REsp Flashcards

1
Q

Hospital acquired pneumonia - antibiotics to use

A

Ceftriaxone (low risk: HA from ward)

High risk: from ICU, ventilator etc (concern about pseudomonas)
Tazosin = piperacillin/tazobactram

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2
Q

Common causes of HA pneumonia

A

Gram neg: klebsiella, E coli, pseudomonas, bacteroides

MRSA

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3
Q

Common causes of community acquired pneumonia (typical)

A

Strep pneumonia (90% cases)
H influenzae
Moraxella
Staph aureus

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4
Q

Common causes of community acquired pneumonia (atypical)

A

Mycoplasma pneumonia
Chlamydia pneumoniae
Legionella

Pneumocystis Jiroveci

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5
Q

What is COPD characterised by?

A

airway inflammation and limitation that IS NOT FULLY reversible (asthma is fully reversible so is not COPD)

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6
Q

What medical conditions does COPD include? Define them

A

Emphysema - dilation and destruction of lung tissue distal to terminal bronchiole (alveolar wall destruction and overinflation)

Chronic bronchitis - persistent PRODUCTIVE cough for at least 3 consecutive months in at least 2 consecutive years (airway inflammation)

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7
Q

Risk factors/causes of COPD

A
Cigarette smoking 
Air pollution
Occupational exposure 
Alpha1 antitrypsin deficiency 
Recurrent RTIs in childhood
Genetics
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8
Q

What pattern would you see on respiratory function test with COPD?

A

Restrictive lung disease.
Forced expiratory ratio (FEV1/FVC) <70% indicating airflow obstruction.
FEV1 is reduced but FVC normal.

With no improvement with bronchodilator (ventolin).

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9
Q

Pathophysiology of emphysema

A

Noxious agent causes release of destructive cytokines and neutrophils, macrophages and CD8+ T cells which cause ongoing destruction of lung parenchyma - destruction of elastin and alveolar membranes -> reduced elastic coil - air trapping during expiration

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10
Q

Pathophysiology of chronic bronchitis

A

Noxious agent causes release of destructive cytokines and neutrophils, macrophages and CD8+ T cells which cause ongoing destruction of lung parenchyma and airway inflammation and remodelling

-> enlarged mucus secreting glands, goblet cell metaplasia, bronchial wall fibrosis, hyper secretion of mucus, inflammation

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11
Q

Clinical features of COPD

A

Chronic productive cough
Wheeze
SOB

HX smoking

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12
Q

What will you find on chest examination for COPD (Non-examination)

A
Auscultation - breath sounds reduced with prolonged expiratory phase, wheeze 
Percussion - normal/hyper-resonance
Vocal resonance - normal or reduced
Hyperinflation (barrel chest)
Decr expansion
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13
Q

Classic CXR findings for COPD

A

hyperinflation (>6 ribs anterior ribs above diaphragm in mid-clavicular line)
Flat hemidiaphragms
Large central pulmonary arteries
Decr peripheral vascular markings

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14
Q

Management plan for COPD

A

CONFIRM diagnosis w pulmonary function tests

  • smoking cessation
  • influenza and pneumococcus vaccine (reduces risk of exacerbations)
  • pulmonary rehab
  • medications (depend on stage of disease)
  • Long-term o2 therapy if chronic resp failure (Stage 4) - must be non-smokers
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15
Q

Pharmacological treatment of COPD

A

Stage 1: Short acting bronchodilators when needed

  • Short acting beta 2 agonists (Salbutamol/Ventolin)
  • SAMAR (ipratropium)

Stage 2: regular treatment with one or more long acting bronchodilators

  • LABAs (Salmeterol/Serevent)
  • LAMAR (Tiotropium/Spiriva)

Stage 3/4: Inhaled glucocorticosteroids if repeated exacerbations

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16
Q

Complications of COPD

A

CHRONIC BRONCHITIS COMPLICAITONS:

  • SCC of lung resulting from squamous metaplasia
  • Infective exacerbations
  • Hypoxia -> pulmonary HTN -> cor pulmonale

EMPHESEMA COMPLCIATIONS

  • Loss of diffusion capacity
  • pneumothorax
  • hypoxia -> pulmonary HTN -> cor pulmonale
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17
Q

Management of exacerbation of COPD

A

Give O2

Bronchodilators

Corticosteroids

Antibiotics

Mobilisation

Non-invasive ventilation - BiPap, VPAP

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18
Q

Why don’t you give high flow O2 with COPD?

