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Acute cor pulmonale


Acute cor pulmonale (pulmonary embolus – PE):

A thrombus formed in the systemic veins may dislodge and embolize into the pulmonary arterial system.

  • After PE, lung tissue is ventilated but not perfused, leading to impaired gaseous exchange
  • After some hours, surfactant is no longer produced by the non-perfused lung
  • Alveolar collapse occurs and exacerbates hypoxaemia
  • The haemodynamic consequence of PE is an elevation of pulmonary arterial pressure and a reduction in cardiac output

Clinical features of PE:

Many Pulmonary emboli occur silently, but there are 3 typical clinical presentations:

Small/medium PE:

  • In this situation, an embolus has impacted in a terminal pulmonary vessel
  • Symptoms are:
    • Pleuritic chest pain
    • Breathlessness
    • Haemoptysis (in ~30%, occurring >3 days after the initial event)
  • On examination:
    • Tachypnoea
    • Localized pleural rub
    • Coarse crackles over the involved area
    • A pleural effusion can develop
    • There may be a fever
    • Normal CVS

Massive PE:

  • Much rarer scenario
  • Sudden collapse occurs due to an acute obstruction of the right ventricular outflow tract
  • Symptoms:
    • Severe central chest pain (cardiac ischaemia due to lack of coronary blood flow)
    • Shock
    • Death can occur
  • On examination:
    • Tachypnoea
    • Tachycardia
    • Hypotension
    • Peripheral vasoconstriction
    • Raised JVP
    • Right ventricular heave
    • Gallop rhythm
    • Widely split second heart sound

Multiple recurrent pulmonary emboli:

  • Symptoms:
    • Increasing breathlessness (often over weeks or months)
    • Weakness
    • Syncope on exertion
    • Angina (occasionally)
  • On examination:
    • Signs of right ventricular overload
    • Right ventricular heave
    • Loud pulmonary second heart sound

Diagnosis of PE:

PE should be considered if patients present with symptoms of new-onset AF (or other tachycardia), unexplained breathlessness or cough, if no other obvious cause is present.


Investigations for PE:

CXR:

  • Usually normal in small/medium PE
  • May show pulmonary oligaemia with a massive PE

ECG:

  • In small/medium PE, there is usually sinus tachycardia or AF
  • In massive PE there is:
    • Tall peaked T waves in lead II
    • Right axis deviation
    • Right bundle branch block

Blood tests:

  • Hypoxia and hypercapnia
  • Raised ESR/LDH due to pulmonary infarction

Plasma D-dimer:

  • If undetectable, it excludes the diagnosis of PE

Radionucleotide ventilation-perfusion scan (V/Q scan):

Ultrasound:

  • To detect clots in pelvic/lower limb veins

Spiral CT scans

MRI


Acute management:

High-flow O2, unless they have significant chronic lung disease

In severe cases:

  • IV fluids
  • Inotropic agents

Analgesia

Dissolution of the thrombus:

  • Streptokinase 250,000U IVI over 30 minutes, followed by streptokinase 100,000U IV hourly is often used following a major embolism

Prevent further emboli:

  • The basis of therapy is IV heparin
  • Give a bolus of 10,000U of unfractionated heparin followed by a continuous infusion of 1000-2000U per hour
  • Oral anticoagulants are usually begun after 48 hours and the heparin is tapered off as the oral anticoagulant becomes effective
  • Oral anticoagulants are continued for 6 weeks to 6 months

 


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