Resp Flashcards
What are the ABG findings in T1RF?
O2 <8 kPa
What are the ABG findings in T2RF?
O2 <8 kPa, CO2 >6.5 kPa
In summary, what sort of problem is T1RF?
Obstruction problem
What is shunting?
Alveoli are perfused but not ventilated, eg due to ARDS or consolidation.
Hypoxia can’t be corrected by increasing FiO2 because poorly-ventilated alveoli will continue to lower systemic pO2
Physiological causes of T1RF
Hypoventilation
V/Q mismatch
Shunting
Decrease in inspired pO2
Causes of T1RF
Severe acute asthma
Pneumonia
PE
Pulmonary oedema
Causes of T2RF
COPD
Asthma
Pneumonia
Pulmonary fibrosis
Obstructive sleep apnoea
Decreased respiratory drive: trauma, CNS trauma, sedatives
Neuromuscular: cervical cord lesion, MG, GBS, diaphragm paralysis
Symptoms and signs of hypoxia
SOB, restless/ agitated, reduced GCS, cyanosis
Symptoms and signs of hypercapnia
Headache, reduced GCS, tachycardia with bounding pulse, tremor in hands, peripheral vasodilatation, papilloedema
Investigations for hypoxia?
ABG
Sputum/ spirometry
ABG
CXR
Management of hypoxia
High-flow oxygen
Re-check ABGs
What are the options for NON-invasive respiratory support?
Humidified supplemental O2 (for T1RF)
CPAP (for T1RF)
NIV (BIPAP) (for T2RF)
Explain CPAP
Expiration against a resistance
opens up alveoli, forces out pulmonary oedema, decreases work of breathing
Explain BIPAP
Positive pressure support for inspiration in addition to patient’s own breathing
(clears CO2, decreases work of breathing)
How is INVASIVE mechanical ventilation different?
Can set a desired pressure, desired tidal volume, desired RR
What are the indications for invasive mechanical respiration?
NIV not tolerated
Severe respiratory failure/ increased work of breathing
Airway protection (eg GCS <8 or burns)
Control pO2 and pCO2 in acute neurological disesase/ increased ICP
Contraindications of invasive mechanical ventilation
Tension pneumothorax
Volutrauma, barotrauma
How is invasive mechanical ventilation provided?
Most will have ETT (requires anaesthesia, sedation)
Long-term need tracheostomy (little/ no sedation, improved comfort, improved nursing/ oral care)
4 types of pulmonary embolism
Thrombosis (usually distant vein)
Fat (fractures)
Amniotic fluid
Air (neck vein cannulation/ bronchial trauma)
Presentation of PE
Large can cause sudden death/ small can be hard to diagnose
Symptoms: SOB, dyspnoea, chest pain (pleuritic or retrosternal), cough, haemoptysis
Signs: tachypnoea, tachycardia, hypotension hypoxia pyrexia pleuritic pain increased JVP, gallop rhythm
Investigations for PE?
Two-level Wells Score:
LIKELY
CTPA + leg USS
anticoag to buy time
[if can’t have contrast/ renal impairment: V/Q spectroscopy]
If UNLIKELY: D-dimer
ABG Bloods: FBC, U&Es, baseline clotting, D-dimers, troponin + BNP may be raised due to strain ECG CXR Echo will show thrombus
Consider:
looking for ca (hx, CXR, mammogram, abdomino-pelvic CT)
antiphospholipid antibodies, thrombophilia screen
How might a PE present on ECG?
Tachy
RBBB
R axis deviation
S1, Q3, T3
Large PE may show ST depression
How do you manage PE?
Ideally LMWH or fondaparinux (at least 5 days whilst awaiting warfarin)
Warfarin for 3 months - INR 2-3
Maybe rivoraxaban (prophylactic) Surgical embolectomy/ IVC filters
What are the signs of pulmonary oedema?
Resp distress: pale, sweaty, tachypnoeic, tachycardic
May be cyanosed, low sats <90% RA
May be signs of associated cause
Basal or widespread crackles
Cardiogenic shock: hypotension, oliguria, low CO2
Investigations for pulmonary oedema
Bloods: FBC, U&Es, glucose, cardiac enzymes
ECG
CXR
Echo (to establish LV function once stable)
How does pulmonary oedema appear on CXR?
Bilateral patchy shadowing
Kerley B lines
Batwings (increased vascular shadowing)
Pleural effusions
If cardiogenic, maybe cardiomegaly
How do you manage pulmonary oedema?