A

Don’t give too much too quickly though, may be in chronic resp failure where their drive to breathe is low O2.
If you increase O2 then you decrease their drive to breathe which leads to hypercapnoea

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19
Q

Definition of bronchiectasis

A

Chronic infection of bronchi and bronchioles leads to permanent dilation of bronchi, as well as inflammatory changes in airway walls and neighbouring parenchyma

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20
Q

Pathophys of bronchiectasis

A

Recurrent inflammation of bronchial walls weakens walls

Fibrosis of surrounding parenchyma puts traction on and weakens walls, causes dilation

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21
Q

Symptoms of bronchiectasis

Signs

A

Cough
Copious purulent foul smelling sputum
intermittent haemoptysis

Signs:

  • Clubbing
  • Exp wheeze
  • Coarse insp crepitations
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22
Q

Causes of bronchiectasis

A

Obstructive

  • tumour
  • foreign body
  • thickened mucus (asthma)

Post-inflammation

  • pneumonia
  • Tb
  • measles etc

Weakened defences
-CF

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23
Q

Common causes of lung abscesses

A
  • Most commonly a complication of aspiration pneumonia (aspirated objects accompanied by bacteria -> inflammation secondary to inflammation -> localised consolidation)
  • Pulmonary infarct
  • malignancy
  • Penetrating trauma
  • Bronchial obstruction
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24
Q

