

Outline presentation of idiopathic pulmonary fibrosis

A

Insidious onset SOB and dry cough >3mths
Usually affects adults >50y

225
Q

What is the prognosis of idiopathic pulmonary fibrosis?

A

Poor
2-5y life expectancy from diagnosis

226
Q

Which medications can slow progression of idiopathic pulmonary fibrosis?

A

Pirfenidone- Reduces fibrosis and inflammation
Nintedanib- Reduces fibrosis and inflammation by inhibiting tyrosine kinase

227
Q

Which drugs can cause secondary pulmonary fibrosis?

A

Amiodarine (also causes grey/blue skin)
Cyclophosphamide
Methotrexate
Nitrofurantoin

228
Q

Which conditions can cause secondary pulmonary fibrosis?

A

Alpha-1 antitrypsin deficiency
RA
SLE
Systemic sclerosis
Sarcoidosis

229
Q

What is hypersensitivity pneumonitis?

A

Extrinsic allergic alveolitis
Involves type III and type IV hypersensitivity reaction to environmental allergen
Inhalation of allergens patient sensitised to causes immune response- Inflammation and damage to lung tissue

230
Q

Outline diagnosis of hypersensitivity pneumonitis

A

Bronchoalveolar lavage performed during bronchoscopy
Airways washed with sterile saline to gather cells- Fluid collected and analysed
Raised lymphocytes

231
Q

List specific examples of causes of hypersensitivity pneumonitis

A

Bird-fancier’s lung- Reaction to bird droppings
Farmer’s lung- Reaction to mouldy spores in hay
Mushroom worker’s lung- Reaction to specific mushroom antigens
Malt worker’s lung- Reaction to mould on barley

232
Q

What is cryptogenic organising pneumonia?

A

Focal area of inflammation of lung tissue
Can be idiopathic or triggered by infection/inflammatory disorders/meds/radiation/environmental toxins/allergens

233
Q

Outline presentation of cryptogenic organising pneumonia

A

SOB
Cough
Fever
Lethargy
Inspiratory crackles on auscultation

234
Q

Outline management of cryptogenic organising pneumonia

A

CXR- Focal consolidation
Lung biopsy- Definitive

235
Q

How is cryptogenic organising pneumonia treated?

A

Systemic corticosteroids

236
Q

What is asbestosis?

A

Lung fibrosis related to asbestos exposure
Oncogenic- Causes cancer

237
Q

What can asbestos inhalation cause?

A

Lung fibrosis
Pleural thickening and pleural plaques
Adenocarcinoma
Mesothelioma

238
Q

What is bronchiectasis?

A

Permanent dilation of bronchi
Sputum collects and grows- Chronic cough, continuous sputum production and recurrent infections

239
Q

What causes bronchiectasis?

A

Results from damage to airways

Idiopathic
Pneumonia
Whooping cough (pertussis)
TB
Alpha-1-antitrypsin deficiency
CT disorder (RA)
CF
Yellow nail syndrome

240
Q

What is yellow nail syndrome?

A

Yellow fingernails
Bronchiectasis
Lymphoedema

241
Q

What are the symptoms of bronchiectasis?

A

SOB
Chronic productive cough
Recurrent chest infections
Weight loss

242
Q

What are the signs of bronchiectasis?

A

Sputum pot by bedside
Oxygen therapy
Weight loss
Finger clubbing
Signs of cor pulmonale (eg: Raised JVP and peripheral oedema)
Scattered crackles throughout chest that change/clear with coughing
Scattered wheezes and squeaks

243
Q

Outline investigations of bronchiectasis

A

Sputum culture- Haemophilus influenza, Pseudomonas aeruginosa

244
Q

What can be seen on CXR of bronchiectasis?

A

Tram-track opacities (parallel markings of side-view of dilated airway)
Ring shadows (dilated airways seen end-on)

High resolution CT (HRCT)- Test of choice for establishing diagnosis

245
Q

Outline general management of bronchiectasis

A

Vaccines (pneumococcal and influenza)
Respiratory physiotherapy- Clear sputum
Pulmonary rehab
Long-term ABs (azithromycin) for frequent exacerbations
Inhaled colistin for Pseudomonas aeruginosa colonisation
Long-acting bronchodilators- For breathlessness
Long-term oxygen therapy- In hypoxia
Surgical lung resection
Lung transplant

246
Q

Outline management of infective exacerbations in bronchiectasis

A

Sputum culture
Extended course of antibiotics- 7-14d
Ciprofloxacin- For exacerbations caused by Pseudomonas aeruginosa

247
Q

What is COPD?

A

Long-term, progressive condition involving airway obstruction, chronic bronchitis and emphysema
Damage to lung tissue obstructs flow of air

248
Q

What is chronic bronchitis?

A

Long-term symptoms of cough and sputum production due to inflammation in bronchi

249
Q

What is emphysema?

A

Involves damage and dilatation of alveolar sacs and alveoli, decreasing surface area for gas exchange

250
Q

Outline presentation of COPD

A

SOB
Cough
Sputum production
Wheeze
Recurrent respiratory infections

Does NOT cause clubbing/haemoptysis/chest pain

251
Q

Outline diagnosis of COPD

A

Based on clinical presentation and spirometry
Spirometry- Shows obstructive picture- FEV1:FVC ratio <70%- Little or no response to reversibility testing with beta-2 agonists
TLCO- Tests diffusion of inhaled gas into blood (reduced in COPD)

252
Q

What is the initial medical treatment of COPD?

