S5 L1 Pulmonary embolism Flashcards
Embolism definition
Pulmonary embolism definition
Types of emboli (i.e. materials)
PE is ___ most common death
Embolus: the movement of a material from one part of the circulation to another. An embolus will usually travel until it reaches a part of the circulation that is too small for it to pass through, at which point it will block that part of the circulation and cause pathology.
Pulmonary embolism:
material that has moved from one part of the vasculature, through the right side of the heart, and lodges in the pulmonary arteries.
-> often an unexpected death, i.e. patient about to go home after big operation, a DVT has formed, but when they start to move and stand -> clot dislodges = can lead to death
Blood clot (thromboembolism), but can also be formed from tumour, air, fat, or amniotic fluid
Third most common
What % of PE arise from DVT?
What is a DVT?
What is Virchow’s Triad?
Examples of ‘conditions’ etc that can lead to DVT
90%
DVT: deep vein thrombosis (DVT), a thrombus that has formed in the deep veins of the lower limb
Virchow’s Triad:
stasis of blood flow, hypercoagulability of blood, and endothelial injury,
e.g.:
- Endothelial injury: e.g. trauma, surgery -cut through/clamped vasculature
- Stasis: clot itself causes stasis e.g. small clot in popliteal vein – still some circulation but turbulent flow – flow decreases = stasis = clot enlarges
- Blood hypercoagulability: surgery increases clotting factors, pregnancy (higher oestrogen state, increases clotting factors, growing foetus -> compresses pelvic veins -> stasis)
- Pregnancy
- Prolonged immobilisation (e.g. post-operatively or on a long-haul flight)
- Previous venous thromboembolism
- Thombophilia
- Severe burns
- Heart failure (stasis of circulation, congestive HF increases stasis)
- HRT
- Age
- Combined oral contraceptive pill
- Cancer
- Obesity
- Hormone replacement therapy
- COVID-19 (especially ICU patients – high inflammation state, virus invades endothelial injury – covid increases risk of PE)
How can inflammation lead to DVT?
Risk factors can be divided into…
inflammation: endothelial injury, activates clotting cascade
The above risk factors can be divided into those that are;
- Temporary; for example, pregnancy, the pill, and immobilisation.
- Permanent; for example, cancer.
Prevention
- Example of prevention of DVT
It is thought that 50% of patients with a PE have a temporary risk factor and that 25% have a permanent, but that 25% don’t have any risk factors at all. It is important to realise that prevention of a PE, for example through the use of compression stockings on a long haul flight, is extremely important, and more easily implemented than treatment
Pathophysiology of clinical outcomes in PE
List 4…
- Acute right ventricular overload
- Respiratory failure
- Pulmonary infarction
- Paradoxical embolism and stroke
- How does PE lead to acute right ventricular overload and what does this mean?
1. Acute right ventricular overload:
If an embolus occludes over 30% of the arterial bed, then pulmonary arterial pressure will increase. This leads to right ventricular dilation and strain (RV pumps blood into low pressure system = low resistance, however obstruction of PE, leads to high pressure and higher resistance, leading to heart strain).
Frank-Starling curve - Also, the release of inotropes (adrenaline and nor-adrenaline) in order to control the blood pressure. However, the release of inotropes causes pulmonary artery vasoconstriction, thus further exacerbating the original problem (increase BP of pulmonary vasculation -> RV needs to pump harder due to increased resistance to flow). Main cause of death in PE is acute right sided heart failure leading to
- Cardiogenic shock with circulatory failure and/or
- Cardiac arrest secondary to arrythmias
- Respiratory failure - How does PE lead to Resp failure? Why? What type of resp failure?
The areas of the lung that used to be perfused by the areas of now-blocked arteries no longer have a blood supply, meaning no gas exchange can take place in these areas, despite the area being well ventilated. This area has now become alveolar dead space, meaning the body will redirect the blood to other areas of the lung to be perfused. If this increased blood flow is not matched by increased ventilation, then pO2 will drop. This drop in O2 leads to hyperventilation, meaning the CO2 is adequately removed from the body. This means the patient will have low pO2 with normal or low pCO2, which can be classified as type 1 respiratory failure.
- Pulmonary Infaction - How does PE lead to Resp failure? Why? What type of resp failure?
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
• Relatively uncommon – approx. 10-20% cases – may be visible on CXR as wedge shape
- Paradoxical embolism - What is this? How does PE lead to this? What does a paradoxical embolism lead to?
