PE Flashcards

1
Q

RED FLAGS

A
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2
Q

DIFFERNTIALS

A
  • AMI
  • Pneumonia
  • Pericarditis
  • Pleurisy
  • Pneumothorax
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3
Q

RISK FACTORS

A
  • Hx. of DVT or PE
  • Prolonged immobilisation
  • Recent surgery/trauma
  • Oral contraceptives
  • Long-haul flights
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4
Q

CAUSES

A

Thrombus from DVT, emboli’s from fat, air, amniotic fluid.

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5
Q

DEFINITION

A

Obstruction of the pulmonary arteries from an embolus, most likely lower extremity DVT.

Virchow’s triad:
1. Endothelial damage – trauma, atherosclerosis, surgery, inflammation
2. Venous stasis – pooling  coagulability, immobility, obesity, venous obstruction
3. Hypercoagulability – clotting disorder, chemotherapy/cancer, pregnancy (particularly after C section), oral contraception.

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6
Q

PATHOPHYSIOLOGY

A

Thrombus breaks off/dislodges  travels into venous blood flow (smallest vessels)  vascular occlusion, local ischaemia  redistribution of blood flow  increased pulmonary circulation pressure (pulmonary hypertension)  hydrostatic pressure out competes oncotic pressure in the blood vessels + ischaemia of the lung tissue  inflammation  increase pulmonary capillary permeability  fluid moves down its pressure gradient into the lungs
Pressure backlogs into R heart  increase HR and contractility that with time will eventually fail as heart is under perfused, + foramen ovale opens and O2 blood mixes with low O2 blood  hypoxaemia
Blood pools in systemic circuit  raised JVP, peripheral oedema, RVF
VQ mismatch- less blood for gas exchange  systemic hypoxaemia.

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7
Q

TREATMENT

A

DRAB: oxygenation. C: 250-500ml IV fluids. DE.
Basic cares: position of comfort, minimising movement (thrombus to travel). Normothermia.
Analgesia: paracetamol. Fentanyl- antianxiety, heart problems.
Management - O2, analgesia, 12-lead ECG, Fluids administered judiciously (250-500ml) as it can put more pressure on an already over stretched R heart, clot may dislodge.
- Anticipate further deterioration (shock  resus, adrenaline)
- CCP: adrenaline

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8
Q

ROLE OF PARAMEDIC

A

Attempt to rule out differential Dx. e.g. as ASC, maximise blood oxygenation.

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9
Q

PHARMACOLOGY

A

Paracetamol mechanism– similar to NSAID:
- Analgesic properties: inhibits COX which blocks the production of prostaglandins. Prostaglandins act on neurons to cause pain response
- Antipyretic properties – directly act on temperature regulation in the hypothalamus

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10
Q

DEFINITIVE CARE

A

Hospital:
- Blood tests: clot-dissolving substance D dimer. High levels suggest increased likelihood of clots. Blood tests measure the amount of O2 & CO2 in blood. A clot in the lungs can lower the level of O2 in the blood. Inherited clotting disorder.
- Chest X-ray: rule out conditions that mimic PE.
- Ultrasound: to check for DVTs.
- CT pulmonary angiography: detect abnormalities such as PE
- Ventilation-perfusion scan (V/Q scan): to avoid radiation exposure or contrast due to a medical condition. Tracer maps perfusion & compares it with ventilation & can be used to determine whether clots are causing symptoms of pulmonary hypertension.
- Pulmonary angiogram: provides a clear picture of the blood flow in lung arteries

Medications:
- Anticoagulants- prevent existing clots from enlarging & new clots from forming while your body works to break up the clots. Heparin + warfarin. Anticoagulant side effects: bleeding.
- Clot dissolvers (thrombolytics). Can cause sudden & severe bleeding, usually reserved for life-threatening situations.

Surgical / other procedures:
- Clot removal.
- Vein filter.

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