A

Short-acting beta-2 agonists (salbutamol)
Short-acting muscarinic antagonists (ipratropium bromide)

253
Q

How is extra management of COPD determined?

A

If symptoms and exacerbations still a problem, measured by:

Previous diagnosis of asthma or atopy
Variation in FEV1 >400mls
Diurnal variability in peak flow >20%
Raised blood eosinophil count

254
Q

Which vaccines should patients with COPD receive?

A

Pneumococcal and annual flu

255
Q

If there are no asthmatic or steroid-responsive features, what is the treatment of COPD?

A

LABA
LAMA

256
Q

If there are asthmatic or steroid-responsive features, what is the treatment of COPD?

A

LABA
ICS

257
Q

What is the final inhaler step for COPD management?

A

LABA
LAMA
ICS

258
Q

What are the specialist management options of COPD?

A

Nebulisers- Salbutamol or ipratropium
Oral theophylline
Oral mucolytic therapy to break down sputum (eg: Carbocisteine)
Prophylactic ABs (azithromycin)
Oral corticosteroids (prednisolone)
Oral phosphodiesterase-4 inhibitors (roflumilast)
Long-term oxygen therapy at home
Lung volume reduction surgery
Palliative care

259
Q

What monitoring is required when taking azithromycin?

A

ECG and liver function before and during treatment

260
Q

When is long-term oxygen therapy an option in COPD?

A

Chronic hypoxia
Polycythaemia
Cyanosis
Cor pulmonale

Smoking is a CI

261
Q

What is cor pulmonale?

A

Right sided HF caused by respiratory disease
Increased pressure and resistance in pulmonary arteries limits RV pumping blood into pulmonary arteries
Causes back pressure into RA, VC, and systemic venous system

262
Q

What are the causes of cor pulmonale?

A

COPD
PE
ILD
CF
Primary pulmonary HTN

263
Q

What are the symptoms of Cor pulmonale?

A

Can be asymptomatic
SOB
Peripheral oedema
Breathlessness of exertion
Syncope
Chest pain

264
Q

What are the signs of cor pulmonale on examination?

A

Hypoxia
Cyanosis
Raised JVP
Peripheral oedema
Parasternal heave
Loud 2nd HS
Murmurs (eg: Pansystolic in tricuspid regurg)
Hepatomegaly (pulsatile in tricuspid regurg)

265
Q

Outline management of cor pulmonale

A

Treat symptoms and underlying cause
LTOT
Prognosis is poor

266
Q

Outline acute exacerbation of COPD

A

Rapidly worsening symptoms
Cough/SOB/Sputum production/wheezing

267
Q

Outline an ABG of COPD acute exacerbation

A

Respiratory acidosis
Low pH- Acidosis
Low pO2- Hypoxia and respiratory failure
Raised CO2- CO2 retention (hypercapnia)
Raised bicarbonate- Chronic retention of CO2

268
Q

Outline diagnosis of a patient with COPD as a CO2 retainer

A

CO2 makes blood acidotic
Low pH with raised pCO2 suggests acutely retaining CO2- Respiratory acidosis
Raised bicarbonate suggests chronically retaining CO2- Maintain normal pH- In acute exacerbation kidneys can’t keep up with rising CO2- Blood acidotic despite raised bicarbonate

269
Q

List investigations used in COPD acute exacerbations

A

ABG
Chest xray- Look for pneumonia
ECG- Look for arrhythmias
FBC- Infection
U&E
Sputum culture
Blood cultures- In signs of sepsis

270
Q

Outline oxygen therapy in COPD

A

CO2 retainers- When treated with oxygen can cause oxygen-induced hypercapnia- Ventilation-perfusion mismatch- Hb binding less well to CO2 when also bound to O2
Target 88-92% if risk of CO2 retention
Target 94-98% if no retention CO2
Venturi masks

271
Q

Outline use of venturi masks

A

Deliver a specific % conc. oxygen
Allow some oxygen to leak out side of mask and normal air to be inhaled alongside O2
Environmental air contains 21% O2
24% (blue), 28% (white), 31% (orange), 35% (yellow), 40% (red), 60% (green)

272
Q

Outline management of an acute exacerbation of COPD

A

1st line:
Regular inhalers or nebulisers (eg: Salbutamol and ipratropium)
Steroids (eg: Prednisolone 30mg once daily 5d)
ABs (if evidence of infection)

Respiratory physio can help clear sputum

Additional:
IV aminophylline
NIV
Intubation and ventilation with admission to intensive care

Doxapram- Used as respiratory stimulant if NIV/intubation not appropriate

273
Q

What are the inclusion criteria for NIV?

A

Persistent respiratory acidosis (pH <7.35 and PaCO2 >6) despite max. medical treatment
Potential to recover
Acceptable to patient

274
Q

What are the main CIs to NIV?

A

Untreated pneumothorax
Any structural abnormality or pathology affecting face/airway/GI tract
All patients have CXR before NIV to exclude pneumothorax

275
Q

What needs monitoring whilst on NIV?

A

ABGs (1h after every change, then 4h until stable)
IPAP increased by 2-5cm increments until acidosis resolves

Final Year (14 decks)

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