S3 Respiratory Flashcards
(7 cards)
Respiratory distress syndrome
Usually seen in premature babies less than 30 weeks old
Have lack of surfactant so lungs are very stiff
As there is a lack of surfactant, surface tension of the alveoli is high as surfactant molecules are usually interspersed between fluid molecules to disrupt interaction between surface molecules
So the lungs are difficult to inflate so baby uses more effort to expand lungs leading to distress
There is widespread collapse of alveoli so these alveoli will not be ventilated and gas exchange does not occur, hypoxaemia (low pO2)
Signs include cyanosis, grunting, intercostal and subcostal recession
Intercostal recession as the newborn has a very soft chest wall and lungs are stuff so infant uses more inspiratory effort to expand stiff lungs resulting in more negative intrapleural pressure
Since the lungs are stiff and cannot expand easily, pliable chest is sucked inwards
Treatment include surfactant replacement by end ot Racheal tub and supportive treatment with oxygen and low pressure assisted ventilation.
Type 2 respiratory failure and some causes
Low arterial pO2 (under 8kPa) and high pCO2
So central chemoreceptors stimulated due to high CO2
Hyperventilation stimulated but due to disease mechanical factors stop this from happening
Breathlessness
Oxygen administration may make hypercapnia worse as
- hypoxia is now stimulus to drive respiration as choroid plexus adjusts composition of CSF so higher pCO2 seen as normal
- main reason: also if oxygen given it would reduce hypoxic pulmonary vasoconstriction in poorly ventilated alveoli so would worsen the V/Q mismatch
You would use titrated oxygen therapy with monitoring
Causes
- acute exacerbation of COPD
- lung fibrosis
- severe obesity
- kyphoscoliosis
Type 1 respiratory failure and some causes
Low pO2 (<8kPa) but normal or low pCO2
Ventilation perfusion mismatch
- some alveoli not getting enough ventilation so vasoconstriction to these areas
- blood going away from bad alveoli have low pO2 and high pCO2 so chemoreceptors stimulate hyperventilation but disease stops this from occurring so alveoli still poorly ventilated
- normal alveoli would get extra ventilation from hyperventilation but you cannot increase oxygen uptake in the blood coming from these alveoli too much as not enough binding spaces to HB so blood from these alveoli have normal pO2 (or bit higher) and low CO2
- Blood mixes from all alveoli and results in low pO2 which would keep hyperventilation going
V/Q mismatching can be due to
- reduced ventilation e.g. Pneumonia, acute asthma, COPD, respiratory distress of newborn
- Reduced perfusion e.g. Pulmonary embolism
Treat with oxygen therapy as increases pO2 in alveoli so increased partial pressure gradient
Clinical features of hypoxia
Tachypnoea
Confusion
Exercise intolerance
Central cyanosis
Features of CO2 retention
Warm hands
Bounding pulse
Flapping tremors
Define
- pneumonia
- lobar pneumonia
- broncho pneumonia
Pneumonia
- inflammation of a gas exchanging region, usually due to infection
Lobar pneumonia
- pneumonia localised to one lobe/s in the lung
Broncho pneumonia
- pneumonia that is diffuse and patchy so the infection starts in the airways and spreads to adjacent to adjacent alveoli and lung tissue
Pneumonia
Signs and symptoms
- fever, cough, pleuritic chest pain, SOB
- consolidation on CXR
Investigations
- FBC, U+Es, CRP, ABG, CXR
- Sputum
- Blood culture before antibiotics
- BAL (broncho alveolar lovage)
Management
- CURB 65
CAP (community acquired)
- main organisms: Streptococcus pneumoniae, Haemophilus influenzae
- mild to moderate treatment: amoxicillin
- moderate to severe: co-amoxiclav and doxycycline
HAP (hospital acquired)
- appears after 48 hours of being in hospital
- main organisms: Staphlyococcus aureus, Haemophilus influenzae (more gram negative)
- First line treatment: co-amoxiclav
- Second line treatment: meropenem
