Respiratory Flashcards
Metabolic acidosis causes
Changes to ABG
Increased H+ production e.g. DKA
Decreased H+ excretion e.g. renal tubular acidosis; renal failure
Bicarbonate loss e.g. intestinal fistula
ABG changes
If uncompensated:
- High H+
- Low bicarbonate
If compensated:
- High H+
- Low bicarbonate
- Low CO2 (can’t compensate if resp failure - H+ will rise more)
Respiratory acidosis
Causes
Changes to ABG
Poor ventilation
Poor perfusion
Impaired gas exchange
If chronic
- COPD
- Emphysema
ABG changes
If uncompensated:
- High CO2; high H+; high HCO3-
If compensated:
High CO2; normalised H+; high HCO3-; PH may be normal now
Metabolic alkalosis causes
- Hypokalaemia
- H+ loss e.g. pyloric stenosis, vomiting
- Ingestion of bicarbonate (tx for GI ulcer)
Causes of respiratory alkalosis
Hyperventilation
- Anxiety
- Hypoglycaemia
Salicyclate poisoning
CNS disorders: stroke, subarachnoid haemorrhage, encephalitis
Aspirin overdose picture on ABG
Mixed metabolic acidosis and respiratory alkalosis
Hyperventilation stimulated
Hydrogen excretion by kidney
Define chronic bronchitis
- symptoms
Complications
Pathology
chronic cough productive of sputum for at least 3 months over at least 2 consecutive years
Symptoms
Repeated infections
Resp failure, reduced exercise tolerance
Increased lung cancer risk (independent of smoking)
Complications Chronic hypoxia results in PULMONARY HTN AND RHF = aka cor-pulmonale - Peripheral oedema - Hepatosplenomegaly - Raised JVP
Pathology
- Dilation of the airways
- Mucus gland hyperplasia
- Goblet cell hyperplasia
- Mild inflammation
Bronchiectasis define
Causes
Complications
Permanent dilation of the bronchi with scarring
Causes
- Inflammatory
- post infection
- immunodeficiency (hypogammoglbulinaeia) or secondary
- obstruction
- post inflammatory (aspiration)
- Secondary to bronchiolar disease and interstitial fibrosis
- systemic disease
- Asthma - Congenital
- CF
- primary ciliary dyskinesia
- hypogammaglobulinemia
- yellow nail syndrome
- young’s syndrome (Rhinosinusitis, Azoospermia, Bronchiectasis)
Complications
- Recurrent infections
- Haemoptysis
- Pulmonary HTN
- Amyloidosis (as producing excessive amyloid A protein)
What does honeycomb lung indicate?
Categories
Interstitial Lung disease
- all have at end stage
Categories
1) Fibrosis
2) Granulomatous
3) Eosinophilic
4) Smoking related
What is a saddle embolus?
What does it lead to
Large pulmonary thrombo-embolism that straddles the main pulmonary arterial trunk at its bifurcation
Leads to
- Acute cor pulmonale
- Cardiogenic shock
- Death If >60% of pulmonary bed occluded
NB - wedge infarct = Pulmonary infarction (commonly after PE), Repeated infarctions can cause pulmonar HTN
What is alpha-1 antitrypsin deficiency
Clinical picture
Management
Common inherited condition caused by a lack of a protease inhibitor (Pi) normally produced by the liver. The role of A1AT is to protect cells from enzymes such as neutrophil elastase.
Clinical picture
lungs: panacinar emphysema, most marked in lower lobes
liver: cirrhosis and hepatocellular carcinoma in adults, cholestasis in children
Management
- no smoking
- supportive: bronchodilators, physiotherapy
- intravenous alpha1-antitrypsin protein concentrates
- surgery: volume reduction surgery, lung transplantation
COPD prophylaxis example
What needs monitoring
Azithromycin prophylaxis
- patients should not smoke, have optimised standard treatments and continue to have exacerbations
other prerequisites include a CT thorax (to exclude bronchiectasis) and sputum culture (to exclude atypical infections and tuberculosis)
Ned to do
LFTs and an ECG to exclude QT prolongation should also be done as azithromycin can prolong the QT interval
Obstructive sleep apnoea
Consequences
Consequences
- HTN
- Day time somnolence
- Compensated respiratory acidosis
ARDS definition
Diagnosis
Causes
Non cardiogenic pulmonary oedema ((i.e. the pulmonary capillary wedge pressure must not be raised) and diffuse pulmonary infiltrates, refractory hypoxaemia, stiff lungs and respiratory distress. ARDS forms part of a systemic inflammatory reaction.