Management of lung abscess

A

Empiracle antibiotics

If non-resolving, surgical intervention

+/- postural drainage
+/- chest physiotherapy

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25
What is the histopath pattern of Tb?
Caseating granulomatous inflammation with epithelial cells, giant cells and lymphocytes and central caseating necrosis.
26
Tests for DIAGNOSIS OF Tb
Quantiferon GOLD test or Mantoux test Ziel-nelson stain
27
When does primary vs progressive vs secondary occur?
Primary Tb is what occurs following first exposure to M. Tb Progressive Tb occurs in less than 10% patients, mostly immunocompromised/malnourished. Rapid spread through lungs/body Secondary: reactivation of a dormant focus of primary infection, often with immunosuppression (steroids and HIV)
28
Possible sequelae of progressive Tb
Caveatting fibrocaseous Tb (erosion of ghon complex into bronchiole) Miliary Tb (haematogenous dissemination) Tuberculous bronchopneumonia (infection spreads rapidly -> diffuse bronchopneumonia or lobar exudative consolidation)
29
Gohn complex vs focus in Tb
Occurs in primary Tb GHON focus - small area of encapsulated granulomatous inflammation (central cassation) GHON complex - involves adjacent lymphatics and lymph nodes
30
What area of lungs do Tb GHON focuses in primary Tb occur in?
Mid zone sub-pleural
31
At what stage in Tb do patients become symptomatic and what are those SX?
Primary Tb usually asymptomatic Progressive- have pulmonary and systemic SX Secondary Tb - systemic symptoms (cough, fever, malaise, weight loss)
32
What area of lungs does secondary tb affect?
Upper lobes
33
Causes of granulomatous inflammation in the lung
``` Tb Sarcoid (non-caseating) Hypersensitivity pneumonitis Wegener's granulomatosis vasculitis Aspiration pneumonia Rheumatoid nodules ```
34
Treatment of Sarcoidosis
Immunosuppression
35
What is sarcoidosis?
Non-caseating granulomatous inflammation - affects lungs, skin - common in young adults 20-40
36
Asthma
- 3 characteristics 1. reversible airflow limitation 2. airway hyperresponsiveness to a variety of stimuli 3. bronchial inflammation (T lypmphocytes, mast cells, eosinophils)
37
Asthma symptoms
Wheeze (exp if mild; exp and insp if severe) Cough Chest tightness SOB Often worse at night
38
Why might asthma become associated with irreversible airflow limitation?
Chronic inflammation leading to airway remodeling (smooth and goblet cell hyperplasia with incr mucus secretion) in chronic asthma patients (60-70)
39
Triggers for asthma
``` Cold Exercise Pollen, dust, pollution Tobacco smoke Animals - cat, dog, birds URTI Medications (NSAIDs, beta blocers) Emotion, stress ```
40
Investigations for asthma
CXR and ABG Lung function tests (forced peak expiratory flow) - decr Spirometry - >15% improvement in FEV1 or peak exp flow rate following bronchodilator Blood or sputum test - large eosinophil titre and IgA/IgE levels Skin prick tests to help identify allergic causes Histamine or methacholine bronchial provocation testing (measures airway hyperresponsiveness). Note: can provoke resp arrest so dont do in individuals w FEV1<1.5L or w brittle asthma
41
Management of chronic asthma
Intermittent asthma § Inhaled SABA (beta 2 agonist) as needed Mild persistent § Use low potency inhaled GC Moderate persistent § Mild dose of inhaled GC + LABA (or leukotriene antagonist) § OR moderate dose of inhaled GC Severe persistent § Med-high dose of inhaled GC + LABA +/- leukotriene antagonist + SABA as needed Salbutamol
42
Management of acute asthma attack (in ED) = status asthmaticus
O2 Nebulise bronchodilators on O2, not air CXR Large dose oral prednisilone or IV hydrocortisone +/- IV Mg (vasodilator/dilates airway) ICU assessment if no improvement in 1 hour DO NOT give IV beta agonists - toxic.
43
Medications used for asthma
Beta 2 agonists - SABA Salbutamol; LABA Salmeterol (SX relief) Inhaled corticosteroids -fluticasone (preventer) Oral coritcosteroids in ED only Combination inhaleds - Seretide (ICS/LABA = fluticasone/salmeterol) Leukotriene R antagonists (oral montelukast) Anti IgE (omalizumab) - SC inj every 2-4 weeks w persistent allergic asthma
44
SE of Inhaled corticosteroids in treatment of asthma
Thrush, hoarse voice Cushingoid syndrome w v high doses
45
Features of life threatening asthma (status asthmaticus)
