Pulmonary embolism Flashcards

1
Q

PE depends on what?

A
  1. Extent of vasculature exclusion
  2. Rate at which obstruction accumulates
  3. Pre-existing cardiopulmonary status of the patient
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2
Q

Discuss the Pathophysiology of the PE

Read pg 10 of slides

A
  1. Decreased in the cross-sectional area of the pulmonary vasculature bed > which will increase vasculature resistance and RV afterload
  2. More than 50% of the pulmonary vasculature bed needs to be obstructed to increase pulmonary resistance
  3. Mediators released from platelets may induce vaso-bronchoconstriction
  4. Increase alveolar dead space > ventilation-perfusion mismatch and hypoxemia
  5. This will stimulate irritant receptors > hypoventilation
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3
Q

Discuss the 4 clinical forms of PE

A
  1. Acute Minor PE > short sudden onset > less then 50% vasculature obstruction (VO) > PST: Dyspnoea ,pleuritic chest pains ,haemoptysis > PAP & RAP normal
  2. Acute massive PE > Short sudden onset > >50% VO and thrombus volume is >30 ml > Right side heart strain ,haemodynamic instability and syncope > PAP Increased & RAP 12
  3. Subacute massive PE > Several weeks > > 50%VO > Dyspnoea with right heartstrain > PAP increases and RAP 8
  4. Chronic thromboembolic pulmonary hypertension > Months to years > >50% VO > Slowly progressing dyspnoea with exercise intolerance and right heart strain > PAP increased & RAP 6
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4
Q

History that might suggest PE

A
  • Dyspnoea at rest or exertion usually onset
  • Pleuritic chest pain
  • calf pain or swelling
  • coagh
  • wheeze
  • haemopytysis
  • syncope
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5
Q

The examination that might suggest PE

A
  • Tachypnoea
  • Signs of DVT
  • Tachycardia
  • pulmonary crackles
  • loud pulmonary component of second heart sound
  • Elevated jugular venous pressure
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6
Q

Investigating PE: Arterial blood gas

A
  • Doesn’t exclude minor PE but it is good evidence against major PE
  • Decreased pO2 and Increased pCO2
  • Widen alveolar-arterial O2 gradient
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7
Q

Investigating PE: Chest X-ray

A
  • Usually abnormal (80%) but it is a nonspecific diagnosis therefore it may provide an alternative diagnosis
  • Normal cardiac shadow with plump pulmonary artery segments
  • Palla sign: Abrupt cut off of pulmonary artery
  • Westermark sign: Oligeamia of the affected segment
  • Hampton s hump: peripheral semicircular / wedge shape in contact with the pleural surface
  • small pleural effusion, atelectasis, and raised hemidiaphragm
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8
Q

Investigating PE: ECG

A

ECG changes are common in PE but are nonspecific

  • Sinus tachycardia
  • S1Q3T3 pattern is uncommon
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9
Q

Investigating PE: Well’s Criteria for a clinical assessment for PE

A
  • Symptoms of DVT (leg swelling with pain ,warmth ,palpation ) : 3
  • Other diagnosis less likely than PE : 3
  • HR > 100 bpm : 1,5
  • Immobalization for more than 3 days or surgery in the past 4 weeks : 1,5
  • Previous DVT / PE : 1,5
  • Hemoptysis : 1
  • malignancy 1

Simplified clinical assessment(mordified Wells criteria)
>4: PE likely
< 4: PE unlikely

Traditional clinicall probability assessment (Wells criteria)

  • High :>6
  • moderate : 2-6
  • Low: <2
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10
Q

What to do when the patient is likely PE and haemodynamically stable after resus

A
  1. Start full anticoagulation and do definitive diagnostic imaging (CTPA) which will give us 2 types of results either PEor no PE
  2. When no PE stop full anticoagulation and investigate other causes for circulatory collapse
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11
Q

What to do when the patient is likely PE and hemodynamically unstable despite resus

A
  1. Bedside transthoracic or oesophagus echo which will give us 2 types of results
    either Clot visualization in RV or proximal pulmonary arteries after considering empiric thrombolysis
  2. Clot visualised no other cause for instability and RV dysfunction
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12
Q

What to expect when performing echocardiography in a likely PE situation

A
  1. Transthroracic: May see clot in RA
  2. Transoesophageal: Allows visualization of proximal pulmonary arteries
  3. Can assess for the presence of RV dysfunction
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13
Q

Using D dimer to determine PE

A

1.Determine if PE likely / PE unlikely

  1. IF PE unlikely :
    * D-dimer assay
    * if <500 ng/mL then exclude PE and offer no treatment
    * if >500 ng/mL then CT pulmonary angiogram (CTPA)
  2. If PE likely
    * CTPA which will give us one of 3 different results
    * Negative > PE excluded
    * Possivtive > PE confirmed > Treatment
    * Inconclusive > Additional testing eg V/Q which will ether confirm PE / not
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14
Q

Are elevated D-dimer levels enough to confirm PE

A
  • NO, however, it should raise suspicions for VTED and prompt further testing even if well s modified criteria is PE unlikely
  • Normal D dimer levels with likely PE is not enough to exclude PE but can exclude PE in patients with PE unlikely
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15
Q

Investigating PE : V/Q scan

A

Mismatch of inhaled and injected compounds on the lung scan suggest PE

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16
Q

When to use Pulmonary angiography

A

when other investigations are inconclusive

17
Q

Treatment of PE: General resuscitation

A
  • Analgesia: caution with opiates
  • Oxygenation: facemask / mechanical ventilation
  • Careful fluid resuscitation
  • Inotropes
  • Empiric anticoagulation depending on clinical suspicion for PE, risk of bleeding, and expected timing of diagnostic tests
18
Q

Treatment of with established diagnosis in severely impaired circulation

A
  1. If thrombolysis contraindication > embolectomy
  2. If not thrombolysis contraindicated > thrombolysis with / without clot fragmentation if susscessful > heparin / LMWH

if not sussessful > embolectomy

19
Q

Treatment of with established diagnosis in stable circulation

A

Either :
heparin / LMWH > oral anticoagulants / recurrent emolism
or
if anticoagulant C/I > vena caval interuption

20
Q

Discuss the goals and agents of parental anticoagulation

A

Goals

  • inhibition of thrombus propagation
  • prevention of early recurrences
  • allows for endogenous fibrinolysis

Agents

  • UFH IV or Protein S/C to maintain PTT 2,5 normal
  • LMWH
  • Fondaparinux

efficacy depends on achieving the therapeutic level of anticoagulation within 24 hrs

21
Q

List the oral anticoagulant agents

A
  • Vitamin k antagonist (warfarin ) ; initiate after parental anticoagulation started for 5 days
  • Factor Xa inhibitors: Do not require monitoring but do not use in haemodynamically unstable patients
22
Q

Long term management of PE

A

Goals: prevent delayed recurrences and sequelae eg Posy thrombotic syndrome and Pulmonary Hypertension

agents

  • Warfarin : INR maintained at 2-3
  • LMWH
  • Rivaroxaban (factor Xa inhibitor )
23
Q

What is thrombolysis and when to use it

A

aCTIVE DISSOLUTION OF THROMBUS WITH PARENTERAL ANTITHROMBOTIC ENZYMES EG STREPTOKINASEE OR ALTEPLASE
*Reserved for patients with hypotension will not survive long enough for spontaneous fibrinolysis and severe hypoxaemia and RV dysfunction

24
Q

When to do embolectomy

A

When other measures have failed and in acute PE to prevent death