Diagnosis = 3 criteria
1) Acute onset (within 1 week)
2) Bilateral opacities on CXR
3. ) PaO2 /FiO2 (arterial to inspired oxygen) ratio of less than/= 300 on PEEP (positive end-expiratory pressure) or CPAP more than/equal 5cm H20
Causes
- Pulmonary: Trauma, shock, infection, gas inhalation, aspiration, mechanical ventilation
- Systemic: Shock/sepsis, pancreatitis, burns, cardiopulmonary bypass, DIC, Oxygen toxicity, drug overdose, ops (eclampsia)
Clinical presentation • Tachypnoea, often unexplained • Dyspnoea • Cyanosis • Peripheral vasodilation • Bilateral fine inspiratory crackles on auscultation
ARDS investigations
Management
Prognosis
•Sputum/Urine cultures:
•Blood tests: FBC, U&Es, LFTs, Amylase, Clotting screen, Blood cultures, BNP
•ABG
•CXR: Bilateral infiltrates
•Pulmonary artery catheter: Measure pulmonary capillary wedge pressure + demonstrate arterial hypoxaemia, refractory to oxygen therapy
o = 18 suggests ARDS but not done routinely
Management
Treat underlying cause whilst giving supportive measures
- PEEP
- Non-ventilatory management: NO/Prostacyclin
- Steroids
- Circulatory support (as in pulmonary oedema)
- Antimicrobials (if infectious cause)
Prognosis
- Mortality is 30-50%: Death most often due to multiple organ failure
- Pts who survive usually have residual decrease in lung function
- Muscle weakness, neuropathies, joint disorders and chronic pain common in survivors
Respiratory failure type 1
Causes
Clinical presentation
Management
PaO2 <8kPa. PaCO2 is normal or low
V/Q mismatch
Causes • Severe acute asthma • Pneumonia • PE • Pulmonary oedema
Clinical presentation • Dyspnoea • Restless and agitated • Confusion • Cyanosis (peripheral and central)
Management
- High flow O2
- Consider CPAP if O2 remains <8kPa despite 60% O2
Type 2 respiratory failure
Causes
Clinical presentation
Management
Low PaO2 <8kPa;
High PaO2 > 6.5kPa
Known as ventilatory failure; the rise in PaCO2 is no longer matched by an increase in ventilation.
Causes
- most common cause is (COPD). Others include chest-wall deformities, respiratory muscle weakness (e.g. Guillain-Barre syndrome) and central depression of the respiratory centre (e.g. heroin overdose)
Clinical presentation:
- As in type 1: Dyspnoea, restless, confusion, cyanosis
- Headache
- Drowsiness
- Confusion
- Tachycardia with a bounding pulse
- Tremor in hands
- Peripheral vasodilation
- Papilloedema
Management
•Use O2 therapy conservatively: start at 24% via facemask
•Recheck PaCO2 after 20 mins (ABG)
•If PaCO2 is stable, oxygen can be increased. If it has risen, consider alternative support i.e. non invasive positive pressure ventilation such as biphasic positive airway pressure
PE definition
Pathophysiology
Obstruction of one or more pulmonary arteries, mostly embolism is caused by blood thrombi, which arise from deep vein system in legs or pelvis (DVT)
Pathophysiology
Thrombus formation –> DVT in leg or pelvis –> embolisation to pulmonary arteries via IVC –> partial or complete pulmonary arteries
Response of lung to arterial obstruction
- Infarction and inflammation: Causes pleuritic chest pain and haemoptysis
- Impaired gas exchange: V/Q mismatch
- Cardiac compromise
PE aetiology
RIsk factors
Presentation
Aetiology
- DVT
- Fat embolism
- Others
Risk factors (SPASMODICAL) •Sex: F •Pregnancy (+ other hypercoagulable states): Caesarean, pre-eclampsia •Age: •Surgery: classically 10s post-op straining at stool. Major abdo/pelvic, orthopaedic •Malignancy •Oestrogen: OCP/HRT •DVT/PE previous hx •Immobility •Colossal size •Antiphospholipid Abs •Lupus Anti-coagulant
Presentation
- Dyspnoea
- Sudden onset pleuritic pain
- Haemoptysis
- Syncope
Signs: Fever, Cyanosis, Tachycardia, Tachypnoea
- RHF ( hypotension, high JVP, RV heave)
- Evidence of DVT
PE Well’s score factors
Action to take
Investigations
3: Signs/symptoms of DVT
3: PE most likely dx
1. 5: Tachycardia >100
1. 5: Immobility/surgery in 4wks
1. 5 Prior DVT/PE
1: Haemoptysis
1: Active malignancy (trt w/in 6months)
PE unlikely 0-4 points - D-dimer
PE likely > 4 points - immediate CTPA
ECG:
- large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III - ‘S1Q3T3’
- New RBB and RAD may occur
D-dimer
- Generated as a result of fibrinolysis
- -ve –> PE v unlikey
- CTPA = gold standard
- CXR: usually normal. May show wedge shaped opacities
- Lower limb US
- ABG: Arterial hypoxaemia and hypocapnia in early stages