Stroke
1/3 of patients with a PE have a patent foramen ovale, a hole between the left and right atria which is normal in the fetus but has not closed properly during infancy. Due to the shunting of blood through the foramen, these patients are at risk of having a paradoxical embolism and stroke, because the clot formed in the venous system can pass through the right side of the heart, into the left side of the heart and be pumped through the aorta to the brain (stroke) or another site (paradoxical embolism).
Signs and Symptoms of PE
Symptoms of a PE include:
- Shortness of breath
- Pleuritic chest pain
- Cough
- Substernal chest pain
- Fever
- Haemoptysis (occurs due to pulmonary infarcts)
- Syncope (clot travelled through pulmonary artery -> R acute strain – induced arrhythmia, decreased cardiac output = syncope)
- Unilateral leg pain (DVT)
Signs of a PE include:
- Dyspnoea
- Tachycardia
- Tachypnea (respiratory rate >16/min)
- Low BP
- Raised jugular venous pressure
- Pleural rub in cases of pulmonary infarction
- Evidence of DVT, e.g. erythema, increased temperature and tenderness on palpation of the leg
- Sweating
- Central cyanosis (hypoxaemia due to V/Q mismatch in PE)
Investigations of PE
- List them
- Arterial Blood gas
- Chest x-ray
- ECG
- D-dimers
- Wells score
- Imaging: CTPA (main), VQ scan
- Arterial Blood Gas
- Chest x-ray
1. Arterial Blood Gas (ABG) – would show respiratory alkalosis and hypoxaemia and hypocapnia due to the patient hyperventilating.
2. Chest X-ray – to exclude differentials such as pneumothorax or pleural effusion.
- ECG
ECG:
- The most common sign of a PE on an ECG is sinus tachycardia
- This could show an S1Q3T3 pattern; a large S wave in lead I, and a Q wave with an inverted T wave in lead III, which are all classic signs of right heart strain. This is a common textbook presentation but is not actually common in clinical practice.
- There could also be no signs on ECG – a normal ECG cannot rule out a PE.
- D-dimers
- Wells Score
- Imaging
-
D-dimers:
- Measured in a blood test, d-dimer is a fibrin degradation product released into the blood when a thrombus is degraded by fibrinolysis.
- In a patient with a low likelihood of PE, a normal d-dimer can rule a PE out. However, if the patient has a high probability of PE a normal D-dimer should not be used to rule a PE out, as its negative predictive value is too low to use.
- This means that if a PE is likely, a D-dimer is not a useful investigation, because it cannot be used to rule in or out a PE, and so a CT pulmonary angiography (CTPA) should be done immediately.
- A Wells Score should be calculated for any patient where a PE is a possible cause of symptoms. The components of a Wells Score are:
- Clinical Signs or Symptoms of a DVT – 3 points
- PE is the most likely clinical diagnosis – 3 points
- Heart rate >100 bpm – 1.5 points
- The patient has been immobilised for more than 3 days or has had surgery in the past 4 weeks – 1.5 points
- Previous PE or DVT – 1.5 points
- Haemoptysis – 1 point
- Malignancy with treatment within the past 6 months or active palliative malignancy –1 point
- A score of >4 indicates a PE is likely
- A score of <= 4 indicates a PE is unlikely
- Imaging: - CT Pulmonary Angiogram (CTPA)***main one - Ventilation Perfusion Lung Scintigraphy (VQ scan)
Treatment PE:
- What should you do first? (for all patients)
- High risk PE patients who are haemodynamically unstable?
- Procedures that remove the embolus
Oxygen, heparin or DOAC immediately:
A patient with a suspected PE should be given O2 immediately to increase pO2, and immediate heparinisation (low molecular weight heparin) or direct oral anticoagulant (DOAC) administration, which reduces mortality by preventing the thrombus from propagating in the pulmonary artery and allowing the body’s fibrinolytic system to lyse the thrombus. It reduces the frequency of further embolism but doesn’t dissolve the clot already present.
High risk PE patients: haemodynamically unstable
Drugs: Streptokinase/tPA.
Patients with a high risk of PE should also be given haemodynamic support, respiratory support, and exogenous fibrinolytics (given via percutaneous catheter into the pulmonary arteries. Drugs: Streptokinase/tPA). Procedures used to remove the embolus include percutaneous catheter directed thrombectomy, or surgical pulmonary embolectomy.
What is heparin-induced thrombocytopenia? What can this lead to?
Main differential diagnoses
