Influence of an acute increase in systemic vascular resistance on transpulmonary thermodilution-derived parameters in critically ill patients.
OBJECTIVE
The transpulmonary thermodilution technique enables measurement of cardiac index (CI), intrathoracic blood volume (ITBV), global end-diastolic volume (GEDV), and extravascular lung water (EVLW). In this study, we analyzed the robustness of this technique during an acute increase in systemic vascular resistance (SVR).


METHODS
Prospective, clinical study.


METHODS
Surgical intensive care unit in a university hospital.


METHODS
Twenty-four mechanically ventilated septic shock patients, who for clinical indications underwent extended hemodynamic monitoring by transpulmonary thermodilution and continuously received norepinephrine.


RESULTS
After baseline measurements, mean arterial pressure was increased briefly by increasing norepinephrine dosage and hemodynamic measurements were repeated before a control measurement was obtained. At each time point, 15 cc of 0.9% saline (< 8 degrees C) was administered by central venous injection in triplicate. Fluid status and respirator adjustments were kept constant. ANOVA with an all-pairwise comparison method was used for statistical analysis. Heart rate, central venous pressure, and EVLW remained constant throughout, while SVR significantly changed from 551 +/- 106 to 746 +/- 91 dyn*s*cm(-5) and again to 566 +/- 138 dyn*s*cm(-5) (p < 0.05). However, CI and central blood volumes showed a reversible significant increase, i.e., ITBV went from 816 +/- 203 to 867 +/- 195 ml/m(2) and then to 821 +/- 205 ml/m(2) and GEDV from 703 +/- 178 to 747 +/- 175 ml/m(2) and finally to 704 +/- 170 ml/m(2), respectively. In eight patients, 2-D echocardiography was applied and revealed a reversible increase in left-ventricular end-diastolic area.


CONCLUSIONS
An acute increase in SVR by increasing norepinephrine dosage results in a reversible increase in central blood volumes (ITBV, GEDV) as measured by transpulmonary thermodilution and supported by echocardiography.
Kozieras
Jan
J
Friedrich-Schiller-University of Jena, Department of Anesthesiology and Intensive Care Medicine, Jena, Germany.
Thuemer
Oliver
O
Sakka
Samir G
SG
D000328:Adult; D000368:Aged; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001810:Blood Volume / Q000187:drug effects / Q000502:physiology*; D002302:Cardiac Output / Q000187:drug effects / Q000502:physiology; D016638:Critical Illness; D003971:Diastole / Q000187:drug effects / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D005260:Female; D006352:Heart Ventricles / Q000000981:diagnostic imaging; D006801:Humans; D007262:Infusions, Intravenous; D007362:Intensive Care Units; D008297:Male; D008875:Middle Aged; D008991:Monitoring, Physiologic; D009638:Norepinephrine / Q000008:administration & dosage*; D011446:Prospective Studies; D012121:Respiration, Artificial; D012772:Shock, Septic / Q000503:physiopathology / Q000628:therapy; D013566:Sympathomimetics / Q000008:administration & dosage*; D013815:Thermodilution / Q000379:methods*; D014463:Ultrasonography; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology*; D016277:Ventricular Function, Left / Q000502:physiology
D013566:Sympathomimetics; D009638:Norepinephrine