Session 6 Flashcards
Draw a Spirogram
- TLC Total lung capacity:
- TV Tidal volume:
- Simple spirometry allows measurement of lung volumes & capacities. Vital capacity is particularly significant. Why?
- As Vital capacity depends on maximal inspiration & maximal expiration, it may be reduced because the lungs are not:
5.
- volume in the lungs at maximal inflation, the sum of VC & RV
- volume of air moved into or out of the lungs during quiet breathing
- measured value is compared to the predicted vital capacity of an individual of the same age, height and sex as obtained from tables or nomogram
- filled normally in inspiration,
- emptied normally in expiration,
- or both.
- filled normally in inspiration,
- Forced expiratory volume (FEV) measures?
- Forced vital capacity (FVC) is ?
- Obstructive & restrictive deficits are distinguished by ?
- What can we learn from forced flow-volume measurements?
- Volume of air exhaled during a forced breath (first (FEV1), second (FEV2), and/or third seconds (FEV3))
- The total volume of air exhaled during a forced breath
- Measuring the Forced Expiratory Volume in one second (FEV1.0)
- Volume of air breathed out (reduced in restrictive disorders, or if there is airway narrowing precipitating early airway closure (e.g. asthma or CF))
- flow (reduced with airway narrowing)
- Pattern of change in flow-volume curve (insp & exp) can indicate site of obstruction
- Response to treatment (e.g. β agonist)
- Change with age or growth
- Progression of disease
- Volume of air breathed out (reduced in restrictive disorders, or if there is airway narrowing precipitating early airway closure (e.g. asthma or CF))
Why is intrathoracic abnormalities detected on expiration and intrathoracic abnormalities detected on expiration?
Why do you hear stridor on inspiration & wheeze on expiration?
Stridor: deep laboured noisy inspiration that’s a sign of upper airway obstruction e.g. epiglottitis.
Recap of inspiration: Take a breath in, your diaphragm moves down and your ribcage moves out to decrease the intrathoracic pressure. This decreases intrapulmonary pressure so it sucks air in. This causes a suction force on the airways by pulling the walls slightly inwards. Now normally this is fine but in a patient with a narrowed airway, this effects becomes exacerbated because that suction force pulls the airway in more and makes that noisy inspiratory stridor sound.
It only affects the upper respiratory tract because… the lower respiratory tract i.e. your bronchioles are enveloped in your pleurae. Do you remember that intrapleural pressure becomes more negative when you inspire? Intrapleural pressure is like at -3mmHg and then it drops to about -7/8mmHg. Well… the pressure from inside the bronchioles moves outwards during that period thus opposing that suction force! So they don’t collapse.
Wheeze: high-pitched noisy expiration sign of lower airway obstruction e.g. asthma.
Recap of expiration: your diaphragm moves up and your ribcage moves in to increase the intrathoracic pressure. This increases intrapulmonary pressure. That pressure is pushing onto the outside of those bronchioles and forcing the air out. This is normal in me and you but bad in a patient with narrowed bronchioles because when that intrapulmonary pressure increases its gonna effectively squeeze the bronchioles, airflow is tight through those bronchioles and you get that high-pitched wheezy sound.
- Embolism:
- Pulmonary embolism means?
- E.g.
- What is this image showing?
- Cause of PE?
- Movement of material from one part of the circulation to another
- The material passes through the right side of the heart and lodges in the pulmonary arteries
- – Thrombus
– Tumour
– Air (cerebrum)
– Fat (long bone fractures)
– Amniotic fluid (post-partum)
– Bullet
- Pulmonary arteriogram showing thrombus in the major branches of the right pulmonary artery
5. 90% DVT
- Risk factors of PE?
- age > 40 (Image)
- 50% have an identifiable ‘temporary’ risk factor (surgery, oestrogen treatment etc…)
- 25% have cancer (permanent risk factor)
- 25% have no identifiable risk factor
Pathophysiology of PE
-
Right ventricular overload
* *Pulmonary artery pressure increases** (> 30% of the total cross section of the pulmonary arterial bed is occluded). Right ventricular dilatation & strain (think of Frank Starling curve). Also inotropes are released in an attempt to maintain systemic BP – these cause pulmonary artery vasoconstriction that further exacerbates the situation.
1/3 right-to-left shunting through a patent foramen ovale is present and may lead to severe hypoxaemia and an increased risk of paradoxical embolization and stroke.
-
Respiratory failure
- Due to areas of ventilation perfusion mismatch & low right ventricle output -
Pulmonary infarction
- Small distal emboli may create areas of alveolar haemorrhage resulting in haemoptysis, pleuritis, and small pleural effusion. This clinical presentation is known as pulmonary infarction.
- Symptoms of PE
- Main differential diagnoses
- Physical signs in PE
- Image
- • Myocardial infarction • Pneumothorax • Pneumonia/pleurisy
- • Pleural rub in cases of pulmonary infarction
• Raised JVP
Investigations
What would the investigations show?
- CXR – normal CXR (common). Exclude other diagnoses. Not useful as a primary diagnostic tool.
- ECG – May show signs of right ventricular strain - T wave inversion in the right precordial leads (V1 - V4 and the inferior leads, II, III and aVF). The ‘classic’ finding is SI QIII TIII . Not useful as a primary diagnostic tool
- Blood gases – May show hypoxaemia and hypocapnia (respiratory alkalosis) due to hyperventilation
- D-dimer – A normal D-dimer effectively rules out PE in those at low likelihood of having a PE. In those at high likelihood the negative predictive value of D-dimer is too low to use
D-dimer is a ?
fibrin degradation product, a small protein fragment released into the blood when a thrombus is degraded by fibrinolysis. D-dimers are not normally present in the blood except when the coagulation system has been activated. A negative D-dimer result practically rules out thrombosis in patients with a low clinical likelihood of PE
no d diners- no thrombolysis - no emboli - no PE
What imaging can be done to check for a PE?
- Pulmonary angiography
- Ventilation perfusion lung scintigraphy
CT Pulmonary Angiography CTPA
What are the different emboli you can get?
What is this image showing?
- Saddle embolus straddling the pulmonary trunk
- What is this image showing?
- How do you assess if a patients at risk of a DVT?
- Embolus in the right PA
- Wells’ score for predicting clinical likelihood of PE
- Pain swelling tenderness
warm skin
ulcerations
skin changes
Treatment of high and low risk patients?
Immediate heparinisation ( Xa, thrombin, s/e thrombocytopenia, hyperkalaemia, haemorrhage)
- What happens after initial heparinisation?
- What is this image showing?
- • Patients are started on an oral anticoagulant (e.g warfarin):
– For 3 months if there is an identifiable ‘temporary’ risk factor (50%)
– Indefinitely if cancer or no identifiable risk factor (50%)
• What about those patients who cannot be safely anticoagulated? (e.g have oesophageal varices, previous haemorrhagic stroke, severe thrombocytopenia)
2. IVC filter
