Intrathoracic blood volume (ITBV) is a reliable indicator of myocardial preload in critically ill patients [1,2]. The single transpulmonary thermodilution technique, which is increasingly used for haemodynamic monitoring, is sufficiently accurate for clinical estimation of ITBV and extravascular lung water (EVLW) [3,4]. We report a patient with low ITBV, despite high central venous pressure (CVP), which was first interpreted erroneously as hypovolaemia.
A 34-yr-old male with abdominal and chest trauma was transferred to our institution. He underwent splenectomy and mini-thoracotomy for removal of a left-sided pleural haematoma that caused compression atelectasis. Unfortunately, the patient developed the adult respiratory distress syndrome (FiO2 60%, with a positive end-expiratory pressure of 10 cmH2O) and septic shock on day 19. At that stage, extended haemodynamic monitoring, including the transpulmonary thermal-dye dilution technique (femoral artery catheter 4-F, Pulsiocath PV 2024L®; Pulsion Medical Systems, Munich, Germany), was instituted. A chest spiral-CT scan was performed in the search for an infectious focus. No pulmonary abscess was found and there were no signs of central pulmonary embolism. Staphylococci were isolated from blood cultures and the antibiotic therapy was changed appropriately. The patient developed an abdominal compartment syndrome that required laparotomy. The abdomen was not closed. Disseminated intravascular coagulation (DIC) with transfusion requirements developed (D-dimers 3 mg L−1) and the cardiopulmonary function deteriorated further. ITBV was very low (Table 1) and fluid challenges were given to optimize myocardial preload. Although CVP increased progressively, ITBV remained low. This was interpreted as persistent hypovolaemia and fluid loading was continued. However, cardiac output (CO) did not increase and even decreased. Echocardiography was performed and revealed right heart failure as indicated by poorly contracting and fluid overloaded right heart chambers. The left heart was markedly underfilled. The arterial to alveolar PCO2 difference was first interpreted - especially in view of the computed tomographic scan findings the day before - as a result of pulmonary gas exchange disturbance and it increased progressively (Table 1). Pulmonary embolism was suspected as an underlying cause, but unfortunately the patient died several hours later in hypodynamic shock despite high vasopressor and inotropic support. Autopsy revealed lung oedema and purulent pneumonia. The epicardial coronary arteries were normal but hypoxia-induced patchy necroses within the myocardium were found. A necrotic area, about 5 cm under the diaphragm, with Gram-positive cocci was found. Pulmonary fat embolism was excluded, but repeated multistage massive peripheral pulmonary thromboembolism was considered as the major cause of death.
In our patient, ITBV was low despite high CVP and this was first erroneously interpreted as hypovolaemia. In fact, pulmonary embolism, which was clinically suspected late in the course, could be confirmed post mortem. A previous study showed that fluid loading might be an appropriate measure in acute massive pulmonary embolism as indicated by an increase in CO in 12 of 13 patients . In that study, the mean right atrial pressure increased from 9 to 17 mmHg after a volume challenge of 500 mL dextran. In contrast to our case, these patients received simultaneously heparin and thrombolytic therapy. In our patient, DIC-related multistage pulmonary artery obstruction was diagnosed by the pathologist from macroanatomical changes at autopsy. The patient did not receive thrombolysis and fluid loading so may therefore have been without positive effects on CO. We used the transpulmonary indicator dilution technique by which ITBV, as an indicator of myocardial preload, can be obtained. In principle, a low ITBV is measured when the perfused intravascular space is actually reduced. Recently obtained animal experimental data show that ITBV, measured by the transpulmonary thermo-dye dilution technique, was reduced following occlusion of large pulmonary artery branches, while EVLW was underestimated . In our patient, repeated pulmonary embolism during sepsis-related DIC may be considered as responsible for the reduced pulmonary perfusion bed. This would explain the reduced ITBV and underestimated EVLW. The observed increase in EVLW during fluid loading may be interpreted as increasing oedema in the remaining perfused pulmonary bed which was still underestimated. This correspondence demonstrates that if the intravascular capacity is reduced, ITBV must consequently decrease. Theoretically, in this case the decrease in pulmonary blood and left heart volumes must have exceeded the increase in right heart volume. In general, ITBV does not differentiate between the different compartments within the chest. It might be normal if the right heart and the pulmonary tree have an excess of volume whilst the pulmonary venous circulation and the left heart are underfilled. Therefore, in the presence of right heart failure, ITBV may not be regarded as representative of left heart preload.
In our patient, right heart overload and poor left heart filling - findings consistent with relatively acutely increased right heart afterload during pulmonary embolism - were found by echocardiography. Accordingly, echocardiography should be considered when other cardiovascular monitoring techniques yield inconclusive or contradictory information. In conclusion, whenever ITBV is low and CVP high, particularly when CO does not increase following fluid loading, other possible reasons for reduced central blood volume (i.e. pulmonary embolism, tension pneumothorax, etc.) should be suspected and further diagnostic measures considered.
S. G. Sakka
Department of Anaesthesiology and Intensive Care Medicine; Friedrich-Schiller-University of Jena; Jena, Germany
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