``` silent chest cyanosis feeble resp effort exhaustion, confusion, coma bradycardia or hypotension peak exp flow rate <30% of predicted normal ``` hypercalaemia, hypoxaemia Low/falling arterial pH
46
Treatment of pulmonary oedema
LMNOPP ``` Lasix (frusemide) Morphine Nitroglycerin (GTN) O2 (hypoxemic) Position (sit upright) Positive airway (CPAP, BiPAP) ```
47
Causes of viral pneumonia . is this a typical or atypical pneumonia ?
Influenza Parainfluenza RSV Atypical presentation
48
Atypical vs typical pneumonia ``` Who does it affect? Time course Pattern Degree of rise - WCC SX ```
Typical (bacterial): - Older people - Sudden onset, lasts 7-10days - Lobar consolidation - High rise WCC - Fatigue, high fever, productive cough (resp Sx only) Atypical: - Younger people - Gradual onset over 2-3 weeks - Diffuse, bilateral - No consolidation; mild incr WCC - SX not as severe - cough w minimal sputum; low grade fever + extrapulm SX (muscle aches, headache, nausea, vomiting diarrhoea, abdo pain)
49
Acute bronchopneumonia vs acute lobar pneumonia
Acute bronchopneumonia - Patchy bilateral distribution involving multiple lobes, multiple foci of inflammation - Bug w low virulence Acute lobar pneumonia -Inflammation of an entire lobe w no part spared -Bug w high virulence +Pleural pain (inflame of pleura)
50
Consolidation - findings on chest examination
``` Decr expansion Dull percussion note Incr vocal resonance Bronchial breathing Pleural rub ```
51
Investigations for suspected pneumonia
Bloods: FBE, U&E (renal baseline), CRP, blood culture CXR Pulse oximetry Sputum sample for MCS If suspected atypical infection: Urine test - legionella and pneumococcal Ag Viral serology Nasopharyngeal swab for influenza PCR
52
Treatment for CA atypical pneumonia
Doxycycline + macrolide
53
Treatment CA typical pneumonia
Augmentin (Strep) Azithromycin (H infl, moraxella) Doxycycline (H infl)
54
What agents, in what context, might cause lung abscess
Strep pygenes, staph aureus, Klebsiella | Secondary to bacterial pneumonia
55
Complications of pneumonia
``` Empyema Pleural effusion Lung abscess Respiratory failure Sepsis ```
56
What is cor pulmonale?
Cor pulmonale is RV enlargement and eventually failure secondary to a lung disorder that causes pulmonary artery hypertension.
57
Causes of pulmonary HTN
Primary pull artery HTN Increased LA pressure - Mitral Stenosis - LV failure - Diastolic dysfunction Increased pulmonary blood flow - L-R shunts - high flow states - Fluids overload Increased pulmonary vascular resistance - Vasoconstriction secondary to hypoxia (COPD, bronchiectasis) - Obstruction (PE) - Obliteration (emphysema, pulmonary fibrosis, arteritis)
58
Signs of pulmonary HTN (without R heart failure)
RV (L parasternal) heave Prominent "v" wave in JVP Cyanosis, tachypnoea
59
How does pulm HTN lead to RV hypertrophy (what sort) and Cor pulmonale?
Pulmonary HTN leads to incr afterload on R ventricle -> R ventricular concentric hypertrophy - > decr CO -> RH failure - > incr systemic venous pressure -> extravasation of fluid into interstitial tissues and peritoneal and/or pleural spaces
60
Type 1 vs Type 2 resp failure
Type 1: Hypoxaemia WITHOUT Co2 in blood. caused by VQ mismatch (failure of blood oxygenation) Type 2: Hypoxaemia WITH hypercapnoea; low pH . caused by inadequate alveolar ventilation or high inspired CO2 or high CO2 production (fever, sepsis, acidosis etc)
61
What is Mesothelioma strongly associated with, in terms of social history?
Asbestos Workers: miners, dockers, masons, plumbers, welders, installation
62
What is the most frequent initial presentation of mesothelioma?
Pleural effusion
63
What is mesothelioma? | What is the life expectancy?
Primary malignancy of pleura, usually occurring 20-30 years after asbestos exposure <1 year after symptom onset
64
Investigations/diagnosis of mesothelioma
CXR/chest CT | Biopsy of pleura with histological confirmation and biomarker staining
65
What are benign manifestations of asbestos exposure?
``` Pleural plaques (asymptomatic radiological finding) Pleural effusion - Self-resolving and exudative ```
66
How do you characterise pleural effusions are what are possible causes under each category?
1. Transudative: - High hydrostatic pressures or low oncotic pressure - Low protein content) - CCF, cirrhosis, renal failure - Hypoproteinemia (nephrotic syndrome, cirrhosis, malabsorption) 2. Exudative: - Incr vasc permeability/damage to vessels - High protein content - Infectious: Pneumonia, Tb - Malignant: Primary cancer, mets - Inflammatory: RA, SLE, PE-> Pulm Infarct 3. Haemothorax (blood, traumatic ) 4. Chylous effusion (lymph in pleural space) 5. Empyema (pus)
