Week 8 Flashcards
Explain a systematic approach to looking at ABGs
- Always look at the P02 first
- is the patient in respiratory failure requiring additional oxygen?
- Then look at PCO2 (type 1 vs type 2 respiratory failure)
- Then consider acid base balance
- Acute respiratory acidosis- elevated pCO2, normal bicarbonate, acidosis
- Compensated respiratory acidosis- elevated pCO2, elevated bicarbonate (renal compensation), not acidotic
- Acute on chronic respiratory acidosis- elevated pCO2, elevated bicarbonate, acidotic
What is the clinical application of the alveolar-air equation?
Arterial pO2 (PaO2) can be directly measured- ABG
The difference between the calculated alveolar pO2 and the arterial pO2 is the alveolar arterial (A-a) oxygen gradient
Difference between alveolar and arterial oxygen partial pressures should be <2-4 kPa- more than this suggests V/Q mismatch
Describe the pathology of COPD:
COPD is characterised by airflow obstruction. Obstruction is usually progressive, not fully reversible and does not change markedly over several months
Can be caused by alpha 1 anti-trypsin deficiency
Emphysema is abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles
Due to emphysema, airways collapse on expiration -> causes air-trapping and hyperinflation -> increased work breathing -> breathlessness
Other changes: goblet cell metaplasia with mucus plugging of lumen, inflammation of airway wall, thickening of bronchiolar wall, smooth muscle hypertrophy and peribronchial fibrosis
How do you differentiate between asthma and COPD?
COPD:
Nearly all smokers
Symptoms under 35 rare
Chronic productive cough common
Persistent and progressive breathlessness
Night waking with wheeze or blessness uncommon
Significant diurnal or variability uncommon with COPD
Asthma: opposite
Explain the serum biochemical adaptation to acute and chronic respiratory failure:
Compensatory changes are usually partial
Respiratory compensations (to metabolic disorders) happen quickly - minutes to hours
Metabolic compensations are slower, many hours - days
Greater compensation in chronic than acute disorders
Describe the indications for the use of non-invasive ventilation in COPD
Provides positive pressure to the airways to support breathing
Recommended as the first line intervention in addition to usual medical care in COPD exacerbations with persistent hypercapniac respiratory failure
Considered if there is a respiratory acidosis (pH <7.35, H+ >45) present or if acidosis persists despite maximal medical therapy
Describe basic anatomy of the lungs:
Bronchus leading to primary, secondary and tertiary bronchi and bronchioles, which open onto alveoli (the site of gas exchange)
Intra-Alveolar pressure same as atmospheric pressure. Chest wall expands, pulling lungs outwards on inspiration- air enters lungs as pressure becomes negative (volume increases)
On expiration, diaphragm relaxes, pushing up lungs decreasing volume and thus pressure
Describe the clinical syndrome of asthma:
Pathological, physiological and clinical syndrome characterised by reversible airflow obstruction, airway inflammation and triggers
Symptoms: wheee, cough, yellow/clear sputum and breathlessness, exercise intolerance
Episodic, triggered and variable- paroxysmal
Triggers: exercise, cats (allergy), chemical/physical (hyper-reactivity), diurnal
Responds to asthma therapies
Describe the clinical syndrome of COPD:
Chronic bronchitis and emphysema
CB: the production of sputum on most days for at least 3 months in at least 2 years
- larger airways >4 mm in diameter
- inflammation leads to scarring and thickening of airways
E: abnormal, permanent enlargement of the airspaces distal to the terminal bronchioles
- centri-acinar; damage around bronchioles
- pan-acinar: uniformly enlarged from level of terminal bronchiole distally, associated with genetic COPD
Define obstructive sleep apnoea syndrome:
Sleep apnoea with daytime tiredness
Sleep apnoea: recurrent episodes of partial or complete upper airway obstruction during sleep, intermittent hypoxia and sleep fragmentation
Symptoms: snore, witnessed apnoeas, disruptive sleep (nocturial/choking/dry mouth/sweating), unrefreshed sleep, daytime somnolence, fatigue/low mood/poor concentration
What factors predispose to OSA?
Obesity: approximately two-thirds of people with OSA are overweight or obese
Family history of OSA or snoring
Small lower jaw and certain other facial configurations
Male gender
Large neck circumference
Large tonsils
Alcohol consumption at bedtime
Post-menopausal (for women)
Hypothyroidism (low levels of thyroid hormone)
Acromegaly (high levels of growth hormone)
What investigations are done in OSA and how is it treated?
Investigations: limited and full polysonography, transcutaneous oxygen sats and CO2 assessment (TOSCA)
- involves ECG, video, audio, thoracic and abdominal bands, position, flow, O2 sats, limb leads and snore
Assessment: history from partner, weight/BMI, BP, neck circumference, tonsils, nasal latency, craniofacial appearance
Treatment:
Continuous positive airways pressure (CPAP)
- splints airway open, stops snoring, stops sleep fragmentation
Mandibular advancement device for mild-moderate OSAS and unable to tolerate CPAP
Describe pathological features in the lung that leads to pneumothorax:
Air within the pleural cavity, can be traumatic, iatrogenic or spontaneous
Spontaneous:
Primary: development of subplueral blebs/bullae at lung apex with possible additional diffuse, microscopic emphysema below the surface of the visceral pleura.
Spontaneous rupture leads to tear in visceral pleura, air flows from airways to pleural space and elastic lung then collapses
Secondary: inherent weakness in the lung tissue, increased airway pressure, increased lung elasticity
Describe treatment of pneumothorax:
Primary spontaneous pneumothorax may be treated conservatively if symptoms are minimal
Secondary pneumothorax more frequently requires treatment by aspiration or ICD
Tension pneuomoth always required ICD
Describe the mechanism of action of anti-fungal drugs:
Azoles are inhibitors an enzyme which produces ergosterol, an essential component of fungal cell membrane
Amphotericin B binds to ergosterol and forms a pore in the fungal cell membrane through which ions can freely pass, killing the cell