Depends on cause but…
Fluid balance
What is a pneumothorax?
Air in pleural space
What are the causes of pneumothorax?
SPONTANEOUS: rupture of pleural pleb (congenital weakness) - tall, slim males - often apical
SECONDARY: COPD (emphysematous bullae), TB, pneumonia, bronchial Ca, sarcoidosis, CF, trauma
Causes of pulmonary oedema: lymphatic obstruction
Mediastinal carcinamatosis
Silicosis
Causes of pulmonary oedema: neurogenic
Status epilepticus
Head injury
Cerebrovascular insult
These happen within a few hours
Causes of pulmonary oedema: increased capillary permeability
ARDS Increased altitude Inhaled/ aspirated toxins Radiation Liver failure Fat/ amniotic embolus
Causes of pulmonary oedema: increased pulmonary capillary pressure
Heart: MI/ ACS, valvular disease (regurg or severe AS), cardiomyopathy, PE, acute arrhythmia, tamponade, dissection, right-output HF (septicaeia, thyrotoxicosis, anaeia)
Renal: AKI, CKD, renal artery stenosis
Iatrogenic: fluid overload
Causes of pulmonary oedema: airway obstruction
Acute or chronic upper airway obstruction
What is ARDS?
Non-cardiogenic pulmonary oedema - 30-45% mortality
What are the causes of ARDS?
Pulmonary causes: mechanical ventilation, trauma, near drowning, smoke inhalation, gastric contents aspiration, infection
Extrapulmonary causes: Gram-negative septicaemia, pancreatitis, burns, CABG, perforated viscus, DIC, O2 toxicity, drug OD
Management of ARDs
Identify cause + support -ve fluid balance, as in pulm oedema PEEP: prevent alveolar walls from collapsing during expiration Vasodilators Steroids (late stages)
Presentation of pneumothorax
Asymptomatic - esp if small or they’re healthy
or
Sudden unilateral chest pain, SOB, sudden deterioration of existing lung problem
How does pneumothorax present on examination?
Reduced chest expansion on that size - hyperresonance - reduced, absent breath sounds
How does pneumothorax present on CXR?
Are of increased lucency without lung markings, edge of lung may be visible away from chest wall
Management of pneumothorax
Small: often no treatment, r/v 7-10 days
Large: admit for aspiration
Common causes of tension pneumothorax
Positive pressure ventilation, stab, rib fracture
Management of tension pneumothorax
Large-bore cannula, 2nd ICS, MCL
How does tension pneumothorax present on examination?
Tracheal deviation (pulled to contralateral side)
Hyperresonance
Absence of breath sounds
Widened ICS spaces on contralateral side
How does tension pneumothorax present?
As pressure increases, venous return to heart is impaired:
Dyspnoea, chest pain, cyanosis, even cardiac arrest
What is a tension pneumothorax?
A chest or lung wall injury allowing air into the pleural space. The air rises above atmospheric pressure, compressing the lung and venous return to the heart. Air enters but doesn’t leave.
Which side do aspirated foreign bodies go?
R
Presentation of foreign body aspiration?
Upper airway: stridor, respiratory distress, cyanosis, resp arrest
Beyond carina: recurrent cough, pneumonia, SOB, haemoptysis
Management of foreign body aspiration
Heimlich - suction - bronchoscopy - abx to treat/ prevent pneumonia
Investigations for foreign body aspiration
Bloods (inflammatory response) - CXR (if radio-opaque, if pneumonia) - bronchoscopy (direct visualisation)
What is OSA?
Intermittent and repeated upper airway collapse during sleep
What should you look for when examining for OSA?
No specific signs
Look for: neck fat deposition, small mouth, big tongue, polyps etc
Gold standard for OSA?
Ix
Mx
Ix Polysomnography (electrodes on eyes and chin)
Mx CPAP
What are the risks associated with OSA?
HTN, CVD, obesity, DM, asthma
What are the options for treating OSA?
Lifestyle/ avoid supine sleeping
CPAP
Consider:
Modafinil for sleepiness
Surgery
What is central sleep apnoea?
Airway patent but no respiratory effort
Causes hypercapnia that arouses pt
What are the causes of pulmonary hypertension?
COPD, interstitial lung disease, others
L cardiac disease, secondary to congenital heart disease
Portal HTN
Idiopathic is rare - poor prognosis - associated with CREST/ autoimmune
How does pulmonary HTN present?