67
Signs of a pleural effusion on chest examination
Chest expansion: decr Percussion: stony dull Vocal resonance: decr Breath sounds: decr If severe, tracheal deviation away from effusion
68
Investigations for pleural effusion
CXR (blunting of costophenic angle +/- meniscus) Pleural tap (diagnostic or therapeutic) -> Protein and LDH -> MCS -> Tb stain -> Cytology -> Immunology if indicated (Rh factor; ANA, C' for SLE) +/- biopsy (if malignancy, Tb suspected) +/- US (locate pleural fluid and guide diagnostic or therapeutic aspiration)
69
Management of pleural effusion
Pleural tap to drain the effusion if symptomatic PLeurodesis for recurrent effusions
70
What is an empyema?
Pus in pleural space or pleural effusion with purulent bacteria seen on Gram stain or culture
71
Causes of empyema?
Complication of pneumonia (contiguous spread) Infection through chest wall (trauma, surgery)
72
definition of Sarcoidosis
Multisystem granulomatous disease of unknown cause, commonly affecting lungs, and skin (but also lymph nodes, liver, spleen, eyes, heart, brain)
73
Diagnosis of Sarcoidosis
Tissue Biopsy showing non-caseating granulomatous inflammation (lung, liver, lymph nodes, skin nodules, lacrimal glands) Bloods: raised serum ACE (60%), +/- hypercalcaemia, raised ESR, incr LFTs CXR: 90% peripheral pulmonary infiltrates +/- bilatera hilar lymphadenopathy
74
Management of Sarcoidosis
1. Bilateral hilar lymphadenopathy alone: no treatment, spontaneous recovery 2. Acute sarcoidosis: bed rest and NSAIDS 3. Pulmonary disease, uveitis, hypercalcaemia, cardiac or neuro involvement - Oral prednisilone - IV steroids or immunosuppressants if severe - Anti TNF alpha or lung transplant if refractory
75
What are the presenting features of acute sarcoidosis? Treatment?
Erythema Nodosum +/- polyarthralgia Treatment: bed rest and NSAIDs
76
What is Cystic Fibrosis? and how does it present?
Autosomal recessive condition (mutation in Cl channel) Chloride transport dysfunction -> defective Cl secretion and increased Na absorption across airway epithelium. This Cl channel involved in fluid production In lungs -> leads to thicker secretions of airway mucus which clogs airways and predisposes to pulm infection and bronchiectasis Also affects pancreas, skin, reproductive organs
77
How does CF usually present? | What else happens w time?
Presenting in childhood with recurrent lung infections that become persistent and chronic. Results in - severe lung disease - pancreatic insufficiency - diabetes - azoospermia
78
Signs on examination of CF (lung disease)
Clubbing Bilateral coarse crackles Cyanosis
79
How do you diagnose CF?
Sweat chloride test (incr [NaCl and K in sweat) Pulmonary function tests (reduced FEV1 - obstructive pattern) ABGs - hypoxaemia, w hypercapnoea later on CXR: hyperinflation, incr pulmonary markings
80
What diseases are associated with industrial dust
Coal Worker's Pneumoconiosis (inhalation of coal dust), can progress to 'Progressive Massive Fibrosis' Silicosis (inhalation of silica which is fibrogenic) Asbestosis (inhalation of asbestos which is fibrogenic), assoc w Mesothelioma Mesothelioma
81
Definition of Interstitial Lung Disease
Inflammatory and/or fibrosing process in the alveolar walls causing distortion and destruction of normal alveoli and microvasculature . Generally BILATERAL.
82
Common causes of interstitial lung disease
Rheumatic - RA, SLE, Scleroderma Drugs -Methotrexate, amiodarone, bleomycin, nitrofurantoin Radiation Environmental/Occupational - Silicosis, asbestosis, coal worker's pneumoconiosis Pulmonary Vasculitis Inherited Sarcoidosis
83
What pattern do you get on spirometry w ILD?
Restrictive due to decr lung compliance (TLC and VC reduced; FEV1/FVC incr/normal)
84
Common causes of acute bronchitis
Mostly viral. Influenza when + fever.
85
Definition of acute bronchitis
Acute bronchitis is suggested by the persistence of cough for more than five days. Cough generally persists two to three weeks, and airway hyperreactivity may last five to six weeks. Fever uncommon and suggests influenza or pneumonia.
86
What are the indications for CXR in patients w acute cough?
To exclude pneumonia: Tachypnoea Tachycardia Fever Chest exam: signs of consolidation, rales Hypoxaemia (pulse oximetry) Altered mental state
