222

INTENSIVE CARE

fever, passage of time (1216 hours) and improvement in

the childs general appearance. Pre-extubation laryngoscopy
is unnecessary. Most can be extubated within 24 hours.

CARDIOGENIC PULMONARY OEDEMA

(see Chapters 3, 5 and 9) (Fig. 8.7)
Treatment
Immediate management of acute left ventricular failure
involves sitting the patient up and administering high-flow

(a)

oxygen, intravenous opiates (e.g. morphine 2.510 mg),

intravenous nitrates (e.g. glyceryl trinitrate or isosorbide
dinitrite) and intravenous diuretics (e.g. furosemide 40
120 mg). Inotropic support or intra-aortic balloon counterpulsation may be required (see Chapter 5). When pulmonary
oedema is resistant to these measures, ultrafiltration or
haemofiltration (see Chapter 13) should be considered.
Some patients may be suitable candidates for heart
transplantation.
Unless pulmonary capillary pressure falls to less than
10 mmHg, hydrostatic oedema resolves slowly by lymphatic
drainage, not by the more rapid process of reversal of fluid
flux.
Patients with severe respiratory distress and exhaustion
due to unresponsive cardiogenic pulmonary oedema may
benefit from a period of CPAP via a face mask or hood or
non-invasive mechanical ventilation (see Chapter 7). Some
may require invasive mechanical ventilation. This is particularly the case in those scheduled for corrective cardiac
surgery (e.g. closure of a ventricular septal defect or replacement of a leaking mitral valve). The low cardiac output and
hypotension often present in these patients need not be a
deterrent to respiratory support since hypoxaemia is usually
very responsive to the application of positive pressure to the
airways, the net effect often being to increase DO2. In one
study, however, high-dose isosorbide dinitrate was found to
be safer and more effective than biphasic positive airway
pressure combined with conventional treatment (Sharon
et al., 2000).

ACUTE LUNG INJURY/ACUTE RESPIRATORY

DISTRESS SYNDROME (Ware and Matthay,
2000; Wyncoll and Evans, 1999, Wheeler and
Bernard, 2007)
In 1967, Ashbaugh et al. described a syndrome of acute
respiratory distress in adults characterized by:

(b)

Fig. 8.7 (a) Cardiogenic pulmonary oedema in a patient with

a left ventricular aneurysm. Notice the prominent upper-lobe
vessels, peribronchial cuffing and Kerley B lines. (b) Batswing pulmonary oedema in a patient with left ventricular
failure.

severe dyspnoea;
tachypnoea;
cyanosis refractory to oxygen therapy;
a reduction in lung compliance;
diffuse alveolar infiltrates seen on the chest radiograph.

They remarked on the similarity between this adult respiratory distress syndrome and that seen in neonates (Ashbaugh
et al., 1967). Before this description the same clinical syndrome had been given a variety of names, such as shock lung,
Da Nang lung (during the Vietnam war), septic lung,
posttraumatic pulmonary insufficiency, respiratory lung
and pump lung (associated with cardiopulmonary bypass).
Because it also occurs in children this condition is now
known as acute respiratory distress syndrome.

Definition
In order to define ARDS more precisely, as well as allow
more accurate assessments and comparisons of outcome, an
expanded three-part definition was proposed in 1988 in

References pp 222

Sharon A, Shpirer I, Kaluski E, et al.

(2000) High-dose intravenous isosorbidedinitrate is safer and better than Bi-PAP
ventilation combined with conventional
treatment for severe pulmonary edema.
Journal of the American College of
Cardiology 36: 832837.

Extracts 2008 Elsevier Limited. All

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