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130 Chapter 3: Respiratory system

ventricular(parasternal)heaveduetoincreasedstroke Right bundle branch block: RSR’ in lead V 1 (may be
work,a raised JVP with a prominent ‘a’ wave due to transient).
increased right atrial pressure.
There may be chest signs resulting from alveolar at-

Management
electasis or complicating pneumonia. Pleural inflam-
1 In massive pulmonary embolism, there is haemody-
mationresultsinapleuralfrictionrubandalow-grade
namic compromise which may require resuscitative
pyrexia.
therapy. With large emboli, thrombolysis or surgical
Clinical signs of a deep vein thrombosis may also be

thrombectomy with cardiac bypass may be life-saving.
present.
2 Prevention of propagation and recurrence: Unfrac-
tionated intravenous heparin is started immediately
Macroscopy titrated according to the APTT. For small or moderate
Blood enters the pulmonary vasculature and thus there emboli subcutaneous low molecular weight heparin is
is congestion proximal to the blockage. Affected areas as effective and does not require monitoring of APTT.
appear haemorrhagic and are frequently wedge shaped. Therapy is converted to warfarin after 48 hours (for 3
Repair results in the formation of a white scar. months minimum – usually 6 months). Lifelong war-
farin may be indicated depending on the underlying
Microscopy cause, or in recurrent embolism.
Typical features include haemorrhage (due to extravasa- 3 If anti-coagulants are unsuccessful or contraindicated
tion of blood), loss of cell architecture, cellular infiltra- a filter may be inserted into the inferior vena cava to
tion and occasionally necrosis. prevent further pulmonary embolism.
4 Standard prophylaxis pre- and postoperatively, and
Complications for bed bound patients or those at risk – subcutaneous
Cardiopulmonary arrest and death in the acute stages. lowmolecularweightheparin,graduatedcompression
Atrial fibrillation and other arrhythmias. Recurrent stockings and early mobilisation if possible.
thromboembolic disease may cause pulmonary hyper-
tension. Prognosis
Tenper cent of symptomatic emboli are fatal.
Investigations
The chest X-ray may be normal. Atelectasis and areas of
hypoperfusion may be seen, and large emboli may cause Pulmonary hypertension
an elevated hemidiaphragm and enlarged proximal pul-
Definition
monary arteries. Blood D-dimers (breakdown products
Apulmonaryarterialpressuregreaterthan30/20mmHg.
of fibrin) are of reasonable sensitivity but high specificity
and are therefore useful for exclusion in cases of low
clinical suspicion. A ventilation perfusion (V/Q) scan is Aetiology
usually diagnostic, but is less helpful if the chest X-ray Pulmonary hypertension may be secondary to a variety
is abnormal. Spiral CT pulmonary angiogram normally of diseases, or more rarely a primary idiopathic form.
demonstrates the clot(s) within the pulmonary vascula- Causes can be divided into
ture. The ECG may be normal or (particularly in larger 1 Increased blood volume passing through the pul-
emboli) reveal: monary circulation as occurs in left to right shunting
Tachycardia. (septal defects, persistent ductus arteriosus).

Acharacteristic S 1 Q 3 T 3 pattern. This refers to an S 2 Increased left atrial pressure, which causes an increase

wave in lead I, and Q and inverted T wave in lead III. in pulmonary venous pressure. This in turn raises
Right ventricular ‘strain’ pattern – T wave inversion the pulmonary capillary and arterial pressures (left

in leads V 1 –V 4 . ventricular failure, mitral valve disease, cardiomyo-
Tall peaked P waves in lead II (p pulmonale). pathy).