87
Treatment of acute bronchitis
Reassurance and symptomatic treatment (NSAIDs, aspirin and/or ipratropium) NOT ANTIBIOTICS.
88
Classifying lung tumours
Benign or malignant Primary or secondary Endobronchial or parencymal
89
What is the most common type of primary lung tumour?
Bronchogenic carcinoma - small cell - non-small cell (SCC, adenocarcinoma, large cell undifferentiated) -Adenocarcinoma the most common overall
90
Which type of lung cancer is most common in NON SMOKERS
non small cell adenocarcinoma
91
Where are bronchogenic non small cell SCCs found in lungs
centrally
92
Where are bronchogenic small cell carcinomas found?
centrally
93
Where are bronchogenic non-small cell adenocarcinomas found?
Peripherally
94
Which type of lung cancer is most aggressive?
Small cell - disseminated at presentation.
95
What are the histological features of : SCC adenocarcinoma
SCC: keratin pearls and intercellular bridges Adenocarcinoma: glandular, mucin-producing
96
What are apical lung tumours called and what are common SX?
Pan coast tumour . Horner Syndrome Brachial plexus palsy (C8, T1 nerve roots -> weak intrinsic hand muscles)
97
What are distant met sites for lung cancer?
Brain Bone Liver
98
What are local sites of spread/obstruction for lung cancer?
``` Hilum, mediastinum, pleura Pericardium Oesophagus Phrenic nerve Recurrent laryngeal nerve SVC Rib and vertebrae ```
99
Investigations for lung cancer
Bloods: UEC, LFTs, Ca CXR, CT chest and abdo +/- PET and bone scan Sputum sample cytology Bronchoscopy -> biopsy
100
Horner's syndrome
Mitosis ANhydrosis Ptosis
101
Treatment for lung cancer
Combination treatment surgery (not for small cell and CI with spread to lymph nodes or distant sites or poor pulm function) radiotherapy chemotherapy palliation
102
Causes of pneumothorax
1. Traumatic - penetrating or non-penetrating injuries 2. Iatrogenic 3. Spontaneous (no HX trauma) ○ Primary (no underlying lung disease) § Generally due to spontaneous rupture of subpleural bleb of lung into pleural space § Common in tall, healthy young males ○ Secondary (underlying lung disease) § Rupture of subpleural bleb § Necrosis of lung tissue adjacent to pleural space (Often w pneumonia, abscess, PCP, lung CA, emphysema )
103
Treatment for pneumothorax
○ Give 100% O2 in all cases Small pneumothoraxes (haem stable) resolve spontaneously Small intercostal tube for spontaneous pneumothoraces Large pneumothoraces or those w secondary causes ○ Chest tube connected to underwater seal +/- suction ○ Treat underlying causes (ex: antibiotic for PCP)
104
Signs on examination of pneumothorax
* Tracheal deviation (if tension -> deviates AWAY from pneumothorax) * Unilateral reduced chest expansion * Decr vocal/tactile fremitus * Hyper-resonant * Unilateral reduced breath sounds
105
What signs make you think that a person might have a tension pneumothorax rather than a simple one and how does this change your management?
* Severe resp distress * Tracheal deviation away from affected lung * Distended neck veins (incr JVP) * Hypotension In this case, do NOT perform CXR -> needs immediate MX
106
Treatment for resp failure.. what investigations would you do?
Investigations: serial ABGs, CXR, chest CT (for underlying cause) 1. Give O2 2. Positive pressure ventilation: BiPAP, CPAP 3. Reverse/manage underlying pathology and/or exacerbators NOTE: in COPD patients w chronic hypercapnoea, give low-flow O2 to achieve target SaO2 of 88-92%
107
What is the different in definition between OSA and central sleep apnea?
OSA: Transient, episodic obstruction of upper airway with reduced or absent airflow despite persistent respiratory effort. CSA: Transient, episodic decreases in CNS drive to breathe with no airflow because no resp effort.
108
Signs and symptoms of sleep apnea
``` • Due to fragmented sleep: ○ Daytime somnolence ○ Personality and cognitive changes ○ Snoring • Due to hypoxemia and hypercapnia ○ Morning headache ○ Polycythemia ○ Pulmonary/systemic HTN ○ Cor pulmonale/CHF ○ Nocturnal angina ○ Arrhythmias ```
109
Investigations and treatment for OSA
Investigate w sleep study Treatment - manage risk factors (weight loss, decr alch and sedatives, nasal decongestion, treat underlying medical conditions) - nasal CPAP - no supine sleeping - dental appliance - surgery (tonsillectomy. uvulopalatopharyngoplasty)