Hemodynamic monitoring in shock aims at identifying and reversing those hemodynamic and metabolic defects that contribute to the shock syndrome and are associated with a poor outcome. The data obtained with the pulmonary artery catheter may be of considerable help in judging the type, severity, and course of shock, and in choosing and evaluating the effect of therapy, even though the importance of various hemodynamic variables in the reflecting severity of disease has been questioned. Moreover, therapy aimed at increased tissue oxygenation may promote survival, although this has also been questioned ( Gro§ne.v§ld.iii§n.diii.Thjis.i.l991.).
Insertion of a pulmonary artery catheter is justified in the management of circulatory failure when difficulties in diagnosis arise, i.e. differentiation of obstructive, hypovolemic, cardiogenic, and distributive types of shock ( GI9.e.D.e.V§.!d.ll.§n.d.ll.Ih.ijs„1.991). Monitoring of hemodynamic and metabolic variables may also help in therapeutic decisions which aim at adequate tissue oxygenation. The clinical situations that may warrant insertion of a pulmonary artery catheter are listed in Tabled Pulmonary hypertension is a relatively frequent phenomenon in critically ill patients, and it may have various etiologies. It may be associated with a fatal outcome, but it is unclear whether pulmonary hypertension is central in circulatory compromise or merely reflects severe underlying lung disease carrying an unfavorable prognosis, such as the acute respiratory distress syndrome.
Table 4 Indications for pulmonary artery catheterization
In the normal heart, the left ventricular filling pressure (PAWP) is usually only a few mmHg higher than the right ventricular filling pressure (right atrial or central venous pressure), so that the latter pressure may reflect cardiac preload. Assessment of cardiac filling from the central venous pressure may be difficult in the diseased heart, even after proper measurement. The central venous pressure may not accurately reflect right ventricular end-diastolic volume, and the pressure (changes in pressure) may not predict (changes in) left ventricular filling pressure (PAWP) in the presence of pre-existing or shock-induced left ventricular dysfunction, pulmonary hypertension, and right ventricular dysfunction.
However, variability and changes in left ventricular distensibility may invalidate PAWP as a measure of ventricular preload, i.e. left ventricular end-diastolic volume
(O;Quinnand..M.arini 1983; Groenevejdand When volume status is in doubt from PAWP measurements, it may be useful to assess left ventricular ejection fraction and end-diastolic volume at the bedside with the help of two-dimensional echocardiography or radionuclide angiography with a mobile gamma-camera or
'nuclear probe' (0'Quinn.and.Marini 1983; Gio®0®y®!.d aDd Ihiiis 184.108.40.206). However, these techniques are not widely available. Irrespective of left ventricular end-diastolic volume, PAWP is an important determinant of microvascular filtration in the lung, even in the case of the 'leaky capillaries' associated with the acute respiratory distress syndrome (0'Quinn...and.M§ri.Di 1983).
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