Non-specific insidious signs (often diagnosed late)
SOB, malaise, presyncopal
Often picked up as signs of cor pulmonale
How is pulmonary HTN investigated?
R heart catheterisation confirms
PAH diagnosed by exclusion: ECG, echo, CXR, CT chest, autoantibodies
How is pulmonary HTN managed?
Warfarin to minimise risk of thrombosis
CCBs to decrease pressure of pulmonary vasculature
HF should be treated aggressively
Poor prognosis (2-3 years) - death usually due to RHF
Incidence of asthma
20% kids
5% adults
Define asthma
Reversible airflow obstruction, airway hyper-responsiveness, inflamed bronchi
What is extrinsic vs intrinsic asthma?
EXTRINSIC: atopic childhood asthma, remits in teens
INTRINSIC: usually adult, progressive, less responsive to treatment
How to diagnose asthma?
at least 15% improvement in FEV1 after bronchodilator use
There will be an obstructive picture (FEV1/ forced vital capacity reduced)
Residual volume may be increased due to air trapping
Management of asthma (adults and children over 5)
Avoid triggers!
STEP 1: inhaled short-acting beta2 agonist - PRN
STEP 2: add inhaled steroid (200-800 mcg) - 400 usually ideal, but titrate
STEP 3: Add LABA
Good response: continue!
Quite good response: continue/ ensure steroids at 800 mcg
No response: steroids at 800 mcg, stop LABA
From this step eligible for SMART (single maintenance and reliever therapy)
STEP 4: add leukotriene receptor antagonist, theophylline, beta2 agonist pill
steroids up to 2000 mcg/day
STEP 5: add daily oral steroid (+ 2000 mcg/day inhaled)
TRY TO STEP DOWN WHERE POSSIBLE
What should every asthmatic have?
Asthma action plan
Definition COPD
airflow obstruction with little or no reversibility
Incidence of COPD
5-15% industrialised countries
What should be considered cause of COPD in under 40s?
alpha-1-antitrypsin deficiency (proteases overwhelm antiproteases = increased compliance)
panacinar picture
What are the traditional forms of COPD?
Blue bloaters: CHRONIC BRONCHITIS - small airways obstructed by mucus plugs & bacterial colonisation - crackles/ wheeze - peripheral oedema
Pink puffers: EMPHYSEMA - proteases overwhell=m antiproteases - cachectic, pursed-lip breathing, accessory muscles, barrel chest, decreased breath sounds
Signs of COPD
I: central cyanosis - barrel chest - use of accessory muscles - pursed lip breathing - flapping tremor - tachypnoea - persistent cough - chronic sputum production - weight loss
P: tacycardia - tracheal tug - reduced expansion
P: hyperresonant lung fields (unless consolidation)
A: wheeze - prolonged expiration
Investigations for COPD
Spirometry (severity based on FEV1) Pulse oximetry Sputum Bloods: FBC, alpha1-antitrypsin level CXR ECG/ Echo for cor pulmonale
Management of COPD
Yearly influenza jab, 5-yearly pneumococcus jab
Pulmonary rehab: 6-12 weeks, work on exercise tolerance
Medications (these are all symptomatic so only continue if iprovement after 4 weeks):
STEP 1 (breathlessness or exercise limitation): SABA or SAMA
STEP 2 (exacerbations or persistent breathlessness)
FEV > 50% - LABA/ LAMA
FEV < 50% - LABA + ICS / or LAMA (combination inhaler - ICS not used alone in COPD)
STEP 3
LABA –> LABA + ICS
Others –> LAMA + LABA + ICS
ORAL: theophylline, carbocisteine (mucolytic), rescue pack abx
SEVERE/ END-STAGE: home O2 (15h/ day)
Lung transplant an option
Complications of COPD
Acute worsening (usually infection, eg influenza or haemophilus influenzae)
T2RF
cor pulmonale
Example SABA
Salbutamol
Example SAMA
Ipratropium
Example LABA
Salmetarol
Example LAMA
Tiotropium
Definition cor pulmonale
Impairment of right ventricular function as a result of respiratory disease - leading to increased resistance to blood flow in the pulmonary vasculature
General two types of pathology leading to interstitial lung disease
Granulomatous or fibrosis
Define pulmonary fibrosis
The irreversible end-stage of many respiratory diseases, characterised by scarring of lung tissue which decreases compliance.
An example of interstitial lung disease